How To - Arms Exercises using Resistance Exercise Bands for C5-C6 Tetraplegia
Myron Wand has a spinal cord injury (C5-C6 tetraplegia). Here he shows some tips and techniques to do arm exercises using resistance band. sci-health.org 2012 by Healthy Tomorrow.From:HealthyTomorrowViews:2 0ratingsTime:01:49More inSports

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Black Male Tosses a 21 Month-Old "Like A Sack of Potatoes"
Newslink: http://www.myfoxtwincities.com MINNEAPOLIS (KMSP) - A 21-month-old girl thrown "like a sack of potatoes" onto a bed by her mother #39;s boyfriend may never walk again after suffering a spinal cord injury. On Oct. 26, Minneapolis police officers were dispatched to the 2400 block of Logan Avenue North on a report of a child not breathing. When they arrived, paramedics had to perform rescue breathing on the girl. On that day, the girl and the couple #39;s newborn child were left alone with the boyfriend, identified by authorities as 21-year-old Eric Paul Boone. When interviewed by police, Boone said he was sleeping in the same bed as the kids and woke up to find the little girl wasn #39;t breathing. He told officers he had pushed down on the girl #39;s stomach while reaching for the newborn before falling asleep. On Oct. 29, a Hennepin County child protection investigator learned Boone had thrown the girl on the bed out of anger because she fell out of his hands when he was walking downstairs with her. When Boone was re-interviewed, police say he admitted he was angry at the girl because she had wriggled out of his grip and fallen on the stairs. He told police he then picked her up and threw her on the bed "like a sack of potatoes." The toddler was transferred from North Memorial Medical Center to Children #39;s Hospital, where specialists determined it was unlikely that the injuries to her face, head and neck were caused by Boone pushing on her stomach or from falling down the stairs. After ...From:TheColourOfCrimeViews:1 0ratingsTime:02:56More inNews Politics

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Call for Nominations: "Stem Cell Person of the Year"
UC Davis stem cell scientist Paul Knoepfler is seeking nominees for the 2012 "Stem Cell Person of the Year." He created the new award to recognize an individual who has made an outstanding difference in the field of stem cell-based cellular and regenerative medicine. Nominees can be scientists, patient advocates, individuals from industry or just about anyone who has made the stem cell field better. The award includes a $1000 cash prize.From:UCDavisHealthViews:60 2ratingsTime:01:48More inScience Technology

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Review Of An Academic Paper Related To Regenerative Medicine
sens.org (The paper that I am reviewing should be second link down within the bibliography section.) The bibliography of it is: Bussel II, Stupple A, Moody KJ, Lefkowitz DM. Call to action: medical students for regenerative medicine. Rejuvenation Res. 2010 Feb;13(1):1-2. PubMed: 20230272. Support abolishing aging. Support regenerative medicine. Considering studying it. Especially young adults should. idea-archive.net http Please subscribe to this channel, share this video with others, visit my websites and watch my other videos. Thanks for watching. Also, please checkout my Etsy store. http://www.etsy.com Comments are welcomed and encouraged. However, if they contain rudeness, disrespect or swear words, then they will likely be deleted.From:APerfectUniverseViews:14 2ratingsTime:04:43More inPeople Blogs

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Bone Marrow Stem cells for Rotator cuff Injury
George Ramsey Describes the road to recovery of his shoulder function using his own bone marrow stemcellsFrom:FLRegenerativeMedViews:0 0ratingsTime:01:55More inEducation

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Placenta Extract
Buy from Amazon US redirect.viglink.com?key=f341fd9454fc162be8b38d504acbd4e1 out=http%3A%2F%2Fwww%2Eamazon%2Ecom%2Fexec%2Fobidos%2FASIN%2FB007250F6K%2Fhealth%5Fhope%2D20 Customer Reviews "My wife has used these Placenta Softgels for 3 months. Not only did she notice a reduction of wrinkles and a new firmness in her skin, she also noticed that she didn #39;t suffer any colds last winter. These softgels are a great booster for the immune system and they revitalize the skin. My wife plans on using them for 3 months every year instead of doing cell therapy injections that cost a lot and require traveling." "I received a box of these Placenta capsules as a gift last december. I usually go through 4 to 5 colds every winter, but not last winter. Not one cold bothered me. I also noticed an improvement of my facial skin. It appears smoother, firmer and revitalized. I will order more of these every autumn and use them to boost my immune system and give my skin a mini spa." Product Description Placenta Extract MFIII of Switzerland PE Softgels Advanced Formula 2009 are fully researched and developed in Switzerland and Germany. The method employed in unique softgel capsules produces cells which remain biologically active [a proven technique for gently conserving biological substances] without damaging the effectiveness of the valuable, big, bio-active matter. The exact dosage of the cell preparations can be accurately measured and the sterility controlled. Cell Therapy is a well known ...From:leonor christyViews:0 0ratingsTime:00:56More inHowto Style

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ZÉLL-V Sheep Placenta Anti Aging Satisfied Customer - Winnie
http://www.zell-v.com We specialise in cell therapy products for anti aging. we are supported by an international medical board of practitioners, biologist and wellness professionals.From:zellvsheepplacentaViews:8 0ratingsTime:01:33More inHowto Style

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Stem Cell Therapy | Stem Cell Malaysia
stemcellmalaysia.com Stem cell therapy is a form of cell therapy that makes use of stem cells harvested from placenta for disease treatment. Stem cell therapy is also used for beauty, anti-aging and health rejuvenation purposes. The efficacy of stem cell therapy has been in practice for decades. Many rich and wealthy individuals and celebrities pay hefty price for stem cell therapy just to maintain youthfulness and vitality. For many severely ill-stricken people who have exhausted all means of conventional therapy look toward stem cell therapy for saving their condition and life. stemcellmalaysia.comFrom:stemcells2012Views:224 2ratingsTime:07:23More inHowto Style

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Mrs. Linda Flournoy
describes ger experience with Stem Cell Therapy PRPFrom:FLRegenerativeMedViews:2 0ratingsTime:02:27More inEducation

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Published: Thursday, November 15, 2012, 12:01 a.m.

The problem gene is not common -- less than 1 percent of people are thought to have it -- but it roughly triples the chances of developing Alzheimer's compared to people with the normal version of the gene. It also seems to harm memory and thinking in older people without dementia.

The main reason scientists are excited by the discovery is what this gene does, and how that might reveal what causes Alzheimer's and ways to prevent it. The gene helps the immune system control inflammation in the brain and clear junk such as the sticky deposits that are the hallmark of the disease. Mutations in the gene may impair these tasks, so treatments to restore the gene's function and quell inflammation may help.

"It points us to potential therapeutics in a more precise way than we've seen in the past," said Dr. William Thies, chief medical and scientific officer of the Alzheimer's Association, which had no role in the research. Years down the road, this discovery will likely be seen as very important, he predicted.

It is described in a study by an international group published online Wednesday by the New England Journal of Medicine.

About 35 million people worldwide have dementia, and Alzheimer's is the most common type. In the U.S., about 5 million have Alzheimer's. Medicines such as Aricept and Namenda just temporarily ease symptoms. There is no known cure.

Until now, only one gene -- ApoE -- has been found to have a big impact on Alzheimer's risk. About 17 percent of the population has at least one copy of the problem version of this gene but nearly half of all people with Alzheimer's do. Other genes that have been tied to the disease raise risk only a little, or cause the less common type of Alzheimer's that develops earlier in life, before age 60.

The new gene, TREM2, already has been tied to a couple other forms of dementia. Researchers led by deCODE Genetics Inc. of Iceland honed in on a version of it they identified through mapping the entire genetic code of more than 2,200 Icelanders.

Further tests on 3,550 Alzheimer's patients and more than 110,000 people without dementia in several countries, including the United States, found that the gene variant was more common in Alzheimer's patients.

"It's a very strong effect," raising the risk of Alzheimer's by three to four times -- about the same amount as the problem version of the ApoE gene does, said Dr. Allan Levey, director of an Alzheimer's program at Emory University, one of the academic centers participating in the research.

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Scientists identify new Alzheimer's gene

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London, November 17 (ANI): Scientists at Manchester University have revealed that they have discovered 14 genes that lead to rheumatoid arthritis, making a major breakthrough in their bid to find a cure for the condition.

Lifestyle and environmental factors, such as smoking, diet, pregnancy and infection may cause the complicated disease, but a person's genetic make-up also influences their susceptibility.

Manchester University scientists believe they now know most of the disease-causing genes with the latest research identifying ones specific to the female X-chromosome.

The discovery, published in the journal Nature Genetics, could explain why three times more women than men develop the illness and scientists can use these findings to try to stop the disease from developing.

"This work will have a great impact on the treatment of arthritis. We have already found three genes that are targets for drugs, leaving 43 genes with the potential for drug development, helping the third of patients who fail to respond well to current medications," the Daily Express quoted study author Dr Stephen Eyre as saying.

"The genetic findings can help divide patients into smaller groups with more similar types of rheumatoid arthritis and assist in the allocation of therapies," he noted.

The team studied 27,000 DNA samples to identify the new genes and move closer to improving the lives of rheumatoid arthritis sufferers.

Professor Alan Silman, medical director of Arthritis Research UK, added: "We hope that this research will lead to a greater understanding of the disease and allow us to develop targeted drug treatments for the people currently living with rheumatoid arthritis. (ANI)

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Scientists have discovered another gene mutation that may indicate if a person is more likely to get Alzheimer's, a remarkable breakthrough in a field that hasn't seen major progress in a decade.

Two independent studies published in the New England Journal of Medicine on Nov. 14 revealed that people who had a certain mutation on their TREM2 gene were shown to be three to five times more likely to get Alzheimer's than those without the mutation. The rate is comparable to the number of people who get late-onset Alzheimer's who have an ApoE4 gene mutation, which is about 40 percent.

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When a person has a working TREM2 gene, their white blood cells get rid of a plaque-forming protein known as beta amyloid that builds up on cells connected to inflammatory response called microglia, the New York Times reported. People who have the genetic mutation variant R47H on the gene aren't able to clean up their cells. Scientists believe that beta amyloid plaque on the brain is one of the markers of the disease.

"This discovery provides an increasingly firm link between brain inflammation and increased risk for Alzheimer's," Dr. Peter St. George-Hyslop, director of University of Toronto's Tanz Centre for Research in Neurodegenerative Diseases, said in a press release. "This is an important step towards unraveling the hidden causes of this disease, so that we can develop treatments and interventions to end one of the 21st century's most significant health challenges."

Alzheimer's disease is the most common form of dementia, affecting 5.4 million Americans according to the Alzheimer's Association. About one in eight elderly people living in the U.S. have the disease. It is the sixth-leading cause of death and the only one in the top 10 that cannot be prevented, cured or slowed. The disease, which usually occurs later in life in people 65 and older, starts with mild memory loss and progresses to the inability to carry a conversation or to recognize one's environment.

Recent studies have shown that Alzheimer's signs may be seen decades before diagnosis in people who have PSEN1 gene mutation, which has been linked to the early-onset form of the disease.

Clinical trials will test new drugs solanezumab from Eli Lilly and gantenerumab from Roche on their effectiveness of preventing the disease. Previously in July, solanezumab and bapineuzumab made by Pfizer were shown to be ineffective in treating people with late-stage and mild-to-moderate forms of Alzheimer's respectively. Solanezumab did show promise in treating mild forms, however.

Scientists came to the conclusion about the TREM2 mutation after two studies showed similar results. One study, which was led by researchers at the University College London among other universities, studied the DNA of 1,092 people with Alzheimer's disease and 1,107 people without the disease. The R47H mutation was found in approximately 1.9 percent of the group with the disease and only 0.37 percent of control group. They then tested a larger pool of about 6,700 Alzheimer's patients and 16,200 people without the disease to confirm their results.

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Gene mutation identified as new risk factor for Alzheimer's

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Scientists have identified a new gene variant that seems to strongly raise the risk for Alzheimers disease, giving a fresh target for research into treatments for the mind-robbing disorder.

The problem gene is not common less than 1 per cent of people are thought to have it but it roughly triples the chances of developing Alzheimers compared to people with the normal version of the gene. It also seems to harm memory and thinking in older people without dementia.

The main reason scientists are excited by the discovery is what this gene does, and how that might reveal what causes Alzheimers and ways to prevent it. The gene helps the immune system control inflammation in the brain and clear junk such as the sticky deposits that are the hallmark of the disease. Mutations in the gene may impair these tasks, so treatments to restore the genes function and quell inflammation may help.

It points us to potential therapeutics in a more precise way than weve seen in the past, said Dr. William Thies, chief medical and scientific officer of the Alzheimers Association, which had no role in the research. Years down the road, this discovery will likely be seen as very important, he predicted.

It is described in a study by an international group published online Wednesday by the New England Journal of Medicine.

About 35 million people worldwide have dementia, and Alzheimers is the most common type. In Canada, about 500,000 people have Alzheimers or related dementia, according to the Alzheimer Society of Canada. Current medicines just temporarily ease symptoms. There is no known cure.

Until now, only one gene ApoE has been found to have a big impact on Alzheimers risk. About 17 per cent of the population has at least one copy of the problem version of this gene but nearly half of all people with Alzheimers do. Other genes that have been tied to the disease raise risk only a little, or cause the less common type of Alzheimers that develops earlier in life, before age 60.

The new gene, TREM2, already has been tied to a couple other forms of dementia. Researchers led by deCODE Genetics Inc. of Iceland honed in on a version of it they identified through mapping the entire genetic code of more than 2,200 Icelanders.

Further tests on 3,550 Alzheimers patients and more than 110,000 people without dementia in several countries found that the gene variant was more common in Alzheimers patients.

Its a very strong effect, raising the risk of Alzheimers by three to four times about the same amount as the problem version of the ApoE gene does, said Dr. Allan Levey, director of an Alzheimers program at Emory University in Atlanta, one of the academic centres participating in the research.

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Gene may triple Alzheimer’s risk

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By Steven Reinberg HealthDay Reporter

WEDNESDAY, Nov. 14 (HealthDay News) -- A rare mutation in a gene called TREM2 appears to nearly triple the risk for Alzheimer's disease in adults, a new study finds.

This gene is involved in immune and inflammatory responses, and may be yet another piece of the mystery of the causes of Alzheimer's disease and a target for treatment, the researchers added.

"We found a mutation that confers a large risk for Alzheimer's disease," said lead researcher Dr. Kari Stefansson, the CEO of deCODE Genetics based in Reykjavik, Iceland.

Although only 1.2 percent of the population has the TREM2 mutation, when comparing adults aged 85 and older with and without it, those who do have it are almost seven times more likely to have Alzheimer's disease, he said.

Of course, having this mutation doesn't mean that one is destined to develop Alzheimer's disease. Alzheimer's is a complex disease and a person probably needs to have several risk factors that combine to produce the condition, Stefansson said.

"This has implications for treatment," he said. The mutation might be a target for new drugs that blunt the mutation's action, he said.

The report was published in the Nov. 14 online edition of the New England Journal of Medicine.

An Alzheimer's expert praised the new study.

"This shows the value of basic research," said William Thies, chief medical and scientific officer at the Alzheimer's Association. "This kind of science is very important, and can accelerate our finding better therapies for Alzheimer's disease."

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Public release date: 16-Nov-2012 [ | E-mail | Share ]

Contact: Bonnie Prescott bprescot@bidmc.harvard.edu 617-667-7306 Beth Israel Deaconess Medical Center

BOSTON Many of the body's processes follow a natural daily rhythm or so-called circadian clock. There are certain times of the day when a person is most alert, when blood pressure is highest, and when the heart is most efficient. Several rare gene mutations have been found that can adjust this clock in humans, responsible for entire families in which people wake up at 3 a.m. or 4 a.m. and cannot stay up much after 8 at night. Now new research has, for the first time, identified a common gene variant that affects virtually the entire population, and which is responsible for up to an hour a day of your tendency to be an early riser or night owl.

Furthermore, this new discovery not only demonstrates this common polymorphism influences the rhythms of people's day-to-day lives -- it also finds this genetic variant helps determine the time of day a person is most likely to die.

The surprising findings, which appear in the November 2012 issue of the Annals of Neurology, could help with scheduling shift work and planning medical treatments, as well as in monitoring the conditions of vulnerable patients.

"The internal 'biological clock' regulates many aspects of human biology and behavior, such as preferred sleep times, times of peak cognitive performance, and the timing of many physiological processes. It also influences the timing of acute medical events like stroke and heart attack," says first author Andrew Lim, MD, who conducted the work as a postdoctoral fellow in the Department of Neurology at Beth Israel Deaconess Medical Center (BIDMC).

"Previous work in twins and families had suggested that the lateness or earliness of one's clock may be inherited and animal experiments had suggested that the lateness or earliness of the biological clock may be influenced by specific genes," adds Lim, who is currently an Assistant Professor in the Division of Neurology at the University of Toronto.

The work originated several years ago while Lim was working in the laboratory of BIDMC Chief of Neurology Clifford Saper, MD, PhD. Lim and the other lab members were studying why older people have trouble sleeping and had joined a research project based at Rush University in Chicago involving 1,200 people who signed on as healthy 65-year-olds and would receive annual neurological and psychiatric examinations.

The cohort's original intent was to determine if there were identifiable precursors to the development of Parkinson's disease or Alzheimer's disease. As part of the research the subjects were undergoing various sleep-wake analyses using a wristband called an actigraph, which provides a reliable record of an individual's pattern of activity. Additionally, in order to provide the scientists with information on sleep-wake patterns within a year of death, the participants had agreed to donate their brains after they died.

But the investigation took a new turn when Lim learned that the same group of subjects had also had their DNA genotyped. Teaming up with investigators from Brigham and Women's Hospital (BWH), Lim and his colleagues compared the wake-sleep behavior of these individuals with their genotypes. These findings were later verified in a group of young volunteers.

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Gene distinguishes early birds from night owls and helps predict time of death

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Food Water Watch Genetic Engineering (GE) Labeling Campaign
DAVENPORT, IOWA | November 14, 2012 - Leann Felder coordinator for Food Water Watch, Russ Neff for Sierra Club, Curtis Rexroth, MA, DC, CCN of the Rexroth Clinic in Moline, IL address a group of concerned citizens regarding a campaign branded, "Let Me Decide: Iowans Campaign to Make the Labeling of Genetically Engineered Foods the Law". The meeting was hosted at Greatest Grains in Davenport, Iowa.From:QCATodayViews:7 0ratingsTime:39:23More inNews Politics

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Genetic Engineering Persuasive Informercial
From:Chloe DurkinViews:7 1ratingsTime:02:49More inNews Politics

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The Day of the Triffids Full Movie HD
Watch full movie : tinyurl.com The Day of the Triffids Full Movie HD, The Day of the Triffids Part 1 Movie, The Day of the Triffids Movie Part 1, The Day of the Triffids Part 1 The Movie, The Day of the Triffids Part 2 Full Movie, The Day of the Triffids Movie Full Movie, The Day of the Triffids (2013) Movie Part 1 English Full, The Day of the Triffids Movie HD trailer. An epic tale of mankind #39;s self-annihilation in the wake of a cosmic event leading to global blindness. His legacy in genetic engineering changed the hierarchy of nature, toppling mankind #39;s place atop the world #39;s food chain.From:doriana dimcevViews:2 0ratingsTime:04:21More inFilm Animation

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The End Of The World - John Leslie
ll4.me The End Of The World - John Leslie Nuclear war, holes in the ozone layer, disease, genetic engineering, asteroids and supernovas - any of these may bring human history to an end. But are we in imminent danger of extinction? John Leslie assesses the risks facing the human race and concludes: yes, we probably are. Leslie pays particular attention to the #39;doomsday argument #39;. This argument, arising from the undeniable fact that we are a very young species, substantially increases the likelihood of our extinction.Author: Leslie, John Publisher: Routledge Illustration: N Language: ENG Title: The End of the World Pages: 00000 (Encrypted PDF) On Sale: 1998-03-12 SKU-13/ISBN: 9780415140430 Category: Education : Teaching Methods Materials - Arts Humanities Nuclear war, holes in the ozone layer, disease, genetic engineering, asteroids and supernovas - any of these may bring human history to an end. But are we in imminent danger of extinction? John Leslie john leslie, education, teaching methods, materials, arts, humanitiesFrom:heathertrull9854Views:0 0ratingsTime:00:10More inPeople Blogs

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Genetic Engineering Controversy
A presentation on genetic modification for our freshmen seminar at Penn State University. We discuss the issues and facts surrounding the controversy about genetically modified foods, animals, and plants.From:Benjamin FowlerViews:8 0ratingsTime:33:08More inScience Technology

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Genetic Engineering Of Mesenchymal Stem Cells
ll4.me Genetic Engineering Of Mesenchymal Stem Cells 1. Mesenchymal Stem Cell Engineering and Transplantation: An introduction; F. Aerts, G. Wagemaker- 2. Establishment and Transduction of primary human Stromal/Mesenchymal Stem Cell Monolayers; T. Meyerrose, I. Rosova, m. Dao, P. Herrbrich, G. Bauer, JA Nolta- 3. Gene Expression Profiles of Mesenchymal Stem Cells; DG Phinney- 4. In Vivo Homing and Regeneration of freshly isolated and culture Murine Mesenchymal Stem Cells; RE Ploemacher- 5. Non-human primate models of Mesenchymal Stem Cell Transplantation; SM Devine, R. Hoffman- 6. Engineering of Human Adipose-derived Mesenchymal Stem-like Cells; JK Fraser, M. Zhu, B. Strem, MH Hedrick- 7. Uncommitted Progenitors in Cultures of Bone Marrow-derived Mesenchymal Stem Cells; JJ Minguell, A. Rices, WD Sierralta- 8. Bone Marrow Mesenchymal Stem Cell Transplantation for Children with severe Osteogenesis Imperfecta; EM Horwitz, PL Gordon- 9. Clinical Trials of Human Mesenchymal Stem Cells to support Hematopoietic Stem Cell Transplantation; ON Ko EAN/ISBN : 9781402039591 Publisher(s): Springer Netherlands Discussed keywords: Stammzelle Format: ePub/PDF Author(s): Nolta, Jan A. 1. Mesenchymal Stem Cell Engineering and Transplantation: An introduction; F. Aerts, G. Wagemaker- 2. Establishment and Transduction of primary human Stromal/Mesenchymal Stem Cell Monolayers; T. MeyerFrom:jonibishop696Views:0 0ratingsTime:00:12More inPeople Blogs

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Precarious World - Steve Quayle - Coast to Coast AM Classic
http://www.jetnews.us Date: 01-06-11 Host: George Noory Guests: Steve Quayle Author and researcher Steve Quayle riffed on a variety of topics such as giants, weather modification, secret aircraft, biblical prophecy, genetic engineering, the Illuminati agenda, and Planet X. The machinery to affect weather has gotten smaller and cheaper over the years, and there are currently 72 ionospheric heaters, in addition climate-controlling technology like Project HAARP, he outlined. Sightings of silent triangular-shaped craft are on the rise, and a battle in outer space is imminent, said Quayle, naming "extra-dimensionals" and black-ops as some of the participants. The "super-soldier" program, Stargate technology, and CERN are involved in efforts to re-animate ancient giants, who were some 12-18 ft. height, he declared. "We are experiencing now the full implementation, in my opinion, of the Luciferian war on humanity. We talk about the New World Order, the Illuminati, the International League, but what is the prime directive of all those entities? It #39;s the destruction of a five and half billion people," he cautioned. Quayle reported his recent conversation with a "high ranking Goldman Sachs official" who #39;d visited one of the elite #39;s underground cities that was being prepared. The official warned him that a "global flu" had already been determined, and a mandatory vaccination will be required, with those who refuse to take it being sent to FEMA camps. On the subject of Planet X, Quayle ...From:C2CPlanetViews:17 3ratingsTime:01:53:01More inEducation

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Public release date: 16-Nov-2012 [ | E-mail | Share ]

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

New Rochelle, NY, November 13, 2012Following an infection, dysregulation of the immune system can result in a systemic inflammatory response and an often fatal condition called severe sepsis or septic shock. Sepsis is not uncommon, yet its cause and underlying immune dysfunction remain poorly understood. Regulatory T cells (Tregs), a component of the immune system, now appear to have an important role in suppressing the immune response in advance of sepsis, and understanding this role may lead to new therapeutic strategies for improving patient outcomes, as described in a review article in Journal of Interferon & Cytokine Research, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available free online on the Journal of Interferon & Cytokine Research website.

Li-Na Jiang, Yong-Ming Yao, and Zhi-Yong Sheng, Chinese PLA General Hospital, Beijing, and Hebei North University, Zhyangjiakou, China, review the growing body of literature supporting a link between alterations in Treg function and the development of sepsis, based on animal studies and preliminary human studies. In the article "The Role of Regulatory T Cells in the Pathogenesis of Sepsis and Its Clinical Implications (http://online.liebertpub.com/doi/full/10.1089/jir.2011.0080)," the authors suggest that accumulating experimental and clinical evidence indicates that manipulating Tregs may offer a promising strategy for treating patients with septic shock.

"Regulatory T cells are receiving much attention as important determinants of both beneficial and detrimental immune responses," says Co-Editor-in-Chief Thomas A. Hamilton, PhD, Chairman, Department of Immunology, Cleveland Clinic Foundation. "This review brings focus to the function of this important cell population in the context of sepsis, a condition more frequently associated with innate immunity."

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About the Journal

Journal of Interferon & Cytokine Research, led by Co-Editors-in-Chief Ganes C. Sen, PhD, Chairman, Department of Molecular Genetics, Cleveland Clinic Foundation, and Thomas A. Hamilton, PhD, is an authoritative peer-reviewed journal published monthly in print and online that covers all aspects of interferons and cytokines from basic science to clinical applications. Journal of Interferon & Cytokine Research is the official journal of the International Society for Interferon and Cytokine Research. Complete tables of content and a sample issue may be viewed online on the Journal of Interferon & Cytokine Research website.

About the Publisher

Mary Ann Liebert, Inc., publishers is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including Viral Immunology, AIDS Research and Human Retroviruses, and DNA and Cell Biology. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 70 journals, books, and newsmagazines is available on the Mary Ann Liebert, Inc., publishers website.

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Are we closer to understanding the cause of deadly sepsis?

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Public release date: 16-Nov-2012 [ | E-mail | Share ]

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

New Rochelle, NY, November 15, 2012Epstein-Barr virus (EBV) is the cause of infectious mononucleosis and a risk for serious disease in liver transplant recipients. Molecular tests that can identify early protein markers produced by EBV may have value for diagnosing active infection. The benefits of this diagnostic approach in patients with mononucleosis and in EBV-infected transplant patients are evaluated in an article published in BioResearch Open Access, a bimonthly peer-reviewed open access journal from Mary Ann Liebert, Inc., publishers. The article is available free on the BioResearch Open Access website.

Andrea Crowley, Jeff Connell, Kirsten Schaffer, William Halla, and Jaythoon Hassan, University College Dublin and St. Vincent's University Hospital, Dublin, Ireland, compared three immunoassay methods for detecting antibodies produced by the body in response to EBV infection and the presence of proteins that comprise the EBV early antigen complex. The researchers determined which of the diagnostic tests could better predict EBV infection in patients with mononucleosis or in immunosuppressed adult liver transplant recipients. The article "Is There Diagnostic Value in Detection of Immunoglobulin G Antibodies to the EpsteinBarr Virus Early Antigen?" presents the complete methodology and results of this study.

"Having the ability to predict the risk of developing EBV-induced lymphoproliferative disorders after a transplant has important consequences for patient care, as it would allow for prompt therapy and could potentially decrease patient mortality," says Editor-in-Chief Jane Taylor, PhD, MRC Centre for Regenerative Medicine, University of Edinburgh, Scotland.

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About the Journal

BioResearch Open Access is a bimonthly peer-reviewed open access journal that provides a new rapid-publication forum for a broad range of scientific topics including molecular and cellular biology, tissue engineering and biomaterials, bioengineering, regenerative medicine, stem cells, gene therapy, systems biology, genetics, biochemistry, virology, microbiology, and neuroscience. All articles are published within 4 weeks of acceptance and are fully open access and posted on PubMedCentral. All journal content is available on the BioResearch Open Access website.

About the Publisher

Mary Ann Liebert, Inc., publishers is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including Tissue Engineering, Stem Cells and Development, Human Gene Therapy and HGT Methods, and AIDS Research and Human Retroviruses. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 70 journals, books, and newsmagazines is available on the Mary Ann Liebert, Inc., publishers website.

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Is the detection of early markers of Epstein Barr virus of diagnostic value?

Recommendation and review posted by Bethany Smith

PHILADELPHIA Fifty years ago, UK researcher John Gurdon demonstrated that genetic material from non-reproductive cells could be reprogrammed into an embryonic state when transferred into an egg. In 2006, Kyoto University researcher Shinya Yamanaka expanded on those findings by expressing four proteins in mouse somatic cells to rewind their genetic clocks, converting them into embryonic-like stem cells called induced pluripotent stem cells, or iPS cells.

In early October, Gurdon and Yamanaka were awarded the 2012 Nobel Prize in Physiology or Medicine for their discoveries. Now, thanks to some careful detective work by a team of scientists led by Kenneth Zaret, PhD, at the Perelman School of Medicine, University of Pennsylvania, researchers can better understand just how iPS cells form and why the Yamanaka process is so inefficient, an important step to work out for regenerative medicine. Zaret is associate director of the Penn Institute for Regenerative Medicine and professor of Cell and Developmental Biology.

The findings, which appear in the Nov. 22 issue of the journal Cell, uncover cellular impediments to iPS cell development that, if overcome, could dramatically improve the efficiency and speed of iPS cell generation.

These studies provide detailed insights into how reprogramming factors interact with the chromatin of differentiated cells and start them down the path toward becoming stem cells, said Susan Haynes, PhD, National Institute of General Medical Sciences, which partially funded the work. Dr. Zarets work also identified a major structural roadblock in the chromatin that the factors must overcome in order to bind DNA.This knowledge will help improve the efficiency of reprogramming, which is important for any future therapeutic applications.

Human iPS cells are generated by expressing four DNA-binding proteins Oct4, Sox2, Klf4, and c-Myc (O, S, K, and M) in human non-reproductive, or somatic cells, such as skin cells. These factors have generated intense interest in the stem cell and medical communities, not least because they offer the promise of embryonic stem cells with none of the messy ethical and moral dilemmas. Just as significantly, patient-specific iPS cells from individuals with genetic disorders can be used to study disease origin and to develop drugs for a range of conditions such as Huntingtons and Parkinsons diseases.

Yet, the process of generating iPS cells is highly inefficient. It can take a month to fully reprogram somatic cells into iPS cells, and as few as one in 10,000 cells that take up the four factors will successfully convert. Whats more, some studies indicate that, for all their plasticity, iPS cells are not precisely equivalent to embryonic stem cells. Zaret, with Penn postdoctoral fellow Abdenous Soufi, PhD, and bioinformatician Greg Donahue, PhD, decided to find out why.

The team analyzed the destination in the human genome of the four reprogramming factors 48 hours after the initiation of iPS cell reprogramming and compared those locations to four cell types: the starting cell population; the fully reprogrammed iPS cells; cells nearing the end of the reprogramming process (pre-iPS); and embryonic stem cells.

They found that at 48 hours the factors tended to bind gene regulatory elements called enhancers, far removed from the genes they regulate, rather than the target genes themselves. That suggests that O, S, and K serve as pioneer factors that open closed chromatin structures on the DNA itself, facilitating the reprogramming process by making target sections of the genome available to be read by messenger RNA.

The team also found large regions of the genome that were refractory to the binding of reprogramming factors at 48 hours, but which were eventually activated in, and are in fact required, for the formation of iPS cells.

Basically, large chunks of the human genome were physically resisting these factors from entering, Zaret explained. That provided some understanding that youve got to overcome the binding impediment to get these factors to their final destination.

Continue reading here:
Penn Study Decodes Molecular Mechanisms Underlying Stem Cell Reprogramming

Recommendation and review posted by Bethany Smith