Thursday, November 7, 2013

Cost-effective method accurately orders DNA sequencing along entire chromosomes

Cost-effective method accurately orders DNA sequencing along entire chromosomes


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7-Nov-2013



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Contact: Leila Gray
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206-685-0381
University of Washington



A major step toward improving the quality of rapid, inexpensive genome assembly



A new computational method has been shown to quickly assign, order and orient DNA sequencing information along entire chromosomes. The method may help overcome a major obstacle that has delayed progress in designing rapid, low-cost -- but still accurate -- ways to assemble genomes from scratch. Data gleaned through this new method can also validate certain types of chromosomal abnormalities in cancer, research findings indicate.


The advance was reported in Nature Biotechnology by several University of Washington scientists led by Dr. Jay Shendure, associate professor of genome sciences.


Existing technologies can quickly produce billions of "short reads" of segments of DNA at very low cost. Various approaches are currently used to put the pieces together to see how DNA segments line up to form larger stretches of the genetic code.


However, current methods produce a highly fragmented genome assembly, lacking long-range information about what sequences are near what other sequences, making further biological analysis difficult.


"Genome science has remained remarkably distant from routinely assembling genomes to the standards set by the Human Genome Project," said the researchers. They noted that the Human Genome Project tapped into many different techniques to achieve its end result. Many of these are too expensive, technically difficult, and impractical for large-scale initiatives such as the Genome 10K Project, which aims to sequence and assemble the genomes of 10,000 vertebrate species.


Members of the Shendure lab that developed what they hope will be a more scalable strategy were Joshua N. Burton, Andrew Adey, Rupali P. Patwardhan, Ruolan Qiu, and Jacob O. Kitzman.


To more completely assemble genomes, they tapped into a technology called Hi-C, which measures the three-dimensional architecture and physical territories of chromosomes within the nuclei of cells. Hi-C maps the physical interactions between regions of the chromosomes in a genome, including contact within a chromosome and with other chromosomes. The results indicate which regions tend to occur near each other within three-dimensional space in a cell's nucleus.


The researchers speculated that this interaction data, because it offers clues about the position of and distances between various regions of the chromosome, might reveal how DNA sequences are grouped and lined up along entire chromosomes. They wondered if the interaction data could show them which regions of the genome are near each other on each chromosome.


Their investigation of this possibility led them to create what they named LACHESIS (an acronym for "ligating adjacent chromatin enables scaffolding in situ"). The map of physical interactions generated by Hi-C was interpreted by the LACHESIS computational program to assign, order and orient genomic sequences into their correct position along chromosomes, including DNA positioned close to the centromere, the "pinch waist" gap in the chromosome shape.


The researchers combined their new approach with other cheap and widely used sequencing methods to generate chromosome-scale assemblies of the human, mouse and fruit fly genomes. The researchers were able to cluster nearly all scaffolds -- collections of short DNA segments whose position relative to each other is unknown -- into groups that corresponded to individual chromosomes.


They then ordered and oriented the scaffolds assigned to each chromosome group, and validated their results by comparing them to the high-quality reference genomes for these species that were generated by the Human Genome Project. In the case of human genomes, they achieved 98 percent accuracy in assigning tens of thousands of sequences of contiguous DNA to chromosome groups and 99 percent accuracy in ordering and orienting these sequences within chromosome groups.


"We think the method may fundamentally change how we approach the assembly of new genomes with next-generation sequencing technologies," noted Shendure.


While he and his team cite many areas in which the computational and experimental methods can be improved, the approach is an important step in his lab's long-term goal to facilitate the assembly, for a variety of species, of low-cost, high-quality genomes that meet the rigorous standards set by the Human Genome Project.


###


The research was supported by grants HG006283 and T32HG000035 from the National Human Genome Research Institute, and graduate research fellowships from the National Science Foundation.




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Cost-effective method accurately orders DNA sequencing along entire chromosomes


[ Back to EurekAlert! ]

PUBLIC RELEASE DATE:

7-Nov-2013



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]


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Contact: Leila Gray
leilag@uw.edu
206-685-0381
University of Washington



A major step toward improving the quality of rapid, inexpensive genome assembly



A new computational method has been shown to quickly assign, order and orient DNA sequencing information along entire chromosomes. The method may help overcome a major obstacle that has delayed progress in designing rapid, low-cost -- but still accurate -- ways to assemble genomes from scratch. Data gleaned through this new method can also validate certain types of chromosomal abnormalities in cancer, research findings indicate.


The advance was reported in Nature Biotechnology by several University of Washington scientists led by Dr. Jay Shendure, associate professor of genome sciences.


Existing technologies can quickly produce billions of "short reads" of segments of DNA at very low cost. Various approaches are currently used to put the pieces together to see how DNA segments line up to form larger stretches of the genetic code.


However, current methods produce a highly fragmented genome assembly, lacking long-range information about what sequences are near what other sequences, making further biological analysis difficult.


"Genome science has remained remarkably distant from routinely assembling genomes to the standards set by the Human Genome Project," said the researchers. They noted that the Human Genome Project tapped into many different techniques to achieve its end result. Many of these are too expensive, technically difficult, and impractical for large-scale initiatives such as the Genome 10K Project, which aims to sequence and assemble the genomes of 10,000 vertebrate species.


Members of the Shendure lab that developed what they hope will be a more scalable strategy were Joshua N. Burton, Andrew Adey, Rupali P. Patwardhan, Ruolan Qiu, and Jacob O. Kitzman.


To more completely assemble genomes, they tapped into a technology called Hi-C, which measures the three-dimensional architecture and physical territories of chromosomes within the nuclei of cells. Hi-C maps the physical interactions between regions of the chromosomes in a genome, including contact within a chromosome and with other chromosomes. The results indicate which regions tend to occur near each other within three-dimensional space in a cell's nucleus.


The researchers speculated that this interaction data, because it offers clues about the position of and distances between various regions of the chromosome, might reveal how DNA sequences are grouped and lined up along entire chromosomes. They wondered if the interaction data could show them which regions of the genome are near each other on each chromosome.


Their investigation of this possibility led them to create what they named LACHESIS (an acronym for "ligating adjacent chromatin enables scaffolding in situ"). The map of physical interactions generated by Hi-C was interpreted by the LACHESIS computational program to assign, order and orient genomic sequences into their correct position along chromosomes, including DNA positioned close to the centromere, the "pinch waist" gap in the chromosome shape.


The researchers combined their new approach with other cheap and widely used sequencing methods to generate chromosome-scale assemblies of the human, mouse and fruit fly genomes. The researchers were able to cluster nearly all scaffolds -- collections of short DNA segments whose position relative to each other is unknown -- into groups that corresponded to individual chromosomes.


They then ordered and oriented the scaffolds assigned to each chromosome group, and validated their results by comparing them to the high-quality reference genomes for these species that were generated by the Human Genome Project. In the case of human genomes, they achieved 98 percent accuracy in assigning tens of thousands of sequences of contiguous DNA to chromosome groups and 99 percent accuracy in ordering and orienting these sequences within chromosome groups.


"We think the method may fundamentally change how we approach the assembly of new genomes with next-generation sequencing technologies," noted Shendure.


While he and his team cite many areas in which the computational and experimental methods can be improved, the approach is an important step in his lab's long-term goal to facilitate the assembly, for a variety of species, of low-cost, high-quality genomes that meet the rigorous standards set by the Human Genome Project.


###


The research was supported by grants HG006283 and T32HG000035 from the National Human Genome Research Institute, and graduate research fellowships from the National Science Foundation.




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Source: http://www.eurekalert.org/pub_releases/2013-11/uow-cma110713.php
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Hangouts 2.0 now rolling out with SMS support

Hangouts

New version lets you use Google's IM app to send and receive texts

As promised at last week's Google+ event, the new version of Hangouts capable of sending and receiving text messages is now rolling out through Google Play. The update to brings things up to speed with the version of Hangouts on the Nexus 5, which is the default SMS app on that device. When you first load up the updated Hangouts you'll be presented with a fullscreen message asking if you want to enable SMS support — tap yes and your messages are imported into the app, and you'll receive future SMS notifications through Hangouts instead of your preloaded SMS app. Tap "Maybe later" and things will stay as they are.

For the most part, the texting experience through Hangouts 2.0 on any other device is the same as it is on the Nexus 5 — SMS conversations are shown in a list alongside your other, and you can choose whether you want to communicate over Hangouts or SMS when starting a new conversation. Want out? At any point you can go to Settings > SMS > Turn on SMS to enable or disable SMS in Hangouts.

The update also adds animated GIF support and a new location-sharing button, which you can tap to tell contacts where you are.

As usual the update is being rolled out gradually across the Android user base, so don't be surprised if you don't see it immediately. If you're updating today, be sure to hit the comments and let us know whether you're opting into SMS in Hangouts or not.


    






Source: http://feedproxy.google.com/~r/androidcentral/~3/V5rJQvS01WI/story01.htm
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'Hunger Games: Catching Fire': The 8 Jams We've Heard So Far


MTV News wraps up what we've heard from film's soundtrack.


By Brenna Ehrlich








Source:
http://www.mtv.comhttp://www.mtv.com/news/articles/1717062/hunger-games-cathing-fire-soundtrack-what-we-know-so-far.jhtml

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Hope builds for a drug that might shut down a variety of cancers

Hope builds for a drug that might shut down a variety of cancers


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PUBLIC RELEASE DATE:

7-Nov-2013



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Contact: Sarah Smith
sas2072@med.cornell.edu
646-317-7401
Weill Cornell Medical College



Cancer cells 'go to sleep' when crucial set of molecules is targeted




NEW YORK (November 7, 2013) -- The most frequently mutated gene across all types of cancers is a gene called p53. Unfortunately it has been difficult to directly target this gene with drugs. Now a multi-institutional research team, led by Dr. Lewis Cantley and investigators at Weill Cornell Medical College, has identified a family of enzymes they say is crucial for the growth of cancers that have genetic aberrations in p53. Targeting these enzymes with novel agents might prevent the growth of p53 mutant cancers, thereby benefiting a broad spectrum of cancer patients, including those with breast, ovarian, lung, colorectal and brain tumors.


In the Nov. 7 issue of Cell, investigators pinpoint two cellular enzymes -- Type 2 phosphatidylinositol-5-phosphate 4-kinases α and β (Type 2 PIP kinases) -- as essential for cancer growth when cells have lost p53, the powerful tumor-suppressor gene long dubbed the "guardian of the genome." More than half of all cancers lose this gene, allowing these cancers to grow at will.


The researchers discovered that the Type 2 PIP kinases are not critical for the growth of normal cells but become essential for cell growth when p53 is lost due to mutations or deletions. The scientists showed, in animal and lab studies of human cancer cells, that targeting these molecules effectively shuts down the growth of p53 mutant cancers.


Although the studies were conducted in human breast cancer cells, the researchers believe Type 2 PIP kinase inhibitors could block the growth of cancers with a mutated or missing p53 gene.


"The fact that one can delete the Type 2 PIP kinases in normal human cells or in mice with essentially no effect on cell survival suggests that inhibitors of these enzymes should have little toxicity," says Dr. Cantley, the study's senior author and director of the Cancer Center at Weill Cornell Medical College and NewYork-Presbyterian Hospital.


Dr. Cantley is already leading an effort to develop drugs to shut down these kinases. "Well-designed Type 2 PIP kinase inhibitors may turn the tide on p53 mutant cancer," he says.


A Crucial Link


Dr. Cantley is known for his discovery of the PI 3-kinase oncogene, and pioneering work in teasing apart how the gene contributes to cancer. PI 3-kinases (PI3K) have been linked to a wide variety of cellular functions, including cell growth and proliferation, and most cancers activate PI3K by one or more mechanisms. Dr. Cantley's discovery led to promising avenues for the development of personalized cancer therapies.


Activity of PI3K is in some cases linked to Type 2 PIP kinases, so in this study, Dr. Cantley sought to understand the function of these enzymes. Because the researchers knew that a subset of breast cancers over-express these molecules, investigators looked at their role in HER2-positive breast cancers, which typically are more aggressive tumors.


The researchers, including those from Harvard Medical School, Beth Israel Deaconess Medical Center and other institutions, discovered that the enzymes are silent in cells that have healthy p53. One critical role of p53 is to "rescue" cells that are producing excess reactive oxygen species (ROS), which are byproducts of cells that are growing too rapidly. The oxidative stress produced by ROS can damage cell structures, so p53 attempts to reduce ROS in affected cells. "If, however, ROS levels exceed the capacity of p53s to rescue it, then p53 takes on a second function, which is to kill the cell," Dr. Cantley says.


"That is why cancers often disable p53. If p53 is mutated or gone, then the cell keeps on growing at a very high rate," he says. "And then ROS begins to damage genes, making the cancer even more aggressive."


The Type 2 PIP kinases are the backup rescue system to p53. But they only reduce ROS enough to keep the cells from dying. (Too much ROS will also kill a cell.)


What this means is that cancer cells become "absolutely dependent on these kinases to be able to grow," Dr. Cantley says.


Taking Advantage of "Synthetic Lethality"


But there is a big and important hitch in this scenario, he adds. If the Type 2 PIP kinases are inhibited, and if p53 is deactivated, the cancer cell essentially "goes to sleep," he says. "It just stops dividing and growing. This is called synthetic lethality: You can get by without one gene or another, but if you lose both of them nothing can grow."


Shutting down these enzymes, as the researchers did in their experiments, puts cancer cells to sleep but has no effect on healthy cells. "A normal cell doesn't need Type 2 PIP kinases at all, so inhibitors of these enzymes should not be toxic to humans," Dr. Cantley says.


Because it is not possible to replace p53 proteins or the gene in cells that have lost it (many attempts have been made), deactivating Type 2 PIP kinases is the next-best thing, he adds. "This would likely be a very powerful advance in the treatment of many cancers."


###


This work was supported by NIH grant R01 GM041890 and by a Stand Up to Cancer Dream Team Translational Research Grant, a Program of the Entertainment Industry Foundation (SU2C-AACR-DT0209).


Co-authors include first author Dr. Brooke M. Emerling, Gary Bellinger and Rayman Choo-Wing from Weill Cornell Medical College; Dr. George Poulogiannis, Kazumi S. Tsukazawa, Hye-Seok Shim, and Dr. Gina M. DeNicola from Harvard Medical School; Dr. Gerburg M. Wulf, Dr. John M. Asara, Xin Yuan, and Dr. Andrea Bullock from Beth Israel Deaconess Medical School; Dr. Jonathan B. Hurov from Agios Pharmaceuticals; Dr. Eric L. Bell from the Massachusetts Institute of Technology; Dr. Katja A. Lamia from The Scripps Research Institute; Dr. Lucia E. Rameh from Boston University School of Medicine; Dr. Atsuo T. Sasaki from the University of Cincinnati College of Medicine; Dr. Jiaxi Song, Dr. Victoria Brown, and Dr. Sabina Signoretti from Dr. Dana-Farber Cancer Institute.


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 Houston Methodist. For more information, visit weill.cornell.edu.



Office of External Affairs

Weill Cornell Medical College

tel: 646.317.7401

email: pr@med.cornell.edu

Follow WCMC on Twitter and Facebook



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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.




Hope builds for a drug that might shut down a variety of cancers


[ Back to EurekAlert! ]

PUBLIC RELEASE DATE:

7-Nov-2013



[


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]


Share Share

Contact: Sarah Smith
sas2072@med.cornell.edu
646-317-7401
Weill Cornell Medical College



Cancer cells 'go to sleep' when crucial set of molecules is targeted




NEW YORK (November 7, 2013) -- The most frequently mutated gene across all types of cancers is a gene called p53. Unfortunately it has been difficult to directly target this gene with drugs. Now a multi-institutional research team, led by Dr. Lewis Cantley and investigators at Weill Cornell Medical College, has identified a family of enzymes they say is crucial for the growth of cancers that have genetic aberrations in p53. Targeting these enzymes with novel agents might prevent the growth of p53 mutant cancers, thereby benefiting a broad spectrum of cancer patients, including those with breast, ovarian, lung, colorectal and brain tumors.


In the Nov. 7 issue of Cell, investigators pinpoint two cellular enzymes -- Type 2 phosphatidylinositol-5-phosphate 4-kinases α and β (Type 2 PIP kinases) -- as essential for cancer growth when cells have lost p53, the powerful tumor-suppressor gene long dubbed the "guardian of the genome." More than half of all cancers lose this gene, allowing these cancers to grow at will.


The researchers discovered that the Type 2 PIP kinases are not critical for the growth of normal cells but become essential for cell growth when p53 is lost due to mutations or deletions. The scientists showed, in animal and lab studies of human cancer cells, that targeting these molecules effectively shuts down the growth of p53 mutant cancers.


Although the studies were conducted in human breast cancer cells, the researchers believe Type 2 PIP kinase inhibitors could block the growth of cancers with a mutated or missing p53 gene.


"The fact that one can delete the Type 2 PIP kinases in normal human cells or in mice with essentially no effect on cell survival suggests that inhibitors of these enzymes should have little toxicity," says Dr. Cantley, the study's senior author and director of the Cancer Center at Weill Cornell Medical College and NewYork-Presbyterian Hospital.


Dr. Cantley is already leading an effort to develop drugs to shut down these kinases. "Well-designed Type 2 PIP kinase inhibitors may turn the tide on p53 mutant cancer," he says.


A Crucial Link


Dr. Cantley is known for his discovery of the PI 3-kinase oncogene, and pioneering work in teasing apart how the gene contributes to cancer. PI 3-kinases (PI3K) have been linked to a wide variety of cellular functions, including cell growth and proliferation, and most cancers activate PI3K by one or more mechanisms. Dr. Cantley's discovery led to promising avenues for the development of personalized cancer therapies.


Activity of PI3K is in some cases linked to Type 2 PIP kinases, so in this study, Dr. Cantley sought to understand the function of these enzymes. Because the researchers knew that a subset of breast cancers over-express these molecules, investigators looked at their role in HER2-positive breast cancers, which typically are more aggressive tumors.


The researchers, including those from Harvard Medical School, Beth Israel Deaconess Medical Center and other institutions, discovered that the enzymes are silent in cells that have healthy p53. One critical role of p53 is to "rescue" cells that are producing excess reactive oxygen species (ROS), which are byproducts of cells that are growing too rapidly. The oxidative stress produced by ROS can damage cell structures, so p53 attempts to reduce ROS in affected cells. "If, however, ROS levels exceed the capacity of p53s to rescue it, then p53 takes on a second function, which is to kill the cell," Dr. Cantley says.


"That is why cancers often disable p53. If p53 is mutated or gone, then the cell keeps on growing at a very high rate," he says. "And then ROS begins to damage genes, making the cancer even more aggressive."


The Type 2 PIP kinases are the backup rescue system to p53. But they only reduce ROS enough to keep the cells from dying. (Too much ROS will also kill a cell.)


What this means is that cancer cells become "absolutely dependent on these kinases to be able to grow," Dr. Cantley says.


Taking Advantage of "Synthetic Lethality"


But there is a big and important hitch in this scenario, he adds. If the Type 2 PIP kinases are inhibited, and if p53 is deactivated, the cancer cell essentially "goes to sleep," he says. "It just stops dividing and growing. This is called synthetic lethality: You can get by without one gene or another, but if you lose both of them nothing can grow."


Shutting down these enzymes, as the researchers did in their experiments, puts cancer cells to sleep but has no effect on healthy cells. "A normal cell doesn't need Type 2 PIP kinases at all, so inhibitors of these enzymes should not be toxic to humans," Dr. Cantley says.


Because it is not possible to replace p53 proteins or the gene in cells that have lost it (many attempts have been made), deactivating Type 2 PIP kinases is the next-best thing, he adds. "This would likely be a very powerful advance in the treatment of many cancers."


###


This work was supported by NIH grant R01 GM041890 and by a Stand Up to Cancer Dream Team Translational Research Grant, a Program of the Entertainment Industry Foundation (SU2C-AACR-DT0209).


Co-authors include first author Dr. Brooke M. Emerling, Gary Bellinger and Rayman Choo-Wing from Weill Cornell Medical College; Dr. George Poulogiannis, Kazumi S. Tsukazawa, Hye-Seok Shim, and Dr. Gina M. DeNicola from Harvard Medical School; Dr. Gerburg M. Wulf, Dr. John M. Asara, Xin Yuan, and Dr. Andrea Bullock from Beth Israel Deaconess Medical School; Dr. Jonathan B. Hurov from Agios Pharmaceuticals; Dr. Eric L. Bell from the Massachusetts Institute of Technology; Dr. Katja A. Lamia from The Scripps Research Institute; Dr. Lucia E. Rameh from Boston University School of Medicine; Dr. Atsuo T. Sasaki from the University of Cincinnati College of Medicine; Dr. Jiaxi Song, Dr. Victoria Brown, and Dr. Sabina Signoretti from Dr. Dana-Farber Cancer Institute.


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 Houston Methodist. For more information, visit weill.cornell.edu.



Office of External Affairs

Weill Cornell Medical College

tel: 646.317.7401

email: pr@med.cornell.edu

Follow WCMC on Twitter and Facebook



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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.




Source: http://www.eurekalert.org/pub_releases/2013-11/wcmc-hbf110713.php
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Scientists Found the Wolverine Healing Gene

Scientists Found the Wolverine Healing Gene

Deep within our bodies are all kinds of genes that turn on and off over the years, including the very genes that make you grow a body in the first place. This is where scientists are looking for the magical code that could enable us to regrow organs and regenerate limbs. A Harvard researcher thinks he might've found it.

Read more...


    






Source: http://feeds.gawker.com/~r/gizmodo/full/~3/vnr9m7gXeH4/scientists-found-the-wolverine-healing-gene-1460379380
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5 ways BYOD is shaking up tech support



November 07, 2013







Amid the clamor of "bring your own device" (BYOD), a question lurks in the background: "What happens to technical service and support?" Concerns for the tech support function encompass the extremes, from agents being overwhelmed with calls, to their becoming inhabitants of a help desk ghost town.


On the one hand, it’s easy to imagine a flood of calls as employees attempt to access wireless networks or synch their e-mail, especially in companies that permit the use of any device type. At the same time, as more people own smartphones, they are increasingly accustomed to resolving issues independently, through online forums, communities and other means of self-support.


By 2016, says Gartner analyst Jarod Greene, help desks will see a 25% to 30% drop in user-initiated call volume, as BYOD drives a companion trend of BYOS, or “bring your own support.”



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Source: http://www.infoworld.com/d/consumerization-of-it/5-ways-byod-shaking-tech-support-230379?source=rss_mobile_technology
Category: lesean mccoy   Eiza González  

Zaatari: Temporary city on desert's edge


"A Day in the Life" is a multi-part documentary joint venture between Yahoo News UK and the United Nations High Commission for Refugees.

The series and special features accompanying it depict daily existence in the Zaatari refugee camp in Jordan, where more than 122,000 people displaced by the Syrian civil war have fled.

Zaatari has grown to become Jordan's fourth largest city, spawning food markets, housewares shops and, some say, drug dealing and prostitution.

"A Day in the Life" video episodes will appear here as they debut.



Source: http://news.yahoo.com/zaatari-refugee-camp/
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Colin Farrell Stars in "Winter's Tale" Trailer: Watch Here!

Sure to bring tears to your eyes, the trailer for “Winter’s Tale” hit the web on Thursday (November 7).


Colin Farrell and Jessica Brown star in the flick as unlikely lovers, battling to stay together through a number of obstacles.


Based on the imaginative novel by Mark Helprin, the flick also stars Jennifer Connelly, William Hurt and Russell Crowe.


It is slated to hit theaters on Valentine’s Day 2014. Check out the trailer below!






Source: http://celebrity-gossip.net/winters-tale/winters-tale-1095195
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Lea Michele and the Cast of "Glee" Are Feeling Festive on Set

Getting into the holiday spirit a little earlier than the rest of us, Lea Michele, Chris Colfer, and Naya Rivera filmed a holiday episode of "Glee" on Thursday (November 7).


While Rachel wore a red tutu with her green top and pointy elf hat, Santana sported a sexy sleeveless ensemble with Kurt stuck in tights with his outfit.


Recently, the 27-year-old actress got a special shoutout from one of her favorite pop stars on Twitter as the gang features her songs on Thursday's episode.


Encouraging her fans to tune in, Lea tweeted, "#Glee is back tonight! Who's excited?! Hope you guys love it! #GleeSeason5 #KatyOrGaga, " to which Katy Perry replied, "I'm sups excited for tonight's episode of #GLEE, who's with me?!" Clearly indicating her side, Ms. Michele wrote, "I am @katyperry! Ps I love you. #fangirling."


Source: http://celebrity-gossip.net/lea-michele/lea-michele-and-cast-glee-are-feeling-festive-set-957485
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Tim Kennedy admits suffering quadriceps injury a week before Rafael Natal bout


Joshua Lindsey-USA TODAY Sports



UFC middleweight Tim Kennedy had one of the most successful nights of his professional mixed martial arts career, but it didn't come without a measure of adversity prior to even entering the cage.


As he admitted in the post-fight press conference for UFC Fight for the Troops (UFC Fight Night 31), Kennedy suffered an injury to his quadriceps muscle just a week prior to Wednesday evening.


"I tore my quad coming into this camp," Kennedy told the media at Fort Campbell, Kentucky. "The very last week of fight camp, just a stupid thing happened. A lady walked over the track and it was either run over a 65 year-old lady - probably kill her - or try to decelerate in about two meters. I chose to decelerate and just fell to the ground, grabbing my leg screaming not great words."


Kennedy, however, remained undeterred. The former special forces operator said, come hell or high water, there was nothing that was going to keep him from competing on Wednesday evening. It didn't matter what condition was ultimately in by fight time.


"If they had to roll me into the cage to fight Natal, I would've fought him," Kennedy continued. "In the cage, once they hoisted me up and lifted me into the cage, Natal would've had to shoot me and bludgeon me to death until I quit.


"I'm too dumb to care."


That doesn't mean, however, the injury wasn't on his mind. Kennedy told the attending press he and his team did everything they could to mitigate the pain, from deep tissue massages to suction cups to ointments and more.


No matter what, though, Kennedy insisted he was fighting. There was no way as a veteran of combat and the armed services, he wasn't going to compete on a card like this.


"We did everything that we could, like crazy, wacko stuff," Kennedy explained. "You would've had to kill me to prevent me from getting in that cage tonight. I swear to god.


"I'd be dead or I'd be in that cage fighting."


Source: http://www.mmafighting.com/2013/11/6/5075874/tim-kennedy-admits-suffering-quadriceps-injury-a-week-before-rafael
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Kerry warns of violence if peace talks fail

U.S. Secretary of State John Kerry speaks his meeting with Palestinian President Mahmoud Abbas in Bethlehem, Wednesday, Nov. 6, 2013. Kerry waded again into the nitty-gritty of faltering Israeli-Palestinian peace talks on Wednesday, saying he was optimistic that tensions and difficulties could be overcome, even between "two proud people" struggling to reach an accommodation. Kerry was upbeat after separate meetings with Israeli Prime Minister Benjamin Netanyahu and Jerusalem and Palestinian President Mahmoud Abbas in the West Bank town of Bethlehem.(AP Photo/Jason Reed, Pool)







U.S. Secretary of State John Kerry speaks his meeting with Palestinian President Mahmoud Abbas in Bethlehem, Wednesday, Nov. 6, 2013. Kerry waded again into the nitty-gritty of faltering Israeli-Palestinian peace talks on Wednesday, saying he was optimistic that tensions and difficulties could be overcome, even between "two proud people" struggling to reach an accommodation. Kerry was upbeat after separate meetings with Israeli Prime Minister Benjamin Netanyahu and Jerusalem and Palestinian President Mahmoud Abbas in the West Bank town of Bethlehem.(AP Photo/Jason Reed, Pool)







U.S. Secretary of State John Kerry, right, is welcomed by Israel's President Shimon Peres in Jerusalem, Wednesday, Nov. 6, 2013. Kerry waded again into the nitty-gritty of faltering Israeli-Palestinian peace talks on Wednesday, saying he was optimistic that tensions and difficulties could be overcome, even between "two proud people" struggling to reach an accommodation.(AP Photo/Jason Reed, Pool)







U.S. Secretary of State John Kerry hugs The Nativity Store owner Victor Tabash as Kerry receives a gift of a baby Jesus figurine at Manger Square in Bethlehem, Wednesday, Nov. 6, 2013. Kerry waded again into the nitty-gritty of faltering Israeli-Palestinian peace talks on Wednesday, saying he was optimistic that tensions and difficulties could be overcome, even as both sides traded barbs about who is to blame for the current poor state of negotiations. (AP Photo/Jason Reed, Pool)







U.S. Secretary of State John Kerry, left, meets with Israel's President Shimon Peres in Jerusalem, Wednesday, Nov. 6, 2013. Kerry waded again into the nitty-gritty of faltering Israeli-Palestinian peace talks on Wednesday, saying he was optimistic that tensions and difficulties could be overcome, even between "two proud people" struggling to reach an accommodation.(AP Photo/Jason Reed, Pool)







(AP) — U.S. Secretary of State John Kerry issued a stark warning to Israel on Thursday, saying it faces international isolation and a possible explosion of violence if it does not make progress in peace efforts with the Palestinians.

Kerry issued the blunt remarks in a joint interview with Israeli and Palestinian television channels, ensuring the message would reach its intended audience.

"The alternative to getting back to the talks is the potential of chaos. I mean does Israel want a third intifada?" Kerry said, using the term for past Palestinian uprisings against Israeli occupation.

Kerry has been shuttling this week among Israel, the Palestinian territories and Jordan in a frantic bid to get the peace negotiations back on track amid rising public anger among Palestinians over Israeli settlement activity and among Israelis over the release of Palestinian prisoners.

In the television interview, Kerry said a failure in the talks could be devastating.

"If we do not find a way to find peace, there will be an increasing isolation of Israel. There will be an increasing campaign of de-legitimization of Israel (that) has been taking place in an international basis," he said.

If Israel cannot reach peace with the current Palestinian leadership, Kerry added, "you may wind up with leadership that is committed to violence." Excerpts of his comments were aired on Israel's Channel 2 TV, hours before the full interview was to be broadcast.

Kerry recorded the interview in Jerusalem early Thursday before heading to neighboring Jordan, where he tried to rally support for his peace efforts from King Abdullah II.

In Amman, Kerry also warned of a return to violence if peace efforts fail, and rejected suggestions that he scale back his ambition to forge a final settlement with an interim agreement. He said he still believed it could be done by an April 2014 target date.

"What is the alternative to peace?" Kerry asked at a joint news conference with Jordanian Foreign Minister Nasser Judeh. "Prolonged continued conflict."

Kerry appealed for Israelis and Palestinians to take the peace process seriously and for their leaders to overcome differences that have hamstrung the talks since they began three months ago.

He acknowledged the hurdles, but said he was convinced that both Israeli Prime Minister Benjamin Netanyahu and Palestinian President Mahmoud Abbas were committed to the negotiations

"I am pleased to say that despite difficulties, and we all understand what they are, these discussions have been productive," he said.

Kerry said he would make an unscheduled return to Jerusalem on Friday morning for a breakfast meeting with Netanyahu.

Earlier Thursday, Kerry told Jordan's king that his meetings had "created some clarity on some of the points."

He did not elaborate, but said at the news conference with Judeh that there was "significant progress in our discussions about a couple of areas of concern in the panorama of concerns that exist."

A statement from Jordan's Royal Palace said Abdullah, a close U.S. Arab ally, said final status talks involve "higher Jordanian interest," mainly a common border with a future Palestinian state, the fate of Jordan-based Palestinian refugees displaced in the 1967 Mideast war and Jerusalem, where the kingdom maintains custody over Christian and Muslim holy sites.

The king also called on the international community to help end unspecified "Israeli unilateral actions in the occupied Palestinian territories because they are illegal, illegitimate and constitute a real obstacle to peace efforts," the statement said.

He was referring to Israeli government plans to build more settlements in the West Bank, the heartland of a future Palestinian state.

Kerry will see Abbas again Thursday night in Amman and then return to Jerusalem on Friday for a third meeting with Netanyahu in two days before continuing with his swing through the Middle East and North Africa in the United Arab Emirates, Algeria and Morocco.

Since Kerry brokered the re-start of Israeli-Palestinian peace talks, little progress has been made.

The secretary has been hit with complaints from both sides during his trip while working to maintain an optimistic tone.

The stalemate has prompted speculation that the U.S. may need to increase its involvement in the talks and present its own outline for peace — or lower expectations and pursue a more limited, interim agreement.

Kerry rejected the idea of an interim agreement, saying it had been tried before and not worked.

"An interim agreement only if it embraces the concept of a final status might be a step on the way, but you cannot just do an interim agreement and pretend you are dealing with the problem," he said. "We've been there before. We've had interim agreements, we've had roadmaps. But if you leave the main issues hanging out there, mischief-makers will make the most of that and bad things will happen in the interval that then make it even harder to get to the final status."

"It is imperative that we keep final status and settle this before it can't be settled because events on the ground or other events interfere with that possibility."

The Palestinians want to establish an independent state in the West Bank, east Jerusalem and Gaza Strip, territories captured by Israel in the 1967 Mideast war. They say they're willing to adjust those borders to allow Israel to keep some West Bank settlements as part of a "land swap."

Netanyahu opposes a withdrawal to Israel's pre-1967 lines, saying such borders would be indefensible.

He has also demanded that the Palestinians recognize Israel as the Jewish homeland, a condition they reject on the grounds that it would harm the rights of Israel's Arab minority and Palestinian refugees who claim lost properties inside what is now Israel. Netanyahu also rejects shared control of east Jerusalem, home to key religious sites and the Palestinians' hoped-for capital.

___

Associated Press reporters Josef Federman in Jerusalem and Jamal Halaby in Amman, Jordan, contributed to this story.

Associated PressSource: http://hosted2.ap.org/APDEFAULT/cae69a7523db45408eeb2b3a98c0c9c5/Article_2013-11-07-Mideast-Kerry/id-9c9583fe7d634732a1a981c4d54dd846
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TUF 18: Wootten vs. Holdsworth Full Fight Video


Watch every punch, kick and submission attempt uncut and unfiltered as the first spot in the final is claimed. Also make sure to check our recap of The Ultimate Fighter 18 – Episode 10 and make sure to tune in each Wednesday at 10PM ET on FS1 for new episodes.




Source: http://mmafrenzy.com/95950/tuf-18-wootten-vs-holdsworth-full-fight-video/
Category: Cricinfo   edward norton   notre dame   Robocop   Espn.com  

Hilary Duff & Corbin Bleu Celebrate #SelenatorHeaven at LA's Hyde Lounge

Stepping out for a fashionable affair, Hilary Duff and Corbin Bleu attended the Fresh-Tops' #SelenatorHeaven Selena Gomez concert viewing party in Los Angeles on Wednesday (November 6).


Working their magic for the cameras at Staples Center's Hyde Lounge, the former Disney stars looked absolutely stylish and chic as they mingled with fellow industry pals.


The massive VIP event was held for not only Selena's LA concert, but also to celebrate the Twitter trending hastag #SelenatorHeaven. The phrase is used to allow fans of the "Come and Get It" singer's clothing brand share their praise.


Guests at the Hyde Lounge were also swooned by 11-year-old DJ Baby Chino who kept the party's energy up until its closing.


Source: http://celebrity-gossip.net/party-pics/hilary-duff-corbin-bleu-celebrate-selenatorheaven-las-hyde-lounge-957037
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CMA Awards, fellow stars salute George Strait


NASHVILLE, Tenn. (AP) — The entertainer of the year trophy at the Country Music Association Awards is one of the most coveted honors in the genre, but sometimes it's OK to lose — like, say, when George Strait is a nominee.

Strait won his third entertainer of the year award and his first since 1990 Wednesday night against country music's current hitmakers, and there wasn't a disappointed person in the house. Heck, Blake Shelton — one of five performers with a leading two victories — was excited to lose to the 61-year-old whose popularity defies his age.

"That's how it needs to be because he's not just entertainer of the year, he's entertainer of the last three decades, I guess, or four decades," Shelton said. "I don't know who's keeping score. I mean, it's George Strait. He's King George. I couldn't be happier with how this turned out."

Shelton was one of five top winners with two trophies apiece, along with Florida Georgia Line and the trio of Taylor Swift, Tim McGraw and Keith Urban, who won music video and music event of the year for their "Highway Don't Care" collaboration. Like Strait, Swift also was going for her third entertainer of the year, which would have been a CMA record for a woman. Like Shelton, she couldn't have cared less when she lost, instead hugging Faith Hill as they cried tears of joy for Strait. She noted they've both opened for Strait in their careers and she recounted a story about how Strait and his wife Norma dropped in to one of her first headlining concerts when she was a teenager just to wish her luck.

"And that's the kind of artist he is," Strait said. "And when you're that kind of person, and you win something, everybody's cheering for you and people are crying. And that's the kind of legacy you want to leave behind.

The crowd gave Strait a standing ovation as he made his way to the stage, and stayed standing throughout his speech — which by the usually reclusive Strait's standards, was long. It wasn't just a special night for those in the arena. It was also the show's top trending moment on Facebook.

His retirement from the road has gained lots of attention, but Strait isn't a relic. He remains relevant, recently earning his record 60th No. 1 and signing a five-album deal with Universal Music Nashville that will keep in making records.

Backstage he shared with reporters how it has felt as he circles the country on his The Cowboy Rides Away tour, his last.

"When I first started out this year, the first few shows, I about lost it every night, you know, leaving the stage ... thinking, This might be the last time I ever play on this stage again,'" Strait said. He joked he had so much fun, "The cowboy might be riding in again."

Strait's victory capped a show that was simultaneously focused on the past, present and future.

Shelton, his wife Miranda Lambert and Swift all continued winning ways. Shelton took album of the year for "Based on a True Story ...," and won his fourth male vocalist of the year. Voters supplied some symmetry when they named Lambert female vocalist of the year, also for the fourth time, tying her with good friend Reba McEntire.

It was the third straight year in which Lambert or Shelton were among the top winners, and capped a year in which they were dogged by tabloid stories about their relationship. Lambert said she wasn't sure why the CMA's 6,000 voters love the couple so much.

"You know, pillow talk, literally, we're like, 'Well, our year was last year,'" Lambert said. "It was great, a great run while we had it. We'll drink tonight and celebrate all of our friends winning, because literally all of my friends won awards tonight. And that's what's great about country music because we are all friends. But I just thank everybody for really understanding that we're real people and that every time they vote for us and that we stand up there on that stage it's like it makes our life."

Swift, who performed a somber, acoustic version of her hit "Red" with Vince Gill, Alison Krauss and Sam Bush, won her eighth and ninth CMA trophies before being honored with the association's Pinnacle Award, given to an artist who has taken country to a worldwide audience.

The CMA brought a star-studded welcoming group out on stage for Swift that included Strait, Rascal Flatts, McGraw and Hill, Urban and Brad Paisley — all of whom gave Swift a chance to open for them on the road a teenager. A video salute followed with appearances by Justin Timberlake, Julia Roberts, Carly Simon, Ethel Kennedy and Mick Jagger — whose appearance made Swift shout.

"You've made me feel so special right now, thank you," Swift said.

Voters also cast an eye to the future, handing trophies to young stars Florida Georgia Line and Kacey Musgraves, who was a top nominee with Swift.

Florida Georgia Line's Tyler Hubbard and Brian Kelley scored single and vocal duo of the year. Their quick wins early in the show was more proof the so-called bro country movement is the sound of the moment in mainstream country. FGL kicked off the show performing a fist-pumping medley with Luke Bryan, and very quickly returned to the stage to take the trophy for single of the year for their "Cruise" remix featuring Nelly. They also played the new song "Round Here."

"It's been a constant thing all year — we've been trying to wrap our minds around what's going on," Hubbard said of the band's platinum success backstage. "It's been a dream come true for us and a huge blessing for us and something we could have never imagined."

Musgraves won the new artist trophy, besting a field that included Florida Georgia Line. With smart songwriting, a progressive bent and a strong sense of self like country's other top women, Musgraves made an auspicious mainstream country debut this year with her album "Same Trailer Different Park." She attended with her grandmother.

"It's amazing what 52 weeks can do to a person," Musgraves said backstage. "... Last year I had really crappy seats. You know, I was just sitting back with my roommate just as a fan. And here I am holding this thing."

Lee Brice's "I'd Drive Your Truck," about a fallen soldier whose father still drives his truck, won song of the year, and Little Big Town took its second straight vocal group of the year.

Collaboration was the theme of the night as Strait and Alan Jackson joined together to salute the late George Jones with a rendition of "She Stopped Loving Him Today." Hunter Hayes and Jason Mraz took a tour of the Bridgestone Arena while performing "Everybody's Got Somebody But Me." And Zac Brown and his band joined in on a growing hard-rock trend in country as Foo Fighter Dave Grohl played drums for new high-powered song "Day for the Dead." Eric Church earlier turned things up to 11 with his new song "The Outsiders." And in one of the night's most anticipated moments, Kenny Rogers received the CMA's Willie Nelson lifetime achievement award and was saluted by Jennifer Nettles, Rucker and Rascal Flatts.

___

http://www.cmaawards.com

___

Follow AP Entertainment for updates from the show: http://twitter.com/APEntertainment. Follow AP Music Writer Chris Talbott: http://twitter.com/Chris_Talbott.

Source: http://news.yahoo.com/cma-awards-fellow-stars-salute-george-strait-083510678.html
Category: Johnny Manziel   FIFA 14   Wally Bayola scandal   jessica biel   Lisa Robin Kelly  

Matt Lauer & Al Roker Receive Prostate Exams Live on "Today"

In an effort to raise awareness for men's health, Matt Lauer and Al Roker received live prostate exams on the "Today Show" Thursday (November 7).


During the unusual segment, the talk show hosts stopped by a local prostate cancer center to prove why getting an exam is extremely important for early detection.


An estimated 238,000 new cases are diagnosed in the US each year and doctors encourage men to get the simple test annually.


While in the exam room, both Lauer and Roker's screening were timed to only take 34 seconds. Although it's not the best half minute of your life, it's crucial for all men.


Check out the video below of Matt and Al's experience!






Source: http://celebrity-gossip.net/today-show/matt-lauer-al-roker-receive-prostate-exams-live-today-1094792
Category: michigan football   dez bryant   nfl standings   Derrick Thomas   Kelly LeBrock  

Clotting protein hardens aging hearts

Clotting protein hardens aging hearts


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PUBLIC RELEASE DATE:

7-Nov-2013



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Contact: David Ruth
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Rice University



Rice U. researchers link von Willebrand factor to heart-valve calcium deposits



Heart valves calcify over time, and Rice University scientists are beginning to understand why.


The Rice lab of bioengineer Jane Grande-Allen found through studies of pigs' heart valves that age plays a critical role in the valves' progressive hardening, and the problem may be due to the infiltration of a protein known as von Willebrand factor (VWF). Tissues from pig valves are commonly used to make human heart-valve replacements.


VWF helps regulate blood clotting in both pigs and humans but, as the Rice team discovered, it finds its way over time into the collagen-rich interior of the valve tissues. Because clotting is not an issue in collagen, there is no apparent need for VWF to be present. The researchers went looking for a connection to the calcium nodules that form in the tissues and make the valves' leaflets less flexible, which decreases blood flow to the heart.


The new work, detailed in the American Heart Association journal Arteriosclerosis, Thrombosis and Vascular Biology, "opens up a huge line of investigation," Grande-Allen said.


The paper's lead author, Liezl Balaoing, a graduate student of Grande-Allen and Rice research scientist Joel Moake, studied valves from pigs of three ages: 6 weeks, 6 months and 2 years (as stand-ins for young, middle-aged and old human hearts). Through staining, Balaoing traced the migration of a number of clotting-related proteins common to pigs and humans from the surface endothelial cells to the inner interstitial cells.


The tests showed that as a valve ages, VWF and other proteins gather in the valve tissue's interior. They then tested how valve interstitial cells that produce calcium nodules in diseased valves respond to VWF. When interstitial cells were intentionally exposed to VWF, "there was a dramatic increase in the size of the nodules at every age," Balaoing said.


"Endothelial cells on the outside of the valve are making most of these (clotting-related) proteins," Grande-Allen said. "We found they don't just float away into the blood or stay on the valve surface. Some of them penetrate down into the tissue."


What remains to be seen is why. Heart valves are in motion from birth to death and are perhaps the most active connective tissue in the body. The researchers suspect the breakdown of collagen over time, as well as the constant stretching of the valve, opens gaps through which the proteins can travel.


"As you get older, collagen becomes less organized," Balaoing said. "Because the distinct arrangement of extracellular matrix disappears, I think proteins like VWF permeate inside the valve more than what you would see in young, healthy adults."


"We clearly know that our bodies and our whole physiology change with age," Grande-Allen said. "Biologically, characteristics like blood-clotting change with age too. The remarkable finding here is that aspects of changes in blood clotting are very strongly linked to the propensity to form calcified heart valves."


Grande-Allen said she saw signs of VWF invasion into the valves' interiors in earlier work, but it took a systematic effort by Balaoing to get to the truth. Now they hope to find the binding mechanism that keeps the proteins in place, as that discovery could lead to treatment. "We want to know if VWF and other clotting-related proteins are doing things to the valve interstitial cells and extracellular matrix that may contribute to calcification and other valve diseases," Grande-Allen said.


###


Co-authors of the paper are Allison Post, a Rice alumna now in graduate studies at the University of Houston, and Rice undergraduates Wendy Liu and Kyung Taeck Minn. Grande-Allen is a professor of bioengineering based at Rice's BioScience Research Collaborative. Moake is a senior research scientist and associate director of the J.W. Cox Laboratory for Biomedical Engineering at Rice and a professor of medicine at Baylor College of Medicine.



The American Heart Association, the National Institutes of Health, the Mary R. Gibson Foundation and the Mabel and Everett Hinkson Memorial Fund supported the research.



Read the abstract at http://atvb.ahajournals.org/content/early/2013/10/31/ATVBAHA.113.301936.abstract


Follow Rice News and Media Relations via Twitter @RiceUNews


Related Materials:


Jane Grande-Allen: http://bioengineering.rice.edu/faculty/Jane_Grande-Allen.aspx


Grande-Allen Integrative Matrix Mechanics Lab: http://grandegroup.blogs.rice.edu


Images for download:


http://news.rice.edu/wp-content/uploads/2013/11/1111_HEART-1-web.jpg


A new study by Rice University researchers shows how the extracellular matrix in heart valve tissues changes with age, including the accumulation of von Willebrand factor (VWF), a blood-clotting protein. At top left is a sample of an elderly pig valve; at right, staining reveals the accumulation of VWF throughout the tissue. At bottom are porcine aortic valve interstitial cells not treated with endothelial cell VWF (left) and treated with endothelial cell VWF (right). The VWF appears to prompt formation of larger calcific nodules. (Credit: Integrative Matrix Mechanics Lab/Rice University)


http://news.rice.edu/wp-content/uploads/2013/11/1111_HEART-2-web.jpg


Rice University researchers have determined that von Willebrand factor, a blood-clotting protein, plays a critical role in the progressive hardening of heart valves in pigs as they age. The researchers believe the same process is occurring in human heart valves. Clockwise from left are Rice senior Kyung Taeck Minn, Professor Jane Grande-Allen, Liezl Balaoing and Rice alumna Allison Post. (Credit: Jeff Fitlow/Rice University)


http://news.rice.edu/wp-content/uploads/2013/11/1111_HEART-3-web.jpg


Rice University researchers have determined that von Willebrand factor, a blood-clotting protein, plays a critical role in the progressive hardening of heart valves in pigs as they age. The researchers believe the same process is occurring in human heart valves. Clockwise from left are Rice senior Kyung Taeck Minn, Professor Jane Grande-Allen, Liezl Balaoing and Rice alumna Allison Post. (Credit: Jeff Fitlow/Rice University)


http://news.rice.edu/wp-content/uploads/2013/11/1111_HEART-4-web.jpg


Rice University bioengineer Jane Grande-Allen, standing, and graduate student Liezl Balaoing led a study that determined the increasing effects of a blood-clotting protein on heart valves as they age. (Credit: Jeff Fitlow/Rice University)


Located on a 300-acre forested campus in Houston, Rice University is consistently ranked among the nation's top 20 universities by U.S. News & World Report. Rice has highly respected schools of Architecture, Business, Continuing Studies, Engineering, Humanities, Music, Natural Sciences and Social Sciences and is home to the Baker Institute for Public Policy. With 3,708 undergraduates and 2,374 graduate students, Rice's undergraduate student-to-faculty ratio is 6-to-1. Its residential college system builds close-knit communities and lifelong friendships, just one reason why Rice has been ranked No. 1 for best quality of life multiple times by the Princeton Review and No. 2 for "best value" among private universities by Kiplinger's Personal Finance. To read "What they're saying about Rice," go to http://tinyurl.com/AboutRiceU.




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Clotting protein hardens aging hearts


[ Back to EurekAlert! ]

PUBLIC RELEASE DATE:

7-Nov-2013



[


| E-mail

]


Share Share

Contact: David Ruth
david@rice.edu
713-348-6327
Rice University



Rice U. researchers link von Willebrand factor to heart-valve calcium deposits



Heart valves calcify over time, and Rice University scientists are beginning to understand why.


The Rice lab of bioengineer Jane Grande-Allen found through studies of pigs' heart valves that age plays a critical role in the valves' progressive hardening, and the problem may be due to the infiltration of a protein known as von Willebrand factor (VWF). Tissues from pig valves are commonly used to make human heart-valve replacements.


VWF helps regulate blood clotting in both pigs and humans but, as the Rice team discovered, it finds its way over time into the collagen-rich interior of the valve tissues. Because clotting is not an issue in collagen, there is no apparent need for VWF to be present. The researchers went looking for a connection to the calcium nodules that form in the tissues and make the valves' leaflets less flexible, which decreases blood flow to the heart.


The new work, detailed in the American Heart Association journal Arteriosclerosis, Thrombosis and Vascular Biology, "opens up a huge line of investigation," Grande-Allen said.


The paper's lead author, Liezl Balaoing, a graduate student of Grande-Allen and Rice research scientist Joel Moake, studied valves from pigs of three ages: 6 weeks, 6 months and 2 years (as stand-ins for young, middle-aged and old human hearts). Through staining, Balaoing traced the migration of a number of clotting-related proteins common to pigs and humans from the surface endothelial cells to the inner interstitial cells.


The tests showed that as a valve ages, VWF and other proteins gather in the valve tissue's interior. They then tested how valve interstitial cells that produce calcium nodules in diseased valves respond to VWF. When interstitial cells were intentionally exposed to VWF, "there was a dramatic increase in the size of the nodules at every age," Balaoing said.


"Endothelial cells on the outside of the valve are making most of these (clotting-related) proteins," Grande-Allen said. "We found they don't just float away into the blood or stay on the valve surface. Some of them penetrate down into the tissue."


What remains to be seen is why. Heart valves are in motion from birth to death and are perhaps the most active connective tissue in the body. The researchers suspect the breakdown of collagen over time, as well as the constant stretching of the valve, opens gaps through which the proteins can travel.


"As you get older, collagen becomes less organized," Balaoing said. "Because the distinct arrangement of extracellular matrix disappears, I think proteins like VWF permeate inside the valve more than what you would see in young, healthy adults."


"We clearly know that our bodies and our whole physiology change with age," Grande-Allen said. "Biologically, characteristics like blood-clotting change with age too. The remarkable finding here is that aspects of changes in blood clotting are very strongly linked to the propensity to form calcified heart valves."


Grande-Allen said she saw signs of VWF invasion into the valves' interiors in earlier work, but it took a systematic effort by Balaoing to get to the truth. Now they hope to find the binding mechanism that keeps the proteins in place, as that discovery could lead to treatment. "We want to know if VWF and other clotting-related proteins are doing things to the valve interstitial cells and extracellular matrix that may contribute to calcification and other valve diseases," Grande-Allen said.


###


Co-authors of the paper are Allison Post, a Rice alumna now in graduate studies at the University of Houston, and Rice undergraduates Wendy Liu and Kyung Taeck Minn. Grande-Allen is a professor of bioengineering based at Rice's BioScience Research Collaborative. Moake is a senior research scientist and associate director of the J.W. Cox Laboratory for Biomedical Engineering at Rice and a professor of medicine at Baylor College of Medicine.



The American Heart Association, the National Institutes of Health, the Mary R. Gibson Foundation and the Mabel and Everett Hinkson Memorial Fund supported the research.



Read the abstract at http://atvb.ahajournals.org/content/early/2013/10/31/ATVBAHA.113.301936.abstract


Follow Rice News and Media Relations via Twitter @RiceUNews


Related Materials:


Jane Grande-Allen: http://bioengineering.rice.edu/faculty/Jane_Grande-Allen.aspx


Grande-Allen Integrative Matrix Mechanics Lab: http://grandegroup.blogs.rice.edu


Images for download:


http://news.rice.edu/wp-content/uploads/2013/11/1111_HEART-1-web.jpg


A new study by Rice University researchers shows how the extracellular matrix in heart valve tissues changes with age, including the accumulation of von Willebrand factor (VWF), a blood-clotting protein. At top left is a sample of an elderly pig valve; at right, staining reveals the accumulation of VWF throughout the tissue. At bottom are porcine aortic valve interstitial cells not treated with endothelial cell VWF (left) and treated with endothelial cell VWF (right). The VWF appears to prompt formation of larger calcific nodules. (Credit: Integrative Matrix Mechanics Lab/Rice University)


http://news.rice.edu/wp-content/uploads/2013/11/1111_HEART-2-web.jpg


Rice University researchers have determined that von Willebrand factor, a blood-clotting protein, plays a critical role in the progressive hardening of heart valves in pigs as they age. The researchers believe the same process is occurring in human heart valves. Clockwise from left are Rice senior Kyung Taeck Minn, Professor Jane Grande-Allen, Liezl Balaoing and Rice alumna Allison Post. (Credit: Jeff Fitlow/Rice University)


http://news.rice.edu/wp-content/uploads/2013/11/1111_HEART-3-web.jpg


Rice University researchers have determined that von Willebrand factor, a blood-clotting protein, plays a critical role in the progressive hardening of heart valves in pigs as they age. The researchers believe the same process is occurring in human heart valves. Clockwise from left are Rice senior Kyung Taeck Minn, Professor Jane Grande-Allen, Liezl Balaoing and Rice alumna Allison Post. (Credit: Jeff Fitlow/Rice University)


http://news.rice.edu/wp-content/uploads/2013/11/1111_HEART-4-web.jpg


Rice University bioengineer Jane Grande-Allen, standing, and graduate student Liezl Balaoing led a study that determined the increasing effects of a blood-clotting protein on heart valves as they age. (Credit: Jeff Fitlow/Rice University)


Located on a 300-acre forested campus in Houston, Rice University is consistently ranked among the nation's top 20 universities by U.S. News & World Report. Rice has highly respected schools of Architecture, Business, Continuing Studies, Engineering, Humanities, Music, Natural Sciences and Social Sciences and is home to the Baker Institute for Public Policy. With 3,708 undergraduates and 2,374 graduate students, Rice's undergraduate student-to-faculty ratio is 6-to-1. Its residential college system builds close-knit communities and lifelong friendships, just one reason why Rice has been ranked No. 1 for best quality of life multiple times by the Princeton Review and No. 2 for "best value" among private universities by Kiplinger's Personal Finance. To read "What they're saying about Rice," go to http://tinyurl.com/AboutRiceU.




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]

 


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Source: http://www.eurekalert.org/pub_releases/2013-11/ru-cph110713.php
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