By Elizabeth Lopatto - Wed May 09 18:00:00 GMT 2012

An experimental therapy that reprograms the immune system then spurs the growth of healthy insulin-producing cells reversed late-stage diabetes in mice and may lead to a cure for people, researchers said.

Mice with Type 1 diabetes, a form of the disease in which the bodys immune system destroys cells that secrete insulin, were free of illness after scientists shut down the immune attack, reprogrammed the errant cells and coaxed the growth of healthy, new insulin-producers. The study was published today in the journal Science Translational Medicine.

About 3 million Americans have Type 1 diabetes, which is usually diagnosed in children, according to the Juvenile Diabetes Research Foundation. The only treatment is insulin injected to replace the bodys naturally-occurring version of the hormone, which is needed to convert blood sugar into energy. The experimental immune system approach appears promising because its the first time diabetes has been cured in mice with advanced disease, said Anita Chong, a medical researcher at the University of Chicago.

Conceptually, each component isnt novel, people have thought about them, but put it together and show it can work? said Chong, who wrote an accompanying editorial to the study. Thats very exciting.

There are many more steps before the treatment will be tested in humans, starting with non-human primate models, she said in a telephone interview.

Type 1 diabetes differs from the more common Type 2 form in that it is an autoimmune disease, in which the immune system kills the cells needed to produce insulin. In Type 2 diabetes, the body produces insulin but cells no longer respond to it.

Diabetics must test their blood sugar several times a day, and sometimes experience hypoglycemia, or dangerously low blood sugar, while they sleep at night.

In the study, the mice were given antibodies to attack two kinds of immune cells that kill the pancreas insulin-producing beta cells. Then the mice had a bone marrow transplant to replenish the vanquished cells. Bone marrow is where blood cells are made, and the transplant let the mice make immune cells that wouldnt attack the beta cells. A treatment with pancreas growth factor spurred creation of new beta cells.

The study was led by Defu Zeng, an endocrinologist at City of Hope medical center in Duarte, California, and funded by the Iacocca Family Foundation, and private donations from Todd and Karen Wanek and the Davis family.

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Immune Cell Therapy Cures Diabetic Mice, Researchers Find

Recommendation and review posted by Bethany Smith

Wed May 9, 2012 3:35pm BST

(Reuters) - Pluristem Therapeutics Inc said a 7-year old girl suffering from a bone marrow disease experienced a reversal of her condition after receiving its experimental stem cell therapy, sending the Israeli company's shares up 32 percent.

The girl, suffering from aplastic bone marrow in which the patient has no blood-forming stem cells, had a significant rise in her red cells, white cells and platelets following an injection of Pluristem's therapy -- PLacental eXpanded cells.

"The results of this unique case indicate that PLX cells may be effective in treating other diseases that affect the bone marrow," Reuven Or, the child's physician at Hadassah Medical Center, was quoted in a statement by Pluristem.

Last September, the company said animal studies showed that the therapy had the potential to treat blood tissue complications related with acute radiation syndrome, commonly called radiation sickness.

Last month, the U.S. health regulators gave a go ahead to the company to start a mid-stage trial of the therapy for treating Intermittent Claudication -- a subset of peripheral artery disease.

Pluristem shares, which have gained 5 percent since receiving the FDA nod for the mid-stage trial, were up 15 percent at $2.70 in morning trade on the Nasdaq. They touched a high of $3.10 earlier.

(Reporting by Esha Dey in Bangalore; Editing by Gopakumar Warrier)

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Pluristem stem cell therapy saves a patient, shares jump

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By Kate Rauch on May 11, 2012

Chronic pain affects an estimated 116 million Americans and costs $635 billion each year in medical treatment and lost productivity.

Aditi Bhargava, PhD

Aditi Bhargava, PhD, associate professor at UCSFs School of Medicine, is using a technique known as RNA interference (RNAi) to develop a gene therapy system that sends specific commands to certain neurons, or nerve cells, telling them to turn off pain, or stop inflammation.

The current treatments for pain dull everything, Bhargava said. You have a little fire in the kitchen, but your only solution is a fire hose that floods the entire house. You put out the fire, but youre affecting the whole house in the process a huge negative side effect.

Likening her method to a Trojan horse, Bhargavas novel therapeutic approach essentially hides the pain-silencing commands, carried by distinct proteins that affect cellular function, inside other proteins which bind only to the troublemaker cells. Once attached, they release their hidden power.

We want to target the small or medium neurons that sense pain, while leaving other neurons unaffected, she said. Were hoping that while you reduce pain, for example, youll still be able to chew or not drool.

The data from her proof-of-concept animal studies look promising, Bhargava said. I believe that this project has tremendous translational potential to turn what we learn into concrete benefits for patients.

Targeted pain and inflammation relief could also be used to treat illnesses, such as Inflammatory Bowel Disease (IBD), an autoimmune condition. This approach has potential to not only minimize unwanted side effects, but save costs, as it sends very small amounts of drug therapies to the targeted cells.

Targeted delivery of drug would reduce the dose required to treat, reduce cost, and most importantly, reduce unwanted side effects.

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Targeted Gene Therapy Offers Relief from Pain and Inflammation

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09-05-2012 19:22 Humanity faces increasing problems around the supply and quality of water. The dual implications of an ever expanding population, combined with the threat of climate change, makes water a precious commodity. Delving deep into the composition of water however, may help its preservation into the future. In this presentation, Professor Chris Saint will share examples from his research where gene technology has been applied to identify and record microorganisms that cause problems in our water supplies. These include blue-green algae and protozoan parasites such as Cryptosporidium. For the first time DNA tests are being developed to rapidly assess the risk that these organisms present to drinking water consumers. Research has also demonstrated that not all bugs in water are bad -- some can be used to breakdown key pollutants, leading to a possibility of using bacteria to clean up our water supplies. Professor Saint will discuss how these discoveries will lead the way in monitoring water quality, and share his thoughts on what the future holds in this area.

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Christopher Saint - Water quality management - it can be in the genes - Knowledge Works - Video

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10-05-2012 04:57 Watch in 1080p or 720p for best experience! I hope you enjoy watching the video. I do not own the music in this video! All rights reserved to DVBBS & Arkasia! Follow Arkasia: Follow DVBBS: Copyright Disclaimer Under Section 107 of the Copyright Act 1976, allowance is made for "fair use" for purposes such as criticism, comment, news reporting, teaching, scholarship, and research. Fair use is a use permitted by copyright statute that might otherwise be infringing. Non-profit, educational or personal use tips the balance in favor of fair use.

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DVBBS - DRVGS ft. Hayley Gene (Arkasia Remix) [Audio React] - Video

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Public release date: 10-May-2012 [ | E-mail | Share ]

Contact: Tracey Peake tracey_peake@ncsu.edu 919-515-6142 North Carolina State University

Imagine being able to control genetic expression by flipping a light switch. Researchers at North Carolina State University are using light-activated molecules to turn gene expression on and off. Their method enables greater precision when studying gene function, and could lead to targeted therapies for diseases like cancer.

Triplex-forming oligonucleotides (TFOs) are commonly used molecules that can prevent gene transcription by binding to double-stranded DNA. NC State chemist Dr. Alex Deiters wanted to find a way to more precisely control TFOs, and by extension, the transcription of certain genes. So Deiters attached a light-activated "cage" to a TFO. When exposed to ultraviolet (UV) light, the cage is removed, and the TFO is free to bind with DNA, inhibiting transcription of the gene of interest.

"In the absence of light, transcription activity is 100 percent," says Deiters. "When we turn on the light, we can take it down to about 25 percent, which is a significant reduction in gene expression."

Additionally, Deiters fine-tuned the process by attaching a caged inhibitor strand to the TFO. In the absence of UV light, the TFO behaves normally, binding to DNA and preventing gene expression. However, when exposed to UV light, the caged inhibitor activates and stops the TFO from binding with DNA, turning gene transcription on.

"We've created a tool that allows for the light-activation of genetic transcription," Deiters says. "By giving researchers greater temporal and spatial control over gene expression, we've expanded their ability to study the behavior of particular genes in whichever environment they choose."

###

The research appears online in ACS Chemical Biology, and was funded by the National Institutes of Health. Deiters worked with NC State graduate students Jeane M. Govan, Rajendra Uprety and James Hemphill and Wake Forest University's Mark O. Lively on the research.

Note to editors: An abstract of the paper follows.

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Researchers use light to switch on gene expression

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ScienceDaily (May 10, 2012) History, science and discovery come together to help family members affected by this syndrome make informed family planning choices.

C5ORF42 was identified as the gene that causes Joubert Syndrome in a number of families in the Lower St. Lawrence region of Quebec where the causal gene had remained unknown since the initial description of the syndrome in 1969. This is what a study in the April issue of The American Journal of Human Genetics reveals. The study was conducted by researchers from the Sainte-Justine University Hospital Research Center and the Centre of Excellence in Neuromics of Universit de Montral (CENUM).

Joubert Syndrome is a condition that affects brain development and manifests itself through delayed psychomotor development, abnormal coordination of eye movements and respiratory abnormalities. Since Dr. Marie Joubert and her colleagues described it for the first time in 1969, a number of related genes have been identified in various populations, but the causal gene of the Quebec form of the syndrome has remained until now unknown.

"No studies had been done to identify the genetic origin of the disease in Quebec, more specifically in the exact area of the Lower St. Lawrence where most cases in Quebec are concentrated," Dr. Jacques Michaud, the study's principal investigator, explained. "This is the first study to present a picture of Joubert syndrome in the Quebec population. It will allow family members affected by the syndrome to assess their children's genetic risks with a simple DNA test."

The finding is interesting, both genetically and historically, since, while Joubert Syndrome is present around the world, genetic strains can vary regionally. Distribution is related to the history of various population groups.

Quebec is no exception. In fact, 6,000 French Canadian settlers from Quebec City and its surroundings settled in the Lower St. Lawrence region about the end of the 17th and beginning of the 18th centuries. The fact that most present day inhabitants of the Lower St. Lawrence region descend from this small group of settlers suggests a genetic founder effects. Indeed, certain founder mutations are transmitted to a large number of descendants, which increases the risk of genetic diseases in offspring.

As a matter of fact, Dr. Michaud's team identified three C5ORF42 mutations that are common to most of the families in the study. In all, seven families that are carriers of the gene were identified in a 400-km area along Route 132.

In the space of about two centuries, the first colonists settled in the Lower St. Lawrence region and from there other families headed out to settle along the river heading east as far as Mont-Joli and then along the Matapedia River. According to Myriam Srour, a doctoral student and co-author of the study, the mutations likely spread in the population along these migration routes.

So far 15 genes that play a role in the expression of the syndrome have been revealed elsewhere in the world. Dr. Michaud and his team will continue their research to better understand the exact function of the gene and the specific effect of each mutation.

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Gene that causes Joubert Syndrome discovered

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Public release date: 10-May-2012 [ | E-mail | Share ]

Contact: William Raillant-Clark w.raillant-clark@umontreal.ca 514-343-7593 University of Montreal

This press release is available in French.

C5ORF42 was identified as the gene that causes Joubert Syndrome in a number of families in the Lower St. Lawrence region of Quebec where the causal gene had remained unknown since the initial description of the syndrome in 1969. This is what a study in the April issue of The American Journal of Human Genetics reveals. The study was conducted by researchers from the Sainte-Justine University Hospital Research Center and the Centre of Excellence in Neuromics of Universit de Montral (CENUM).

Joubert Syndrome is a condition that affects brain development and manifests itself through delayed psychomotor development, abnormal coordination of eye movements and respiratory abnormalities. Since Dr. Marie Joubert and her colleagues described it for the first time in 1969, a number of related genes have been identified in various populations, but the causal gene of the Quebec form of the syndrome has remained until now unknown.

"No studies had been done to identify the genetic origin of the disease in Quebec, more specifically in the exact area of the Lower St. Lawrence where most cases in Quebec are concentrated," Dr. Jacques Michaud, the study's principal investigator, explained. "This is the first study to present a picture of Joubert syndrome in the Quebec population. It will allow family members affected by the syndrome to assess their children's genetic risks with a simple DNA test."

The finding is interesting, both genetically and historically, since, while Joubert Syndrome is present around the world, genetic strains can vary regionally. Distribution is related to the history of various population groups.

Quebec is no exception. In fact, 6,000 French Canadian settlers from Quebec City and its surroundings settled in the Lower St. Lawrence region about the end of the 17th and beginning of the 18th centuries. The fact that most present day inhabitants of the Lower St. Lawrence region descend from this small group of settlers suggests a genetic founder effects. Indeed, certain founder mutations are transmitted to a large number of descendants, which increases the risk of genetic diseases in offspring.

As a matter of fact, Dr. Michaud's team identified three C5ORF42 mutations that are common to most of the families in the study. In all, seven families that are carriers of the gene were identified in a 400-km area along Route 132.

In the space of about two centuries, the first colonists settled in the Lower St. Lawrence region and from there other families headed out to settle along the river heading east as far as Mont-Joli and then along the Matapedia River. According to Myriam Srour, a doctoral student and co-author of the study, the mutations likely spread in the population along these migration routes.

Continued here:
Discovery of a gene that causes Joubert Syndrome

Recommendation and review posted by Bethany Smith

ScienceDaily (May 9, 2012) For the first time, scientists at Fred Hutchinson Cancer Research Center have transplanted brain cancer patients' own gene-modified blood stem cells in order to protect their bone marrow against the toxic side effects of chemotherapy. Initial results of the ongoing, small clinical trial of three patients with glioblastoma showed that two patients survived longer than predicted if they had not been given the transplants, and a third patient remains alive with no disease progression almost three years after treatment.

"We found that patients were able to tolerate the chemotherapy better and without negative side effects after transplantation of the gene-modified stem cells than patients in previous studies who received the same type of chemotherapy without a transplant of gene-modified stem cells," said Hans-Peter Kiem, M.D., senior and corresponding author of the study published in the May 9 issue of Science Translational Medicine.

Kiem, a member of the Clinical Research Division at the Hutchinson Center, said that a major barrier to effective use of chemotherapy to treat cancers like glioblastoma has been the toxicity of chemotherapy drugs to other organs, primarily bone marrow. This results in decreased blood cell counts, increased susceptibility to infections and other side effects. Discontinuing or delaying treatment or reducing the chemotherapy dose is generally required, but that often results in less effective treatment.

In the current study, Kiem and colleagues focused on patients with glioblastoma, an invariably fatal cancer. Many of these patients have a gene called MGMT (O6-methylguanine-DNA-methyltransferase) that is turned on because the promoter for this gene is unmethylated. MGMT is a DNA repair enzyme that counteracts the toxic effect of some chemotherapy agents like temozolomide. Patients with such an unmethylated promoter status have a particularly poor prognosis.

A drug called benzylguanine can block the MGMT gene and make tumor cells sensitive to chemotherapy again, but when given with chemotherapy, the toxic effects of this combination are too much for bone marrow cells, which results in marrow suppression.

By giving bone marrow stem cells P140K, which is a modified version of MGMT, those cells are protected from the toxic effects of benzylguanine and chemotherapy, while the tumor cells are still sensitive to chemotherapy. "P140K can repair the damage caused by chemotherapy and is impervious to the effects of benzylguanine," Kiem said.

"This therapy is analogous to firing at both tumor cells and bone marrow cells, but giving the bone marrow cells protective shields while the tumor cells are unshielded," said Jennifer Adair, Ph.D., who shares first authorship of the study with Brian Beard, Ph.D., both members of Kiem's lab.

The three patients in this study survived an average of 22 months after receiving transplants of their own circulating blood stem cells. One, an Alaskan man, remains alive 34 months after treatment. Median survival for patients with this type of high-risk glioblastoma without a transplant is just over a year.

"Glioblastoma remains one of the most devastating cancers with a median survival of only 12 to 15 months for patients with unmethylated MGMT," said Maciej Mrugala, M.D., the lead neuro oncologist for this study.

As many as 50 percent to 60 percent of glioblastoma patients harbor such chemotherapy-resistant tumors, which makes gene-modified stem cell transplant therapy applicable to a large number of these patients. In addition, there are also other brain tumors such as neuroblastoma or other solid tumors with MGMT-mediated chemo resistance that might benefit from this approach.

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Gene-modified stem cell transplant protects patients from toxic side effects of chemotherapy, study suggests

Recommendation and review posted by Bethany Smith

Study is first to show feasibility and efficacy of a new use for autologous stem cell transplant

Newswise SEATTLE For the first time, scientists at Fred Hutchinson Cancer Research Center have transplanted brain cancer patients own gene-modified blood stem cells in order to protect their bone marrow against the toxic side effects of chemotherapy. Initial results of the ongoing, small clinical trial of three patients with glioblastoma showed that two patients survived longer than predicted if they had not been given the transplants, and a third patient remains alive with no disease progression almost three years after treatment.

We found that patients were able to tolerate the chemotherapy better and without negative side effects after transplantation of the gene-modified stem cells than patients in previous studies who received the same type of chemotherapy without a transplant of gene-modified stem cells, said Hans-Peter Kiem, M.D., senior and corresponding author of the study published in the May 9 issue of Science Translational Medicine.

Kiem, a member of the Clinical Research Division at the Hutchinson Center, said that a major barrier to effective use of chemotherapy to treat cancers like glioblastoma has been the toxicity of chemotherapy drugs to other organs, primarily bone marrow. This results in decreased blood cell counts, increased susceptibility to infections and other side effects. Discontinuing or delaying treatment or reducing the chemotherapy dose is generally required, but that often results in less effective treatment.

In the current study, Kiem and colleagues focused on patients with glioblastoma, an invariably fatal cancer. Many of these patients have a gene called MGMT (O6-methylguanine-DNA-methyltransferase) that is turned on because the promoter for this gene is unmethylated. MGMT is a DNA repair enzyme that counteracts the toxic effect of some chemotherapy agents like temozolomide. Patients with such an unmethylated promoter status have a particularly poor prognosis.

A drug called benzylguanine can block the MGMT gene and make tumor cells sensitive to chemotherapy again, but when given with chemotherapy, the toxic effects of this combination are too much for bone marrow cells, which results in marrow suppression.

By giving bone marrow stem cells P140K, which is a modified version of MGMT, those cells are protected from the toxic effects of benzylguanine and chemotherapy, while the tumor cells are still sensitive to chemotherapy. P140K can repair the damage caused by chemotherapy and is impervious to the effects of benzylguanine, Kiem said.

This therapy is analogous to firing at both tumor cells and bone marrow cells, but giving the bone marrow cells protective shields while the tumor cells are unshielded, said Jennifer Adair, Ph.D., who shares first authorship of the study with Brian Beard, Ph.D., both members of Kiems lab.

The three patients in this study survived an average of 22 months after receiving transplants of their own circulating blood stem cells. One, an Alaskan man, remains alive 34 months after treatment. Median survival for patients with this type of high-risk glioblastoma without a transplant is just over a year.

Glioblastoma remains one of the most devastating cancers with a median survival of only 12 to 15 months for patients with unmethylated MGMT, said Maciej Mrugala, M.D., the lead neuro oncologist for this study.

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Transplanted Gene-Modified Blood Stem Cells Protect Brain Cancer Patients From Toxic Side Effects of Chemotherapy

Recommendation and review posted by Bethany Smith

Public release date: 9-May-2012 [ | E-mail | Share ]

Contact: Dean Forbes dforbes@fhcrc.org 206-667-2896 Fred Hutchinson Cancer Research Center

SEATTLE For the first time, scientists at Fred Hutchinson Cancer Research Center have transplanted brain cancer patients' own gene-modified blood stem cells in order to protect their bone marrow against the toxic side effects of chemotherapy. Initial results of the ongoing, small clinical trial of three patients with glioblastoma showed that two patients survived longer than predicted if they had not been given the transplants, and a third patient remains alive with no disease progression almost three years after treatment.

"We found that patients were able to tolerate the chemotherapy better and without negative side effects after transplantation of the gene-modified stem cells than patients in previous studies who received the same type of chemotherapy without a transplant of gene-modified stem cells," said Hans-Peter Kiem, M.D., senior and corresponding author of the study published in the May 9 issue of Science Translational Medicine.

Kiem, a member of the Clinical Research Division at the Hutchinson Center, said that a major barrier to effective use of chemotherapy to treat cancers like glioblastoma has been the toxicity of chemotherapy drugs to other organs, primarily bone marrow. This results in decreased blood cell counts, increased susceptibility to infections and other side effects. Discontinuing or delaying treatment or reducing the chemotherapy dose is generally required, but that often results in less effective treatment.

In the current study, Kiem and colleagues focused on patients with glioblastoma, an invariably fatal cancer. Many of these patients have a gene called MGMT (O6-methylguanine-DNA-methyltransferase) that is turned on because the promoter for this gene is unmethylated. MGMT is a DNA repair enzyme that counteracts the toxic effect of some chemotherapy agents like temozolomide. Patients with such an unmethylated promoter status have a particularly poor prognosis.

A drug called benzylguanine can block the MGMT gene and make tumor cells sensitive to chemotherapy again, but when given with chemotherapy, the toxic effects of this combination are too much for bone marrow cells, which results in marrow suppression.

By giving bone marrow stem cells P140K, which is a modified version of MGMT, those cells are protected from the toxic effects of benzylguanine and chemotherapy, while the tumor cells are still sensitive to chemotherapy. "P140K can repair the damage caused by chemotherapy and is impervious to the effects of benzylguanine," Kiem said.

"This therapy is analogous to firing at both tumor cells and bone marrow cells, but giving the bone marrow cells protective shields while the tumor cells are unshielded," said Jennifer Adair, Ph.D., who shares first authorship of the study with Brian Beard, Ph.D., both members of Kiem's lab.

The three patients in this study survived an average of 22 months after receiving transplants of their own circulating blood stem cells. One, an Alaskan man, remains alive 34 months after treatment. Median survival for patients with this type of high-risk glioblastoma without a transplant is just over a year.

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Gene-modified stem cell transplant protects patients from toxic side effects of chemotherapy

Recommendation and review posted by Bethany Smith

Public release date: 9-May-2012 [ | E-mail | Share ]

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

New Rochelle, NY, May 9, 2012Disorders of consciousness such as coma or a vegetative state caused by severe brain injury are poorly understood and their diagnosis has relied mainly on patient responses and measures of brain activity. However, new functional and imaging-based diagnostic tests that measure communication and signaling between different brain regions may provide valuable information about the potential for consciousness in patients unable to communicate. These innovative approaches are described and compared in a Review article in the groundbreaking neuroscience journal Brain Connectivity, a bimonthly peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available free on the Brain Connectivity website at http://www.liebertpub.com/brain.

Mlanie Boly and coauthors from University of Lige (Belgium), University of Milan (Italy), and University College London (UK) compare the benefits and limitations of three methods for studying the dynamics of brain communication and connectivity in response to internal and external stimulation: functional magnetic resonance imaging f(MRI); transcranial magnetic stimulation (TMS) combined with electroencephalograpy (EEG); and response to neuronal perturbation, measuring, for example, sensory evoked potentials (ERP). They report their findings and propose future research directions in the article "Brain Connectivity in Disorders of Consciousness."

"In recent years, there has been a tremendous interest in gaining a better understanding of the various disorders of consciousness. A variety of methods including fMRI and PET have been used to study these disorders," says Bharat Biswal, PhD, Co-Editor-in-Chief of Brain Connectivity and Associate Professor, University of Medicine and Dentistry of New Jersey. "This article provides a comprehensive analysis using three new and innovative methods to study disorders of consciousness."

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About the Journal

Brain Connectivity is the journal of record for researchers and clinicians interested in all aspects of brain connectivity. The Journal is under the leadership of Founding and Co-Editors-in-Chief Christopher Pawela, PhD, Assistant Professor, Medical College of Wisconsin, and Bharat Biswal, PhD. It includes original peer-reviewed papers, review articles, point-counterpoint discussions on controversies in the field, and a product/technology review section. To ensure that scientific findings are rapidly disseminated, articles are published Instant Online within 72 hours of acceptance, with fully typeset, fast-track publication within 4 weeks. Tables of content and a sample issue may be viewed on the Brain Connectivity website at http://www.liebertpub.com/brain.

About the Publisher

Mary Ann Liebert, Inc. 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, Human Gene Therapy and HGT Methods, and Rejuvenation Research. 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, newsmagazines, and books is available on the Mary Ann Liebert, Inc. website at http://www.liebertpub.com.

Link:
Can new diagnostic approaches help assess brain function in unconscious, brain-injured patients?

Recommendation and review posted by Bethany Smith

Hematoxylin and eosin (H&E) staining of sections of wild-type (top row) and H1 triple-knockout (bottom row) embryoid bodies. After 14 days in rotary suspension culture, the wild-type embryoid bodies showed more differentiated morphologies with cysts forming (black arrows) and the knockout embryoid bodies failed to form cavities (far right). (Credit: Yuhong Fan)

(Phys.org) -- New research findings show that embryonic stem cells unable to fully compact the DNA inside them cannot complete their primary task: differentiation into specific cell types that give rise to the various types of tissues and structures in the body.

Researchers from the Georgia Institute of Technology and Emory University found that chromatin compaction is required for proper embryonic stem cell differentiation to occur. Chromatin, which is composed of histone proteins and DNA, packages DNA into a smaller volume so that it fits inside a cell.

A study published on May 10, 2012 in the journal PLoS Genetics found that embryonic stem cells lacking several histone H1 subtypes and exhibiting reduced chromatin compaction suffered from impaired differentiation under multiple scenarios and demonstrated inefficiency in silencing genes that must be suppressed to induce differentiation.

While researchers have observed that embryonic stem cells exhibit a relaxed, open chromatin structure and differentiated cells exhibit a compact chromatin structure, our study is the first to show that this compaction is not a mere consequence of the differentiation process but is instead a necessity for differentiation to proceed normally, said Yuhong Fan, an assistant professor in the Georgia Tech School of Biology.

Fan and Todd McDevitt, an associate professor in the Wallace H. Coulter Department of Biomedical Engineering at Georgia Tech and Emory University, led the study with assistance from Georgia Tech graduate students Yunzhe Zhang and Kaixiang Cao, research technician Marissa Cooke, and postdoctoral fellow Shiraj Panjwani.

The work was supported by the National Institutes of Healths National Institute of General Medical Sciences (NIGMS), the National Science Foundation, a Georgia Cancer Coalition Distinguished Scholar Award, and a Johnson & Johnson/Georgia Tech Healthcare Innovation Award.

Enlarge

Phase contrast images showing that H1 triple-knockout (bottom) embryonic stem cells were unable to adequately form neurites and neural networks compared to wild-type embryonic stem cells (top). (Click image for high-resolution version. Credit: Yuhong Fan)

Enlarge

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Genetic packing: Successful stem cell differentiation requires DNA compaction, study finds

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Public release date: 9-May-2012 [ | E-mail | Share ]

Contact: Nicole Davis ndavis@broadinstitute.org 617-714-7152 Broad Institute of MIT and Harvard

Melanoma the deadliest and most aggressive form of skin cancer has long been linked to time spent in the sun. Now a team led by scientists from the Broad Institute and Dana-Farber Cancer Institute has sequenced the whole genomes of 25 metastatic melanoma tumors, confirming the role of chronic sun exposure and revealing new genetic changes important in tumor formation.

In an article published online May 9 in Nature, the authors provide the first high-resolution view of the genomic landscape of human melanoma tumors. Previous genetic analyses have focused on the exomes of many types of cancer tumors, concentrating on the tiny fraction of the genome that provides the genetic code for producing proteins. Whole genomes contain a wealth of genetic information, and by sequencing and analyzing 25 metastatic melanoma tumors a significant technical and computational feat scientists can learn vastly more about the variety of genetic alterations that matter in melanoma.

"Sequencing the whole genome certainly adds a richness of discovery that can't be fully captured with a whole exome," said Levi A. Garraway, a senior associate member of the Broad Institute, an associate professor at Dana-Farber Cancer Institute and Harvard Medical School, and co-senior author of the paper.

"By looking across the entire genome you can more accurately determine the background mutation rate and the different classes of mutations, and more confidently describe the pattern of ultraviolet-induced mutagenesis in melanoma," said Michael F. Berger, co-first author of the paper. He worked in the Broad's cancer genome analysis group and with Garraway as a research scientist and computational biologist before moving to Memorial Sloan-Kettering Cancer Center.

When the scientists explored the whole genome data generated and analyzed at the Broad, they found that the rates of genetic mutations rose along with chronic sun exposure in patients, confirming the role of sun damage in disease development.

"Whole-genome analysis of human melanoma tumors shows for the first time the existence of many structural rearrangements in this tumor type," said Lynda Chin, a senior associate member of the Broad and co-senior author of the paper. Formerly at Dana-Farber and Harvard Medical School, she is now chair of the Department of Genomic Medicine at the University of Texas MD Anderson Cancer Center.

As expected, the scientists detected known BRAF and NRAS mutations in 24 of the 25 tumors. Both genes are involved in sending signals important in cell growth.

One other gene leaped out: PREX2, previously implicated in breast cancer for blocking a tumor-suppressor pathway, was altered in 44 percent of patients. In a larger validation cohort of 107 tumors, the frequency of the mutation was 14 percent.

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New under the sun: Recurrent genetic mutations in melanoma

Recommendation and review posted by Bethany Smith

Public release date: 10-May-2012 [ | E-mail | Share ]

Contact: Dr. Hilary Glover hilary.glover@biomedcentral.com 44-020-319-22370 BioMed Central

Chemotherapy is a major first line defense against breast cancer. However a patient's response is often variable and unpredictable. A study published in BioMed Central's open access journal BMC Medical Genomics shows that 'gene expression signatures' for TOP2A and -tubulin can be used to predict the outcome of chemotherapy.

The goal of personalized medicine in cancer treatment is to target therapy to the characteristics of the individual tumor. For example Herceptin treatment is of most benefit to patients whose cancer is driven by HER2 and antiestrogens benefit patients whose breast cancer is hormonally driven. Gene signatures are increasingly available for different cancer types and can be used to predict patient prognosis.

Researchers from McMaster University, in association with the Juravinski Hospital and Cancer Center, analyzed the expression of the enzyme TOP2A (DNA topoisomerase) and -tubulin, which are the targets of commonly used chemotherapy drugs (anthracycline and taxane) in hundreds of breast tumors. Combining the results from the tumor samples analyses allowed the researchers to build gene expression 'signatures' that measure the susceptibility of tumor cells to chemotherapy.

Both of the 'signatures' were separately able to predict which patients achieved a complete response (where invasive or metastatic cancer could no longer be detected) and together the two indices together were even more accurate at predicting response to chemotherapy.

Prof John Hassell, who led this study, commented, " Our results clearly demonstrate the practicality of using gene expression to personalize chemotherapy treatment for breast cancer patients. Identifying patients who will not benefit from a specific treatment means that they can be moved to a different treatment plan, and the earlier appropriate treatment is started the more likely it is that the patients will benefit from it."

###

Media Contact Dr Hilary Glover Scientific Press Officer, BioMed Central Tel: +44 (0) 20 3192 2370 Mob: +44 (0) 778 698 1967 Email: hilary.glover@biomedcentral.com

Notes to Editors

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Genetic predictor of breast cancer response to chemotherapy

Recommendation and review posted by Bethany Smith

By Sean Williams | More Articles May 9, 2012 |

Although we don't believe in timing the market or panicking over market movements, we do like to keep an eye on big changes -- just in case they're material to our investing thesis.

What: Shares of biotech company Seattle Genetics (Nasdaq: SGEN) have had a wild ride this morning following its first-quarter earnings results. After being down 10% early in the trading session, shares are up more than 2% as of this writing.

So what: For the quarter, Seattle Genetics reported a near-quadrupling in sales to $48.2 million as the company sold $34.5 million worth of its cancer drug Adcetris, which was approved by the Food and Drug Administration in August for the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Its quarterly loss came in at $0.11 per share. Although the loss met Wall Street's estimates, sales estimates for Adcetris fell about $3 million shy of the consensus. For the year, Seattle Genetics forecast Adcetris sales of $140 million-$150 million and collaboration/licensing revenue of $55 million-$65 million.

Now what: Despite the sales miss, RBC Capital told investors this morning that any dip in Seattle Genetics shares is a buying opportunity, as it expects the company to report positive data at the ASCO conference. That may be partly responsible for the strength in its share price since it opened significantly lower this morning. As for me, I see Seattle Genetics as largely range-bound until it can produce that elusive quarterly profit.

Craving more input? Start by adding Seattle Genetics to your free and personalized watchlist so you can keep up on the latest news with the company.

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Why Seattle Genetics Shares Dropped Then Rallied

Recommendation and review posted by Bethany Smith

LOS ANGELES--(BUSINESS WIRE)--

Response Genetics Inc. (Nasdaq:RGDX - News), (the Company), a company focused on the development and sale of molecular diagnostic tests for cancer, today announced its consolidated financial results for the first quarter ended March 31, 2012.

Total revenues for the quarter ended March 31, 2012 were $4.0 million, compared to $5.9 million for the quarter ended March 31, 2011 was largely as a result of the expected decrease in pharmaceutical client revenue. The Companys ResponseDX revenue decreased slightly to $3.0 million for the quarter ended March 31, 2012, compared to $3.1 million for the quarter ended March 31, 2011.

The Companys first quarter 2012 net loss increased compared to the first quarter of 2011, while the sequential net loss decreased for the quarter ended March 31, 2012. Net loss for the quarter ended March 31, 2012 was $3.1 million, compared with a net loss of $0.3 million for the quarter ended March 31, 2011 and net loss of $3.9 million for the quarter ended December 31, 2011.

Cash and cash equivalents at March 31, 2012, were $5.7 million, compared to $1.7 million at December 31, 2011.

In the first quarter of 2012 we accomplished what needed to be done first we strengthened our balance sheet when we raised $7.8 million of cash, said Thomas Bologna, the Companys recently appointed Chairman & Chief Executive Officer. We also began implementing programs to put our company on the right track and took action to recover from the transition that the Company faced in 201l. While we appreciate that it will take time to achieve the results that we fully expect to deliver to our shareholders, we believe we are making good progress on what needs to be done and putting the team in place to make it happen. We believe our company is in the right space and we have the foundation and wherewithal to capitalize on our strengths and the opportunities in front of us.

Excluding cost of revenue, total operating expenses for the first quarter were $4.4 million, compared to $3.5 million for the same period last year. The increase in total operating expenses of $0.9 million was due to an increase in general and administrative expenses of $0.5 million and research and development expenses of $0.4 million.

The increase in general and administrative expenses was a result of an increase of $0.2 million in stock based compensation expense, $0.1 million in bad debt expense, $0.1 million in consulting expense, $0.1 million of equipment/maintenance expense and $0.1 million in legal fees, offset by a decrease in business tax of $0.1 million.

The increase in research and development expenses was due to an increase in personnel expenses and associated laboratory supplies and reagents related to increased research and development activity.

CONFERENCE CALL DETAILS

Link:
Response Genetics, Inc. Announces First Quarter Financial Results

Recommendation and review posted by Bethany Smith

BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (Nasdaq: SGEN - News) today announced that interim results from an investigator-sponsored phase II clinical trial of ADCETRIS (brentuximab vedotin) in patients with relapsed cutaneous T-cell lymphoma (CTCL) were presented at the Society for Investigative Dermatology annual meeting being held May 9-12, 2012 in Raleigh, NC. ADCETRIS is an antibody-drug conjugate (ADC) directed to CD30. ADCETRIS has not been approved for use in CTCL.

The trial enrolled CTCL patients with mycosis fungoides (MF) or Sezary syndrome. At the time of data analysis, 17 patients had been enrolled, including 16 with MF and one with Sezary syndrome. Patients had received a median of six prior therapies, including a median of four prior systemic therapies. The primary endpoint of the trial is clinical response rate. Secondary endpoints include correlation of clinical response with CD30 expression levels, duration of response, progression-free survival and safety. The study is led by principal investigator Dr. Youn H. Kim, Professor, Department of Dermatology, and Director, Multidisciplinary Cutaneous Lymphoma Program at Stanford University School of Medicine in Stanford, CA. Key findings include:

This is the second data set reported with ADCETRIS in CTCL patients. At the T-Cell Lymphoma Forum in January 2012, interim data were presented from a phase II investigator-sponsored trial in CD30-positive CTCL patients, including lymphomatoid papulosis, primary cutaneous anaplastic large cell lymphoma (pcALCL) or MF. In the trial, which is being conducted by Dr. Madeleine Duvic at The University of Texas MD Anderson Cancer Center, 11 of 17 evaluable patients (65 percent) achieved an objective response, including seven complete remissions (CRs) and four partial remissions (PRs). The most common adverse events were Grade 1, including diarrhea, chest tightness, alopecia, nausea, elevated liver enzymes and peripheral neuropathy.

Seattle Genetics and Millennium: The Takeda Oncology Company recently initiated a randomized phase III clinical trial of ADCETRIS for relapsed CD30-positive CTCL patients. The trial will assess ADCETRIS versus investigators choice of methotrexate or bexarotene in patients with CD30-positive CTCL, including those with pcALCL or MF. The primary endpoint of the study is overall response rate lasting at least 4 months. Approximately 124 patients will be enrolled in the pivotal trial. The phase III trial is being conducted under a Special Protocol Assessment agreement from the U.S. Food and Drug Administration (FDA). The study also received European Medicines Agency scientific advice.

About CTCL

Lymphoma is a general term for a group of cancers that originate in the lymphatic system. There are two major categories of lymphoma: Hodgkin lymphoma and non-Hodgkin lymphoma. Cutaneous lymphomas are a category of non-Hodgkin lymphomas that primarily involve the skin. According to the Cutaneous Lymphoma Foundation, CTCL is the most common type of cutaneous lymphoma and typically presents with red, scaly patches or thickened plaques of skin that often mimic eczema or chronic dermatitis. Progression from limited skin involvement is variable and may be accompanied by tumor formation, ulceration and exfoliation, complicated by itching and infections. Advanced stages are defined by involvement of lymph nodes, peripheral blood and internal organs. According to published literature, up to 50 percent of CTCL patients lesions express CD30.

About ADCETRIS

ADCETRIS (brentuximab vedotin) is an ADC comprising an anti-CD30 monoclonal antibody attached by a protease-cleavable linker to a microtubule disrupting agent, monomethyl auristatin E (MMAE), utilizing Seattle Genetics proprietary technology. The ADC employs a linker system that is designed to be stable in the bloodstream but to release MMAE upon internalization into CD30-expressing tumor cells.

ADCETRIS (brentuximab vedotin) received accelerated approval from the U.S. Food and Drug Administration for two indications: (1) the treatment of patients with Hodgkin lymphoma after failure of autologous stem cell transplant (ASCT) or after failure of at least two prior multi-agent chemotherapy regimens in patients who are not ASCT candidates, and (2) the treatment of patients with systemic anaplastic large cell lymphoma (sALCL) after failure of at least one prior multi-agent chemotherapy regimen. The indications for ADCETRIS are based on response rate. There are no data available demonstrating improvement in patient-reported outcomes or survival with ADCETRIS.

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Seattle Genetics Announces Data from Investigator Trial of ADCETRIS™ in Relapsed Cutaneous T-Cell Lymphoma

Recommendation and review posted by Bethany Smith

AMES, Iowa, May 10, 2012 (GLOBE NEWSWIRE) -- NewLink Genetics Corporation (Nasdaq:NLNK - News), a biopharmaceutical company focused on discovering, developing and commercializing cancer therapeutics, today reported consolidated financial results for the first quarter of 2012, and provided an update on the progress of its clinical development programs.

"During the first quarter of 2012 we continued to advance our pivotal trial in pancreatic cancer and are also moving forward on a number of other HyperAcute immunotherapy development programs including those to treat melanoma and lung and kidney cancers," commented Dr. Charles Link, Chairman and Chief Executive Officer of NewLink. "We also made strides in our IDO pathway inhibitor program and are looking forward to presenting new data for a number of these programs at both DDW and ASCO. We believe that the receipt of patent allowances in both of our core programs will also facilitate our business development activities."

First quarter 2012 Financial Results

Financial Guidance

NewLink is maintaining its financial guidance and continues to expect to end 2012 with about $20 million in cash, cash equivalents and marketable securities. NewLink continues to anticipate that this capital should allow it to fund its operations through 2013 based on its current operating plans.

2012 Key Accomplishments to Date

Upcoming Activities

NewLink expects to present at the following investor conferences:

NewLink expects to present at the following oncology and pharmacology meetings:

About NewLink Genetics Corporation

Original post:
NewLink Genetics Corporation Reports First Quarter 2012 Financial Results

Recommendation and review posted by Bethany Smith

BOTHELL, Wash.--(BUSINESS WIRE)--

Seattle Genetics, Inc. (NASDAQ:SGEN - News) announced today that management will present at the Bank of America Merrill Lynch 2012 Health Care Conference on Tuesday, May 15, 2012 at 1:00 p.m. Pacific Time. The presentation will be webcast live and available for replay from Seattle Genetics website at http://www.seattlegenetics.com in the Investors and News section.

About Seattle Genetics

Seattle Genetics is a biotechnology company focused on the development and commercialization of monoclonal antibody-based therapies for the treatment of cancer. The U.S. Food and Drug Administration granted accelerated approval of ADCETRIS in August 2011 for two indications. ADCETRIS is being developed in collaboration with Millennium: The Takeda Oncology Company. In addition, Seattle Genetics has three other clinical-stage antibody-drug conjugate (ADC) programs: SGN-75, ASG-5ME and ASG-22ME. Seattle Genetics has collaborations for its ADC technology with a number of leading biotechnology and pharmaceutical companies, including Abbott, Bayer, Celldex Therapeutics, Daiichi Sankyo, Genentech, GlaxoSmithKline, Millennium, Pfizer and Progenics, as well as ADC co-development agreements with Agensys, an affiliate of Astellas, and Genmab. More information can be found at http://www.seattlegenetics.com.

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Seattle Genetics to Present at Bank of America Merrill Lynch Health Care Conference

Recommendation and review posted by Bethany Smith

WALTHAM, Mass.--(BUSINESS WIRE)--

Interleukin Genetics,Inc. (OTCQB: ILIU.PK - News) today announced financial and operational results for the first quarter ended March 31, 2012.

Total revenue for the three months ended March 31, 2012 was $678,000, compared to $719,000 for the same period in the prior year. The decrease was attributable to lower genetic test revenue.

Research and development expenses were $446,000 for the three months ended March 31, 2012, compared to $305,000 for the same period in the prior year. The Company continues its work in its weight management and periodontal disease programs.

Selling, general, and administrative expenses were $1.1 million for the three months ended March 31, 2012, compared to $1.2 million for the same period in the prior year. The decrease was primarily attributable to decreased corporate professional fees and patent-related legal fees offset in part by increased compensation, consulting and sales commissions paid to Amway.

The Company reported a net loss of $1.4 million, or $(0.04) per basic and diluted common share, for the first quarter of 2012, compared to a loss of $1.3 million, or $(0.03) per basic and diluted share, for the same period in the prior year. On March 31, 2012, the Company had cash and cash equivalents of $732,000 and had $1.3 million available under its credit facility with Pyxis Innovations, Inc.

The Company expects that its current and anticipated financial resources, including the $1.3 million available as of March 31, 2012 under the credit facility, which was borrowed on April 13, 2012, are adequate to maintain current and planned operations at least through June 30, 2012. The Companys independent registered public accounting firm has included an explanatory paragraph in their opinion in connection with the 2011 audit, relating to the Company's ability to continue as a going concern.

While recognized genetic test revenue this quarter was lower than last years for this corresponding quarter, our deferred revenue increased by over 35% or more than $300,000 in this quarter indicating that unit test sales are continuing to grow nicely, said Lewis H. Bender, Chief Executive Officer of Interleukin Genetics. In addition, enrollment in our clinical study in collaboration with Renaissance Health and the University of Michigan to demonstrate the utility of using our PST genetic test in the management of dental patients was completed and we successfully delivered 5,186 genotypes to the University thereby completing our portion of the program.

Conference Call and Webcast Information

Interleukin Genetics will host a live conference call and webcast today at 4:30 p.m. EDT to review the Companys new business developments and first quarter financial results. To access the live call, dial 877-324-1976 (domestic) or 631-291-4550 (international). The live webcast and replay access will be available on the Investors section of the Companys Website at: http://www.ilgenetics.com.

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Interleukin Genetics Reports First Quarter 2012 Financial Results

Recommendation and review posted by Bethany Smith

The study involved painstaking molecular analysis of blood samples taken annually from the patients, who participated in separate studies begun in 2000, 2002, and 2004.

"We were astonished that we could detect the modified cells for so long. It's a relatively small number of patients, but more than 500 years of patient data," said University of Pennsylvania pathologist Bruce Levine, a leader of the research. "But it's difficult to separate with certainty the effectiveness of this treatment from the antiretrovirals."

Gene therapy harnesses the insidious ability of viruses to slip their DNA into the cells they infect. By neutralizing a virus and then using it as a "vector" to insert DNA that is helpful rather than harmful, gene therapy can theoretically treat ailments ranging from arthritis to infections and cancer.

Levine, his Penn colleague Carl June, and their team have tested a variety of ways to outwit HIV with gene therapy. Their approach has focused on T cells, which are the big guns of the immune system but also the cells that HIV infects. The researchers took some of the patients' T cells and inserted a gene that makes them better at recognizing and killing HIV-infected cells. Then these super-T cells were multiplied using growth-stimulation technology and put back into the patient.

Over the years, many other research groups have tried using modified T cells, but the patient's immune system perceived them as invaders and wiped them out, sometimes within hours.

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Penn researchers report a gene-therapy success

Recommendation and review posted by Bethany Smith

Dr. Julio C. Voltarelli, who made a significant impact in cell transplantation, dies at 63

Distinguished Brazilian professor pioneered bone marrow transplantation

Newswise Tampa, Fla. (May. 9th , 2012) Julio C. Voltarelli, MD, PhD, professor at the Ribeiro Preto School of Medicine at the University of So Paulo, Brazil, died March 21, 2012 at the age of 63. Dr. Voltarelli, who was on the editorial board of the Cell Transplantation journal, published by Cognizant Communication Corporation, and an important factor in the journals success, was a distinguished stem cell researcher and head of the bone marrow transplantation unit at the Ribeiro Preto School of Medicine.

Dr. Voltarelli had a significant impact on Brazilian stem cell transplantation science, said Dr. Maria C. O. Rodrigues, Dr. Voltarellis longtime colleague. He was driven to bring the benefits of the newest cellular therapies to those with ALS, MS and type 1 diabetes. His efforts and dedication will be greatly missed.

Dr. Voltarelli, a graduate of the Ribeiro Preto School of Medicine, served post-doctoral fellowships at the University of California San Francisco, the Fred Hutchinson Cancer Research Center in Seattle, and the Scripps Research Institute in San Diego. He returned to Brazil in 1992 and started a highly ranked bone marrow transplantation program at the Ribeiro Preto School of Medicine. In 2002, Dr. Voltarelli initiated the schools research efforts in stem cell transplantation for autoimmune diseases, later focusing on diabetes, graft-versus-host disease and sickle cell anemia.

At the time of his death, Dr. Voltarelli, in addition to serving as head of the bone marrow transplantation unit, also served as research coordinator for the Center for Cellular Therapy at the So Paulo Research Foundation and the National Institute of Science and Technology in Stem Cells and Cell Therapy. He was recently elected president of the Brazilian Society of Bone Marrow Transplantation.

His publications included the first books on stem cell transplantation and clinical immunology written in Portuguese. He also founded the Brazilian Society of Stem Cell Transplantation.

His colleagues in Brazil called his lifelong contributions priceless and remembered him for his leadership skills, vision, and sense of humor.

# The Coeditor-in-chiefs for CELL TRANSPLANTATION are at the Center for Neuropsychiatry, China Medical University Hospital, TaiChung, Taiwan, and the Diabetes Research Institute, University of Miami Miller School of Medicine. Contact, Shinn-Zong Lin, MD, PhD at shinnzong@yahoo.com.tw or Camillo Ricordi, MD at ricordi@miami.edu or David Eve, PhD at celltransplantation@gmail.com #

News release by Florida Science Communications http://www.sciencescribe.net

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Julio C. Voltarelli, Pioneer in Cell Transplantation, Dies at 63

Recommendation and review posted by simmons

ScienceDaily (May 10, 2012) This summer's action film, "The Amazing Spider-Man," is another match-up between the superhero and his nemesis the Lizard. Moviegoers and comic book fans alike will recall that the villain, AKA Dr. Curt Connors, was a surgeon who, after losing an arm, experimented with cell generation and reptilian DNA and was eventually able to grow back his missing limb.

The latest issue of the journal Physiology contains a review article that looks at possible routes that unlock cellular regeneration in general, and the principles by which hair and feathers regenerate themselves in particular.

The authors apply what is currently known about regenerative biology to the emerging field of regenerative medicine, which is being transformed from fantasy to reality.

Review Article

While the concept of regenerative medicine is relatively new, animals are well known to remake their hair and feathers regularly by normal regenerative physiological processes. In their review, the authors focus on (1) how extrafollicular environments can regulate hair and feather stem cell activities and (2) how different configurations of stem cells can shape organ forms in different body regions to fulfill changing physiological needs.

The review outlines previous research on the role of normal regeneration of hair and feathers throughout the lifespan of various birds and mammals. The researchers include what is currently known about the mechanism behind this re-growth, as well as what gaps still exist in the knowledge base and remain ripe for future research.

The review examines dozens of papers on normal "physiological regeneration" -- the re-growth that happens over the course of an animal's life and not in response to an injury. This regeneration takes place to accommodate different stages in an animal's life (e.g., replacing downy chick feathers with an adult chicken's, or replacing the fine facial hair of a young boy with the budding beard of an adolescent), or in response to various environmental conditions (e.g., cats shedding a thick winter coat in the summer heat but re-growing it when the seasons change again, or snowshoe hares switching from brown in the summer to white in the winter for camouflage).

These changes seem to respond both to internal cues such as physiology of the hair follicle itself, or external cues such as the environment, but the mechanisms behind these normal alterations are largely unknown. Stem cells inside the follicle prompt hair and feather regeneration, but researchers are still unsure how to guide those cells to form the shape, size, and orientation of these "skin appendages" so that controlled re-growth is possible. Additionally, scientists are still unsure how to re-grow hair on skin in people after severe injuries that lead to scar tissue.

Importance of the Findings

The reviewed studies suggest that while researchers are making headway in understanding how and why hair and feathers regenerate after normal loss or in response to different life stages, much still remains unknown. This missing knowledge could hold valuable clues to learning how to regenerate much more complicated and valuable structures after loss to injury, such as fingers and toes.

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Regenerative medicine: Could the ways animals regenerate hair and feathers help restore human fingers and toes?

Recommendation and review posted by simmons

Connie K. Ho for RedOrbit.com

A new study by researchers at the University of California, Los Angeles (UCLA) has discovered two adult stem cell-like subpopulations in adult human skin.

The findings allow for further research to be done in the area of personalized medicine and patient-specific cellular therapies.

The study, using technology from Fibrocell Science, allowed the researchers to identify and confirm two types of cells in human skin cell cultures; the possible source of stem cell-like subpopulations from skin biopsies would be faster to perform, painless, and less invasive than current extractions from adipose tissues and bone marrow.

The research, featured in the inaugural issue of BioResearch Open Access, discusses two subtypes of cells. BioResearch Open Access is a bimonthly, peer-reviewed journal. It features scientific topics like biochemistry, bioengineering, gene therapy, genetics, microbiology, neuroscience, regenerative medicine, stem cells, systems biology, tissue engineering and biomaterials, and virology.

Being able to identify two sub-populations of rare, viable and functional cells that behave like stem cells from within the skin is an important finding because both cell types have the potential to be investigated for diverse clinical applications, commented Dr. James A. Bryne, lead author of the report.

Brynes research, first at Stanford University then at UCLA, focused on reprogramming beginnings of cells from animals and then humans. A graduate of Cambridge University, Bryne studied the intra- and inter-species of epigenetic reprogramming. His work also highlighted how primate embryonic stem cells could be derived from somatic cell nuclear transfers.

The study published in BioResearch Open Access confirmed previous research that identified a rare population of cells in adult human skin that had a marker called stage-specific embryonic antigen 3 (SSEA3). Bryne and his colleagues found that there was an increase in the amount of SSEA3 expressing cells after injury to the human skin. It showed that the SSEA3 biomarker could be used to help identify and isolate cells with tissue-regenerative traits.

Finding these rare adult stem cell-like subpopulations in human skin is an exciting discovery and provides the first step towards purifying and expanding these cells to clinically relevant numbers for application to a variety of potential personalized cellular therapies for osteoarthritis, bone loss, injury and/or damage to human skin as well as many other diseases, remarked Bryne, an Assistant Professor of Molecular and Medical Pharmacology at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

Bryne and his team used Fibrocell technology to collect cells from skin samples, cultured the cells in the lab, and purified them by fluorescence-activated cell sorting (FACS). The FACS tagged suspended cells with fluorescent markers for undifferentiated stem cells. The researchers were able to separate the rare cell subpopulations from other kinds of cells.

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Study Identifies Cell Subtypes For Potential Personalized Cellular Therapies

Recommendation and review posted by simmons