A new technology that reveals cellular gene transcription in greater detail has been developed by Dr. Daniel Kaufmann of the University of Montreal Hospital Research Centre (CRCHUM) and the research team he directed. "This new research tool offers us a more profound view of the immune responses that are involved in a range of diseases, such as HIV infection. At the level of gene transcription, this had been difficult, complex and costly to do with current technologies, such as microscopy," explained the University of Montreal professor.

The technology is known as the "FISH investigation protocol" (Fluorescent in situ hybridization) -- it optimises current flow cytometry processes, resulting in a greater visibility of the transcription of RNA, a key step in the transmission of cellular information. The researchers published their breakthrough in Nature Communications' online edition. Flow cytometry itself enables the simultaneous measurement of hundreds of thousands of cells as they quickly pass through laser beams. This technology dates back to 1934, when it was used to count the cells making up organs and blood, before being developed across the decades to enable the analysis of cells' various physical characteristics. Today, flow cyclometers are standard equipment for immunology and cancer research labs.

However, the tool's major barrier was that it could only be used for the study of proteins, as specific antibodies that recognize these molecules make them visible by marking. Unfortunately, there are many proteins for which no specific antibodies are available, and so it has been impossible to study them with flow cytometry. Moreover, cancer, HIV and other diseases are caused by a problem that precedes cells' creation of proteins -- the deregulation of the transcription of DNA information to the RNA messenger. Classic flow cytometry cannot examine what is happening during this process.

Dr Kaufmann's team worked with Affymetrix, a company, to break through this barrier by applying their technology to a fundamental step in the transmission of genetic information within the cell. The technology, which is now patented, involves carefully mixing chemical reactants by following a two day long handling protocol. Using a standard flow cyclometer, a hybridization oven and a variety of meticulously dosed solutions (which act as microscopic fluorescent probes), the cells can be coaxed to deliver information that has been previously unavailable.

The application of the technology promises to have a huge impact as ultimately it will enable researchers to better understand the mechanisms that cause diseases and to establish the efficacy of the drugs used to treat them. "In principle, our technology can be applied to any species. We can detect a very wide variety of RNA molecules produced by the human body and animals," Dr. Kaufmann explained.

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Technology breakthrough reveals cellular transcription process

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CONFERENCE COVERAGE

The 25th annual meeting of the American Academy of Addiction Psychiatry (AAAP), will feature a symposium titled Pharmacogenetically Driven Treatments Of Drug and Alcohol Dependence on December 4, 2014. The symposium will highlight work of presenters: Dr Henry Kranzler (University of Pennsylvania, Perelman School of Medicine), Dr David Oslin (University of Pennsylvania), and Dr Thomas Kosten (Baylor College of Medicine).

This brief communication will focus on the recently completed randomized, controlled trials by Drs Kranzler and Oslin that studied the utility of pharmacogenetics in predicting treatment outcome for subjects with alcohol use disorders.

Dr Oslin presents the latest in his line of addiction research which has not been published yet. The research investigates usefulness of genetic variation in the gene encoding the -opioid receptor (OPRM1) in predicting treatment response to naltrexone among alcoholics. The research highlights a functional single-nucleotide polymorphism in exon 1 of the OPRM1 gene, rs1799971, also referred to as Asn40Asp (or A118G), which is one of the best-studied functional genetic variants relevant to alcoholism treatment.

The variant G allele is associated with a phenotype characterized by increased alcohol reward and reinforcement in healthy and heavy drinking subjects. In addition, this phenotype has a greater attenuation to alcohol-induced reward and reinforcement (including craving) with the administration of naltrexone. Evidence from clinical trials suggests that the presence of the variant G allele of rs1799971 may predict better treatment response to opioid receptor antagonists such as naltrexone, though findings to date have been inconsistent.1

Another important gene associated with alcohol dependence is the glutamate receptor, ionotropic, kainate 1 (GRIK1) gene that encodes the Gluk1 (GluR5) subunit of the kainate glutamate receptor. One GRIK1 single nucleotide polymorphism (SNP), rs2832407, a C to A transition, was significantly associated with alcohol dependence, with the C allele being more common in subjects with the disorder.2

Building on the importance of this gene, Dr Kranzler presents findings of a published randomized controlled trial (RCT)3 in which a total of 138 heavy drinking participants (men > 24 drinks/week, women > 18 drinks/week) with an alcohol use disorder whose goal was not abstinence, rather to reduce the amount of drinking to safe levels. Subjects in this study were randomized to receiving a maximal topiramate dose of 200 mg or placebo.3 The primary outcome was heavy drinking days per week. Both groups received counseling to reduce drinking, and multiple assessments were done to monitor change in self-reported alcohol related problem, Beck Depression Inventory, and blood work (Kidney and liver functions including gamma-glutamyl transferase [GGT]).

The study found that the topiramate group had fewer heavy drinking days, and subjects in the topiramate group reduced drinking more rapidly compared with placebo. By the end of treatment weeks, subjects in placebo group were five times more likely to experience heavy drinking days compared to treatment group. Also subjects in the medication group had lower GGT levels compared to controls.

What adds to the merit of this study is the pharmacogenetics analysis that was done on the European American subsample, which represents the majority of the sample (83% of medication group, 93% of placebo group). Topiramate in Kranzlers RCT was efficacious only in patients with CC allele of rs2832407, reducing heavy drinking days to on average one drinking day per week compared to three days per week in controls. There was no difference in response between medication and placebo among subjects with the A alleles. The authors conclude that studies with larger sample sizes and studies in samples different that European Americans are needed.

This brief communication highlights the importance of genetic predictors and moderators of treatment research in the field of substance use. The ability to predict response based on pharmacogenetic factors, among others, would allow for more efficacious personalized treatment plans for patients with substance use disorders. Much more translational research is needed before pharmacogentically guided treatments are a mainstay of regular clinical practice. Results to date have been promising, though there have been a number of inconsistent findings. Some of the discrepant findings to date may result from analyses focusing largely on single candidate genes, often only a single variant, while ignoring the effects of variation in other genes that could be affecting treatment response.

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Pharmacogenetics to Predict Treatment Outcome in Substance Use Disorders

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A new study shows that increasing sugar in the diet of male fruit flies for just 1 or 2 days before mating can cause obesity in their offspring through alterations that affect gene expression in the embryo. There is also evidence that a similar system regulates obesity susceptibility in mice and humans. The research, which is published online December 4 in the Cell Press journal Cell, provides insights into how certain metabolic traits are inherited and may help investigators determine whether they can be altered.

Research has shown that various factors that are passed on by parents or are present in the uterine environment can affect offspring's metabolism and body type. Investigators led by Dr. J. Andrew Pospisilik, of the Max Planck Institute of Immunobiology and Epigenetics in Germany, and team member Dr. Anita st, now at Linkoping University in Sweden, sought to understand whether normal fluctuations in a parent's diet might have such an impact on the next generation.

Through mating experiments in Drosophila melanogaster, or fruit flies, the scientists found that dietary interventions in males could change the body composition of offspring, with increased sugar leading to obesity in the next generation. High dietary sugar increased gene expression through epigenetic changes, which affect gene activity without changing the DNA's underlying sequence. "To use computer terms, if our genes are the hardware, our epigenetics is the software that decides how the hardware is used," explains Dr. st. "It turns out that the father's diet reprograms the epigenetic 'software' so that genes needed for fat production are turned on in their sons."

Because epigenetic programs are somewhat plastic, the investigators suspect that it might be possible to reprogram obese epigenetic programs to lean epigenetic programs. "At the moment, we and other researchers are manipulating the epigenetics in early life, but we don't know if it is possible to rewrite an adult program," says Dr. st.

The fruit fly models and experiments that the team designed will be valuable resources for the scientific community. Because the flies reproduce quickly, they can allow investigators to quickly map out the details of how nutrition and other environmental stimuli affect epigenetics and whether or not they can be modulated, both early and later in life.

"It's very early days for our understanding of how parental experiences can stably reprogram offspring physiology, lifelong. The mechanisms mapped here, which seem in some way to be conserved in mouse and man, provide a seed for research that has the potential to profoundly change views and practices in medicine," says Dr. Pospisilik.

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BETHESDA, Md., Dec. 4 (UPI) -- Two is often better than one, but not when it comes to the DNA and RNA that make up the human chromosome. Researchers now believe gene duplication in a specific region, key in the regulation of childhood growth, is responsible for the rare disorder known as gigantism.

"Finding the gene responsible for childhood overgrowth would be very helpful, but the much wider question is what regulates growth," Constantine Stratakis, lead author of the new study, said in a press release.

Gigantism is a rare medical condition whereby children grow rapidly. Those affected typically grow to be abnormally tall; gigantism patients may also have delayed puberty, outsized hands and feet, and double vision.

To locate the offending genes, researchers at the National Institutes of Health used whole-genome analysis to study the DNA of 43 people with gigantism. The chromosomes of those afflicted with the rare disorder were then compared to family members who were born without the defect.

The analysis showed that gene duplication varied among the study participants, but researchers were able to narrow down the offending portion of the X chromosome to a stretch containing four duplicated genes. Scientists determined the gene most likely responsible for gigantism was GPR101.

"We believe GPR101 is a major regulator of growth," Stratakis said.

The gene duplication that causes gigantism results in a malfunctioning pituitary, the pea-sized gland that produces growth hormones. Researchers found activity of GPR101 was up to 1,000 times stronger than normal in children with enlarged and overactive pituitary glands.

The research was published this week in the New England Journal of Medicine.

2014 United Press International, Inc. All Rights Reserved. Any reproduction, republication, redistribution and/or modification of any UPI content is expressly prohibited without UPI's prior written consent.

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Duplication of gene on X chromosome causes gigantism

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Discussion Starters Human Genetic Engineering
Discussion Starters Human Genetic Engineering.

By: Alen Zilic

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Discussion Starters Human Genetic Engineering - Video

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Convergent Evolution - Genetic Engineering [Evolutio]
http://www.beatport.com/release/evolutio/1406055 https://www.facebook.com/pages/Convergent-Evolution/327176334122235.

By: The Psychedelic Muse

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Seoul, South Korea (PRWEB) December 05, 2014

Imagine yourself as a mad scientist on a quest to breed the perfect beast. Thats exactly the premise behind Remimorys latest release D.N.Age.

Set inside a fantasy world, players take on the role of a lost adventurer who finds himself transported to an alternate dimension. In order to get back home, he must search for magical items in forests, deserts, and dungeons with the help of a team of monsters.

D.N.Age strikes a perfect balance between a dungeon-crawler RPG and monster raising simulator with a very unique twist. The upgrade system is unlike anything seen before, based around genetics and DNA manipulation. Players can collect monsters on dungeon raids, then analyze their DNA for specific traits and breed them with other monsters to improve their traits and make them stronger.

The game brings a whole range of customization options including the ability to dress and style your virtual assistant a rather attractive elf who guides you on your quest; a medicine crafting clinic; and a lab to grow special herbs.

Remimory has gone with a premium model, pricing the game at $4.99 USD, to avoid pushy free-to-play monetization strategies. The game can is now available on Google Play and the App Store.

Google Play: https://play.google.com/store/apps/details?id=com.remimory.projectd

App Store: https://itunes.apple.com/ca/app/d.n.age/id941496594?mt=8

For more information contact Curtis File at curtis.file@latisglobal.com.

About Remimory: Remimory is a small, indie game studio based out of Seoul South Korea. They are known for the game Color Symphony, a simple side scrolling RPG for PC. D.N.Age marks the companys foray into the premium mobile sphere.

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Duke University has signed an exclusive licensing agreement with Editas Medicine, a leading genome editing company, for genetic engineering technologies developed in the lab of Charles Gersbach, assistant professor of biomedical engineering. The agreement focuses on Gersbachs work with genome engineering technologies known as CRISPR/Cas9 and TALENs.

Charles Gersbach

The agreement allows broad use of the technology developed in Gersbachs lab for the prevention or treatment of human disease. To this point, Gersbachs most notable work in that field is on Duchenne muscular dystrophy, a genetic disease affecting one in 3,500 newborn males that currently has no approved treatment and causes muscular deterioration, paralysis and eventual death, usually by age 25. Gersbachs work is focused on using gene editing to correct the mutated gene that causes the disease, in contrast to treating the resulting symptoms of the disease. Gersbach has also pioneered the use of both CRISPR/Cas9 and TALEs for turning on genes in a way that could be used to treat degenerative disorders or compensate for genetic defects.

Charlies deep expertise in both genome editing and in this area of biology is a tremendous asset as we begin to understand how to apply genome editing technologies to specific diseases, said Katrine Bosley, chief executive officer of Editas Medicine. Gersbach is also serving as a scientific advisor to Editas.

Editas is a leading genome editing company and part of a transformational new area of healthcaregenomic medicine. The company was founded by the pioneers and world leaders in genome editing bringing specific expertise in CRISPR/Cas9 and TALENs technologies. The companys mission is to translate its proprietary technology into novel solutions to treat a broad range of genetically-driven diseases.

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PUBLIC RELEASE DATE:

4-Dec-2014

Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News @LiebertOnline

New Rochelle, NY, December 4, 2014--Recommendations by physician groups to avoid bedsharing among mothers and their babies are intended to reduce sleep-related infant deaths. But evidence suggests that the risks of bedsharing have been over-emphasized, advice never to bedshare is unrealistic, and avoiding bedsharing may interfere with breastfeeding, according to an article in Breastfeeding Medicine, the official journal of the Academy of Breastfeeding Medicine published by Mary Ann Liebert, Inc., publishers. The article is available free on the Breastfeeding Medicine website at http://online.liebertpub.com/doi/full/10.1089/bfm.2014.0113 until January 4, 2015.

In "Speaking Out on Safe Sleep: Evidence-Based Infant Sleep Recommendations, Melissa Bartick, MD, MSC, Cambridge Health Alliance and Harvard Medical School (Cambridge, MA), and Linda Smith, MPH, IBCLC, Boonshoft School of Medicine, Wright State University (Dayton, OH), discuss the American Academy of Pediatrics' (AAP) recommendations against all bedsharing for sleep, the leading modifiable risk factors for preventing Sudden Infant Death Syndrome (SIDS), and the potential for the AAP's bedsharing recommendations to interfere with the frequency, duration, and exclusivity of breastfeeding.

"The alternatives to feeding an infant in bed, such as on a couch, lounge chair, or rocker are far greater risks for SIDS," says Ruth Lawrence, MD, Editor-in-Chief of Breastfeeding Medicine and Professor of Pediatrics, University of Rochester School of Medicine. "Bed-sharing increases the risk of SIDS when the infant is bottle fed or the mother is obese or impaired by smoking, alcohol, or illicit drugs. These are correctable risks of SIDS. Breastfeeding is protective, and the editors of Breastfeeding Medicine are pleased that the AAP Task Force on SIDS is strongly supporting breastfeeding."

###

About the Journal

Breastfeeding Medicine, the official journal of the Academy of Breastfeeding Medicine, is an authoritative, peer-reviewed, multidisciplinary journal published 10 times per year in print and online. The Journal publishes original scientific papers, reviews, and case studies on a broad spectrum of topics in lactation medicine. It presents evidence-based research advances and explores the immediate and long-term outcomes of breastfeeding, including the epidemiologic, physiologic, and psychological benefits of breastfeeding. Tables of content and a sample issue may be viewed on the Breastfeeding Medicine website at http://www.liebertpub.com/bfm.

About the Publisher

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5-Dec-2014

Contact: Sandy Van sandy@prpacific.com 808-526-1708 Cedars-Sinai Medical Center @cedarssinai

LOS ANGELES (Dec. 4, 2014) - Genetics may play a larger role in causing Lou Gehrig's disease than previously believed, potentially accounting for more than one-third of all cases, according to one of the most comprehensive genetic studies to date of patients who suffer from the condition also known as amyotrophic lateral sclerosis, or ALS.

The study, conducted by investigators at Cedars-Sinai and Washington University in St. Louis, also showed that patients with defects in two or more ALS-associated genes experience disease onset about 10 years earlier than patients with single-gene mutations.

"These findings shed new light on the genetic origins of ALS, especially in patients who had no prior family history of the disease," said Robert H. Baloh, MD, PhD, director of neuromuscular medicine in the Department of Neurology and director of the ALS Program at Cedars-Sinai. Baloh is senior author of the study, published online in Annals of Neurology.

Typically, researchers classify 90 percent of ALS cases as "sporadic," meaning they occur in patients without a family history of the disease. In their study, however, the researchers found a significant degree of genetic involvement in patients with no family history. Examining DNA from 391 individuals, they identified numerous new or very rare ALS gene mutations in such people. Added to the 10 percent of cases already known to be genetic because of family history, the study suggested that more than one-third of all ALS could be genetic in origin.

Baloh said the presence of the new and rare mutations, found among 17 genes already known to be associated with ALS, does not necessarily mean they all cause the disease. But they are considered likely suspects - especially in combination. ALS often is caused by well-known defects in single genes, but recent studies have suggested that some cases could be brought on by the simultaneous occurrence of two or more "lesser" genetic defects. In theory, each mutation alone might be tolerated without initiating disease, but in combination they exceed the threshold required for disease development.

This study strengthens that possibility: Fifteen patients - nine of whom had no previous family history of ALS - had mutations in two or more ALS-associated genes. The research also takes an important next step, showing that multiple genetic defects can influence the way disease manifests in individual patients. Those with mutations in two or more genes had onset about 10 years earlier than those with defects in only one gene.

Matthew B. Harms, MD, assistant professor of neurology at Washington University and co-corresponding author of the article, said that unknown factors still accounted for the majority of ALS cases.

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PUBLIC RELEASE DATE:

5-Dec-2014

Contact: Michael C. Purdy purdym@wustl.edu 314-286-0122 Washington University School of Medicine @WUSTLmed

Genetic mutations may cause more cases of amyotrophic lateral sclerosis (ALS) than scientists previously had realized, according to researchers at Washington University School of Medicine in St. Louis and Cedars-Sinai Medical Center in Los Angeles. The scientists also showed that the number of mutated genes influences the age when the fatal paralyzing disorder first appears.

ALS, also known as Lou Gehrig's disease, destroys the nerve cells that control muscles, leading to loss of mobility, difficulty breathing and swallowing, and eventually paralysis and death. Understanding the many ways genes contribute to ALS helps scientists seek new treatments.

The study appears online in Annals of Neurology.

Scientists have linked mutations in more than 30 genes to ALS. Alone or in combination, mutations in any of these genes can cause the disease in family members who inherit them.

Roughly 90 percent of patients with ALS have no family history of the disease, and their condition is referred to as sporadic ALS. Scientists had thought mutations contributed to barely more than one in every 10 cases of sporadic ALS.

But researchers recently started to suspect that patients with sporadic ALS carry mutations in the 30 genes linked to ALS more often than previously thought. The new study is among the first to prove this suspicion correct.

"To our surprise, we found that 26 percent of sporadic ALS patients had potential mutations in one of the known ALS genes we analyzed," said co-senior author Matthew Harms, MD, assistant professor of neurology at Washington University. "This suggests that mutations may be contributing to significantly more ALS cases."

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Newswise LOS ANGELES (Dec. 4, 2014) Genetics may play a larger role in causing Lou Gehrigs disease than previously believed, potentially accounting for more than one-third of all cases, according to one of the most comprehensive genetic studies to date of patients who suffer from the condition also known as amyotrophic lateral sclerosis, or ALS.

The study, conducted by investigators at Cedars-Sinai and Washington University in St. Louis, also showed that patients with defects in two or more ALS-associated genes experience disease onset about 10 years earlier than patients with single-gene mutations.

These findings shed new light on the genetic origins of ALS, especially in patients who had no prior family history of the disease, said Robert H. Baloh, MD, PhD, director of neuromuscular medicine in the Department of Neurology and director of the ALS Program at Cedars-Sinai. Baloh is senior author of the study, published online in Annals of Neurology.

Typically, researchers classify 90 percent of ALS cases as sporadic, meaning they occur in patients without a family history of the disease. In their study, however, the researchers found a significant degree of genetic involvement in patients with no family history. Examining DNA from 391 individuals, they identified numerous new or very rare ALS gene mutations in such people. Added to the 10 percent of cases already known to be genetic because of family history, the study suggested that more than one-third of all ALS could be genetic in origin.

Baloh said the presence of the new and rare mutations, found among 17 genes already known to be associated with ALS, does not necessarily mean they all cause the disease. But they are considered likely suspects especially in combination. ALS often is caused by well-known defects in single genes, but recent studies have suggested that some cases could be brought on by the simultaneous occurrence of two or more lesser genetic defects. In theory, each mutation alone might be tolerated without initiating disease, but in combination they exceed the threshold required for disease development.

This study strengthens that possibility: Fifteen patients nine of whom had no previous family history of ALS had mutations in two or more ALS-associated genes. The research also takes an important next step, showing that multiple genetic defects can influence the way disease manifests in individual patients. Those with mutations in two or more genes had onset about 10 years earlier than those with defects in only one gene.

Matthew B. Harms, MD, assistant professor of neurology at Washington University and co-corresponding author of the article, said that unknown factors still accounted for the majority of ALS cases.

This tells us that more research is needed to identify other genes that influence ALS risk, and that ultimately, individuals may have more than one gene contributing toward developing disease, Harms said.

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Study Shows More Patients With Lou Gehrig's Disease Have Genetic Origin Than Previously Thought

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The Role of Genetics in Alcoholism
A short video describing the role that genetics can play in alcoholism.-- Created using PowToon -- Free sign up at http://www.powtoon.com/join -- Create animated videos and animated presentations...

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Asymmetrex Stem Cell Medicine

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Posted by Dana Sparks (@danasparks) 3 day(s) ago

Uniting the Global Stem Cell Community

The World Stem Cell Summit, December 3-5 in San Antonio, unites and educates the global stem cell community. With more than 1,200 attendees from more than 40 countries, the annual World Stem Cell Summits interdisciplinary agenda explores disease updates, research directions, cell standardization, regulatory pathways, reimbursements, financing, venture capital and economic development.

Throughout the week, the Mayo Clinic Center for Regenerative Medicine will use social media to connect using the hashtag #WSCS14. At the end of the week, we'll let the tweets, Google+ posts, Flickr photos, Facebook posts and YouTube videos tell the story.

The World Stem Cell Summit includes in-depth programming and more than 200 international speakers, including leaders from theMayo Clinic Center for Regenerative Medicine:

About the World Stem Cell SummitMayo Clinic, The University of Texas Health Science Center at San Antonio, Kyoto University Institute for Integrated Cell-Material Sciences (iCeMS), BioBridge Global, Baylor College of Medicine and the Regenerative Medicine Foundation have joined the Genetics Policy Institute to organize the10th Annual World Stem Cell Summit the largest and most comprehensive multi-track interdisciplinary stem cell conference.

Related LinksMayo Clinic at World Stem Cell Summit 2013Mayo Clinic at World Stem Cell Summit 2012

Regenerative MedicineWorld Stem Cell Summit

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Uniting the Global Stem Cell Community

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Bone Marrow Stem Cell Treatment (BMAC) for Knee Osteoarthritis - Mayo Clinic
Shane Shapiro, M.D., orthopedic physician at Mayo Clinic in Florida, discusses a regenerative medicine clinical research trial to treat knee arthritis, which is the bone marrow stem cell treatment...

By: Mayo Clinic

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Peptide shows great promise for treating spinal cord injury
Case Western Reserve scientists have developed a new chemical compound that shows extraordinary promise in restoring function lost to spinal cord injury. The compound, which the researchers...

By: Thomas Barnes

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MIAMI (PRWEB) December 04, 2014

After a successful first run in Spain last month, Global Stem Cells Group, has announced the decision to take the biotech companys hands-on stem cell training course to additional European cities in 2015. GSCG subsidiary Stem Cell Training, Inc. and Dr. J. Victor Garcia conducted the Adipose Derived Harvesting, Isolation and Re-integration Training Course for medical professionals in Barcelona Nov. 22-23, 2014.

The two-day, hands-on intensive training course was developed for physicians and high-level practitioners to learn techniques in harvesting and reintegrating stem cells derived from adipose tissue and bone marrow. The objective of the training is to bridge the gap between bench science in the laboratory and the doctors office by teaching effective, in-office regenerative medicine techniques.

Global Stem Cells Group will release a schedule of cities and dates for future training classes in upcoming weeks.

For more information, visit the Stem Cell Training, Inc. website, email info(at)stemcelltraining(dot)net, or call 305-224-1858.

About Global Stem Cells Group: Global Stem Cells Group, Inc. is the parent company of six wholly owned operating companies dedicated entirely to stem cell research, training, products and solutions. Founded in 2012, the company combines dedicated researchers, physician and patient educators and solution providers with the shared goal of meeting the growing worldwide need for leading edge stem cell treatments and solutions.

With a singular focus on this exciting new area of medical research, Global Stem Cells Group and its subsidiaries are uniquely positioned to become global leaders in cellular medicine.

Global Stem Cells Groups corporate mission is to make the promise of stem cell medicine a reality for patients around the world. With each of GSCGs six operating companies focused on a separate research-based mission, the result is a global network of state-of-the-art stem cell treatments.

About Stem Cell Training, Inc.:

Stem Cell Training, Inc. is a multi-disciplinary company offering coursework and training in 35 cities worldwide. Coursework offered focuses on minimally invasive techniques for harvesting stem cells from adipose tissue, bone marrow and platelet-rich plasma. By equipping physicians with these techniques, the goal is to enable them to return to their practices, better able to apply these techniques in patient treatments.

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Global Stem Cells Group Hands-on Training Course in Barcelona Heading to Additional Euro Cities in 2015

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PUBLIC RELEASE DATE:

3-Dec-2014

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

HOUSTON - (Dec. 3, 2014) - A novel mechanism - similar to how normal tissue stem cells respond to wounding - might explain why bladder cancer stem cells actively contribute to chemo-resistance after multiple cycles of chemotherapy drug treatment. Targeting this "wound response" of cancer stem cells can potentially provide a novel approach for therapeutic invention, said researchers from the National Cancer Institute-designated Dan L. Duncan Cancer Center at Baylor College of Medicine.

The results of their study appear online in the journal Nature today.

"Treatment for advanced bladder cancer is limited to surgery and chemotherapy. There are no targeted treatments available," said Dr. Keith Syson Chan, an assistant professor of molecular and cellular biology and of urology and the corresponding author on the report. "The chemotherapy response is far from ideal so the clinical goal is to advance research into this area and uncover a much more targeted approach."

Together with co-lead authors Antonina Kurtova, a graduate student in the Translational Biology and Molecular Medicine Program at Baylor, and Dr. Jing Xiao, research assistant in urology at Baylor, Chan and his team sought out to identify mechanisms underlying the development of resistance in bladder cancer that has invaded the muscles. They found that regrowth of cancer stem cells actively contributes to therapy resistance between drug treatment cycles.

"This is a paradoxical mechanism leading to resistance, one we didn't expect," said Chan. "The cancer stem cells actively regrow and respond to the induced damage or apoptosis (cell death) caused by chemotherapy in between the different cycles, similar to how normal tissue stem cells respond to wound-induced damages."

The proliferation is stimulated by the release of a metabolite (or factor) called prostaglandin E2 or PGE2 from the dying cells, which causes the cancer stem cells to repopulate tumors that were reduced in size by chemotherapy, they found.

In normal cells, this is a part of the wound repair process when PGE2 induces tissues stem cells to regrow; in cancer PGE2 ironically induces regrowth of more cancer stem cells in between chemotherapy cycles, Kurtova and Xiao said.

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'Wound response' of cancer stem cells may explain chemo-resistance in bladder cancer

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Released: 1-Dec-2014 1:00 PM EST Embargo expired: 3-Dec-2014 5:00 AM EST Source Newsroom: McMaster University Contact Information

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Newswise Hamilton, ON (Dec. 3, 2014) Scientists at McMaster University have discovered that human stem cells made from adult donor cells remember where they came from and thats what they prefer to become again.

This means the type of cell obtained from an individual patient to make pluripotent stem cells, determines what can be best done with them. For example, to repair the lung of a patient with lung disease, it is best to start off with a lung cell to make the therapeutic stem cells to treat the disease, or a breast cell for the regeneration of tissue for breast cancer patients.

Pluripotency is the ability stem cells have to turn into any one of the 226 cell types that make up the human body.The work challenges the previously accepted thought that any pluripotent human stem cell could be used to similarly to generate the same amount of mature tissue cells.

This finding, published today in the prestigious science journal Nature Communications, will be used to further drug development at McMaster, and potentially improve transplants using human stem cell sources.

The study was led by Mick Bhatia, director of the McMaster Stem Cell and Cancer Research Institute. He holds the Canada Research Chair in Human Stem Cell Biology and he is a professor in the Department of Biochemistry and Biomedical Sciences of the Michael G. DeGroote School of Medicine.

Its like the stem cell we make wants to become a doctor like its grandpa or an artist like its great-grandma, said Bhatia.

Weve shown that human induced pluripotent stem cells, called iPSCs, have a memory that is engraved at the molecular/genetic level of the cell type used to make them, which increases their ability to differentiate to the parent tissue type after being put in various stem cell states.

So, not all human iPSCs are made equal, Bhatia added. Moving forward, this means that iPSC generation from a specific tissue requiring regeneration is a better approach for future cellular therapies. Besides being faster and more cost-efficient in the development of stem cell therapy treatments, this provides a new opportunity for use of iPSCs in disease modeling and personalized drug discovery that was not appreciated before.

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Not All Induced Pluripotent Stem Cells Are Made Equal

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PUBLIC RELEASE DATE:

3-Dec-2014

Contact: Veronica McGuire vmcguir@mcmaster.ca 90-552-591-402-2169 McMaster University @mcmasteru

Hamilton, ON (Dec. 3, 2014) - Scientists at McMaster University have discovered that human stem cells made from adult donor cells "remember" where they came from and that's what they prefer to become again.

This means the type of cell obtained from an individual patient to make pluripotent stem cells, determines what can be best done with them. For example, to repair the lung of a patient with lung disease, it is best to start off with a lung cell to make the therapeutic stem cells to treat the disease, or a breast cell for the regeneration of tissue for breast cancer patients.

Pluripotency is the ability stem cells have to turn into any one of the 226 cell types that make up the human body.The work challenges the previously accepted thought that any pluripotent human stem cell could be used to similarly to generate the same amount of mature tissue cells.

This finding, published today in the prestigious science journal Nature Communications, will be used to further drug development at McMaster, and potentially improve transplants using human stem cell sources.

The study was led by Mick Bhatia, director of the McMaster Stem Cell and Cancer Research Institute. He holds the Canada Research Chair in Human Stem Cell Biology and he is a professor in the Department of Biochemistry and Biomedical Sciences of the Michael G. DeGroote School of Medicine.

"It's like the stem cell we make wants to become a doctor like its grandpa or an artist like its great-grandma," said Bhatia.

"We've shown that human induced pluripotent stem cells, called iPSCs, have a memory that is engraved at the molecular/genetic level of the cell type used to make them, which increases their ability to differentiate to the parent tissue type after being put in various stem cell states.

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Not all induced pluripotent stem cells are made equal: McMaster researchers

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

3-Dec-2014

Contact: Robert Bock or Meredith Daly dalym@mail.nih.gov 301-496-5133 NIH/National Institute of Child Health and Human Development @@NICHDPress

Researchers at the National Institutes of Health have found a duplication of a short stretch of the X chromosome in some people with a rare disorder that causes excessive childhood growth. They believe that a single gene within the region likely has a large influence on how much children grow. The research comes from a lab at NIH's Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), which seeks to understand growth.

"Finding the gene responsible for childhood overgrowth would be very helpful, but the much wider question is what regulates growth," said Constantine Stratakis, M.D., D.Sc., lead author of the new paper and the scientific director of the Division of Intramural Research at NICHD.

In theory, the causes of overgrowth and undergrowth in children should be regulated by the same mechanisms, Dr. Stratakis explained. "As pediatricians and endocrinologists, we look at growth as one of the hallmarks of childhood. Understanding how children grow is extraordinarily important, as an indicator of their general health and their future well-being."

The study, appearing in the New England Journal of Medicine, was part of the intramural research program at the NICHD. Support also came from NIH's National Institute of Neurological Disorders and Stroke and the National Human Genome Research Institute.

The research started with a family who came to the NIH Clinical Center for treatment in the mid-1990s. A mother who had been treated for gigantism had two sons who were also growing rapidly. People with this condition are abnormally tall and may have delayed puberty, large hands and feet, and double vision. A second family, with an affected daughter, came to NIH from Australia. The girl had the same duplication the researchers saw in the first family. Dr. Stratakis then contacted Albert Beckers, M.D., Ph.D., at the University of Liege, Belgium. For more than 30 years, Dr. Beckers has been following people with gigantism and acromegaly, a disorder in which excessive growth begins after adulthood. Dr. Beckers agreed to test these patients and identified the same duplication in a group of his patients as well.

Gigantism results from a defect in the pituitary, a pea-sized gland at the base of the brain that makes growth hormones and controls the activity of other glands in the body. Some people with gigantism have a tumor in the pituitary that secretes extra hormone; others just have an oversized pituitary. Gigantism is often treated by removing the tumor, or even the entire pituitary, but can sometimes be treated with medication alone.

"Giants are very rare. If you have three cases in the same family, that is very rare," Dr. Stratakis said. He explained that most of the pituitary gland of the mother in the first family was removed when she was 3 years old, and in adulthood she was only a little above average height. Both of her sons had gigantism, too, and had pituitary surgery.

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NIH researchers link chromosome region to duplication of gene on X chromosome appears to cause excessive growth

Recommendation and review posted by Bethany Smith

CSHL Keynote Series, Dr. Christopher Voight, Massachusetts Institute of Technology
"Pushing the scale of genetic engineering" from the Synthetic Biology meeting in Suzhou China, CSHL-Asia 12/2/2014.

By: CSHL Leading Strand

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CSHL Keynote Series, Dr. Christopher Voight, Massachusetts Institute of Technology - Video

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

3-Dec-2014

Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News @LiebertOnline

New Rochelle, NY, December 3, 2014--Hereditary angioedema (HAE), a rare genetic disease that causes recurrent swelling under the skin and of the mucosal lining of the gastrointestinal tract and upper airway, usually first appears before 20 years of age. A comprehensive review of the therapies currently available to treat HAE in adults shows that some of these treatments are also safe and effective for use in older children and adolescents. Current and potential future therapies are discussed in a Review article in a special issue of Pediatric Allergy, Immunology, and Pulmonology, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Pediatric Allergy, Immunology, and Pulmonology website at http://online.liebertpub.com/doi/full/10.1089/ped.2014.0412 until January 3, 2015.

Based on the current medical literature, Eveline Wu, University of North Carolina at Chapel Hill, and Michael Frank, Duke University Medical Center (Durham, NC), report that additional therapies are now approved for use in the pediatric age group. In their article "Management of Hereditary Angioedema in Childhood: A Review" they also discuss clinical trials and published experience among younger age groups for which data are most limited.

"HAE is a potentially life-threatening disease that until recently had very limited therapeutic options for children," says Pediatric Allergy, Immunology, and Pulmonology Editor-in-Chief Mary Cataletto, MD, Professor of Clinical Pediatrics, State University of New York at Stony Brook (Stony Brook, NY). "This special issue of Pediatric Allergy, Immunology, and Pulmonology, developed in collaboration with Guest Editor Dr. Timothy Craig, has been created for physicians who care for children. It focuses on recent advances in HAE-related immunophysiology, as well as current and future therapies for acute and chronic care and prophylaxis."

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About the Journal

Pediatric Allergy, Immunology, and Pulmonology is a quarterly, peer-reviewed journal published in print and online. The Journal synthesizes the pulmonary, allergy, and immunology communities in the advancement of the respiratory health of children. The Journal provides comprehensive coverage to further the understanding and optimize the treatment of some of the most common and costly chronic illnesses in children. It includes original translational, clinical, and epidemiologic research; public health, quality improvement, and case control studies; patient education research; and the latest research and standards of care for functional and genetic immune deficiencies and interstitial lung diseases. Tables of content and a sample issue may be viewed on the Pediatric Allergy, Immunology, and Pulmonology website at http://www.liebertpub.com/ped.

About the Publisher

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Are there safe and effective treatments for hereditary angioedema in children?

Recommendation and review posted by Bethany Smith

December 3, 2014

Provided by Dr. Jennifer Kuzma and Matt Shipman, North Carolina State University

New research from North Carolina State University and the University of Minnesota shows that the majority of consumers will accept the presence of nanotechnology or genetic modification (GM) technology in foods but only if the technology enhances the nutrition or improves the safety of the food.

In general, people are willing to pay more to avoid GM or nanotech in foods, and people were more averse to GM tech than to nanotech, says Dr. Jennifer Kuzma, senior author of a paper on the research and co-director of the Genetic Engineering in Society Center at NC State. However, its not really that simple. There were some qualifiers, indicating that many people would be willing to buy GM or nanotech in foods if there were health or safety benefits.

The researchers conducted a nationally representative survey of 1,117 US consumers. Participants were asked to answer an array of questions that explored their willingness to purchase foods that contained GM tech and foods that contained nanotech. The questions also explored the price of the various foods and whether participants would buy foods that contained nanotech or GM tech if the foods had enhanced nutrition, improved taste, improved food safety, or if the production of the food had environmental benefits.

The researchers found that survey participants could be broken into four groups.

Eighteen percent of participants belonged to a group labeled the new technology rejecters, which would not by GM or nanotech foods under any circumstances. Nineteen percent of participants belonged to a group labeled the technology averse, which would buy GM or nanotech foods only if those products conveyed food safety benefits. Twenty-three percent of participants were price oriented, basing their shopping decisions primarily on the cost of the food regardless of the presence of GM or nanotech. And 40 percent of participants were benefit oriented, meaning they would buy GM or nanotech foods if the foods had enhanced nutrition or food safety.

This tells us that GM or nanotech food products have greater potential to be viable in the marketplace if companies focus on developing products that have safety and nutrition benefits because a majority of consumers would be willing to buy those products, Kuzma says.

From a policy standpoint, it also argues that GM and nanotech foods should be labeled, so that the technology rejecters can avoid them, Kuzma adds.

The paper, Heterogeneous Consumer Preferences for Nanotechnology and Genetic-modification Technology in Food Products, is published online in the Journal of Agricultural Economics. Lead author of the paper is Dr. Chengyuan Yue of the University of Minnesota. The paper was co-authored by Shuoli Zhao, a graduate student at UM. The research was supported by a grant from the U.S. Department of Agriculture.

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Consumer Acceptance of Nanotech, Genetic Modification In Foods Depends On Nutrition, Safety

Recommendation and review posted by Bethany Smith