Those who want to use an unlocked iPhone 5 in the US beyond AT&T have had relatively few places to go for an exodus, T-Mobile and Straight Talk usually being the two carriers on the short list. It's time to add a third: Solavei is now carrying nano-SIMs for its T-Mobile-based virtual network. There's not much mystery to what's involved after that, since you're still getting the singular, all-unlimited $49 plan and no guarantee of 3G when even T-Mobile's own spectrum refarming is still young. If you can live with those potential caveats for the sake of network and contract independence, Solavei is waiting.
South Carolina defensive end Jadeveon Clowney is ready for the NFL.? But thanks to an NFL rule aimed at protecting the free farm system known as college football, he can?t join the NFL until he is three years removed from high school.
Clowney, who reportedly ran the 40 recently in 4.5 seconds (or maybe it was a 4.19), tells Tom Rinaldi of ESPN that Clowney never considered taking 2013 off to protect his body for the next level.
?My mom was the first person to call me, and was like, ?I hope you ain?t talking about doing nothing crazy like this.?? I?m not gonna do that.? Nobody would like me here in South Carolina,? Clowney said, laughing.
?I?m not leaving school.? I don?t really think I?m taking a big risk.? You can get hurt anywhere.? I can get in a car accident any given day outside of playing football.? I can trip off a curb and tear my ACL.? Anything can happen to you.? It don?t matter where you at you can get hurt.? You can get hurt at your own house, fall, trip and fall.? I?ve been doing this since I was five years old, playing football.? If it?s my time to get hurt, it?s my time to get hurt.? I?m just gonna play like I?ve been playing.?
He?s right, but the normal, everyday risk of injury is slightly higher when playing major college football.? And the point was, is, and will be that, for a guy who isn?t getting paid and who is playing football to ultimately get paid, playing for free when he?s already at a point where he?d enter the NFL at the top of the draft pool creates a grossly unnecessary risk.
We like Clowney?s attitude.? But most kids that age would feel that way.? Clowney, and everyone else in his position, needs someone who understands the real risks to give him objective advice that takes into account the player?s best interests, and no one else?s.
We won?t hold our breath, or any other bodily function, waiting for his head coach to have that conversation with him.? And that?s not a specific rip on Steve Spurrier.
We?d be shocked if any Division I head coach would give advice to a player that makes the coach?s team weaker in the coming season.
WASHINGTON (AP) ? Lawmakers are pushing for tougher U.S. financial restrictions on North Korea even as the U.N. Security Council moves closer to a new resolution tightening international sanctions in response to Pyongyang's latest nuclear test.
The U.S. is expected to present a draft resolution to the council Tuesday, after reaching agreement with China following three weeks of deliberations on how to respond to the North's third atomic test, U.N. diplomats said.
That's a sign of Beijing's disapproval of its troublesome ally's behavior and will be welcomed in Washington. The text of the resolution has not been made public, but there has been speculation the U.N.'s most powerful body could move to toughen financial restrictions and cargo inspections, as well as blacklisting more companies and individuals.
Earlier Tuesday, North Korea's military vowed to cancel the 1953 Korean War cease-fire, saying Washington and others are going beyond mere economic sanctions and expanding into blunt aggression and military acts. The Korean People's Army Supreme Command also warned that it will block a communications line at the border village separating the two Koreas.
In the U.S., the foreign affairs panels of both houses of Congress will consider the Obama administration's next policy options to impede Pyongyang's development of missile and nuclear weapons that are increasingly viewed as a direct threat to the United States.
On Tuesday, the Republican-led House foreign affairs panel will examine how criminal activities support North Korea's authoritarian regime. That could buttress the case for leveraging the vast reach of the U.S. financial system to pressure international banks that deal with the North.
North Korea long has been believed to have derived hundreds of millions of dollars a year from criminal activities such as counterfeiting of cigarettes and U.S. currency, drug trafficking and insurance scams. Its sales of missiles and conventional weaponry are also outlawed under existing U.N. resolutions.
Targeted U.S. financial sanctions have been tried before and have had a significant impact but upset China, the North's main source of economic support and the country where it conducts most of its trade and financial transactions. The U.S. wants Beijing to exert more pressure on North Korea, and China's willingness to agree to more U.N sanctions shows its patience is wearing thin. It remains to be seen, however, whether diplomatic action on more sanctions translates into their implementation on the ground.
There is deep frustration in Congress over the international diplomatic efforts aimed at persuading Pyongyang to end its nuclear weapons program in exchange for aid. The talks, hosted by China, have been stalled since 2009. A U.S. attempt to offer food aid in exchange for nuclear concessions last year fell flat.
New North Korean leader Kim Jong Un has adopted a confrontational approach toward Washington, although he did deign to meet last week with former professional basketball star Dennis Rodman.
House Foreign Affairs Committee Chairman Ed Royce said that since the Bill Clinton administration, U.S. policy toward North Korea has been a "bipartisan failure" based on the hope that North Korea would do the right thing.
The California Republican said Tuesday's hearing "will identify the best strategy for cutting off North Korea's access to hard currency in order to see real change."
Sung-Yoon Lee, professor of Korea studies at Tufts University, who was scheduled to testify, said the North's "shadowy palace economy" makes the Kim regime vulnerable to actions targeting money laundering. He suggests the Treasury Department require American banks to restrict their dealings with foreign individuals, banks, entities and even entire governments that are linked to North Korea's government.
"The Obama administration has apparently not decided on this approach, but the political climate is conducive to trying something like it," Lee said.
Marcus Noland, an expert on North Korea's economy at the Peterson Institute for International Economics, said the North's illicit activities continue, although their overall importance for the North's economy has declined as its international trade, particularly with China, has grown sharply. China accounts for 70 percent to 80 percent of North Korea's trade and totaled more than $7 billion in 2011.
In a rough estimate, Noland estimated that arms and illicit exports accounted for just under 10 percent of the merchandise the North traded in 2011, compared with more than 30 percent in 1999, when the economy was at a low point after years of famine. International interdiction efforts have also impeded the illicit trade, he said.
The North's improved financial standing could help explain its recent provocative behavior in conducting rocket and nuclear tests.
"If you are running a surplus and China is in your corner and won't implement U.N. embargos, then you can be provocative," Noland said. "But North Korea is heavily dependent on China, particularly for energy, and if China changes policy and literally cuts off the pipeline, then they're in real trouble."
In 2005, the U.S. Treasury sanctioned Banco Delta Asia, a bank in the Chinese territory of Macau which held about $25 million in North Korean funds. Treasury accused the bank of introducing counterfeit notes and laundering funds on behalf of North Korean enterprises linked to weapons of mass destruction programs.
The 2005 action caused a ripple effect among other banks worried about being closed out of the international financial system. Yet the sanction annoyed Beijing ? as well as enraging Pyongyang ? and proved complicated to undo when nuclear negotiations with North Korea finally got back on track.
The U.S. could also target the North's shipping by declaring the country a criminal enterprise, making vessels carrying its goods difficult to insure and subject to search and seizure, Noland said.
____
Associated Press writer Edith Lederer at the United Nations contributed to this report.
Mar. 3, 2013 ? A study led by St. Jude Children's Research Hospital has discovered mutations in two genes that lead to the death of nerve cells in amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, and related degenerative diseases.
The same mutation occurred in both genes and led to the abnormal build-up of the proteins inside cells. These proteins play an essential role in normal RNA functioning and have also been linked to cancer, including the Ewing sarcoma, the second most common type of bone cancer in children and adolescents. The finding is the latest in a series of discoveries suggesting degenerative diseases and cancer may have common origins. RNA is the molecule that directs protein assembly based on instructions carried in DNA.
The study also adds to evidence that seemingly unrelated neurodegenerative diseases may involve similar defects in RNA metabolism. Researchers linked the problems to a specific region of the mutated proteins whose normal function was unclear. The study was published today in the advanced online edition of the scientific journal Nature.
"I hope this study helps to build the foundation for desperately needed treatments for ALS and perhaps a broad range of diseases caused by abnormal RNA metabolism," said J. Paul Taylor, M.D., Ph.D., an associate member of the St. Jude Department of Developmental Neurobiology and senior author of the study. Taylor and James Shorter, Ph.D., an assistant professor in the biochemistry and biophysics department at the University of Pennsylvania's Perelman School of Medicine, are the study's corresponding authors.
Each year approximately 5,600 people in the U.S. are found to have ALS. The disease is nearly always fatal, often within five years. Patients suffer muscle wasting and paralysis that affects their limbs and trunk as well as their ability to talk, swallow and breathe. There is no cure.
For this project, St. Jude sequenced just the portion of the genome called the exome, which carries instructions for making proteins. Researchers sequenced the exomes of two families affected by rare inherited degenerative disorders that target cells in the muscle, bone and brain. Neither family carried mutations previously tied to ALS or related diseases. The project built on the infrastructure developed by the St. Jude Children's Research Hospital -- Washington University Pediatric Cancer Genome Project, which played an important role in finding the mutations.
Researchers found the families carried a single, previously unknown mutation in a pair of RNA-binding proteins named hnRNPA2B1 and hnRNPA1. The proteins both bind RNA and help regulate its function. When researchers checked for the same mutations in 517 ALS patients they found hnRNPA1 protein mutated in two patients. One patient had the inherited form of ALS. The other ALS patient had no family history of the disease.
The new mutations occurred in a region of the proteins Taylor refers to as a prion-like domain because it has similarities with yeast proteins called prions. Prions are proteins that can alternate between shapes as needed for different functions. "Until recently we did not know these domains existed in humans and now we realize that hundreds of human proteins have them," Taylor said. "We're only beginning to understand their function in human cells."
Researchers showed the prion-like domains are responsible for the shape change that occurs when these proteins convert into slender threads called fibrils. The mutations accelerate fibril formation and recruit normal proteins to form fibrils. This phenomenon called propagation may explain how ALS and related diseases spread throughout the nervous system.
Taylor speculated that the normal function of prion-like domains is to assemble RNAs into temporary structures called granules, which are part of the cell's normal protein production machinery. Granules are normally short lived, and the RNA-binding proteins involved in their formation are recycled. But in cells with hnRNPA2B1 or hnRNPA1 mutation, RNA granules accumulated in the cytoplasm instead of being disassembled. "That's bad news for RNA regulation, which is bad news for those cells," Taylor said.
The study has several important implications, Taylor said. Recognition that the mutations adversely impact regulation of RNA could lead to targeted therapy to correct the problem. The mutation's location in the prion-like domain might also prove significant. Although the mutations in hnRNPA2B1 or hnRNPA1 appear to be rare, hundreds of other RNA-binding proteins have prion-like domains. Taylor said patients with unexplained neurodegenerative diseases may have mutations in these proteins.
The study's first authors are Hong Joo Kim, Nam Chul Kim, Yong-Dong Wang and Jennifer Moore, all of St. Jude; and Emily Scarborough and Zamia Diaz, both of the University of Pennsylvania. The other authors are Kyle MacLea and Eric Ross, both of Colorado State University; Brian Freibaum, Songqing Li, Amandine Molliex, Anderson Kanagaraj and Robert Carter, all of St. Jude; Kevin Boylan, Aleksandra Wojtas and Rosa Rademakers, all of the Mayo Clinic, Jacksonville, Fla.; Jack Pinkus and Steven Greenberg, both of Brigham and Women's Hospital and Harvard Medical School; John Trojanowski, Bradley Smith, Yun Li and Alice Flynn Ford, all of the University of Pennsylvania; Bryan Traynor, of the National Institute of Aging, National Institutes of Health, Bethesda, Md.; Simon Topp, Athina-Soragia Gkazi, Jack Miller and Christopher Shaw, all of the Institute of Psychiatry, London; Michael Kottlors and Janbernd Kirschner, both of University Children's Hospital Freiburg, Germany; Alan Pestronk and Conrad Weihl, both of the Washington University School of Medicine, St. Louis; Aaron Gitler, Stanford University School of Medicine; Michael Benatar, University of Miami Miller School of Medicine; Oliver King, Boston Biomedical Research Institute, Watertown, Mass.; and Virginia Kimonis, University of California-Irvine.
The research was supported in part by the Packard Foundation, by grants (NS053825, AG032953, DP2OD002177 and NS067354) from the National Institutes of Health, the ALS Association, the Ellison Medical Foundation, a grant (MCB-1023771) from the National Science Foundation and ALSAC.
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The above story is reprinted from materials provided by St. Jude Children's Research Hospital.
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Hong Joo Kim, Nam Chul Kim, Yong-Dong Wang, Emily A. Scarborough, Jennifer Moore, Zamia Diaz, Kyle S. MacLea, Brian Freibaum, Songqing Li, Amandine Molliex, Anderson P. Kanagaraj, Robert Carter, Kevin B. Boylan, Aleksandra M. Wojtas, Rosa Rademakers, Jack L. Pinkus, Steven A. Greenberg, John Q. Trojanowski, Bryan J. Traynor, Bradley N. Smith, Simon Topp, Athina-Soragia Gkazi, Jack Miller, Christopher E. Shaw, Michael Kottlors, Janbernd Kirschner, Alan Pestronk, Yun R. Li, Alice Flynn Ford, Aaron D. Gitler, Michael Benatar, Oliver D. King, Virginia E. Kimonis, Eric D. Ross, Conrad C. Weihl, James Shorter, J. Paul Taylor. Mutations in prion-like domains in hnRNPA2B1 and hnRNPA1 cause multisystem proteinopathy and ALS. Nature, 2013; DOI: 10.1038/nature11922
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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.
Biking down to the store to pick up a two liter of soda is one thing. Bombing down a steep street at full speed, throwing all caution to the wind is another, and Marcelo Gutierrez is a pro at it. This is is winning run from the recent Valparaiso Urban Downhill competition, and it's enough to make your palms sweat. Good job Marcelo, but next time I want to see some unicycling. [Reddit] More »
Researchers discover how to shutdown cancer's powerful master proteinPublic release date: 3-Mar-2013 [ | E-mail | Share ]
Contact: Lauren Woods Law2014@med.cornell.edu 646-317-7401 Weill Cornell Medical College
Weill Cornell research offers patients hope for new treatments for an aggressive and common lymphoma
NEW YORK (March 3, 2013) -- The powerful master regulatory transcription factor called Bcl6 is key to the survival of a majority of aggressive lymphomas, which arise from the B-cells of the immune system. The protein has long been considered too complex to target with a drug since it is also crucial to the healthy functioning of many immune cells in the body, not just B cells gone bad.
But now, in the journal Nature Immunology, researchers at Weill Cornell Medical College report that it is possible to shut down Bcl6 in the cancer, known as diffuse large B-cell lymphoma (DLBCL), while not affecting its vital function in T cells and macrophages that are needed to support a healthy immune system.
"The finding comes as a very welcome surprise," says the study's lead investigator, Dr. Ari Melnick, Gebroe Family Professor of Hematology/Oncology and director of the Raymond and Beverly Sackler Center for Biomedical and Physical Sciences at Weill Cornell.
"This means the drugs we have developed against Bcl6 are more likely to be significantly less toxic and safer for patients with this cancer than we realized," says Dr. Melnick, who is also a hematologist-oncologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.
If Bcl6 is completely inhibited, patients might suffer from systemic inflammation and atherosclerosis. Weill Cornell researchers conducted this new study to help clarify possible risks, as well as to understand how Bcl6 controls the various aspects of the immune system.
DLBCL is the most common subtype of non-Hodgkin lymphoma -- the seventh most frequently diagnosed cancer -- and many of these patients are resistant to currently available treatments.
"Scientists have been searching for the right answer to treat this difficult lymphoma, which, after initial treatment, can be at high risk of relapse and resistant to current therapies," Dr. Melnick says. "Believing that Bcl6 could not be targeted, some researchers have been testing alternative therapeutic approaches. This study strongly supports the notion of using Bcl6-targeting drugs."
In fact, the findings in this study were inspired from preclinical testing of two Bcl6-targeting agents that Dr. Melnick and his Weill Cornell colleagues have developed to treat DLBCLs. These experimental drugs are RI-BPI, a peptide mimic, and the small molecule agent 79-6.
Dr. Melnick says the discovery that a master regulatory transcription factor can be targeted offers implications beyond just treating DLBCL. Recent studies from Dr. Melnick and others have revealed that Bcl6 plays a key role in the most aggressive forms of acute leukemia, as well as certain solid tumors.
Transcription factors are responsible for either inhibiting or promoting the expression of genes, and master regulatory transcription factors are the equivalent of the CPU of a computer their actions regulate thousands of genes in different kinds of cells. For example, Bcl6 can control the type of immune cell that develops in the bone marrow -- playing many roles in the development of B cells, T cells, macrophages and other cells -- including a primary and essential role in enabling B-cells to generate specific antibodies against pathogens.
"When cells lose control of Bcl6, lymphomas develop in the immune system. Lymphomas are 'addicted' to Bcl6, and therefore Bcl6 inhibitors powerfully and quickly destroy lymphoma cells," Dr. Melnick says.
The big surprise in the current study is that rather than functioning as a single molecular machine, Bcl6 instead seems to function more like a Swiss Army knife, using different tools to control different cell types. This multi-function paradigm could represent a general model for the functioning of other master regulatory transcription factors.
"In this analogy, the Swiss Army knife, or transcription factor, keeps most of its tools folded, opening only the one it needs in any given cell type," Dr. Melnick says. "For B cells, it might open and use the knife tool; for T cells, the cork screw; for macrophages, the scissors. The amazing thing from a medical standpoint is that this means that you only need to prevent the master regulator from using certain tools to treat cancer. You don't need to eliminate the whole knife," he says. "In fact, we show that taking out the whole knife is harmful since the transcription factor has many other vital functions that other cells in the body need."
Prior to these study results, it was not known that a master regulator could separate its functions so precisely.
"Now we know we can take out a specific tool -- to shut down a specific part of the protein -- that causes the disease we want to treat."
Researchers hope this will be a major benefit to the treatment of DLBCL and perhaps other disorders that are influenced by Bcl6 and other master regulatory transcription factors.
###
Study co-authors include Dr. Chuanxin Huang and Dr. Katerina Chatzi from the Division of Hematology and Oncology at Weil Cornell Medical College.
The research was funded by grants from the National Cancer Institute, The Burroughs Wellcome Foundation and the Chemotherapy Foundation. The research was initially supported by a March of Dimes Scholar Award and facilitated by the Sackler Center for Biomedical and Physical Sciences at Weill Cornell.
The Raymond and Beverly Sackler Center for Biomedical and Physical Sciences
The Raymond and Beverly Sackler Center for Biomedical and Physical Sciences of Weill Cornell Medical College brings together a multidisciplinary team of scientists for the purpose of catalyzing major advances in medicine. By harnessing the combined power of experimental approaches rooted in the physical and biological sciences, Sackler Center investigators can best accelerate the pace of discovery and translate these findings for the benefit of patients with various medical conditions, including but not limited to cancer.
Weill Cornell Medical College
Weill Cornell Medical College, Cornell University's medical school located in New York City, is committed to excellence in research, teaching, patient care and the advancement of the art and science of medicine, locally, nationally and globally. Physicians and scientists of Weill Cornell Medical College are engaged in cutting-edge research from bench to bedside, aimed at unlocking mysteries of the human body in health and sickness and toward developing new treatments and prevention strategies. In its commitment to global health and education, Weill Cornell has a strong presence in places such as Qatar, Tanzania, Haiti, Brazil, Austria and Turkey. Through the historic Weill Cornell Medical College in Qatar, the Medical College is the first in the U.S. to offer its M.D. degree overseas. Weill Cornell is the birthplace of many medical advances -- including the development of the Pap test for cervical cancer, the synthesis of penicillin, the first successful embryo-biopsy pregnancy and birth in the U.S., the first clinical trial of gene therapy for Parkinson's disease, and most recently, the world's first successful use of deep brain stimulation to treat a minimally conscious brain-injured patient. Weill Cornell Medical College is affiliated with NewYork-Presbyterian Hospital, where its faculty provides comprehensive patient care at NewYork-Presbyterian Hospital/Weill Cornell Medical Center. The Medical College is also affiliated with the Methodist Hospital in Houston. For more information, visit weill.cornell.edu.
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Researchers discover how to shutdown cancer's powerful master proteinPublic release date: 3-Mar-2013 [ | E-mail | Share ]
Contact: Lauren Woods Law2014@med.cornell.edu 646-317-7401 Weill Cornell Medical College
Weill Cornell research offers patients hope for new treatments for an aggressive and common lymphoma
NEW YORK (March 3, 2013) -- The powerful master regulatory transcription factor called Bcl6 is key to the survival of a majority of aggressive lymphomas, which arise from the B-cells of the immune system. The protein has long been considered too complex to target with a drug since it is also crucial to the healthy functioning of many immune cells in the body, not just B cells gone bad.
But now, in the journal Nature Immunology, researchers at Weill Cornell Medical College report that it is possible to shut down Bcl6 in the cancer, known as diffuse large B-cell lymphoma (DLBCL), while not affecting its vital function in T cells and macrophages that are needed to support a healthy immune system.
"The finding comes as a very welcome surprise," says the study's lead investigator, Dr. Ari Melnick, Gebroe Family Professor of Hematology/Oncology and director of the Raymond and Beverly Sackler Center for Biomedical and Physical Sciences at Weill Cornell.
"This means the drugs we have developed against Bcl6 are more likely to be significantly less toxic and safer for patients with this cancer than we realized," says Dr. Melnick, who is also a hematologist-oncologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.
If Bcl6 is completely inhibited, patients might suffer from systemic inflammation and atherosclerosis. Weill Cornell researchers conducted this new study to help clarify possible risks, as well as to understand how Bcl6 controls the various aspects of the immune system.
DLBCL is the most common subtype of non-Hodgkin lymphoma -- the seventh most frequently diagnosed cancer -- and many of these patients are resistant to currently available treatments.
"Scientists have been searching for the right answer to treat this difficult lymphoma, which, after initial treatment, can be at high risk of relapse and resistant to current therapies," Dr. Melnick says. "Believing that Bcl6 could not be targeted, some researchers have been testing alternative therapeutic approaches. This study strongly supports the notion of using Bcl6-targeting drugs."
In fact, the findings in this study were inspired from preclinical testing of two Bcl6-targeting agents that Dr. Melnick and his Weill Cornell colleagues have developed to treat DLBCLs. These experimental drugs are RI-BPI, a peptide mimic, and the small molecule agent 79-6.
Dr. Melnick says the discovery that a master regulatory transcription factor can be targeted offers implications beyond just treating DLBCL. Recent studies from Dr. Melnick and others have revealed that Bcl6 plays a key role in the most aggressive forms of acute leukemia, as well as certain solid tumors.
Transcription factors are responsible for either inhibiting or promoting the expression of genes, and master regulatory transcription factors are the equivalent of the CPU of a computer their actions regulate thousands of genes in different kinds of cells. For example, Bcl6 can control the type of immune cell that develops in the bone marrow -- playing many roles in the development of B cells, T cells, macrophages and other cells -- including a primary and essential role in enabling B-cells to generate specific antibodies against pathogens.
"When cells lose control of Bcl6, lymphomas develop in the immune system. Lymphomas are 'addicted' to Bcl6, and therefore Bcl6 inhibitors powerfully and quickly destroy lymphoma cells," Dr. Melnick says.
The big surprise in the current study is that rather than functioning as a single molecular machine, Bcl6 instead seems to function more like a Swiss Army knife, using different tools to control different cell types. This multi-function paradigm could represent a general model for the functioning of other master regulatory transcription factors.
"In this analogy, the Swiss Army knife, or transcription factor, keeps most of its tools folded, opening only the one it needs in any given cell type," Dr. Melnick says. "For B cells, it might open and use the knife tool; for T cells, the cork screw; for macrophages, the scissors. The amazing thing from a medical standpoint is that this means that you only need to prevent the master regulator from using certain tools to treat cancer. You don't need to eliminate the whole knife," he says. "In fact, we show that taking out the whole knife is harmful since the transcription factor has many other vital functions that other cells in the body need."
Prior to these study results, it was not known that a master regulator could separate its functions so precisely.
"Now we know we can take out a specific tool -- to shut down a specific part of the protein -- that causes the disease we want to treat."
Researchers hope this will be a major benefit to the treatment of DLBCL and perhaps other disorders that are influenced by Bcl6 and other master regulatory transcription factors.
###
Study co-authors include Dr. Chuanxin Huang and Dr. Katerina Chatzi from the Division of Hematology and Oncology at Weil Cornell Medical College.
The research was funded by grants from the National Cancer Institute, The Burroughs Wellcome Foundation and the Chemotherapy Foundation. The research was initially supported by a March of Dimes Scholar Award and facilitated by the Sackler Center for Biomedical and Physical Sciences at Weill Cornell.
The Raymond and Beverly Sackler Center for Biomedical and Physical Sciences
The Raymond and Beverly Sackler Center for Biomedical and Physical Sciences of Weill Cornell Medical College brings together a multidisciplinary team of scientists for the purpose of catalyzing major advances in medicine. By harnessing the combined power of experimental approaches rooted in the physical and biological sciences, Sackler Center investigators can best accelerate the pace of discovery and translate these findings for the benefit of patients with various medical conditions, including but not limited to cancer.
Weill Cornell Medical College
Weill Cornell Medical College, Cornell University's medical school located in New York City, is committed to excellence in research, teaching, patient care and the advancement of the art and science of medicine, locally, nationally and globally. Physicians and scientists of Weill Cornell Medical College are engaged in cutting-edge research from bench to bedside, aimed at unlocking mysteries of the human body in health and sickness and toward developing new treatments and prevention strategies. In its commitment to global health and education, Weill Cornell has a strong presence in places such as Qatar, Tanzania, Haiti, Brazil, Austria and Turkey. Through the historic Weill Cornell Medical College in Qatar, the Medical College is the first in the U.S. to offer its M.D. degree overseas. Weill Cornell is the birthplace of many medical advances -- including the development of the Pap test for cervical cancer, the synthesis of penicillin, the first successful embryo-biopsy pregnancy and birth in the U.S., the first clinical trial of gene therapy for Parkinson's disease, and most recently, the world's first successful use of deep brain stimulation to treat a minimally conscious brain-injured patient. Weill Cornell Medical College is affiliated with NewYork-Presbyterian Hospital, where its faculty provides comprehensive patient care at NewYork-Presbyterian Hospital/Weill Cornell Medical Center. The Medical College is also affiliated with the Methodist Hospital in Houston. For more information, visit weill.cornell.edu.
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AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
TRIPOLI, Libya (AP) ? Transport of natural gas from Libya to Italy through a major pipeline in the country's west was halted Sunday after clashes between tribesmen and forces guarding the natural gas complex, a security official said.
The unrest was just the latest instance of tribal clashes disrupting efforts to bring Libya under control of the central government.
A company official said foreign staff of the Mettillah Oil and Gas complex near Zwara, about 110 kilometers (70 miles) from the capital Tripoli, were evacuated following the clashes which broke out Saturday.
The security official said the move to halt exports was a security measure, but no pipelines were affected. He said one of the company staff was injured during the clashes, which ended on Sunday.
Both officials spoke on condition of anonymity because they were not authorized to speak to reporters.
The complex is a joint venture between Libya's National Oil Corporation and Italy's largest energy company, Eni SpA.
A lawmaker from Zwara, Nouri Abu-Sahmein, blamed the guards at the complex.
Abu-Sahmein said the clashes broke out after guards refused to stop at a local checkpoint. Clashes erupted with the local ethnic Berber tribesmen early Saturday, killing a tribesman.
The guards are from Zintan, home of the rebels who were first to sweep into the capital, Tripoli, in August last year, dealing the decisive blow to the regime of former dictator Moammar Gadhafi.
The empowered militiamen took charge of guarding the natural gas complex, raising the anger and jealousy of local tribesmen. Turf wars between different tribes in post-Gadhafi Libya over control of strategic areas are common, as the central government struggles to impose order.
After the first clashes, three guards were arrested, prompting them to call in their supporters from Zintan, who surrounded the natural gas complex and fired at the local tribesmen, killing one, Abu-Sahmein said.
Many of the tribal conflicts are along ethnic lines between Arab and ethnic Berbers.
Abu-Sahmein said local tribes, including some Arab tribes, have called on the government to send the military to guard the complex to stave off disputes and protect the country's resources.
The Mettillah complex is one of Libya's largest oil and gas production facilities. Exports to Italy were halted during the civil war in 2011.
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