#39;The results are profound #39;; Stem cell therapy used to treat animal ailments
#39;The results are profound #39;; Stem cell therapy used to treat animal ailments.

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'The results are profound'; Stem cell therapy used to treat animal ailments - Video

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HONOLULU (HawaiiNewsNow) -

Breakthrough research has created excitement in the genetics field. The University of Massachusetts Medical School has found a way to turn off the chromosome that causes down syndrome.

In Hawaii five to eight babies a year are born with Down syndrome. It is the most common birth defect. Doctors say the new research is exciting because it's the first time someone has been able to shut off a gene, although not everyone agrees that's the right thing to do.

"Not too high," said Emily Keane, as her father Darryl pushed her on a swing.

Emily is 22 years old and brings a world of joy to her family.

"She is very social, she likes to have friends," said Karen Keane, Emily's mom.

Emily was born with Down syndrome and cerebral palsy which makes it difficult for her to have a job. So when the family heard about the breakthrough research that doctors found a way to turn off the extra chromosome that causes the Down syndrome they were excited and would have done it had it been an option for Emily.

"Yes absolutely because it would open up more possibilities for her. She wants to do everything, she wants to be like everybody else and that would make that possible for her," said Karen Keane.

"The universal thing is that the kids are a blessing but the other side of it is we're always looking for ways to help improve their quality of life," said Darryl Keane, Emily's dad. "The medical research if it can help we are definitely open to that."

We also met five year old Gracie McComas.

The rest is here:
New Down syndrome research gets mixed reactions from parents

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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 - Boston.com

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Toronto, ON (PRWEB) July 20, 2013

Bel Marra Health, who offers high-quality, specially formulated vitamins and nutritional supplements, reports on a new study revealing a gene found to determine prognosis of breast cancer.

As Bel Marra Health reports in its article, (http://www.belmarrahealth.com/cancer/breast-cancer-prognosis-determined-by-this-one-gene/) receiving a confirmed breast cancer diagnosis is difficult, and discovering an aggressive form of this disease can be utterly devastating. But new research just published in Cell may provide some hope for those diagnosed with aggressive forms of breast cancer. The researchers identified a particular gene, called ZEB1, with the power to convert non-cancer stem cells into cancer stem cells, and thus ultimately influence whether a breast cancer will exhibit as a benign form or as an aggressive and rapidly spreading form. This discovery has major implications on the future of breast cancer treatment, allowing brand new options to begin to be devised for patients fighting this devastating disease.

There are various categories of breast cancer, differing according to their molecular structure. Less aggressive types of breast cancer are grouped into the luminal category, while more aggressive types are categorized into the basal category. Patients that are diagnosed with a luminal type of breast cancer have a better prognosis than those diagnosed with a basal type of the disease. Aggressive basal types of breast cancer often metastasize, spreading and creating tumors in other areas of the body. This may be due to the fact that non-cancer stems cells from basal type breast cancer are able to turn into cancer stem cells relatively easily, while those from luminal types of breast cancer usually stay in a non-cancer stem cell state.

Genes that control the expression of other genes are known as transcriptor factors. Therefore, they have a significant role in various cell activities. ZEB1 is one type of transcriptor factor, responsible for transitioning certain types of cells into other forms. The researchers found that the ZEB1 gene is found in a poised state in basal non-cancer stem cells, which means that they are ready to respond to environmental cues that would put them into action. Essentially, the ZEB1 gene converts non-cancer stem cells into cancer stem cells. This may be the basis that determines whether breast cancer cells will exhibit benign or aggressive behavior in the future. The researchers discovered that the ZEB1 gene acts differently in luminal and basal breast cancer cells. In luminal breast cancer cells, the ZEB1 gene is basically shut down whereas, in basal breast cancer cells, the ZEB1 gene is more active, allowing for easier conversion of non-cancer stem cells into cancer stem cells.

The results from the current research suggest that breast cancer cells are very adaptable. Treatment options for breast cancer should look at targeting cancer stem cells and preventing non-cancer stem cells from transitioning into cancer stem cells. One way in which this may be accomplished is by discovering new treatment options that inhibit the adaptability of breast cancer cells. This may help to control the spread of cancer throughout the body, resulting in a better prognosis.

The recent research brings hope to the future prevention and treatment of breast cancer. The fact that a specific gene has been identified as the gene responsible for the aggressive nature of certain breast cancers will allow scientists to study new treatment options for this devastating disease. Additionally, researchers can investigate whether the ZEB1 gene reacts that same way in other forms of cancer, which could possibly change the future of cancer treatment.

(SOURCE: Christine L. Chaffer, et al. Poised chromatin at the ZEB1 promoter enables breast cancer cell plasticity and enhances tumorigenicity. Cell, 2013)

Bel Marra Health is the maker of CoQ10 Premium Plus, a high-quality nutritional supplement that helps maintain and support cardiovascular health. All ingredients are backed with scientific evidence. Every product is tested for safety, quality, and purity at every stage of the manufacturing process. Furthermore, Bel Marra Health products are produced only in Health Canada approved facilities, going the extra mile to ensure that our health-conscious customers are getting top quality products. For more information on Bel Marra Health visit belmarrahealth.com or call 1-866-531-0466.

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Bel Marra Health Reports on New Research Discovering Aggressiveness of Breast Cancer Determined by Gene

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Two studies zero in on DNA-based drivers of weight. Is obesity written in our genes?

In two separate papers, published in the journal Science and in the Journal of Clinical Investigation (JCI), researchers describe new genetic factors that could explain weight gain in some people. In the Science study, researchers at Boston Childrens Hospital studying mice found a rare genetic mutation that prevented the animals from burning off fat calories. They also found the same gene was mutated in a group of obese people. And a team based at University College London reported in JCI that a specific form of a gene previously linked to obesity, FTO, can increase craving for high-fat foods.

The discoveries add to the growing body of knowledge about the biology behind weight, and the results confirm that while its represented by a single number, weight is the complex combination of a multitude of different metabolic processes, from brain systems that regulate appetite to enzymes that control how efficiently calories are turned from food into energy that the body needs. Making matters even more confusing, these factors are also likely influenced by environmental contributors such as diet and lifestyle.

In the mouse study, the research team determined that mutations in theMrap2 gene led the animals to eat less initially but still gain about twice as much weight as they normally would. While their appetites returned, these mice continued to gain weight despite being fed the same number of calories as a group of control animals. That led the scientists to figure out that the mice with the mutated gene were simply sequestering fat rather than breaking it down for energy. The mice, like people, possessed two copies of the gene, and mice with even one defective copy experienced significant weight gain, although not as much as those who had two mutated versions of Mrap2.

The scientists found a similar pattern among a group of 500 obese people; they detected four mutations in the human version of Mrap2, and each of the obese individuals possessed only one bad version of the gene.

(MORE: Study Identifies Four New Genetic Markers For Severe Childhood Obesity)

In the British study, the researchers divided a group of 359 healthy men of normal weight by their FTO gene status. The majority of the men had low-risk versions of the gene, while 45 of the participants had mutations that have been linked to greater appetite and caloric consumption. To figure out how the altered genes were affecting appetite, the team measured levels of the hunger hormone ghrelin both before and after meals that the participants ate; the men with the mutated form of FTO did not show the same drop in ghrelin levels, signifying that they were full, as the men with the low-risk form of FTO.

Genome wide association studies, which compare genetic makeups of obese individuals to those of normal weight, are making it easier to flesh out important genetic factors contributing to weight, and researchers at the Harvard School of Public Health say that to date, these studies haveidentified over 30 candidate genes on 12 chromosomes associated with body mass index.

Thus far mutations in about eight genes are known to cause obesity in humans. But these mutations account for under five percent of the obesity in our society, and certainly are not, by themselves, responsible for the current obesity epidemic, since the mutation rate in these genes could not have changed dramatically during the past twenty years, says Dr.Joseph Majzoub, the chief of the division of endocrinology at BostonChildrens Hospital and an author on the Science paper. However, mutations in these genes have led to the discovery of pathways that are important in energy balance in humans, giving us hope that drugs can be developed that affect these pathways to prevent excessive weight gain, either by curbing appetite or increased burning of calories.

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The Obesity Gene: Is Weight Coded in DNA?

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OMD 1983 Interview (Dazzle Ships)
Interview with Andy McCluskey in 1983 speaking about the "Dazzle Ships" album, the science of genetic engineering, OMD becoming a four member band and more.....

By: abcautoindustry

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OMD 1983 Interview (Dazzle Ships) - Video

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NUC Ops - Apex Genetics: Resecure + Defense - Planetside 2
Apex Genetics: Resecure + Defense - 7/16/13 Perspective: [NUC]Enemy http://www.nucgaming.com Server: Waterson.

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NUC Ops - Apex Genetics: Resecure + Defense - Planetside 2 - Video

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Genetics: The Study of Heredity - How Traits are Inherited
To access a comprehensive array of complete multimedia lessons visit http://www.newpathlearning.com -Genetics: The Study of Heredity http://newpathlive.com/h...

By: NewPathLearning

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Genetics: The Study of Heredity - How Traits are Inherited - Video

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Genetics: The Study of Heredity - Gregor Mendel
To access a comprehensive array of complete multimedia lessons visit http://www.newpathlearning.com -Genetics: The Study of Heredity http://newpathlive.com/h...

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Genetics: The Study of Heredity - Gregor Mendel - Video

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Genetics: The Study of Heredity - Phenotypes and Genotypes
To access a comprehensive array of complete multimedia lessons visit http://www.newpathlearning.com -Genetics: The Study of Heredity http://newpathlive.com/h...

By: NewPathLearning

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Genetics: The Study of Heredity - Phenotypes and Genotypes - Video

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gen 101
this is the first video in our study of genetics.

By: B Curtis

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gen 101 - Video

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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...

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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.

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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...

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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.

Originally posted here:
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

Recommendation and review posted by Bethany Smith

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."

Read the original:
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.

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Genetic key to conquering cholera

Recommendation and review posted by Bethany Smith