ScienceDaily (Nov. 25, 2012) A newly discovered gene that is essential for embryo survival could also hold the key to treating and potentially controlling chronic infections such as HIV, hepatitis and tuberculosis.

The gene, called Arih2, is fundamental to the function of the immune system -- making critical decisions about whether to switch on the immune response to an infection.

Its discovery has implications for the treatment of chronic overwhelming infections, such as HIV, that 'exhaust' and switch off the immune system, as well as for chronic inflammatory (also known as autoimmune) conditions such as rheumatoid arthritis and sepsis.

Dr Marc Pellegrini, Dr Greg Ebert and colleagues from the institute's Infection and Immunity division, with collaborators from the University of Toronto, Canada, led the research. Their findings were published November 26 in the journal Nature Immunology.

Infectious disease specialist and researcher Dr Pellegrini said that Arih2 is found in dendritic cells, the sentinels of the immune system that play an essential role in raising the alarm about the presence of foreign invaders in the body. "Arih2 is responsible for the most fundamental and important decision that the immune system has to make -- whether the immune response should be initiated and progressed or whether it should be switched off to avoid the development of chronic inflammation or autoimmunity," Dr Pellegrini said. "If the wrong decision is made, the organism will either succumb to the infection, or succumb to autoimmunity."

Dr Pellegrini said although our immune system works well against many infections, some organisms have developed mechanisms to evade or counteract the immune system, allowing them to persist in the body. "During evolution, some organisms have evolved ways of exhausting our immune system to the point where the immune system just switches off, and this is what happens in HIV, hepatitis B and tuberculosis," he said. "These organisms counter the immune response -- exhausting T cells which are stimulated over and over again by the infection and becoming exhausted or paralysed. With this current discovery, what we should be able to do is circumvent these mechanisms and reinvigorate the immune response temporarily to boost the immune system and help clear these infections."

Dr Ebert said the research team was now looking at the effect on the immune response of switching off Arih2 for short periods of time during chronic infections. "We are investigating how manipulating Arih2 and associated pathways promotes immunity in chronic overwhelming infections, where we know the immune response is inadequate," Dr Ebert said.

He said Arih2 had significant promise as a drug target. "Arih2 has a unique structure, which we believe make it an excellent target for a therapeutic drug, one that is unlikely to affect other proteins and cause unwanted side-effects," Dr Ebert said. "Because Arih2 is critical for survival, we now need to look at the effect of switching off the gene for short periods of time, to see if there is a window of opportunity for promoting the immune response to clear the infection without unwanted or collateral damage or autoimmunity."

Dr Pellegrini said it would take many years to translate the discovery to a drug that could be used in humans. "We are very excited about this discovery," Dr Pellegrini said. "Arih2 is the one of the most important genes involved in the most fundamental and vital decisions that the immune system has to make: whether or not to switch on the immune response to an infection. This discovery has significant implications for manipulating the immune response to infections and suppressing chronic inflammation or autoimmunity because we can target this gene to try to push immune responses in one or other direction -- either promoting it or suppressing it," Dr Pellegrini said. "It is probably one of the few genes and pathways that is very targetable and could lead to a drug very quickly."

The study was supported by the National Health and Medical Research Council of Australia and the Victorian Government.

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Survival gene may be key to controlling HIV and hepatitis

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Chromosomes must 'huddle' together to ensure an eggs healthy development and fertilisation But when the gene SRPK is missing, they cannot do this, say Edinburgh scientists

By Anna Hodgekiss

PUBLISHED: 10:57 EST, 26 November 2012 | UPDATED: 10:57 EST, 26 November 2012

Scientists have identified a gene which could help solve the problem of infertility in humans.

The team at the University of Edinburgh conducted a study with fruit flies, during which they found that when the gene SRPK is missing, chromosomes do not 'huddle' together.

They believe the huddling process is necessary to ensure the eggs healthy development and fertilisation.

When the SRPK gene is missing, chromosomes do not 'huddle' together, something necessary for the egg's healthy development and fertilisation

Chromosomes are thread-like structures which contain a persons DNA, and when they divide it can lead to sterility and low fertility, according to the study.

Previous research in mice has shown that the huddling process is essential in order for eggs to remain fertile, the scientists said.

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Could a problematic gene be the key to solving infertility problems?

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The completion of human and primate genome sequences (including some close, extinct relatives) reveals a great deal about the evolutionary innovations behind modern humans. All indications are a large collection of relatively subtle genetic changesadded up to considerable differences in our brains and anatomy.

So, it was a bit shocking to see a headline claiming a single gene separated us from our fellow apes. The article behind the headline turned out to be wrong, of course. But there was an additional research paper behind that article. The story this told turned out to be rather interesting, even after the hype was stripped away.

The second paper was the product of a research group studying the evolution of human micro RNAs. These are short pieces of RNA that form a "hairpin" structure: two stretches of complementary sequence that can base pair to form a double helix, separated by a short loop that lets the RNA fold back on itself.

Micro RNAs, unlike messenger RNAs, don't code for other proteins. Instead, they help control which messenger RNAs do get made into proteins. The hairpin structure is recognized by a complex of proteins inside the cell, which process it in a way that leaves a short guide sequence exposed. The guide sequence can then base pair with sequences on messenger RNAs, leading the protein complex to them. The complex will typically either block the messenger RNA from being translated into protein or cause it to be destroyed altogether.

The net result of this: a single micro RNA can determine whether a much larger number of genes are made into proteins. In that sense, they act a lot like the proteins that bind to DNA and regulate the activity of large collections of genes.

To find micro RNAs that might be involved in human evolution, the authors of the new study identified over 1,400 micro RNAs known to be active in human cells. Next they searched for the equivalent sequences in the genomes of 10 other mammalian species (as well as, for some reason, the chicken). Most of these seem to have appeared in our ancestors' genomes long before humans were a species, but 10 of them appeared to be unique to us. And another dozen have mutations in key regions that help determine their activity.

Since the authors were interested in human-specific activity, they looked in an organ that's got distinctive features in humans: the brain. Most of the collection wasn't active there, but one wasmiR-941.

Looking at the region in the human genome that contains miR-941 showed it's an area with a series of repeats of the same sequence, arranged in tandem. Chimps and macaques have similar sequences, but the duplications aren't arranged in a way that allows the production of a hairpin structure. Somewhere after we split off from chimps 6 million years ago, a rearrangement in the area (an event that's common in areas with duplicated sequences) created the human form of miR-941. It was already in place a million years ago, when the Denisovan population branched off.

But the rearrangements didn't end there, as there have been a series of duplications that created as many as 11 extra copies of miR-941 (the numbers vary in different populations, but average is about six or seven copies in most). The extra copies should help ensure it's expressed at higher levels than it would be otherwise.

A variety of evidence indicated it's likely to be having a significant impact on gene regulation. miR-941 is expressed in a variety of tissues, and the sequences it recognizes are present in two important signaling pathways that contribute to the growth and structures of the brain (hedgehog and insulin) and other tissues. And, if you express it in the cells from other primates, it is able to shut a variety of genes down. In humans, several of those genes no longer respond to miR-941 due to mutations in their sequence. This suggests the appearance of the micro RNA caused a period of fine-tuning of its targets (in order to more precisely control its regulation of gene expression).

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Sydney, Nov 27 (IANS) A gene that protects the human embryo could possibly treat and subdue chronic infections such as HIV, hepatitis and tuberculosis.

The newly discovered gene, called Arih2, is basic to the immune system making critical decisions about whether to switch it on during an infection or not.

Marc Pellegrini, Greg Ebert and colleagues from the Walter and Eliza Hall Institute of Medical Research's infection and immunity division, Australia, with collaborators from the University of Toronto, Canada, led the research, the journal Nature Immunology reported.

Infectious disease specialist Pellegrini said that Arih2 is found in dendritic cells, the sentinels of the immune system that play an essential role in raising the alarm about the presence of foreign invaders in the body, according to a Walter Eliza Institute statement.

"Arih2 is responsible for the most fundamental and important decision that the immune system has to make whether the immune response should be initiated and progressed or whether it should be switched off to avoid the development of chronic inflammation or autoimmunity," Pellegrini said.

"If the wrong decision is made, the organism will either succumb to the infection, or succumb to autoimmunity."

"During evolution, some organisms have evolved ways of exhausting our immune system to the point where the immune system just switches off, and this is what happens in HIV, Hepatitis B and tuberculosis," he said.

"These organisms counter the immune response exhausting T cells which are stimulated over and over again by the infection and becoming exhausted or paralysed," said Pellegrini.

"With this current discovery, what we should be able to do is circumvent these mechanisms and reinvigorate the immune response temporarily to boost the immune system and help clear these infections," he added.

Ebert said the research team was now looking at the effect on the immune response of switching off Arih2 for short periods of time during chronic infections.

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Key immune system gene could subdue HIV

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A gene that keeps embryos alive appears to control the immune system and determine how it fights chronic diseases like hepatitis and HIV, and autoimmune diseases like rheumatoid arthritis, scientists said on Monday.

Although the experts have only conducted studies on the gene Arih2 using mice, they hope it can be used as a target for drugs eventually to fight a spectrum of incurable diseases.

Lead author Marc Pellegrini at the Walter and Eliza Hall Institute of Medical Research in Australia said the gene appears to act like a switch, flipping the immune system on and off.

"If the gene is on, it dampens ... the immune response. And if you switch it off, it greatly enhances immune responses," Pellegrini said in a telephone interview.

"It is probably one of the few genes and pathways that is very targetable and could lead to a drug very quickly."

Arih2 was first identified by another group of scientists in the fruit fly but it drew the interest of Pellegrini's team because of its suspected links to the immune system.

In a paper published in Nature Immunology, Pellegrini and his team described how mice embryos died when the gene was removed.

Next, they removed the gene from adult mice and noticed how their immune systems were boosted for a short period of time. But it quickly went into an overdrive and started attacking the rodents' own healthy cells, skin and organs.

"The mice survived for six weeks quite well. Then they started developing this very hyperactive immune responses and if you leave it for too long, it starts reacting against the body itself," Pellegrini said.

Pellegrini and his colleagues hope that scientists can study the gene further and use it as a drug target to fight a large spectrum of diseases.

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Embryo survival gene may fight range of diseases

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HONG KONG (Reuters) - A gene that keeps embryos alive appears to control the immune system and determine how it fights chronic diseases like hepatitis and HIV, and autoimmune diseases like rheumatoid arthritis, scientists said on Monday.

Although the experts have only conducted studies on the gene Arih2 using mice, they hope it can be used as a target for drugs eventually to fight a spectrum of incurable diseases.

Lead author Marc Pellegrini at the Walter and Eliza Hall Institute of Medical Research in Australia said the gene appears to act like a switch, flipping the immune system on and off.

"If the gene is on, it dampens ... the immune response. And if you switch it off, it greatly enhances immune responses," Pellegrini said in a telephone interview.

"It is probably one of the few genes and pathways that is very targetable and could lead to a drug very quickly."

Arih2 was first identified by another group of scientists in the fruit fly but it drew the interest of Pellegrini's team because of its suspected links to the immune system.

In a paper published in Nature Immunology, Pellegrini and his team described how mice embryos died when the gene was removed.

Next, they removed the gene from adult mice and noticed how their immune systems were boosted for a short period of time. But it quickly went into an overdrive and started attacking the rodents' own healthy cells, skin and organs.

"The mice survived for six weeks quite well. Then they started developing this very hyperactive immune responses and if you leave it for too long, it starts reacting against the body itself," Pellegrini said.

Pellegrini and his colleagues hope that scientists can study the gene further and use it as a drug target to fight a large spectrum of diseases.

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Embryo survival gene may fight range of diseases: study

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Genetic Engineering - A Level Biology - Unit 5
For A Level Biology, suited for Unit 5 of the OCR exam board.From:ocrbiologya2Views:3 0ratingsTime:03:06More inEducation

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Ancient ET Intervention - Marshall Klarfeld - Coast to Coast AM Classic
http://www.jetnews.us Date: 11-07-10 Host: George Noory Guests: Marshall Klarfeld Mechanical engineer Marshall Klarfeld discussed his relationship with the late Zecharia Sitchin and his theories of how humans were created by genetic engineering of the Annunaki. Sitchin arrived at his conclusions after translating the ancient cuneiform tablets of the Sumerians, telling Klarfeld, "It #39;s not a secret, I #39;m just a reporter." While some have not concurred with Sitchin #39;s interpretations, Klarfeld said five major scholars agreed with his translations. Klarfeld recounted the 6000 year-old Epic of Gilgamesh which tells in cuneiform the history of Earth #39;s first contact with extraterrestrial beings-- the Annunaki, who mixed their DNA with Homo erectus to create the human race. The story involved Gilgamesh, the king of Uruk, who was part Annunaki, a cloned counterpart, Enkidu, and Ishtar, an Annunaki princess who traveled in a shuttlecraft to the space platform (the huge stone ruins in Baalbek, Lebanon). She was said to control a weapon "the Bull of Heaven," which Klarfeld likened to a laser beam. The Epic also tells the story of the Great Flood (associated with the arrival of the planet Nibiru in between Mars and Jupiter), and how the Annunaki wanted to use it to wipe out humans, said Klarfeld. Yet, some opted to save humankind, and Noah #39;s Ark was developed as a submersible, and rather than containing actual animals, it held the DNA of all living creatures, which was later reconstituted ...From:C2CPlanetViews:18 1ratingsTime:01:52:47More inEducation

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Ancient Giants Cosmic War - Joseph P. Farrell - Coast to Coast AM Classic
http://www.jetnews.us Date: 04-20-11 Host: George Noory Guests: Joseph P. Farrell, Richard C. Hoagland Renowned researcher with a PhD from Oxford University, Joseph P. Farrell presented evidence for a hidden history of mankind that involved tyrannical giants and an elite race bent on genetic mutation. The Greeks, Hopi, Mayans, Iroquois, Aztecs, and the Bible all recorded an ancient war against giants in the dim past. "I was astounded at the parallels between all these very, very divergent cultures,"-- there seems to be some kind of worldwide or civil war against the giants, for different reasons including their sexual practices and/or cannibalism. This "cosmic war" may have involved something far more destructive than nuclear bombs-- torsion or scalar-based weapons that effectively annihilated both sides, he said. Farrell cited ancient cuneiform tablets that suggest some type of genetic manipulation took place in which prototypical Earth females and Annunaki-type males were mixed to form modern humans, to serve as a slave race. This is particularly problematic, as our "cousins" may return one day to claim us as their property, he warned. Such ancient genetic engineering also produced chimerical beings composed of various human and animal components, he continued. We #39;re looking at the activity of one elite group, if not more, "that has been in continual existence more or less since ancient times," and their behavior is to try and preserve knowledge just for themselves, he said ...From:C2CPlanetViews:139 3ratingsTime:02:34:57More inEducation

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Ancient Giants

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Top of the Pops 3rd March 1983 Icehouse OMD Forrest Bananarama Peel Jensen.
Top Of the Pops 3rd March 1983 Presented by John Peel David Jensen, Featuring Performances By Icehouse ( Hey Little Girl ) OMD ( Genetic Engineering ) Forrest ( Rock The Boat ) Bananarama ( Na Na Hey Hey Kiss Him Goodbye ).From:marfun2Views:0 0ratingsTime:15:44More inMusic

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Interior of an incubator showing cells growing in culture flasks, petri dishes, and microtiter plates.

Cell lines are standard tools in biomedical research, and yet when it comes to their genetic identity, they are remarkably unstable. That volatility comes with their defining traitimmortality. Over time, cells accumulate mutations that may ultimately change the structure of chromosomes and alter cellular functions.

A number of those genetic changes can be detected with cell line authentication, although despite the authority implied by its name, such testing is not yet performed routinely in many laboratories. In fact, for the better part of the 60 years since its inception, authentication has not featured prominently on scientists to-do lists. It was even actively dismissed for a time, because the manner in which attention had been called to scientists mistakes (in many cases committed unknowingly) was perceived as career-threatening.

By the 1960s, it was clear that authentication would be an effective way to catch obvious mix-ups and contamination between cell lines. But it would have been difficult to predict its usefulness for detecting the many diverse genetic variations that bear so critically on cell line identity over time, since those variations were unknown then. And even now, equipped with relatively advanced technologies and with an understanding that genetic variation can be both powerful in effect and subtle in form, they are still able to escape detection.

The elusiveness of variation is a fascinating aspect of cell biology, and its significance is emphasized particularly by the widespread use of immortalized cell lines in laboratory research and by the fact that genetic variation is now a cornerstone of biomedical science. Curiosity about variation in nature is not a new phenomenon, of course. Observations of plants, notably those recorded by Gregor Mendel and Dutch botanist Hugo De Vries in the 19th century, were critical to the realization that genetic variation is the basis for evolution by natural selection. Knowledge of induced mutation, or mutagenesis, introduced in the 1920s with the work of German geneticist Hermann Joseph Mller, piqued the interest of not only scientists but also writers and the general public, notably in the form of science fiction and comics, which are rife with mutant characters.

Types of chromosomal mutations.

Still today it is difficult not to be amazed by genetic variation and mutagenesis. The depth of variation that exists in the human genome, for instance, is astonishing. In 2006 scientists reported that copy number variations, which include relatively large deletions, duplications, and insertions of genetic material that alter the structure of DNA, affect from 6 to 19 percent of any given chromosome in the human genome. Prior to that study, it had been estimated that just 0.1 percent of the human genome was affected by genetic variation, much of which had been attributed to single nucleotide polymorphisms, which alter individual building blocks of DNA (changing an A to a T, for example).

The sheer diversity of variation in humans is illustrated further by cancer. Scientists have identified nearly 225,000 unique variants for this disease alone. Presumably many of those represent acquired mutations, or changes that have occurred as a result of time or exposure to cellular stressors, such as certain chemicals.

Which brings us back to cell lines.

The longer cells are kept in culture, and the more stressors they are exposed to, the more mutations they acquire. Eventually, they gain the mutations they need to make them immortal, giving rise to a cell line. A cell line, then, is an established lineage of continuously dividing cells, one in which the cells have effectively surpassed the Hayflick limit, or the finite number of cell divisions that normally would bring about replicative senescence (a state in which cells are metabolically active but not capable of division).

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Authenticating Cells Out of Curiosity, Not Fear

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Newswise Researchers at the Georgia Institute of Technology have received a five-year, $1.8 million grant from the National Science Foundation (NSF) to study how complex microbial systems use their genetic diversity to respond to human-induced change. The work is important because these microbial communities play critical roles in the environment, breaking down pollutants, recycling nutrients and serving as major sources of nitrogen and carbon.

Despite the importance of the microbes, relatively few among the thousands of species that make up a typical microbial community have been studied extensively. The relatively unknown organisms within these communities may have genes that could help address critical environmental, energy and other challenges.

We are all dependent on these microbes, said Kostas Konstantinidis, an assistant professor in Georgia Techs School of Civil and Environmental Engineering and the grants principal investigator. There are many different species and a huge amount of diversity out there. This project will allow us to look at the details of how this diversity is generated, how redundant it is and how these microbes are changing in response to perturbations in the environment.

The funding, from the NSFs Dimensions of Biodiversity program, will support a collaborative effort involving Konstantinidis and two other Georgia Tech researchers: Eberhardt Voit and Jim Spain. Voit holds the David D. Flanagan Chair in Biological Systems within the Department of Biomedical Engineering at Georgia Tech and Emory University, and is a Georgia Research Alliance Eminent Scholar. Spain is a professor in the School of Civil and Environmental Engineering.

The research will initially focus on Lake Lanier, a large man-made lake located near Atlanta. Beyond the experimental work, the research will involve extensive mathematical modeling of the complex microbial communities.

We want to see how the microbial communities of the lake change over time, and how the perturbations affect that, said Konstantinidis, who holds the Carlton S. Wilder Chair in Environmental Engineering at Georgia Tech. We then want to extend our understanding to other ecosystems, such as the Gulf of Mexico.

The researchers will set up mesocosms bioreactors in the laboratory with microbial populations from Lake Lanier. They will feed these populations pollutants such as hydrocarbons, antibiotics and pesticides to see how they respond and how they deal with compounds to which they may not have been exposed.

Sometimes they may not have the genes to break down the pollutants and may not encode the right enzymes, Konstantinidis said. But if you give them enough time, these microbes somehow innovate. We want to understand the genetic mechanisms that allow the microbes to break down a compound that they are seeing for the first time.

The grant will allow the Georgia Tech researchers to expand knowledge of rare microbes, largely unknown organisms that may harbor useful genes.

We think these unusual microbes may be the key ones, Konstantinidis said. Though they may be low in abundance, the whole community may depend on them. When you have a new pollutant, these rare microbes may become more important by providing the genetic diversity needed.

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ScienceDaily (Nov. 26, 2012) Researchers at the Georgia Institute of Technology have received a five-year, $1.8 million grant from the National Science Foundation (NSF) to study how complex microbial systems use their genetic diversity to respond to human-induced change. The work is important because these microbial communities play critical roles in the environment, breaking down pollutants, recycling nutrients -- and serving as major sources of nitrogen and carbon.

Despite the importance of the microbes, relatively few among the thousands of species that make up a typical microbial community have been studied extensively. The relatively unknown organisms within these communities may have genes that could help address critical environmental, energy and other challenges.

"We are all dependent on these microbes," said Kostas Konstantinidis, an assistant professor in Georgia Tech's School of Civil and Environmental Engineering and the grant's principal investigator. "There are many different species and a huge amount of diversity out there. This project will allow us to look at the details of how this diversity is generated, how redundant it is and how these microbes are changing in response to perturbations in the environment."

The funding, from the NSF's "Dimensions of Biodiversity" program, will support a collaborative effort involving Konstantinidis and two other Georgia Tech researchers: Eberhardt Voit and Jim Spain. Voit holds the David D. Flanagan Chair in Biological Systems within the Department of Biomedical Engineering at Georgia Tech and Emory University, and is a Georgia Research Alliance Eminent Scholar. Spain is a professor in the School of Civil and Environmental Engineering.

The research will initially focus on Lake Lanier, a large human-made lake located near Atlanta. Beyond the experimental work, the research will involve extensive mathematical modeling of the complex microbial communities.

"We want to see how the microbial communities of the lake change over time, and how the perturbations affect that," said Konstantinidis, who holds the Carlton S. Wilder Chair in Environmental Engineering at Georgia Tech. "We then want to extend our understanding to other ecosystems, such as the Gulf of Mexico."

The researchers will set up mesocosms -- bioreactors -- in the laboratory with microbial populations from Lake Lanier. They will feed these populations pollutants such as hydrocarbons, antibiotics and pesticides to see how they respond and how they deal with compounds to which they may not have been exposed.

"Sometimes they may not have the genes to break down the pollutants and may not encode the right enzymes," Konstantinidis said. "But if you give them enough time, these microbes somehow innovate. We want to understand the genetic mechanisms that allow the microbes to break down a compound that they are seeing for the first time."

The grant will allow the Georgia Tech researchers to expand knowledge of "rare" microbes, largely unknown organisms that may harbor useful genes.

"We think these unusual microbes may be the key ones," Konstantinidis said. "Though they may be low in abundance, the whole community may depend on them. When you have a new pollutant, these rare microbes may become more important by providing the genetic diversity needed."

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How diversity helps microbial communities respond to change

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Public release date: 26-Nov-2012 [ | E-mail | Share ]

Contact: Bill Ferguson bferguson@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, November 20, 2012Mary Ann Liebert, Inc., publishers announces the launch of Soft Robotics, a peer-reviewed journal dedicated to the science and engineering of soft materials in mobile machines. The Journal breaks new ground as the first to answer the urgent need for research on robotic technology that can safely interact with living systems and function in complex natural or human-built environments. Soft Robotics will be published in print and online with Open Access options.

Multidisciplinary in scope, Soft Robotics combines advances in biomedical engineering, biomechanics, mathematical modeling, biopolymer chemistry, computer science, and tissue engineering to provide comprehensive coverage of new approaches to constructing devices that can undergo dramatic changes in shape and size in order to adapt to various environments. This new technology delivers vital applications for a variety of purposes, including surgery, assistive healthcare devices, search and rescue in emergency situations, space instrument repair, mine detection, and more. The Journal covers topics related to device development 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.

Soft Robotics is led by Editor-in-Chief Barry A. Trimmer, PhD, Henry Bromfield Pearson Professor of Natural Sciences and the Director of the Neuromechanics and Biomimetic Devices Laboratory at Tufts University. A distinguished team of Associate Editors includes John H. Long, Jr., Vassar College (biomechanics); Josh Bongard, University of Vermont (computer science and controls); Fumiya Iida, Swiss Institute of Robotics and Intelligence Systems (biorobotics); Qibing Pei, UCLA (materials development and applications); and Nanshu Lu, University of Texas (flexible electronics). Bill Ferguson, PhD from the Publisher will serve as Managing Editor.

"This powerful new journal provides a much-needed cross-discipline forum on the rapidly advancing science and engineering of Soft Robotics which has great potential for benefit to mankind and our world," says Dr. Trimmer.

Company founder and CEO Mary Ann Liebert comments, "Soft Robotics is an important and growing field with great promise; the Journal will make a significant contribution to the literature and also advance the field. Under the leadership of Dr. Barry Trimmer, this journal will play an important role in the advancement of soft robotic technologies and applications."

###

To sign up to receive email alerts for Soft Robotics, please email journalmarketing2@liebertpub.com.

About the Publisher

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'Soft Robotics': A groundbreaking new journal on engineered soft devices that Interact with Living Systems

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ScienceDaily (Nov. 26, 2012) Johns Hopkins researchers report concrete steps in the use of human stem cells to test how diseased cells respond to drugs. Their success highlights a pathway toward faster, cheaper drug development for some genetic illnesses, as well as the ability to pre-test a therapy's safety and effectiveness on cultured clones of a patient's own cells.

The project, described in an article published November 25 on the website of the journal Nature Biotechnology, began several years ago, when Gabsang Lee, D.V.M., Ph.D., an assistant professor at the Johns Hopkins University School of Medicine's Institute for Cell Engineering, was a postdoctoral fellow at Sloan-Kettering Institute in New York. To see if induced pluripotent stem cells (iPSCs) could be used to make specialized disease cells for quick and easy drug testing, Lee and his colleagues extracted cells from the skin of a person with a rare genetic disease called Riley-Day syndrome, chosen because it affects only one type of nerve cell that is difficult if not impossible to extract directly from a traditional biopsy. These traits made Riley-Day an ideal candidate for alternative ways of generating cells for study.

In a so-called "proof of concept" experiment, the researchers biochemically reprogrammed the skin cells from the patient to form iPSCs, which can grow into any cell type in the body. The team then induced the iPSCs to grow into nerve cells. "Because we could study the nerve cells directly, we could for the first time see exactly what was going wrong in this disease," says Lee. Some symptoms of Riley-Day syndrome are insensitivity to pain, episodes of vomiting, poor coordination and seizures; only about half of affected patients reach age 30.

In the recent research at Johns Hopkins and Memorial Sloan-Kettering, Lee and his co-workers used these same lab-grown Riley-Day nerve cells to screen about 7,000 drugs for their effects on the diseased cells. With the aid of a robot programmed to analyze the effects, the researchers quickly identified eight compounds for further testing, of which one -- SKF-86466 -- ultimately showed promise for stopping or reversing the disease process at the cellular level.

Lee says a clinical trial with SKF-86466 might not be feasible because of the small number of Riley-Day patients worldwide, but suggests that a closely related version of the compound, one that has already been approved by the U.S. Food and Drug Administration for another use, could be employed for the patients after a few tests.

The implications of the experiment reach beyond Riley-Day syndrome, however. "There are many rare, 'orphan' genetic diseases that will never be addressed through the costly current model of drug development," Lee explains. "We've shown that there may be another way forward to treat these illnesses."

Another application of the new stem cell process could be treatments tailored not only to an illness, but also to an individual patient, Lee says. That is, iPSCs could be made for a patient, then used to create a laboratory culture of, for example, pancreatic cells, in the case of a patient with type 1 diabetes. The efficacy and safety of various drugs could then be tested on the cultured cells, and doctors could use the results to help determine the best treatment. "This approach could move much of the trial-and-error process of beginning a new treatment from the patient to the petri dish, and help people to get better faster," says Lee.

Other authors of the paper are Christina N. Ramirez, Ph.D., Nadja Zeltner, Ph.D., Becky Liu, Constantin Radu, M.S., Bhavneet Bhinder, Hakim Djaballah, Ph.D., and Lorenz Studer, Ph.D., of the Sloan-Kettering Institute; and Hyesoo Kim, Ph.D., Young Jun Kim, M.D., Ph.D., InYoung Choi, Ph.D., and Bipasha Mukherjee-Clavin of the Johns Hopkins University School of Medicine.

The work was supported by funds from New York State Stem Cell Science (NYSTEM), the New York Stem Cell Foundation (NYSCF), the state of Maryland (TEDCO, MSCRF), the Commonwealth Foundation for Cancer Research, the Experimental Therapeutics Center at Memorial Sloan-Kettering Cancer Center, the William Randolph Hearst Fund in Experimental Therapeutics, the L.S. Wells Foundation, and the National Cancer Institute (grant number 5 P30 CA008748-44).

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Use of stem cells in personalized medicine

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Public release date: 26-Nov-2012 [ | E-mail | Share ]

Contact: Shawna Williams shawna@jhmi.edu 410-955-8236 Johns Hopkins Medicine

Johns Hopkins researchers report concrete steps in the use of human stem cells to test how diseased cells respond to drugs. Their success highlights a pathway toward faster, cheaper drug development for some genetic illnesses, as well as the ability to pre-test a therapy's safety and effectiveness on cultured clones of a patient's own cells.

The project, described in an article published November 25 on the website of the journal Nature Biotechnology, began several years ago, when Gabsang Lee, D.V.M., Ph.D., an assistant professor at the Johns Hopkins University School of Medicine's Institute for Cell Engineering, was a postdoctoral fellow at Sloan-Kettering Institute in New York. To see if induced pluripotent stem cells (iPSCs) could be used to make specialized disease cells for quick and easy drug testing, Lee and his colleagues extracted cells from the skin of a person with a rare genetic disease called Riley-Day syndrome, chosen because it affects only one type of nerve cell that is difficult if not impossible to extract directly from a traditional biopsy. These traits made Riley-Day an ideal candidate for alternative ways of generating cells for study.

In a so-called "proof of concept" experiment, the researchers biochemically reprogrammed the skin cells from the patient to form iPSCs, which can grow into any cell type in the body. The team then induced the iPSCs to grow into nerve cells. "Because we could study the nerve cells directly, we could for the first time see exactly what was going wrong in this disease," says Lee. Some symptoms of Riley-Day syndrome are insensitivity to pain, episodes of vomiting, poor coordination and seizures; only about half of affected patients reach age 30.

In the recent research at Johns Hopkins and Memorial Sloan-Kettering, Lee and his co-workers used these same lab-grown Riley-Day nerve cells to screen about 7,000 drugs for their effects on the diseased cells. With the aid of a robot programmed to analyze the effects, the researchers quickly identified eight compounds for further testing, of which one SKF-86466 ultimately showed promise for stopping or reversing the disease process at the cellular level.

Lee says a clinical trial with SKF-86466 might not be feasible because of the small number of Riley-Day patients worldwide, but suggests that a closely related version of the compound, one that has already been approved by the U.S. Food and Drug Administration for another use, could be employed for the patients after a few tests.

The implications of the experiment reach beyond Riley-Day syndrome, however. "There are many rare, 'orphan' genetic diseases that will never be addressed through the costly current model of drug development," Lee explains. "We've shown that there may be another way forward to treat these illnesses."

Another application of the new stem cell process could be treatments tailored not only to an illness, but also to an individual patient, Lee says. That is, iPSCs could be made for a patient, then used to create a laboratory culture of, for example, pancreatic cells, in the case of a patient with type 1 diabetes. The efficacy and safety of various drugs could then be tested on the cultured cells, and doctors could use the results to help determine the best treatment. "This approach could move much of the trial-and-error process of beginning a new treatment from the patient to the petri dish, and help people to get better faster," says Lee.

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