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Executive Producers: Sir Greg and Dame Kathy Simunich, Earl Melancon, Parker Snyder
Associate Executive Producers: Stephen Agarhutty, Daniel Serbus, Sir Jan Persiel
513 Club Members: Sir Greg and Dame Kathy Simunich
Art By: Bomb-o-Bot
ShowNotes Archive of links and Assets (clips etc) 513.nashownotes.com
New: Directory Archive of Shownotes (includes all audio and video assets used) nashownotes.com
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Torrents of each episode via BitLove
Sir Lauri and I are getting together for an NA Knights Luncheon on Mon., May 20 (coming Mon.) at noon in Keilaranta 1, Espoo.
Other Knights / Producers are hereby invited as well of course! I think there is one more Knight in the Greater Helsinki Metropolitan Area at least.
Perhaps you could mention it on the show?
Wed, 15 May 2013 21:22
Benghazigate might have derailed Ambassador Susan Rice's bid to be Secretary of State, but the ''extraordinary'' Rice might have a promotion in her future after all. Foreign Policy reports today that Rice ''has become the heir apparent to National Security Advisor Tom Donilon '-- a post at the epicenter of foreign-policy decision making and arguably more influential than secretary of state.'' Writer John Hudson quotes an unnamed source as saying ''it's definitely happening.''
Wed, 15 May 2013 21:22
Insiders with ties tothe Obama administration tell The Cablethat U.S. ambassador to the United Nations SusanRice has become the heir apparent to National Security Advisor Tom Donilon -- a post at the epicenterof foreign-policy decision making and arguably more influential than secretaryof state, a job for which she withdrew her candidacy last fall amid severepolitical pressure.
"It's definitelyhappening," a source who recently spoke with Rice told The Cable. "She is sure she iscoming and so too her husband and closest friends."
"Susan is a verylikely candidate to replace him whenever he would choose to leave," agreed Dennis Ross, a former special assistantto President Obama and counselor at the Washington Institute. "She is close tothe president, has the credentials, and has a breadth of experience."
Both sources said thetiming of succession was uncertain. "I don't believe Tom Donilon is about toleave but would be surprised if he were to remain for the whole second term," Rosssaid. "But in answer to your question, [Rice's appointment] is very logical."
Rice's candidacy forsecretary of state imploded in November after she recited talking points aboutthe Sept. 11 attack in Benghazi on five Sunday talk shows that turned out to beerroneous.
The question now iswhether Benghazi's return to the spotlight will affect her potentialappointment at a time when the White House is reeling from revelations about theIRS's scrutiny of conservative groups and the Justice Department's subpoena ofthe calling records of AP journalists.
For now, prominentRepublicans don't seem inclined to make a fuss.
In November, ArizonaSen. John McCain pledged to "do everything in my power to blockher from becoming secretary of state"; South Carolina Sen. Lindsey Grahamsaid, "I don't think she deserves to bepromoted"; and Tennessee Sen. Bob Corkersaid she'd make a better DNC chair: "I think most of us want someone who is more independentminded."
But now -- even asBenghazi fever reaches a crescendo following last week's dramatic"whistleblower" hearing and Wednesday's release of 100pages of Benghazi emails -- the GOP's desire to check her rise has seeminglyevaporated, and Republicans have few tools to prevent her appointment, whichwould not require Senate confirmation.
When asked if he wasconcerned about a future National Security Adviser Susan Rice, Corker, the rankingmember of the Senate Foreign Relations Committee, told The Cable he was sitting this one out.
"In the case ofnational security advisor," he said, "whomever serves in that position servesat the pleasure of the president. So it's totally his prerogative." When The Cable asked Graham and McCain thesame question, their spokesmen declined to comment.
In some ways, thedeflated interest in Rice is only natural. Though the testimony of State Department witnesses lastweek served to highlight the inaccuracy of Rice's talk-show appearances, new details of the editing process of hertalking points show her nowhere near the drafting process -- just as theadministration has long maintained.
Meanwhile, a more tantalizingGOP target has emerged in the form of HillaryClinton, the overwhelming favorite to assume the Democratic presidentialnomination in 2016. Democrats, Republicans and witnesses fixated on Clinton 32 times during discussionsin last week's hearing.
Rice spokeswoman Erin Pelton declined to comment forthis article. White House National Security Council Spokeswoman Caitlin Hayden said, "We don't have anypersonnel announcements to make at this time, and Mr. Donilon has no plans todepart at this point." She added that Donilon is "fully engaged in managing ournational security agenda, from his recent trip to Moscow and major address onglobal energy, to planning for a trip to China in late May and more upcomingspeaking events."
The administrationhasn't shied away from heaping praise on Rice. Last week, at a gala for theJoint Center for Political and Economic Studies, Vice President Joe Bidentold the audience that the U.N. ambassador has"the absolute, total, complete confidence of the president," and that when shespeaks on issues of foreign policy, nobody doubts she's speaking for Obama.
Back in March, whencolleague Colum Lynch first reported whispers of Rice'scomeback, Ben Rhodes, deputynational security adviser for strategic communications, spoke glowingly ofRice's relationship with the president. "Susan always maintains close relationswith the president and his national security team, and that continues to be thecase," he said. "If anything, the way she handled the Benghazi situation -- andthen the withdrawal -- only enhanced her relations here, because she did sowith grace and good humor."
The president himselfhas gone out of his way to wink at an expanded role for Rice within hisadministration. "I have every confidence that Susan has limitless capability toserve our country now and in the years to come, and know that I will continueto rely on her as an advisor and friend," Obama said in a December statement.
Thu, 16 May 2013 07:19
May 14, 2013Jack Flash
Excerpted from EO-History: The now-retired general counsel and chief of staff of the House Judiciary Committee, who supervised Hillary when she worked on the Watergate investigation, says Hillary's history of lies and unethical behavior goes back farther '' and goes much deeper '' than anyone realizes.
Jerry Zeifman, a lifelong Democrat, supervised the work of 27-year-old Hillary Rodham on the committee. Hillary got a job working on the investigation at the behest of her former law professor, Burke Marshall, who was also Sen. Ted Kennedy's chief counsel in the Chappaquiddick affair. When the investigation was over, Zeifman fired Hillary from the committee staff and refused to give her a letter of recommendation '' one of only three people who earned that dubious distinction in Zeifman's 17-year career.
''Because she was a liar,'' Zeifman said in an interview last week. ''She was an unethical, dishonest lawyer. She conspired to violate the Constitution, the rules of the House, the rules of the committee and the rules of confidentiality.''
How could a 27-year-old House staff member do all that? She couldn't do it by herself, but Zeifman said she was one of several individuals '' including Marshall, special counsel John Doar and senior associate special counsel (and future Clinton White House Counsel) Bernard Nussbaum '' who engaged in a seemingly implausible scheme to deny Richard Nixon the right to counsel during the investigation.
Why would they want to do that? Because, according to Zeifman, they feared putting Watergate break-in mastermind E. Howard Hunt on the stand to be cross-examined by counsel to the president. Hunt, Zeifman said, had the goods on nefarious activities in the Kennedy Administration that would have made Watergate look like a day at the beach '' including Kennedy's purported complicity in the attempted assassination of Fidel Castro.
The actions of Hillary and her cohorts went directly against the judgment of top Democrats, up to and including then-House Majority Leader Tip O'Neill, that Nixon clearly had the right to counsel. Zeifman says that Hillary, along with Marshall, Nussbaum and Doar, was determined to gain enough votes on the Judiciary Committee to change House rules and deny counsel to Nixon. And in order to pull this off, Zeifman says Hillary wrote a fraudulent legal brief, and confiscated public documents to hide her deception.
The brief involved precedent for representation by counsel during an impeachment proceeding. When Hillary endeavored to write a legal brief arguing there is no right to representation by counsel during an impeachment proceeding, Zeifman says, he told Hillary about the case of Supreme Court Justice William O. Douglas, who faced an impeachment attempt in 1970.
''As soon as the impeachment resolutions were introduced by (then-House Minority Leader Gerald) Ford, and they were referred to the House Judiciary Committee, the first thing Douglas did was hire himself a lawyer,'' Zeifman said.
The Judiciary Committee allowed Douglas to keep counsel, thus establishing the precedent. Zeifman says he told Hillary that all the documents establishing this fact were in the Judiciary Committee's public files. So what did Hillary do?
''Hillary then removed all the Douglas files to the offices where she was located, which at that time was secured and inaccessible to the public,'' Zeifman said. Hillary then proceeded to write a legal brief arguing there was no precedent for the right to representation by counsel during an impeachment proceeding '' as if the Douglas case had never occurred.
The brief was so fraudulent and ridiculous, Zeifman believes Hillary would have been disbarred if she had submitted it to a judge.
Wed, 15 May 2013 15:47
What's got Eric Holder's panties in a bunch? It's Rep. Darrell Issa and his pursuit of the truth. During this afternoon's House Judiciary Committee hearing, the scandal-plagued AG lashed out at the House Oversight Committee chair:
Let's go to the videotape (via The Washington Examiner):
No kidding. And Holder's not doing himself or his boss any favors:
No. No it isn't. Then again, this is the Obama administration we're talking about. Sound strategy is not their fort(C).
Anyone have a mirror Holder can borrow?
Bonehead move, bro.
In the battle of Holder vs. Issa, it's pretty clear how things are gonna end.
Editor's note: This post has been updated with video of Holder's outburst.
Wed, 15 May 2013 22:58
Photograph by Melodie McDaniel / Trunk ArchiveAngelina Jolie has never lacked for influence. When she adopted a baby from Ethiopia, inquiries at U.S. adoption agencies about other Ethiopian orphans doubled. When she named other children Vivienne or Maddox, those names shot up the popularity charts for American newborns. So this week, when a woman known for her powerfully iconic beauty announced that she had undergone an elective double mastectomy to reduce her genetically high risk of breast cancer, it was a cultural and medical earthquake '-- a revelation so arresting it became the subject of TIME's newest cover story, which will be publish on TIME.com Thursday morning, before hitting newsstands on Friday (visit time.com/angelina; free for subscribers or purchase a digital pass).
(MORE:The Tricky Calculus of Cancer Testing)
Jolie, by nearly universal agreement, made the right choice for her. She tested positive for the breast-cancer-related BRCA1 gene, putting the probability that she would develop the disease at a terrifying 87%; after her surgery, her doctors put that number at just 5%. But a lot of experts worry that we may overread the lessons. Genetic screening is a young science, and while we may have detected genes linked to a host of ills '-- Alzheimer's disease, prostate cancer, rheumatoid arthritis, diabetes, heart disease '-- we often do a terrible job of calculating our resulting risks. Just over one-tenth of 1% of all women carry the same BRCA mutation Jolie has, and yet doctors expect a stampede of women requesting the test. In the U.S., 36% of women who test positive opt for preventive mastectomy, but some doctors argue that regular MRIs and other screening tests may be sufficient to detect the disease, and that less radical procedures, like lumpectomies, may be sufficient to treat it if it does occur.
Similar misunderstanding of risks is common in the case of prostate cancer too. The familiar PSA screening test detects blood antigens related to the disease, but levels of the marker can rise as a result of inflammation, infection and even riding a bicycle. Still, many men who test positive begin a cascade of subsequent tests and treatments that can often lead to a radical prostatectomy, sometimes with no real sign that they have the disease, or at least not a slow-growing case they could live with.
Human beings are very good at worrying'--it's what keeps us alive and out of harm's way. But we're also good at over-worrying, making irreversible decisions to reduce or avoid risks that don't really exist at all. Jolie's brave example can make us all smarter and help keep us all healthier'--but only if we take the right lessons from it.
MORE:Hard Choices About Gene Testing Kids
Jeffrey KlugerJeffrey Kluger, senior editor, oversees TIME's science and technology reporting.
Kluger's latest book is The Sibling Effect: What the Bonds Among Brothers and Sisters Reveal About Us.
Wed, 15 May 2013 15:43
Angelina Jolie has earned praise from breast cancer experts for highlighting the heightened predisposition of some women to the disease. Photograph: Jon Kopaloff/FilmMagic.com
Angelina Jolie was back at work preparing for her next film just four days after having a double mastectomy, her doctor has revealed in a detailed description of the actor's months of treatment.
The Oscar-winner underwent her double mastectomy on 16 February at the Pink Lotus Breast Centre in Beverly Hills, California, as the second of three operations to reduce her risk of breast cancer from 87% to 5%.
"On day four after her mastectomies I was pleased to find her not only in good spirits with bountiful energy, but with two walls in her house covered with freshly assembled storyboards for the next project she is directing.
"All the while she spoke, six drains dangled from her chest, three on each side, fastened to an elastic belt around her waist," wrote Dr Kristi Funk in a lengthy and intimate blogpost on the centre's website that explained what Jolie underwent before, during and after her three surgeries.
Despite her fame and constant trailing by the media, Jolie's medical treatment had remained a secret until Tuesday, when she wrote about her decision in an article in the New York Times.
She earned praise from breast cancer experts for flagging up the heightened genetic predisposition to the disease run by women who have inherited a faulty version of either the BRCA1 or BRCA2 gene from one of their parents.
Jolie approved Funk's account of her treatment to help women at high risk because of their family history of either breast or ovarian cancer to understand what is involved if they opt to undergo surgery rather than regular scans and preventive drugs as a way of managing their risk.
Jolie's first operation, on 2 February, was a "nipple delay", a procedure to rule out the presence of cancerous cells in the milk ducts around the nipple in women who have decided to preserve their nipples while almost all their breast tissue is removed during the mastectomy.
"Her partner [Brad Pitt] was on hand to greet her as soon as she came around from the anaesthetic, as he was during each of the operations," said Funk.
Tests showed no sign of cancer.
During the mastectomy a fortnight later, a plastic surgeon called Dr Jay Orringer also "performed the first stage breast reconstruction by placing tissue expanders with allograft", which Funk describes as "synthetic sheets of material, that create a more natural look" for women having their breasts rebuilt.
Despite an extra operation being involved to fit the tissue expanders, Jolie chose to have them, because they help maximise blood flow to the breast skin and nipple, said Funk.
Ten weeks later, on 27 April, Jolie received breast implants during her third and final surgery, the reconstruction, "which went extremely well, bringing an end to her surgical journey".
Funk also detailed the myriad medications and supplements which Jolie took to help her wounds heal after each operation, reduce the risk of infection, lessen post-operative nausea, vomiting, swelling and bruising, get the anaesthetics out of her system, increase the amount of oxygen reaching her skin and minimise scarring.
Wed, 15 May 2013 14:03
Angelina Jolie announced yesterday that she had both of her breasts surgically removed even though she had no breast cancer. She carries the BRCA1 gene, and she has been tricked into believing that genetic code is some sort of absolute blueprint to disease expression -- which it most certainly is not. Countless millions of women carry the BRCA1 gene and never express breast cancer because they lead healthy, anti-cancer lifestyles based on smart nutrition, exercise, sensible sunlight exposure and avoidance of cancer-causing chemicals.Jolie, like many other women who have been deluded by cancer quackery, decided the best way to prevent the risk of breast cancer was not to lead a healthy, anti-cancer lifestyle, but rather to surgically remove her breasts in what she describes as "three months of medical procedures."
...just in case, you know. Because you can never be too careful these days, with the cancer industry scaring women half to death at every opportunity. "My breasts might murder me!" seems to be the slogan of many women these days, all of whom are victims of outrageous cancer industry propaganda and fear mongering.
Let me set the record straight: Your breasts are not your enemy! The cancer industry is far more likely to kill you than your breasts. (But more on that later...)
Women's liberation crusade: Off with your breasts!
Worse than merely maiming herself in an act of outright medical quackery, Angelina Jolie has positioned her decision as some sort of women's liberation crusade, acting and talking as if her "choice" to remove her breasts somehow blazes a new path of female power for all women. (How sick is this, really?)Oh, what a mess Jolie has made of herself. She has maimed her own body with no medical justification whatsoever, then celebrated this horrible disfiguration through some sort of twisted perception of what womanhood really is. Being an empowered woman doesn't mean cutting off your breasts and aborting live babies -- even though both of these things are often celebrated by delusional women's groups. Being an empowered woman means protecting your health, your body and your womanhood by honoring and respecting your body, not maiming it.
A vivacious, confident, healthy woman who protects her fertility and nourishes her unborn child is far more heroic and empowering than someone who maims her own body as some sort of sick sacrifice to the cancer industry. Angelina Jolie, as much as she is often viewed as a symbol of female power, seems to have completely lost touch with the core truths of honoring the "temple" of your own female body.
Cancer is never limited to just the breast
Cancer, by the way, is a systemic problem when it emerges, not a local problem limited to just the breasts or other organs. It may be diagnosed in breast tissues, but that's not the only place it's growing. The idea that someone can prevent cancer by just removing their breasts is absurd. If the conditions of cancer are present in the body -- due to nutritional deficiencies, exposure to chemicals, radiation, etc. -- cancer will develop in many different places, not just breast tissues. Removing an organ that might possibly someday be one of the many locations in which cancer is diagnosed is completely irrational and medically abhorrent. Logically, it's a lot like arguing that you can avoid flat tires on your car by removing all the tires!
If you really want to learn the truth about cancer -- and SAVE your breasts! -- get our "New Cancer Solutions" CD set. The third CD is absolutely amazing, offering astounding information that can literally help save your life. You can also hear the entire collection for free during our New Cancer Solutions Healing Summit launching next Monday, May 20th.
If Angelina Jolie had heard the information on these CDs, she would have said, "NO!" to the cancer fear mongers and learned that there are far more effective and empowering ways to protect yourself from cancer. Women everywhere need to hear truly empowering, honoring, holistic information about cancer and stop listening to the insanity of the cancer industry and its delusional, victimized spokespeople like Angelina Jolie.
Celebrating the medical abuse of women
The mainstream media is heralding Jolie's decision to cut off both her perfectly healthy breasts, announcing Jolie is "admired for bravery." In a NYT op-ed, Jolie wrote, "I hope that other women can benefit from my experience." (No, I'm not making this up. She literally wants other healthy women to cut off their breasts, too...)
The medical industry, never known to back down from an opportunity to physically abuse women for profit, is jumping on the double mastectomy bandwagon. In a Businessweek article, a genetic counselor named Rebecca Nagy declares, "Having this conversation empowers us all. It's wonderful what she's done."
Wonderful? To cut off parts of your body that have NO disease? With this logic, abortions are cancer prevention, too, because those babies might one day grow up and develop tumors. Better to kill them early and "prevent cancer," right?
The irrationality of Jolie's decision is truly sickening. Even worse is that idea that she may inspire other women to have their healthy bodies maimed, too. If Jolie cut off both legs and called it a "choice" to prevent leg cancer, I have little doubt many women would follow her lead and cut off their legs, too. Jolie herself says she may have her ovaries cut out in the future because they, too, might someday get cancer.
You don't have to be a rocket scientist to see where this medical insanity ultimately leads. Got a risk of kidney cancer? Remove your kidneys. Risk of colon cancer? Take out your colon. Lung cancer, perhaps? Remove your lungs, just in case! That's the logic of Angelina Jolie who has been completely deceived by the cancer industry into maiming her own body based on nothing for medical fear mongering and cancer quackery.
Never doubt the fact that fear can be an effective marketing tool when it comes to breast cancer, by the way. The cancer industry rakes in billions of dollars a year based on irrational fears spread by misinformed women.
Medical maiming going viral across the population of sheeple
There's nothing quite as exciting and heroic as having your body parts chopped off by surgeons and then declaring yourself to be a "pre-vivor" of cancer. Yep, that's the new term. You're not really a "survivor" of cancer, since you never had it. You're a "pre-vivor" because you preempted the cancer.
Or, just as likely, you got suckered into the most delusional decision of your life and had a bunch of quacks slice off pieces of your body that were perfectly healthy to begin with. This is medical insanity at its worst... especially given that a woman's risk of breast cancer can be reduced by 78% using nothing but vitamin D. Yeah, take some vitamin D and keep your breasts! What a deal, eh?
Why aren't male cancer doctors cutting off their own testicles?
You'll note, by the way, that men never have their testicles removed to lower the risk of testicular cancer. Not even the male cancer doctors, oncologists and surgeons who are slicing off women's breasts all day long. Sure, they think cutting off breasts is a great idea, but ask one of them to part with their own testicles to "prevent" cancer, and they'll look at you like you've gone, well, nuts.
Because cutting off your testicles to prevent testicular cancer that you don't even have would be stupid, of course. Pure quackery. Suggest it to a man you know and you'll either be laughed at or punched in the mouth. No ethical doctor would ever remove a perfectly healthy set of testicles from a man who has no symptoms of testicular cancer. The very idea is absurd and possibly even risking a medical malpractice lawsuit.
So why is it somehow acceptable to cut off the breasts of "empowered women" who think they are making some sort of social statement by maiming their own perfectly healthy bodies?
(SNIP story here if you are publishing this on another site. You do not need to include the cancer CD mentioned below...)
Get answers for cancer... and save your breasts!
Inform yourself and you can protect your body from the insane, knife-wielding cancer surgeons. Get the New Cancer Solutions CD set and empower yourself with real answers rather than cancer industry disinformation and deadly propaganda.
The CD includes the following discussions:
The Consciousness of Cancer - The Health Ranger, Mike AdamsMike Adams, the founder and editor of NaturalNews.com presents, "The Consciousness of Cancer" -- a new way of looking at cancer.
The Compassionate Oncologist - James Forsythe, M.D., H.M.DJames W. Forsythe, M.D., H.M.D., has long been considered one of the most respected physicians in the United States. Dr. Forsythe graduated with honors from UC Berkeley and earned his medical degree at UCSF. This presentation reveals a NEW way of caring for cancer patients with an amazing success rate. You'll learn about the most important cancer test available today; Dr. Forsythe's 3-week cancer treatment program plus much more!
Stop Making Cancer - Thomas Lodi, M.D.Thomas Lodi, M.D. completed his medical degree in 1985 from the University of Hawaii. This program will help you understand cancer - like you've never heard before. Discover the best ways to stop making cancer; eliminate cancer cells without harming the body and effectively strengthen the immune system - our ultimate defense against cancer. As Dr. Lodi says, the "bioterrain is everything". This show will teach you how to prevent disease from the inside out.
Life Over Cancer - Keith I. Block, M.D.Keith Block, M.D. is an internationally recognized expert in integrative oncology. Referred to by many as the "father of integrative oncology", Dr. Block has published more than 75 scientific papers and his model of individualized integrative oncology continues to set the standard for the practice of comprehensive cancer care in the United States. This presentation goes way beyond "early detection" and teaches you about the best diet, supplement and exercise routines to promote optimal health.
Six Pillars of Health - Richard Linchitz, M.D.Dr. Richard Linchitz graduated with honors from Cornell University Medical College, and completed his residency at the famed University of California, San Francisco, Moffit Hospital. In 1998, after being diagnosed with lung cancer, Dr. Linchitz changed everything about his life, career and overall perspective about medicine. Killing cancer cells is not enough - learn about detoxification, stress reduction techniques, hormone balancing plus much more! Dr. Linchitz believes his 6-step program is the best way to stay healthy - always!
The Regeneration Effect - John Apsley, MD(E), ND, DCDr. John Apsley is a physician and researcher who for the past 30 years has specialized in the rehabilitation and reversal of chronic degenerative illnesses through accelerated tissue repair and cellular regeneration. Dr. Apsley teaches cancer patients about "The Regeneration Effect - Curing versus Controlling Advanced Cancer". There's a NEW chemistry of cancer remedies - find out about the latest advances in cancer testing; non-toxic cancer treatments plus scientifically proven ways to prevent cancer. The power is in your hands to get healthy today.
Get the full CD set by clicking here.
Or listen to the entire seminar for free on May 20th, as we launch our New Cancer Solutions Healing Summit.
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Wed, 15 May 2013 11:22
Myriad Genetics, Inc. is a molecular diagnostic company based in Salt Lake City, Utah. Myriad employs a number of proprietary technologies that permit doctors and patients to understand the genetic basis of human disease and the role that genes play in the onset, progression and treatment of disease. This information is used to guide the development of new molecular diagnostic products that assess an individual's risk for developing disease later in life (predictive medicine), identify a patient's likelihood of responding to a particular drug therapy and tailor a patient's drug dose to ensure optimal treatment (personalized medicine), and assess a patient's risk of disease progression and disease recurrence (personalized medicine). Myriad was the subject of scrutiny after it became involved in a lengthy lawsuit over its controversial patenting practices.
HistoryThe global search for a genetic basis for breast and ovarian cancer began in earnest in 1988. In 1990, at an American Society of Human Genetics Meeting, a team of scientists led by Mary-Claire King, Ph.D., from University of California at Berkeley announced the localization through linkage analysis of a gene associated with increased risk for breast cancer (BRCA1) to the long arm of chromosome 17. In August 1994, Mark Skolnick and researchers at Myriad, along with colleagues at the University of Utah, the U.S National Institutes of Health (NIH), and McGill University sequenced BRCA1.
FoundersThe founders of Myriad are Mark Skolnick (Adjunct Professor in the Department of Medical Informatics at the University of Utah), Walter Gilbert (1980 Nobel Laureate in chemistry and Professor in the Department of Molecular and Cellular Biology at Harvard University) and Peter Meldrum (past President and CEO of Agridyne and current CEO and President of Myriad Genetics, Inc) and Kevin Kimberlin of Spencer Trask & Company
SubsidiaryMyriad Genetic Laboratories, Inc., a wholly owned subsidiary of Myriad Genetics, Inc., has launched eight commercial molecular diagnostic products, including four predictive medicine, three personalized medicine products and one prognostic medicine product.
Myriad currently offers the following predictive medicine products based on DNA testing from blood: BRACAnalysis (assesses risk for hereditary breast and ovarian cancer), COLARIS (assesses risk for hereditary colorectal and uterine cancer), COLARIS AP (assesses risk for hereditary familial adenomatous polyposis colon cancer syndromes) and MELARIS (assesses risk for hereditary melanoma) and PANEXIA (assess risk for hereditary pancreatic cancer).
Myriad currently offers the following personalized medicine tests based on the investigation of blood or tissues: TheraGuide (predicts toxicity to Fluorouracil (5-FU)-based chemotherapy), OnDose (measures a patient's exposure to 5-FU chemotherapy), PREZEON (assesses the status of the PTEN gene) and a prognostic medicine product: PROLARIS (assesses the aggressiveness of prostate cancer).
Timeline1991 - BRCA1 was linked to chromosome 17 by UC Berkeley scientists1991 - Myriad Genetics was founded by Dr. Walter Gilbert, Mark Skolnick, Kevin Kimberlin and Peter Meldrum1994 - BRCA1 was cloned at the University of Utah in Mark Skolnick's lab and published by 40 collaborators1994 - First BRCA1 U.S. patent was filed by the University of Utah, National Institute of Environmental Health Sciences (NIEHS) and Myriad Genetics1994/1995 - Development of process and laboratory to perform high throughput sequencing by Myriad1995 - BRCA2 was resequenced based on unpublished information at the Myriad facility and the University of Utah by Mark Skolnick and collaborators1995 - First BRCA2 patent filed in the U.S. by the University of Utah and other institutions1996 - Myriad launched BRACAnalysis, a predictive medicine product for hereditary breast and ovarian cancer1997 - First BRCA1 patent was granted in the U.S. to the University of Utah, NIEHS and Myriad Genetics1998 - First BRCA2 patent was granted in the U.S. to the University of Utah, NIEHS and Myriad Genetics2000 - Myriad launched COLARIS, a predictive medicine product for hereditary colorectal and uterine cancer2002 - Myriad launched COLARIS AP, a predictive medicine product for adenomatous polyposis colon cancer syndromes2002 - Myriad launched MELARIS, a predictive medicine product for hereditary melanoma2007 - Myriad launched TheraGuide 5-FU, a personalized medicine product to predict toxicity to 5-FU-based chemotherapy2008 - Myriad launched PREZEON, a personalized medicine product to assess the status of the PTEN gene2009 - Myriad launched OnDose, a personalized medicine product to measure a patient's exposure to 5-FU chemotherapy2010 - Myriad launched PANEXIA, a predictive medicine product for hereditary pancreatic and related cancersIn July, 2009, the spin off, Myriad Pharmaceuticals, was completed. Myriad Pharmaceuticals is a biopharmaceutical company focused on the discovery and development of therapeutic products.
BRCA1 Co-discoverersNational Institute of Environmental Health Sciences (NIEHS)University of Utah Research FoundationUniversity of Laval/Endo Research '' QuebecHospital for Sick Children '' University of TorontoUniversity of TokyoMyriad Genetics, Inc.BRCA2 Co-discoverersUniversity of Utah Research FoundationHospital for Sick Children '' University of TorontoUniversity of PennsylvaniaMyriad Genetics, Inc.Legislation and LitigationMyriad Genetics is a defendant in the case Association for Molecular Pathology v. Myriad Genetics (formerly Association For Molecular Pathology et al. v. United States Patent and Trademark Office). Lawyers at the ACLU serve as counsel for the plaintiffs. In the suit, medical associations, doctors, and patients sued Myriad Genetics to challenge seven United Statespatents on genes related to breast cancer and ovarian cancer.
Two of the company's patents on the BRCA1 and BRCA2 genes were ruled invalid on March 29, 2010 by Judge Robert W. Sweet in the U.S. District Court for the Southern District of New York. This was the first time a U.S. court had declared a gene patent invalid. On appeal, the Court of Appeals for the Federal Circuit reversed the trial court in an opinion dated July 29, 2011 and held that the genes were eligible for patents.
On December 7, 2011, the ACLU filed a petition for a writ of certiorari to the Supreme Court. On March 26, 2012, the Supreme Court vacated the Federal Circuit's judgment and remanded the case for further consideration in light of Mayo Collaborative Services v. Prometheus Laboratories, Inc., in which the Supreme Court had ruled, just six days earlier, that more restrictive rules were required to patent observations about natural phenomena.
On August 16, 2012, the Federal Circuit reaffirmed Myriad's right to patent the genes although they denied rights to patent comparisons of DNA sequences. On November 30, 2012, The Supreme Court agreed to hear a second challenge to the two gene patents held by Myriad. Oral argument is scheduled for April 15, 2013, with a decision expected by the end of the Supreme Court's term in June.
See alsoReferences^ abcBegley, Sharon (March 29, 2010). "In Surprise Ruling, Court Declares Two Gene Patents Invalid". Newsweek. Retrieved March 29, 2010. ^ abSchwartz, John and Pollack, Andrew (March 29, 2010). "Judge Invalidates Human Gene Patent". The New York Times. Retrieved March 29, 2010. ^ ab"ACLU v. Myriad Genetics opinion". 2010-03-29. Retrieved 2010-03-30. ^Hall, J.; Lee, M.; Newman, B.; Morrow, J.; Anderson, L.; Huey, B.; King, M. (1990). "Linkage of early-onset familial breast cancer to chromosome 17q21". Science250 (4988): 1684''1689. doi:10.1126/science.2270482. PMID 2270482. edit^Miki, Y.; Swensen, J.; Shattuck-Eidens, D.; Futreal, P. A.; Harshman, K.; Tavtigian, S.; Liu, Q.; Cochran, C. et al. (1994). "A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1". Science266 (5182): 66''71. doi:10.1126/science.7545954. PMID 7545954. edit^"Breakthrough: The Race to Find the Breast Cancer Gene," page 199, by Kevin Davies and Michael White John Wiley & Sons.^Staff (2 July 2009) Myriad Pharmaceuticals, Inc. Established As An Independent Pharmaceutical Development Company Pharmaceutical Online, Retrieved 21 January 2013^"Association For Molecular Pathology et al v. United States Patent and Trademark Office et al". Justia.com. May 12, 2009. ^"ACLU Challenges Patents on Breast Cancer Genes". American Civil Liberties Union. June 6, 2008. ^"Myriad Applauds the Court of Appeals' Decision to Uphold Gene Patenting". Myriad Genetics. 2011-07-29. Retrieved 2011-11-20. ^http://jurist.org/paperchase/2011/12/aclu-ask-supreme-court-to-rule-on-gene-patent-case.php^Pollack, Andrew (March 26, 2012). "Supreme Court Orders New Look at Gene Patents". The New York Times. ^"Court Reaffirms Right of Myriad Genetics to Patent Genes". New York Times. August 16, 2012. ^"Myriad Genetics slips on Supreme Court review". Bloomberg Business Week. December 3, 2012. External links
Wed, 15 May 2013 11:22
Breast cancer 1, early onsetPDB rendering based on 1jm7.Available structuresPDBOrtholog search: PDBe, RCSBList of PDB id codes1JM7, 1JNX, 1N5O, 1OQA, 1T15, 1T29, 1T2U, 1T2V, 1Y98, 2ING, 3COJ, 3K0H, 3K0K, 3K15, 3K16, 3PXA, 3PXB, 3PXC, 3PXD, 3PXE
IdentifiersSymbolsBRCA1; BRCAI; BRCC1; BROVCA1; IRIS; PNCA4; PPP1R53; PSCP; RNF53External IDsOMIM: 113705MGI: 104537HomoloGene: 5276ChEMBL: 5990GeneCards: BRCA1 GeneRNA expression patternMore reference expression dataOrthologsSpeciesHumanMouseEntrez67212189EnsemblENSG00000012048ENSMUSG00000017146UniProtP38398P48754RefSeq (mRNA)NM_007294NM_009764RefSeq (protein)NP_009225NP_033894Location (UCSC)Chr 17:41.2 '' 41.32 MbChr 11:101.49 '' 101.55 MbPubMed searchBRCA1 (pron.:/Ëbr...kÉ/;breast cancer 1, early onset) is a human caretaker gene that produces a protein called breast cancer type 1 susceptibility protein, responsible for repairing DNA. The first evidence for the existence of the gene was provided by the King laboratory at UC Berkeley in 1990. Four years later, after an international race to find it, the gene was cloned in 1994 by scientists at University of Utah, National Institute of Environmental Health Sciences (NIEHS) and Myriad Genetics.
BRCA1 is expressed in the cells of breast and other tissue, where it helps repair damaged DNA, or destroy cells if DNA cannot be repaired. If BRCA1 itself is damaged, damaged DNA is not repaired properly and this increases risks for cancers (see BRCA mutation).
The protein encoded by the BRCA1 gene combines with other tumor suppressors, DNA damage sensors, and signal transducers to form a large multi-subunit protein complex known as the BRCA1-associated genome surveillance complex (BASC). The BRCA1 protein associates with RNA polymerase II, and through the C-terminal domain, also interacts with histone deacetylase complexes. Thus, this protein plays a role in transcription, DNA repair of double-stranded breaksubiquitination, transcriptional regulation as well as other functions.
Methods to diagnose the likelihood of a patient with mutations in BRCA1 and BRCA2 getting cancer were covered by patents owned or controlled by Myriad Genetics. Myriad's business model of exclusively offering the diagnostic test led from Myriad being a startup in 1994 to being a publicly traded company with 1200 employees and about $500M in annual revenue in 2012; it also led to controversy over high prices and the inability to get second opinions from other diagnostic labs, which in turn led to the landmark Association for Molecular Pathology v. Myriad Genetics lawsuit.
Gene locationThe human BRCA1 gene is located on the long (q) arm of chromosome 17 at region 2 band 1, from base pair 41,196,312 to base pair 41,277,500 (Build GRCh37/hg19) (map).BRCA1orthologs have been identified in most mammals for which complete genome data are available.
Protein structureThe BRCA1 protein contains the following domains:
This protein also contains nuclear localization signal and nuclear export signal motifs.
The human BRCA1 protein consists of four major protein domains; the Znf C3HC4- RING domain, the BRCA1 serine domain and two BRCT domains. These domains encode approximately 27% of BRCA1 protein. There are six known isoforms of P38398 BRCA1, with isoforms 1 and 2 comprising 1863 amino acids each.
Zinc ring finger domainThe RING motif, a Zn finger found in eukaryotic peptides, is 40-60 amino acids long and consists of eight conserved metal-binding residues, two quartets of cysteine or histidine residues that coordinate two zinc atoms. This motif contains a short anti-parallel beta-sheet, two zinc binding loops and a central alpha helix in a small domain. This RING domain interacts with associated proteins including BARD1, which also contains a RING motif, to form a heterodimer. The BRCA1 RING motif is flanked by alpha helices formed by residues 8-22 and 81-96 of the BRCA1 protein. It interacts with a homologous region in BARD1 also consisting of a RING finger flanked by two alpha-helices formed from residues 36-48 and 101-116. These four helices combine to form a heterodimerization interface and stabilise the BRCA1-BARD1 heterodimer complex. Additional stabilisation is achieved by interactions between adjacent residues in the flanking region and hydrophobic interactions. The BARD1/BRCA1 interaction is disrupted by tumorigenic amino acid substitutions in BRCA1, implying that the formation of a stable complex between these proteins may be an essential aspect of BRCA1 tumor suppression.
The ring domain is an important element of ubiquitin E3 ligases which catalyse protein ubiquitination2. Ubiquitin is a small regulatory protein found in all tissues which directs proteins to compartments within the cell. BRCA1 polypeptides, in particular Lys-48-linked polyubiquitin chains, are dispersed throughout within the resting cell nucleus but when DNA replication begins they gather in restrained groups that also contain BRCA2 and BARD1. BARD1 is thought to be involved in the recognition and binding of protein targets for ubiquitination. It attaches to proteins and labels them for destruction. Ubiquitination occurs via the BRCA1 fusion protein and is abolished by zinc chelation. The enzyme activity of the fusion protein is dependent on the proper folding of the ring domain.
Serine cluster domainThe BRCA1 serine cluster domain (SCD) spans amino acids 1280-1524. A portion of the domain is located in exons 11-13. High rates of mutation occur in exons 11-13. Reported phosphorylation sites of BRCA1 are concentrated in the SCD where they are phosphorylated by ATM/ATR kinases both in vitro and in vivo. ATM/ATR are kinases activated by DNA damage. Mutation of serine residues may affect localization of BRCA1 to sites of DNA damage and DNA damage response function.
BRCT domainsThe dual repeat BRCT domain of the BRCA1 protein is an elongated structure approximately 70 long and 30-35 wide. The 85-95 amino acid domains in BRCT can be found as single modules or as multiple tandem repeats containing two domains. Both of these possibilities can occur in a single protein in a variety of different conformations. The C-terminal BRCT region of the BRCA1 protein is essential for repair of DNA, transcription regulation and tumor suppressor function. In BRCA1 the dual tandem repeatBRCT domains are arranged in a head-to-tail-fashion in the three-dimensional structure, burying 1600 of hydrophobic, solvent accessible surface area in the interface. These all contribute to the tightly packed knob-in-hole structure that comprises the interface. These homologous domains interact to control cellular responses to DNA damage. It is therefore no surprise, that a missense mutation at the interface of these two proteins can have devastating consequences on the cell cycle, resulting in protein dysfunction and a greater risk of developing cancer. The linker that joins these two homologs also needs to be considered, since its poorly defined electron density alludes to a possible complex function; the ability to flex.
Function and mechanismBRCA1 repairs double-strand breaks in DNA. The strands of the DNA double helix are continuously breaking from damage. Sometimes one strand is broken, and sometimes both strands are broken simultaneously. DNA cross linking agents are an important source of chromosome/DNA damage. Double strand breaks occur as intermediates after the cross links are removed. BRCA1 is part of a protein complex that repairs DNA when both strands are broken. When both strands are broken, it is difficult for the repair mechanism to "know" how to replace the correct DNA sequence, and there are multiple ways to attempt the repair. The double-stranded repair mechanism that BRCA1 participates in is homologous recombination, in which the repair proteins utilize homologous intact sequence from a sister chromatid, from a homologous chromosome, or from the same chromosome (depending on cell cycle phase) as a template. This DNA repair takes place with the DNA in the cell nucleus, wrapped around the histone. Several proteins, including BRCA1, arrive at the histone-DNA complex for this repair. Regulatory aspect to BRCA1 nuclear ' non-nuclear distribution was first shown by Dr Rao laboratory in 1997
In the nucleus of many types of normal cells, the BRCA1 protein interacts with RAD51 during repair of DNA double-strand breaks. These breaks can be caused by natural radiation or other exposures, but also occur when chromosomes exchange genetic material (homologous recombination, e.g., "crossing over" during meiosis). The BRCA2 protein, which has a function similar to that of BRCA1, also interacts with the RAD51 protein. By influencing DNA damage repair, these three proteins play a role in maintaining the stability of the human genome.
BRCA1 directly binds to DNA, with higher affinity for branched DNA structures. This ability to bind to DNA contributes to its ability to inhibit the nuclease activity of the MRN complex as well as the nuclease activity of Mre11 alone. This may explain a role for BRCA1 to promote lower fidelity DNA repair by non-homologous end joining (NHEJ). BRCA1 also colocalizes with Î"-H2AX (histone H2AX phosphorylated on serine-139) in DNA double-strand break repair foci, indicating it may play a role in recruiting repair factors.
Formaldehyde and acetaldehyde are common environmental sources of DNA cross links that often require repairs mediated by BRCA1 containing pathways.
TranscriptionBRCA1 was shown to co-purify with the human RNA Polymerase II holoenzyme in HeLa extracts, implying it is a component of the holoenzyme. Later research, however, contradicted this assumption, instead showing that the predominant complex including BRCA1 in HeLa cells is a 2 megadalton complex containing SWI/SNF. SWI/SNF is a chromatin remodeling complex. Artificial tethering of BRCA1 to chromatin was shown to decondense heterochromatin, though the SWI/SNF interacting domain was not necessary for this role. BRCA1 interacts with the NELF-B (COBRA1) subunit of the NELF complex.
Other rolesResearch suggests that both the BRCA1 and BRCA2 proteins regulate the activity of other genes and play a critical role in embryo development. The BRCA1 protein probably interacts with many other proteins, including tumor suppressors and regulators of the cell division cycle.
Mutations and cancer riskCertain variations of the BRCA1 gene lead to an increased risk for breast cancer as part of a hereditary breast-ovarian cancer syndrome. Researchers have identified hundreds of mutations in the BRCA1 gene, many of which are associated with an increased risk of cancer. Women with an abnormal BRCA1 or BRCA2 gene have up to a 80% risk of developing breast cancer by age 90; increased risk of developing ovarian cancer is about 55% for women with BRCA1 mutations and about 25% for women with BRCA2 mutations.
These mutations can be changes in one or a small number of DNA base pairs (the building-blocks of DNA). Those mutations can be identified with PCR and DNA sequencing.
In some cases, large segments of DNA are rearranged. Those large segments, also called large rearrangements, can be a deletion or a duplication of one or several exons in the gene. Classical methods for mutations detection (sequencing) are unable to reveal those mutations. Other methods are proposed: Q-PCR,Multiplex Ligation-dependent Probe Amplification (MLPA), and Quantitative Multiplex PCR of Shorts Fluorescents Fragments (QMPSF). New methods have been recently proposed: heteroduplex analysis (HDA) by multi-capillary electrophoresis or also dedicated oligonucleotides array based on comparative genomic hybridization (array-CGH).
Some results suggest that hypermethylation of the BRCA1 promoter, which has been reported in some cancers, could be considered as an inactivating mechanism for BRCA1 expression.
A mutated BRCA1 gene usually makes a protein that does not function properly because it is abnormally short. Researchers believe that the defective BRCA1 protein is unable to help fix mutations that occur in other genes. These defects accumulate and may allow cells to grow and divide uncontrollably to form a tumor.
BRCA1 mRNA 3' UTR can be bound by an miRNA, Mir-17 microRNA. It has been suggested that variations in this miRNA along with Mir-30 microRNA could confer susceptibility to breast cancer.
In addition to breast cancer, mutations in the BRCA1 gene also increase the risk of ovarian, fallopian tube, and prostate cancers. Moreover, precancerous lesions (dysplasia) within the Fallopian tube have been linked to BRCA1 gene mutations. Pathogenic mutations anywhere in a model pathway containing BRCA1 and BRCA2 greatly increase risks for a subset of leukemias and lymphomas.
Women having inherited a defective BRCA1 or BRCA2 gene have risks for breast and ovarian cancer that are so high and seem so selective that many mutation carriers choose to have prophylactic surgery. There has been much conjecture to explain such apparently striking tissue specificity. Major determinants of where BRCA1/2 hereditary cancers occur are related to tissue specificity of the cancer pathogen, the agent that causes chronic inflammation or the carcinogen. The target tissue may have receptors for the pathogen, become selectively exposed to an inflammatory process or to a carcinogen. An innate genomic deficit in a tumor suppressor gene impairs normal responses and exacerbates the susceptibility to disease in organ targets. This theory also fits data for several tumor suppressors beyond BRCA1 or BRCA2. A major advantage of this model is that it suggests there may be some options in addition to prophylactic surgery.
Germ line mutations and founder effectAll germ-line BRCA1 mutations identified to date have been inherited, suggesting the possibility of a large ''founder'' effect in which a certain mutation is common to a well-defined population group and can, in theory, be traced back to a common ancestor. Given the complexity of mutation screening for BRCA1, these common mutations may simplify the methods required for mutation screening in certain populations. Analysis of mutations that occur with high frequency also permits the study of their clinical expression. Examples of manifestations of a founder effect are seen among Ashkenazi Jews. Three mutations in BRCA1 have been reported to account for the majority of Ashkenazi Jewish patients with inherited BRCA1-related breast and/or ovarian cancer: 185delAG, 188del11 and 5382insC in the BRCA1 gene. In fact, it has been shown that if a Jewish woman does not carry a BRCA1 185delAG, BRCA1 5382insC founder mutation, it is highly unlikely that a different BRCA1 mutation will be found. Additional examples of founder mutations in BRCA1 are given in Table 1 (mainly derived from ).
Population or subgroupBRCA1 mutation(s)Reference(s)African-Americans943ins10, M1775RAfrikanersE881XAshkenazi Jewish185delAG, 188del11, 5382insCAustrians2795delA, C61G, 5382insC, Q1806stopBelgians2804delAA, IVS5+3A>GDutchExon 2 deletion, exon 13 deletion, 2804delAAFinns3745delT, IVS11-2A>GFrench3600del11, G1710XFrench CanadiansC4446TGermans5382insC, 4184del4Greeks5382insCHungarians300T>G, 5382insC, 185delAGItalians5083del19JapaneseL63X, Q934XNative North Americans1510insG, 1506A>GNorthern Irish2800delAANorwegians816delGT, 1135insA, 1675delA, 3347delAGPakistanis2080insA, 3889delAG, 4184del4, 4284delAG, IVS14-1A>GPolish300T>G, 5382insC, C61G, 4153delARussians5382insC, 4153delAScottish2800delAASpanishR71GSwedishQ563X, 3171ins5, 1201del11, 2594delCPatents, enforcement, litigation, and controversyA patent application for the isolated BRCA1 gene and cancer-cancer promoting mutations discussed above, as well as methods to diagnose the likelihood of getting breast cancer, was filed by the University of Utah, National Institute of Environmental Health Sciences (NIEHS) and Myriad Genetics in 1994; over the next year, Myriad, in collaboration with investigators at Endo Recherche, Inc., HSC Research & Development Limited Partnership, and University of Pennsylvania, isolated and sequenced the BRCA2 gene and identified key mutations, and the first BRCA2 patent was filed in the U.S. by Myriad and other institutions in 1995. Myriad is the exclusive licensee of these patents and has enforced them in the US against clinical diagnostic labs. This business model led from Myriad being a startup in 1994 to being a publicly traded company with 1200 employees and about $500M in annual revenue in 2012; it also led to controversy over high prices and the inability to get second opinions from other diagnostic labs, which in turn led to the landmark Association for Molecular Pathology v. Myriad Genetics lawsuit. The patents begin to expire in 2014.
According to an article published in the journal, Genetic Medicine, in 2010, "The patent story outside the United States is more complicated.... For example, patents have been obtained but the patents are being ignored by provincial health systems in Canada. In Australia and the UK, Myriad's licensee permitted use by health systems, but announced a change of plans in August 2008. ... Only a single mutation has been patented in Myriad's lone European-wide patent, although some patents remain under review of an opposition proceeding. In effect, the United States is the only jurisdiction where Myriad's strong patent position has conferred sole-provide status." Peter Meldrum, CEO of Myriad Genetics, has acknowledged that Myriad has "other competitive advantages that may make such [patent] enforcement unnecessary" in Europe.
Legal decisions surrounding the BRCA1 and BRCA2 patents will affect the field of genetic testing in general.
InteractionsBRCA1 has been shown to interact with
UCSC Gene details page
See alsoReferences^Hamel PJ (2007-05-29). "BRCA1 and BRCA2: No Longer the Only Troublesome Genes Out There". HealthCentral. Retrieved 2010-07-02. ^Check W (2006-09-01). "BRCA: What we know now". College of American Pathologists. Retrieved 2010-08-23. ^Hall JM, Lee MK, Newman B, Morrow JE, Anderson LA, Huey B, King MC (December 1990). "Linkage of early-onset familial breast cancer to chromosome 17q21". Science250 (4988): 1684''9. doi:10.1126/science.2270482. PMID 2270482. ^High-Impact Science: Tracking down the BRCA genes (Part 1) - Cancer Research UK science blog, 2012^ abcUS patent 5747282, Skolnick HS, Goldgar DE, Miki Y, Swenson J, Kamb A, Harshman KD, Shattuck-Eidens DM, Tavtigian SV, Wiseman RW, Futreal PA, "7Q-linked breast and ovarian cancer susceptibility gene", issued 1998-05-05, assigned to Myraid Genetics, Inc., The United States of America as represented by the Secretary of Health and Human Services, and University of Utah Research Foundation ^Miki Y, Swensen J, Shattuck-Eidens D, Futreal PA, Harshman K, Tavtigian S, Liu Q, Cochran C, Bennett LM, Ding W, et al. (October 1994). "A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1". Science266 (5182): 66''71. doi:10.1126/science.7545954. PMID 7545954. ^"Breast and Ovarian Cancer Genetic Screening". Palo Alto Medical Foundation. Archived from the original on 4 October 2008. Retrieved 2008-10-11. ^ abcFriedenson B (2007). "The BRCA1/2 pathway prevents hematologic cancers in addition to breast and ovarian cancers". BMC Cancer7: 152. doi:10.1186/1471-2407-7-152. PMC 1959234. PMID 17683622. ^ abcdefgWang Y, Cortez D, Yazdi P, Neff N, Elledge SJ, Qin J (April 2000). "BASC, a super complex of BRCA1-associated proteins involved in the recognition and repair of aberrant DNA structures". Genes Dev.14 (8): 927''39. PMC 316544. PMID 10783165. ^ abStarita LM, Parvin JD (2003). "The multiple nuclear functions of BRCA1: transcription, ubiquitination and DNA repair". Current Opinion in Cell Biology15 (3): 345''350. doi:10.1016/S0955-0674(03)00042-5. PMID 12787778. ^ abUS patent 5837492, Tavtigian SV, Kamb A, Simard J, Couch F, Rommens JM, Weber BL, "Chromosome 13-linked breast cancer susceptibility gene", issued 1998-11-17, assigned to Myriad Genetics, Inc., Endo Recherche, Inc., HSC Research & Development Limited Partnership, Trustees of the University of Pennsylvaina ^ abMyriad Investor Page'--see "Myriad at a glance" accessed October 2012^ abcSchwartz J (2009-05-12). "Cancer Patients Challenge the Patenting of a Gene". Health. New York Times. ^National Center for Biotechnology Information, U.S. National Library of Medicine EntrezGene reference information for BRCA1 breast cancer 1, early onset (Homo sapiens)^"OrthoMaM phylogenetic marker: BRCA1 coding sequence". ^Paterson JW (February 1998). "BRCA1: a review of structure and putative functions". Dis. Markers13 (4): 261''74. PMID 9553742. ^Henderson BR (September 2005). "Regulation of BRCA1, BRCA2 and BARD1 intracellular trafficking". BioEssays27 (9): 884''93. doi:10.1002/bies.20277. PMID 16108063. ^ abClark SL, Rodriguez AM, Snyder RR, Hankins GD, Boehning D (April 2012). "Structure-Function Of The Tumor Suppressor BRCA1". Comput Struct Biotechnol J1 (1). doi:10.5936/csbj.201204005. PMC 3380633. PMID 22737296. ^ abcdBrzovic PS, Rajagopal P, Hoyt DW, King MC, Klevit RE (October 2001). "Structure of a BRCA1-BARD1 heterodimeric RING-RING complex". Nat. Struct. Biol.8 (10): 833''7. doi:10.1038/nsb1001-833. PMID 11573085. ^Baer R (October 2001). "With the ends in sight: images from the BRCA1 tumor suppressor". Nat. Struct. Biol.8 (10): 822''4. doi:10.1038/nsb1001-822. PMID 11573079. ^ abcWilliams RS, Green R, Glover JN (October 2001). "Crystal structure of the BRCT repeat region from the breast cancer-associated protein BRCA1". Nat. Struct. Biol.8 (10): 838''42. doi:10.1038/nsb1001-838. PMID 11573086. ^Huyton T, Bates PA, Zhang X, Sternberg MJ, Freemont PS (August 2000). "The BRCA1 C-terminal domain: structure and function". Mutat. Res.460 (3-4): 319''32. PMID 10946236. ^ abJoo WS, Jeffrey PD, Cantor SB, Finnin MS, Livingston DM, Pavletich NP (March 2002). "Structure of the 53BP1 BRCT region bound to p53 and its comparison to the Brca1 BRCT structure". Genes Dev.16 (5): 583''93. doi:10.1101/gad.959202. PMC 155350. PMID 11877378. ^Kimball's Biologh Pages^ abWang H, Shao N, Ding QM, Cui J, Reddy ES, Rao VN (Jul 1997). "BRCA1 proteins are transported to the nucleus in the absence of serum and splice variants BRCA1a, BRCA1b are tyrosine phosphoproteins that associate with E2F, cyclins and cyclin dependent kinases". Oncogene15 (2): 143''57. doi:10.1038/sj.onc.1201252. PMID 9244350. ^Boulton SJ (November 2006). "Cellular functions of the BRCA tumour-suppressor proteins". Biochem. Soc. Trans.34 (Pt 5): 633''45. doi:10.1042/BST0340633. PMID 17052168. ^Paull TT, Cortez D, Bowers B, Elledge SJ, Gellert M (2001). "Direct DNA binding by Brca1". Proceedings of the National Academy of Sciences98 (11): 6086''6091. doi:10.1073/pnas.111125998. PMC 33426. PMID 11353843. ^Durant ST, Nickoloff JA (2005). "Good timing in the cell cycle for precise DNA repair by BRCA1". Cell Cycle4 (9): 1216''22. doi:10.4161/cc.4.9.2027. PMID 16103751. ^ abcYe Q, Hu YF, Zhong H, Nye AC, Belmont AS, Li R (2001). "BRCA1-induced large-scale chromatin unfolding and allele-specific effects of cancer-predisposing mutations". The Journal of Cell Biology155 (6): 911''922. doi:10.1083/jcb.200108049. PMC 2150890. PMID 11739404. ^Friedenson B (November 2011). "A common environmental carcinogen unduly affects carriers of cancer mutations: carriers of genetic mutations in a specific protective response are more susceptible to an environmental carcinogen". Med. Hypotheses77 (5): 791''7. doi:10.1016/j.mehy.2011.07.039. PMID 21839586. ^Ridpath JR, Nakamura A, Tano K, Luke AM, Sonoda E, Arakawa H, Buerstedde JM, Gillespie DA, Sale JE, Yamazoe M, Bishop DK, Takata M, Takeda S, Watanabe M, Swenberg JA, Nakamura J (December 2007). "Cells deficient in the FANC/BRCA pathway are hypersensitive to plasma levels of formaldehyde". Cancer Res.67 (23): 11117''22. doi:10.1158/0008-5472.CAN-07-3028. PMID 18056434. ^Scully R, Anderson SF, Chao DM, Wei W, Ye L, Young RA, Livingston DM, Parvin JD (1997). "BRCA1 is a component of the RNA polymerase II holoenzyme". Proceedings of the National Academy of Sciences94 (11): 5605''10. doi:10.1073/pnas.94.11.5605. PMC 20825. PMID 9159119. ^Bochar DA, Wang L, Beniya H, Kinev A, Xue Y, Lane WS, Wang W, Kashanchi F, Shiekhattar R (2000). "BRCA1 Is Associated with a Human SWI/SNF-Related Complex Linking Chromatin Remodeling to Breast Cancer". Cell102 (2): 257''265. doi:10.1016/S0092-8674(00)00030-1. PMID 10943845. Retrieved 2008-05-05. ^"Genetics". Breastcancer.org. 2012-09-17. ^Mazoyer S (May 2005). "Genomic rearrangements in the BRCA1 and BRCA2 genes". Hum. Mutat.25 (5): 415''22. doi:10.1002/humu.20169. PMID 15832305. ^Barrois M, Bi¨che I, Mazoyer S, Champ¨me MH, Bressac-de Paillerets B, Lidereau R (February 2004). "Real-time PCR-based gene dosage assay for detecting BRCA1 rearrangements in breast-ovarian cancer families". Clin. Genet.65 (2): 131''6. doi:10.1111/j.0009-9163.2004.00200.x. PMID 14984472. ^Hogervorst FB, Nederlof PM, Gille JJ, McElgunn CJ, Grippeling M, Pruntel R, Regnerus R, van Welsem T, van Spaendonk R, Menko FH, Kluijt I, Dommering C, Verhoef S, Schouten JP, van't Veer LJ, Pals G (April 2003). "Large genomic deletions and duplications in the BRCA1 gene identified by a novel quantitative method". Cancer Res.63 (7): 1449''53. PMID 12670888. ^Casilli F, Di Rocco ZC, Gad S, Tournier I, Stoppa-Lyonnet D, Frebourg T, Tosi M (September 2002). "Rapid detection of novel BRCA1 rearrangements in high-risk breast-ovarian cancer families using multiplex PCR of short fluorescent fragments". Hum. Mutat.20 (3): 218''26. doi:10.1002/humu.10108. PMID 12203994. ^Rouleau E, Lefol C, Tozlu S, Andrieu C, Guy C, Copigny F, Nogues C, Bieche I, Lidereau R (September 2007). "High-resolution oligonucleotide array-CGH applied to the detection and characterization of large rearrangements in the hereditary breast cancer gene BRCA1". Clin. Genet.72 (3): 199''207. doi:10.1111/j.1399-0004.2007.00849.x. PMID 17718857. ^Tapia T, Smalley SV, Kohen P, Mu±oz A, Solis LM, Corvalan A, Faundez P, Devoto L, Camus M, Alvarez M, Carvallo P (2008). "Promoter hypermethylation of BRCA1 correlates with absence of expression in hereditary breast cancer tumors". Epigenetics3 (3): 157''63. doi:10.1186/bcr1858. PMID 18567944. ^Shen J, Ambrosone CB, Zhao H (March 2009). "Novel genetic variants in microRNA genes and familial breast cancer". Int. J. Cancer124 (5): 1178''82. doi:10.1002/ijc.24008. PMID 19048628. ^ abLacroix M, Leclercq G (2005). "The "portrait" of hereditary breast cancer". Breast Cancer Research and Treatment89 (3): 297''304. doi:10.1007/s10549-004-2172-4. PMID 15754129. ^ abStruewing JP, Abeliovich D, Peretz T, Avishai N, Kaback MM, Collins FS, Brody LC (1978). "Isolation of two human tumor epithelial cell lines from solid breast carcinomas". Journal of the National Cancer Institute61 (2): 967''978. doi:10.1038/ng1095-198. PMID 7550349. ^ abTonin P, Serova O, Lenoir G, Lynch H, Durocher F, Simard J, Morgan K, Narod S (1995). "BRCA1 mutations in Ashkenazi Jewish women". American Journal of Human Genetics57 (1): 189. PMC 1801236. PMID 7611288. ^Narod SA, Foulkes WD (2004). "BRCA1 and BRCA2: 1994 and beyond". Nature Reviews on Cancer4 (9): 665''676. doi:10.1038/nrc1431. PMID 15343273. ^den Dunnen JT, Antonarakis SE (2000). "Mutation nomenclature extensions and suggestions to describe complex mutations: a discussion". Human Mutation15 (1): 7''12. doi:10.1002/(SICI)1098-1004(200001)15:13.0.CO;2-N. PMID 10612815. ^ abNeuhausen SL (2000). "Founder populations and their uses for breast cancer genetics". Cancer Research2 (2): 77''81. doi:10.1186/bcr36. PMC 139426. PMID 11250694. ^Reeves MD, Yawitch TM, van der Merwe NC, van den Berg HJ, Dreyer G, van Rensburg EJ (July 2004). "BRCA1 mutations in South African breast and/or ovarian cancer families: evidence of a novel founder mutation in Afrikaner families". Int. J. Cancer110 (5): 677''82. doi:10.1002/ijc.20186. PMID 15146556. ^Wagner TM, M¶slinger RA, Muhr D, Langbauer G, Hirtenlehner K, Concin H, Doeller W, Haid A, Lang AH, Mayer P, Ropp E, Kubista E, Amirimani B, Helbich T, Becherer A, Scheiner O, Breiteneder H, Borg A, Devilee P, Oefner P, Zielinski C (1998). "BRCA1-related breast cancer in Austrian breast and ovarian cancer families: specific BRCA1 mutations and pathological characteristics". International Journal of Cancer77 (3): 354''360. doi:10.1002/(SICI)1097-0215(19980729)77:33.0.CO;2-N. PMID 9663595. ^ abPeelen T, van Vliet M, Petrij-Bosch A, Mieremet R, Szabo C, van den Ouweland AM, Hogervorst F, Brohet R, Ligtenberg MJ, Teugels E, van der Luijt R, van der Hout AH, Gille JJ, Pals G, Jedema I, Olmer R, van Leeuwen I, Newman B, Plandsoen M, van der Est M, Brink G, Hageman S, Arts PJ, Bakker MM, Devilee P, et al. (1997). "A high proportion of novel mutations in BRCA1 with strong founder effects among Dutch and Belgian hereditary breast and ovarian cancer families". American Journal of Human Genetics60 (5): 1041''1049. PMC 1712432. PMID 9150151. ^Claes K, Machackova E, De Vos M, Poppe B, De Paepe A, Messiaen L. (1999). "Mutation analysis of the BRCA1 and BRCA2 genes in the Belgian patient population and identification of a Belgian founder mutation BRCA1 IVS5 + 3A > G". Disease Markers15 (1''3): 69''73. PMID 10595255. ^Petrij-Bosch A, Peelen T, van Vliet M, van Eijk R, Olmer R, Dr¼sedau M, Hogervorst FB, Hageman S, Arts PJ, Ligtenberg MJ, Meijers-Heijboer H, Klijn JG, Vasen HF, Cornelisse CJ, van 't Veer LJ, Bakker E, van Ommen GJ, Devilee P (1997). "BRCA1 genomic deletions are major founder mutations in Dutch breast cancer patients". Nature Genetics17 (3): 341''345. doi:10.1038/ng1197-341. PMID 9354803. ^Verhoog LC, van den Ouweland AM, Berns E, van Veghel-Plandsoen MM, van Staveren IL, Wagner A, Bartels CC, Tilanus-Linthorst MM, Devilee P, Seynaeve C, Halley DJ, Niermeijer MF, Klijn JG, Meijers-Heijboer H (2001). "Large regional differences in the frequency of distinct BRCA1/BRCA2 mutations in 517 Dutch breast and/or ovarian cancer families". European Journal of Cancer37 (16): 2082''2090. doi:10.1016/S0959-8049(01)00244-1. PMID 11597388. ^Huusko P, P¤¤kk¶nen K, Launonen V, P¶yh¶nen M, Blanco G, Kauppila A, Puistola U, Kiviniemi H, Kujala M, Leisti J, Winqvist R (1998). "Evidence of founder mutations in Finnish BRCA1 and BRCA2 families". American Journal of Human Genetics62 (6): 1544''1548. doi:10.1086/301880. PMC 1377159. PMID 9585608. ^P¤¤kk¶nen K, Sauramo S, Sarantaus L, Vahteristo P, Hartikainen A, Vehmanen P, Ignatius J, Ollikainen V, K¤¤ri¤inen H, Vauramo E, Nevanlinna H, Krahe R, Holli K, Kere J (2001). "Involvement of BRCA1 and BRCA2 in breast cancer in a western Finnish sub-population". Genetic Epidemiology20 (2): 239''246. doi:10.1002/1098-2272(200102)20:23.0.CO;2-Y. PMID 11180449. ^Muller D, Bonaiti-Pelli(C) C, Abecassis J, Stoppa-Lyonnet D, Fricker JP (2004). "BRCA1 testing in breast and/or ovarian cancer families from northeastern France identifies two common mutations with a founder effect". Familial Cancer3 (1): 15''20. doi:10.1023/B:FAME.0000026819.44213.df. PMID 15131401. ^Tonin PN, Mes-Masson AM, Narod SA, Ghadirian P, Provencher D (1999). "Founder BRCA1 and BRCA2 mutations in French Canadian ovarian cancer cases unselected for family history". Clinical Genetics55 (5): 318''324. doi:10.1034/j.1399-0004.1999.550504.x. PMID 10422801. ^Backe J, Hofferbert S, Skawran B, D¶rk T, Stuhrmann M, Karstens JH, Untch M, Meindl A, Burgemeister R, Chang-Claude J, Weber BH (1999). "Frequency of BRCA1 mutation 5382insC in German breast cancer patients". Gynecologic Oncology72 (3): 402''406. doi:10.1006/gyno.1998.5270. PMID 10053113. ^"Mutation data of the BRCA1 gene". KMDB/MutationView (Keio Mutation Databases). Keio University. ^Ladopoulou A, Kroupis C, Konstantopoulou I, Ioannidou-Mouzaka L, Schofield AC, Pantazidis A, Armaou S, Tsiagas I, Lianidou E, Efstathiou E, Tsionou C, Panopoulos C, Mihalatos M, Nasioulas G, Skarlos D, Haites NE, Fountzilas G, Pandis N, Yannoukakos D (2002). "Germ line BRCA1 and BRCA2 mutations in Greek breast/ovarian cancer families: 5382insC is the most frequent mutation observed". Cancer Letters185 (1): 61''70. doi:10.1016/S0304-3835(01)00845-X. PMID 12142080. ^Van Der Looij M, Szabo C, Besznyak I, Liszka G, Csokay B, Pulay T, Toth J, Devilee P, King MC, Olah E (2000). "Prevalence of founder BRCA1 and BRCA2 mutations among breast and ovarian cancer patients in Hungary". International Journal of Cancer86 (5): 737''740. doi:10.1002/(SICI)1097-0215(20000601)86:53.0.CO;2-1. PMID 10797299. ^Baudi F, Quaresima B, Grandinetti C, Cuda G, Faniello C, Tassone P, Barbieri V, Bisegna R, Ricevuto E, Conforti S, Viel A, Marchetti P, Ficorella C, Radice P, Costanzo F, Venuta S (2001). "Evidence of a founder mutation of BRCA1 in a highly homogeneous population from southern Italy with breast/ovarian cancer". Human Mutation18 (2): 163''164. doi:10.1002/humu.1167. PMID 11462242. ^Sekine M, Nagata H, Tsuji S, Hirai Y, Fujimoto S, Hatae M, Kobayashi I, Fujii T, Nagata I, Ushijima K, Obata K, Suzuki M, Yoshinaga M, Umesaki N, Satoh S, Enomoto T, Motoyama S, Tanaka K; Japanese Familial Ovarian Cancer Study Group (2001). "Mutational analysis of BRCA1 and BRCA2 and clinicopathologic analysis of ovarian cancer in 82 ovarian cancer families: two common founder mutations of BRCA1 in Japanese population". Clinical Cancer Research7 (10): 3144''3150. PMID 11595708. ^Liede A, Jack E, Hegele RA, Narod SA (2002). "A BRCA1 mutation in Native North American families". Human Mutation19 (4): 460. doi:10.1002/humu.9027. PMID 11933205. ^ abThe Scottish/Northern Irish BRCA1/BRCA2 Consortium (2003). "BRCA1 and BRCA2 mutations in Scotland and Northern Ireland". British Journal of Cancer88 (8): 1256''1262. doi:10.1038/sj.bjc.6600840. PMC 2747571. PMID 12698193. ^Borg A, D¸rum A, Heimdal K, Maehle L, Hovig E, M¸ller P (1999). "BRCA1 1675delA and 1135insA account for one third of Norwegian familial breast-ovarian cancer and are associated with later disease onset than less frequent mutations". Disease Markers15 (1''3): 79''84. PMID 10595257. ^Heimdal K, Maehle L, Apold J, Pedersen JC, M¸ller P (2003). "The Norwegian founder mutations in BRCA1: high penetrance confirmed in an incident cancer series and differences observed in the risk of ovarian cancer". Europen Journal of Cancer39 (15): 2205''2213. doi:10.1016/S0959-8049(03)00548-3. PMID 14522380. ^Liede A, Malik IA, Aziz Z, Rios Pd Pde L, Kwan E, Narod SA (2002). "Contribution of BRCA1 and BRCA2 Mutations to Breast and Ovarian Cancer in Pakistan". American Journal of Human Genetics71 (3): 595''606. doi:10.1086/342506. PMC 379195. PMID 12181777. ^G"rski B, Byrski T, Huzarski T, Jakubowska A, Menkiszak J, Gronwald J, PluzaÅska A, Bebenek M, Fischer-Maliszewska L, Grzybowska E, Narod SA, LubiÅski J (2000). "Founder mutations in the BRCA1 gene in Polish families with breast-ovarian cancer". American Journal of Human Genetics66 (6): 1963''1968. doi:10.1086/302922. PMC 1378051. PMID 10788334. ^Perkowska M, BroZek I, Wysocka B, Haraldsson K, Sandberg T, Johansson U, Sellberg G, Borg A, Limon J (May 2003). "BRCA1 and BRCA2 mutation analysis in breast-ovarian cancer families from northeastern Poland". Hum. Mutat.21 (5): 553''4. doi:10.1002/humu.9139. PMID 12673801. ^Gayther SA, Harrington P, Russell P, Kharkevich G, Garkavtseva RF, Ponder BA (May 1997). "Frequently occurring germ-line mutations of the BRCA1 gene in ovarian cancer families from Russia". Am. J. Hum. Genet.60 (5): 1239''42. PMC 1712436. PMID 9150173. ^Liede A, Cohen B, Black DM, Davidson RH, Renwick A, Hoodfar E, Olopade OI, Micek M, Anderson V, De Mey R, Fordyce A, Warner E, Dann JL, King MC, Weber B, Narod SA, Steel CM (February 2000). "Evidence of a founder BRCA1 mutation in Scotland". Br. J. Cancer82 (3): 705''11. doi:10.1054/bjoc.1999.0984. PMC 2363321. PMID 10682686. ^Vega A, Campos B, Bressac-De-Paillerets B, Bond PM, Janin N, Douglas FS, Dom¨nech M, Baena M, Pericay C, Alonso C, Carracedo A, Baiget M, Diez O (June 2001). "The R71G BRCA1 is a founder Spanish mutation and leads to aberrant splicing of the transcript". Hum. Mutat.17 (6): 520''1. doi:10.1002/humu.1136. PMID 11385711. ^Campos B, Dez O, Odefrey F, Dom¨nech M, Moncoutier V, Martnez-Ferrandis JI, Osorio A, Balma±a J, Barroso A, Armengod ME, Bentez J, Alonso C, Stoppa-Lyonnet D, Goldgar D, Baiget M (April 2003). "Haplotype analysis of the BRCA2 9254delATCAT recurrent mutation in breast/ovarian cancer families from Spain". Hum. Mutat.21 (4): 452. doi:10.1002/humu.9133. PMID 12655574. ^Bergman A, Einbeigi Z, Olofsson U, Taib Z, Wallgren A, Karlsson P, Wahlstr¶m J, Martinsson T, Nordling M (October 2001). "The western Swedish BRCA1 founder mutation 3171ins5; a 3.7 cM conserved haplotype of today is a reminiscence of a 1500-year-old mutation". Eur. J. Hum. Genet.9 (10): 787''93. doi:10.1038/sj.ejhg.5200704. PMID 11781691. ^"ACLU sues over patents on breast cancer genes". CNN. Archived from the original on 15 May 2009. Retrieved 2009-05-14. ^Robert Cook-Deegan, MD et al (2010) Impact of Gene Patents and Licensing Practices on Access to Genetic Testing for Inherited Susceptibility to Cancer: Comparing Breast and Ovarian Cancers to Colon Cancers: Patents and Licensing for Breast, Ovarian and Colon Cancer Testing Genet Med.12(4 Suppl): S15''S38.^Benowitz S (January 2003). "European groups oppose Myriad's latest patent on BRCA1". J. Natl. Cancer Inst.95 (1): 8''9. doi:10.1093/jnci/95.1.8. PMID 12509391. ^Conley J, Vorhous D, Cook-Deegan J (2011-03-01). "How Will Myriad Respond to the Next Generation of BRCA Testing?". Robinson, Bradshaw, and Hinson. Retrieved 2012-12-09. ^"Genetics and Patenting". Human Genome Project Information. U.S. Department of Energy Genome Programs. 2010-07-07. ^Foray N, Marot D, Randrianarison V, Venezia ND, Picard D, Perricaudet M, Favaudon V, Jeggo P (June 2002). "Constitutive association of BRCA1 and c-Abl and its ATM-dependent disruption after irradiation". Mol. Cell. Biol.22 (12): 4020''32. doi:10.1128/MCB.22.12.4020-4032.2002. PMC 133860. PMID 12024016. ^Altiok S, Batt D, Altiok N, Papautsky A, Downward J, Roberts TM, Avraham H (November 1999). "Heregulin induces phosphorylation of BRCA1 through phosphatidylinositol 3-Kinase/AKT in breast cancer cells". J. Biol. Chem.274 (45): 32274''8. doi:10.1074/jbc.274.45.32274. PMID 10542266. ^Xiang T, Ohashi A, Huang Y, Pandita TK, Ludwig T, Powell SN, Yang Q (December 2008). "Negative Regulation of AKT Activation by BRCA1". Cancer Res.68 (24): 10040''4. doi:10.1158/0008-5472.CAN-08-3009. PMC 2605656. PMID 19074868. ^Yeh S, Hu YC, Rahman M, Lin HK, Hsu CL, Ting HJ, Kang HY, Chang C (October 2000). "Increase of androgen-induced cell death and androgen receptor transactivation by BRCA1 in prostate cancer cells". Proc. Natl. Acad. Sci. U.S.A.97 (21): 11256''61. doi:10.1073/pnas.190353897. PMC 17187. PMID 11016951. ^ abKim ST, Lim DS, Canman CE, Kastan MB (December 1999). "Substrate specificities and identification of putative substrates of ATM kinase family members". J. Biol. Chem.274 (53): 37538''43. doi:10.1074/jbc.274.53.37538. PMID 10608806. ^ abTibbetts RS, Cortez D, Brumbaugh KM, Scully R, Livingston D, Elledge SJ, Abraham RT (December 2000). "Functional interactions between BRCA1 and the checkpoint kinase ATR during genotoxic stress". Genes Dev.14 (23): 2989''3002. doi:10.1101/gad.851000. PMC 317107. PMID 11114888. ^ abChen J (September 2000). "Ataxia telangiectasia-related protein is involved in the phosphorylation of BRCA1 following deoxyribonucleic acid damage". Cancer Res.60 (18): 5037''9. PMID 11016625. ^ abGatei M, Zhou BB, Hobson K, Scott S, Young D, Khanna KK (May 2001). "Ataxia telangiectasia mutated (ATM) kinase and ATM and Rad3 related kinase mediate phosphorylation of Brca1 at distinct and overlapping sites. In vivo assessment using phospho-specific antibodies". J. Biol. Chem.276 (20): 17276''80. doi:10.1074/jbc.M011681200. PMID 11278964. ^Gatei M, Scott SP, Filippovitch I, Soronika N, Lavin MF, Weber B, Khanna KK (June 2000). "Role for ATM in DNA damage-induced phosphorylation of BRCA1". Cancer Res.60 (12): 3299''304. PMID 10866324. ^Cortez D, Wang Y, Qin J, Elledge SJ (November 1999). "Requirement of ATM-dependent phosphorylation of brca1 in the DNA damage response to double-strand breaks". Science286 (5442): 1162''6. doi:10.1126/science.286.5442.1162. PMID 10550055. ^Houvras Y, Benezra M, Zhang H, Manfredi JJ, Weber BL, Licht JD (November 2000). "BRCA1 physically and functionally interacts with ATF1". J. Biol. Chem.275 (46): 36230''7. doi:10.1074/jbc.M002539200. PMID 10945975. ^Ouchi M, Fujiuchi N, Sasai K, Katayama H, Minamishima YA, Ongusaha PP, Deng C, Sen S, Lee SW, Ouchi T (May 2004). "BRCA1 phosphorylation by Aurora-A in the regulation of G2 to M transition". J. Biol. Chem.279 (19): 19643''8. doi:10.1074/jbc.M311780200. PMID 14990569. ^ abCantor SB, Bell DW, Ganesan S, Kass EM, Drapkin R, Grossman S, Wahrer DC, Sgroi DC, Lane WS, Haber DA, Livingston DM (April 2001). "BACH1, a novel helicase-like protein, interacts directly with BRCA1 and contributes to its DNA repair function". Cell105 (1): 149''60. doi:10.1016/S0092-8674(01)00304-X. PMID 11301010. ^ abcMallery DL, Vandenberg CJ, Hiom K (December 2002). "Activation of the E3 ligase function of the BRCA1/BARD1 complex by polyubiquitin chains". EMBO J.21 (24): 6755''62. doi:10.1093/emboj/cdf691. PMC 139111. PMID 12485996. ^ abBrzovic PS, Keeffe JR, Nishikawa H, Miyamoto K, Fox D, Fukuda M, Ohta T, Klevit R (May 2003). "Binding and recognition in the assembly of an active BRCA1/BARD1 ubiquitin-ligase complex". Proc. Natl. Acad. Sci. U.S.A.100 (10): 5646''51. doi:10.1073/pnas.0836054100. PMC 156255. PMID 12732733. ^ abNishikawa H, Ooka S, Sato K, Arima K, Okamoto J, Klevit RE, Fukuda M, Ohta T (February 2004). "Mass spectrometric and mutational analyses reveal Lys-6-linked polyubiquitin chains catalyzed by BRCA1-BARD1 ubiquitin ligase". J. Biol. Chem.279 (6): 3916''24. doi:10.1074/jbc.M308540200. PMID 14638690. ^ abKentsis A, Gordon RE, Borden KL (November 2002). "Control of biochemical reactions through supramolecular RING domain self-assembly". Proc. Natl. Acad. Sci. U.S.A.99 (24): 15404''9. doi:10.1073/pnas.202608799. PMC 137729. PMID 12438698. ^ abcChen A, Kleiman FE, Manley JL, Ouchi T, Pan ZQ (June 2002). "Autoubiquitination of the BRCA1*BARD1 RING ubiquitin ligase". J. Biol. Chem.277 (24): 22085''92. doi:10.1074/jbc.M201252200. PMID 11927591. ^ abcdefgDong Y, Hakimi MA, Chen X, Kumaraswamy E, Cooch NS, Godwin AK, Shiekhattar R (November 2003). "Regulation of BRCC, a holoenzyme complex containing BRCA1 and BRCA2, by a signalosome-like subunit and its role in DNA repair". Mol. Cell12 (5): 1087''99. doi:10.1016/S1097-2765(03)00424-6. PMID 14636569. ^ abcSato K, Hayami R, Wu W, Nishikawa T, Nishikawa H, Okuda Y, Ogata H, Fukuda M, Ohta T (July 2004). "Nucleophosmin/B23 is a candidate substrate for the BRCA1-BARD1 ubiquitin ligase". J. Biol. Chem.279 (30): 30919''22. doi:10.1074/jbc.C400169200. PMID 15184379. ^ abcVandenberg CJ, Gergely F, Ong CY, Pace P, Mallery DL, Hiom K, Patel KJ (July 2003). "BRCA1-independent ubiquitination of FANCD2". Mol. Cell12 (1): 247''54. doi:10.1016/S1097-2765(03)00281-8. PMID 12887909. ^ abWu-Baer F, Lagrazon K, Yuan W, Baer R (September 2003). "The BRCA1/BARD1 heterodimer assembles polyubiquitin chains through an unconventional linkage involving lysine residue K6 of ubiquitin". J. Biol. Chem.278 (37): 34743''6. doi:10.1074/jbc.C300249200. PMID 12890688. ^ abHashizume R, Fukuda M, Maeda I, Nishikawa H, Oyake D, Yabuki Y, Ogata H, Ohta T (May 2001). "The RING heterodimer BRCA1-BARD1 is a ubiquitin ligase inactivated by a breast cancer-derived mutation". J. Biol. Chem.276 (18): 14537''40. doi:10.1074/jbc.C000881200. PMID 11278247. ^ abKleiman FE, Manley JL (March 2001). "The BARD1-CstF-50 interaction links mRNA 3' end formation to DNA damage and tumor suppression". Cell104 (5): 743''53. doi:10.1016/S0092-8674(01)00270-7. PMID 11257228. ^ abKleiman FE, Manley JL (September 1999). "Functional interaction of BRCA1-associated BARD1 with polyadenylation factor CstF-50". Science285 (5433): 1576''9. doi:10.1126/science.285.5433.1576. PMID 10477523. ^ abcdeWang Q, Zhang H, Guerrette S, Chen J, Mazurek A, Wilson T, Slupianek A, Skorski T, Fishel R, Greene MI (August 2001). "Adenosine nucleotide modulates the physical interaction between hMSH2 and BRCA1". Oncogene20 (34): 4640''9. doi:10.1038/sj.onc.1204625. PMID 11498787. ^Wu LC, Wang ZW, Tsan JT, Spillman MA, Phung A, Xu XL, Yang MC, Hwang LY, Bowcock AM, Baer R (December 1996). "Identification of a RING protein that can interact in vivo with the BRCA1 gene product". Nat. Genet.14 (4): 430''40. doi:10.1038/ng1296-430. PMID 8944023. ^Fabbro M, Rodriguez JA, Baer R, Henderson BR (June 2002). "BARD1 induces BRCA1 intranuclear foci formation by increasing RING-dependent BRCA1 nuclear import and inhibiting BRCA1 nuclear export". J. Biol. Chem.277 (24): 21315''24. doi:10.1074/jbc.M200769200. PMID 11925436. ^Rodriguez JA, Sch¼chner S, Au WW, Fabbro M, Henderson BR (March 2004). "Nuclear-cytoplasmic shuttling of BARD1 contributes to its proapoptotic activity and is regulated by dimerization with BRCA1". Oncogene23 (10): 1809''20. doi:10.1038/sj.onc.1207302. PMID 14647430. ^ abcdefChiba N, Parvin JD (October 2001). "Redistribution of BRCA1 among four different protein complexes following replication blockage". J. Biol. Chem.276 (42): 38549''54. doi:10.1074/jbc.M105227200. PMID 11504724. ^Morris JR, Keep NH, Solomon E (March 2002). "Identification of residues required for the interaction of BARD1 with BRCA1". J. Biol. Chem.277 (11): 9382''6. doi:10.1074/jbc.M109249200. PMID 11773071. ^Brzovic PS, Meza JE, King MC, Klevit RE (November 2001). "BRCA1 RING domain cancer-predisposing mutations. Structural consequences and effects on protein-protein interactions". J. Biol. Chem.276 (44): 41399''406. doi:10.1074/jbc.M106551200. PMID 11526114. ^Xia Y, Pao GM, Chen HW, Verma IM, Hunter T (February 2003). "Enhancement of BRCA1 E3 ubiquitin ligase activity through direct interaction with the BARD1 protein". J. Biol. Chem.278 (7): 5255''63. doi:10.1074/jbc.M204591200. PMID 12431996. ^Meza JE, Brzovic PS, King MC, Klevit RE (February 1999). "Mapping the functional domains of BRCA1. Interaction of the ring finger domains of BRCA1 and BARD1". J. Biol. Chem.274 (9): 5659''65. doi:10.1074/jbc.274.9.5659. PMID 10026184. ^Fabbro M, Savage K, Hobson K, Deans AJ, Powell, SN, McArthur GA, Khanna KK (July 2004). "BRCA1-BARD1 complexes are required for p53Ser-15 phosphorylation and a G1/S arrest following ionizing radiation-induced DNA damage". J. Biol. Chem.279 (30): 31251''8. doi:10.1074/jbc.M405372200. PMID 15159397. ^ abYu X, Wu LC, Bowcock AM, Aronheim A, Baer R (September 1998). "The C-terminal (BRCT) domains of BRCA1 interact in vivo with CtIP, a protein implicated in the CtBP pathway of transcriptional repression". J. Biol. Chem.273 (39): 25388''92. doi:10.1074/jbc.273.39.25388. PMID 9738006. ^Jin Y, Xu XL, Yang MC, Wei F, Ayi TC, Bowcock AM, Baer R (October 1997). "Cell cycle-dependent colocalization of BARD1 and BRCA1 proteins in discrete nuclear domains". Proc. Natl. Acad. Sci. U.S.A.94 (22): 12075''80. doi:10.1073/pnas.94.22.12075. PMC 23707. PMID 9342365. ^Scully R, Ganesan S, Vlasakova K, Chen J, Socolovsky M, Livingston DM (December 1999). "Genetic analysis of BRCA1 function in a defined tumor cell line". Mol. Cell4 (6): 1093''9. doi:10.1016/S1097-2765(00)80238-5. PMID 10635334. ^Tascou S, Kang TW, Trappe R, Engel W, Burfeind P (September 2003). "Identification and characterization of NIF3L1 BP1, a novel cytoplasmic interaction partner of the NIF3L1 protein". Biochem. Biophys. Res. Commun.309 (2): 440''8. doi:10.1016/j.bbrc.2003.07.008. PMID 12951069. ^ abcBenezra M, Chevallier N, Morrison DJ, MacLachlan TK, El-Deiry WS, Licht JD (July 2003). "BRCA1 augments transcription by the NF-kappaB transcription factor by binding to the Rel domain of the p65/RelA subunit". J. Biol. Chem.278 (29): 26333''41. doi:10.1074/jbc.M303076200. PMID 12700228. ^ abWang Q, Zhang H, Kajino K, Greene MI (October 1998). "BRCA1 binds c-Myc and inhibits its transcriptional and transforming activity in cells". Oncogene17 (15): 1939''48. doi:10.1038/sj.onc.1202403. PMID 9788437. ^Ryser S, Dizin E, Jefford CE, Delaval B, Gagos S, Christodoulidou A, Krause KH, Birnbaum D, Irminger-Finger I (February 2009). "Distinct roles of BARD1 isoforms in mitosis: full-length BARD1 mediates Aurora B degradation, cancer-associated BARD1beta scaffolds Aurora B and BRCA2". Cancer Res.69 (3): 1125''34. doi:10.1158/0008-5472.CAN-08-2134. PMID 19176389. ^Nishikawa H, Wu W, Koike A, Kojima R, Gomi H, Fukuda M, Ohta T (January 2009). "BRCA1-associated protein 1 interferes with BRCA1/BARD1 RING heterodimer activity". Cancer Res.69 (1): 111''9. doi:10.1158/0008-5472.CAN-08-3355. PMID 19117993. ^ abChen J, Silver DP, Walpita D, Cantor SB, Gazdar AF, Tomlinson G, Couch FJ, Weber BL, Ashley T, Livingston DM, Scully R (September 1998). "Stable interaction between the products of the BRCA1 and BRCA2 tumor suppressor genes in mitotic and meiotic cells". Mol. Cell2 (3): 317''28. doi:10.1016/S1097-2765(00)80276-2. PMID 9774970. ^ abReuter TY, Medhurst AL, Waisfisz Q, Zhi Y, Herterich S, Hoehn H, Gross HJ, Joenje H, Hoatlin ME, Mathew CG, Huber PA (October 2003). "Yeast two-hybrid screens imply involvement of Fanconi anemia proteins in transcription regulation, cell signaling, oxidative metabolism, and cellular transport". Exp. Cell Res.289 (2): 211''21. doi:10.1016/S0014-4827(03)00261-1. PMID 14499622. ^Sarkisian CJ, Master SR, Huber LJ, Ha SI, Chodosh LA (October 2001). "Analysis of murine Brca2 reveals conservation of protein-protein interactions but differences in nuclear localization signals". J. Biol. Chem.276 (40): 37640''8. doi:10.1074/jbc.M106281200. PMID 11477095. ^ abcdRodriguez M, Yu X, Chen J, Songyang Z (December 2003). "Phosphopeptide binding specificities of BRCA1 COOH-terminal (BRCT) domains". J. Biol. Chem.278 (52): 52914''8. doi:10.1074/jbc.C300407200. PMID 14578343. ^ abcdWada O, Oishi H, Takada I, Yanagisawa J, Yano T, Kato S (August 2004). "BRCA1 function mediates a TRAP/DRIP complex through direct interaction with TRAP220". Oncogene23 (35): 6000''5. doi:10.1038/sj.onc.1207786. PMID 15208681. ^Botuyan MV, Nomin(C) Y, Yu X, Juranic N, Macura S, Chen J, Mer G (July 2004). "Structural basis of BACH1 phosphopeptide recognition by BRCA1 tandem BRCT domains". Structure12 (7): 1137''46. doi:10.1016/j.str.2004.06.002. PMC 1817811. PMID 15242590. ^Yu X, Chini CC, He M, Mer G, Chen J (October 2003). "The BRCT domain is a phospho-protein binding domain". Science302 (5645): 639''42. doi:10.1126/science.1088753. PMID 14576433. ^Clapperton JA, Manke IA, Lowery DM, Ho T, Haire LF, Yaffe MB, Smerdon SJ (June 2004). "Structure and mechanism of BRCA1 BRCT domain recognition of phosphorylated BACH1 with implications for cancer". Nat. Struct. Mol. Biol.11 (6): 512''8. doi:10.1038/nsmb775. PMID 15133502. ^ abcHu YF, Li R (June 2002). "JunB potentiates function of BRCA1 activation domain 1 (AD1) through a coiled-coil-mediated interaction". Genes Dev.16 (12): 1509''17. doi:10.1101/gad.995502. PMC 186344. PMID 12080089. ^Lee JS, Collins KM, Brown AL, Lee CH, Chung JH (March 2000). "hCds1-mediated phosphorylation of BRCA1 regulates the DNA damage response". Nature404 (6774): 201''4. doi:10.1038/35004614. PMID 10724175. ^Chabalier-Taste C, Racca C, Dozier C, Larminat F (December 2008). "BRCA1 is regulated by Chk2 in response to spindle damage". Biochim. Biophys. Acta1783 (12): 2223''33. doi:10.1016/j.bbamcr.2008.08.006. PMID 18804494. ^Lin SY, Li K, Stewart GS, Elledge SJ (April 2004). "Human Claspin works with BRCA1 to both positively and negatively regulate cell proliferation". Proc. Natl. Acad. Sci. U.S.A.101 (17): 6484''9. doi:10.1073/pnas.0401847101. PMC 404071. PMID 15096610. ^Ye Q, Hu YF, Zhong H, Nye AC, Belmont AS, Li R (December 2001). "BRCA1-induced large-scale chromatin unfolding and allele-specific effects of cancer-predisposing mutations". J. Cell Biol.155 (6): 911''21. doi:10.1083/jcb.200108049. PMC 2150890. PMID 11739404. ^ abPao GM, Janknecht R, Ruffner H, Hunter T, Verma IM (February 2000). "CBP/p300 interact with and function as transcriptional coactivators of BRCA1". Proc. Natl. Acad. Sci. U.S.A.97 (3): 1020''5. doi:10.1073/pnas.97.3.1020. PMC 15508. PMID 10655477. ^ abChai YL, Cui J, Shao N, Shyam E, Reddy P, Rao VN (January 1999). "The second BRCT domain of BRCA1 proteins interacts with p53 and stimulates transcription from the p21WAF1/CIP1 promoter". Oncogene18 (1): 263''8. doi:10.1038/sj.onc.1202323. PMID 9926942. ^ abcFan S, Ma YX, Wang C, Yuan RQ, Meng Q, Wang JA, Erdos M, Goldberg ID, Webb P, Kushner PJ, Pestell RG, Rosen EM (January 2002). "p300 Modulates the BRCA1 inhibition of estrogen receptor activity". Cancer Res.62 (1): 141''51. PMID 11782371. ^Neish AS, Anderson SF, Schlegel BP, Wei W, Parvin JD (February 1998). "Factors associated with the mammalian RNA polymerase II holoenzyme". Nucleic Acids Res.26 (3): 847''53. doi:10.1093/nar/26.3.847. PMC 147327. PMID 9443979. ^O'Brien KA, Lemke SJ, Cocke KS, Rao RN, Beckmann RP (July 1999). "Casein kinase 2 binds to and phosphorylates BRCA1". Biochem. Biophys. Res. Commun.260 (3): 658''64. doi:10.1006/bbrc.1999.0892. PMID 10403822. ^Chen Y, Farmer AA, Chen CF, Jones DC, Chen PL, Lee WH (July 1996). "BRCA1 is a 220-kDa nuclear phosphoprotein that is expressed and phosphorylated in a cell cycle-dependent manner". Cancer Res.56 (14): 3168''72. PMID 8764100. ^Ruffner H, Jiang W, Craig AG, Hunter T, Verma IM (July 1999). "BRCA1 is phosphorylated at serine 1497 in vivo at a cyclin-dependent kinase 2 phosphorylation site". Mol. Cell. Biol.19 (7): 4843''54. PMC 84283. PMID 10373534. ^Schlegel BP, Starita LM, Parvin JD (February 2003). "Overexpression of a protein fragment of RNA helicase A causes inhibition of endogenous BRCA1 function and defects in ploidy and cytokinesis in mammary epithelial cells". Oncogene22 (7): 983''91. doi:10.1038/sj.onc.1206195. PMID 12592385. ^Anderson SF, Schlegel BP, Nakajima T, Wolpin ES, Parvin JD (July 1998). "BRCA1 protein is linked to the RNA polymerase II holoenzyme complex via RNA helicase A". Nat. Genet.19 (3): 254''6. doi:10.1038/930. PMID 9662397. ^Chai Y, Chipitsyna G, Cui J, Liao B, Liu S, Aysola K, Yezdani M, Reddy ES, Rao VN (March 2001). "c-Fos oncogene regulator Elk-1 interacts with BRCA1 splice variants BRCA1a/1b and enhances BRCA1a/1b-mediated growth suppression in breast cancer cells". Oncogene20 (11): 1357''67. doi:10.1038/sj.onc.1204256. PMID 11313879. ^Zheng L, Annab LA, Afshari CA, Lee WH, Boyer TG (August 2001). "BRCA1 mediates ligand-independent transcriptional repression of the estrogen receptor". Proc. Natl. Acad. Sci. U.S.A.98 (17): 9587''92. doi:10.1073/pnas.171174298. PMC 55496. PMID 11493692. ^Fan S, Ma YX, Wang C, Yuan RQ, Meng Q, Wang JA, Erdos M, Goldberg ID, Webb P, Kushner PJ, Pestell RG, Rosen EM (January 2001). "Role of direct interaction in BRCA1 inhibition of estrogen receptor activity". Oncogene20 (1): 77''87. doi:10.1038/sj.onc.1204073. PMID 11244506. ^Kawai H, Li H, Chun P, Avraham S, Avraham HK (October 2002). "Direct interaction between BRCA1 and the estrogen receptor regulates vascular endothelial growth factor (VEGF) transcription and secretion in breast cancer cells". Oncogene21 (50): 7730''9. doi:10.1038/sj.onc.1205971. PMID 12400015. ^Folias A, Matkovic M, Bruun D, Reid S, Hejna J, Grompe M, D'Andrea A, Moses R (October 2002). "BRCA1 interacts directly with the Fanconi anemia protein FANCA". Hum. Mol. Genet.11 (21): 2591''7. doi:10.1093/hmg/11.21.2591. PMID 12354784. ^Yan J, Zhu J, Zhong H, Lu Q, Huang C, Ye Q (October 2003). "BRCA1 interacts with FHL2 and enhances FHL2 transactivation function". FEBS Lett.553 (1-2): 183''9. doi:10.1016/S0014-5793(03)00978-5. PMID 14550570. ^Yan JH, Ye QN, Zhu JH, Zhong HJ, Zheng HY, Huang CF (December 2003). "[Isolation and characterization of a BRCA1-interacting protein]". Yi Chuan Xue Bao (in Chinese) 30 (12): 1161''6. PMID 14986435. ^Paull TT, Rogakou EP, Yamazaki V, Kirchgessner CU, Gellert M, Bonner WM (2000). "A critical role for histone H2AX in recruitment of repair factors to nuclear foci after DNA damage". Curr. Biol.10 (15): 886''95. doi:10.1016/S0960-9822(00)00610-2. PMID 10959836. ^Sutherland KD, Visvader JE, Choong DY, Sum EY, Lindeman GJ, Campbell IG (October 2003). "Mutational analysis of the LMO4 gene, encoding a BRCA1-interacting protein, in breast carcinomas". Int. J. Cancer107 (1): 155''8. doi:10.1002/ijc.11343. PMID 12925972. ^Sum EY, Peng B, Yu X, Chen J, Byrne J, Lindeman GJ, Visvader JE (March 2002). "The LIM domain protein LMO4 interacts with the cofactor CtIP and the tumor suppressor BRCA1 and inhibits BRCA1 activity". J. Biol. Chem.277 (10): 7849''56. doi:10.1074/jbc.M110603200. PMID 11751867. ^Gilmore PM, McCabe N, Quinn JE, Kennedy RD, Gorski JJ, Andrews HN, McWilliams S, Carty M, Mullan PB, Duprex WP, Liu ET, Johnston PG, Harkin DP (June 2004). "BRCA1 interacts with and is required for paclitaxel-induced activation of mitogen-activated protein kinase kinase kinase 3". Cancer Res.64 (12): 4148''54. doi:10.1158/0008-5472.CAN-03-4080. PMID 15205325. ^Chiba N, Parvin JD (August 2002). "The BRCA1 and BARD1 association with the RNA polymerase II holoenzyme". Cancer Res.62 (15): 4222''8. PMID 12154023. ^ abScully R, Anderson SF, Chao DM, Wei W, Ye L, Young RA, Livingston DM, Parvin JD (May 1997). "BRCA1 is a component of the RNA polymerase II holoenzyme". Proc. Natl. Acad. Sci. U.S.A.94 (11): 5605''10. doi:10.1073/pnas.94.11.5605. PMC 20825. PMID 9159119. ^ abcZhong Q, Chen CF, Li S, Chen Y, Wang CC, Xiao J, Chen PL, Sharp ZD, Lee WH (July 1999). "Association of BRCA1 with the hRad50-hMre11-p95 complex and the DNA damage response". Science285 (5428): 747''50. doi:10.1126/science.285.5428.747. PMID 10426999. ^Paull TT, Cortez D, Bowers B, Elledge SJ, Gellert M (May 2001). "Direct DNA binding by Brca1". Proc. Natl. Acad. Sci. U.S.A.98 (11): 6086''91. doi:10.1073/pnas.111125998. PMC 33426. PMID 11353843. ^ abLi H, Lee TH, Avraham H (June 2002). "A novel tricomplex of BRCA1, Nmi, and c-Myc inhibits c-Myc-induced human telomerase reverse transcriptase gene (hTERT) promoter activity in breast cancer". J. Biol. Chem.277 (23): 20965''73. doi:10.1074/jbc.M112231200. PMID 11916966. ^Xiong J, Fan S, Meng Q, Schramm L, Wang C, Bouzahza B, Zhou J, Zafonte B, Goldberg ID, Haddad BR, Pestell RG, Rosen EM (December 2003). "BRCA1 inhibition of telomerase activity in cultured cells". Mol. Cell. Biol.23 (23): 8668''90. doi:10.1128/MCB.23.23.8668-8690.2003. PMC 262673. PMID 14612409. ^Zhou C, Liu J (March 2003). "Inhibition of human telomerase reverse transcriptase gene expression by BRCA1 in human ovarian cancer cells". Biochem. Biophys. Res. Commun.303 (1): 130''6. doi:10.1016/S0006-291X(03)00318-8. PMID 12646176. ^Park JJ, Irvine RA, Buchanan G, Koh SS, Park JM, Tilley WD, Stallcup MR, Press MF, Coetzee GA (November 2000). "Breast cancer susceptibility gene 1 (BRCAI) is a coactivator of the androgen receptor". Cancer Res.60 (21): 5946''9. PMID 11085509. ^Cabart P, Chew HK, Murphy S (July 2004). "BRCA1 cooperates with NUFIP and P-TEFb to activate transcription by RNA polymerase II". Oncogene23 (31): 5316''29. doi:10.1038/sj.onc.1207684. PMID 15107825. ^Abramovitch S, Werner H (2003). "Functional and physical interactions between BRCA1 and p53 in transcriptional regulation of the IGF-IR gene". Horm. Metab. Res.35 (11-12): 758''62. doi:10.1055/s-2004-814154. PMID 14710355. ^Ouchi T, Monteiro AN, August A, Aaronson SA, Hanafusa H (March 1998). "BRCA1 regulates p53-dependent gene expression". Proc. Natl. Acad. Sci. U.S.A.95 (5): 2302''6. doi:10.1073/pnas.95.5.2302. PMC 19327. PMID 9482880. ^Zhang H, Somasundaram K, Peng Y, Tian H, Zhang H, Bi D, Weber BL, El-Deiry WS (April 1998). "BRCA1 physically associates with p53 and stimulates its transcriptional activity". Oncogene16 (13): 1713''21. doi:10.1038/sj.onc.1201932. PMID 9582019. ^Sy SM, Huen MS, Chen J (April 2009). "PALB2 is an integral component of the BRCA complex required for homologous recombination repair". Proc. Natl. Acad. Sci. U.S.A.106 (17): 7155''60. doi:10.1073/pnas.0811159106. PMC 2678481. PMID 19369211. ^Krum SA, Miranda GA, Lin C, Lane TF (December 2003). "BRCA1 associates with processive RNA polymerase II". J. Biol. Chem.278 (52): 52012''20. doi:10.1074/jbc.M308418200. PMID 14506230. ^Krum SA, Womack JE, Lane TF (September 2003). "Bovine BRCA1 shows classic responses to genotoxic stress but low in vitro transcriptional activation activity". Oncogene22 (38): 6032''44. doi:10.1038/sj.onc.1206515. PMID 12955082. ^Liu Y, Virshup DM, White RL, Hsu LC (November 2002). "Regulation of BRCA1 phosphorylation by interaction with protein phosphatase 1alpha". Cancer Res.62 (22): 6357''61. PMID 12438214. ^Scully R, Chen J, Plug A, Xiao Y, Weaver D, Feunteun J, Ashley T, Livingston DM (January 1997). "Association of BRCA1 with Rad51 in mitotic and meiotic cells". Cell88 (2): 265''75. doi:10.1016/S0092-8674(00)81847-4. PMID 9008167. ^ abcYarden RI, Brody LC (April 1999). "BRCA1 interacts with components of the histone deacetylase complex". Proc. Natl. Acad. Sci. U.S.A.96 (9): 4983''8. doi:10.1073/pnas.96.9.4983. PMC 21803. PMID 10220405. ^Chen GC, Guan LS, Yu JH, Li GC, Choi Kim HR, Wang ZY (June 2001). "Rb-associated protein 46 (RbAp46) inhibits transcriptional transactivation mediated by BRCA1". Biochem. Biophys. Res. Commun.284 (2): 507''14. doi:10.1006/bbrc.2001.5003. PMID 11394910. ^ abYarden RI, Brody LC (2001). "Identification of proteins that interact with BRCA1 by Far-Western library screening". J. Cell. Biochem.83 (4): 521''31. PMID 11746496. ^Li S, Chen PL, Subramanian T, Chinnadurai G, Tomlinson G, Osborne CK, Sharp ZD, Lee WH (April 1999). "Binding of CtIP to the BRCT repeats of BRCA1 involved in the transcription regulation of p21 is disrupted upon DNA damage". J. Biol. Chem.274 (16): 11334''8. doi:10.1074/jbc.274.16.11334. PMID 10196224. ^Wong AK, Ormonde PA, Pero R, Chen Y, Lian L, Salada G, Berry S, Lawrence Q, Dayananth P, Ha P, Tavtigian SV, Teng DH, Bartel PL (November 1998). "Characterization of a carboxy-terminal BRCA1 interacting protein". Oncogene17 (18): 2279''85. doi:10.1038/sj.onc.1202150. PMID 9811458. ^Li S, Ting NS, Zheng L, Chen PL, Ziv Y, Shiloh Y, Lee EY, Lee WH (July 2000). "Functional link of BRCA1 and ataxia telangiectasia gene product in DNA damage response". Nature406 (6792): 210''5. doi:10.1038/35018134. PMID 10910365. ^Wu-Baer F, Baer R (November 2001). "Effect of DNA damage on a BRCA1 complex". Nature414 (6859): 36. doi:10.1038/35102118. PMID 11689934. ^Yu X, Baer R (June 2000). "Nuclear localization and cell cycle-specific expression of CtIP, a protein that associates with the BRCA1 tumor suppressor". J. Biol. Chem.275 (24): 18541''9. doi:10.1074/jbc.M909494199. PMID 10764811. ^ abcFan S, Yuan R, Ma YX, Xiong J, Meng Q, Erdos M, Zhao JN, Goldberg ID, Pestell RG, Rosen EM (August 2001). "Disruption of BRCA1 LXCXE motif alters BRCA1 functional activity and regulation of RB family but not RB protein binding". Oncogene20 (35): 4827''41. doi:10.1038/sj.onc.1204666. PMID 11521194. ^Aprelikova ON, Fang BS, Meissner EG, Cotter S, Campbell M, Kuthiala A, Bessho M, Jensen RA, Liu ET (October 1999). "BRCA1-associated growth arrest is RB-dependent". Proc. Natl. Acad. Sci. U.S.A.96 (21): 11866''71. doi:10.1073/pnas.96.21.11866. PMC 18378. PMID 10518542. ^ abBochar DA, Wang L, Beniya H, Kinev A, Xue Y, Lane WS, Wang W, Kashanchi F, Shiekhattar R (July 2000). "BRCA1 is associated with a human SWI/SNF-related complex: linking chromatin remodeling to breast cancer". Cell102 (2): 257''65. doi:10.1016/S0092-8674(00)00030-1. PMID 10943845. ^Hill DA, de la Serna IL, Veal TM, Imbalzano AN (April 2004). "BRCA1 interacts with dominant negative SWI/SNF enzymes without affecting homologous recombination or radiation-induced gene activation of p21 or Mdm2". J. Cell. Biochem.91 (5): 987''98. doi:10.1002/jcb.20003. PMID 15034933. ^Ouchi T, Lee SW, Ouchi M, Aaronson SA, Horvath CM (May 2000). "Collaboration of signal transducer and activator of transcription 1 (STAT1) and BRCA1 in differential regulation of IFN-gamma target genes". Proc. Natl. Acad. Sci. U.S.A.97 (10): 5208''13. doi:10.1073/pnas.080469697. PMC 25807. PMID 10792030. ^Cable PL, Wilson CA, Calzone FJ, Rauscher FJ, Scully R, Livingston DM, Li L, Blackwell CB, Futreal PA, Afshari CA (October 2003). "Novel consensus DNA-binding sequence for BRCA1 protein complexes". Mol. Carcinog.38 (2): 85''96. doi:10.1002/mc.10148. PMID 14502648. ^Zhang H, Wang Q, Kajino K, Greene MI (May 2000). "VCP, a weak ATPase involved in multiple cellular events, interacts physically with BRCA1 in the nucleus of living cells". DNA Cell Biol.19 (5): 253''63. doi:10.1089/10445490050021168. PMID 10855792. ^Ganesan S, Silver DP, Drapkin R, Greenberg R, Feunteun J, Livingston DM (January 2004). "Association of BRCA1 with the inactive X chromosome and XIST RNA". Philos. Trans. R. Soc. Lond., B, Biol. Sci.359 (1441): 123''8. doi:10.1098/rstb.2003.1371. PMC 1693294. PMID 15065664. ^Ganesan S, Silver DP, Greenberg RA, Avni D, Drapkin R, Miron A, Mok SC, Randrianarison V, Brodie S, Salstrom J, Rasmussen TP, Klimke A, Marrese C, Marahrens Y, Deng CX, Feunteun J, Livingston DM (November 2002). "BRCA1 supports XIST RNA concentration on the inactive X chromosome". Cell111 (3): 393''405. doi:10.1016/S0092-8674(02)01052-8. PMID 12419249. ^Zheng L, Pan H, Li S, Flesken-Nikitin A, Chen PL, Boyer TG, Lee WH (October 2000). "Sequence-specific transcriptional corepressor function for BRCA1 through a novel zinc finger protein, ZBRK1". Mol. Cell6 (4): 757''68. doi:10.1016/S1097-2765(00)00075-7. PMID 11090615. External linksPDB gallery
1jm7: Solution structure of the BRCA1/BARD1 RING-domain heterodimer
1jnx: Crystal structure of the BRCT repeat region from the breast cancer associated protein, BRCA1
1n5o: Structural consequences of a cancer-causing BRCA1-BRCT missense mutation
1oqa: Solution structure of the BRCT-c domain from human BRCA1
1t15: Crystal Structure of the Brca1 BRCT Domains in Complex with the Phosphorylated Interacting Region from Bach1 Helicase
1t29: Crystal structure of the BRCA1 BRCT repeats bound to a phosphorylated BACH1 peptide
1t2u: Structural basis of phosphopeptide recognition by the BRCT domain of BRCA1: structure of BRCA1 missense variant V1809F
1t2v: Structural basis of phospho-peptide recognition by the BRCT domain of BRCA1, structure with phosphopeptide
1y98: Structure of the BRCT repeats of BRCA1 bound to a CtIP phosphopeptide.
Wed, 15 May 2013 11:21
BRCA2 (breast cancer type 2 susceptibility protein) is a protein found inside cells. In humans it is encoded by the geneBRCA2.BRCA2 belongs to the tumor suppressor gene family, and orthologs have been identified in most mammals for which complete genome data are available. The protein encoded by this gene is involved in the repair of chromosomal damage with an important role in the error-free repair of DNA double strand breaks.
The BRCA2 gene is located on the long (q) arm of chromosome 13 at position 12.3 (13q12.3). The human reference BRCA 2 gene contains 27 exons, and the cDNA has 10,254 base pairs coding for a protein of 3418 amino acids.
The gene was first cloned by scientists at Myriad Genetics, Endo Recherche, Inc., HSC Research & Development Limited Partnership, and University of Pennsylvania.
Methods to diagnose the likelihood of a patient with these mutations getting cancer were covered by patents owned or controlled by Myriad Genetics. Myriad's business model of exclusively offering the diagnostic test led from Myriad being a startup in 1994 to being a publicly traded company with 1200 employees and about $500M in annual revenue in 2012; it also led to controversy over high prices and the inability to get second opinions from other diagnostic labs, which in turn led to the landmark Association for Molecular Pathology v. Myriad Genetics lawsuit.
FunctionAlthough the structures of the BRCA1 and BRCA2 genes are very different, at least some functions are interrelated. The proteins made by both genes are essential for repairing damaged DNA. BRCA2 binds the single strand DNA and directly interacts with the recombinase RAD51 to stimulate strand invasion a vital step of homologous recombination. The localization of RAD51 to the DNA double-strand break requires the formation of BRCA1-PALB2-BRCA2 complex. PALB2 (Partner and localizer of BRCA2) can function synergistically with a BRCA2 chimera (termed piccolo, or piBRCA2) to further promote strand invasion. These breaks can be caused by natural and medical radiation or other environmental exposures, but also occur when chromosomes exchange genetic material during a special type of cell division that creates sperm and eggs (meiosis). Double strand breaks are also generated during repair of DNA cross links. By repairing DNA, these proteins play a role in maintaining the stability of the human genome and prevent dangerous gene rearrangements that can lead to hematologic and other cancers.
Like BRCA1, BRCA2 probably regulates the activity of other genes and plays a critical role in embryo development.
Clinical significanceCertain variations of the BRCA2 gene increase risks for breast cancer as part of a hereditary breast-ovarian cancer syndrome. Researchers have identified hundreds of mutations in the BRCA2 gene, many of which cause an increased risk of cancer. BRCA2 mutations are usually insertions or deletions of a small number of DNA base pairs in the gene. As a result of these mutations, the protein product of the BRCA2 gene is abnormal and does not function properly. Researchers believe that the defective BRCA2 protein is unable to help fix mutations that occur in other genes. As a result, mutations build up and can cause cells to divide in an uncontrolled way and form a tumor.
People who have two mutated copies of the BRCA2 gene have one type of Fanconi anemia. This condition is caused by extremely reduced levels of the BRCA2 protein in cells, which allows the accumulation of damaged DNA. Patients with Fanconi anemia are prone to several types of leukemia (a type of blood cell cancer); solid tumors, particularly of the head, neck, skin, and reproductive organs; and bone marrow suppression (reduced blood cell production that leads to anemia). A pathogenic mutation almost anywhere in a model pathway for DNA double strand break repair containing BRCA1 and BRCA2 greatly increases the risks for a subgroup of lymphomas and leukemia.
In addition to breast cancer in men and women, mutations in BRCA2 also lead to an increased risk of ovarian, Fallopian tube, prostate, and pancreatic cancers, as well as malignant melanoma. In some studies, mutations in the central part of the gene have been associated with a higher risk of ovarian cancer and a lower risk of prostate cancer than mutations in other parts of the gene. Several other types of cancer have also been seen in certain families with BRCA2 mutations.
In general, strongly inherited gene mutations (including mutations in BRCA2) account for only 5-10% of breast cancer cases; the specific risk of getting breast or other cancer for anyone carrying a BRCA2 mutation depends on many factors.
HistoryGerm line BRCA2 mutations and founder effectAll germ line BRCA2 mutations identified to date have been inherited, suggesting the possibility of a large ''founder'' effect in which a certain mutation is common to a well-defined population group and can theoretically be traced back to a common ancestor. Given the complexity of mutation screening for BRCA2, these common mutations may simplify the methods required for mutation screening in certain populations. Analysis of mutations that occur with high frequency also permits the study of their clinical expression. A striking example of a founder mutation is found in Iceland, where a single BRCA2 (999del5) mutation accounts for virtually all breast/ovarian cancer families. This frame-shift mutation leads to a highly truncated protein product. In a large study examining hundreds of cancer and control individuals, this 999del5 mutation was found in 0.6% of the general population. Of note, while 72% of patients who were found to be carriers had a moderate or strong family history of breast cancer, 28% had little or no family history of the disease. This strongly suggests the presence of modifying genes that affect the phenotypic expression of this mutation, or possibly the interaction of the BRCA2 mutation with environmental factors. Additional examples of founder mutations in BRCA2 are given in the table below.
Population or subgroupBRCA2 mutation(s)Reference(s)Ashkenazi Jewish6174delTDutch5579insAFinns8555T>G, 999del5, IVS23-2A>GFrench Canadians8765delAGGermansC61GHungarians9326insAIcelandics999del5Italians8765delAGNorthern Irish6503delTTPakistanis3337C>TScottish6503delTTSloveniansIVS16-2A>GSpanish3034delAAAC(codon936), 9254del5Swedish4486delGInteractionsBRCA2 has been shown to interact with
BRE,BARD1,BCCIP,BRCA1,BRCC3,BUB1B,CREB-binding protein,C11orf30,FANCD2,FANCG,FLNA,HMG20B,P53,PALB2,PCAF,PLK1,RAD51,RPA1,SHFM1 andSMAD3.Domain architectureBRCA2 contains a number of 39 amino acidrepeats that are critical for binding to RAD51 (a key protein in DNA recombinational repair) and resistance to methyl methanesulphonate treatment.
The BRCA2 helical domain adopts a helical structure, consisting of a four-helix cluster core (alpha 1, alpha 8, alpha 9, alpha 10) and two successive beta-hairpins (beta 1 to beta 4). An approximately 50-amino acid segment that contains four short helices (alpha 2 to alpha 4), meanders around the surface of the core structure. In BRCA2, the alpha 9 and alpha 10 helices pack with the BRCA2 OB1 domain through van der Waals contacts involving hydrophobic and aromatic residues, and also through side-chain and backbone hydrogen bonds. This domain binds the 70-amino acid DSS1 (deleted in split-hand/split foot syndrome) protein, which was originally identified as one of three genes that map to a 1.5-Mb locusdeleted in an inherited developmental malformation syndrome.
The BRCA OB1 domain assumes an OB fold, which consists of a highly curved five-stranded beta-sheet that closes on itself to form a beta-barrel. OB1 has a shallow groove formed by one face of the curved sheet and is demarcated by two loops, one between beta 1 and beta 2 and another between beta 4 and beta 5, which allows for weak single strand DNA binding. The domain also binds the 70-amino acid DSS1 (deleted in split-hand/split foot syndrome) protein.
The BRCA OB3 domain assumes an OB fold, which consists of a highly curved five-stranded beta-sheet that closes on itself to form a beta-barrel. OB3 has a pronounced groove formed by one face of the curved sheet and is demarcated by two loops, one between beta 1 and beta 2 and another between beta 4 and beta 5, which allows for strong ssDNAbinding.
The Tower domain adopts a secondary structure consisting of a pair of long, antiparallelalpha-helices (the stem) that support a three-helix bundle (3HB) at their end. The 3HB contains a helix-turn-helix motif and is similar to the DNA bindingdomains of the bacterial site-specific recombinases, and of eukaryoticMyb and homeodomaintranscription factors. The Tower domain has an important role in the tumour suppressor function of BRCA2, and is essential for appropriate binding of BRCA2 to DNA.
Patents, enforcement, litigation, and controversyA patent application for the isolated BRCA1 gene and cancer-cancer promoting mutations, as well as methods to diagnose the likelihood of getting breast cancer, was filed by the University of Utah, National Institute of Environmental Health Sciences (NIEHS) and Myriad Genetics in 1994; over the next year, Myriad, in collaboration with other investigators, isolated and sequenced the BRCA2 gene and identified relevant mutations, and the first BRCA2 patent was filed in the U.S. by Myriad and the other institutions in 1995. Myriad is the exclusive licensee of these patents and has enforced them in the US against clinical diagnostic labs. This business model led from Myriad being a startup in 1994 to being a publicly traded company with 1200 employees and about $500M in annual revenue in 2012; it also led to controversy over high prices and the inability to get second opinions from other diagnostic labs, which in turn led to the landmark Association for Molecular Pathology v. Myriad Genetics lawsuit. The patents begin to expire in 2014.
According to an article published in the journal, Genetic Medicine, in 2010, "The patent story outside the United States is more complicated.... For example, patents have been obtained but the patents are being ignored by provincial health systems in Canada. In Australia and the UK, Myriad's licensee permitted use by health systems, but announced a change of plans in August 2008. ... Only a single mutation has been patented in Myriad's lone European-wide patent, although some patents remain under review of an opposition proceeding. In effect, the United States is the only jurisdiction where Myriad's strong patent position has conferred sole-provide status." Peter Meldrum, CEO of Myriad Genetics, has acknowledged that Myriad has "other competitive advantages that may make such [patent] enforcement unnecessary" in Europe.
Legal decisions surrounding the BRCA1 and BRCA2 patents will affect the field of genetic testing in general.
See alsoReferences^ abcWooster R, Neuhausen SL, Mangion J, Quirk Y, Ford D, Collins N, Nguyen K, Seal S, Tran T, Averill D, et al (September 1994). "Localization of a breast cancer susceptibility gene, BRCA2, to chromosome 13q12-13". Science265 (5181): 2088''90. doi:10.1126/science.8091231. PMID 8091231. ^Duncan JA, Reeves JR, Cooke TG (October 1998). "BRCA1 and BRCA2 proteins: roles in health and disease". Molecular pathology : MP51 (5): 237''47. doi:10.1136/mp.51.5.237. PMC 395646. PMID 10193517. ^Yoshida K, Miki Y (November 2004). "Role of BRCA1 and BRCA2 as regulators of DNA repair, transcription, and cell cycle in response to DNA damage". Cancer science95 (11): 866''71. doi:10.1111/j.1349-7006.2004.tb02195.x. PMID 15546503. ^"OrthoMaM phylogenetic marker: BRCA2 coding sequence". ^ abFriedenson B (2008-06-08). "Breast cancer genes protect against some leukemias and lymphomas" (video). SciVee. ^"BRCA2 breast cancer 2, early onset [Homo sapiens]". EntrezGene. National Center for Biotechnology Information, U.S. National Library of Medicine. ^"Breast cancer type 2 susceptibility protein - Homo sapiens (Human)". P51587. UniProt. ^Williams-Jones B (2002). Genetic testing for sale: Implications of commercial brca testing in Canada (Ph.D.). The University of British Columbia.^ abcUS patent 5837492, Tavtigian SV, Kamb A, Simard J, Couch F, Rommens JM, Weber BL, "Chromosome 13-linked breast cancer susceptibility gene", issued 1998-11-17, assigned to Myriad Genetics, Inc., Endo Recherche, Inc., HSC Research & Development Limited Partnership, Trustees of the University of Pennsylvaina ^ abUS patent 5747282, Skolnick HS, Goldgar DE, Miki Y, Swenson J, Kamb A, Harshman KD, Shattuck-Eidens DM, Tavtigian SV, Wiseman RW, Futreal PA, "7Q-linked breast and ovarian cancer susceptibility gene", issued 1998-05-05, assigned to Myraid Genetics, Inc., The United States of America as represented by the Secretary of Health and Human Services, and University of Utah Research Foundation ^ abMyriad Investor Page'--see "Myriad at a glance" accessed October 2012^ abcSchwartz J (2009-05-12). "Cancer Patients Challenge the Patenting of a Gene". Health. New York Times. ^ abXia B, Sheng Q, Nakanishi K, Ohashi A, Wu J, Christ N, Liu X, Jasin M, Couch FJ, Livingston DM (June 2006). "Control of BRCA2 cellular and clinical functions by a nuclear partner, PALB2". Mol. Cell22 (6): 719''29. doi:10.1016/j.molcel.2006.05.022. PMID 16793542. ^Buisson R, Dion-C´t(C) A.M, et al. (2010). "Cooperation of breast cancer proteins PALB2 and piccolo BRCA2 in stimulating homologous recombination.". Nature Structural & molecular biology17 (10): 1247''54. doi:10.1038/nsmb.1915. PMID 20871615. ^"High-Penetrance Breast and/or Ovarian Cancer Susceptibility Genes". National Cancer Institute. Retrieved 7 December 2012. ^High-Impact Science: Tracking down the BRCA genes (Part 2) - Cancer Research UK science blog, 2012^Route information board^ abLacroix M, Leclercq G (2005). "The "portrait" of hereditary breast cancer". Breast Cancer Research and Treatment89 (3): 297''304. doi:10.1007/s10549-004-2172-4. PMID 15754129. ^ abThorlacius S, Olafsdottir G, Tryggvadottir L, Neuhausen S, Jonasson JG, Tavtigian SV, Tulinius H, Ogmundsdottir HM, Eyfjord JE (1996). "A single BRCA2 mutation in male and female breast cancer families from Iceland with varied cancer phenotypes". Nature Genetics13 (1): 117''119. doi:10.1038/ng0596-117. PMID 8673089. ^ abThorlacius S, Sigurdsson S, Bjarnadottir H, Olafsdottir G, Jonasson JG, Tryggvadottir L, Tulinius H, Eyfjord JE (1997). "Study of a single BRCA2 mutation with high carrier frequency in a small population". American Journal of Human Genetics60 (5): 1079''1085. PMC 1712443. PMID 9150155. ^den Dunnen JT, Antonarakis, SE. (2000). "Mutation nomenclature extensions and suggestions to describe complex mutations: a discussion.". Human Mutation15 (1): 7''12. doi:10.1002/(SICI)1098-1004(200001)15:13.0.CO;2-N. PMID 10612815. ^Neuhausen S, Gilewski T, Norton L, Tran T, McGuire P, Swensen J, Hampel H, Borgen P, Brown K, Skolnick M, Shattuck-Eidens D, Jhanwar S, Goldgar D, Offit K (1996). "Recurrent BRCA2 6174delT mutations in Ashkenazi Jewish women affected by breast cancer". Nature Genetics13 (1): 126''128. doi:10.1038/ng0596-126. PMID 8673092. ^Verhoog LC, van den Ouweland AM, Berns E, van Veghel-Plandsoen MM, van Staveren IL, Wagner A, Bartels CC, Tilanus-Linthorst MM, Devilee P, Seynaeve C, Halley DJ, Niermeijer MF, Klijn JG, Meijers-Heijboer H (2001). "Large regional differences in the frequency of distinct BRCA1/BRCA2 mutations in 517 Dutch breast and/or ovarian cancer families". European Journal of Cancer37 (16): 2082''2090. doi:10.1016/S0959-8049(01)00244-1. PMID 11597388. ^Huusko P, P¤¤kk¶nen K, Launonen V, Poyhonen M, Blanco G, Kauppila A, Puistola U, Kiviniemi H, Kujala M, Leisti J, Winqvist R (1998). "Evidence of founder mutations in Finnish BRCA1 and BRCA2 families". American Journal of Human Genetics62 (6): 1544''1548. doi:10.1086/301880. PMC 1377159. PMID 9585608. ^P¤¤kk¶nen K, Sauramo S, Sarantaus L, Vahteristo P, Hartikainen A, Vehmanen P, Ignatius J, Ollikainen V, Kaariainen H, Vauramo E, Nevanlinna H, Krahe R, Holli K, Kere J (2001). "Involvement of BRCA1 and BRCA2 in breast cancer in a western Finnish sub-population". Genetic Epidemiology20 (2): 239''246. doi:10.1002/1098-2272(200102)20:23.0.CO;2-Y. PMID 11180449. ^Tonin PN, Mes-Masson AM, Narod SA, Ghadirian P, Provencher D (1999). "Founder BRCA1 and BRCA2 mutations in French Canadian ovarian cancer cases unselected for family history". Clinical Genetics55 (5): 318''324. doi:10.1034/j.1399-0004.1999.550504.x. PMID 10422801. ^Backe, J; Hofferbert, S; Skawran, B; Dork, T; Stuhrmann, M; Karstens, JH; Untch, M; Meindl, A; Burgemeister, R; Chang-Claude, J; Weber, BH. (1999). "Frequency of BRCA1 mutation 5382insC in German breast cancer patients". Gynecologic Oncology72: 402 '' 406. PMID 10053113. ^Van Der Looij M, Szabo C, Besznyak I, Liszka G, Csokay B, Pulay T, Toth J, Devilee P, King MC, Olah E (2000). "Prevalence of founder BRCA1 and BRCA2 mutations among breast and ovarian cancer patients in Hungary". International Journal of Cancer86 (5): 737''740. doi:10.1002/(SICI)1097-0215(20000601)86:53.0.CO;2-1. PMID 10797299. ^Pisano M, Cossu A, Persico I, Palmieri G, Angius A, Casu G, Palomba G, Sarobba MG, Rocca PC, Dedola MF, Olmeo N, Pasca A, Budroni M, Marras V, Pisano A, Farris A, Massarelli G, Pirastu M, Tanda F (2000). "Identification of a founder BRCA2 mutation in Sardinia". British Journal of Cancer82 (3): 553''559. doi:10.1054/bjoc.1999.0963. PMC 2363305. PMID 10682665. ^ abScottish/Northern Irish BRCAI/BRCA2 Consortium (2003). "BRCA1 and BRCA2 mutations in Scotland and Northern Ireland". British Journal of Cancer88 (8): 1256''1262. doi:10.1038/sj.bjc.6600840. PMC 2747571. PMID 12698193. ^Liede A, Malik IA, Aziz Z, Rios PD, Kwan E, Narod, SA (2002). "Contribution of BRCA1 and BRCA2 mutations to breast and ovarian cancer in Pakistan". American Journal of Human Genetics71 (3): 595''606. doi:10.1086/342506. PMC 379195. PMID 12181777. ^Krajc M, De Greve J, Goelen G, Teugels E (2002). "BRCA2 founder mutation in Slovenian breast cancer families". European Journal of Human Genetics10 (12): 879''882. doi:10.1038/sj.ejhg.5200886. PMID 12461697. ^Osorio A, Robledo M, Martinez B, Cebrian A, San Roman JM, Albertos J, Lobo F, Benitez J (1998). "Molecular analysis of the BRCA2 gene in 16 breast/ovarian cancer Spanish families". Clinical Genetics54 (7): 142''147. doi:10.1054/bjoc.1999.1089. PMC 2374482. PMID 10755399. ^Neuhausen SL (2000). "Founder populations and their uses for breast cancer genetics". Cancer Research2 (2): 77''81. doi:10.1186/bcr36. PMC 139426. PMID 11250694. ^ abcdefDong Y, Hakimi Mohamed-Ali, Chen Xiaowei, Kumaraswamy Easwari, Cooch Neil S, Godwin Andrew K, Shiekhattar Ramin (November 2003). "Regulation of BRCC, a holoenzyme complex containing BRCA1 and BRCA2, by a signalosome-like subunit and its role in DNA repair". Mol. Cell12 (5): 1087''99. doi:10.1016/S1097-2765(03)00424-6. PMID 14636569. ^Ryser S, Dizin Eva, Jefford Charles Edward, Delaval B(C)n(C)dicte, Gagos Sarantis, Christodoulidou Agni, Krause Karl-Heinz, Birnbaum Daniel, Irminger-Finger Irmgard (February 2009). "Distinct roles of BARD1 isoforms in mitosis: full-length BARD1 mediates Aurora B degradation, cancer-associated BARD1beta scaffolds Aurora B and BRCA2". Cancer Res.69 (3): 1125''34. doi:10.1158/0008-5472.CAN-08-2134. PMID 19176389. ^ abLiu J, Yuan Y, Huan J, Shen Z (January 2001). "Inhibition of breast and brain cancer cell growth by BCCIPalpha, an evolutionarily conserved nuclear protein that interacts with BRCA2". Oncogene20 (3): 336''45. doi:10.1038/sj.onc.1204098. PMID 11313963. ^ abSarkisian CJ, Master S R, Huber L J, Ha S I, Chodosh L A (October 2001). "Analysis of murine Brca2 reveals conservation of protein-protein interactions but differences in nuclear localization signals". J. Biol. Chem.276 (40): 37640''8. doi:10.1074/jbc.M106281200. PMID 11477095. ^ abChen J, Silver D P, Walpita D, Cantor S B, Gazdar A F, Tomlinson G, Couch F J, Weber B L, Ashley T, Livingston D M, Scully R (September 1998). "Stable interaction between the products of the BRCA1 and BRCA2 tumor suppressor genes in mitotic and meiotic cells". Mol. Cell2 (3): 317''28. doi:10.1016/S1097-2765(00)80276-2. PMID 9774970. ^Reuter TY, Medhurst Annette L, Waisfisz Quinten, Zhi Yu, Herterich Sabine, Hoehn Holger, Gross Hans J, Joenje Hans, Hoatlin Maureen E, Mathew Christopher G, Huber Pia A J (October 2003). "Yeast two-hybrid screens imply involvement of Fanconi anemia proteins in transcription regulation, cell signaling, oxidative metabolism, and cellular transport". Exp. Cell Res.289 (2): 211''21. doi:10.1016/S0014-4827(03)00261-1. PMID 14499622. ^Futamura M, Arakawa H, Matsuda K, Katagiri T, Saji S, Miki Y, Nakamura Y (March 2000). "Potential role of BRCA2 in a mitotic checkpoint after phosphorylation by hBUBR1". Cancer Res.60 (6): 1531''5. PMID 10749118. ^Siddique H, Rao VN, Reddy ES (August 2009). "CBP-mediated post-translational N-glycosylation of BRCA2". Int J Oncol.35 (2): 16387''91. PMID 19578754. ^Hughes-Davies L, Huntsman David, Ruas Margarida, Fuks Francois, Bye Jacqueline, Chin Suet-Feung, Milner Jonathon, Brown Lindsay A, Hsu Forrest, Gilks Blake, Nielsen Torsten, Schulzer Michael, Chia Stephen, Ragaz Joseph, Cahn Anthony, Linger Lori, Ozdag Hilal, Cattaneo Elena, Jordanova E S, Schuuring Edward, Yu David S, Venkitaraman Ashok, Ponder Bruce, Doherty Aidan, Aparicio Samuel, Bentley David, Theillet Charles, Ponting Chris P, Caldas Carlos, Kouzarides Tony (November 2003). "EMSY links the BRCA2 pathway to sporadic breast and ovarian cancer". Cell115 (5): 523''35. doi:10.1016/S0092-8674(03)00930-9. PMID 14651845. ^Wang XZ, Andreassen Paul R, D'Andrea Alan D (July 2004). "Functional interaction of monoubiquitinated FANCD2 and BRCA2/FANCD1 in chromatin". Mol. Cell. Biol.24 (13): 5850''62. doi:10.1128/MCB.24.13.5850-5862.2004. PMC 480901. PMID 15199141. ^Hussain S, Wilson James B, Medhurst Annette L, Hejna James, Witt Emily, Ananth Sahana, Davies Adelina, Masson Jean-Yves, Moses Robb, West Stephen C, de Winter Johan P, Ashworth Alan, Jones Nigel J, Mathew Christopher G (June 2004). "Direct interaction of FANCD2 with BRCA2 in DNA damage response pathways". Hum. Mol. Genet.13 (12): 1241''8. doi:10.1093/hmg/ddh135. PMID 15115758. ^Hejna J, Holtorf Megan, Hines Jennie, Mathewson Lauren, Hemphill Aaron, Al-Dhalimy Muhsen, Olson Susan B, Moses Robb E (April 2008). "Tip60 is required for DNA interstrand cross-link repair in the Fanconi anemia pathway". J. Biol. Chem.283 (15): 9844''51. doi:10.1074/jbc.M709076200. PMC 2398728. PMID 18263878. ^Hussain S, Witt Emily, Huber Pia A J, Medhurst Annette L, Ashworth Alan, Mathew Christopher G (October 2003). "Direct interaction of the Fanconi anaemia protein FANCG with BRCA2/FANCD1". Hum. Mol. Genet.12 (19): 2503''10. doi:10.1093/hmg/ddg266. PMID 12915460. ^Yuan Y, Shen Z (December 2001). "Interaction with BRCA2 suggests a role for filamin-1 (hsFLNa) in DNA damage response". J. Biol. Chem.276 (51): 48318''24. doi:10.1074/jbc.M102557200. PMID 11602572. ^Marmorstein LY, Kinev A V, Chan G K, Bochar D A, Beniya H, Epstein J A, Yen T J, Shiekhattar R (January 2001). "A human BRCA2 complex containing a structural DNA binding component influences cell cycle progression". Cell104 (2): 247''57. doi:10.1016/S0092-8674(01)00209-4. PMID 11207365. ^Hakimi M-A, Bochar Daniel A, Chenoweth Josh, Lane William S, Mandel Gail, Shiekhattar Ramin (May. 2002). "A core-BRAF35 complex containing histone deacetylase mediates repression of neuronal-specific genes". Proc. Natl. Acad. Sci. U.S.A.99 (11): 7420''5. doi:10.1073/pnas.112008599. PMC 124246. PMID 12032298. ^ abcMarmorstein LY, Ouchi T, Aaronson S A (November 1998). "The BRCA2 gene product functionally interacts with p53 and RAD51". Proc. Natl. Acad. Sci. U.S.A.95 (23): 13869''74. doi:10.1073/pnas.95.23.13869. PMC 24938. PMID 9811893. ^"Entrez Gene: PALB2 partner and localizer of BRCA2". ^ abcLin H-R, Ting Nicholas S Y, Qin Jun, Lee Wen-Hwa (September 2003). "M phase-specific phosphorylation of BRCA2 by Polo-like kinase 1 correlates with the dissociation of the BRCA2-P/CAF complex". J. Biol. Chem.278 (38): 35979''87. doi:10.1074/jbc.M210659200. PMID 12815053. ^Fuks F, Milner J, Kouzarides T (November 1998). "BRCA2 associates with acetyltransferase activity when bound to P/CAF". Oncogene17 (19): 2531''4. doi:10.1038/sj.onc.1202475. PMID 9824164. ^Lee MY, Daniels Matthew J, Venkitaraman Ashok R (January 2004). "Phosphorylation of BRCA2 by the Polo-like kinase Plk1 is regulated by DNA damage and mitotic progression". Oncogene23 (4): 865''72. doi:10.1038/sj.onc.1207223. PMID 14647413. ^Sharan SK, Morimatsu M, Albrecht U, Lim D S, Regel E, Dinh C, Sands A, Eichele G, Hasty P, Bradley A (April 1997). "Embryonic lethality and radiation hypersensitivity mediated by Rad51 in mice lacking Brca2". Nature386 (6627): 804''10. doi:10.1038/386804a0. PMID 9126738. ^Yu DS, Sonoda Eiichiro, Takeda Shunichi, Huang Christopher L H, Pellegrini Luca, Blundell Tom L, Venkitaraman Ashok R (October 2003). "Dynamic control of Rad51 recombinase by self-association and interaction with BRCA2". Mol. Cell12 (4): 1029''41. doi:10.1016/S1097-2765(03)00394-0. PMID 14580352. ^ abChen PL, Chen C F, Chen Y, Xiao J, Sharp Z D, Lee W H (April 1998). "The BRC repeats in BRCA2 are critical for RAD51 binding and resistance to methyl methanesulfonate treatment". Proc. Natl. Acad. Sci. U.S.A.95 (9): 5287''92. doi:10.1073/pnas.95.9.5287. PMC 20253. PMID 9560268. ^ abWong AK, Pero R, Ormonde P A, Tavtigian S V, Bartel P L (December 1997). "RAD51 interacts with the evolutionarily conserved BRC motifs in the human breast cancer susceptibility gene brca2". J. Biol. Chem.272 (51): 31941''4. doi:10.1074/jbc.272.51.31941. PMID 9405383. ^Katagiri T, Saito H, Shinohara A, Ogawa H, Kamada N, Nakamura Y, Miki Y (March 1998). "Multiple possible sites of BRCA2 interacting with DNA repair protein RAD51". Genes Chromosomes Cancer21 (3): 217''22. doi:10.1002/(SICI)1098-2264(199803)21:33.0.CO;2-2. PMID 9523196. ^Pellegrini L, Yu David S, Lo Thomas, Anand Shubha, Lee MiYoung, Blundell Tom L, Venkitaraman Ashok R (November 2002). "Insights into DNA recombination from the structure of a RAD51-BRCA2 complex". Nature420 (6913): 287''93. doi:10.1038/nature01230. PMID 12442171. ^Tarsounas M, Davies Adelina A, West Stephen C (January 2004). "RAD51 localization and activation following DNA damage". Philos. Trans. R. Soc. Lond., B, Biol. Sci.359 (1441): 87''93. doi:10.1098/rstb.2003.1368. PMC 1693300. PMID 15065660. ^Wong JMS, Ionescu Daniela, Ingles C James (January 2003). "Interaction between BRCA2 and replication protein A is compromised by a cancer-predisposing mutation in BRCA2". Oncogene22 (1): 28''33. doi:10.1038/sj.onc.1206071. PMID 12527904. ^Marston NJ, Richards W J, Hughes D, Bertwistle D, Marshall C J, Ashworth A (July 1999). "Interaction between the product of the breast cancer susceptibility gene BRCA2 and DSS1, a protein functionally conserved from yeast to mammals". Mol. Cell. Biol.19 (7): 4633''42. PMC 84261. PMID 10373512. ^ abcdeYang H, Jeffrey Philip D, Miller Julie, Kinnucan Elspeth, Sun Yutong, Thoma Nicolas H, Zheng Ning, Chen Phang-Lang, Lee Wen-Hwa, Pavletich Nikola P (September 2002). "BRCA2 function in DNA binding and recombination from a BRCA2-DSS1-ssDNA structure". Science297 (5588): 1837''48. doi:10.1126/science.297.5588.1837. PMID 12228710. ^Preobrazhenska O, Yakymovych Mariya, Kanamoto Takashi, Yakymovych Ihor, Stoika Rostyslav, Heldin Carl-Henrik, Souchelnytskyi Serhiy (August 2002). "BRCA2 and Smad3 synergize in regulation of gene transcription". Oncogene21 (36): 5660''4. doi:10.1038/sj.onc.1205732. PMID 12165866. ^Bork P, Blomberg N, Nilges M (May 1996). "Internal repeats in the BRCA2 protein sequence". Nat. Genet.13 (1): 22'¬''3. doi:10.1038/ng0596-22. PMID 8673099. ^"ACLU sues over patents on breast cancer genes". CNN. Archived from the original on 15 May 2009. Retrieved 2009-05-14. ^Robert Cook-Deegan, MD et al (2010) Impact of Gene Patents and Licensing Practices on Access to Genetic Testing for Inherited Susceptibility to Cancer: Comparing Breast and Ovarian Cancers to Colon Cancers: Patents and Licensing for Breast, Ovarian and Colon Cancer Testing Genet Med.12(4 Suppl): S15''S38.^Benowitz S (January 2003). "European groups oppose Myriad's latest patent on BRCA1". J. Natl. Cancer Inst.95 (1): 8''9. doi:10.1093/jnci/95.1.8. PMID 12509391. ^Conley J, Vorhous D, Cook-Deegan J (2011-03-01). "How Will Myriad Respond to the Next Generation of BRCA Testing?". Robinson, Bradshaw, and Hinson. Retrieved 2012-12-09. ^"Genetics and Patenting". Human Genome Project Information. U.S. Department of Energy Genome Programs. 2010-07-07. Further readingZou JP, Hirose Y, Siddique H, Rao VN, Reddy ES (1999). "Structure and expression of variant BRCA2a lacking the transactivation domain". Oncology reports6 (2): 437''40. PMID 10023017. Venkitaraman AR (2001). "Chromosome stability, DNA recombination and the BRCA2 tumour suppressor". Curr. Opin. Cell Biol.13 (3): 338''43. doi:10.1016/S0955-0674(00)00217-9. PMID 11343905. Orelli BJ, Bishop DK (2001). "BRCA2 and homologous recombination". Breast Cancer Res.3 (5): 294''8. doi:10.1186/bcr310. PMC 138691. PMID 11597317. Daniel DC (2002). "Highlight: BRCA1 and BRCA2 proteins in breast cancer". Microsc. Res. Tech.59 (1): 68''83. doi:10.1002/jemt.10178. PMID 12242698. Tutt A, Ashworth A (2003). "The relationship between the roles of BRCA genes in DNA repair and cancer predisposition". Trends in molecular medicine8 (12): 571''6. doi:10.1016/S1471-4914(02)02434-6. PMID 12470990. Gon§alves A, Viens P, Sobol H, et al. (2005). "[Molecular alterations in breast cancer: clinical implications and new analytical tools]". La Revue de m(C)decine interne / fond(C)e ... Par la Soci(C)t(C) nationale francaise de m(C)decine interne26 (6): 470''8. doi:10.1016/j.revmed.2004.11.012. PMID 15936476. Hay T, Clarke AR (2005). "DNA damage hypersensitivity in cells lacking BRCA2: a review of in vitro and in vivo data". Biochem. Soc. Trans.33 (Pt 4): 715''7. doi:10.1042/BST0330715. PMID 16042582. Domchek SM, Weber BL (2006). "Clinical management of BRCA1 and BRCA2 mutation carriers". Oncogene25 (43): 5825''31. doi:10.1038/sj.onc.1209881. PMID 16998496. Honrado E, Osorio A, Palacios J, Benitez J (2006). "Pathology and gene expression of hereditary breast tumors associated with BRCA1, BRCA2 and CHEK2 gene mutations". Oncogene25 (43): 5837''45. doi:10.1038/sj.onc.1209875. PMID 16998498. External linksPDB gallery
1n0w: Crystal structure of a RAD51-BRCA2 BRC repeat complex
This article incorporates text from the public domainPfam and InterProIPR002093
This article incorporates text from the public domainPfam and InterProIPR015252
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This article incorporates text from the public domainPfam and InterProIPR015205
Wed, 15 May 2013 11:20
In an article in the New York Times today, My Medical Choice, Angelina Jolie promised to share some background about her medical treatment with women seeking more information about BRCA gene mutations and what it might mean for them.
This blog describes the main stages of her treatment. It is important to emphasize that each woman's case is different. Surgery will not necessarily be the right choice for everyone, and there are alternatives available. As Angelina says in her article, the important thing is to be aware of your options.
STAGE 1. Gathering Data and Information
BRCA stands for BReast CAncer. BRCA genes help you fight cancer when it happens in your body. But some families carry mutated or broken BRCA genes that can be passed down from one generation to the next. Approximately 5-10% of all breast cancers and 14% of ovarian cancers occur from a BRCA1 or BRCA2 genetic mutation that is inherited from either parent.Women carrying BRCA1 or BRCA2 gene mutations have up to an 87% lifetime chance of breast cancer and 54% chance of ovarian cancer vs. a general population risk of 12% for breast cancer and less than 1% for ovarian cancer. Prevention does not yet exist. More details about the risks of breast and ovarian cancer, including how risk changes with each decade of life, can be found in our BRCA Gene Mutations blog post.Given the high likelihood of getting breast or ovarian cancer with BRCA mutations, family history usually triggers testing for the gene. Angelina's mother had breast cancer, and sadly passed away from ovarian cancer. Her maternal grandmother was also diagnosed with ovarian cancer. This family history would certainly meet any insurance carrier's criteria to cover genetic testing. To find out if there is enough risk for you to consider a BRCA mutation genetic test, we encourage you to take our Genetics Quiz that reviews a variety of information, including your family history.STAGE 2. After diagnosis: Traveling the Road of Surveillance
We follow a standard surveillance plan at our center for BRCA mutation carriers, which I used for Angelina:
Beginning at age 18, or 10 years younger than the youngest relative with breast cancer, every 3 months, you have breast imaging or an exam. An example plan follows:
Month 10:Clinical breast exam with a breast specialistEvery month:Self breast exams (cycle days 7-10). If you don't know how to do a self breast exam, please watch our how-to video.For those who prefer twice-a-year surveillance, we combine the imaging with clinical breast exams, and meet every 6 months.
Ovarian surveillance begins at age 35, or 10 years prior to youngest relative with ovarian cancer, and includes the following:
Transvaginal Pelvic ultrasound every 6 months (cycle days 1-10)CA-125 blood marker testing every 6 months (after cycle day 5)Pelvic exam by gynecologist every 6 monthsFor additional screening details, including risk reduction strategies and holistic and integrative medicine, see our blog on BRCA Gene Mutations.
STAGE 3.Committing to an operation
When first meeting a woman newly diagnosed with a BRCA mutation, my immediate goal is to learn about her, including her family situation, whether she is in a stable relationship, and whether she is planning to have children. In the course of these discussions, it becomes clear whether the patient will proceed to a mastectomy.
STAGE 4.Preparing for the operations
The questions any patient needs to address at this stage include: (1) whether or not to preserve the nipples, (2) if so, whether or not to perform a ''nipple delay'' procedure, (3) where to place the incision, (4) whether or not to test sentinel nodes, (5) what kind of reconstruction will be done, (6) what supplements might enhance healing and recovery, and finally (7) where should we operate.
NIPPLE: Women undergoing preventive mastectomies can always consider keeping their nipples. While no one can guarantee that the nipples will survive an operation, much can be done to ensure the greatest chance of success.
NIPPLE DELAY: The delay, performed 1-2 weeks prior to the actual mastectomies, uses the planned mastectomy incision and lifts half of the skin off of the breast surface. A small disc of the tissue directly behind the nipple and areola is also removed and analyzed by a pathologist. This is done to rule out the presence of any disease directly behind the nipples, which would make preserving them a dangerous proposition. Additionally, it recruits extra blood flow to the area, lessening the chances of nipple and skin loss due to insufficient blood supply after the mastectomy. Since starting this technique in 2008, my loss of skin and nipple after mastectomy has decreased to less than 2%. In Angelina's case, she judged it worth taking this extra step of caution.
INCISION: Incision locations must take into consideration a cancer location (if cancer is present), any prior incisions, breast size reduction (if desired), and the technical skill of the surgeon (smaller incisions make for a harder and longer operation). For Angelina, her optimal incision choices were around the areola, or underneath the breast in the inframammary fold '' the latter was chosen.
SENTINEL NODE BIOPSY/PBDI: Whenever a breast contains cancer and the armpit lymph nodes cannot be felt on exam, we routinely perform a sentinel node biopsy, which is the removal of the first nodes that receive breast lymphatic drainage. By injecting blue dye into the breast, which then travels to the lymph node(s), we find out if cancer spread beyond the breast. Until now, the trend has been not to perform sentinel node biopsies in conjunction with prophylactic (preventive) mastectomies since the discovery of cancer in breasts removed prophylactically only ranges from 2-8%. Therefore, most women do not want to take the additional risks associated with a sentinel node biopsy, especially since they can have complications, such as pain, numbness, arm swelling (lymphedema), fluid buildup (seroma), limited arm movement, and infection. This dilemma has been resolved with a new technique that was pioneered at the Pink Lotus Breast Center, called Prophylactic Breast Dye Injection, or PBDI. PBDI allows the sentinel node to be identified, but not surgically removed, giving more control and peace of mind to women. I developed this technique while treating Angelina, and I hope other women will now benefit from it. It was at her friendly insistence that I wrote the rationale for it in our blog post, Prophylactic Breast Dye Injection.
RECONSTRUCTION: Reconstruction options vary depending on a number of factors. The two broad categories of reconstruction include implants and flaps. Implants are the most common reconstruction, often requiring two stages, whereby a tissue expander is placed prior to the final implant. A tissue expander is a deflated implant that goes behind the pectoral muscles and gets slowly inflated with saline over a period of 2-3 months, until the chosen volume is reached. A second operation is performed to swap the expander for the final implant (usually silicone). A different implant option can be a ''one-step'' operation, where the final implant is placed at the time of mastectomy, skipping the expander phase.
Two improvements which I believe can enhance the final outcome for those patients choosing implants include: (1) the newly FDA-approved anatomic implants, which are teardrop shaped, and (2) allograft, or synthetic sheets of material, that create a more natural look.
Autologous flaps use your own skin, fat and sometimes muscle from the abdomen, back (latissimus), thigh (gracilis), or buttock to create a potentially more natural breast reconstruction than implants can achieve. Flaps, however, create scars at the donor site, potential weakness in the donor area, and involve a longer operation than implants, with longer recovery periods and associated hospital stays.
Angelina's body type was best suited to an implant reconstruction with allograft. Although tissue expanders required an additional operation, she preferred to use them. Expanders maximize blood flow to the breast skin and nipple (because they are not fully expanded right after placement, they do not compress the tiny blood vessels in the skin), and they allow us to optimize the final implant size, location and appearance.
SUPPLEMENTS AND PREP: To prepare for and to recover from operations, patients can use a variety of supplements. Angelina followed the regimen below, written onto a calendar:
To enhance wound healing (for each operation):
A) Vitamin C: 1000mg tablets; one tablet once daily for one week before and one week after surgery.
B) Multi-Vitamin: one tablet once daily for one week before and one week after surgery.
C) Zinc: 50 mg; one tablet once daily for one week before and one week after surgery.
To reduce the risk of infection (operations 2 and 3):
D) Bactroban ointment: Applied twice a day beginning 3 days prior to surgery x 7 days.
E) Hibiclens shower: Hibiclens soap applied to upper torso and abdomen '' left on for 5 minutes, then rinsed. Applied once a day for 3 days prior to surgery.
F) Keflex: 250mg (antibiotic); one tablet 4x a day for 7 days, beginning with 2 doses the day of the operation.
To reduce postoperative nausea and vomiting (for each operation):
G) Emend: 40mg; one tablet by mouth the night before surgery
To reduce postoperative swelling and bruising (for each operation):
H) Arnica Forte (Arnica and Bromelain): two capsules daily x 7 days, beginning one day prior to surgery.
To help eliminate anesthesia from the system (for each operation):
I) Exchem: 10 drops in water or directly in the mouth twice daily, beginning the day before surgery and continuing for one week after surgery.
J) Lymphomyosat: 10 drops in water or directly in the mouth twice daily, beginning the day before surgery and continuing for one week after surgery.
To increase oxygen to the skin (operations 1 and 2):
K) Cutagenix: Applied to breast every 6 hours x 3 days. Skin care specialists use this topical cream after laser resurfacing to increase oxygen flow to the outer layers of skin. We decided in Angelina's case to apply it to the mastectomy skin to give it an oxygen boost and to help ensure adequate blood flow to her skin postoperatively.
To minimize scarring(after operation 3):
L) BioCorneum: Rubbed into scars twice a day for 12 weeks '' begin after the third operation once steri strips are removed.
Medications ''as needed'' for comfort:
Percocet: 1-2 tablets every 4-6 hours as needed for pain
Colace: 250mg twice a day
MiraLax: One tablespoon diluted in 8oz water once a day
Ativan: 1mg every 8 hours as needed for muscle spasm
Zofran: 8mg oral dissolving tablet placed on tongue every 6 hours as needed for nausea
LOCATION: Angelina chose to have her care, including her three operations, performed at the Pink Lotus Breast Center. Some people might think that a hospital is the only place to have a mastectomy. However, outpatient surgery centers provide an attractive, peaceful alternative when coupled with attentive nursing care at recovery facilities. You can learn more about our comprehensive and integrative breast center by exploring this website.
STAGE 5. Recovering from the operations
On February 2, 2013, Angelina was in the operating room for the first operation, the nipple delay. Her partner was on hand to greet her as soon as she came around from the anesthetic, as he was during each of the operations.
After the operation, her skin was slightly bruised but soon returned to normal. Two days after her procedure, great news arrived: the tissue behind both nipples came back completely normal.
On February 16 she had the main surgery, which can last up to eight hours. The mastectomies went smoothly, with sentinel nodes identified but not removed. After the mastectomies, I assisted plastic surgeon, Dr. Jay Orringer, as we performed the first stage breast reconstruction by placing tissue expanders with allograft.
To a large extent, I believe recovery reflects expectation. Angelina expected to feel well, to be active. On Monday, the pathology returned and I called Angelina to confirm our biggest hope: all of the breast tissue was benign. On day four after her mastectomies, I was pleased to find her not only in good spirits with bountiful energy, but with two walls in her house covered with freshly assembled storyboards for the next project she is directing. All the while she spoke, six drains dangled from her chest, three on each side, fastened to an elastic belt around her waist.
The next day she had her first injection of saline into the expanders, thus beginning the process that would gradually prepare the tissues for the final stage of her operations, reconstruction. Four of the six drains were removed. Four days after that, on postoperative day nine, the last two drains were removed. A second saline fill occurred on March 4. Over the next four weeks she was hard at work.
The final operation occurred on April 27, 2013, ten weeks after the mastectomies: reconstruction of the breasts with implant, which went extremely well, bringing an end to her surgical journey.
Many women unfortunately do not know that BRCA gene mutations exist and could affect them. Breast and ovarian cancers take lives every day '' knowledge and action can help prevent the premature loss of those who love us, and whom we deeply love in return.
Like Angelina, I urge women who feel they might have reason to be at risk for a BRCA gene mutation '' perhaps because of a strong family history of cancer '' to seek medical advice and to take control of their futures.
Wed, 15 May 2013 11:19
MY MOTHER fought cancer for almost a decade and died at 56. She held out long enough to meet the first of her grandchildren and to hold them in her arms. But my other children will never have the chance to know her and experience how loving and gracious she was.
We often speak of ''Mommy's mommy,'' and I find myself trying to explain the illness that took her away from us. They have asked if the same could happen to me. I have always told them not to worry, but the truth is I carry a ''faulty'' gene, BRCA1, which sharply increases my risk of developing breast cancer and ovarian cancer.
My doctors estimated that I had an 87 percent risk of breast cancer and a 50 percent risk of ovarian cancer, although the risk is different in the case of each woman.
Only a fraction of breast cancers result from an inherited gene mutation. Those with a defect in BRCA1 have a 65 percent risk of getting it, on average.
Once I knew that this was my reality, I decided to be proactive and to minimize the risk as much I could. I made a decision to have a preventive double mastectomy. I started with the breasts, as my risk of breast cancer is higher than my risk of ovarian cancer, and the surgery is more complex.
On April 27, I finished the three months of medical procedures that the mastectomies involved. During that time I have been able to keep this private and to carry on with my work.
But I am writing about it now because I hope that other women can benefit from my experience. Cancer is still a word that strikes fear into people's hearts, producing a deep sense of powerlessness. But today it is possible to find out through a blood test whether you are highly susceptible to breast and ovarian cancer, and then take action.
My own process began on Feb. 2 with a procedure known as a ''nipple delay,'' which rules out disease in the breast ducts behind the nipple and draws extra blood flow to the area. This causes some pain and a lot of bruising, but it increases the chance of saving the nipple.
Two weeks later I had the major surgery, where the breast tissue is removed and temporary fillers are put in place. The operation can take eight hours. You wake up with drain tubes and expanders in your breasts. It does feel like a scene out of a science-fiction film. But days after surgery you can be back to a normal life.
Nine weeks later, the final surgery is completed with the reconstruction of the breasts with an implant. There have been many advances in this procedure in the last few years, and the results can be beautiful.
I wanted to write this to tell other women that the decision to have a mastectomy was not easy. But it is one I am very happy that I made. My chances of developing breast cancer have dropped from 87 percent to under 5 percent. I can tell my children that they don't need to fear they will lose me to breast cancer.
It is reassuring that they see nothing that makes them uncomfortable. They can see my small scars and that's it. Everything else is just Mommy, the same as she always was. And they know that I love them and will do anything to be with them as long as I can. On a personal note, I do not feel any less of a woman. I feel empowered that I made a strong choice that in no way diminishes my femininity.
I am fortunate to have a partner, Brad Pitt, who is so loving and supportive. So to anyone who has a wife or girlfriend going through this, know that you are a very important part of the transition. Brad was at the Pink Lotus Breast Center, where I was treated, for every minute of the surgeries. We managed to find moments to laugh together. We knew this was the right thing to do for our family and that it would bring us closer. And it has.
For any woman reading this, I hope it helps you to know you have options. I want to encourage every woman, especially if you have a family history of breast or ovarian cancer, to seek out the information and medical experts who can help you through this aspect of your life, and to make your own informed choices.
I acknowledge that there are many wonderful holistic doctors working on alternatives to surgery. My own regimen will be posted in due course on the Web site of the Pink Lotus Breast Center. I hope that this will be helpful to other women.
Breast cancer alone kills some 458,000 people each year, according to the World Health Organization, mainly in low- and middle-income countries. It has got to be a priority to ensure that more women can access gene testing and lifesaving preventive treatment, whatever their means and background, wherever they live. The cost of testing for BRCA1 and BRCA2, at more than $3,000 in the United States, remains an obstacle for many women.
I choose not to keep my story private because there are many women who do not know that they might be living under the shadow of cancer. It is my hope that they, too, will be able to get gene tested, and that if they have a high risk they, too, will know that they have strong options.
Life comes with many challenges. The ones that should not scare us are the ones we can take on and take control of.
Angelina Jolie is an actress and director.
A bill to amend the Public Health Service Act to raise awareness of, and to educate breast cancer patients anticipating surgery, especially patients who are members of racial and ethnic minority groups, regarding the availability and coverage of breast reconstruction, prostheses, and other options.
Tue, 14 May 2013 12:17
GovTrack's Bill SummaryWe don't have a summary available yet.
Library of Congress SummaryThe summary below was written by the Congressional Research Service, which is a nonpartisan division of the Library of Congress.
No summary available.
House Republican Conference SummaryThe summary below was written by the House Republican Conference, which is the caucus of Republicans in the House of Representatives.
No summary available.
House Democratic Caucus SummaryThe House Democratic Caucus does not provide summaries of bills.
So, yes, we display the House Republican Conference's summaries when available even if we do not have a Democratic summary available. That's because we feel it is better to give you as much information as possible, even if we cannot provide every viewpoint.
We'll be looking for a source of summaries from the other side in the meanwhile.
Wed, 15 May 2013 22:16
Last year's hugely successful Indiegogo campaign to raise $850,000 for the nonprofit Tesla Science Center to build a museum dedicated to the genius inventor Nikola Tesla at his Wardenclyffe laboratory in Shoreham, New York, has borne fruit. The 15.69-acre laboratory site and all its buildings are no longer the property of Belgian multinational Agfa. As of May 2nd, the last laboratory of Nikola Tesla still standing anywhere in the world officially belongs to the Tesla Science Center at Wardenclyffe (TSCW). Agfa, who put the property up for sale for $1.6 million and was reportedly entertaining an offer from real estate developers to demolish the historic structures and build condos on the site, now says via its North American general counsel Christopher Santomassimo that it ''is proud to be associated, albeit in a small way, with this historic event.''
It took two decades of unrelenting effort from the Tesla Science Center at Wardenclyffe to pay Agfa off so this historic event could take place. New York State had offered matching funds to make the purchase, so the TSCW needed to come up with $850,000 to meet Agfa's asking price. When they found out that an interested developer was looming on the horizon last summer, they kicked off a public fundraising campaign. Matthew Inman of the massively popular website The Oatmeal, an avowed Tesla fan, got involved. He started an Indiegogo fundraiser entitled ''Operation Let's Build a Goddamn Tesla Museum,'' offered extensive donation incentives and promoted the campaign heavily on his high-traffic site. Within a week, the campaign raised a million dollars. The final tally was $1,370,000.
It's been almost nine months since then. Finally owning the property is a major milestone for the Tesla Science Center, but they don't have time to rest on their laurels because the buildings are dilapidated, the grounds a wilderness and it's going to take a great deal more money and time to convert this former Superfund hazardous waste site into a museum.
The TSCW has ambitious plans. They want to take advantage of the complex to create a museum about Tesla and his work, a hands-on science learning center where workshops will be held for inventors, a replica of the 187-foot power tower which was destroyed by the government in 1917 and, perhaps the coolest idea of them all, a physics-themed playground. The estimated cost to make this vision a reality is $10,000,000. The extra $520,000 raised on Indiegogo on top of the $850,000 used for the purchase gives them a little breathing room to get cleanup started, but isn't even a dent on the total costs for the creation of the museum.
They're not wasting any time doing what they can do, though. They's already begun to board up the buildings to keep destructive human and animal elements out. Next on the agenda is a thorough assessment of their condition. Not all buildings can be saved, which is fine because many of them were built after Tesla sold the lab in 1915. The ones that are structurally viable will be restored and integrated into the design of the museum. The rest will be demolished.
Clean-up and construction will take an estimated five years. The TSCW plans to further fundraising to raise the $10 million. They expect corporate donors to provide the bulk of the amount, although considering that the Veronica Mars movie raised a record-breaking $5 million on Kickstarter, who knows what might be accomplished with crowdfunding these days?
Here's video of the press conference announcing the purchase held at the New Yorker Hotel in Manhattan, where Tesla spent the last ten years of his life in Suite 3327 feeding pigeons and meeting the occasional dignitary. He died there on January 7th, 1943.
The video includes talks from the ''Angel Investors,'' three people who donated key large amounts that helped the campaign meet its goals. The first to speak around the 15 minute mark is Joe Sikorski, a filmmaker who shot a Tesla documentary Fragments from Olympus and is working on a second documentary called Tower to the People about the inventor's Wardenclyffe laboratory. The Sikorskis donated $33,000, all their seed money for the film, to the fundraising campaign. That was the donation that took them over the top to the $850,000 necessary to secure matching funds.
Next around the 20 minute mark is a great talk from Greg and Meredith Tally of the Best Western Denver Southwest who are awesomely turning the hotel into a paleontologically correct dinosaur resort. Big fans of Tesla and science boosters in general, they donated $35,000 to the Indiegogo campaign, which earned them a custom comic by Matthew Inman dedicated to the greatness that is the Dino hotel. They have a great bit describing Tesla's laboratory in Colorado.
The last Angel is venture capitalist Dusan Stojanovic who gives an animated, passionate speech at the 26 minute mark encouraging wealthy companies to ''put some cash into the future.'' He is actually distantly related to Tesla. He shows his family tree and the piles of Tesla cousins that include his little branch. He will plans to put that kickass family tree online as part of the museum project.
He's not the only Tesla relative to speak at the press conference. William Turbo, Tesla's great grandnephew (his grandmother was Nikola Tesla's sister) who knew him personally speaks around the 44 minute mark. He's the Executive Secretary of the Tesla Memorial Society and notes there's been a marked spike in interest in the inventor who was famous until his death but then faded into relative obscurity.
This entry was posted on Wednesday, May 8th, 2013 at 1:18 PM and is filed under Modern(ish). You can follow any responses to this entry through the RSS 2.0 feed. You can skip to the end and leave a response. Pinging is currently not allowed.
Thu, 16 May 2013 08:56
From the UK's Daily Mail:
Obama fires acting IRS commissioner as pressure grows surrounding political targeting of conservative groups that sought tax-exempt statusBy David Martosko | 15 May 2013
In a hastily called press conference in the East Room of the White House, Obama told reporters that he had asked Treasury Secretary Jacob Lew to find out who was responsible for a program that targeted tea party groups and other conservative organizations for a special level of intrusive questioning after they applied for tax-exempt charitable statuses'...
Why should the Treasury Department be in charge of investigating how it broke the law? Why not appoint a special counsel?
Lest we forget, a special counsel was appointed to investigate the Valerie Plame (non) scandal, even though everyone knew beforehand who had leaked her (non-classified) information.
'Lew took the first step by requesting and accepting the resignation of the acting director of the IRS,' Obama said. 'It's important,' he added, 'to institute new leadership that can help restore confidence going forward.'
But in an email to IRS employees, Miller claimed he would only be leaving next month because his assignment would be over.
'It is with regret that I will be departing from the IRS as my acting assignment ends in early June,' Miller wrote. 'This has been an incredibly difficult time for the IRS given the events of the past few days, and there is a strong and immediate need to restore public trust in the nation's tax agency.'
In fact, Mr. Miller was not the acting director when this illegal activity occurred. He was appointed November 10, 2012. The IRS had been scrutinizing conservative groups since March 2010. And we are supposed to believe that they had stopped by late 2012. (After the elections were over.)
However, Miller had been the Deputy Commissioner for Services and Enforcement, which put him directly in charge of the Tax Exempt Entities Division. And, before that, Millar had been the Commissioner of the Tax Exempt and Government Entities Division. '-- So, in fact he might have been promoted in November for his fine work there, suppressing the Tea Party.
In fact, it turns out that Miller has a long history of being involved in these kind of IRS shenanigans.
From the Washington Examiner:
Deja vu: IRS boss of Tea Party probes targeted anti-Clinton group in 1990sBy Paul Bedard | May 14, 2013
Steven T. Miller, the acting IRS commissioner who managed the division that has admitted targeting anti-Obama Tea Party groups, was one of several agents who investigated anti-Clinton organizations including Judicial Watch during that Democrat's administration, according to court documents and interviews.
Miller, who headed the IRS Services and Enforcement Division from 2009 until the end of last year, is named in court documents as part of a trio of Internal Revenue Service officials who allegedly characterized the 1998-2001 investigation of Judicial Watch as politically motivated.
According to court papers, one agent in the case reportedly told the legal watchdog group, "What do you expect when you sue the president?" Miller reportedly added that the Judicial Watch audit, coming after the group sent the White House a lengthy Freedom of Information Act request, "had created at least the appearance of a problem." '...
At the time, several groups probing various Clinton administration scandals were being audited, leading to charges that the president was manipulating the IRS to target his enemies'...
According to the IRS website, Miller, a lawyer, joined the IRS in the office of chief counsel in 1987 and "has served most of his 25 years at the IRS, an agency in the Treasury Department, in its Tax Exempt and Government Entities Division." That division is the one involved in the current scandal.
Judicial Watch President Tom Fitton said that the audit his group faced in the 1990s came from a complaint sent by a citizen and sent to the White House which forwarded it to the IRS. "This was all part of the pattern of the Clinton years," he said, adding that it cost his group "a lot of money" to fight the audit'...
So history may be repeating itself with some of the very same players.
This article was posted by Steve Gilbert on Thursday, May 16th, 2013. You can leave a response.
Thu, 16 May 2013 08:50
(CNN) '' In a letter to Internal Revenue Service employees, acting IRS Commissioner Steven Miller announced "with regret" that he'll be leaving the agency in early June.
"This has been an incredibly difficult time for the IRS given the events of the past few days, and there is a strong and immediate need to restore public trust in the nation's tax agency," said Miller, a 25-year IRS veteran. "I believe the Service will benefit from having a new acting commissioner in place during this challenging period."
Read the full letter below.CNN obtained the memo shortly after President Barack Obama announced from the White House that Treasury Secretary Jack Lew requested Miller's resignation.
May 15, 2013The internal message to IRS Employees from Acting IRS Commissioner Steven T. Miller
It is with regret that I will be departing from the IRS as my acting assignment ends in early June. This has been an incredibly difficult time for the IRS given the events of the past few days, and there is a strong and immediate need to restore public trust in the nation's tax agency. I believe the Service will benefit from having a new Acting Commissioner in place during this challenging period. As I wrap up my time at the IRS, I will be focused on an orderly transition.
While I recognize that much work needs to be done to restore faith in the IRS, I don't want anyone to lose sight of the fact that the IRS is comprised of incredibly dedicated and hard-working public servants. During my 25-year IRS career, I am profoundly proud to have worked alongside you and to be part of an institution that has worked hard to support the nation. I have strong confidence in the IRS leadership team to continue the important work of our agency.
I want to thank everyone for all of their support and friendship during my career in government service. And I especially want to thank each and every one of you for your continued commitment to the nation's taxpayers.
Thu, 16 May 2013 07:50
Conservatives are howling about the IRS targeting Tea Party groups applying for nonprofit tax exemptions.
Well, welcome to our world. Nonprofit journalism has been going through the same thing for the last few years, with almost none of the screeching'--even though journalism organizations had a much better case for tax exemptions than did the Tea Party groups.
Tell me if this sounds familiar: The IRS targets a particular kind of nonprofit applicant for special scrutiny. Scrutiny comes from the Cincinnati office, works upward to Washington, D.C., and leaves applicants in limbo for years. After years of rubber-stamping approvals, the review comes amid a surge in applications in a murky part of the tax code. Some suggest politics plays a role in favoring some applications. The IRS itself specifically questions applicants about their political activities.
That's what happened to the nonprofit-news movement for the better part of three years, something I reported on last fall. But there's been little-to-no uproar over the First Amendment implications of selecting journalism startups for special scrutiny.
San Francisco Public Press, El Paso's Newspaper Tree, New Orleans's The Lens, Rhode Island's Johnston Insider, the Investigative News Network, San Diego News Room, Virginia's The Arlington Mercury, and the Chicago News Cooperative all had to run the IRS gamut'--and those are just the ones we know about. (The right-wing provocateur James O'Keefe III's Project Veritas, by contrast, breezed through 501(c)(3) approval while legitimate news organizations who had applied earlier waited years, answering repeated (and repetitive) inquiries from IRS agents.)
The INN's Kevin Davis told me last November that ''The IRS has preemptively suggested that we modify our procedures, change our policies, and modify our articles of incorporation to remove the word 'journalism' because that is not a charitable cause.'' Agents asked the SF Public Press, repeatedly, to sign forms promising not to make political endorsements, according to Steven Waldman's Council on Foundations report two months ago.
Why did the IRS suddenly start putting nonprofit journalism startups through the wringer, and why did it take so long to finally approve them? The Cincinnati IRS office noticed a surge in activity in the sector a few years ago as for-profit journalism took a beating, and while the IRS had typically put up little resistance to nonprofit news applicants (at least since it threatened Mother Jones's tax-exempt status in 1981 and was defeated), Congress has never specifically protected journalism in the 501(c)(3) section of the law.
Journalism organizations, including this one, get in under the educational activity exemption, which requires ''the instruction of the public on subjects useful to individuals and beneficial to the community.'' While the IRS's fumbled the handling of nonprofit news in the last few years, the need for an updated code specifically exempting journalism is clear.
Why the nonprofit news mess took so long to sort out is less clear, though it's worth noting, as David Cay Johnston has, that the IRS is seriouslyunderstaffed. The Transactional Records Access Clearinghouse at Syracuse University says IRS staffing is down 23 percent in the last two decades, while tax returns are up 27 percent. Do the math.
The Tea Party story is awfully similar. There's a surge in applications from these groups, except they're applying under the 501(c)(4) section, which allows groups ''operated exclusively to promote social welfare'' to operate without taxes. The code specifically prohibits political organizations, but with a loophole big enough to drive an American Crossroads and a Priorities USA through:
The promotion of social welfare does not include direct or indirect participation or intervention in political campaigns on behalf of or in opposition to any candidate for public office. However, a section 501(c)(4) social welfare organization may engage in some political activities, so long as that is not its primary activity. However, any expenditure it makes for political activities may be subject to tax under section 527(f).
It's unsurprising that the sudden increase in Tea Party-related 501(c)(4) applicants would raise red flags at the IRS since these groups, by their nature, likely had political objectives. None of their applications ultimately were denied (read an IRS expert, David Cay Johnston, for more on this).
Ryan Chittum , a former Wall Street Journal reporter, is deputy editor of The Audit, CJR's business section. If you see notable business journalism, give him a heads-up at email@example.com.
Thu, 16 May 2013 00:27
The Internal Revenue Service (IRS) official who apologized for targeting conservative nonprofit groups for extra scrutiny is married to an attorney whose firm hosted a voter registration organizing event for the 2012 Obama re-election campaign, praised Obama's policy work, and had one of its partners appointed by Obama to a key ambassadorship.
IRS Exempt Organizations Division director Lois G. Lerner, who has been described as ''apolitical'' in mainstream press coverage of the IRS scandal, is married to tax attorney Michael R. Miles, a partner at the law firm Sutherland Asbill & Brennan. The firm is based in Atlanta but has a number of offices including in Washington, D.C., where Miles works.
The 400-attorney firm hosted an organizing meeting at its Atlanta office for people interested in helping with voter registration for the Obama re-election campaign.
Read more: http://dailycaller.com/2013/05/16/em...#ixzz2TQYeqHc2The more we learn, the more I'm not surprised. A-political my ass.
Sen. Max Baucus, D-Mont. (a primary author of Obamacare, by the way), head of the Senate Finance Committee, has promised his panel would conduct a "full investigation" into who was responsible for the targeting of conservative , "Tea Party" and "patriot" groups and if they were targeted specifically because of their political beliefs. "These actions by the IRS are an outrageous abuse of power and a breach of the public's trust. Targeting groups based on their political views is not only inappropriate but it is intolerable," said Baucus in a statement - perhaps acutely aware that, under a Republican administration, the same thing could happen to liberal groups in the future if lawmakers from both parties don't nip this in the bud.
Wed, 15 May 2013 22:07
The Internal Revenue Service (IRS) will arm its agents with Remington 870 pump-action shotguns, according to a solicitation request by the agency.
The federal tax collector posted an acquisition notice earlier this month on FedBizOpps.gov. The IRS will close its acquisition request on Wednesday.
The IRS will purchase 60 Remington Model 870 Police, 12-gauge pump-action shotguns for its Criminal Investigation Division. The Remington parkerized shotguns will include a 14-inch barrel, modified choke, Wilson Combat ghost-ring rear sight and XS4 contour-bead front sight, Knoxx reduced-recoil adjustable stock, and Speedfeed ribbed black forend, according to the notice.
The shotguns are designated as the only shotguns authorized for IRS duty, based on compatibility with existing IRS shotguns, certification by an armorer, combat training and protocol, maintenance and parts.
Quotes are submitted including an 11 percent Firearms and Ammunition Excise Tax (FAET) and shipping costs to D.C.
Thu, 16 May 2013 08:53
The office of Commissioner of Internal Revenue was created by an Act of Congress on July 1, 1862. The Commissioner is appointed by the President with the advice and consent of the Senate. With no set tenure, Commissioners served as long as they and the President chose. The IRS Restructuring and Reform Act of 1998 amended Code section 7803 to set a five-year term of office. The first such term was applied to the Commissioner serving when this Act became law, Charles Rossotti, beginning with the date of his appointment. He served the full five years, from November 1997 to November 2002.
Not counting those who served as Acting Commissioner between permanent appointees, these Commissioners served the shortest times in office, less than one year:
Robert E. Hannegan3 months, 14 days10/9/1943 '-- 1/22/1944 William Orton4 months 7/1/1865 '-- 10/31/1865 Alfred Pleasonton7 months, 6 days 1/3/1871 '-- 8/8/1871George S. Boutwell7 months, 16 days 7/17/1862 '-- 3/4/1863 Shirley D. Peterson 11months, 18 days2/3/1992 '-- 1/20/1993
These Commissioners served the longest terms, five years or more:
Guy T. Helvering
10 years, 4 months6/6/1933 '-- 10/8/1943David H. Blair8 years5/27/1921 '-- 5/31/1929 Joseph S. Miller7 years, 7 months3/20/1885 '-- 3/20/1889 and4/19/1893 '-- 11/26/1896
Green B. Raum6 years, 9 months8/2/1876 '-- 4/30/1883John W. Yerkes6 years, 4 months12/20/1900 '-- 4/30/1907Roscoe L. Egger, Jr.5 years, 1 month3/14/1981 '-- 4/30/1986Charles O. Rossotti5 years11/13/1997 '-- 11/12/2002 Page Last Reviewed or Updated: 14-Mar-2013
Wed, 15 May 2013 15:57
Call me crazy but I don't think Holder is being all that truthful.
Attorney General Eric Holder testified Wednesday that his recusal from a criminal investigation into an administration leak of classified information last year was not done in writing.
Asked by Rep. Spencer Bachus (R-AL) whether he thought it might be appropriate to memorialize such an action as a matter of record, Holder said he agreed.
''I guess it might be helpful,'' he said.
Wed, 15 May 2013 14:09
Today the Associated Press reported that the Department of Justice has collected the telephone calling records of many of its reporters and editors. By obtaining these records, the DOJ has struck a terrible blow against the freedom of the press and the ability of reporters to investigate and report the news. As James Madison understood, "a popular government without popular information or the means of acquiring it is but a prologue to a farce or tragedy, or perhaps both." AP had it right when it told Attorney General Holder that it was "a serious interference with AP's constitutional rights to gather and report the news."
The DOJ's decision to dive deep into these call records also shows the growing need to update our privacy laws to eliminate the outmoded Third Party Doctrine and to recognize that datamining has now reached the point where it no longer makes sense to treat calling records and other metadata related to our communications as if they aren't fully protected by the Constitution.
According to the AP, "the records obtained by the Justice Department listed outgoing calls for the work and personal phone numbers of individual reporters, for general AP office numbers in New York, Washington and Hartford, Conn., and for the main number for the AP in the House of Representatives press gallery." In all it included more than 20 telephone lines from April and May 2012.
While the government has not confirmed, the subpoenas appear to stem from an investigation into a government leak of information to the AP. This is not a sufficient excuse. Imagine if "Deep Throat," the informant critical to Woodward and Bernstein's investigation of the 1972 Watergate burglary, knew that his identity could be obtained through legal process. His career, and perhaps his life, would have been in serious jeopardy, and a cautious individual would have kept silent.
The widespread collection of information, as well as the apparent delay in notifying AP, both appear to be yet another violation the government's own regulations, 28 C.F.R. sec. 50.10. In 2010, the DOJ Inspector General reported on three other violation, involving the Washington Post and New York Times. The regulations require that, "wherever possible" subpoenas of records of the news media should be "directed at material information regarding a limited subject matter, should cover a reasonably limited period of time and should avoid requiring production of a large volume of unpublished material."
None of those limits appear to have been observed here. It seems impossible to imagine how a subpoena for all the records of call to and from AP's main switchboard, for example, is as narrowly tailored as the law required. Importantly, the regulations anticipate negotiation with the news media prior to subpoena, which also didn't occur. And in any event the regulations require notification to the news media within 45 days of any receipt of any information, with another 45 days possible with additional authorization. Since the timeframe of the records is a year ago, it seems likely that the government did not abide by this regulation either. While the regulations do not allow a lawsuit, violations of them can be grounds for discipline for governmental officials.
It is disturbing enough that the government appears to have violated its own regulations for subpoenas to the news media. However, this revelation also shows that we have a severe problem in protecting the privacy of our communications. It is critical to update our privacy laws and our understanding of the Constitution, and reflect the realities of what law enforcement can determine from our records and other metadata about our communications stored with our communications providers, be they phone companies, ISPs or social networks.
First, the third party doctrine is wholely inadequate for protecting privacy in the modern era. Citing this doctrine, the government consistently argues that any information given to a third party'--like a phone company'--has no Constitutional protection. Here, it's clear that the government was able to get the calling record information, secretly and in large quantities, because it didn't have to go to AP to get it. Instead, it went to the phone companies, who have little incentive to stand up for their customers and who may not have even realized that the information pertained to news media and so was protected by an extra regulation.
Justice Sotomayor recognized the growing problem with the third party doctrine in the recent U.S. v. Jones Supreme Court case, and signaled that it's the time that the Fourth Amendment caselaw be updated:
People disclose the phone numbers that they dial or text to their cellular providers, the URLS that they visit and the e-mail addresses with which they correspond to their Internet service providers, and the books, groceries and medications they purchase to online retailers . . . I would not assume that all information voluntarily disclosed to some member of the public for a limited purpose is, for that reason alone, disentitled to Fourth Amendment protection.
Second, this incident underscores that government access to records'--information about our communications and movements over time'--does impact our privacy. AP President Pruitt noted: "These records potentially reveal communications with confidential sources across all of the newsgathering activities undertaken by the AP during a two-month period, provide a road map to AP's newsgathering operations, and disclose information about AP's activities and operations that the government has no conceivable right to know." This sentiment was echoed by the Appellate Court in the Jones (then called U.S. v. Maynard) case in the context of GPS information: "A person who knows all of another travels can deduce whether he is a weekly church goer, a heavy drinker, a regular at the gym, an unfaithful husband, an outpatient receiving medical treatment, an associate of particular individuals or political groups and not just one such fact about a person, but all such facts."
Overall, this revelation of government's secret access to huge amounts of calling records as part of its leak investigation should not be such a surprise. The DOJ has long maintained that no one has any privacy interests in their call data records and has also engaged in unprecedented and aggressive prosecutions around government leaks.
But it should sound a wake-up call for the rest of us, including members of Congress and the courts. Government datamining of Americans' calling records and other metadata held by phone companies and ISPs should require more than a mere subpoena and should be protected by more than a hortatory regulation, whether the target is the news media or an ordinary citizen. Whether we get there by legislation or by updating our understanding of the Constitution to reflect the power of datamining to reveal the content of our "papers," we need to get there soon. Because it's clear that the DOJ remains firmly headed in the opposite direction.
Wed, 15 May 2013 14:08
In the war on terror, the Obama administration has eschewed putting military forces on the ground in favor of surgically precise drone strikes. The campaign is constitutionally dubious, although the program's backers say it is more humane, as it means the loss of fewer innocent lives, and more effective. That the drone program is waged mostly in the shadows, and thus keeps gruesome images off television screens, is considered by the administration to be a benefit as well.
Eric Holder holds a news conference at which he tries to explain the probe of Associated Press journalists. (Chip Somodevilla/Getty Images)
The drone program comes to mind as the Department of Justice fends off questions this week about its decision to subpoena two months of phone and email records from reporters and editors at the Associated Press. Typically, when federal agents want a reporter to disclose a source, the reporter is subpoenaed and forced to name names or face jail time. That happened to Judith Miller and, more recently, to Jeffrey Sterling.
But like the drone strikes, Justice Department officials say the subpoena method is, in the end, more efficient and more humane. It keeps reporters loath to give up their sources out of jail, and it permits federal officials to track down leakers more quickly. And the surgical strike on newsroom records avoids months and months of high-profile court cases, with every news outlet in the country screaming about the First Amendment.
''From the department's perspective, this is a much less aggressive step than putting someone in front of a grand jury or putting them on trial,'' said Matthew Miller, a former spokesman for Attorney General Eric Holder. ''You're trying to balance reporters' needs and ability to do their job and the department's need to fully investigate a crime, and this step achieves that balance.''
Miller noted that Justice officials wanted to avoid the subpoena. They interviewed 550 people in connection with the AP case, he said, but the May 2012 leak, which disclosed a CIA operation in Yemen that disrupted an al Qaeda plot to blow up a U.S.-bound airplane, was serious.
''I know Adam Goldman and Matt Apuzzo [the two AP reporters who wrote the original stories], and they would rather sit in jail [rather than reveal their sources], as would a lot of really good reporters,'' he said. ''Having reporters sit in jail is a problem with moving forward with this case.''
But others disagree that the subpoena approach is preferred.
Alberto Gonzales, a former attorney general for the Bush administration, said that while he did not know the particulars of the case, the decision was ''highly unusual.'' It is likely, he added, that someone was killed or some critical piece of intelligence compromised due to the leak.
''When I was the attorney general, the department, both before and after [my tenure], tried to be very respectful in dealing with the media, because we understood that the media has a special place in the society,'' he said. ''So we try to accommodate the competing interests of the media and the competing interests of the criminal-justice system.''
Eric Holder said the reason behind the subpoena was a "very serious leak" that "put the American people at risk."
In such situations, Gonzales, who as attorney general investigated The New York Times for publishing classified information about a domestic wiretapping program, said the government has to be careful that anger at leakers does not lead to irrational decision making.
''It is certainly one of the most intense intrusions by the government into a pressroom that I can remember,'' said Floyd Abrams.
''Obviously the government goes to great lengths to protect our intelligence, to protect sensitive law-enforcement information, and when it leaks, it is frustrating, there is no question about that,'' he said. ''And it puts the government in the very difficult position of trying to balance what we are going to do here. This is against the law, and we want to discourage lawbreaking, we want to prosecute lawbreakers, and we can't do that without this information. But we are also mindful of the fact that the media, quite candidly, generally writ large is going to be very unhappy by this kind of action, and they are going to be quite critical.''
First Amendment advocates and attorneys are comparing the actions by the Department of Justice not to a drone strike but to a dragnet. If the department needed the information, they say, it should have gone through the embarrassment of hauling reporters and editors before judges and sending them off to jail if they failed to name their sources. Yes, it would have been embarrassing, but a free press requires it.
''It is certainly one of the most intense intrusions by the government into a pressroom that I can remember,'' said Floyd Abrams, the First Amendment lawyer who most famously represented The New York Times in the Pentagon papers case. He compared the Justice Department's action to the FBI storming the AP's newsroom and seizing telephone and computer records. Unless an agent is on the verge of being killed, he added, ''this is an egregious overreaction.''
''Why couldn't they put this issue before a judge? What they have done is foreclose any meaningful response by the AP. This isn't just seeking a record of one journalist for one day. This is breaking and entering into the heart of the journalistic process of the Associated Press.''
few shows back a listener talked about getting to verge of donating,
only to be put off by your ignorance of a particular subject that he was
knowledgeable about and the undermining effect that had on everything
else you say.
I knew exactly what he meant, and I couldn't have
written a better example than the recent farce with John's blog getting
I could barely listen as you both flew
off the handle, calling foul play, slamming Matt Cutts â "It's NOT TRUE
people! Pay no attention to the browser warnings. Google is out to get
us!" â it was cringeworthy in the extreme. (All this, by the way, before
continuing to hypocritically use Google's search engine for the rest of
It's exactly this sort of paranoid narcissistic
nonsense that turns people off the show. What reasonable person would
consider the options â A) Google is specifically targeting one web site
for malicious reasons, and B) a Wordpress site got hacked â and decide
that option A was the better explanation of what happened? Come on!
If you'd been less apt to fly off the handle, you could have found the iframe in 5mins and ended up with less egg on your face.
real doozy is not only that the issue was resolved in a couple of days
(despite your suggestion it would take weeks), but the site actually WAS
hacked! It even got a mention on Matt Cutts' blog. http://www.mattcutts.com/blog/malware-warning/
The following show was the turning point for me. I'd
listened to it before I saw the Matt Cutts post, and when I later
recollected how quickly and sheepishly you glossed over the suject, I
lost all respect on the spot. To have been so wrong on so many counts,
to have confidently told listeners to ignore warnings and infect their
machines with malware, and yet in the face of the truth you look in the
I've not been a doner, but I've turned a few people
on to the show over the years. I stuck with things through through the
"I don't want to play all these jingles, I get tiiired" period, and this
recent bullshit dinner party tales of "Listen to how I totally told
these enemies of my worldview what was what".
That's it for me. I'm out.
Google Panda is a change to Google's search results ranking algorithm that was first released in February 2011. The change aimed to lower the rank of "low-quality sites" or "thin sites", and return higher-quality sites near the top of the search results. CNET reported a surge in the rankings of news websites and social networking sites, and a drop in rankings for sites containing large amounts of advertising. This change reportedly affected the rankings of almost 12 percent of all search results. Soon after the Panda rollout, many websites, including Google's webmaster forum, became filled with complaints of scrapers/copyright infringers getting better rankings than sites with original content. At one point, Google publicly asked for data points to help detect scrapers better. Google's Panda has received several updates since the original rollout in February 2011, and the effect went global in April 2011. To help affected publishers, Google published an advisory on its blog, thus giving some direction for self-evaluation of a website's quality. Google has provided a list of 23 bullet points on its blog answering the question of "What counts as a high-quality site?" that is supposed to help webmasters "step into Google's mindset".
Hey Adam (Heil Everybody!),
I was just listening to last Thursday's episode and was listening to you reading about Lock Down drills and just had to chime in on my experience. Right after the Columbine "massacree," I, in particular, was singled out as a potential shoot 'em up nutjob because, I suppose, I wore black all the time, listened to metal bands, and it was widely known that until 10th grade (the year before Columbine), I was often the victim of physical and emotional bullying. Unlike modern bullying campaigns, I ended this by stomping the ever-living shit out of the last person that bullied me, just as my father had told me too, finally, and that pretty much ended it.
Anyway, moving on, after Columbine I was called down to the guidance office all the time. A county brownie (sheriff's officer) was present at all meetings. At one of these intellectually exhaustive meetings I was asked "if" I were to go on a rampage like the kids at Columbine, how would I go about it. Tired of these overt, conspicuous meetings that made me even more of an outcast amongst the school populace, I decided to see if I could make these two assholes crap themselves like Al Roker in the White House. I told them that since they've instituted these lockdown procedures, I'd found out that the principal's office area (a group of offices for the Principal, Vice Principal, and Guidance Counselors) was where I'd go first because there was a single button unlocked by a key the Principal and Vice Principal had that magnetically sealed all classroom doors in the building. I told them that'd be the first place I'd hit, lock down the school, and cut the outside phone and network lines (cell phones weren't something every kid had at the time). Then, using the Principal's master key, and knowing the windows didn't open, I'd go from room to room, opening them up, and chucking in a grenade or something, finishing off anyone who was left. This way, I told them, I'd get the maximum kill count.
The look on their faces was priceless. I told them that in locking down the school, they were in fact putting everyone in MORE danger and would essentially be responsible for a school full of dead kids. Then I told them that doing that would be easy, but I'm way to lazy to carry it out so they had nothing to fear from me, but every reason to fear their own procedures. After that, it was "Adios Mofos," and they sent me on my way, never to interrogate me again. They changed lockdown procedures after that by way of never having them again, but I DID notice that two more police were stationed there giving a total of 3. So this has been going on for some time, at least over a decade, in regards to lockdown procedures. Just had to chime in and share my experience.
Aaron J. Howell
Hi Adam, I've been a listener to the show for a year now,
but I am a high school junior, so I have no money to donate. I'll donate
once I have money to spend.
At our school, they used to have drills similar to what was talked about
on show 512, where the principal would come on the intercom and tell us
"Code Blue" to trigger a lockdown. We would then all hide in a corner,
like the subservient slaves that we are, until the principal would say
This school year, as apparently district policy, we have been told to
adopt a new strategy for combating any potential threat... Arming
ourselves! Not with guns, of course, but with textbooks and calculators,
pencils and pens, We arm ourselves to attack an invader with whatever
means necessary. We also barricade the door with desks. Apparently they
didn't think that a school shooter could break the glass window right
next to the door!
Needless to say, I prefer the new strategy better than cowering like
slaves in a corner. I like the concept of armed resistance in schools
Living the Mac 'n cheese life,
(Hopefully soon to be) producer Nikhil (pronounced Nih-kill)
I really enjoyed your analysis of the anti-bullying epidemic. I was talking to my dad about the issue of taunting (him being a sports fan) he told me that the Ohio State Buckeyes frequently get the taunting penalty pulled on them. Apparently they have an "O" for Ohio printed on the underside of their gloves that they flash after scoring touchdowns. They are prohibited from flashing this at the crowd as it arouses their fans and in term hurts the other football team's feelings.
After thinking more on this, I realized that my school is just as bad with their "see something say something" bully policy. I go to the elitist white school (Mattawan) in the right-wing hillbilly Capitol of the communist republic of Michigan (Kalamazoo.) I realize that you two are completely correct about it being a slave training camp. And they have only upped the gun! (not literally cause guns are bad when the slaves have them.) My French teacher, for example, has locked her door everyday since columbine, which makes bathroom breaks a bitch, especially when one is late for class after the Giant Voice System has given us a "final warning." The teachers are also required to wear name tags and drills are very frequent. In order to strike fear into us slaves, we are ordered to turn the lights off, crawl into the corner of the room on the same side of the door, so that there are no "peepers" through the window in the door. We then crouch down (or as we refer to it, "bend over,") and SHUT UP for 15 minutes.
My English teacher tells a story of when he was first teaching, the Swat team came to perform a safety drill at the school and teachers were informed not to open their doors or speak at all. Ten minutes went by, and assuming the drill was finished, he heard a knock at the door, and proceeded to open it. When he did, the staged shooter proceeded to shoot him with a blank in front of the class! But that is nothing compared to the slave-food lunches that are served. Every day "nachos" are served. They are essentially stale tortillas, with cheap-as-wet-cigarette-butts horse meat and cheap cheddar melted on the top. I have suggested to the office many times that they should be serving Tuna Ã La King. They haven't responded so I'm assuming that it doesn't fit their budget. The staff seems to have taken suggestion this just as well as they took NA CD's I gave them. Love the show and wish you two the best of luck!
Hookers and Blow,
Heil! I'm a high school senior who has been
awakened for a few years now, having been listening to No Agenda since
somewhere near its beginning. I decided I ought contribute to the
different stories from schools and add my own experiences.
some of the other listeners who have wrote in, my school also practices
these "lockdown" (scare-quotes intended) drills once a quarter. Doors
are locked, lights shut off, and students are forced into a corner of
the room. Administrators go around the school jiggling the doorknobs and
knocking on windows outside the classrooms, successfully wasting
fifteen to twenty minutes of valuable time. All the while, we are being
conditioned into feeling utterly helpless while we are at school.
our textbooks are inundated with various cheap shots at the political
groups the textbook authors don't like. Discussions in class never get
any further than ad hominem attacks and repeating talking points from
the political playbooks, but these kids are made to think that they are
practicing critical thinking. In reality, the whole thing is simply
teaching us to allow ourselves to be distracted and get drunk on
passionate debates about social issues instead of opening our eyes and
thinking outside the box a little.
As a brief
comment, I go to a private religious school (not necessarily of my own
choosing), and I wanted to point out that it's not just government-run
schools who are attempting to brainwash us and condition us into obeying
and keeping our noses down. Private schools and public schools alike
are doping us up so we can go out into the world and behave like good
slaves do. In fact, I would argue that the private school system is more
effective at its job, because the people here tend to be even more
determinedly, dogmatically blind.
If you have
any more questions, or if there is any new interesting information from
inside the modern education world, I'd be glad to pass that on. Thank
you both for the superb content. Someday when I have money I'll be sure
to backpay my great debt to you both.
Wed, 15 May 2013 15:51
A woman poses for a picture while cleaning the destroyed main market in Gao, March 2, 2013.
Credit: Reuters/Joe Penney
By Ethan Bilby and Adrian Croft
BRUSSELS | Wed May 15, 2013 4:24pm EDT
BRUSSELS (Reuters) - International donors pledged 3.25 billion euros ($4.22 billion) on Wednesday to help Mali recover from a conflict with al Qaeda-linked Islamists, exceeding the West African country's target.
The development drive for Mali, one of the world's poorest countries, is aimed at halting a resurgence of the rebels driven out of major northern towns by a French-led offensive this year.
"More than 3.25 billion euros have been mobilized at this conference," French President Francois Hollande told the meeting, organized jointly by France and the European Union.
More than 100 delegations took part in the conference, including 10 presidents or prime ministers.
The EU's executive Commission will allocate 524 million euros to Mali. Large pledges by France, the United States, Britain, Germany, Denmark, the Netherlands, the Islamic Development Bank and others enabled the West African country to exceed its goal of raising two billion euros.
It needs the money to fill a funding gap in a 4.34 billion euro plan to keep the peace and build infrastructure over this year and next.
EU, French and Malian officials declared the conference a success. "It went beyond what we could have hoped for ... This conference marks a new chapter in the fight of civilization against terrorism," Malian President Dioncounda Traore told a news conference.
French and EU officials said that releasing the bulk of the money was dependent on Mali fulfilling its commitment to holding presidential elections on July 28.
"We cannot wait for the elections. One third of the EU commitment will be financed before, but two thirds depends on the elections," French Development Minister Pascal Canfin told Reuters.
He also said Mali must push through reforms in justice, fighting corruption, public finances and decentralizing power.
NO BLANK CHEQUE
Mali's implementation of reforms will be strictly monitored by the donors.
"Nothing is a blank check, everything is covered by this plan for 2013-2014 and the progress will be evaluated based on the objectives of this plan," Andris Piebalgs, the EU's development commissioner, told Reuters.
Aid group Oxfam welcomed the pledges, but said they should be seen as "a down payment, not a one-off check".
France launched a ground and air operation in its former colony in January to break the Islamist rebel hold on the northern two-thirds of the country, saying the militants posed a threat to the security of West Africa and Europe.
The rapid offensive took back most of the territory seized by the militants but has failed to stop them from waging a guerrilla war.
Hollande dismissed comparisons between Mali and Afghanistan.
"In Mali, the terrorists have been beaten. I don't say there are none left, I don't say there is no risk, but there is no longer any fighting," he said.
Mali continues to suffer a humanitarian crisis, with more than 174,000 refugees in neighboring countries and 300,000 internally displaced.
Some 750,000 Malians need food assistance and 660,000 children face malnutrition, according to Kristalina Georgieva, the EU's humanitarian aid commissioner.
"At the moment conditions are better in the camps than they are at home," Georgieva told Reuters.
"This is why this focus on the early recovery of basic services is so crucial. As long as people live better in the camps than they live at home, they're not going to go back."
(Additional reporting by Justyna Pawlak; editing by Mike Collett-White)
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Just wanted to let you know that today i sat in on a series of presentations at NA T
O HQ for all the Chiefs of Defence Staff and without giving too much away, you are
so absolutely spot on with your pipeline theories. It really is all about the pipes.
Also you may be interested to know that I had I 'I am awake' moment too. The French
gave a brief about M A L I and one of the slides about 'the weapons arsenal' they
found in M A L I that consisted of a few boxes of rounds and 27 (i counted them)
rocket launcher grenades. I said to the guy (sarcastically) that was scanning for
illicit communication devices in the room"OMG look at all those weapons" to which he
replied with an open mouth, aghast at what he was seeing, "that's really serious
I thank you both oh and God that i am awake. Knowledge is power!
John, sorry, I'm the douchebag who never got back to you when you asked for those
European Slingbox details (i confess that i didn't know what a Slingbox was and
presumed you could use the details of my box), and will as a result, make my first
donation and set up a monthly payment plan.
Love you guys
PS thought you may want to know that General Dempsey, got up, and walked around the
room for no apparent reason (most unusual btw) during a brief and just sat back
down, everyone and i mean everyone was captivated by this bizarre occurrence. Any
stories of him losing his marbles over there?
Wed, 15 May 2013 15:45
Four months after an EU-backed French force halted an advance by militants in the country's north, the EU hosted the donor conference to help finance the Malian government's plan to improve health, education, the economy and food security.
It also pledged to rebuild its impoverished northern region where skirmishes between foreign-backed government troops and militants continue.
The European Commission and the 27 member states have pledged to provide '¬1.35 billion for Mali through 2014, one-third of the international commitment. The pledges included '¬50,000 from Greece and '¬18 million from Spain, two troubled eurozone countries that have themselves turned to Brussels for financial aid.
European leaders made clear at the Brussels meeting that the aid comes as part of broader efforts to stabilise a West African region that has endured repeated food crises, political instability and armed conflicts.
French President Fran§ois Hollande welcomed the financial commitments but said it was up to leaders in the former French colony to follow through with its commitments.
"We need transparency and good governance," Hollande said at the end of the conference.
Earlier, French Foreign Minister Laurent Fabius emphasised the regional dimension of the conflict, saying that ''through Mali, it is the future of the subregion and beyond which is at play''. But he also warned that the aid provided by the international community comes with strings attached.
Fabius said particular attention would be paid to the traceability of aid and the followup of projects, with conditions on disbursement of funds linked to transparency, governance, democracy and the fight against corruption.
The war in Mali ''is being won,'' Fabius said but, ''now we must win the peace''.
Aid in stages
EU representatives repeatedly said aid must be tied to the Malian authorities' adherence to the political stabilisation roadmap they presented to donors, and free elections due in July. Dirk Niebel, the German development minister, said his country would provide at least '¬100 million in aid over the next two years. But it will be released in stages if Mali ''continues to implement its roadmap '... and if the transition process goes well," Niebel said.
EU development aid Commissioner Andris Piebalgs said the stabilisation roadmap for Mali was the cornerstone of the international community's commitment to the country and had to be followed resolutely.
Piebalgs insisted that beyond Mali, ''the EU's commitment is regional'' and extends to the wider Sahel area. ''We are investing considerable means'', he said, referring to the European Commission's '¬520 million commitment. An extra '¬200 million is also available under the EU's strategy for the security and development of Sahel, the Commission said.
Foreign aid was expected to lead to the creation of 20,000 local jobs in the next two years in areas like water, sanitation, justice and education, Piebalgs said.
Big boost for poor nation
The international aid pledged by 108 countries and international organisations is a major boost for Mali, coming a year after a brief military coup and flare-up of sectoral violence led the EU and other donors to freeze aid and ultimately back the French military operation.
Mali's foreign minister, Tieman Hubert Coulibaly, promised ''effective management'' of the aid. ''We need money,'' he pleaded, adding: ''Money is the sinews of war.''
He also said stabilising his own nation would help the region, referring to the Economic Community of West African States, which has pledged support for a forthcoming United Nations peacekeeping mission in Mali. "We believe that a stable Mali is a stable ECOWAS [and] a little more stable Sahel."
But the nation of 16 million faces high hurdles, including continued fighting, pressure from Islamist groups and drug traders, and refugee and food crises.
Mali must also tackle its reputation for corruption and mismanagement of aid. The Business Anti-Corruption portal, an EU-funded project, reports that bribery and graft are widespread. In 2010, the Global Fund to Fight AIDS, Truberculosis and Malaria halted funding to Mali amid allegations of fraud and mismanagement.
The Global Fund has since resumed aid and in November announced '¬110 million in new funding.
Human rights concerns
Europe and its global partners were under pressure ahead of the conference to ensure that the Malian government address reports of extrajudicial executions, torture and reprisals carried out by government forces.
Mali has been torn for decades by divisions between its northern Islamic and Arab communities and the African south. Attacks by northern insurgents, backed by regional Islamic groups, surged in early 2012, leading the military to temporarily seize control of the government.
United Nations rights officials and advocacy groups, including Human Rights Watch and Amnesty International, have accused insurgents and Islamic militants of pillaging and rape, while government forces have been linked to reprisals and torture.
Amnesty International has accused government forces in the north of carrying out executions and Islamic rebels of recruiting child soldiers.
Mon, 13 May 2013 20:42
Rebel is believed to be Abu Sakkar, a founder of the rebel Farouq BrigadeSakkar rants: 'I swear we'll eat from your hearts and livers, you dogs'He then raises one of the organs to his mouth and takes a biteCameron warns he may send troops as evidence of chemical weapons growsBy Matt Blake
PUBLISHED: 10:17 EST, 13 May 2013 | UPDATED: 12:44 EST, 13 May 2013
A video that appears to show a Syrian rebel cutting out and eating the heart of a dead government soldier has been posted online in a horrific new propaganda stunt.
The unverified clip, posted by a pro-government campaign group, claims to show a man - believed to be Abu Sakkar, the well-known founder of Homs' Farouq Brigade - standing over the uniformed corpse in a ditch while ranting against President Bashar al Assad.
Using a knife, the man hacks open the torso and removes two organs before holding them up to the camera and declaring: 'I swear to God we will eat your hearts and your livers, you soldiers of Bashar the dog.' He then raises one to his mouth and takes a bite.
It comes as David Cameron warned today he may still sanction military intervention in the war-torn nation amid growing evidence that Assad is using chemical weapons against his own people.
GRAPHIC CONTENT WARNING:Scroll down for video.
Horrific: The amateur video posted on the Internet on Sunday shows Abu Sakkar, a founder of the rebel Farouq Brigade who is well known to journalists as an insurgent from Homs, cutting into the torso of a dead soldier
Remorseless: After removing what appears to be the dead man's heart, Sakkar then reaches into the chest cavity and draws a lung into view
The video, posted on YouTube by and billed as proof of a war crime, is the latest installment of a propaganda war that is growing fast behind the scenes of this bloody conflict.
Last month, a photograph was released by a pro-Assad group based in Lebanon that appeared to show a young rebel fighter barbecuing the severed head of a government soldier.
Experts say such images demonstrate that the battlefield has spread from rubble-strewn streets and war-churned fields to the internet as both sides vie to control their public image and discredit that of their opposition.
Meanwhile, human rights groups say it is emblematic of a civil war that has rapidly descended into sectarian hatred and revenge killings.
In the most recent video, Sakkar tells the camera: 'I swear to God we will eat your hearts and your livers, you soldiers of Bashar the dog,'
His rant is greeted by offscreen cheers of his comrades shouting 'Allahu akbar (God is great)'.
Gory: Brandishing the organs for the camera to see, Sakkar continues his rant against Assad's government
'Soldier's heart cut out and eaten' in horrific propaganda video
Controversial: The video has caused outrage among both supporters of President Bashar al-Assad and opposition figures
PR war: The video, posted on YouTube by and billed as proof of a war crime, is the latest installment of a propaganda war that is growing fast behind the scenes of this bloody conflict
Peter Bouckaert of Human Rights Watch said that he had seen an original, unedited copy of the video and that Abu Sakkar's identity had been confirmed by rebel sources in Homs and by images of him in other videos wearing the same black jacket as in the latest clip and with the same rings on his fingers.
'The mutilation of the bodies of enemies is a war crime. But the even more serious issue is the very rapid descent into sectarian rhetoric and violence,' said Bouckaert.
He said that in the unedited version of the film, Abu Sakkar instructs his men to 'slaughter the Alawites and take their hearts out to eat them', before biting into the heart.
Abu Sakkar has been seen in previous videos firing rockets at Lebanese Shi'ite villages on the border and posing with the body of a soldier purportedly from the Lebanese Shi'ite militant Hezbollah group, which is helping Assad's forces.
Big talks: Meanwhile, British Prime Minister David Cameron said he wasn't ruling out taking tougher action against Syria over growing evidence it was using chemical weapons, saying he planned to raise the matter with Barack Obama as he met the US president today
MailOnline cannot independently verify videos from Syria, where access is restricted by the government and security constraints.
Meanwhile, British Prime Minister David Cameron said on Monday he wasn't ruling out taking tougher action against Syria over growing evidence it was using chemical weapons, saying he planned to raise the matter with U.S. President Barack Obama.
'Certainly we haven't ruled out stepping up action in response to what seems to be happening on the ground,' Cameron told NPR radio. 'The evidence is growing; the lack of room for doubt is shrinking, and I think this is extremely serious.'
Cameron's comments came two days after he urged Russian President Vladimir Putin to do more to stop the bloodshed in Syria, after failing to make any major progress towards ending the two-year conflict.
Speaking at a press conference in Sochi, the Prime Minister said: 'The history of Syria is being written in the blood of her people.
But Mr Cameron's visit to the Russian president's summer residence in the Black Sea resort ended with an admission that they still have 'differing views' about how to deal with the situation.
Shaky start: David Cameron and Russian President Vladimir Putin exchanged pleasantries before a press conference today but failed to make real progress on resolving the Syrian conflict
Mr Cameron said Britain and Russia have 'differing views' on how to resolve the conflict
The UK is leading the argument to amend or lift restrictions to allow weapons to be passed to forces opposed to Bashar Assad's regime.
But Russia has remained supportive of the Syrian government, with Mr Putin determined to defend the country's 'sovereignty'.
The visit came as details emerged of Britain's arguments in favour of lifting the arms embargo.
Ahead of his visit Mr Cameron said the atrocities in Syria 'continue to mount' and growing evidence that the Asad regime has used chemical weapons.
He told MPs: 'There is a growing body of limited but persuasive information showing that the regime has used, and continues to use, chemical weapons including sarin. The room for doubt about that continues to diminish.'
The Syrian conflict started with peaceful protests in March 2011, but when these were suppressed it gradually turned into an increasingly sectarian civil war which, according to one opposition monitoring group, has cost more than 80,000 lives.
Majority Sunni Muslims lead the revolt, while Assad - whose family have ruled for over four decades - gets his core support from his own Alawite sect, an offshoot of Shi'ite Islam.
Wed, 15 May 2013 15:51
TweetShare thisEmailPrintPeople wait for their turn to register for unemployment benefits at a local jobs centre in Nicosia April 23, 2013.
Credit: Reuters/Andreas Manolis
WASHINGTON | Wed May 15, 2013 2:50pm EDT
WASHINGTON (Reuters) - The IMF's executive board approved a $1.3 billion, three-year loan to Cyprus on Wednesday, part of a larger international bailout to help the Mediterranean country avoid defaulting on its debt.
Cyprus had to comply with certain conditions - including winding down its second-largest bank and imposing losses on large depositors - in order to receive the funds, which total 10 billion euros ($13 billion). The approval of the IMF's board means Cyprus immediately gets $110.7 million.
The financing package "is intended to stabilize the country's financial system, achieve fiscal sustainability and support the recovery of economic activity to preserve the welfare of the population," the IMF said in a statement.
($1 = 0.7705 Euro)
(Reporting by Anna Yukhananov, editing by G Crosse)
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Wed, 15 May 2013 12:34
Wed, 15 May 2013 11:02
The 39th G8 summit will be held on 17''18 June 2013 at the Lough Erne Resort, a five-star hotel and golf resort on the shore of Lough Erne (Irish: Loch irne) in County Fermanagh, Northern Ireland. It will be the sixth G8 summit to be held in the United Kingdom. The earlier G8 summits hosted by the United Kingdom were held at London (1977, 1984, 1991), Birmingham (1998) and Gleneagles (2005).
The decision to hold the summit in Northern Ireland has been criticized. This is mainly due to the threat from Irish republican 'dissident' groups, such as the Real IRA, who are waging a low-level paramilitary campaign in Northern Ireland. The summit also coincides with a protest campaign by loyalists and with the Protestant loyalist "marching season".
Location and preparationThe date and location of the summit was announced by British Prime Minister David Cameron in November 2012. According to Mark Simpson, the BBC's Ireland Correspondent, the British Government chose Fermanagh for two main reasons: history and geography. Since the formation of Northern Ireland in 1921, there has been tension and violence between its two main communities. The unionist/loyalist community (who are mostly Protestant) generally want Northern Ireland to remain within the United Kingdom, while the Irish nationalist/republican community (who are mostly Catholic) generally want it to leave the United Kingdom and join a united Ireland. From the late 1960s until the late 1990s, these two communities and the British State were involved an ethno-nationalist conflict known as The Troubles, in which over 3,500 people were killed. A peace process led to the Belfast Agreement and ceasefires by the British State,and the paramilitary groups involved (such as the republican Provisional IRA, the loyalist Ulster Volunteer Force). The Conservative Party government of David Cameron is a unionist one. By holding it in Northern Ireland, Cameron "will hope it sends the message to the rest of the world that the peace process has worked and normality has returned". The second reason is geography. G8 summits have always drawn large demonstrations, but Fermanagh's geography will make it hard for protesters. Much of the Lough Erne Resort is surrounded by water and almost all of the roads within 30 miles are single carriageway.
However, some have criticized the decision to hold the summit in Northern Ireland, due to ongoing protests and small-scale violence by both republicans and loyalists. Since the Provisional IRA called a ceasefire at the end of The Troubles, dissident republican splinter groups have continued its paramilitary campaign. The main groups involved in this low-intensity campaign are the Real IRA, Continuity IRA and 'glaigh na hireann. Security sources expect that these groups will try to launch an attack during the summit, which "would hijack global headlines".
There is also the likelihood of disruption and violence involving loyalists. The summit will take place during the "marching season", when Protestant and loyalist groups (such as the Orange Order) hold many parades throughout Northern Ireland and Protestant loyalist areas are bedecked with Union Jacks and bunting. This is a tense time in Northern Ireland and it often results in clashes between the two main communities. Furthermore, since December 2012, loyalists have been holding daily street protests. They have been protesting against the decision to lessen the number of days the Union Jack flies from Belfast City Hall. Some of these protests have sparked rioting. Protesters have discussed holding a Union Jack protest at the G8 summit.
On 23 March 2013, a car bomb was defused 16 miles (26 km) from the Lough Erne Resort. Republican group 'glaigh na hireann said it had planned to detonate it at the hotel but had to abort the attack.
ReferencesCoordinates: 54°23'²52'"N7°41'²36'"W>> / >>54.3978°N 7.6933°W>> / 54.3978; -7.6933
Wed, 15 May 2013 11:02
Barack Obama is welcomed to his ancestral home, Moneygall, during his trip to the Irish Republic in 2011. Photograph: Getty Images
The White House has confirmed that Barack Obama is to visit Belfast as well as the G8 summit taking place in the border county of Fermanagh next month.
During the US president's first trip to the city he is expected to express support for the peace process and the power-sharing political settlement at Stormont.
In a statement from Washington on Friday, a spokesman said: "The president's trip will begin in Belfast, where he will engage with the people of Northern Ireland and highlight the hard work, dialogue, and institutional development they have undertaken together."
Obama's press secretary said the summit would provide world leaders with an opportunity to "address pressing economic, political, and security challenges around the globe and to promote the advancement of trade and greater transparency among G8 members and the developing world".
The trip will be Obama's first to Northern Ireland. Two years ago, he went to the Republic and visited Dublin and his ancestral home of Moneygall in County Offaly. During his main address outside Dublin's Trinity College he was mobbed by thousands of well wishers.
The visit will also be the first by a US president since George Bush went to Belfast in 2008. Bill and Hillary Clinton were frequent visitors to Northern Ireland, making three visits in the 1990s to show their support for the peace process.
On Friday Eamon McCann, one of the civil rights movement's leading figures in Northern Ireland, denounced plans to open up an entire prison block and former army base to detain anti-G8 demonstrators next month.
The veteran Derry socialist campaigner and writer said Northern Ireland was going back in time to a repressive law and order situation such as existed in the days of one-party unionist rule.
McCann was responding to reports that a wing of the top-security Maghagerry jail outside Belfast had been opened to cope with any mass arrests when the G8 meeting begins on 17 June in Fermanagh.
Northern Ireland's justice minister David Ford also announced on Friday that a former British Army barracks in Omagh, known as Lisanelly, would be used as a temporary holding centre for any arrested demonstrators.
Ford, leader of the liberal Alliance Party, said the Lisanelly barracks could hold up to 300 people. It is understood the block at Maghaberry prison, County Antrim, has 108 cells and could accommodate up to 200 prisoners.
Barack Obama, Vladimir Putin, David Cameron and the other world leaders, are to hold their two-day global summit at the Lough Erne hotel resort close to Enniskillen.
The Police Service of Northern Ireland announced this month that a four-mile stretch of road from the Fermanagh town to the hotel on Lough Erne would be closed for almost a month as part of a security operation to protect the world's eight most powerful politicians.
An extra 3,600 police officers are to be drafted into the lakeland region for the duration of the summit. There will also by a no-fly and no-sailing regime imposed on the area during that period.
McCann, who was active in Derry during the Battle of the Bogside between civil rights supporters and the unionist-dominated police force in 1969 at the advent of the Troubles, called the security operation a remarkable turn of events.
He said: "We are headed for as repressive a law-and-order situation as there was in the days of one-party unionist rule and the old unreformed RUC [Royal Ulster Constabulary]. PSNI chiefs speak on the media full of confidence that their plans to stamp on civil liberties won't draw any condemnation from the DUP-Sinn Fein coalition.
"Three hundred new places in prisons, the women's prison and in youth detention centres are being readied for an influx of protesters. The cops [are] equipped with drones, with no opposition from the policing board, which includes representative of all the main parties.
"Thousands of British police are being shipped in. The British army is on stand-by. Military helicopters will be flitting above Fermanagh ferrying the leaders and their entourages. MI5 is all over the plans.
"One of the reasons all this has gone virtually unchallenged is that support for the police is seen as crucial to the survival of the Belfast agreement. It's almost seen blasphemy. Criticise the justice establishment or the police and you can easily be denounced as an enemy of peace. It's mad."
Thousands of people are expected to go to Enniskillen during the gathering of the governmental heads to highlight issues such as world poverty, the arms trade and the war in Afghanistan.
Some charities have expressed concern about getting access to Enniskillen to highlight their causes.
In listening to the Sunday May 12th NA episode, I honestly had never heard of "3D
Printing" let alone that in conjunction with Gun manufacturing. I heard you discuss
there not being any real info in the Book of Knowledge about "Cody R. Wilson"
outside of a bio supposedly about him. American Born, blah, blah, Blah....
So I went onto the Video Book of Knowledge (You Tube) and found the 3D Printed Guns
Documentary. But in watching the doc, I picked up on what I believe to be an
accent. I LISTENED to Cody Speak.
(I believe) he is from Australia, or somewhere in the UK. I am pretty good at
detecting accents, even disguised ones. Like you always say, "Words Matter" but what
also matters to me is pronunciation. Take another look at the Documentary. I think
it holds more clues as to where this gentleman is really from, and from there, what
his (and his backers) true intentions are. I would be willing to bet he is not
American Born, as it states in the Book Of Knowledge.
Mon, 13 May 2013 22:03
The FP-45 Liberator was a pistol manufactured by the United States military during World War II for use by resistance forces in occupied territories. The Liberator was never issued to American or Allied troops and there is no documented instance of the weapon being used for their intended purpose. Many FP-45 pistols were never distributed and were destroyed by Allied forces after the war; and most of those distributed were lost or disposed of without any combat use.
Project HistoryThe concept was suggested by a Polish military attache in March 1942. The project was assigned to the US Army Joint Psychological Warfare Committee and was designed for the United States Army two months later by the Inland Manufacturing Division of the General Motors Corporation in Dayton, Ohio. Production was undertaken by General Motors Guide Lamp Division to avoid conflicting priorities with Inland Division production of the M1 carbine. The army designated the weapon the Flare Projector Caliber .45 hence the designation FP-45. This was done to disguise the fact that a pistol was being mass produced. The proposed intent was to drop these weapons at concentration camps where internees would pick up these weapons, overcome Nazi Guards, and hopefully liberate the camp. The original engineering drawings label the barrel as "tube", the trigger as "yoke", the firing pin as "control rod", and the trigger guard as "spanner". The Guide Lamp Division plant in Anderson, Indiana assembled a million of these weapons. The Liberator project took about 6 months from conception to end of production with about 11 weeks of actual manufacturing time, done by 300 workers.
DesignThe FP-45 was a crude, single-shot pistol designed to be cheaply and quickly mass produced. The Liberator had just 23 largely stamped and turned steel parts that were cheap and easy to manufacture. It fired a .45 caliber pistol cartridge from an unrifled barrel. Due to the unrifled barrel, it was intended for very close ambush, 1''4 yd (0.91''3.7 m). Its maximum effective range was only about 25 ft (7.6 m). At longer range, the bullet would begin to tumble and stray off course. Because of the low quality, it was nicknamed the "Woolworth gun."
Wartime useThe Liberator was shipped in a cardboard box with 10 rounds of .45 ACP ammunition, a wooden dowel to remove the empty cartridge case, and an instruction sheet in comic strip form showing how to load and fire the weapon. Extra rounds of ammunition could be stored in the pistol grip. The Liberator was a crude and clumsy weapon, never intended for front line service. It was originally intended as an insurgency weapon to be mass dropped behind enemy lines to resistance fighters in occupied territory. A resistance fighter was to recover the weapon, sneak up on an Axis occupier, kill or incapacitate him, and retrieve his weapons.
The weapon was valued as much for its psychological warfare effect as its actual field performance. It was believed that if vast quantities of these weapons could be delivered into Axis-occupied territory, it would have a devastating effect on the morale of occupying troops. The plan was to drop the weapon in such great quantities that occupying forces could never capture or recover all the weapons. It was hoped that the thought of thousands of these unrecovered weapons potentially in the hands of the citizens of occupied countries would have a deleterious effect on enemy morale.
General Eisenhower's staff never saw the practicality in mass dropping the Liberator over occupied Europe, and authorized distribution of fewer than 25,000 of the half million FP-45 pistols shipped to Great Britain for the French resistance. Generals Joseph Stillwell and Douglas MacArthur were similarly unenthusiastic about the other half of the pistols scheduled for shipment to the Pacific. The Army then turned 450,000 Liberators over to the OSS. Resistance fighters in both theatres were supplied with more effective weapons whenever possible, and French use of the FP-45 remains undocumented; although OSS distributed a few to Greek resistance forces in 1944. 100,000 FP-45 pistols were shipped to China in 1943, but the number actually distributed remains unknown. A few were distributed to Philippine troops under the Commonwealth Army and Constabulary and resistance fighters.
Firearms collectorsThe original delivered cost for the FP-45 was $2.40/unit ($32 in 2010). A Liberator in good condition today can fetch approximately $1200, with the original box bringing an additional $500, with an original extremely rare paper instruction sheet the value could exceed $2000 to a collector of rare World War II militaria. Fakes of these sheets exist, but authentic copies have a watermark that can be seen clearly, which is difficult to duplicate.
The Concept RevivedThe Liberator was replaced with the Deer gun in 1964 when a modernized equivalent was designed for possible use in Vietnam. This was because the CIA needed a weapon of this type, and most Liberators were scrapped after World War II. The Deer Gun was chambered for 9x19mm Parabellum and was loaded by unscrewing the barrel and inserting a round to fire.
Wed, 15 May 2013 22:06
Ajankohtainen kakkonen 15.5.2013 klo 16:57 | p¤ivitetty 15.5.2013 klo 18:34All the gun parts except part of the hammer were produced by a 3D printer. The material used was ABS plastic. It took a veteran gunsmith a little over an hour to assemble the 9mm gun.
Once fired, the barrel of the gun split in half. The cartridge case cracked and the gun's frame fell apart.
The gun was printed at Aalto University with a printer costing some 15,000 euros. The manager of the facility, Kivi Sotamaa, believes that printing high-quality plastic will become considerably cheaper within the next few years.
This plastic gun broke after a single shot, but more durable 'instant' weapons could become available soon. The next big step for home 3D printing is the ability to print metal. Sotamaa believes that printing metal objects at home will become a reality within a few years.
Police stunnedFinnish researcher and 3D-printing entrepreneur Jarkko Moilanen says there is no way to stop gun instructions from circulating on the internet.
"You can't stop piracy, just slow it down," Moilanen says.
Finnish police officials expressed shock at the results of the test.
"Legislators should be concerned now," said Inspector Ossi Kujanp¤¤ of the Tampere Police. "Producing these should not be allowed under any circumstances."
The gun test was performed in a controlled testing facility in Ikaalinen, near Tampere, for the Yle TV investigative programme Ajankohtainen kakkonen. Police were notified of the test in advance.
Instructions for producing the 'Liberator' plastic handgun were removed from their original website two days after being released. By then, though the instructions had been downloaded more than 100,000 times.
Defense Distributed, a Texas nonprofit that promotes the open-source development of firearms using 3D printers, withdrew the files needed to make the single-shot Liberator at the behest of the US State Department on May 9.
L¤hteet:Yle, AFP188.8.131.52.201226.7.201107:21The Finnish Broadcasting Company Yle successfully printed and fired a shot with the "Liberator", the first 3D-printed plastic handgun. 15.5.
Unkarin oikeistopopulistinen hallitus ulottaa valtansa sek¤ mediaan ett¤ kulttuuriin. Kriitikoiden mielest¤ nyt halutaan muuttaa mieli¤: kansalaistensa ajattelua maasta, sen historiasta, sosialismin j¤lkeisest¤ ajasta ja ulkopuolella olevasta Euroopasta. 15.5.
VideoAjankohtainen kakkonen tulosti 3D-printterill¤ aseen. Ase koottiin Ikaalisten asesepp¤koulussa ja vietiin testiradalle. Lopputulos selvi¤¤ videolla. 14.5.
VideoAjankohtainen kakkonen tulosti 3D-printterill¤ aseen. Lis¤ksi ase koottiin ja testattiin. Tulos n¤ytet¤¤n tiistai-illan l¤hetyksess¤. 14.5.
Lauantai-illaksi suunniteltu laskuvarjohypyn Suomenenn¤tysyritys jouduttiin perumaan kovien tuulenpuuskien vuoksi. Enn¤tyst¤ tavoitteleva ryhm¤ odotti sopivaa keli¤ koko lauantain Lahdessa Launeen perhepuistossa. 11.5.
VideoPerussuomalaisten puheenjohtaja Timo Soini otti voimakkaasti kantaa hallituksen sote-uudistukseen, Euroopan liittovaltiokehitykseen ja Suomen liittoutumattomuuteen tiistain Ajankohtaisen kakkosessa. 8.5.
VideoErja Lyytinen luonnehtii itse¤¤n "r¶nsyilev¤ksi, monipuoliseksi blues-pop -artistiksi". Kitaristi-laulaja sanoo, ett¤ blues on h¤nen musiikissaan se kaikkein olennaisin, mutta "kyll¤h¤n m¤ pusken niit¤ rajoja tosi vahvasti". Blues on kuitenkin Erjalle "tunnetila, ihan puhtaasti, v¤lill¤ voisi puhua jopa katharsiksesta". Katso Ajankohtaisen kakkosen l¤hikuva Erja Lyytisest¤. 8.5.
VideoSosiaalisen median palvelut ovat monille kehitysvammaisille liian vaikeita. Suomessa kehitetty sivusto auttaa lukemisessa ja kirjoittamisessa, kertoo Ajankohtainen kakkonen. 7.5.
Suomen olympiaurheilijat joutuvat jatkossa palautumaan suorituksistaan ilman s¤hk¶magneettiseen s¤teilyyn perustuvaa verisuoniterapiaa. Olympiakomitea on p¤¤tt¤nyt lopettaa yhteisty¶n terapialaitteita valmistavan Bemer-yhti¶n kanssa. Ajankohtaisen kakkosen haastattelemien tutkijoiden mukaan Bemer on uskomushoitoa. 7.5.
Peruspalveluministeri Maria Guzenina-Richardson (sd.) vastustaa kovin sanoin hallituksen aikeita leikata S¤teilyturvakeskuksen tutkimusm¤¤r¤rahoja. 30.4.
Kotimaa 24.4.Tapan. Raiskaan. Hakkaan. H¤p¤isen sinut. Miksi anonyymist¤ vihasta on tullut arkip¤iv¤¤? Vihapuheen tarkoitus on h¤p¤ist¤ ja vaientaa. T¤h¤n asti sen sis¤ll¶st¤ on vaiettu, koska se on liian likaista.
Talous 23.4.Tiukan talouskurin puolesta puhuvat poliitikot ja talousasiantuntijat saivat nenilleen, kun yliopisto-opiskelija osoitti, ett¤ heid¤n taajaan siteeraamansa tutkimus oli t¤ynn¤ virheit¤.
Kotimaa 28.4.V¤h¤hiilihydraattinen ruokavalio eli karppaus villitsi suomalaiset pari vuotta sitten. Lihaa ja rasvaa saa sy¶d¤ oikein luvan kanssa - vai saako sittenk¤¤n? Asiantuntijan mukaan Suomessa ja Ruotsissa karppaus on ymm¤rretty osittain v¤¤rin.
Kotimaa 1.5.Kielto on voimassa siihen saakka kunnes asia on lopullisesti ratkaistu.
Internet 6.5.Hidastelevan laajakaistan syy voi piill¤ esimerkiksi langattomassa l¤hiverkossa tai liian pitk¤ss¤ kuparikaapelissa. Mobiilinetin nopeusongelmat ovat oma lukunsa.
Kotimaa 15.5.Punkkien aiheuttamat puutiaisaivotulehdukset ja borrelioosi ovat lis¤¤ntyneet voimakkaasti viime vuosina. Eniten vakavampia TBE-tartuntoja ilmeni viime vuonna Helsingin ja Uudenmaan sairaanhoitopiirin alueella. Asukaslukuun suhteutettuna tartuntoja oli eniten Ahvenanmaan j¤lkeen Kemin ja Simon alueilla.
Ulkomaat 6.4.Azzam on maailman suurin huvijahti. Paljon muuta siit¤ ei tiedet¤k¤¤n.
Kulttuuri 22.4.Yle on aloittanut ensimm¤isen¤ suomalaisena tv-yhti¶n¤ tv-kanaviensa suoran verkkojakelun. Kanavien suoraa tarjontaa voi katsella t¤st¤ p¤iv¤st¤ l¤htien tv:n lis¤ksi tableteilla, tietokoneilla ja ¤lypuhelimilla.
Liikenne 6.3.Turun Kaskenm¤ess¤ on yksi Suomen kummallisimmista liikennemerkeist¤. T¤t¤ mielt¤ ovat monet autoilijat. Keskell¤ tiet¤ m¶ll¶tt¤v¤st¤ liikenteenopastimesta monet autoilijat eiv¤t piittaakaan tuon taivaallista. Kaskenm¤ess¤ on ollut jatkuvia vaaratilanteita.
Viihde 5.5.Krista Siegfrids sanoo, ettei h¤nen Marry me -laulunsa kannanotto ole poliittinen, vaan vetoomus sen puolesta, ettei rakkaudelle pit¤isi asettaa sukupuolirajoja.
Tiede 13.4.Toistaiseksi tutkijat eiv¤t tied¤, mik¤ rakennelma on tai miksi se on tehty. Teoriat vaihtelevat muinaisesta kalojen kasvatuslaitoksesta aikansa mahtavimpaan kaupunkiin.
Ulkomaat 7.5.0:58Clevelandin asukkaat riemuitsevat kadonneiden tytt¶jen l¶ytymisest¤. Sieppaus kesti yli kymmenen vuotta. Vahvistamattomat tiedot kertovat sieppaajien talossa olleen my¶s nuoria lapsia.
Ulkomaat 12.5.01:00L¤ntiseen Manitobaan on julistettu paikallinen h¤t¤tila, kertoo yleisradioyhti¶ CBC.
Ulkomaat 10.4.Internetin suosituimmat pornosivustot altistavat k¤ytt¤j¤ns¤ yh¤ pahemmin haittaohjelmille. Alan asiantuntijan mukaan yli puolet tunnetun pornosivuston k¤vij¶ist¤ joutuu tekemisiin haittaohjelmien kanssa.
Kotimaa 3.5.Kerrostalon parvekkeelta kantautuva melu ja grillink¤ry poikivat valituksia herk¤sti kev¤isin. Auringonpalvontakin voi kismitt¤¤, kertoo lakiasiantuntija Marina Furuhjelm Is¤nn¶intiliitosta.
Kotimaa 25.4.My¶s eurooppalaisessa vertailussa Suomi on hintak¤rjess¤.
Kotimaa 27.4.Kauppojen kassoilta l¶ytyy jo laitteita, joilla voi tulevaisuudessa maksaa vain korttia vilauttamalla. L¤himaksamiseen sopivia maksukortteja saa my¶s jo pankeista.
Politiikka 29.4.Hallituksen kompurointi sote- ja kuntauudistuksessa ja kehysriihen p¤¤t¶sten korjailuissa n¤kyy puolueiden kannatusluvissa. Vuosia gallup-k¤rjess¤ ollut kokoomus on menett¤nyt ykk¶spaikkansa ja SDP:n suosion lasku jatkuu.
Kotimaa 1.5.0:59Zeppeliini tekee tutkimuslentoja Suomessa kes¤kuun puoleen v¤liin asti.
Tiede 18.4.Nasan mukaan tutkijat eiv¤t tied¤, voisiko l¶ydetyill¤ planeetoilla esiinty¤ el¤m¤¤, mutta niiden paljastuminen vie meid¤t askelen l¤hemm¤s Maan kaltaisen planeetan l¶ytymist¤.
Wed, 15 May 2013 10:27
The Department of Homeland Security has apparently shut down a key mobile payments account associated with Mt. Gox, the largest Bitcoin exchange.
Chris Coyne, the co-founder of online dating service OKCupid, tweeted out an e-mail he received from Dwolla this afternoon. The e-mail states that neither Coyne, nor presumably any other Dwolla user, will be able to transfer funds to Mt. Gox.
Dwolla confirmed the change to the New York Observer, which first reported the story. Dwolla received a seizure warrant from a federal court.
"The Department of Homeland Security and US District Court for the District of Maryland issued a 'Seizure Warrant' for the funds associated with Mutum Sigillum's Dwolla account (a.k.a. Mt. Gox)," a Dwolla spokesperson told NYO's BetaBeat. "Dwolla has ceased all account activities... for Mutum Sigillum while Dwolla's holding partner transferred Mutum Sigillum's balance, per the warrant."
It isn't yet clear why this seizure happened, and Dwolla isn't saying anything beyond confirming the court order. Mt. Gox didn't immediately responded to an inquiry from Ars about the seizure. A user on Bitcoin StackExchange published this short reply received from an inquiry to Mt. Gox about the shut-down: "Thank you for the e-mail. We can see that the Dwolla transactions are not getting processed right now. We will contact Dwolla and post an announcement regarding this. Your patience is appreciated till then."
A DHS spokeswoman declined to comment on the case, "in order not to compromise this ongoing investigation being conducted by ICE Homeland Security Investigations (HSI) Baltimore."
Using a payment service like Dwolla is one of the easiest ways for US residents to buy Bitcoins. More popular payments services can't be used to buy on the Mt. Gox exchange'--PayPal, for instance, can't be used to perform currency exchanges. Mt. Gox is the largest Bitcoin exchange, handling about 63 percent of all Bitcoin purchases.
Thu, 16 May 2013 09:04
A move by the U.S. government to rein in the unregulated use of Bitcoin involved the seizure of a Japanese company's account at Wells Fargo (WFC).
Mt. Gox, the world's largest exchange for trading the virtual currency, has operated as an unlicensed money transmitting business in violation of federal law, the Department of Homeland Security charged in warrants issued recently by the U.S. District Court in Baltimore.
The warrants authorize the government to seize funds held in accounts that Mt. Gox, based in Tokyo, allegedly maintains at Wells Fargo, the nation's fourth-biggest bank, and at Dwolla, an alternative payments provider in Des Moines, Iowa.
While opening a Wells Fargo account for a subsidiary in 2011, Mt. Gox's chief executive allegedly answered "no" when asked by the bank if his company dealt in, exchanged or transmitted money.
A Wells Fargo spokesman would not discuss the warrant on Wednesday.
U.S. law requires businesses that transmit money to adhere to state licensing laws and to register with the Treasury Department's Financial Crimes Enforcement Network, which enforces laws that aim to prevent money laundering.
Businesses that register with Fincen also must authenticate the identity of customers and report suspicious activity, a requirement that runs counter to the setup of Bitcoin, which enables users to transact anonymously.
In March, Fincen issued rules "clarifying" that registration requirements apply to certain businesses that deal in bitcoins and other cryptocurrencies. Neither Mt. Gox nor Mutum Sigillum, the Delaware-based subsidiary of the exchange that banked at Wells Fargo, has registered with Fincen as a money services business, the government charged.
"The moment an exchanger is considered a money transmitter a whole slew of regulations fall on you," says Juan Llanos, a risk management expert. "This should be seen as a huge red flag by Bitcoin entrepreneurs."
Mt. Gox said in a Facebook post early Wednesday that it had not seen the warrant but that it would "provide further reports when additional information becomes known."
Dwolla spokesman Jordan Lampe said in an email to PaymentsSource that because of the warrant the company "has ceased all account activated associated with Dwolla services for Mutum Sigillum while Dwolla's holding partner transferred Mutum Sigillum's balance to the proper authorities."
Nicole Navas, a spokeswoman for U.S. Immigration and Customs Enforcement in Baltimore, declined to comment to PaymentsSource.
The seizure means that people who want to convert dollars to bitcoins or vice versa will be unable to do so through Dwolla, which provided settlement accounts for Mt. Gox customers.
Mt. Gox allegedly used the account at Wells Fargo to route funds from overseas to and from accounts at Dwolla at customers' requests.
The seizure also seems calculated to undermine the anonymity of Bitcoin, which serves as a medium of exchange for people who choose to not have their transactions tracked. Because Bitcoin has no central issuing authority, law enforcement agencies view it as a way for people to hide or launder the proceeds of illegal activity.
"Bitcoin offers many of the same challenges associated with other virtual currencies '... and adds unique complexities for investigators because of its decentralized nature," the FBI wrote in a report published last year.
Mon, 13 May 2013 22:59
The White House
Office of the Press Secretary
For Immediate Release
May 12, 2013
I congratulate the people of Pakistan on the successful completion of yesterday's parliamentary elections. The United States stands with all Pakistanis in welcoming this historic peaceful and transparent transfer of civilian power, which is a significant milestone in Pakistan's democratic progress. By conducting competitive campaigns, freely exercising your democratic rights, and persevering despite intimidation by violent extremists, you have affirmed a commitment to democratic rule that will be critical to achieving peace and prosperity for all Pakistanis for years to come.
The United States and Pakistan have a long history of working together on mutual interests, and my Administration looks forward to continuing our cooperation with the Pakistani government that emerges from this election as equal partners in supporting a more stable, secure, and prosperous future for the people of Pakistan.
From Awais Kahn
I am soo depressed right now. It was election day yesterday in pakistan.
The popular vote should have gone to imran khan, the former cricketer.
But on election day, there was rampant corruption. Some examples are:
Armed people walking into polling stations and
shooting into the air. When everyone ran away, they filled in ballot
papers and stuffed boxed.
In certain polling stations, the doors were locked to stop people from entering building.
In certain areas, there was a 100%
voter turnout, and all of these magical 100% voter turn out stations
went to the defending govt.
were people stationed at polling stations, to "guide" people in the
voting process (meaning take the ballot, stamp the right candidate, and
put in ballot for them)
Videos on internet showing whole boxes of ballots being thrown out or burnt
video showing women voters so mad at the police and army rangers
assigned to stop corruption who were not doing anything, that they took
off their jewelary and presented it to the cops and army to shame them
and say you should wear these and stay home......
here is a link: for you to check out...
I know you guys are probably wrapping up sundays show if not already
done so. Maybe you can take a look at this before thursday... I wish I
could show you the support that Imran Khan has, Only candidate that has
not made his money in politics. Only candidate that does his speeches
without a bullet proof shield infront of his face. Only candidate to
actually break bread with the people and sitting on the ground with
them, which is the right way to do it in pakistan. The actual choice of
the people, and somehow he did not win... It truly is one of the worst
most depressing days EVER. When you hope and you pray and you do, but
corrruption still wins, it is really heartbreaking.
Wed, 15 May 2013 10:14
Emails describe how Osama bin Laden's body was washed, wrapped in a white sheet and slid into the sea after religious remarks in ArabicDefense Department says it cannot find any images or videos of bin Laden's aboard USS Carl Vinson Pentagon failed to produce autopsy report, death certificate or results of DNA testsMilitary officials referred to bin Laden's body as 'package' in coded missives Release of emails mark first public disclosure of information about bin Laden's May 1, 2011 deathBy Daily Mail Reporter
PUBLISHED: 19:17 EST, 21 November 2012 | UPDATED: 19:17 EST, 21 November 2012
Enemy No 1: Internal emails released by the Defense Department show that no U.S. sailors witnessed Osama bin Laden's burial at sea aboard USS Carl Vinson
Internal emails among U.S. military officers indicate that no American sailors watched Osama bin Laden's burial at sea from the USS Carl Vinson, and traditional Islamic procedures were followed during the secret ceremony.
The emails, obtained by The Associated Press through the Freedom of Information Act, are heavily blacked out, but are the first public disclosure of government information about the al-Qaida leader's death. The emails were released Wednesday by the Defense Department.
Bin Laden was killed on May 1, 2011, by a Navy SEAL team that assaulted his compound in Abbottabad, Pakistan.
One email stamped secret and sent on May 2 by a senior Navy officer briefly describes how bin Laden's body was washed, wrapped in a white sheet, and then placed in a weighted bag.
According to another message from the Vinson's public affairs officer, only a small group of the ship's leadership was informed of the burial.
'Traditional procedures for Islamic burial was followed,' the May 2 email from Rear Adm. Charles Gaouette reads. 'The deceased's body was washed (ablution) then placed in a white sheet. The body was placed in a weighted bag.
'A military officer read prepared religious remarks, which were translated into Arabic by a native speaker. After the words were complete, the body was placed on a prepared flat board, tipped up, whereupon the deceased's body slid into the sea.'
Final destination: Bin Laden's body was taken to an unknown location aboard USS Carl Vinson and dropped into the sea, but the Defense Department says that it cannot find any images showing the terrorist mastermind's remains on the ship
Fallen mastermind: In this undated file image from video seized from bin Laden's walled compound in Abbottabad, Pakistan, the al Qaeda leader watches TV
Stronghold: Members of the anti-terrorism squad are seen surrounding the compound where bin Laden was killed by Navy SEAL Team 6 in Abbottabad May 4, 2011
The email also included a cryptic reference to the intense secrecy surrounding the mission.
'The paucity of documentary evidence in our possession is a reflection of the emphasis placed on operational security during the execution of this phase of the operation,' Gaouette's message reads.
Long-awaited news: U.S. President Barack Obama is pictured after announcing live on television the death of Osama bin Laden from the East Room of the White House in Washington May 1, 2011
Recipients of the email included Adm. Mike Mullen, then the chairman of the Joint Chiefs of Staff, and Gen. James Mattis, the top officer at U.S. Central Command. Mullen retired from the military in September 2011.
Earlier, Gaouette, then the deputy commander of the Navy's Fifth Fleet, and another officer used code words to discuss whether the helicopters carrying the SEALs and bin Laden's body had arrived on the Vinson.
'Any news on the package for us?' he asked Rear Adm. Samuel Perez, commander of the carrier strike group that included the Vinson.
'FEDEX delivered the package,' Perez responded. 'Both trucks are safely enroute home base.'
Although the Obama administration has pledged to be the most transparent in American history, it is keeping a tight hold on materials related to the bin Laden raid.
In a response to separate requests from the AP for information about the mission, the Defense Department said in March that it could not locate any photographs or video taken during the raid or showing bin Laden's body. It also said it could not find any images of bin Laden's body on the Vinson.
The Pentagon also said it could not find any death certificate, autopsy report or results of DNA identification tests for bin Laden, or any pre-raid materials discussing how the government planned to dispose of bin Laden's body if he were killed.
Historic moment: In this May 1, 2011, image, Secretary of State Hillary Rodham Clinton, President Barack Obama and Vice President Joe Biden receive an update on the bin Laden mission in the Situation Room
The Defense Department also refused to confirm or deny the existence of helicopter maintenance logs and reports about the performance of military gear used in the raid.
One of the stealth helicopters that carried the SEALs to Abbottabad crashed during the mission and its wreckage was left behind. People who lived near bin Laden's compound took photos of the disabled chopper.
The CIA, which ran the bin Laden raid and has special legal authority to keep information from ever being made public, has not responded to AP's request for records about the mission.
Wed, 15 May 2013 10:24
Submitted by Michael Krieger of Liberty Blitzkrieg blog,
In what may be the strangest story I have seen in a while related to the gold market, it appears $982 million worth of gold has left JFK international airport in New York to some undisclosed location in South Africa. While it remains unclear what purpose this gold serves, it seems the most likely explanation is to fulfill demand for Krugerrands (South Africa's popular gold bullion coin) to meet elevated demand in the face of constricted mine production. This story is timely coming on the heels of the article I posted yesterday about how Dubai's gold demand is running at 10x normal levels. This is a bizarre story, so if anyone has further color I'd love to hear it.
Examining US trade data, we were surprised to see that South Africa's $402 million trade surplus with the United States in January had turned into a $689 million deficit by March.
It turns out the $1.1 billion swing is entirely due to unusual shipments of gold from the US to South Africa in February and March. So far this year, 20,013 kg of unwrought gold, worth $982 million, has left John F. Kennedy International Airport (JFK), in New York, for somewhere in South Africa, according to the US Census Bureau's foreign trade division. (Unwrought gold includes bars created from scrap as well as cast bars, but not bullion, jewelry, powder, or currency.)
The shipments from JFK were the only unwrought gold to leave the US for South Africa in 2013; another large shipment occurred in September 2012.
However, the strikes that rocked South Africa's mining industry last year briefly caused gold output to fall sharply, around the same time as last autumn's big gold shipment from JFK. Overall 2012 production declined by a relatively modest 6% (pdf) over the year before, according to a preliminary figure from the US Geological Survey; but those first estimates have sometimes proven wide of the mark. (In 2009 the USGS estimated South Africa's 2008 production to be 250 tons; it subsequently revised the figure to 213 tons.) So it could be that the strikes dealt a more severe blow to the country's gold industry than the data show.
Still, even if gold output did fall precipitously, it's not clear why South Africa would need to start importing it. One possible destination for the gold is the South African Mint, which produces legal-to-own gold coins called Krugerrands; the gold used in them is first refined by the Rand refinery. Calls to the South African embassy in Washington, DC were not returned.
Meanwhile how about this chart, courtesy of the Quartz article.
Full article here.
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Wed, 15 May 2013 16:30
U.S. diplomat named as Ryan Christopher Fogle was arrested on MondayRussia claim he was attempting to recruit a Russian secret services officialLetter allegedly found on him offers agents $1million per year to defectU.S. ambassador summoned to Russian foreign ministry to explain todayBy Daily Mail Reporter
PUBLISHED: 06:44 EST, 15 May 2013 | UPDATED: 07:20 EST, 15 May 2013
The arrest of a US diplomat accused of being a CIA spy was linked to the Boston bombing, sources revealed today.
Russian security officials reported on Tuesday that they had briefly detained Ryan Fogle in Moscow for allegedly trying to recruit a Russian intelligence officer.
Today sources revealed the man Mr Fogle was trying to 'recruit' was an FSB agent who specialised in Islamic extremism in Russia and may even have travelled to the region where the bombing suspects came from.
Lure: Sources today said that Ryan Fogle, right, was seeking to lure into treachery an FSB agent who had knowledge of Russian intelligence operations on suspected Boston terrorist Tamerlan Tsarnaev, left
It is thought that he was part of a team who went to Dagestan and provided intelligence to the United States about an extremist threat in 2011.
Fogle, a third secretary at the U.S. Embassy, who was carrying special technical equipment, disguises, written instructions and a large sum of money. Fogle was later handed over to U.S. Embassy officials.
This morning the Russian foreign ministry today issued a formal protest to American ambassador Michael McFaul who was summoned to explain the alleged espionage mission of one of his diplomats.
As he left after the brief session with Deputy Foreign Minister Sergei Ryabkov, the envoy waved to reporters but refused to comment.
Relations: U.S. Ambassador Michael McFaul walks outside as he leaves the Russian Foreign Ministry headquarters in Moscow. He was summoned to explain the alleged espionage mission of one of his diplomats
The Ministry hit out at 'provocative acts in the spirit of the Cold War' and has ordered the expulsion of Fogle, arrested wearing a blond wig under his baseball cap.
'This does not contribute to the further process of building mutual trust between Russia and the United States and bringing our relations to a qualitatively new level,' warned Dmitry Peskov, spokesman for Russian president Vladimir Putin.
But it was becoming clearer today that the US was seeking to lure into treachery an FSB agent who had knowledge of Russian intelligence operations on suspected Boston terrorist Tamerlan Tsarnaev, who lived in America but had travelled to Dagastan where he was believed to have met Islamic extremists.
Arrested: The US diplomat - suspected by the Russian of being a CIA agent - was named as Ryan Christopher Fogle. He was arrested last night in Moscow
Claims: The FSB counter intelligence service said the envoy, a third secretary in the political section of the American embassy was caught red handed seeking to recruit a Russian intelligence officer
Detained: The FSB said Fogle was in possession of two floppy wigs, three pairs of glasses, a map of Moscow and a folding knife when he was detained
Seized: After his arrest, he was taken to the FSB headquarters at the Lubyanka, in Moscow, and later handed over to the US embassy in keeping with diplomatic protocols
Just call me James... blond? Russian intelligence services parade the 'CIA spy', named as Ryan Christopher Fogle, for cameras on Monday
The FSB had earlier warned the FBI about his potential extremist links.
In material released by the FSB, it is clear the Americans had phone numbers for one or more Russian intelligence agents involved in anti-terrorism work in the Caucasus.
They obtained these during trip involving FBI agents to Dagestan in search of intelligence on Tamerlan's trip.
'After the first call he refused to meet, but this man called again and insisted on a meeting,' said a recording of a FSB officer addressing three US diplomats who came to collect the alleged CIA agent from FSB headquarters.
'At first we did not believe it was happening, because recently the FSB has been actively helping to investigate the Boston blasts, and was also providing some other information about threats to US national security'.
Today Kommersant newspaper said: 'It is likely that during the trip in April the US side obtained the phone numbers of Federal Security Service (FSB) agents.'
'Clearly, they then decided to use it to have personal contacts with anti-terror agents, given that the exchange of information in the form of question and answers between special services is not always quick and smooth,' it said.
Russia has not named the target of the US co-operation, and it is not known whether the agent has faced any problems or even arrest over the US interest in him.
Fogle apparently hinted at an initial payment of $100,000 followed up a salary of up to $1 million a year plus bonuses if the Russian intelligence official handed over secrets to the CIA.
Russian Foreign Minister Sergei Lavrov said he had opted not to bring up the case at talks with US Secretary of State John Kerry on Tuesday in Sweden.
'I decided that talking about it would be superfluous, since it is already made public and everyone already understands everything,' he said.
Statement: 'Recently, the US intelligence service has made repeated attempts to recruit the staff of Russian law enforcement agencies and special services,' according to the FSB
Stash: He was detained with 'special technical devices, written instructions for the person he was recruiting, a lot of cash, and things to help change one's appearance,' according to the FSB
Mission: The website of the American embassy in Russia informs that its Political Section is engaged in 'bringing to the attention of the Russian government the US position on the issues of foreign policy and security'
Questions: A letter the agent carried suggested the US government was willing to pay up to $1 million a year plus bonuses to his unidentified potential Russian recruit, if the letter released by the FSB is genuine
Release: Fogle was held overnight before being released to U.S. officials and expelled from Russia
Fogle was the first American diplomat to be publicly accused of spying in Russia in about a decade.
While relations between the two countries have been strained, officials in both Washington and Moscow sought to play down the incident.
Fogle was caught in Vorontsovski Park, an area in south-east Moscow, the FSB said.
A letter in Russian which Fogle carried suggests '' if genuine '' that the CIA hoped to reel in a big fish.
Addressed 'Dear friend', it states: 'We are ready to offer you $100,000 [£65,000] and discuss your experience, expertise and co-operation, and the payment may go much higher if you are ready to answer certain questions.
'For long-term co-operation we offer $1million [£650,000] per year.'
The recruit is instructed to use an internet cafe to 'create a new Gmail mailbox which you will use only for staying in touch with us'.
The incident is the biggest spy scandal since the arrest of glamorous agent Anna Chapman and nine other Russians in the US in 2010.
The FSB stated: 'Recently, the US intelligence community has made repeated attempts to recruit employees of Russia's law-enforcement bodies and special agencies.'
Many details remained shrouded in mystery last night. It is not known whether the target was part of the sting operation or if they have been arrested.
Russia's haste to make the news public could mean either that the attempt was so audacious that it shocked leaders, or that hardliners have seized on it to stop a move towards detente with the US.
Yesterday Patty Fogle, the diplomat's mother, refused to comment at her home in St Louis, Missouri.
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Tue, 14 May 2013 11:49
A woman walks on a street, as the headquarters (L) of the Federal Security Service is seen in the background, in central Moscow, May 14, 2013.
Credit: Reuters/Maxim Shemetov
By Steve Gutterman
MOSCOW | Tue May 14, 2013 3:46pm BST
MOSCOW (Reuters) - Russia said on Tuesday it had caught an American red-handed as he tried to recruit a Russian intelligence officer to work for the CIA, a throwback to the Cold War era that risks upsetting efforts to improve relations.
The announcement came at an awkward time, just days after a visit by U.S. Secretary of State John Kerry during which Washington and Moscow agreed to try to bring the warring sides in Syria together for an international peace conference.
The Federal Security Service said Ryan Fogle, a third secretary at the U.S. Embassy in Moscow, had been detained overnight carrying "special technical equipment", a disguise, a large sum of money and instructions for recruiting his target.
The Russian Foreign Ministry said it had summoned U.S. Ambassador Michael McFaul over the case and a Russian television station published photographs which it said showed Fogle being detained, apparently wearing a blond wig.
A successor of the Soviet-era KGB, the FSB said Fogle worked for the Central Intelligence Agency and that he had been handed over to embassy officials at some point after his detention.
Diplomats accused of espionage are usually expelled or withdrawn.
"On the night of May 13-14, a staff employee of the CIA, Ryan Christopher Fogle ... was detained by counter-espionage organs of the Russian FSB while attempting to recruit an employee of one of the Russian special services," the FSB said.
"Recently American intelligence has made multiple attempts to recruit employees of Russian law enforcement organs and special agencies, which have been detected and monitored by Russian FSB counterintelligence," it said in a statement.
The embassy declined comment. McFaul, a former adviser to President Barack Obama, was holding a live question-and-answer session on Twitter as news of the detention was announced, but refused to take questions on the matter.
Russia Today television published photographs on its website which it said showed Fogle being detained. In one photograph, a man lies face-down on the ground with his arms held behind his back by another man, and apparently wearing a blond wig.
Another image showed two wigs, apparently found on him, as well as three pairs of glasses, a torch, a mobile phone and a compass. Aldo displayed was a wad of 500-euro (425.36 pounds) notes and an envelope addressed to a "dear friend".
The United States and Russia are still involved in espionage, more than two decades after the collapse of the Soviet Union and the end of the Cold War, and the FSB said such incidents were not unusual.
The last major espionage scandal occurred in 2010, when 10 Russian agents including Anna Chapman were arrested in the United States and later deported in exchange for four Russians imprisoned on charges of spying for the West.
U.S.-Russian relations turned colder after former KGB spy Vladimir Putin returned to the presidency a year ago.
The United States and Russia are also trying to improve counterterrorism cooperation following the Boston Marathon bombings on April 15. FBI chief Robert Mueller visited Moscow for talks last week.
(Writing by Steve Gutterman and Timothy Heritage, Editing by Elizabeth Piper)
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Why are our spies not hot like the russian babes?
Title I General provisions Definitions of variety and its maintenance, variety with official description or variety with officially recognised description, clone as well as of the different marketing categories are laid down. Title II Production and making available on the market of listed species In general, the basic approach on registration of varieties/material and certification/inspection of lots before making available on the market will be maintained. However, more flexibility will be given to the professional operators so that they may decide to carry out the necessary examination for variety registration or inspections, sampling and analysis of plant reproductive material for certification under the official supervision of the competent authorities. In addition, secondary acts will be adopted setting out the specific requirements for the production and making available on the market of particular species and their categories (pre-basic, basic, certified and standard material). This is important to increase flexibility for changes due to technical and scientific developments and at the same time respecting proportionality and sustainability in regulatory approach. The requirements for making available on the market of plant reproductive material may be summarised as follows: -- it belongs to a variety or clone registered in accordance the provisions of this Regulation; -- it complies with the specific requirements adopted for the marketing category concerned per genera and species; -- it bears an official label for pre-basic, basic or certified material, or an operator's label in case of standard material; -- it complies with the handling requirements; -- it complies with the requirements for certification and identification.
Thu, 16 May 2013 07:15
By Sarah Frier and Ari LevyMay 16, 2013 12:01 AM EDTInternational Business Machines Corp. (IBM) will offer its Watson technology, which beat humans in ''Jeopardy!,'' as a building block for startup companies making business software.
''We'll launch an ecosystem where Watson is a service and you build applications around it,'' Chief Executive Officer Ginni Rometty said in a speech at the annual meeting of the National Venture Capital Association in San Francisco.
Rometty has been taking steps to commercialize Watson, a high-powered computer that can answer questions after being preloaded with documents and websites. It has been deployed in the health and finance markets since its debut on the trivia show ''Jeopardy!'' in 2011, with its first products for the doctors and medical researchers announced this year.
Soon, other businesses will be able to design software that takes advantage of Watson's cognitive computing technology. Rometty said the move would help usher in an era of ''systems that learn on their own.''
''That's what will be of value in the future, this domain expertise,'' Rometty said yesterday. ''It's a question-and-answer, it's not a search.''
IBM has already worked with doctors to build applications using Watson's technology, including one that can be used to help diagnose and treat certain types of cancer. The doctor inputs information about the patient's condition, and then Watson responds with a possible diagnosis and treatment plan, displaying the evidence and percentage of confidence for each theory.
In 2012, Watson became 240 percent faster and 75 percent smaller so it can run on a single server, IBM said in February. The Armonk, New York-based company now can install a Watson machine on-site for a business or remotely via cloud computing to a personal computer, tablet or smartphone.
Rometty didn't indicate how many developers would get access to Watson's technology.
To contact the reporters on this story: Sarah Frier in New York at firstname.lastname@example.org; Ari Levy in San Francisco at email@example.com
To contact the editor responsible for this story: Nick Turner at firstname.lastname@example.org
I'm sure you've seen the media push to get the legal drunk blood alcohol level down
to 0.05%, which is 1 beer for the average woman. Perhaps they should just issue
tickets for being "pre-drunk".
Sir Dr Sharkey
The NTSB also called for higher penalties for first and repeat offenders and arming police officers with technology such as "sniffing flashlights" to detect alcohol. The agency does not have the authority to impose its recommendations on states, but its opinion carries weight with policymakers.
The NTSB's recommendation even drew lukewarm support from the national president of Mothers Against Drunk Driving, who said the effort would take too long and undercut more effective programs. MADD President Jan Withers, an Upper Marlboro resident, said her organization's three-pronged campaign could save many more lives. The plan is built around high-visibility law enforcement, ignition locks to prevent convicted drunken drivers from getting on the road and passive technology that measures the blood alcohol content of motorists. "We want to save as many lives as possible as soon as possible," Withers said. "We respect the NTSB and its research, but it will take 15 to 20 years to change the laws in each state. We're already moving forward on our campaign, and it will happen sooner than what the NTSB can accomplish."
Wed, 15 May 2013 00:13
Even moderate drinking before driving could become illegal if a federal safety panel's recommendation Tuesday is enacted eventually by the states.
The National Transportation Safety Board recommended that states cut their thresholds for drunken driving by more than a third '-- from a blood-alcohol content of .08 percent to .05 percent '-- to reduce highway fatalities. A 180-pound man would reach 0.05 BAC by consuming three beers in one hour, according to a Wisconsin Department of Transportation online calculator.
The proposal, among others by the board, faces a long road before, if ever, becoming the law of the land. It took more than 20 years for all the states to act after the NTSB recommended reducing the drunk driving threshold in 1982.
Lowering the blood-alcohol benchmark could reduce the annual drunken-driving death toll of nearly 10,000 lives by as much as 10 percent, the board said.
The NTSB's recommendation even drew lukewarm support from the national president of Mothers Against Drunk Driving, who said the effort would take too long and undercut more effective programs.
MADD President Jan Withers, an Upper Marlboro resident, said her organization's three-pronged campaign could save many more lives. The plan is built around high-visibility law enforcement, ignition locks to prevent convicted drunken drivers from getting on the road and passive technology that measures the blood alcohol content of motorists.
"We want to save as many lives as possible as soon as possible," Withers said. "We respect the NTSB and its research, but it will take 15 to 20 years to change the laws in each state. We're already moving forward on our campaign, and it will happen sooner than what the NTSB can accomplish."
In 2011, the most recent year of federal statistics, 33 percent of Maryland's 485 traffic fatalities involved alcohol, an increase of 2 percentage points over the previous year.
The NTSB also called for higher penalties for first and repeat offenders and arming police officers with technology such as "sniffing flashlights" to detect alcohol. The agency does not have the authority to impose its recommendations on states, but its opinion carries weight with policymakers.
"Most Americans think that we've solved the problem of impaired driving, but in fact, it's still a national epidemic," said NTSB Chairman Deborah A.P. Hersman in a statement. "On average, every hour one person is killed and 20 more are injured."
NTSB studies indicate that at 0.05, depth perception and other visual skills begin deteriorating in some drivers and the risk of having an accident jumps by 39 percent. At 0.08 BAC, the risk of having an accident increases by more than 100 percent.
Most European and South American countries have set BAC levels at 0.05 for drunken-driving charges.
Withers cautioned that the same forces behind the prolonged fight against lowering the BAC from 0.10 to 0.08 are sure to oppose any further changes. Already, the American Beverage Institute, a restaurant trade association, blasted the recommendation as "ludicrous." The Governors Highway Safety Association said it would review the recommendations, but supports the 0.08 level.
In 1982, the NTSB recommended that states reduce the drunken-driving limit from 0.10 BAC. Utah became the first state to lower its limit the following year, but Maryland didn't take the step until 2001, just three years before 0.08 became enacted by every state.
The General Assembly has shown a deep reluctance to pass new laws cracking down on drunken driving. Each year, many bills on alcohol and driving are proposed, but few succeed.
Annapolis lobbyist Bruce Bereano, who has represented alcohol distributors, said a decrease to 0.05 would be "like going back to the Prohibition era."
"Nobody wants drunken-driving accidents," Bereano said. "But 0.08 has worked very well. I assume it will be brought up next session, in an election-year session. It would take hard, reliable data to convince [lawmakers] that the current laws and enforcement are not adequate."
Historically, the highest hurdle for such bills has been the House Judiciary Committee.
Del. Kathleen Dumais, vice chairman of the committee, said that the legislature acted in 2001 only under the threat of the loss of federal highway funds.
Dumais, a Montgomery County Democrat who was not a legislator at the time, said lawmakers will have to examine how the 0.05 standard would be implemented and what the implications would be.
"I do see some opposition." she said.
In the past, proposals to lower the blood-alcohol level have been fought especially hard by restaurant and tavern owners.
Dumais, who served on a 2007-2008 task force on Maryland drunken-driving laws, said she's willing to take a look at the proposal but is not convinced that a 0.05 standard would be a "panacea." She said lawmakers might want to consider other remedies such as stricter ignition interlock laws, tougher penalties and stepped-up enforcement of current laws.
Gov. Martin O'Malley's office referred a question about the proposal to the sate Department of Transportation. Department spokeswoman Erin Henson said the governor's highway safety representative, Motor Vehicle Administration chief John Kuo, is evaluating the recommendation.
"We are focused on making sure that our roads are as safe as possible for Maryland families," Henson said.
Lon Anderson, the chief lobbyist for AAA Mid-Atlantic, said that while there has been a "sea change in how we view drunken driving, moving the needle again on blood-alcohol content will be a major struggle."
"It's the beginning of a national discussion that will include the need to educate the American people, who will have to be convinced this is a beneficial thing" Anderson said. "It's not something that's going to happen today or tomorrow."
Sun reporter Michael Dresser contributed to this article.
Wed, 15 May 2013 00:13
Ramin Rahimian for The New York Times
A police officer in San Jose, Calif., administering a breathalyzer test in 2010. The current standard of 0.08 percent blood-alcohol concentration was established a decade ago at the instigation of Congress.
WASHINGTON '-- Thousands of people are killed or injured every year by drivers who have not reached the legal standard for being drunk but who have a reduced ability to see, make decisions or operate a vehicle, the National Transportation Safety Board said on Tuesday, and it recommended that the states reduce the allowable blood-alcohol concentration by more than a third, to 0.05 percent from 0.08 percent.
The current standard was established a decade ago at the instigation of Congress, and progress has stalled, the board said, with about 10,000 fatalities a year.
''There are at least 10,000 reasons to tackle this issue,'' said Deborah A. P. Hersman, the chairwoman of the board. Foreign countries with stricter standards have had substantially more success, according to the board.
The board voted for a variety of recommendations. Some, like requiring that everyone convicted of drunken driving be required to install a Breathalyzer interlock in their car, which would prevent the vehicle from starting without an alcohol test, were focused on heavy drinkers and repeat offenders.
Officials said they hoped that a stricter standard would reduce drinking and driving both among social drinkers and among heavy drinkers.
Blood-alcohol concentration varies by body weight, gender, stomach contents and other factors, but generally speaking, a 180-pound man could consume four beers or glasses of wine in 90 minutes without reaching the current limit. At a limit of 0.05 percent, he could legally consume only three. A 130-pound woman could probably consume three drinks in 90 minutes and be legal under the existing standard; if the limit were lowered, she could consume only two.
The blood-alcohol recommendation faces opposition. Sarah Longwell, the managing director at the American Beverage Institute, a restaurant trade association, called the idea ''ludicrous.''
''Moving from 0.08 to 0.05 would criminalize perfectly responsible behavior,'' she said. And ''further restriction of moderate consumption of alcohol by responsible adults prior to driving does nothing to stop hard-core drunk drivers from getting behind the wheel.''
The board is already on record favoring research on built-in alcohol detectors, which could measure blood-alcohol content through a driver's palms on the steering wheel or some other unobtrusive way. Those could be available as an option on new cars or could be universally required. Either would affect drinkers who have never been caught driving, who make up more than 90 percent of those involved in fatal alcohol-related crashes.
People with a blood-alcohol level of 0.05 percent are 38 percent more likely to be involved in a crash than those who have not been drinking, according to government statistics. People with a blood-alcohol level of 0.08 percent are 169 percent more likely.
The standard in most of the industrialized world is 0.05 percent. All 50 states and the District of Columbia switched to 0.08 percent after President Bill Clinton signed a law in 2000 that withheld highway construction money from states that did not agree to that standard.
''These tragedies affect both sides,'' said Robert J. Sumwalt, one of the board members. He said his wife's first cousin was killed by a drunken driver who was traveling down a highway in the wrong direction. And his own cousin, he said, goes on Sundays to visit her 21-year-old daughter who was sentenced to 15 years in prison for drunken driving.
Progress is mostly a matter of political will, board members said.
About 30 percent of all vehicle fatalities are tied to drunken driving, down from 50 percent when President Ronald Reagan raised the issue 30 years ago. The number of deaths is down to about 10,000 a year from about 21,000 over the same period. Highway deaths are decreasing over all because of better-designed cars, seat belt use and better highways.
The board has the support of other safety advocates, but not Mothers Against Drunk Driving. That group said it favored many parts of the board's agenda, including the mandatory installation of the Breathalyzer interlock for anyone convicted of driving drunk, research on the passive alcohol sensors and ''administrative license revocation,'' which gives police officers on the highway the authority to seize a driver's license at the time of an arrest. Those show strong potential for reducing the death toll, said J. T. Griffin, a Washington representative of the group.
The discussion of changing the definition of drunk, Mr. Griffin said, was the safety board's ''trying to focus on a group of people who are more social drinkers, who haven't been targeted in a while.'' MADD would not oppose the change, he said, but would pursue other remedies.
Mon, 13 May 2013 17:20
The White House
Office of the Press Secretary
For Immediate Release
May 13, 2013
Dear Mr. Speaker: (Mr. President:)
Section 202(d) of the National Emergencies Act (50 U.S.C. 1622(d)) provides for the automatic termination of a national emergency unless, within 90 days prior to the anniversary date of its declaration, the President publishes in the Federal Register and transmits to the Congress a notice stating that the emergency is to continue in effect beyond the anniversary date. In accordance with this provision, I have sent to the Federal Register for publication the enclosed notice stating that the national emergency declared in Executive Order 13611 of May 16, 2012, with respect to Yemen is to continue in effect beyond May 16, 2013.
The actions and policies of certain members of the Government of Yemen and others continue to threaten Yemen's peace, security, and stability, including by obstructing the implementation of the agreement of November 23, 2011, between the Government of Yemen and those in opposition to it, which provided for a peaceful transition of power that meets the legitimate demands and aspirations of the Yemeni people for change, and by obstructing the political process in Yemen. For this reason, I have determined that it is necessary to continue the national emergency declared in Executive Order 13611 with respect to Yemen.
Mon, 13 May 2013 16:39
Official U.S. Navy file photo shows Sailors aboard the aircraft carrier USS Kitty Hawk (CV 63) raising the First Navy Jack.
A group of New York veterans is preparing to march into court after a town ordered the Gadsden flag removed from a military armory.
The city of New Rochelle, N.Y., has removed the Gadsden ''Don't Tread on Me'' flag from the New Rochelle Armory after the city council refused to let a veterans organization display the flag, World Net Daily reported.
The United Veterans Memorial and Patriotic Association of New Rochelle is fighting the decision, ordered by City Manager Chuck Strome after complaints that the flag is a symbol of the Tea Party movement, according to World Net Daily.
''Many Americans fought and died for our independence under that flag. . ."
- Richard Thompson, of the Thomas More Law Center
But Strome did an about-face after Peter Parente, president of United Veterans Memorial, sent Strome the history of the Gadsden flag, which is flown beneath the U.S. flag on many military sites, according to World Net Daily.
Then the New Rochelle City Council overruled Strome, voting 5-2 to have the flag removed.
According to the Washington Examiner, the council objected to the flag because they said Parente is a member of the Tea Party and wants to display the flag to push a political agenda.
Parente said no one in the veterans group is a Tea Party member. ''I'm a proud Republican,'' he told the council, according to the Examiner.
Now, the veterans have found an ally in the Thomas More Law Center and are ready to go to court.
''Their outrageous decision to confiscate a cherished symbol of our War for Independence smacks of pure partisan politics,'' Richard Thompson, chief counsel of the Thomas More Law Center, told World Net Daily.
''Many Americans fought and died for our independence under that flag, and the law center will take available means to return the Gadsden flag back on the veterans' flag pole. As one Revolutionary War hero said, we 'have just begun to fight,''' he added.
According to the U.S. Navy website, beginning Sept. 11, 2002, all U.S. Navy ships have flown the First Navy Jack flag. The flag, first used by the Continental Navy in 1775, consists of a rattlesnake superimposed across 13 alternating red and white stripes with the motto, ''Don't Tread On Me.''
According to the site, Commodore Esek Hopkins used the First Navy Jack as a signal to engage the British in the American Revolution. The Jack in today's fleet represents a historic reminder of the nation's origin.
Click for more from World Net Daily.
Mon, 13 May 2013 17:20
A new United Nations report say the health benefits of consuming nutritious insects could help fight obesity and world hunger.
More than 1,900 species of insects are eaten around the world, mainly in Africa and Asia, but people in the West generally turn their noses up at the likes of grasshoppers, termites and other crunchy fare.
The authors of the study, which was published on Monday, by the Forestry Department, part of the UN Food and Agriculture Organisation (FAO), said many insects contained the same amount of protein and minerals as meat and more healthy fats doctors recommend in balanced diets.
Al Jazeera's Jessica Baldwin, reporting from London, said that there is no shortage in supply as there are 1,900 edible insect species on the planet, 40 tonnes of insects to every human.
"But it's not for everyone. Getting over people's squeamishness the UN admits will be a big challenge," she said.
Eva Muller of the FAO said restaurants in Europe were starting to offer insect-based dishes, presenting them to diners as exotic delicacies.
As well as helping in the costly battle against obesity, which the World Health Organisation estimates has nearly doubled since 1980 and affects around 500 million people, the report said insect farming was likely to be less lan -dependent than traditional livestock and produce fewer greenhouse gases.
It would also provide business and export opportunities for poor people in developing countries, especially women, who are often responsible for collecting insects in rural communities.
Mon, 13 May 2013 15:48
Hunger strikers being force-fed at Guantanamo Bay must wear masks over their mouths while being shackled to a restraint chair for up to two hours. Authorities have revised the way they feed the strikers, comparing their techniques to battlefield tactics.
Nasal tubes are jammed up the prisoners' noses until a liquid supplement reaches their stomachs. The tubes, which are 61cm in length or even longer, stay in the prisoners' nostrils until a chest X-ray or a test dose of water show that the nutritional supplement has reached the prisoner's stomach.
The shocking procedure doesn't stop there. Detainees are then sent to a ''dry cell'' with no running water while they undergo supervision to make sure they don't vomit. If they regurgitate their supplement, they're sent right back to the restraint chair.
Details of the "chair restraint system clinical protocol" were published in a newly revised Standard Operating Procedure (SOP) for Guantanamo hunger strikers. The document was obtained by Al Jazeera, from the United States Southern Command (SOUTHCOM), which has oversight over the joint task force that operates the highly controversial prison.
The new policy went into effect March 5, just one month after Guantanamo detainees launched the hunger strike in response to alleged mistreatment and mishandling of their Korans.
"Just as battlefield tactics must change throughout the course of a conflict, the medical responses to GTMO detainees who hunger strike has evolved with time," the revised SOP says. Two weeks ago, 40 more nurses were sent to Guantanamo Bay to assist with force-feedings.
Force-feeding is an extremely invasive and highly controversial practice which many human rights activists - and the UN - say is torturous. But what's perhaps even more shocking than the procedure itself is that the final decision regarding who will be force-fed is left up to Guantanamo Commander John Smith - not physicians.
''In the event a detainee refrains from eating or drinking to the point where it is determined by the medical assessment that continued fasting will result in a threat to life or seriously jeopardize health, and involuntary feeding is required, no direct action will be taken without the knowledge and written approval of Commander [Navy Rear Adm. John Smith, Jr.],'' the document says.
While doctors are, in fact, present at the site, they exist solely to carry out the military's commands.
According to Leonard Rubenstein, a lawyer at the Center of Public Health and Human Rights at Johns Hopkins University and the Berman Institute of Bioethics, the document is alarming because it makes clear that doctors and nurses are simply ''adjuncts of the security apparatus.''
"The clinical judgment of a doctor or a nurse is basically trumped by this policy and protocol. Doctors are not acting with the kind of professional medical independence,'' he said.
Giving Cmdr. Smith such extreme power to decide who gets force-fed ''violates core ethical values of the medical profession,'' American Medical Association president Dr. Jeremy Lazarus wrote in a letter to Secretary of Defense Chuck Hagel last month.
''Every competent patient has the right to refuse medical intervention, including life-sustaining interventions,'' he wrote. ''The AMA has long endorsed the World Medical Association Declaration of Tokyo, which is unequivocal on the point: 'Where a prisoner refuses nourishment and is considered by the physician as capable of forming an unimpaired and rational judgment concerning the consequences of such a voluntary refusal of nourishment, he or she shall not be fed artificially.'''
But authorities seem to place less value on the rules and ethics of the World Medical Association Declaration than Lazarus does. According to the SOP, medical professionals will make ''reasonable efforts'' to gain consent from prisoners, but will perform the procedure without being granted such permission.
According to one detainee, Kuwaiti-born Fayiz al-Kandari, the nasal tubes used in the procedure are large, painful and come with hazardous side effects.
"It takes several attempts to get the tube into the right place,'' his lawyer, Carlos Warner, said. ''Once it goes down his throat he has a difficult time breathing. There's a gag reflex.''
But the SOP says otherwise, claiming that the force-feeding can "be completed comfortably over 20 to 30 minutes."
Guantanamo spokesman Lt. Col. Samuel House said that medical professionals who conduct the force feedings ''carefully evaluate each patient to determine the appropriate size of tube to use.'' He added that the sizes of the tubes used ''should not be a big problem in an adult.''
Those on the receiving end of the force-feeding disagree. However, they have no option but to sit shackled to the restraint chair and let the procedure take place against their will - because the anti-spitting and biting masks are in place to prevent them from interrupting the process.
If the inmates do succeed in biting the feeding tubes, they face even more force and discomfort.
''If the detainee is able to get the [enteral feeding] tube between his teeth, the RN [registered nurse] shall'...direct the guard staff to stabilize the detainee's head in the midline position'...hold traction on the tube for as long as necessary for the detainee to relax his jaw; then continue safe removal of the tube. This may take considerable time,'' the document says.
While the detainees show no signs of ending their hunger strike, US authorities at the prison remain determined to follow the practices outlined in the SOP - despite any criticism from human rights activists or the UN.
And it seems US President Barack Obama doesn't have a problem with the force-feeding techniques.
Less than two weeks ago, the President said he believes the ''Pentagon is trying to manage the situation as best as they can,'' adding that he doesn't want ''these individuals to die.''
Obama vowed to close down Guantanamo at the beginning of his first term in office in 2009. However, he was blocked from fulfilling that promise by legislation passed by the US Congress.
Less than two weeks ago, Obama vowed to ''re-engage with Congress to try to make the case [Guantanamo] is not something that's in the best interests of the American people.''
There are currently 100 inmates participating in the hunger strike at Guantanamo Bay, 29 of whom are receiving enteral feeds. Five of those prisoners are being observed in the detainee hospital, Lt. Col. Samuel House said in a Monday statement. The official numbers differ from those of human rights activists, who have put the number of strikers up to 130.
Mon, 13 May 2013 13:26
Detroit '-- Federal agents arrested a Saudi Arabian traveler who arrived at Detroit Metropolitan Airport with a pressure cooker, a key component used in the Boston Marathon bombings last month.
Hussain Al Kwawahir will be arraigned at 1 p.m. in federal court for allegedly using an altered passport and lying to a Customs and Border Protection Agent about the pressure cooker.
Al Kwawahir arrived at the airport Saturday from Saudi Arabia, via Amsterdam, according to a criminal complaint filed Monday in federal court.
He told agents he was visiting his nephew, who attends the University of Toledo.
During baggage inspection, officers noticed a page missing from his passport.
Al Kwawahir told officers he did not know how the page was removed from the passport.
During the baggage exam, officers found a pressure cooker.
Al Kwawahir said he brought the pressure cooker for his nephew because the devices are not sold in the United States, according to the complaint.
Later, he changed his story and admitted that his nephew had purchased a pressure cooker in the U.S. but it was cheap and broken.
Come back to www.detroitnews.com for more on this developing story.
Tue, 14 May 2013 14:38
TORONTO - On any given day, about one in 12 adults in hospitals across Canada are either colonized or infected with a superbug, the first national survey to determine the prevalence of antibiotic-resistant organisms has found.
The survey of 176 acute-care hospitals looked at rates of infection or colonization in patients from three bacterial microbes that have become immune to the killing effects of most or all antibiotics '-- MRSA (methicillin-resistant Staphylococcus aureus), VRE (vancomycin-resistant Enterococci) and Clostridium difficile.
"And that by itself is a substantial burden of disease," said principal researcher Dr. Andrew Simor, head of infectious diseases at Sunnybrook Health Sciences Centre in Toronto.
"About one in 12 adults ... are going to have one of these three antibiotic-resistant organisms, and clearly the rate would be even higher if you started to add on other resistant organisms that we were not able to measure," Simor added.
Patients can carry, or be colonized by, a microbe like MRSA, but have no signs of active disease, while those who are infected are sick and have symptoms. (All patients with C. diff in the study were infected and had diarrhea and other symptoms.)
However, those who carry a bug can go on to become infected. For example, from one-quarter to one-third of patients colonized with MRSA become infected with the superbug, which can attack the skin and soft tissue, cause a form of pneumonia or invade the bloodstream. About 30 to 60 per cent of MRSA pneumonia patients and 20 to 40 per cent of those with MRSA bloodstream infections die.
Carriers can also spread a superbug to other patients, especially the elderly and those with weakened immune systems due to other illnesses and whose hospital beds are in close proximity.
In Canada, most patients with VRE are colonized rather than infected, said Simor, noting that isn't the case in the United States, where the pathogen causes a "huge burden of disease."
Findings from the November 2010 survey, published Monday in the journal Infection Control and Hospital Epidemiology, provide a snapshot of superbug prevalence in Canada, but also suggest which measures seem to help reduce their spread.
"Number 1, there's no doubt that antibiotic use drives the development of antibiotic resistance," said Simor, explaining that overuse of antibiotics can wipe out susceptible bacterial strains, allowing resistant strains to proliferate.
"So one factor is how antibiotics are used, both in the community and in hospital settings, and also in the agricultural and veterinary sections as well. So it's the cumulative antibiotic utilization that is still at substantially high levels that drives resistance."
In hospitals, the internal mechanisms that make superbugs drug-resistant can be transmitted between different bacteria as well as from patient to patient, he said.
There are two main strategies to prevent people getting infected or colonized with microbes like MRSA: eliminating inappropriate use of antibiotics '-- which kill bacteria but have no effect on viruses such as those that cause colds '-- and ensuring high standards of infection control in hospitals.
Those measures include keeping patients found to be carrying or infected with a superbug in a private room along with strict enforcement of environmental cleaning policies, both of which are designed to prevent the diseases spreading to other patients and hospital staff.
Researchers found lower prevalence rates of superbug infection and colonization in hospitals where potentially infectious patients were cared for in isolation and where there were strong policies for cleaning and disinfecting the hospital environment.
Higher rates were found in health-care institutions that did not routinely isolate infectious patients or had less stringent cleaning policies.
However, Simor stressed that the study showed only an "association" between the existence of those policies and lower superbug rates '-- and doesn't prove cause and effect.
"I can't say that those hospitals have lower rates because of these policies," he said. "But it is clear that the association exists and it deserves further study to confirm whether there is a cause-and-effect relationship.
"In the meantime, it certainly provides additional evidence that these are appropriate infection control policies for hospitals to be following."
The study also looked at regional variations across country '-- hospitals in all 10 provinces and the Northwest Territories took part '-- and found one notable difference: VRE rates were significantly lower in Eastern Canada than elsewhere in the country.
The prevalence of MRSA and C. diff cases did not vary much by province or region, although C. difficile rates were lowest in Eastern hospitals.
"We have to determine what can we learn from that because I don't have an answer right now as to why there is that difference," Simor said of the VRE rates in particular. "But the difference exists and it's real."
Compared with other countries, Canada has a lower prevalence of cases than the U.S., but the rates exceed those in such countries as Sweden and Denmark.
"I think that suggests that we have a certain measure of success because we're not as bad off as the United States, for example, but that there's still an opportunity for us to do an even better job, and we still have a way to go," he said.
The study involved only acute-care hospitals with at least 50 beds and did not include pediatric, psychiatric or long-term care facilities.
Simor said the survey provides a baseline of prevalence rates that will allow researchers to monitor both national and regional trends in subsequent studies and help tease out which infection control measures are having the most impact.
Mon, 13 May 2013 16:49
Cocaine addicts may soon have a 'cure' for their unhealthy dependence: researchers have successfully created a vaccine that prevents cocaine particles from reaching the brain and inducing feelings of euphoria, thereby helping users break their addiction.
''The vaccine eats up the cocaine in the blood like a little Pac-Man before it can reach the brain,'' Dr. Ronald G. Crystal, the lead investigator of the Weill Cornell Medical College study said in a press release.
''We believe this strategy is a win-win for those individuals, among the estimated 1.4 million cocaine users in the United States, who are committed to breaking their addiction to the drug,'' he added. ''Even if a person who receives the anti-cocaine falls off the wagon, cocaine will have no effect.''
Cornell researchers have successfully administered the vaccine to non-human primates and are now much closer to launching human clinical trials. Human testing is expected to begin within a year, Dr. Crystal believes.
Cocaine blocks the recycling of dopamine '' a neurotransmitter that is responsible for feelings of pleasure. The drug prevents the reuptake of dopamine by the neuron that releases it, causing higher concentrations of dopamine to remain in the synapse and create a 'high'.
''You get this massive flooding of dopamine and that is the feel good part of the cocaine high,'' Dr. Crystal said.
The new vaccine prevents dopamine accumulation at the brain's nerve endings. The vaccine consists of particles of the common cold virus and particles that mimic the structure of cocaine. Once the body receives an injection, it recognizes the cold virus and creates an immune response against both the common cold and the cocaine 'impersonator'.
''The immune system learns to see cocaine as an intruder,'' Dr. Crystals said.
In order to feel the drug high that cocaine users seek to achieve, at least 47 percent of the dopamine transporter needs to be occupied by cocaine. The Cornell researchers found that in vaccinated primates, cocaine occupied less than 20 percent of dopamine receptors '' making it impossible for the animals to be affected by the drug.
Researchers expect that the vaccine will work in humans, but do not know how often it needs to be administered to maintain its effect. The vaccine continued to work effectively for 13 weeks in mice and seven weeks in primates.
''An anti-cocaine vaccination will require booster shots in humans, but we don't know yet how often these booster shots will be needed,'' Dr. Crystal said. ''I believe that for those people who desperately want to break their addiction, a series of vaccinations will help.''
There are about 1.9 million current and past-month cocaine users in the US, 1.4 million of which are considered addicts or abusers, according to the latest data from the National Institute on Drug Abuse. About one in five people who use cocaine will become addicted. There are about 2 million visits to US emergency departments for drug abuse each year, 480,000 of which come are a result of cocaine use.
A vaccine preventing cocaine-induced feelings of euphoria would help drug users break free from their addiction, thereby drastically reducing emergency room visits and health problems in the US.
''Cocaine addiction is a major social problem. It causes changes to behavior, it's expensive and it's illegal,'' Dr. Crystal told LiveScience in 2012. ''It's very difficult to stop. If we could successfully develop a cocaine vaccine it would really be a very positive social advance.''
Mon, 13 May 2013 16:30
British scientists plan to harness the power of the internet to catch outbreaks of killer infections before they spread.
The researchers will use online surveillance to monitor millions of web searches where people have looked up symptoms related to conditions such as HIV, MRSA or dangerous strains of flu.
They say this will help them to locate in ''real time'' exactly where the next epidemic is emerging. It is hoped that this will ''revolutionise'' Britain's ability to respond to deadly infections and prevent millions of deaths.
The £17million government-funded Interdisciplinary Research Collaboration (IRC) centre, where the technologies will be advanced, is expected to be operational by October.
The Health Protection Agency currently relies on medical testing which can take up to two weeks to determine where an outbreak is happening.
Dr Rachel McKendry, from UCL, said online tracking of infectious diseases could identify epidemics before patients even visit a doctor.
She said it is ''crucial'' the online surveillance be linked to the mobile testing being developed at the IRC to be used in GP surgeries and even care homes.
''In a single visit someone can be diagnosed, get the result and get treatment,'' said Dr McKendry.
Wed, 15 May 2013 21:21
Somewhere between scandals this week, the president found time to sign financial disclosure forms indicating that he and the first lady held assets totaling somewhere between $1.8 and $6.8 million last year. Five million dollars seems like a pretty big range to those of us in the oppressed 47 percent, but if you're one of the rich, what's a few million here or there? It's not like he's going to be #FlaggedForAudit.
ABC News reports that President Obama collected between $250,000 and $2.1 million in book royalties. We're tempted to make a ''you didn't build write that'' joke, but we'll let it slide.
Wed, 15 May 2013 21:05
The White House
Office of the Press Secretary
For Immediate Release
May 15, 2013
- - - - - - -
2013 AMENDMENTS TO THE MANUAL FOR COURTS-MARTIAL, UNITED STATES
By the authority vested in me as President by the Constitution and the laws of the United States of America, including chapter 47 of title 10, United States Code (Uniform Code of Military Justice, 10 U.S.C. 801-946), and in order to prescribe amendments to the Manual for Courts-Martial, United States, prescribed by Executive Order 12473, as amended, it is hereby ordered as follows:
Section1. Parts III and IV of the Manual for Courts-Martial, United States, are amended as described in the Annex attached and made a part of this order
Sec. 2. These amendments shall take effect as of the date of this order, subject to the following:
(a) Nothing in these amendments shall be construed to make punishable any act done or omitted prior to the effective date of this order that was not punishable when done or omitted.
(b) Nothing in these amendments shall be construed to invalidate any nonjudicial punishment proceedings, restraint, investigation, referral of charges, trial in which arraignment occurred, or other action begun prior to the effective date of this order, and any such nonjudicial punishment, restraint, investigation, referral of charges, trial, or other action may proceed in the same manner and with the same effect as if these amendments had not been prescribed.
THE WHITE HOUSE, May 15, 2013.
Mon, 13 May 2013 16:17
The same researchers previously mapped racist Tweets about President Obama. In both cases there's reason to be a little skeptical.
Candian researchers have created a ''hate map'' that splashes a U.S. map with color-coding showing the proportion of all Tweets that contain common hateful words about race, sexual orientation, or disabilities.
The group responsible, based at California's Humboldt State University, previously faced some criticism for their methodology in mapping racist Tweets concerning President Obama; in that project the researchers identified racist terms algorithmically, meaning the context might sometimes be misconstrued. They say they answered past criticism in part by analyzing tweets by hand to make sure certain words were really used in a derogatory way. In the new study, human readers reviewed 150,000 Tweets in the study sample to confirm the context was derogatory. The results arehere.
While the new effort may accurately find hate in Tweets, there are reasons to doubt that the results accurately map hate in the United States. For starters, the concentration of Twitter users is not even across the country, and not all Tweets are geotagged (they only looked at the geotagged ones). Moreover, a lot of Twitter accounts are marketing-based and wouldn't contain hate words, so those would drown out the signal. Some Twitter accounts are phony. Perhaps most of all, the number of times an individual person Tweets can vary greatly. One guy spewing 1,000 hateful Tweets will make his county look pretty bad.
Overall, the map puts the midwest and southeast in a generally harsh light. By contrast, it says there seems to be very little hate in California, Colorado or Alabama '-- but lots of it in angry red splashes such as one between Davenport and Iowa City, Iowa. My skepticism is tempered by the unbroken corridor in light blue (denoting ''some hate'') generally along the New Jersey Turnpike. When I'm stuck there I don't like my fellow man either.
To make up your own mind, read more about the methodology here.
Thu, 16 May 2013 07:33
Remember when several months ago Wal-Mart leaked just how weak the economy was and that sales had been a "total disaster" (a piece of truthiness that promptly led to the termination of the leak source)? Guess what: they were not lying. Moments ago WMT reported Q1 results, which at the easily fudged bottom line were just in line with expectations, ot $1.14 driven by $2.2 billion in stock repurchases (30 million shares). However, it was sales, as warned, that came in well weaker than expected, posting at $114.2 billion on expectations of $116.1 - just as the guy warned. It gets worse:
Q2 EPS expected in the range $1.22-$1.27, on expectations of $1.29Q1 comps ex-fuel -1.2% vs Exp. 0.4%Comps in Canada and Japan declinedSam's Club implements first fee increase since 2006: raises membership fee to $45 nationwideDuring the 13-week period, the Walmart U.S. comp was negatively impacted by a delay in tax refund checks, challenging weather conditions, less grocery inflation than expected and the payroll tax increase. Comp traffic was down 1.8 percent, while average ticket increased 0.4 percent.From the CFO, Charles Holley: "Although we believe our company will leverage expenses for the year, the second quarter will be challenging, given expense pressures in International and our corporate area. Expense leverage may not be delivered evenly across the quarters, but we believe that by executing our plans, we will continue to reduce expenses and improve productivity."
And with this bad news to close the retail reporting season, we now fully expect the S&P to explode higher out of the gates on zero volume, with Kevin Henry's blessing of course, to such manipulated highs that even Joe Sixpack can do nothing but laugh.
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Wed, 15 May 2013 21:58
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Wed, 15 May 2013 21:50
PALMS, Calif. (KTLA) '-- Police evacuated an area in Palms on Wednesday morning after finding multiple explosive devices inside an apartment.
The LAPD bomb squad was at the scene in the 3800 block of Overland Avenue.
It all began around 10 p.m. Tuesday night, when police pulled over a man for a routine traffic stop, according to the LAPD.
Officers discovered narcotics and a handgun inside the car, police said.
That prompted police to search the man's apartment.
Authorities said he cooperated fully with the search.
The apartment was ''cluttered'' and a least a dozen explosives were found inside, police said.
They would not elaborate on the type of explosives, but residents said police told them they were pipe bombs.
The man was identified by authorities as Robert Wilson.
Investigators described him as a ''lone wolf'' who was intrigued by explosives, and said the incident did not appear to be terrorism-related.
He was booked on suspicion of possessing an explosive device.
Several apartment buildings in the area were evacuated, as well as local businesses.
Overland Avenue was expected to be closed between Venice and Washington for much of the day as the investigation continued.
Tue, 14 May 2013 12:17
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Tue, 14 May 2013 15:16
MRC TV is an online platform for people to share and view videos, articles and opinions on topics that are important to them -- from news to political issues and rip-roaring humor.
MRC TV is brought to you by the Media Research Center, a 501(c) 3 nonprofit research and education organization. The MRC is located at: 325 South Patrick Street, Alexandria, VA 22314. For information about the MRC, please visit www.MRC.org.
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Mon, 13 May 2013 17:19
MRC TV is an online platform for people to share and view videos, articles and opinions on topics that are important to them -- from news to political issues and rip-roaring humor.
MRC TV is brought to you by the Media Research Center, a 501(c) 3 nonprofit research and education organization. The MRC is located at: 325 South Patrick Street, Alexandria, VA 22314. For information about the MRC, please visit www.MRC.org.
Copyright (C) 2013, Media Research Center. All Rights Reserved.
Mon, 13 May 2013 17:17
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In a clip aired on MSNBC's "Andrea Mitchell Reports," President Obama is seen pronouncing the name of Syrian dictator Bashir Assad as "Bassar Ashad."