A.B.Series Apple Stem Cell Serum
A.B.Series Apple Stem Cell Serum A natural way to rejuvenate and revitalize your skin for a younger you. Apple Stem Cell Serum is formulated from Switzerland...

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Midsummer Nights #39; Science: Progress in psychiatric genetics
Copyright Broad Institute, 2013. All rights reserved. To find genes that underlie traits or diseases, scientists often conduct genome-wide association studie...

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X-men gene therapy session (ASMR)
My first attempt at an ASMR video after lurking for so long. A huge thanks to Heatherfeather for making her amazing videos and answering all of my messages. ...

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X-men gene therapy session (ASMR) - Video

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Treating Disease in Babies Before Birth: The Third Option - Anna David at TEDxUCLWomen
Is there a way to treat disease in babies before birth? In this informative talk, Anna David, Associate Professor at the UCL Institute for Women #39;s Health, di...

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Changing the Culture of Cancer Care, Part 1
UW Medicine #39;s 2014 Mini-Medical School is a series of lectures and demonstrations designed to teach viewers about medical science, patient care and leading-edge research underway at the University...

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Clinical Use of Telomere Measurement in Preventive and Personalized Medicine
Clinical Use of Telomere Measurement in Preventive and Personalized Medicine Dave Woynarowski, MD Watch the full presentation at http://www.fleetwoodonsite.com/a4m Recorded at the A4M May 2014...

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The accident of breaking neck completely (2) - Spinal Cord Injury Patient Stories
This patient #39;s story is edited and made out into a short film, which is published on a TV programme, named Approaching science of CCTV channel and can be w...

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Make@OSU: Nanotechnology: From Materials Science to Regenerative Medicine
Make@OSU: Nanotechnology: From Materials Science to Regenerative Medicine presented by Jed Johnson, PhD.

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PUBLIC RELEASE DATE:

31-Jul-2014

Contact: Roberta Gottlieb roberta.gottlieb@cshs.org PLOS

There is epidemiological evidence that links type B coxsackie virus (CVB) infection with heart disease, and research published on July 31st in PLOS Pathogens now suggests a mechanism by which early infection impairs the heart's ability to tolerate stress at later stages of life.

CVB infection is very common and affects mostly children. The symptoms range widely: over half of the infections are thought to be asymptomatic, the majority of children who get sick have only a mild fever, and a very small proportion get inflammation of the heart or brain. On the other hand, 70 80% of patients with heart failure show signs of a previous CVB infection but have no history of viral heart disease, raising the possibility that even a mild earlier infection makes them more vulnerable to get heart disease later on.

To investigate this, researchers from San Diego State University, USA, led by Roberta Gottlieb and Ralph Feuer, first established a mouse model of mild juvenile CVB infection. Mice infected with a non-lethal dose of the virus shortly after birth did not develop any heart disease symptoms during the infection or into adulthood, but they had a predisposition to heart disease later in life.

Detailed analysis of the mice after infection showed that the virus does indeed target the heart and is found in cardiac stem cells. When comparing the numbers of cardiac stem cells in previously infected adult mice with uninfected ones, the researchers found significantly smaller numbers in the infected mice.

To test whether the childhood infection and stem cell depletion had any effect on the adult heart, the researchers exposed infected mice to two different types of cardiac stress. They treated some of the mice with a drug known to overstimulate the heart, and they challenged another group by making them swim for 90 minutes every day for 14 days. Following both treatments, the infected mice showed clear signs of early heart disease whereas uninfected controls showed little or no symptoms.

Analyzing the stressed mice in more detail, the researchers found that the hearts from previously infected mice had impaired ability to re-arrange their heart blood vessels and grow new ones. This process, called vascular remodeling, is critical for the heart to respond to changes in the environment, including stress.

As discussed in the article, important open questions remain. For example, does CVB infection affect cardiac stem cells at any age, or is there a vulnerable period in early childhood? It is also not clear whether other strains of CVB have similar properties to the one used here, which was isolated from a patient with heart disease.

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Childhood coxsackie virus infection depletes cardiac stem cells and might compromise heart health in adults

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Newswise La Jolla, Calif., July 31, 2014 A new study by researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) has found that a peptide called caerulein can convert existing cells in the pancreas into those cells destroyed in type 1 diabetesinsulin-producing beta cells. The study, published online July 31 in Cell Death and Disease, suggests a new approach to treating the estimated 3 million people in the U.S., and over 300 million worldwide, living with type 1 diabetes.

We have found a promising technique for type 1 diabetics to restore the bodys ability to produce insulin. By introducing caerulein to the pancreas we were able to generate new beta cellsthe cells that produce insulinpotentially freeing patients from daily doses of insulin to manage their blood-sugar levels. said Fred Levine, M.D., Ph.D., professor and director of the Sanford Childrens Health Research Center at Sanford-Burnham.

The study first examined how mice in which almost all beta cells were destroyedsimilar to humans with type 1 diabetesresponded to injections of caerulein. In those mice, but not in normal mice, they found that caerulein caused existing alpha cells in the pancreas to differentiate into insulin-producing beta cells. Alpha cells and beta cells are both endocrine cells meaning they synthesize and secret hormonesand they exist right next to one another in the pancreas in structures called islets. However, alpha cells do not normally become beta cells.

The research team then examined human pancreatic tissue from type 1 diabetics, finding strong evidence that the same process induced by caerulein also occurred in the pancreases of those individuals. The process of alpha cells converting to beta cells does not appear to have any age limitationsit occurred in young and old individualsincluding some that had type 1 diabetes for decades.

When caerulein is administered to humans it can cause pancreatitis. So our next step is to find out which molecule(s) caerulein is targeting on alpha cells that triggers their transformation into beta cells. We need to know this to develop a more specific drug, said Levine.

Caerulein is a peptide originally discovered in the skin of Australian Blue Mountains tree frogs. It stimulates gastric, biliary, and pancreatic secretions, and has been used in humans as a diagnostic tool in pancreatic diseases.

In addition to creating new beta cells, another issue that needs to be addressed to achieve a cure for type 1 diabetes is that any new beta cells will be attacked by the autoimmune response present in every patient with type 1 diabetes. We are currently working with Linda Bradley, Ph.D., professor in the Immunity and Pathogenesis Program, and co-author of the study, to couple our approach with an approach to reining in the autoimmune response, added Levine.

The study was funded by the Sanford Childrens Health Research Center, BetaBat (in the Framework Program 7 of the European Community) and CIRM grant TG2-01162.

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A New Way to Generate Insulin-Producing Cells in Type 1 Diabetes

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What clinical trials for gene and stem cell therapy are under way in your London laboratory?
Robin Ali, BSc, PhD, FMedSci, internationally known for his research in gene and cell-based therapy for the treatment of retinal degeneration, has joined the U-M Department of Ophthalmology...

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PUBLIC RELEASE DATE:

31-Jul-2014

Contact: Lynn Celmer lcelmer@aasmnet.org 630-737-9700 American Academy of Sleep Medicine

DARIEN, IL Researchers who studied 100 twin pairs have identified a gene mutation that may allow the carrier to function normally on less than six hours of sleep per night. The genetic variant also appears to provide greater resistance to the effects of sleep deprivation.

Results show that a participant with p.Tyr362His a variant of the BHLHE41 gene had an average nightly sleep duration of only five hours, which was more than one hour shorter than the non-carrier twin, who slept for about six hours and five minutes per night. The twin with the gene mutation also had 40 percent fewer average lapses of performance during 38 hours without sleep and required less recovery sleep afterward sleeping only eight hours after the period of extended sleep deprivation compared with his twin brother, who slept for 9.5 hours.

According to the authors, this is only the second study to link a mutation of the BHLHE41 gene also known as DEC2 - to short sleep duration. The study provides new insights into the genetic basis of short sleep in humans and the molecular mechanisms involved in setting the duration of sleep that individuals need.

"This work provides an important second gene variant associated with sleep deprivation and for the first time shows the role of BHLHE41 in resistance to sleep deprivation in humans," said lead author Renata Pellegrino, PhD, senior research associate in the Center for Applied Genomics at The Children's Hospital of Philadelphia. "The mutation was associated with resistance to the neurobehavioral effects of sleep deprivation."

Study results are published in the Aug. 1 issue of the journal Sleep.

The study group comprised 100 twin pairs 59 monozygotic pairs and 41 dizygotic pairs who were recruited at the University of Pennsylvania. All twin pairs were the same sex and were healthy with no chronic conditions. Nightly sleep duration was measured at home by actigraphy for seven to eight nights. Response to 38 hours of sleep deprivation and length of recovery sleep were assessed in a sleep lab. During sleep deprivation, cognitive performance was measured every two hours using the Psychomotor Vigilance Test.

Although individual sleep needs vary, the American Academy of Sleep Medicine recommends that adults get about seven to nine hours of nightly sleep. However, a small percentage of adults are normal short sleepers who routinely obtain less than six hours of sleep per night without any complaints of sleep difficulties and no obvious daytime dysfunction.

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Study of twins discovers gene mutation linked to short sleep duration

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PUBLIC RELEASE DATE:

31-Jul-2014

Contact: Glenna Picton picton@bcm.edu 713-798-4710 Baylor College of Medicine

HOUSTON (July 31, 2014) Scientists have long speculated that mosaicism a biological phenomenon, in which cells within the same person have a different genetic makeup plays a bigger role in the transmission of rare disease mutations than is currently known. A study conducted by an international team of scientists led by Baylor College of Medicine sheds new light on the frequency of mosaicism in genomic disorders and its influence on recurrence risk.

The study, which was published today in the American Journal of Human Genetics, also included scientists from the University of Leuven in Belgium, St. George's Healthcare Trust in London, Radbound University Medical Center in Nijmegen, Netherlands, the Institute of Mother and Child in Warsaw, Poland, and Trinity University in San Antonio, Texas.

One human, multiple genomes

With recent advances in genome technology, it is becoming increasingly apparent that a human individual is made up of a population of cells, each with its own "personal genome," said Dr. James Lupski, the Cullen Professor of Molecular and Human Genetics at Baylor, and a senior and corresponding author on the report. "Before this study, we understood very little about the centrality of mosaicism in the development of human disease."

In 2011, realizing the suspected importance of this, Lupski and his colleague Dr. Pawe Stankiewicz, associate professor of molecular and human genetics at Baylor and also a senior and corresponding author on the report, tasked graduate students in their labs Ian Campbell and Bo Yuan both currently fourth-year graduate students and co-first authors on the paper with providing a deeper understanding of the role of mosaicism and how it may contribute to genomic disorders.

It turns out Lupski and Stankiewicz's hunch was right: the study found that mosaicism is much more common than originally thought and contributes to recurrence risk in future offspring.

Mutations and mosaicism

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Mosaicism: Study clarifies parents as source of new disease mutations

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"Genetics", Supernumerary Chromosomes

By: MyCyberCollege

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"Genetics", Supernumerary Chromosomes - Video

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Practical Importance of Human Evolution - Genetics, Phylogenetics Health - Natural Selection
Practical Importance of Human Evolution" is a free online course on Janux that is open to anyone. Learn more athttp://janux.ou.edu. Created by the University of Oklahoma, Janux is an interactiv...

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Beef + Lamb New Zealand Genetics is developing research and development genetic research projects and tools to provide additional genetic gains for sheep and beef farmers. Photo from SRL Files

The sheep and beef sector stands to gain by a potential $845 million in added value during the next 20 years once a new Dunedin-based genetics research and development entity hits its stride. Yvonne O'Hara reports.

Upgrading the Sheep Improvement Limited (SIL) database, developing a ram and bull selection app, and contracting out genetics research projects for both sheep and beef are expected to begin later this year for the Dunedin-based Beef + Lamb Genetics (BLNZG).

BLNZG signed a $15 million funding contract for the next five years with the Ministry of Business, Innovation and Employment earlier this month.

The balance of BLNZG's $44 million five-year budget will come from sheep and beef farmers and the wider red meat industry.

BLNZG general manager Graham Alder, of Dunedin, said the contract signing meant it could move ahead with its research and development programmes between now and Christmas.

''The next few months are going to be busy,'' Mr Alder said.

''We intend to employ an additional one or two people [at this point] in the next 12 to 18 months.''

BLNZG's goals included developing the traits and breeding objectives - including ewe and cow efficiency, productivity and longevity - that the New Zealand sheep and beef farmers were going to need in their herds and flocks in the future and what was needed for the delivery of those traits.

''We have to make sure the rams and bulls [available] in the future are the right ones for their farms,'' he said.

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Golden times for genetics firm

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Boston, MA (PRWEB) July 31, 2014

Bostons Adult Stem Cell Technology Center, LLC (ASCTC) finds itself flush with innovative adult stem cell biotechnologies. Currently the company holds seven recently issued patents and has three additional patent applications currently under examination by the U.S. Patent and Trademarks Office.

The patented inventions address two of the most vexing problems in adult stem cell biology research and regenerative medicine. Adult stem cells are difficult to identify; and they have been difficult to multiply to sufficient numbers to support regenerative medicine applications.

ASCTC has addressed the identity problem by developing patented biomarkers that are found exclusively on adult stem cells. The biomarkers are based on ASCTCs expertise in defining properties of adult stem cells that are not shared by any other normal cell types in the body. The patented biomarkers also identify some types of cancer stem cells. Therefore, they have applications in both stem cell medicine and cancer medicine.

ASCTCa success in developing procedures for producing adult stem cells in large numbers is due to the companys expertise in adult stem cell growth control. ASCTCs technology uses natural compounds found in the body to instruct adult stem cells to multiply in a controlled manner as during normal body growth.

The companys patented method for controlling adult stem cells to multiply without losing their stem cell properties has applications for many different types of adult stem cells. ASCTCs approved patents demonstrate the application of the method for production of human liver stem cells, hair follicle stem cells, and human pancreatic stem cells; but the technology has general application to adult stem cells found in many other types of organs and tissues.

In addition to the main focus on adult stem cell technologies, ASCTCs most recently issued patent applies its cell multiplication methods to produce induced pluripotent stem cells (iPSCs) without transferring exogenous genes. This gene-free single agent method should offer significant value to the many mushrooming companies that supply iPSCs and iPSC production reagents.

As a small start-up, ASCTC is employing a social media marketing strategy. In the past week, the company has launched patent licensing ads on LinkedIn, Vocus, and Facebook, as well increased its advertising references within its recently established Twitter presence.

It would be a shame for these technologies to lie dormant, just because our hands are full with other projects at the moment. James Sherley, director of ASCTC, relates that the companys two main business efforts require only a fraction of its available intellectual property. ASCTC is currently focused on bringing laboratory-scale production of human liver stem cells to manufacturing scales and developing a computer simulation assay for preclinical detection of drug candidates with intolerable toxicity due to adverse effects on adult stem cells.

Sherley adds, We already have a few companies that have expressed interest in licensing. But we could do a lot better at reaching others whose development efforts would benefit from ASCTCs unique technologies. Love to hear from ViaCyte!

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The Adult Stem Cell Technology Center, LLC Launches A Marketing Campaign To License Adult Stem Cell Biotechnologies

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"Bubble boy" David Vetter lived in a protective environment designed by NASA engineers. He died of complications after receiving a bone marrow transplant in 1984, at the age of 12. Baylor College of Medicine Photo Archives

Babies born with so-called "bubble boy" disease can often be cured with a stem cell transplant, regardless of the donor -- but early treatment is critical, a new study finds.

Severe combined immunodeficiency (SCID), as the condition is medically known, actually refers to a group of rare genetic disorders that all but eliminate the immune system. That leaves children at high risk of severe infections.

The term "bubble boy" became popular after a Texas boy with SCID lived in a plastic bubble to ward off infections. The boy, David Vetter, died in 1984 at the age of 12, after an unsuccessful bone marrow transplant -- an attempt to give him a functioning immune system.

15 Photos

Immune disorder forced David Vetter to live in bubble - but breakthroughs from his story now enable similar kids to live free

In the best-case scenario, a child would get stem cells -- the blood-forming cells within bone marrow -- from a sibling who is a perfect match for certain immune-system genes.

But that's not always an option, partly because kids with SCID are often their parents' first child, said Dr. John Cunningham, director of hematopoietic stem cell transplantation at the University of Chicago Comer Children's Hospital. He was not involved in the study.

In those cases, doctors typically turn to a parent -- who is usually a "half" match, but whose stem cells can be purified to improve the odds of success. Sometimes, stem cells from an unrelated, genetically matched donor can be used.

The good news: Regardless of the donor, children with SCID can frequently be cured, according to the new findings. But early detection and treatment is vital.

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Early stem cell transplant may cure "bubble boy" disease

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PUBLIC RELEASE DATE:

28-Jul-2014

Contact: Meng Zhao eic@nrren.org 86-138-049-98773 Neural Regeneration Research

MicroRNAs (miRNAs) play an important regulatory role in the self-renewal and differentiation of stem cells. Dr. Defeng Zou and co-workers from the First Affiliated Hospital of China Medical University, China focuses on the effect of miRNA overexpression on the differentiation of bone marrow-derived mesenchymal stem cells into neurons. In the study released on the Neural Regeneration Research (Vol. 9, No. 12, 2014), researchers used GeneChip technology to analyze the expression of miRNAs in bone marrow-derived mesenchymal stem cells, neural stem cells and neurons. They constructed a lentiviral vector overexpressing miR-124 and transfected it into bone marrow-derived mesenchymal stem cells. Intracellular expression levels of the neuronal early markers -III tubulin and microtubule-associated protein-2 were significantly increased, and apoptosis was reduced in transfected cells. After miR-124-transfected bone marrow-derived mesenchymal stem cells were transplanted into the injured rat spinal cord, a large number of cells positive for the neuronal marker neurofilament-200 were observed in the transplanted region. The Basso-Beattie-Bresnahan locomotion scores showed that the motor function of the hind limb of rats with spinal cord injury was substantially improved. These results suggest that miR-124 plays an important role in the differentiation of bone marrow-derived mesenchymal stem cells into neurons, providing novel strategies for enhancing the therapeutic efficacy of bone marrow-derived mesenchymal stem cell transplantation for spinal cord injury.

###

Article: "Overexpression of microRNA-124 promotes the neuronal differentiation of bone marrow-derived mesenchymal stem cells" by Defeng Zou1, Yi Chen2, Yaxin Han1, Chen Lv1, Guanjun Tu1 (1 Department of Orthopedics, First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China; 2 Department of Orthopedics, Jinhua Central Hospital of Zhejiang University, Jinhua, Zhejiang Province, China)

Zou DF, Chen Y, Han YX, Lv C, Tu GJ. Overexpression of microRNA-124 promotes the neuronal differentiation of bone marrow-derived mesenchymal stem cells. Neural Regen Res. 2014;9(12):1241-1248.

Contact: Meng Zhao eic@nrren.org 86-138-049-98773 Neural Regeneration Research http://www.nrronline.org/

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

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How does microRNA-124 promote the neuronal differentiation of BMSCs?

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Theres a good reason people over 60 are not donor candidates for bone marrow transplantation. The immune system ages and weakens with time, making the elderly prone to life-threatening infection and other maladies, and a UC San Francisco research team now has discovered a reason why.

Emmanuelle Passegu, PhD

We have found the cellular mechanism responsible for the inability of blood-forming cells to maintain blood production over time in an old organism, and have identified molecular defects that could be restored for rejuvenation therapies, said Emmanuelle Passegu, PhD, a professor of medicine and a member of the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF. Passegu, an expert on the stem cells that give rise to the blood and immune system, led a team that published the new findings online July 30, 2014 in the journal Nature.

Blood and immune cells are short-lived, and unlike most tissues, must be constantly replenished. The cells that must keep producing them throughout a lifetime are called hematopoietic stem cells. Through cycles of cell division these stem cells preserve their own numbers and generate the daughter cells that give rise to replacement blood and immune cells. But the hematopoietic stem cells falter with age, because they lose the ability to replicate their DNA accurately and efficiently during cell division, Passegus lab team determined.

Especially vulnerable to the breakdown, the researchers discovered in their new study of old mice, are transplanted, aging, blood-forming stem cells, which lack the ability to make B cells of the immune system. These B cells make antibodies to help us fight all sorts of microbial infections, including bacteria that cause pneumonia, a leading killer of the elderly.

In old blood-forming stem cells, the researchers found a scarcity of specific protein components needed to form a molecular machine called the mini-chromosome maintenance helicase, which unwinds double-stranded DNA so that the cells genetic material can be duplicated and allocated to daughter cells later in cell division. In their study the stem cells were stressed by the loss of activity of this machine and as a result were at heightened risk for DNA damage and death when forced to divide.

The researchers discovered that even after the stress associated with DNA replication, surviving, non-dividing, resting, old stem cells retained molecular tags on DNA-wrapping histone proteins, a feature often associated with DNA damage. However, the researchers determined that these old survivors could repair induced DNA damage as efficiently as young stem cells.

"Old stem cells are not just sitting there with damaged DNA ready to develop cancer, as it has long been postulated" Passegu said.

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Key to Aging Immune System Is Discovered

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The fact that China hasnt approved of any commercial GMO planting since 2009 reflects public fears.

Growing future: China is the worlds largest producer of wheat; here a farmer harvests from fields in Jiangsu province.

Despite recent research advances, such as a new strain of wheat that resists destructive mildew (see Chinese Researchers Stop Wheat Disease with Gene Editing), commercial planting of genetically modified food crops has stalled in China, the worlds most populous nation and one with a fast-tightening food supply.

In 2009, the nations Ministry of Agriculture issued a so-called safety certificate to two strains of insect-resistant rice, known as Bt rice, pioneered by Qifa Zhang, a scientist at Huazhong Agricultural University in Wuhan. The ministry also approved a type of corn that helps livestock digest phosphates.

Prior to that, a few minor crop varieties were approved for commercial planting. But to date only nonfood crops, an insect-resistant cotton and a virus-resistant papaya, have been commercially planted on a large scale in China.

The rice approval seemed to have hit a public nerve. Rumors spread on social media chat rooms of claimed health and environmental dangers of homegrown GMOs and of the nations vast imports of GMO grains. (Military officials in one Chinese province even recently banned GMO-sourced cooking oil from troops food supply.) We need the GMOs, but we face severe issues so far in China, meaning the public fears. This is a problem, says Dafang Huang, former director of the Institute of Biotechnology within the Chinese Academy of Agricultural Sciences.

Meanwhile, the government is also trying to wean itself from imports by building its own GMO corn and soybean seed-producing capacity at state companies such as DBN, which runs a biotech center in Beijing.

Long-term food security trends are worrisome. China is home to 1.3 billion people. Its population is rising, its available arable land is slowly decreasing, and yield per acre has stayed essentially flat over the past decade. Its going to be hard to increase the food supply with the traditional crop technology, adds Huang, who spent time planting wheat during the Cultural Revolution.

Against a nationalist and popular backlash, none of the modified rice is officially planted, though reports of illegal plantings abound. Strictly speaking, even though rice has a biosafety certificate, it needs a final step, called varietal trials. For the varietal trials for all major crops except cotton, there are no government guidelines on how to do it. It seems the government is not in a rush. It probably has more challenging issues on its hands, so this is not one to deal with at the moment, says Xing-Wang Deng, who heads a joint research center for plant molecular genetics and agricultural biotech at Peking University and Yale. Deng was one of the prominent experts China lured back to establish labs in China under a government plan called the 1,000 Talent Program.

Despite the regulatory uncertainties, Chinese researchers have quintupled their output of plant science papers in the past decade amid annual funding increases that are the envy of counterparts in other nations. We can do researchwe have enough of financial supportbut I dont know if Chinese scientists can produce the product. The government should give us clearer guidelines or information on which direction we could go further, says Caixia Gao, who heads a gene-editing research group at the State Key Laboratory of Plant Cell and Chromosome Engineering at the Institute of Genetics and Developmental Biology in Beijing.

Excerpt from:
Chinese GMO Research Outpaces Approvals

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Gene research and Silicon Valley-style computing are starting to merge.

J. Craig Venter

Genome scientist and entrepreneur J. Craig Venter is best known for being the first person to sequence his own genome, back in 2001.

This year, he started a new company, Human Longevity, which intends to sequence one million human genomes by 2020, and ultimately offer Web-based programs to help people store and understand their genetic data (see Microbes and Metabolites Fuel an Ambitious Aging Project).

Venter says that hes sequenced 500 peoples genomes so far, and that volunteers are starting to also undergo a battery of tests measuring their strength, brain size, how much blood their hearts pump, and, says Venter, just about everything that can be measured about a person, without cutting them open. This information will be fed into a database that can be used to discover links between genes and these traits, as well as disease.

But thats going to require some massive data crunching. To get these skills, Venter recruited Franz Och, the machine-learning specialist leading Google Translate. Now Och will apply similar methods to studying genomes in a data science and software shop that Venter is establishing in Mountain View, California.

The hire comes just as Google itself has launched a similar-sounding effort to start collecting biomedical data (see Whats a Moon Shot Worth These Days). Venter calls Googles plans for a biomedical database a baby step, a much smaller version of what we are doing.

Whats clear is that genome research and data science are coming together in new ways, and at a much larger scale than ever before. We asked Venter why.

How are we doing in genomics?

In my view there have not been a significant number of advances. One reason for that is that genomics follows a law of very big numbers. Ive had my genome for 15 years, and theres not much I can learn because there are not that many others to compare it to.

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Three Questions for J. Craig Venter

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PUBLIC RELEASE DATE:

29-Jul-2014

Contact: Meng Zhao eic@nrren.org 86-138-049-98773 Neural Regeneration Research

Wallerian degeneration is a subject of major interest in neuroscience. A large number of genes are differentially regulated during the distinct stages of Wallerian degeneration: transcription factor activation, immune response, myelin cell differentiation and dedifferentiation. Although gene expression responses in the distal segment of the sciatic nerve after peripheral nerve injury are known, differences in gene expression between the proximal and distal segments remain unclear. Dr. Dengbing Yao and co-workers from Nantong University, China used microarrays to analyze changes in gene expression, biological processes and signaling pathways in the proximal and distal segments of sciatic nerves undergoing Wallerian degeneration. More than 6,000 genes were differentially expressed and 20 types of expression tendencies were identifed, mainly between proximal and distal segments at 7-14 days after injury. The differentially expressed genes were those involved in cell differentiation, cytokinesis, neuron differentiation, nerve development and axon regeneration. Furthermore, 11 biological processes were represented, related to responses to stimuli, cell apoptosis, inflammatory response, immune response, signal transduction, protein kinase activity, and cell proliferation. Using real-time quantitative PCR, western blot analysis and immunohistochemistry, microarray data were verified for four genes: aquaporin-4, interleukin 1 receptor-like 1, matrix metalloproteinase-12 and periaxin.

Their study, reported in the Neural Regeneration Research (Vol. 9, No. 12, 2014), identifies differential gene expression in the proximal and distal segments of a nerve during Wallerian degeneration, analyzes dynamic biological changes of these genes, and provides a useful platform for the detailed study of nerve injury and repair during Wallerian degeneration.

###

Article: " Differential gene expression in proximal and distal nerve segments of rats with sciatic nerve injury during Wallerian degeneration " by Nan Jiang1, 2, Huaiqin Li1, Yi Sun2, Dexin Yin2, Qin Zhao3, Shusen Cui2, Dengbing Yao1 (1 Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong 226001, Jiangsu Province, China; 2 China-Japan Union Hospital of Jilin University, Changchun 130033, Jilin Province, China; 3 Key Laboratory of People's Liberation Army, Institute of Orthopedics, Chinese PLA General Hospital, Beijing 100853, China)

Jiang N, Li HQ, Sun Y, Yin DX, Zhao Q, Cui SS, Yao DB. Differential gene expression in proximal and distal nerve segments of rats with sciatic nerve injury during Wallerian degeneration. Neural Regen Res. 2014;9(12):1186-1194.

Contact: Meng Zhao eic@nrren.org 86-138-049-98773 Neural Regeneration Research http://www.nrronline.org/

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Differential gene expression in proximal and distal nerve segments after sciatic nerve injury

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A UC San Francisco physician who treats birth defects affecting the face has teamed up with a European expert on animal evolution to create rodent teeth that harken back in evolutionary time.

By making a molar that mimics features found in an ancestral uber-rodent that roamed the earth 60 million years ago, the scientists successfully demonstrated a new way to explore how genetic changes affect mammalian development and how advantageous genetic mutations that spontaneously arise in new generations might take hold over time in an evolving population.

Ophir Klein, MD, PhD

Its not Jurassic Park, but the research team showed that real-time lab experiments are relevant to paleontologists, who typically are stuck working on mysteries of evolution equipped with little more than bits of fossilized bone or teeth. Especially for mammals, the fine features of teeth are used to determine how fossil species are related to each other and to modern animals.

A key gene manipulated by the researchers in their new study, published online July 30, 2014 in Nature, already had been a clinical research focus of study co-senior author Ophir Klein, MD, PhD, Larry L. Hillblom Distinguished Professor in Craniofacial Anomalies at UCSF.The gene, Eda, encodes a developmental protein called ectodysplasin. It is defective in a rare human birth defect that results in a shortage or absence of sweat glands, misshapen and absent teeth, and loss of hair follicles all appendages that develop from the same embryonic tissue. The syndrome was even described by Charles Darwin in The Variation of Animals and Plants Under Domestication, published in 1868.

Researchers in Switzerland had previously found that the syndrome in mice can be treated during the mothers gestation by administering the missing ectodysplasin the first demonstration that a structural birth defect could be prevented with a medical approach, Klein said.

Klein led the first phase I clinical trial to similarly treat the condition in humans, and this past November treated the first North American baby in an ongoing phase II study.

But Klein and collaborator Jukka Jernvall, PhD, Academy Professor of evolution and development at the University of Helsinki, Finland, had also been wondering if the same biochemical pathway also could be manipulated to study evolution.

In the past, biologists have studied fine features of teeth in mutant animals to try to help them reconstruct evolutionary history. However, the changes in the mutants are often too dramatic to be very informative. We wanted to know if we could play with these biochemical pathways to recapitulate changes that are seen in the fossil record, Klein said.

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Gene Behind Rare Birth Abnormality Is a Window on Evolution

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

29-Jul-2014

Contact: Samuel Antenor samuel@fapesp.br 55-113-838-4381 Fundao de Amparo Pesquisa do Estado de So Paulo

Researchers from the University of So Paulo (USP) have identified an RNA known as INXS that, although containing no instructions for the production of a protein, modulates the action of an important gene in the process of apoptosis, or programmed cell death.

According to Sergio Verjovski-Almeida, professor at the USP Chemistry Institute and coordinator of a research funded by So Paulo Research Foundation (FAPESP), INXS expression is generally diminished in cancer cells, and methods that are capable of stimulating the production of this non-coding RNA can be used to treat tumors.

In experiments on mice, the USP scientists were able to effect a 10-fold reduction in the volume of subcutaneous malignant tumors by administering local injections of a plasmid a circular DNA molecule containing INXS. The findings were published in the most recent issue of the journal Nucleic Acids Research.

The group headed by Verjovski-Almeida at USP has devoted the past five years to investigating the regulatory role of so-called intronic non-protein-coding genes those found in the same region of the genome as a coding gene but on the opposite DNA strand. INXS, for example, is an RNA expressed on the opposite strand of a gene coding for a protein known as BCL-X.

"We were studying several protein-coding genes involved in cell death in search of evidence that one of them was regulated by intronic non-coding RNA. That was when we found the gene for BCL-X, which is located on chromosome 20," he explained.

The researcher explained that BCL-X is present in cells in two different forms: one that inhibits apoptosis (BCL-XL) and one that induces the process of cell death (BCL-XS). The two isoforms act on the mitochondria but in opposite ways. The BCL-XS isoform is considered a tumor suppressor because it activates protein complexes known as caspases, which are required for the activation of other genes that cause cell death.

"In a healthy cell, there is a balance between the two BCL-X isoforms. Normally, there is already a smaller number of the pro-apoptotic form (BCL-XS). However, in comparing tumor cells to non-tumor cells, we observed that tumor cells contain even fewer of the pro-apoptotic form, as well as reduced levels of INXS. We suspect that one thing affects the other," the researcher said.

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Brazilian researchers identify RNA that regulates cell death

Recommendation and review posted by Bethany Smith