THURSDAY, Feb. 26, 2015 (HealthDay News) -- Hormone therapy for transgender adults is generally safe, according to a new review.

The findings should ease the concerns of some doctors and transgender people who've wondered about the safety of such therapy, the researchers said. These findings may also help reduce some of the barriers faced by transgender people.

The review analyzed existing research on the subject.

"Although many of the studies identified were small and will need to be replicated with larger numbers of patients involved, the overall trend of the findings is reassuring," review corresponding author Dr. Joshua Safer, an associate professor of medicine and molecular medicine at Boston University School of Medicine, said in a university news release.

"Notably, there was no evidence of a significant increase in cancer risk from transgender hormone treatment despite that being a common fear that is actually listed in most current guidelines," he added.

The review did find that hormone therapy was associated with an increased risk of blood clots in male to female transgender adults, and increased blood counts in female to male transgender adults.

However, there was little evidence that hormone therapy was associated with other serious health concerns, including increased risk of cancer or death.

The findings were published Feb. 24 in the Journal of Clinical and Translational Endocrinology.

"Although the review uncovers numerous areas in transgender hormone treatment that require more research, it should already help put to rest unnecessary anxiety about hormone safety for transgender individuals," Safer said.

"Thus, one additional barrier to care for transgender individuals can be substantially reduced relative to what is still thought by many," he concluded.

Continued here:

Transgender Hormone Therapy Doesn't Seem to Pose Major Risks

HOUSTON -- (Feb. 26, 2015) - For more than 50 years, Dr. Bert O'Malley, chair of Baylor College of Medicine's department of molecular and cellular biology, has worked to understand the estrogen receptor, how it works and how it partners with other molecules in the cell.

In a recent study with Dr. Wah Chiu, professor of biochemistry and molecular biology at Baylor, O'Malley for the first time visualized the 900 kiloDalton molecular machine (kiloDalton is a measurement of mass) made up of the receptor, its coactivator SRC-3 (steroid receptor coactivator 3), another coactivator called p300, and the DNA that it controls, through the use of an electron cryo-microscope and advanced computational analysis. That 3-D image revealed the spatial relationships among these molecules as never seen before and immediately suggests how the receptor recruits the co-activators and activates genes.

A report on their work appears online in the journal Molecular Cell.

The estrogen receptor is a transcription factor - one of those cellular workhorses that alone or together with other proteins binds to specific sequences of DNA, thus controlling the rate at which the information in DNA is transcribed into the messenger RNA to synthesize new proteins for the cell. Estrogen receptor-, in particular, drives growth in cells.

"It is one of the main drivers of breast cancer and other female cancers," said O'Malley. "It is quite important that we understand how this works. No one has ever seen an intact estrogen receptor before - either attached to DNA or in a functional state with coactivators, which can drive growth in cells."

Chiu, who has pioneered the technique of electron cryomicroscopy, said this molecular machine itself presented major technical challenges in solving and validating the results, because of the structural variability that is in fact intrinsic to its function.

"Usually, most proteins assume consistent configurations in space," he said. "But in this case, proteins in this machine appear to assume different conformations. We have developed a novel computational procedure to classify the images so that we are averaging only those that have a uniform conformation in order to compute its 3-D image."

O'Malley is inspired by this 3-D photo and since has designed multiple biochemical experiments to validate this model and extend the understanding of the mechanism of its function.

"This was a two-part success," said O'Malley. "We, in my laboratory, made the proteins, checked their functions and formed the complex on the DNA. But we would not understand what they look like and how they work without Wah's expert technology."

"Bert has developed a biochemical way to purify a number of proteins, which function together as a molecular machine. In this case, the machine is made up of three different proteins, and DNA. For the first time, we found out how these molecules assemble to form the functional machine," said Chiu.

Link:

Interaction of estrogen receptor and coactivators seen for first time

Allele Frequency Community formed to significantly address need to improve the interpretation of DNA findings on disease-causing gene variants and rare diseases

A coalition of 13 leading life science and diagnostics organizations recently announced the formation of the Allele Frequency Community, a landmark initiative that is creating an extensive, high-quality and ethnically diverse collection of human genomes to address a key challenge in interpreting sequencing data for research and clinical applications. The announcement coincides with the start of the 16th annual Advances in Genome Biology and Technology (AGBT) scientific meeting in Marco Island, Florida.

The Allele Frequency Community was recently formed after the 13 organizations agreed to pool their extensive human exome- and genome-wide variant call datasets in a secure, anonymized, pooled fashion to create the most ethnically diverse, freely-accessible, hosted community database of allele frequencies available. Until now, labs often collected their own, private allele frequency libraries, but did not have the infrastructure and incentives to integrate their resources into a freely-available community asset.

Increasing participation in this community-based resource is expected to create greater value over time. In particular, the Allele Frequency Community has the potential to create increasing value for life sciences and clinical research since information on observed allele frequencies can create important benchmarks that significantly increase the accuracy of findings from data generated by molecular analyses, such as Next-Generation Sequencing (NGS).

To enable this resource to grow, users have the opportunity to opt-in to join the Allele Frequency Community and benefit from the extensive database, agreeing in return to contribute statistics from their sequences to the database. Only anonymous, pooled allele frequencies are provided, protecting patient privacy.

The Allele Frequency Community database already holds more than 70,000 variant call datasets including 8,000 whole genomes and has been shown in internal benchmarking studies to generate a 43% average reduction in false positive rates in causal variant identification.

The founding collaborators of the Allele Frequency Community are:

QIAGEN N.V. is one of the founding collaborators of the Allele Frequency Community, and is providing bioinformatics infrastructure and software for the development of this community-based resource.

Over the last few years, access to allele frequency data from large populations has been the most useful resource for the interpretation of human variation, said Dr. Heidi Rehm, Ph.D., Director of the Laboratory for Molecular Medicine at Partners Healthcare Personalized Medicine. The Allele Frequency Community is a really valuable project. I am happy to share data through this new resource and excited that many other people have agreed to do so as well.

An allele is an alternative form of a gene found in a persons DNA. Scientists need diverse, large-scale data on allele frequencies to accurately identify potential disease-causing DNA changes in a population. Information on allele frequency also tells clinicians how common certain changes are within the population, helping to distinguish rare, disease-causing DNA changes from more common variations. A key challenge has been the lack of extensive collections of human genomes as a reference set. A prospective disease-causing variant that appears to be rare based on publicly available data may in fact be more prevalent in an ethnic population under-represented in public databases.

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QIAGEN Collaborates With Allele Frequency Community To Advance Translational Medicine And Clinical Diagnostics

Obesity causes inflammation, which can in turn lead to type 2 diabetes. What isn't well established is how inflammation causes diabetes -- or what we can do to stop it. Researchers at University of California, San Diego School of Medicine have discovered that the inflammatory molecule LTB4 promotes insulin resistance, a first step in developing type 2 diabetes. What's more, the team found that genetically removing the cell receptor that responds to LTB4, or blocking it with a drug, improves insulin sensitivity in obese mice. The study is published Feb. 23 by Nature Medicine.

"This study is important because it reveals a root cause of type 2 diabetes," said Jerrold M. Olefsky, MD, professor of medicine, associate dean for scientific affairs and senior author of the study. "And now that we understand that LTB4 is the inflammatory factor causing insulin resistance, we can inhibit it to break the link between obesity and diabetes."

Here's what's happening in obesity, according to Olefsky's study. Extra fat, particularly in the liver, activates resident macrophages, the immune cells living there. These macrophages then do what they're supposed to do when activated -- release LTB4 and other immune signaling molecules to call up an influx of new macrophages. Then, in a positive feedback loop, the newly arriving macrophages also get activated and release even more LTB4 in the liver.

This inflammatory response would be a good thing if the body was fighting off an infection. But when inflammation is chronic, as is the case in obesity, all of this extra LTB4 starts activating other cells, too. Like macrophages, nearby liver, fat and muscle cells also have LTB4 receptors on their cell surfaces and are activated when LTB4 binds them. Now, in obesity, those cells become inflamed as well, rendering them resistant to insulin.

Once Olefsky and his team had established this mechanism in their obese mouse models, they looked for ways to inhibit it. First, they genetically engineered mice that lack the LBT4 receptor. When that approach dramatically improved the metabolic health of obese mice, they also tried blocking the receptor with a small molecule inhibitor. This particular compound was at one time being tested in clinical trials, but was dropped when it didn't prove all that effective in treating its intended ailment. Olefsky's team fed the prototype drug to their mice and found that it worked just as well as genetic deletion at preventing -- and reversing -- insulin resistance.

"When we disrupted the LTB4-induced inflammation cycle either through genetics or a drug, it had a beautiful effect -- we saw improved metabolism and insulin sensitivity in our mice," Olefsky said. "Even though they were still obese, they were in much better shape."

Story Source:

The above story is based on materials provided by University of California, San Diego Health Sciences. Note: Materials may be edited for content and length.

Link:

Molecular Link between Obesity, Type 2 Diabetes Reveals Potential Therapy

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Newswise Obesity causes inflammation, which can in turn lead to type 2 diabetes. What isnt well established is how inflammation causes diabetes or what we can do to stop it. Researchers at University of California, San Diego School of Medicine have discovered that the inflammatory molecule LTB4 promotes insulin resistance, a first step in developing type 2 diabetes. Whats more, the team found that genetically removing the cell receptor that responds to LTB4, or blocking it with a drug, improves insulin sensitivity in obese mice. The study is published Feb. 23 by Nature Medicine.

This study is important because it reveals a root cause of type 2 diabetes, said Jerrold M. Olefsky, MD, professor of medicine, associate dean for scientific affairs and senior author of the study. And now that we understand that LTB4 is the inflammatory factor causing insulin resistance, we can inhibit it to break the link between obesity and diabetes.

Heres whats happening in obesity, according to Olefskys study. Extra fat, particularly in the liver, activates resident macrophages, the immune cells living there. These macrophages then do what theyre supposed to do when activated release LTB4 and other immune signaling molecules to call up an influx of new macrophages. Then, in a positive feedback loop, the newly arriving macrophages also get activated and release even more LTB4 in the liver.

This inflammatory response would be a good thing if the body was fighting off an infection. But when inflammation is chronic, as is the case in obesity, all of this extra LTB4 starts activating other cells, too. Like macrophages, nearby liver, fat and muscle cells also have LTB4 receptors on their cell surfaces and are activated when LTB4 binds them. Now, in obesity, those cells become inflamed as well, rendering them resistant to insulin.

Once Olefsky and his team had established this mechanism in their obese mouse models, they looked for ways to inhibit it. First, they genetically engineered mice that lack the LBT4 receptor. When that approach dramatically improved the metabolic health of obese mice, they also tried blocking the receptor with a small molecule inhibitor. This particular compound was at one time being tested in clinical trials, but was dropped when it didnt prove all that effective in treating its intended ailment. Olefskys team fed the prototype drug to their mice and found that it worked just as well as genetic deletion at preventing and reversing insulin resistance.

When we disrupted the LTB4-induced inflammation cycle either through genetics or a drug, it had a beautiful effect we saw improved metabolism and insulin sensitivity in our mice, Olefsky said. Even though they were still obese, they were in much better shape.

Co-authors of this study include Pingping Li, Da Young Oh, Gautam Bandyopadhyay, William S. Lagakos, Saswata Talukdar, Olivia Osborn, Andrew Johnson, Heekyung Chung, Rafael Mayoral, Michael Maris, Jachelle M Ofrecio, Sayaka Taguchi, Min Lu, all at UC San Diego.

This research was funded, in part, by the National Institute of Diabetes and Digestive and Kidney Diseases (DK033651, DK074868, DK063491, DK09062), the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and Merck, Inc.

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Molecular Link between Obesity and Type 2 Diabetes Reveals Potential Therapy

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Newswise An international team of scientists, led by researchers at the University of California, San Diego School of Medicine, has identified the microtubule-associated protein tau (MAPT) gene as increasing the risk for developing Alzheimers disease (AD). The MAPT gene encodes the tau protein, which is involved with a number of neurodegenerative disorders, including Parkinsons disease (PD) and AD. These findings provide novel insight into Alzheimers neurodegeneration, possibly opening the door for improved clinical diagnosis and treatment.

The findings are published in the February 18 online issue of Molecular Psychiatry.

Alzheimers disease, which afflicts an estimated 5 million Americans, is typically characterized by progressive decline in cognitive skills, such as memory and language and behavioral changes. While some recent AD genome-wide association studies (GWAS), which search the entire human genome for small variations, have suggested that MAPT is associated with increased risk for AD, other studies have found no association. In comparison, a number of studies have found a strong association between MAPT and other neurodegenerative disorders, such as PD.

Though a tremendous amount of work has been conducted showing the involvement of the tau protein in Alzheimers disease, the role of the tau-associated MAPT gene is still unclear, said Rahul S. Desikan, MD, PhD, research fellow and radiology resident at the UC San Diego School of Medicine and the studys first author.

In the new Molecular Psychiatry paper, conducted with collaborators across the country and world, Desikan and colleagues narrowed their search. Rather than looking at all possible loci (specific gene locations), the authors only focused on loci associated with PD and assessed whether these loci were also associated with AD, thus increasing their statistical power for AD gene discovery.

By using this approach, they found that carriers of the deleterious MAPT allele (an alternative form of the gene) are at increased risk for developing AD and more likely to experience increased brain atrophy than non-carriers.

"This study demonstrates that tau deposits in the brains of Alzheimer's disease subjects are not just a consequence of the disease, but actually contribute to development and progression of the disease," said Gerard Schellenberg, PhD, professor of pathology and laboratory medicine at the University of Pennsylvania, principal investigator of the Alzheimers Disease Genetics Consortium and a study co-author.

An important aspect was the collaborative nature of this work. Thanks to our collaborators from the Consortium, the International Parkinsons Disease Genetics Consortium, the Genetic and Environmental Risk in Alzheimers Disease, the Cohorts for Heart and Aging Research in Genomic Epidemiology, deCODE Genetics and the DemGene cohort, we had tremendous access to a large number of Alzheimers and Parkinsons genetic datasets that we could use to identify and replicate our MAPT finding, said Ole A. Andreassen, MD, PhD, professor of biological psychiatry at the University of Oslo and a senior co-author.

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Tau-Associated MAPT Gene Increases Risk for Alzheimer's Disease

Personalized Cancer Care: A Conversation with Cleveland Clinics Brian Bolwell, MD (Video 3 of 4)
With advances in genomics and molecular medicine, what might cancer care look like in 15 or 20 years? Taussig Cancer Institute Chairman Brian Bolwell, MD, ta...

By: Cleveland Clinic

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Personalized Cancer Care: A Conversation with Cleveland Clinics Brian Bolwell, MD (Video 3 of 4) - Video

The Lerner Research Institute is home to all laboratory-based research at Cleveland Clinic. Our mission is to understand the underlying causes of human diseases and to develop new treatments and cures.

The Department of Molecular Medicine focuses on the fundamentals of Biochemistry, Molecular Biology and Cell Biology in the context of human health and disease.

Molecular Medicine Faculty have academic appointments in Cleveland Clinic's Lerner Research Institute (LRI) and the Cleveland Clinic Lerner College of Medicine (CCLCM). The LRI is home to all laboratory-based research at Cleveland Clinic, and the Faculty are the foundation of the Institute's integrated research community consisting of 11 Departments and more than a dozen Centers of Research. Faculty work in basic, translational and clinical research. CCLCM is a unique medical school program partnership between Cleveland Clinic and Case Western Reserve University (CWRU) that trains physician/scientists through integrating laboratory research and clinical medicine.

The Department Chair is Paul E. DiCorleto, Ph.D., who is also Chair of the Lerner Research Institute.

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Department of Molecular Medicine - Cleveland Clinic Lerner ...

DUBLIN, Feb .10, 2015 /PRNewswire/ --Research and Markets

(http://www.researchandmarkets.com/research/mggz6b/molecular) has announced the addition of Jain PharmaBiotech's new report "Molecular Diagnostics - Technologies, Markets and Companies" to their offering.

This report describes and evaluates the molecular diagnostics technologies that will play an important role in practice of medicine, public health, pharmaceutical industry, forensics and biological warfare in the 21st century. This includes several polymerase chain reaction (PCR)-based technologies, fluorescent in situ hybridization (FISH), peptide nucleic acids (PNA), electrochemical detection of DNA, sequencing, mitochondrial DNA, biochips, nanotechnology and proteomic technologies.

Initial applications of molecular diagnostics were mostly for infections but are now increasing in the areas of genetic disorders, preimplantation screening and cancer. Genetic screening tests, despite some restrictions is a promising area for future expansion of in vitro diagnostic market. Molecular diagnostics is being combined with therapeutics and forms an important component of integrated healthcare. Molecular diagnostic technologies are also involved in development of personalized medicine based on pharmacogenetics and pharmacogenomics. Currently, there has been a considerable interest in developing rapid diagnostic methods for for point-of-care and biowarfare agents such as anthrax.

The number of companies involved in molecular diagnostics has increased remarkably during the past few years. More than 1,000 companies have been identified to be involved in developing molecular diagnostics and 339 of these are profiled in the report along with tabulation of 802 collaborations. Despite the strict regulation, most of the development in molecular diagnostics has taken place in the United States, which has the largest number of companies.

The markets for molecular diagnostics technologies are difficult to estimate. Molecular diagnostics markets overlap with markets for non-molecular diagnostic technologies in the in vitro diagnostic market and are less well defined than those for pharmaceuticals. Molecular diagnostic markets are analyzed for 2014 according to technologies, applications and geographical regions. Forecasts are made up to 2024. A major portion of the molecular diagnostic market can be attributed to advances in genomics and proteomics. Biochip and nanobiotechnology are expected to make a significant contribution to the growth of molecular diagnostics.

Key Topics Covered:

Executive Summary

1. Introduction

2. Molecular Diagnostic Technologies

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Molecular Diagnostics Technologies 2015-2024 - Markets and Companies Report

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Trends in Molecular Medicine

"One thing that was really great about the program was the combination of theory in the morning and practical work in the afternoon. This helped me keep everything in perspective and I found it highly motivating. In the lab I also learned so much; not only a lot of new techniques, but also how to approach and tackle a scientific question, and how to go about designing an experiment to specifically answer the question. Of course I had some idea about this before I began the program, but the lab placements enabled me to really practice this at a professional level. In my thesis right now, for example, I have a great deal of flexibility over the work Im doing, but I also have the chance to consistently check back with my supervisor to discuss next steps and possible future experiments. This combination of working independently but with support is essential for me to mature on the scientific level. In all, it also gives me the feeling that I am a researcher and not just another student."

Radwa Sharaf, graduate 2013, pursuing her PhD at Harvard soon.

Click here to find more about the International Master Program Molecular Medicine

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International Masters Program Molecular Medicine ...

2/12 (Thursday) 11:00 - 12:00 Noon B1B Lecture Room, IBMS Topic PI3 Kinases in Cellular Homeostasis. Speaker Wei-Xing Zong, Ph.D. Professional Title Professor Department of Molecular Genetics & Microbiology Stony Brook University, USA 2/13 (Friday) 11:00 - 12:00 Noon B1B Lecture Room, IBMS Topic Epigenetic Regulation of Vascular Mechanotransduction. Speaker Shu Chien, Ph.D. Professional Title Professor & Director Institute of Engineering In Medicine Departments of Bioengineering and Medicine University of California, San Diego, USA 2/13 (Friday) 3:00 - 4:00 PM B1B Lecture Room, IBMS Topic Recent Developments in Modeling and Docking for GPCRs. Speaker Art Cho, Ph.D. Professional Title Professor, Department of Biotechnology and Bioinformatics, Korea University Co-Founder, President and CSO, Quantum Bio Solutions Korea 2/26 (Thursday) 11:00 - 12:00 Noon B1B Lecture Room, IBMS Topic Mitochondrial ion dynamics and energetics: Computational and experimental approaches to study mitochondrial ion circuits in the heart. Speaker An-Chi Wei, Ph.D. Professional Title Postdoctoral Research Fellow Division of Cardiology Department of Medicine The Johns Hopkins University, USA 3/2 (Monday) 11:00 - 12:00 Noon B1B Lecture Room, IBMS Topic How the Cell Makes Mitochondria from Proteins and Lipids. Speaker Toshiya Endo, Ph.D. Professional Title Professor Faculty of Life Sciences Kyoto Sangyo University, Japan

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Welcome to the Molecular Medicine Program

Seeking to Cure Diseases of Our Time in Our Time

The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases (IMM) at The University of Texas Health Science Center at Houston was established in 1995 in the heart of the Texas Medical Center - the world's largest. The IMM is focused on studying and preventing diseases at the genetic, cellular and molecular levels using DNA and protein technologies and animal models. The IMM is part of the Texas Therapeutics Institute, a multi-institutional collaboration encouraging drug discovery.

Opened in 2006, the 229,000-square-foot Fayez S. Sarofim Research Building houses the IMM's research centers:

We're looking for the best and brightest. Visit http://www.uthouston.edu/imm/career-opportunities.htm

For additional information, contact:

John F. Hancock, MA, MB, BChir, PhD Email: Ms. Naomi Pinkney, MBA 1825 Pressler Street Houston, Texas 77030 Phone: 713-500-2401, Fax: 713-500-2420

IMM: http://www.uthouston.edu/imm/

Photo: Fayez S. Sarofim Research Building and University Center Tower by Richard Payne 2006

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The Brown Foundation Institute of Molecular Medicine ( IMM )

Das MDC im Profil - Max Delbrck Center for Molecular Medicine
English version: http://youtu.be/9en3g8DiPy4 Das Max-Delbrck-Centrum fr Molekulare Medizin (MDC) in Berlin-Buch ist eines der grten und wichtigsten Zentr...

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Das MDC im Profil - Max Delbrck Center for Molecular Medicine - Video

Durham, NC (PRWEB) February 04, 2015

STEM CELLS Translational Medicine (SCTM) presented Marc H. Dahlke, M.D., Ph.D. its second annual STEM CELLS Translational Medicine Young Investigator Award. The award fosters advancements in the field of stem cells and regenerative medicine by honoring a young researcher who is principle author of an article published in SCTM over the course of a year that is deemed to have the most impact and to push the boundaries of novel and insightful research.

Dr. Dahlkes paper describes the discovery of a universal stem cell product that not only seems to increase the long-term survival of organ transplants in instances when the donor is not related to the recipient, but also retains that immunological privileged state when the organ is then transplanted into yet another unrelated recipient. The paper was published in the August 2013 issue of SCTM.

This excellent study by Dr. Dahlke and his co-authors demonstrate the potential for multipotent adult progenitor cells to serve as a universal cell product. Being able to reduce the level of immunosuppressant drugs post-transplant could have significant benefits to patients, said Anthony Atala, M.D., Editor-in-Chief of SCTM. This study represents a promising pathway for clinical immunotherapy, and I congratulate our Young Investigator Award winner on this important accomplishment.

Dr. Dahlke is a lecturer for experimental surgery at Regensburg University, Germany, and an attending surgeon at Regensburg University Medical Center. He received both his M.D. (in 2002) and his Ph.D. (2004) from Hannover Medical School, where he was enrolled in the program for molecular medicine. He went on to receive specialty training in surgery as a fellow at the University of Sydney (Australia) and at Memorial Sloan Kettering Cancer Center in New York (US).

Currently, his lab in Regensburg focuses on the immunobiology of mesenchymal stem cells and the use of stem cell products for clinical application in solid organ transplantation and other indications. His group publishes regularly in this field, and Dr. Dahlke is the principal investigator of the first phase I study applying a mesenchymal stem cell product to liver transplant recipients.

He also is the founder of the MiSOT network (http://www.misot.eu), which aims to bring together academic and commercial research with the goal of bringing mesenchymal stem cell therapies to the transplantation clinic. He also serves as a reviewer for numerous journals in the immunology field.

The STEM CELLS Translational Medicine Young Investigator Award, which includes a $10,000 cash incentive, is co-sponsored by CIRM and Quintiles in cooperation with the Regenerative Medicine Foundation. Its winner is selected each year by the journals editorial board, made up of leading experts in the field of regenerative medicine worldwide.

###

About STEM CELLS Translational Medicine: STEM CELLS TRANSLATIONAL MEDICINE (SCTM), published by AlphaMed Press, is a monthly peer-reviewed publication dedicated to significantly advancing the clinical utilization of stem cell molecular and cellular biology. By bridging stem cell research and clinical trials, SCTM will help move applications of these critical investigations closer to accepted best practices.

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Paper Describing Universal Stem Cell Product Earns Author the 2014 SCTM Young Investigator Award

A complex interplay of molecular components governs almost all aspects of biological sciences -- healthy organism development, disease progression, and drug efficacy are all dependent on the way life's molecules interact in the body. Understanding these bio-molecular interactions is critical for the discovery of new, more effective therapeutics and diagnostics to treat cancer and other diseases, but currently requires scientists to have access to expensive and elaborate laboratory equipment.

Now, a new approach developed by researchers at the Wyss Institute for Biologically Inspired Engineering, Boston Children's Hospital and Harvard Medical School promises a much faster and more affordable way to examine bio-molecular behavior, opening the door for scientists in virtually any laboratory world-wide to join the quest for creating better drugs. The findings are published in February's issue of Nature Methods.

"Bio-molecular interaction analysis, a cornerstone of biomedical research, is traditionally accomplished using equipment that can cost hundreds of thousands of dollars," said Wyss Associate Faculty member Wesley P. Wong, Ph.D., senior author of study. "Rather than develop a new instrument, we've created a nanoscale tool made from strands of DNA that can detect and report how molecules behave, enabling biological measurements to be made by almost anyone, using only common and inexpensive laboratory reagents."

Wong, who is also Assistant Professor at Harvard Medical School in the Departments of Biological Chemistry & Molecular Pharmacology and Pediatrics and Investigator at the Program in Cellular and Molecular Medicine at Boston Children's Hospital, calls the new tools DNA "nanoswitches."

Nanoswitches comprise strands of DNA onto which molecules of interest can be strategically attached at various locations along the strand. Interactions between these molecules, like the successful binding of a drug compound with its intended target, such as a protein receptor on a cancer cell, cause the shape of the DNA strand to change from an open and linear shape to a closed loop. Wong and his team can easily separate and measure the ratio of open DNA nanoswitches vs. their closed counterparts through gel electrophoresis, a simple lab procedure already in use in most laboratories, that uses electrical currents to push DNA strands through small pores in a gel, sorting them based on their shape

"Our DNA nanoswitches dramatically lower barriers to making traditionally complex measurements," said co-first author Ken Halvorsen, formerly of the Wyss Institute and currently a scientist at the RNA Institute at University of Albany. "All of these supplies are commonly available and the experiments can be performed for pennies per sample, which is a staggering comparison to the cost of conventional equipment used to test bio-molecular interactions."

To encourage adoption of this method, Wong and his team are offering free materials to colleagues who would like to try using their DNA nanoswitches.

"We've not only created starter kits but have outlined a step-by-step protocol to allow others to immediately implement this method for research in their own labs, or classrooms" said co-first author Mounir Koussa, a Ph.D. candidate in neurobiology at Harvard Medical School.

"Wesley and his team are committed to making an impact on the way bio-molecular research is done at a fundamental level, as is evidenced by their efforts to make this technology accessible to labs everywhere," said Wyss Institute Founding Director Donald Ingber, M.D., Ph.D., who is also the Judah Folkman Professor of Vascular Biology at Boston Children's Hospital and Harvard Medical School and a Professor of Bioengineering at Harvard SEAS. "Biomedical researchers all over the world can start using this new method right away to investigate how biological compounds interact with their targets, using commonly-available supplies at very low cost."

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DNA nanoswitches reveal how life's molecules connect

TORONTO, ON--(Marketwired - January 28, 2015) - The webinar will examine how rapid molecular stool pathogen diagnostic testing may minimize the burden of diarrheal illness throughout the entire hospital and to healthcare providers worldwide. Featured speakers include David Peaper, Assistant Professor of Laboratory Medicine, Yale School of Medicine; Director ofClinical Microbiology Laboratory, Yale-New Haven Hospital; and Director of Virology Reference Laboratory, VA Connecticut Healthcare System. Dr. Peaper will be joined by Marilyn Mitchell, Supervisor, Microbiology Laboratory, Community Regional Medical Center, Fresno, California.

Diarrhea caused by bacterial, viral, and/or parasitic infection represents a significant worldwide healthcare burden. Though most cases of diarrheal disease are generally self-resolving and not life-threatening in immunocompetent individuals, certain bacterial and viral infections can result in serious clinical morbidity and even death.

The current diagnostic challenge associated with detection of community-acquired diarrhea is twofold. Since clinical presentation of diarrheal disease does not narrow down the potentially responsible pathogen(s), physicians often end up taking the "shotgun" approach to diagnostic testing by ordering testing for a majority of stool pathogens. If physicians are able to characterize the patient's history, it could greatly narrow the number of diagnostic tests necessary for a given patient. On the diagnostic end, stool culture and ova and parasite (O&P) remain the gold standard diagnostics. Though generally considered sensitive and specific, these procedures are labor-intensive, unpleasant for technicians, can take as long as 5-7 days to produce definitive results in the case of stool cultures, and require a high degree of technical skill in the case of performing O&Ps.

Together, the excessive ordering of stool pathogen testing by physicians paired with less-than-ideal diagnostic options has led to what some consider significant inefficiencies in the clinical laboratory. As a result, medical technologists can spend unnecessary time working up negative stools, which can account for upwards of 95% of stools samples submitted for testing. Confirmation of a negative stool sample takes as few as 1-2 hours with a rapid diagnostic test, allowing laboratories to reallocate medical technologist time to other priorities.

The presenters will discuss rapid diagnostics for stool pathogens, which only recently emerged as viable options for testing for community-acquired diarrhea; infections caused by environmental enteric bacteria, viruses, or parasites. Since treatment decisions can vary depending on the identity of the infectious agent and the overall health of the patient, rapid identification of pathogenic bacteria, viruses, and parasites from a stool specimen is crucial.

The live broadcast takes place on Wednesday, February 18, 2015 at 1pm EST. To learn more about this event visit: Molecular Testing for Gastrointestinal Pathogens

P.A.C.E. Accreditation

Xtalks is approved as a provider of continuing education programs in the clinical laboratory sciences by the ASCLS P.A.C.E. Program -- Attendees will receive further details after the event.

About Nanosphere

Nanosphere is enhancing medicine through targeted molecular diagnostics that result in earlier disease detection, optimal patient treatment and improved healthcare economics. The Company's versatile technology platform, the Verigene System, enables clinicians to rapidly detect the most complex, costly and deadly infectious diseases through a low cost and simple-to-use multiplex molecular diagnostic test. The combination of this innovative technology and Nanosphere's customer-driven solutions keeps commitment to the patient at the forefront of its business.

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Molecular Testing for GI Pathogens: Cost-Effectiveness, Clinical Impact and Lab Implementation, New Webinar Hosted by ...

Profile of the MDC - Max Delbrck Center for Molecular Medicine
Deutsche Version: http://youtu.be/zXmn6wKokQ8 The Max Delbrck Center for Molecular Medicine (MDC) is a leading national research institute for biomedicine in Berlin, Germany. It is a member...

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The British cell biologist Professor Amanda Gay Fisher of Imperial College London (ICL) has been honored with the Helmholtz International Fellow Award for her excellent research. Fisher is one of seven outstanding researchers from abroad who received the award, each of which is endowed with 20,000 euros. According to the Helmholtz Association, Germany's largest scientific organization, the award also includes an invitation to visit one or several Helmholtz research centers. Professor Fisher wishes in particular to strengthen her existing collaborations with the Berlin Institute of Medical Systems Biology (BIMSB) of the Max Delbrck Center for Molecular Medicine (MDC) Berlin-Buch.

In her research, Professor Fisher focuses on gene regulation, a fundamental process of life which controls every biological function, including cell division, cell differentiation and regeneration. Professor Fisher, who started her research career in the 1980s, has earned an international reputation in this field. She is known for her pioneering work on HIV, the AIDS virus, describing the function of several of its genes. She also is an expert in epigenetic gene regulation - a process in which molecular biological information not contained in the DNA regulates which genes are turned on and which genes are kept silent. She also has an expertise in T lymphocyte development (immune cells) and in embryonic stem cells.

Professor Fisher is director of the MRC (Medical Research Council) Clinical Sciences Centre (CSC), which forms part of the Institute for Clinical Sciences (ICS) at Imperial College London. In addition, she is a member of the Scientific Advisory Board of the Berlin Institute of Health (BIH), which was founded by the MDC and the Charit - Universittsmedizin Berlin in 2013. All these institutions have a strong interest in "bench-to-bedside" research employing translational and systems biological approaches.

In 2014 Professor Fisher was elected Fellow of the Royal Society for her outstanding achievements in biomedical research. In 2010 she received the Women of Outstanding Achievement in SET (Science, Engineering & Technology) Award, and in 2003 she became a Fellow of the Academy of Medical Sciences in Britain. In 2002 she was honored with the EMBO Gold Medal for her AIDS research.

Since 2012 a total of 43 Fellows including the seven scientists of this selection round have received the Helmholtz International Fellow Award.

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A photo of Professor Fisher can be downloaded from the internet at: https://www.mdc-berlin.de/44046890/en/news/2015

Contact: Barbara Bachtler Press Department Max Delbrck Center for Molecular Medicine (MDC) Berlin-Buch in the Helmholtz Association Robert-Rssle-Strae 10; 13125 Berlin; Germany Phone: +49 (0) 30 94 06 - 38 96 Fax: +49 (0) 30 94 06 - 38 33 e-mail: presse@mdc-berlin.de http://www.mdc-berlin.de/en

Further information:

http://www.helmholtz.de/en/ http://www.imperial.ac.uk/study/pg/courses/clinical-sciences/ http://csc.mrc.ac.uk/ https://www.mdc-berlin.de/13800178/en/bimsb

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Helmholtz International Fellow Award for Prof. Amanda Fisher from London

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Newswise PHILADELPHIA Tens of millions of people around the world have abnormal, leak-prone sproutings of blood vessels in the brain called cerebral cavernous malformations (CCMs). These abnormal growths can lead to seizures, strokes, hemorrhages, and other serious conditions, yet their precise molecular cause has never been determined. Now, cardiovascular scientists at the Perelman School of Medicine at the University of Pennsylvania have studied this pathway in heart development to discover an important set of molecular signals, triggered by CCM-linked gene defects, that potentially could be targeted to treat the disorder.

We hope that these findings will lead to a better understanding of the origins of CCM, and thus to treatment possibilities, says Mark L. Kahn, MD, a professor of Cardiovascular Medicine, and senior author of the new study, published in Developmental Cell.

Although CCM has a relatively high prevalence of 1 in 200 people worldwide, it typically goes undiagnosed until symptoms arise and can only be treated by brain surgery.

Research on CCM has been slowed by the difficulty of recreating the disease in lab animals. About 20 percent of CCM patients have a highly aggressive, inherited form of the disorder that is caused by inactivating one of three genes, whose protein products normally work together in a complex. But knockout mice bred without a full set of those genes dont mature to have CCMs in their brainsthey die in the womb, having failed to develop a working vascular system.

Those animals die so early in their development that you just dont get enough information about what the genes normally should be doing, Kahn says.

Studies by Kahns lab and others have shown that CCM gene knockouts remain lethal to fetal mice even when they are limited to the endothelial cells that line blood vessels and the heart.

In the new study, Kahn and colleagues used advanced techniques to restrict CCM gene disruption to the endothelial cells of the developing heart, leaving the mouse vascular system to develop otherwise normally.

The resulting mice still died before birth, this time from a failure of normal heart development, which is not seen in human CCM patients. But they survived in the womb about a week longer than standard CCM knockout mice. That allowed Kahns team to learn more about the effects of the gene disruptions, and ultimately to find a previously unknown CCM-related signaling pathway.

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Possible Therapeutic Target for Common, But Mysterious Brain Blood Vessel Disorder