Washington, July 20 : A team of Harvard scientists has now uncovered evidence of genetic changes that might help protect some people from contracting cholera.

Based on genetic data gathered from hundreds of people in Bangladesh, a research team made up of Harvard faculty and scientists from the Broad Institute and Massachusetts General Hospital were able to a number of areas in the genome - some of which are responsible for certain immune system functions, while others are related to fluid loss - that appear to be related to cholera resistance.

Later tests showed genetic differences between people who had contracted the disease and those who had been exposed, but did not become ill.

"This study is exceptionally exciting for us because it shows the power of this approach," Associate Professor of Organismic and Evolutionary Biology Pardis Sabeti, one of two senior co-authors of the paper, said.

"This is the first time we've taken a genomic-wide approach to understanding cholera resistance. But it's a first step, and there is a lot of exploration to go from here. For a disease that's so ancient and widespread there's very little that's known about host immunity," the researcher said.

The hope, Sabeti added, is that by better understanding why some people appear to be immune, it will help in our efforts to develop vaccines and therapies, so outbreaks like those that occurred in recent years in Haiti and Africa might one-day be avoided. The study is published in the journal Science Translational Medicine.

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Genetics' key role behind cholera revealed

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VISIONS 2013 - Llura Liggett Gund Award
http://www.FightBlindness.org/visions | Ed Gollob, Dr. Eric Pierce and Dr. Stephen Rose present the Foundation #39;s highest research award, the Llura Liggett Gund Awar...

By: FndFightingBlindness

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VISIONS 2013 - Llura Liggett Gund Award - Video

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Stem Cell Therapy Treatment for Friedreichs Ataxia by Dr Alok Sharma, Mumbai, India.
Improvement seen in just 5 day after Stem Cell Therapy Treatment for Friedreichs Ataxia by Dr Alok Sharma, Mumbai, India. After Stem Cell Therapy 1. Speech has become much smoother and easier,...

By: Neurogen Brain and Spine Institute

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Stem Cell Therapy Treatment for Friedreichs Ataxia by Dr Alok Sharma, Mumbai, India. - Video

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Personalized Medicine Coalition: How medical progress happens
Learn more about how medical progress happens from the Personalized Medicine Coalition.

By: personalizedmedicine

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Personalized Medicine Coalition: How medical progress happens - Video

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Can New Bone Be Made From Skin Stem Cells?
Cartilage can be made from skin stem cells and now bone! In this video, Sharecare expert Michael Roizen, MD, chief wellness officer for Cleveland Clinic, exp...

By: SharecareVideo

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Can New Bone Be Made From Skin Stem Cells? - Video

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DUBLIN, July 18, 2013 /PRNewswire/ --

Research and Markets (http://www.researchandmarkets.com/research/qc7zk2/stem_cell_therapy) has announced the addition of the "Stem Cell Therapy Market in Asia-Pacific to 2018 - Commercialization Supported by Favorable Government Policies, Strong Pipeline and Increased Licensing Activity" report to their offering.

(Logo: http://photos.prnewswire.com/prnh/20130307/600769 )

Commercialization Supported by Favorable Government Policies, Strong Pipeline and Increased Licensing Activity

Stem Cell Research in Asia-Pacific a Growth Engine for Region's Scientific Ambitions

The stem cell therapy market in Asia-Pacific is poised to offer significant contributions in the future, thanks to renewed interest by the respective governments of India, China, Japan, South Korea and Singapore to provide cures for a range of diseases, states a new report by healthcare experts GBI Research.

Stem cells are unique body cells that possess the ability to divide and differentiate into diverse cell types, and can be used to produce more stem cells. The use of adult stem cells has been successfully employed to treat bone and blood related disorders such as leukemia, through bone marrow transplants. Stem cell therapy is used to repair and regenerate the damaged tissue, though the actual mechanism of action is largely unknown.

The growth in the stem cell therapy market will not only provide treatment options but will also contribute significantly to the countries' Gross Domestic Product (GDP), with the President of South Korea only last year referring to stem cell research as a new growth engine for the nation's economy. In order to support the stem cell industry, regulatory guidelines in Asia-Pacific countries allow stem cell research, and this has led to its commercialization. India and South Korea are the leaders in the commercialization of stem cell therapy, with approved products for Acute Myocardial Infarction (AMI), osteoarthritis and anal fistula in Crohn's disease, amongst others. The countries allow the use of human embryonic stem cells and provide adequate funding support for the research.

Stem cell therapy is an emerging field, and a large amount of research is currently being carried out by institutions such as hospitals, universities and medical colleges. According to GBI Research's analysis of the stem cell therapy research in Asia-Pacific, 63% of pipeline molecules were being researched by academia. The emergence of institutional research has boosted stem cell discoveries, as companies can be put off conducting research due to uncertain therapeutic outcomes. China and Japan witness only a negligible industry presence in stem cell research, as academic institutions dominate - however in contrast, India has the presence of both industry and academia. The major institutions engaged in stem cell research in India are LV Prasad Eye Institute (LYPEI) for Limbal Stem Cell Technology (LSCT), and the Post Graduate Institute of Medical Education and Research (PGIMER) for stem cell therapy for type 2 diabetes mellitus.

The market is poised for significant growth in the future, due to the anticipated launch of JCR Pharmaceuticals' JR-031 in Japan in 2014, and FCB Pharmicell's Cerecellgram (CCG) in South Korea in 2015. GBI Research therefore predicts that the stem cell therapy market will grow in value from $545m in 2012 to $972m in 2018, at a Compound Annual Growth Rate (CAGR) of 10%.

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Stem Cell Therapy Market in Asia-Pacific to 2018

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Public release date: 18-Jul-2013 [ | E-mail | Share ]

Contact: Cyndi Lepore 617-919-3110 Boston Children's Hospital

Boston, Mass., July 18, 2013 - Researchers at Boston Children's Hospital have identified a genetic cause of severe obesity that, though rare, raises new questions about weight gain and energy use in the general obese population. The research, published in the journal Science on July 19, involved genetic surveys of several groups of obese humans and experiments in mice.

Mice with the genetic mutation gained weight even while eating the same amount of food as their normal counterparts; the affected gene, Mrap2, has a human counterpart (MRAP2) and appears to be involved in regulating metabolism and food consumption.

"These mice aren't burning the fat, they're somehow holding onto it," says the study's lead investigator Joseph Majzoub, MD, chief of endocrinology at Boston Children's. "Mice with the genetic mutation gained more weight, and we found similar mutations in a cohort of obese humans."

The protein created by the Mrap2 gene appears to facilitate signaling to a receptor in the brain called Mc4r, which helps increase metabolism and decrease appetite as part of a larger signaling chain involved in energy regulation. Fat cells produce the hormone leptin, prompting receptors in the brain to instigate production of a second hormone, MSH. Mc4r detects this hormone with the aid of Mrap2, leading to a decrease in appetite and weight. Mutations in this signaling chain, including mutations in Mc4r, are known to increase the likelihood of obesity.

Majzoub, first author Masato Asai, MD, PhD, now at Nagoya University in Japan, and colleagues studied mice with the Mrap2 gene knocked out both overall and just in the brain. In both cases, the mice grew to about twice their normal size. Weight gain was greatest when both copies of Mrap2 were knocked out, but the mice still showed weight gain and appetite increase with one working copy of the gene. The weight gain was more pronounced in males than females. In addition, the mice without Mrap2 had more exaggerated weight gain when fed a high-fat diet than normal mice.

Surprisingly, while the mice without Mrap2 didn't eat more at first, they still gained weight faster than the controls. Later, their appetites increased and they continued to gain more weight than the controls, even when held to the same diet and quantity of food. In the end, the mutant mice had to be underfed by 10 to 15 percent to show the same weight gain as their normal peers. As soon as they were let off the restricted diet, their weight gain increased.

To investigate the gene in humans, Majzoub collaborated with Sadaf Farooqi, MD, PhD, of the University of Cambridge, and others to investigate groups of obese patients from around the world. The team found four mutations in the human equivalent of Mrap2 among the 500 people, all in patients with severe, early-onset obesity; each of the four affected patients had only one copy of the mutation.

While the finding suggests that these rare mutations directly cause obesity in less than 1 percent of the obese population, the researchers suspect that other mutations in the gene might occur more commonly and might interact with other mutations and environmental factors to cause more common forms of obesity. "We found other mutations that weren't as clearly damaging to the gene," notes Majzoub. "It's possible that some of these more common mutations actually are pathogenic, especially in combination with other genes in the same pathway."

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Gene mutation linked to obesity

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Public release date: 19-Jul-2013 [ | E-mail | Share ]

Contact: Caroline Marin crmarin@umn.edu 612-624-5680 University of Minnesota Academic Health Center

MINNEAPOLIS/ST. PAUL (July 19, 2013) Researchers at the University of Minnesota have identified infection-fighting and inflammation-suppressing functions for a gene associated with human autoimmune disease.

The discovery, centered on a gene known as PTPN22, could set into motion new treatment approaches for autoimmune diseases like lupus, rheumatoid arthritis and type 1 diabetes. The key to these advances may lie with a better understanding of how a variant of PTPN22, known as a "risk variant," impacts autoimmune disease development and the behavior of myeloid cells that act as the body's "first responders."

The study appears in the journal Immunity.

In launching their latest research project, University of Minnesota Center for Immunology researchers set out to determine how PTPN22 could regulate immune system function in health and disease.

"Almost a decade ago, researchers at the University of Minnesota and other institutions discovered that people carrying a variant form of the PTPN22 gene bear an increased risk of becoming sick with certain autoimmune diseases. However, we have lacked a deep understanding how the variant creates that increased risk," said Erik J. Peterson, M.D., one of the study's lead authors and a University of Minnesota Medical School associate professor in the Division of Rheumatic and Autoimmune Diseases. "We wanted to understand the molecular basis for PTPN22 association with disease."

Much of the work carried out in the latest study took place in Peterson's laboratory, which utilizes genetic, biochemical, and primary human sample-based approaches to investigate how "risk" genes predispose to development of autoimmune disease.

According to the study's authors, previous research showed that PTPN22 works in immune cells, but few studies had specifically examined PTPN22's function in infection-fighting cells called myeloid cells.

"Myeloid cells are among the body's 'first responders' to a challenge with a virus or bacterium," said Yaya Wang, Ph.D., one of the study's co-first authors and a research associate in the Center for Immunology. "Upon recognizing the presence of an infection, myeloid cells produce chemicals that increase inflammation and help fight the invading microbe. We were intrigued by the idea that PTPN22 and its disease-associated variant might have a role in myeloid cell functions."

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U of M researchers identify new functions for autoimmune disease 'risk' gene

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July 19, 2013 Researchers at the University of Minnesota have identified infection-fighting and inflammation-suppressing functions for a gene associated with human autoimmune disease.

The discovery, centered on a gene known as PTPN22, could set into motion new treatment approaches for autoimmune diseases like lupus, rheumatoid arthritis and type 1 diabetes. The key to these advances may lie with a better understanding of how a variant of PTPN22, known as a "risk variant," impacts autoimmune disease development and the behavior of myeloid cells that act as the body's "first responders."

The study appears in the journal Immunity.

In launching their latest research project, University of Minnesota Center for Immunology researchers set out to determine how PTPN22 could regulate immune system function in health and disease.

"Almost a decade ago, researchers at the University of Minnesota and other institutions discovered that people carrying a variant form of the PTPN22 gene bear an increased risk of becoming sick with certain autoimmune diseases. However, we have lacked a deep understanding how the variant creates that increased risk," said Erik J. Peterson, M.D., one of the study's lead authors and a University of Minnesota Medical School associate professor in the Division of Rheumatic and Autoimmune Diseases. "We wanted to understand the molecular basis for PTPN22 association with disease."

Much of the work carried out in the latest study took place in Peterson's laboratory, which utilizes genetic, biochemical, and primary human sample-based approaches to investigate how "risk" genes predispose to development of autoimmune disease.

According to the study's authors, previous research showed that PTPN22 works in immune cells, but few studies had specifically examined PTPN22's function in infection-fighting cells called myeloid cells.

"Myeloid cells are among the body's 'first responders' to a challenge with a virus or bacterium," said Yaya Wang, Ph.D., one of the study's co-first authors and a research associate in the Center for Immunology. "Upon recognizing the presence of an infection, myeloid cells produce chemicals that increase inflammation and help fight the invading microbe. We were intrigued by the idea that PTPN22 and its disease-associated variant might have a role in myeloid cell functions."

Researchers found that both mouse and human myeloid cells carrying the PTPN22 "risk" variant show decreased production of molecules called type 1 Interferons. Type 1 Interferons are needed to boost immune responses to viruses and other infections. In mice lacking the PTPN22 gene, reduced type 1 Interferon production correlates with an impaired ability to fight infections.

But the PTPN22 gene does more than simply fight infection, the study showed.

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New functions for autoimmune disease 'risk' gene identified

Recommendation and review posted by Bethany Smith

Medically, obesity is now considered a disease. Socially, the condition is regarded differently. In the latter realm, being extremely overweight can seem like a symptom of laziness or lack of willpower.

Research into the genetics of obesity, however, is revealing that judgment may be unfair. Researchers at Boston Childrens Hospital have discovered a gene that, when deleted, causes extreme obesity in mice. Although an initial survey showed that disease-causing mutations in the gene are quite rare in people, scientists think that less severe mutations in this and other rare genes associated with obesity may cause subtle differences in energy regulation and metabolism. Those differences may cause some people to be predisposed to weight gain.

In an unusual twist, the mice in the study published Thursday in the journal Science didnt gain weight simply because they ate more. Rodents lacking the gene must be fed about 15 percent less than normal mice to have the same amount of weight gain.

The mice we have made that are obese, while theyre children and adolescents and in that phase, theyre getting very obese, but not eating more than brothers and sisters, said Dr. Joseph Majzoub, chief of endocrinology at Childrens Hospital. Its quite different from other types of obesity.

Dr. Michael Schwartz, director of the Diabetes and Obesity Center of Excellence at the University of Washington, said that the new study was a valuable addition to the growing knowledge about the genetic underpinnings of obesity. Schwartz, who was not involved in the work, said that in addition to genes that cause severe obesity, there are genes that protect against gaining weight. The genetic predisposition to gain weight was probably influenced not only by genes that make people gain weight, he said, but in flaws in those that protect against gaining weight.

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New gene associated with severe obesity

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Public release date: 18-Jul-2013 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 x2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, July 18, 2013Mary Ann Liebert, Inc., publishers (http://www.liebertpub.com) has introduced a preview issue of Soft Robotics (SoRo), a new peer-reviewed journal dedicated to the science and engineering of soft materials in mobile machines. The scope and contents of the Journal capture the innovative research on robotic technology that is enabling robots to interact safely with living systems and to function in complex natural or human-built environments. Soft Robotics will be available online with Open Access options and in print. The articles in the preview issue are available free on the Soft Robotics website (http://www.liebertpub.com/soro)

The insightful Roundtable Discussion included in the preview issue, "At the Crossroads: Interdisciplinary Paths to Soft Robots," brings together experts in the many diverse fields needed for the successful development, integration, and application of this complex technology. The panelists discuss the challenges, opportunities, state-of-the-field, and future promise of soft robotics.

Participants in the Roundtable, who also contributed review articles to the preview issue, included Randy Ewoldt, University of Illinois at Urbana-Champaign ("Extremely Soft: Design with Rheologically-Complex Fluids"), Mirko Kova, Imperial College London, UK ("The Bioinspiration Design Paradigm: A Perspective for Soft Robotics"), Hod Lipson, Cornell University, Ithaca, NY ("Challenges and Opportunities for Design, Simulation, and Fabrication of Robots"), Nanshu Lu, University of Texas at Austin ("Flexible and Stretchable Electronics Paving the Way for Soft Robotics"), Mohsen Shahinpoor, University of Maine, Orono ("A Review of Ionic Polymeric Soft Actuators and Sensors"), and Carmel Majidi, Carnegie Mellon University, Pittsburgh, PA ("Soft RoboticsA Perspective: Current Trends and Prospects for the Future").

The preview issue also includes the original research article "A Hybrid Combining Hard and Soft Robots" by A.A. Stokes et al., University of Edinburgh.

"The next frontier in robotics is to make machines that can assist us in everyday activities, at home, in the office, in hospitals, and even in natural environments," says Editor-in-Chief Barry A. Trimmer, PhD, Henry Bromfield Pearson Professor of Natural Sciences and Director, Neuromechanics and Biomimetic Devices Laboratory, Tufts University, Medford, MA. "Soft Robotics provides a forum, for the first time, for scientists and engineers across diverse fields to work together to build the next generation of interactive robots. This journal provides biologists, engineers, materials specialists, and computer scientists a common meeting place, and we are very excited about this new forum."

###

About the Journal

Soft Robotics (SoRo), a new peer-reviewed journal published quarterly online with Open Access options and in print, combines advances in biomedical engineering, biomechanics, mathematical modeling, biopolymer chemistry, computer science, and tissue engineering to present new approaches to the creation of robotic technology and devices that can undergo dramatic changes in shape and size in order to adapt to various environments. Led by Editor-in-Chief Barry A. Trimmer, PhD and a distinguished team of Associate Editors, the Journal provides the latest research and developments on topics such as soft material creation, characterization, and modeling; flexible and degradable electronics; soft actuators and sensors; control and simulation of highly deformable structures; biomechanics and control of soft animals and tissues; biohybrid devices and living machines; and design and fabrication of conformable machines. Complete information is available on the SoRo website (http://www.liebertpub.com/soro).

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Soft Robotics -- preview issue of groundbreaking journal on engineered soft devices that interact with living systems

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Topics: editors picks, laughter, maryborough, medicine, rieters disease

DANIEL Gassman was diagnosed with the rare, incurable genetic disorder Rieters syndrome but he believes the best medicine for him is laughter.

The gene is triggered by a viral infection and Daniel said he believed the disease kicked in after enduring a four-month stint with the flu in 2000.

"I would bump myself and the pain would last two or more weeks and then my vision started to blur," Daniel said.

"For two-and-a-half years I went from doctor to doctor trying to find out what was going on.

"My current GP is absolutely brilliant - he did a few tests and sent me to a specialist.

"I visited Professor Nash in Maroochydore - he asked me a couple of questions, got me to walk and said I know what you've got, I just have to do a blood test to prove it."

The 37-year-old said he was diagnosed with Reiters disease - a roaming rheumatoid arthritis.

"I can wake up one morning and my knees aren't working and the next morning my knees are fine and then my hands aren't working," he said.

"There could be days were I was scared to shake people's hands because the amount of pain - I couldn't clench a fist.

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Laughter the best medicine for incurable disorder

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Public release date: 19-Jul-2013 [ | E-mail | Share ]

Contact: Peter Reuell preuell@fas.harvard.edu 617-496-8070 Harvard University

Researchers have long understood that genetics can play a role in how susceptible people are to contracting cholera, but a team of Harvard scientists is now uncovering evidence of genetic changes that might also help protect some people from contracting the deadly disease.

Based on genetic data gathered from hundreds of people in Bangladesh, a research team made up of Harvard faculty and scientists from the Broad Institute and Massachusetts General Hospital were able to a number of areas in the genome some of which are responsible for certain immune system functions, while others are related to fluid loss that appear to be related to cholera resistance. Later tests showed genetic differences between people who had contracted the disease and those who had been exposed, but did not become ill. Their results are described in a paper published earlier this month in Science Translational Medicine.

"This study is exceptionally exciting for us because it shows the power of this approach," said Associate Professor of Organismic and Evolutionary Biology Pardis Sabeti, one of two senior co-authors of the paper. "This is the first time we've taken a genomic-wide approach to understanding cholera resistance. But it's a first step, and there is a lot of exploration to go from here. For a disease that's so ancient and widespread there's very little that's known about host immunity."

The hope, Sabeti added, is that by better understanding why some people appear to be immune, it will help in our efforts to develop vaccines and therapies, so outbreaks like those that occurred in recent years in Haiti and Africa might one-day be avoided.

"It is a very scary disease," she said. "We now have treatments with oral rehydration therapy, but it is still devastating, and in extreme cases, cholera can kill in hours."

"We also haven't been able to develop a particularly effective vaccine," added Elinor Karlsson, a Post-Doctoral Fellow in Organismic and Evolutionary Biology, the first author of the paper. "The vaccine that's available wears off after a few years, whereas people who are exposed to the disease develop a long-lasting immunityand nobody is quite sure why that is. This research is another way of tackling that problem, and it's a way no one has come at it before."

To understand the genetic differences between those with and without resistance, researchers first gathered genetic data on 42 family groups called "trios" that included a mother, father and child. Using that data, researchers identified more than 300 areas of the genome that appeared to be under pressure due to natural selection, suggesting that genes in those regions might be adapting to deal with the threat of cholera.

"We found 305 areas or about two percent of the genome that appeared to be under selection," Karlsson said. "That's great, but unfortunately, all our tests can tell us is that a region is under selection, it doesn't tell us why."

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The genetic key to conquering cholera

Recommendation and review posted by Bethany Smith

July 19, 2013 Researchers have long understood that genetics can play a role in how susceptible people are to contracting cholera, but a team of Harvard scientists is now uncovering evidence of genetic changes that might also help protect some people from contracting the deadly disease.

Based on genetic data gathered from hundreds of people in Bangladesh, a research team made up of Harvard faculty and scientists from the Broad Institute and Massachusetts General Hospital were able to a number of areas in the genome -- some of which are responsible for certain immune system functions, while others are related to fluid loss -- that appear to be related to cholera resistance. Later tests showed genetic differences between people who had contracted the disease and those who had been exposed, but did not become ill. Their results are described in a paper published earlier this month in Science Translational Medicine.

"This study is exceptionally exciting for us because it shows the power of this approach," said Associate Professor of Organismic and Evolutionary Biology Pardis Sabeti, one of two senior co-authors of the paper. "This is the first time we've taken a genomic-wide approach to understanding cholera resistance. But it's a first step, and there is a lot of exploration to go from here. For a disease that's so ancient and widespread there's very little that's known about host immunity."

The hope, Sabeti added, is that by better understanding why some people appear to be immune, it will help in our efforts to develop vaccines and therapies, so outbreaks like those that occurred in recent years in Haiti and Africa might one-day be avoided.

"It is a very scary disease," she said. "We now have treatments with oral rehydration therapy, but it is still devastating, and in extreme cases, cholera can kill in hours."

"We also haven't been able to develop a particularly effective vaccine," added Elinor Karlsson, a Post-Doctoral Fellow in Organismic and Evolutionary Biology, the first author of the paper. "The vaccine that's available wears off after a few years, whereas people who are exposed to the disease develop a long-lasting immunityand nobody is quite sure why that is. This research is another way of tackling that problem, and it's a way no one has come at it before."

To understand the genetic differences between those with and without resistance, researchers first gathered genetic data on 42 family groups -- called "trios" -- that included a mother, father and child. Using that data, researchers identified more than 300 areas of the genome that appeared to be under pressure due to natural selection, suggesting that genes in those regions might be adapting to deal with the threat of cholera.

"We found 305 areas -- or about two percent of the genome -- that appeared to be under selection," Karlsson said. "That's great, but unfortunately, all our tests can tell us is that a region is under selection, it doesn't tell us why."

To find those answers, Karlsson turned to a process called "gene set enrichment" testing to determine whether any particular groups of genes showed up in those regions more often than others.

"We found two strong patterns," Karlsson said. "We found a whole set of genes that are related to a gene called IKBKG, which plays a key role in immunity. But what we found was not the gene itself, but a whole group of genes that regulate IKBKG. We also found a whole set of genes for potassium channels, which are the channels in the walls of our cells that regulate fluid loss.

Originally posted here:
Genetic key to conquering cholera

Recommendation and review posted by Bethany Smith

Meditation for Rewiring the Brain and Genetics
Meditation can rewire the brain and it can change our genetics Watch and Find Out More.

By: Paul Haider

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Meditation for Rewiring the Brain and Genetics - Video

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Update on og kush , dna genetics kush dream
On this one running og kush , dna genetics kush dream and chem dog from progressive options.

By: jm9300

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Update on og kush , dna genetics kush dream - Video

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MVRF-Macular Degeneration: Vitamin Supplements and Genetics
Dr. Emily Chew gives a lecture about vitamin supplements and genetics, and how they relate to Macular Degeneration at the Macula Vision Research Foundation #39;s...

By: MVRFoundation

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MVRF-Macular Degeneration: Vitamin Supplements and Genetics - Video

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Teaming Up: Imaging and Genetics
Dr. Paul Thompson discusses the possibilities of combining the latest brain imaging technology with the study of genetics. For more information visit: http:/...

By: NIBIBTV

Follow this link:
Teaming Up: Imaging and Genetics - Video

Recommendation and review posted by Bethany Smith

A prominent technology columnist got science journalists into a tizzy last week when she proclaimed that she was a creationist. She probably didnt really mean it, but the next time someone expresses doubt over basic, empirically validated facts of how living things evolve, point them toward a portrait collection called "Genetics Are Awesome"-- it could help you show them the light.

Genetics Are Awesome isnt an educational visualization like the Punnett squares you used to learn about genetic inheritance in high school. Instead, photographer Ulric Collette simply took portraits of two people who are directly related--say, a father and a daughter or pair of twins--and placed them in a split-screen combination. This basic juxtaposition dramatically visualizes the power that genes--just tiny coiled bits of nucleic acids--exert over the design of an entire organism. Sure, its no great epiphany that a baby girl has mommys eyes and daddys chin. But something about these split-screen combinations breaks out of the humdrum abstraction of heritability and snaps your awareness toward the, yes, awesomeness (in the cosmic sense, not the Lolcat-GIF sense) of this basic fact of life.

Some of the resemblances between parents and offspring are so striking that the photos look like they have leaped into the future (or past) of one persons life. But the differences are even more intriguing: Its like seeing jump cuts in genetic code come to life. Its enough to make me hope that Collette might do a more longitudinal follow-up project, perhaps with an interactive element, that could let me slide one half of each portrait forward or backward in "generations" (say, from a teenager all the way to her great grandparent), and literally visualize the genetic variation over more than just one "cut." But even as it stands, Genetics Are Awesome is a great piece of science-communication design--not because it didactically teaches you anything but because it reaches into you and makes you want to learn more.

[See Ulrich Collettes photos here]

John Pavlus is a writer and filmmaker focusing on science, tech, and design topics. His writing has appeared in Wired, New York, Scientific American, ... Continued

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Uncanny Portraits Visualize The Power of Genetics

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BACKGROUND: Back pain affects 80 percent of Americans at some point in their lives. In fact, back pain problems are the most common physical complaints among American adults and are a leading cause of lost job time. It can include sore tendons and muscles, fractures, herniated discs, and other problems. The most common back pain causes include nerve and muscular problems, arthritis, and degenerative disc disease. It is important to understand that back pain is a symptom of a medical condition; it is not a diagnosis itself. (Source: http://www.webmd.com)

MEDICAL PROBLEMS: Medical problems that cause back pain can include:

TREATMENT: Most back pain gets better with home treatment and careful attention. A short period of bed rest is recommended, but too many days can actually do more harm than good. When it is more severe, physical therapy is the cornerstone of back pain treatment. A physical therapist can apply a variety of treatments, like ultrasound, heat, electrical stimulation, and muscle-release techniques. If that doesnt work, injections are another option. The doctor may inject cortisone into the space around the spinal cord. (Source: http://www.mayoclinic.com)

NEW TECHNOLOGY: For some patients, traditional treatment just doesnt work. So, one of the newest breakthroughs in managing back pain is coming from stem cells. A company called Mesoblast released the latest news in a string of studies examining the ability of a specific type of stem cell to treat back pain. In the earliest tests, the company injected mesenchymal precursor cells (MPCs) into three adjacent lumbar discs in 24 adult male sheep. The sheep were injected with chrondroitinase in order to mimic disc degeneration and other discs were left alone. The degenerated discs had 45 to 50 percent less height before treatment with MPCs. After the discs were injected, they rehydrated and increased in height at statistically significant rates. Mesoblast has now released its second round of preliminary results from a phase 2 human study. For this phase, researchers injected allogeneic MPCs into damaged intervertebral discs. Researchers at IPM Medical Group in Walnut Creek, California; The Spine Institute in Santa Monica, California; Carolina Neurosurgery & Spine in Charlotte, North Carolina; Arizona Pain Specialists in Phoenix, Arizona; Virginia I-Spine Physicians in Richmond, Virginia, and Emory Orthropaedics & Spine Center in Atlanta, Georgia, report that a single low-dose injection of MPC significantly reduced low back pain in the treated patients and did so at a statistically significant way when compared to the control group. The study has enrolled 100 patients in 13 sited in the U.S. and Australia. At the six month follow-up, 71 percent of patients who received a low dose of MPCs met the pre-specified treatment success criteria. Twenty and thirty percent of the patients in the two control arms who received hyaluronic acid and saline met the pre-specified success criteria. (Source: http://ryortho.com/breaking/major-study-update-stem-cells-ease-back-pain/) "Stem cell research within the disc is very exciting. It focuses on addressing the source of the pain, rather than solely the treatment, Dr. Tory McJunckin was quoted as saying. As an interventional pain doctor I have seen incredible advances in the specialty during the past 10 years and this study shows we are still at the tip of the iceberg for major advances in pain medicine. (Source: http://www.prweb.com/releases/2011/10/prweb8917784.htm

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Oh, my back!

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Stem Cell Therapy Docere Clinics

By: KeysToYoungerLiving

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Stem Cell Therapy Docere Clinics - Video

Recommendation and review posted by simmons

Public release date: 18-Jul-2013 [ | E-mail | Share ]

Contact: Tara Womersley tara.womersley@ed.ac.uk 44-131-650-9836 University of Edinburgh

Research into multiple sclerosis and motor neurone disease is to be boosted with an international collaboration to further understanding of these illnesses.

Experts from the University of Edinburgh and the Massachusetts-based biotechnology company Biogen Idec will work together to seek greater insight into the cell processes behind these debilitating conditions.

This will include identifying drug compounds that could potentially be used as treatments.

The three-year collaboration will combine the University's expertise in translational medicine which develops laboratory discoveries into treatments for patients with Biogen Idec's strength in drug discovery and development.

Siddharthan Chandran, Professor of Neurology at the University of Edinburgh's College of Medicine and Veterinary Medicine, said: "This landmark partnership is a brilliant example of academic-industrial collaboration in the field of discovery science. Only by better understanding the biological processes behind these devastating diseases can we hope to discover new and effective therapies."

Clinicians and scientists, based at Edinburgh BioQuarter Scotland's flagship lifesciences project will be involved in the project, which will draw on the University's strength in neuroscience, stem cell research and regeneration.

The initiative is being funded by Biogen Idec, which is known for its strength in developing therapies for neurological disorders, particularly its portfolio of treatments for patients with multiple sclerosis.

"We have embraced academic collaborations as a part of our strategy to maintain a vibrant and innovative research organization and better understand the underlying biology of neurodegenerative disease. Our research partnership with the University of Edinburgh is an excellent example of this strategy," said Ken Rhodes, Vice President of Neurology Research at Biogen Idec. "We are committed to continuing to improve the treatment of people with MS and motor neuron diseases, and this collaboration is expected to provide an in-depth portrait of their pathophysiology, and identify important new targets for potential therapies."

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Transatlantic partnership to tackle neurodegenerative disease

Recommendation and review posted by simmons

1 Year Spinal Cord Injury Update
EXPAND FOR AWESOME STUFF: ------------------------------------------------------------------ my links: #9825; my blog: http://sabrinadellinger.com/ #9825; my twitter: ...

By: sabrina dellinger

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1 Year Spinal Cord Injury Update - Video

Recommendation and review posted by sam

Avascular necrosis treatment with bone marrow stem cells.
Avascular necrosis treatment with stem cells from bone marrow. Visit http://www.blog.hipsurgery.in to get details of types of treatment. Visit http://www.hipsurgery...

By: ALAMPALLAM VENKATACHALAM

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Avascular necrosis treatment with bone marrow stem cells. - Video

Recommendation and review posted by Bethany Smith

Public release date: 17-Jul-2013 [ | E-mail | Share ]

Contact: Matthew Levine mlevine@rpbusa.org 212-752-4333 Research to Prevent Blindness

New York, NY, July 17, 2013 -- Research to Prevent Blindness (RPB), the world's leading voluntary health organization supporting eye research, has awarded 43 grants totaling $5,308,000 for research into the causes, treatment, and prevention of all blinding diseases. RPB will award additional grants in December.

The latest RPB awards were conveyed to 28 leading medical institutions. They include unrestricted grants to departments of ophthalmology at 24 medical schools and 17 awards to individual scientists, including Career Development Awards, Physician Scientist Awards, Special Scholar Awards, a Walt and Lilly Disney Award for Amblyopia Research, Medical Student Eye Research Fellowships, an International Research Scholar Award, and a special grant to the Association of University Professors of Ophthalmology. They also include a prestigious, one-time laboratory grant of $600,000 to the Department of Ophthalmology at the University of Florida, College of Medicine, to be named the RPB Mildred Krahmer Sanders and William Clifford Sanders Laboratory for Vision Research Laboratory.

"RPB has an outstanding track record of funding excellence in vision research," said RPB's new President, Brian F. Hofland, PhD. "We expect the recipients of these grants to build on that tradition by making significant contributions to the body of knowledge on eye diseases and developing new treatments for vision disorders."

RPB grants are highly flexible, allowing researchers to pursue new discoveries mid- project. The organization places a premium on innovation in awarding these grants which, this year, include investigations into: the pharmacological manipulation of microorganisms that live in the digestive tract and affect ocular inflammation via the immune system; a single-dose gene therapy for age-related macular degeneration using a virus that expresses therapeutic molecules at levels sufficient for long-term treatment; and the action mechanism of DHA (a fatty acid with neuroprotective properties) in the retina along with possible recommendations for its safe use in specific eye diseases.

Across the nation, RPB-supported laboratories investigate the entire spectrum of eye disease from cataracts, glaucoma, and diabetic retinopathy to macular degeneration, retinitis pigmentosa and eye movement disorders. Among the vision scientists fighting these diseases are five active Jules and Doris Stein RPB Professors who receive up to $1.025 million each over seven years (including a possible two-year extension and a matching grant for laboratory construction).

Since it was founded in 1960, RPB has channeled more than $310 million into eye research. As a result, RPB has been identified with nearly every major breakthrough in vision research in that time, including the development of laser surgery now used to treat diabetic retinopathy, glaucoma, macular degeneration, myopia, retinal detachment and astigmatism.

RPB currently supports a comprehensive grants program at 56 medical institutions throughout the United States. RPB grants nurture vibrant vision-research environments, further the careers of vision scientists and advance the development of thought leaders in the vision research field.

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Original post:
Research to Prevent Blindness awards $5.3 million in grants to support eye research

Recommendation and review posted by Bethany Smith