Gene-editing companies say research on altering the DNA of human reproductive cells is dangerous and unethical.

Officials of a biotechnology industry group have called for a voluntary moratorium on using new DNA-editing techniques to change the genetic characteristics of human embryos in laboratory research.

In an editorial published today by the journal Nature, Edward Lanphier, CEO of the biotechnology company Sangamo Biosciences, and four colleagues write that scientists should agree not to modify the DNA of human reproductive cells because it raises safety and ethical risks including the danger of unpredictable effects on future generations.

New gene-editing techniques, in particular one called CRISPR, have given scientists powerful and useful new ways to swap and change DNA letters inside of living cells for the first time (see Genome Surgery).

Recently, some scientific teams have started to study whether CRISPR would be able to correct disease genes in future generations of peoplefor instance, by repairing genes during in vitro fertilization, or in eggs or sperm. The idea of such germ line modification would be to install healthy versions of genes, which children would be born with.

The emergence of active research around germ-line editing, which is taking place in China, at Harvard University, and at a publicly traded biotechnology company called OvaScience, were described last week by MIT Technology Review (see Engineering the Perfect Baby).

But the idea of using editing technology to improve children is as controversial as it is medically powerful. In their editorial, Lanphier, whose coauthors include Fyodor Urnov, co-developer of a different gene-editing system, raise the concern that such techniques might be exploited for non-therapeutic modifications. That could mean, for instance, changing the physical traits of children.

The availability of technology to carry out genetic engineering in human germ-line cells is driving intense debate in scientific circles and may eventually become a legal issue in the United States and other countries.

The authors call for a cessation of basic research is unusual and likely to be opposed by scientists as an intrusion on the quest for scientific knowledge.

George Church, a professor at Harvard Medical School whose laboratory studies CRISPR and germ-line editing, says a voluntary moratorium would be weak compared with existing regulations that nearly all countries impose on the use of new medical technologies until they are proven safe and effective in animals or human [tests]. Church was referring to rules governing the birth of actual gene-edited children, not basic research.

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Industry Body Calls for Gene-Editing Moratorium

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What can be done to make life easier for paraplegics and their loved ones? | The Cagle Law Firm
http://www.allinjuryattorney.com If you or a loved one has suffered a spinal cord injury, there has been a serious change in your lifestyle. Medical advancements and technology influence long-term...

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WSCS 2014: DEVELOPMENT OF JAPANESE REGENERATIVE MEDICINE INDUSTRY
Presenter - Takuya Yokokawa, FujiFilm.

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WSCS 2014: DEVELOPMENT OF JAPANESE REGENERATIVE MEDICINE INDUSTRY - Video

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Kansas Regenerative Medicine
2015 Emerging Existing Business Award Winner with the Kansas Small Business Development Center.

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The growing number of biological structures being grown on chips in various laboratories around the world is rapidly replicating the entire gamut of major human organs. Now one of the most important of all a viable functioning heart has been added to that list by researchers at the University of California at Berkeley (UC Berkeley) who have taken adult stem cells and grown a lattice of pulsing human heart tissue on a silicon device.

Sourced from human-induced pluripotent stem cells able to be persuaded into forming many different types of tissue, the human heart device cells are not simply separate groups of cells existing in a petri dish, but a connected series of living cells molded into a structure that is able to beat and react just like the real thing.

"This system is not a simple cell culture where tissue is being bathed in a static bath of liquid," said study lead author Anurag Mathur, a postdoctoral researcher at UC Berkeley. "We designed this system so that it is dynamic; it replicates how tissue in our bodies actually gets exposed to nutrients and drugs."

Touted as a possible replacement for living animal hearts in drug-safety screening, the ability to easily access and rapidly analyze a heart equivalent in experiments presents appealing advantages.

"Ultimately, these chips could replace the use of animals to screen drugs for safety and efficacy," said professor of bioengineering at UC Berkeley, and leader of the research team, Kevin Healy.

The cardiac microphysiological system, as the team calls its heart-on-a-chip, has been designed so that its silicon support structure is equivalent to the arrangement and positioning of conjoining tissue filaments in a human heart. To this supporting arrangement, the researchers loaded the engineered human heart cells into the priming tube, whose cone-shaped funnel assisted in aligning the cells in a number of layers and in one direction.

In this setup, the team created microfluidic channels on each side of the cell holding region to replicate blood vessels to imitate the interchange of nutrients and drugs by diffusion in human tissue. The researchers believe that this arrangement may also one day provide the ability to view and gauge the expulsion of metabolic waste from the cells in future experiments.

"Many cardiovascular drugs target those channels, so these differences often result in inefficient and costly experiments that do not provide accurate answers about the toxicity of a drug in humans," said Professor Healy. "It takes about US$5 billion on average to develop a drug, and 60 percent of that figure comes from upfront costs in the research and development phase. Using a well-designed model of a human organ could significantly cut the cost and time of bringing a new drug to market."

The use of animal organs to forecast human reactions to new drugs is problematic, the UC Berkeley researchers note, citing the fundamental differences between species as being responsible for high failure rates in using these models. One aspect responsible for this failure is to be found in the difference in the ion channel structure between human and other animals where heart cells conduct electrical currents at different rates and intensities. It is the standardized nature of using actual human heart cells that the team sees as the heart-on-a-chip's distinct advantage over animal models.

The UC Berkeley device is certainly not the first replication of an organ-on-a-chip, but potentially one of the first successful ones to integrate living cells and artificial structures in a single functioning unit. Harvard's spleen-on-a-chip, for example, replicates the operation of the spleen, but does so by using a set of circulatory tubes containing magnetic nanobeads.

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Heart-on-a-chip beats a steady rhythm

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IMAGE:The success of the new technique suggests the possibility of implanting these tweaked cells back into a patient so they can generate an immune system. Though the new work, published... view more

LA JOLLA--For infants with severe combined immunodeficiency (SCID), something as simple as a common cold or ear infection can be fatal. Born with an incomplete immune system, kids who have SCID--also known as "bubble boy" or "bubble baby" disease--can't fight off even the mildest of germs. They often have to live in sterile, isolated environments to avoid infections and, even then, most patients don't live past a year or two. This happens because stem cells in SCID patients' bone marrow have a genetic mutation that prevents them from developing critical immune cells, called T and Natural Killer (NK) cells.

Now, Salk researchers have found a way to, for the first time, convert cells from x-linked SCID patients to a stem cell-like state, fix the genetic mutation and prompt the corrected cells to successfully generate NK cells in the laboratory.

The success of the new technique suggests the possibility of implanting these tweaked cells back into a patient so they can generate an immune system. Though the new work, published March 12, 2015 in Cell Stem Cell, is preliminary, it could offer a potentially less invasive and more effective approach than current options.

"This work demonstrates a new method that could lead to a more effective and less invasive treatment for this devastating disease," says senior author Inder Verma, Salk professor and American Cancer Society Professor of Molecular Biology. "It also has the potential to lay the foundation to cure other deadly and rare blood disorders."

Previous attempts to treat SCID involved bone marrow transplants or gene therapy, with mixed results. In what began as promising clinical trials in the 1990s, researchers hijacked virus machinery to go in and deliver the needed genes to newly growing cells in the patient's bone marrow. While this gene therapy did cure the disease at first, the artificial addition of genes ended up causing leukemia in a few of the patients. Since then, other gene therapy methods have been developed, but these are generally suited for less mild forms of the disease and require bone marrow transplants, a difficult procedure to perform on critically sick infants.

To achieve the new method, the Salk team secured a sample of bone marrow from a deceased patient in Australia. Using that small sample, the team developed the new method in three steps. First, they reverted the patient cells into induced pluripotent stem cells (iPSCs)--cells that, like embryonic stem cells, have the ability to turn into any type of tissue and hold vast promise for regenerative medicine.

"Once we had patient-derived stem cells, we could remove the genetic mutation, essentially fixing the cells," explains one of the first authors and Salk postdoctoral researcher Amy Firth.

The second innovation was to use new gene editing technology to correct the SCID-related genetic deficiency in these iPSCs. To remove the mutation, the researchers used a technology called TALEN (similar to the better known CRISPR method). This set of enzymes act as molecular scissors on genes, letting researchers snip away at a gene and replace the base pairs that make up DNA with other base pairs.

"Unlike traditional gene therapy methods, we aren't putting a whole new gene into a patient, which can cause unwanted side effects," says Tushar Menon, first author and Salk postdoctoral researcher. "We use TALEN-based genome editing to change just one nucleotide in one gene to correct the deficiency. The technique is literally that precise."

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Immune system-in-a-dish offers hope for 'bubble boy' disease

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March 12, 2015 // R. Colin Johnson

Living beating hearts on-a-chip were recently created from pluripotent stem cells discovered by 2010 Kyoto Prize Winner, Shinya Yamanaka.

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Bioengineers at the University of Berkeley aim to create all of the human organs on-a-chip then connect them with micro-fluidic channels to create a complete human-being on-a-wafer.

"We have learned how to derive almost any type of human tissue from skin stem cells as was first discovered by Yamanaka," professor Kevin Healy told EE Times. "Our initial application is drug screening without having to use animals, but putting organs-on-a-chip using the stem cells of the patient could help with genetic diseases as well."

"For instance, one drug might solve a heart problem, but create toxins in the liver," Healy told us. "Which would be much better to find out before administering to the patient."

As to creating living robots in this way, Healy said that was not their mission on the current project, since their funding in coming from the National Institutes of Health's (NIH's) Tissue Chip for Drug Screening Initiative, an interagency collaboration specifically aimed at developing 3-D human tissue chips for drug screening.

However, the technology being creating, especially the microfluidic channels connecting the organs-on-a-chip so that they interact, could someday serve as a basis for making robot-like creatures.

"What we would need for that is sensors and actuators. Sensors would be the easiest, but MIT in particular is working on artificial muscles to serve as actuators," Healy told us.

Living beating hearts on-a-chip were recently created from pluripotent stem cells discovered by 2010 Kyoto Prize Winner, Shinya Yamanaka.

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Heart on-a-chip beats

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IMAGE:Brain tumor stem cells (orange) in mice express a stem cell marker (green). Researchers at Washington University School of Medicine in St. Louis are studying how cancer stem cells make... view more

Credit: Yi-Hsien Chen

Scientists are eager to make use of stem cells' extraordinary power to transform into nearly any kind of cell, but that ability also is cause for concern in cancer treatment. Malignant tumors contain stem cells, prompting worries among medical experts that the cells' transformative powers help cancers escape treatment.

New research proves that the threat posed by cancer stem cells is more prevalent than previously thought. Until now, stem cells had been identified only in aggressive, fast-growing tumors. But a mouse study at Washington University School of Medicine in St. Louis shows that slow-growing tumors also have treatment-resistant stem cells.

The low-grade brain cancer stem cells identified by the scientists also were less sensitive to anticancer drugs. By comparing healthy stem cells with stem cells from these brain tumors, the researchers discovered the reasons behind treatment resistance, pointing to new therapeutic strategies.

"At the very least, we're going to have to use different drugs and different, likely higher dosages to make sure we kill these tumor stem cells," said senior author David H. Gutmann, MD, PhD, the Donald O. Schnuck Family Professor of Neurology.

The research appears online March 12 in Cell Reports.

First author Yi-Hsien Chen, PhD, a senior postdoctoral research associate in Gutmann's laboratory, used a mouse model of neurofibromatosis type 1 (NF1) low-grade brain tumors to identify cancer stem cells and demonstrate that they could form tumors when transplanted into normal, cancer-free mice.

NF1 is a genetic disorder that affects about 1 in every 2,500 babies. The condition can cause an array of problems, including brain tumors, impaired vision, learning disabilities, behavioral problems, heart defects and bone deformities.

The most common brain tumor in children with NF1 is the optic glioma. Treatment for NF1-related optic gliomas often includes drugs that inhibit a cell growth pathway originally identified by Gutmann. In laboratory tests conducted as part of the new research, it took 10 times the dosage of these drugs to kill the low-grade cancer stem cells.

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Stem cells lurking in tumors can resist treatment

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A new study by University of Alberta law researchers reveals sometimes overly optimistic news coverage of clinical translation of stem cell therapies--and as spokespeople, scientists need to be mindful of harnessing public expectations.

"As the dominant voice in respect to timelines for stem cell therapies, the scientists quoted in these stories need to be more aware of the importance of communicating realistic timelines to the press," said researcher Kalina Kamenova, who co-authored the study with professor Timothy Caulfield in the University of Alberta's Health Law Institute, based in the Faculty of Law.

Their analysis of media coverage showed that most news reports were highly optimistic about the future of stem cell therapies and forecasted unrealistic timelines for clinical use. The study, published in the latest issue of Science Translational Medicine, examined 307 news reports covering translational stem cell research in major daily newspapers in Canada, the United States and the United Kingdom between 2010 and 2013.

While the field of stem cell research holds tremendous promise, "it has also been surrounded by tremendous hype, and we wanted to quantify that in some degree," Caulfield said. "Pop culture representations have an impact on how the public perceives the readiness of stem cell research, and that in turn feeds into stem cell tourism, marketing of unproven therapies and even the public's trust in research. We wanted to provide findings that would help inform the issue."

Their study found that 69 per cent of all news stories citing timelines predicted that therapies would be available within five to 10 years or even sooner. At the same time, the press overlooked challenges and failures in therapy translation, such as the discontinuation of the first FDA-approved clinical trial of an embryonic stem cell-derived therapy for spinal cord injuries in 2011. The biotech company conducting the trial was a leader in embryonic stem cell therapies and its decision to stop its work on stem cells was considered a significant setback for the field.

As well, ethical concerns about the use of human embryonic stem cells were displaced from the forefront of news coverage, while the clinical translation of stem cell therapies and new discoveries, such as hockey star Gordie Howe's recent treatment, grabbed the headlines instead.

"Our findings showed that many scientists have often provided either by implication or direct quotes, authoritative statements regarding unrealistic timelines for stem cell therapies and media hype can foster unrealistic public expectations about clinical translation and increased patient demand for unproven stem cell therapies," Caulfield noted.

While stem cell therapy research is progressing and has seen a dramatic increase in the past decade of clinical trials for treatments, the vast majority of these studies are still in the safety-testing stage and involve a limited number of participants, Kamenova noted.

"The approval process for new treatments is long and complicated, and only a few of all drugs that enter pre-clinical testing are approved for human clinical trials. It takes on average 12 years to get a new drug from the lab to the market, and additional 11 to 14 years of post-market surveillance," she added.

The science world is under pressure to come up with cures for what ails us, but "care needs to be taken by the media and the research community so that advances in research and therapy are portrayed in a realistic manner," Caulfield said.

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Media portray unrealistic timelines for stem cell therapies

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Stem Cell Therapy Network
Stem Cell Therapy Network connects patients and providers through a global Stem Cell Therapy Network using our Patient Advocate System, Medical Tourism and Personal Injury Network. We have...

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Stem Cell Therapy Network - Video

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1 Control of Pluripotency Laboratory, Department of Physiological Sciences I, Faculty of Medicine, University of Barcelona, Hospital Clinic, Casanova 143, 08036, Barcelona, Spain 2 Faculty of Medicine, University of Sydney Medical School, Division of Pediatrics and Child Health, Westmead Children's Hospital, Locked Bag 4001, Westmead NSW 2145, Sydney, Australia 3 School of Anatomy Physiology & Human Biology and The Harry Perkins Institute for Medical Research (CCTRM), the University of Western Australia, 6 Verdun St, Nedlands WA 6009, Perth, Australia

* Author to whom correspondence should be addressed.

Received: 1 October 2014 / Accepted: 3 December 2014 / Published: 29 January 2015

Abstract: The use of adult myogenic stem cells as a cell therapy for skeletal muscle regeneration has been attempted for decades, with only moderate success. Myogenic progenitors (MP) made from induced pluripotent stem cells (iPSCs) are promising candidates for stem cell therapy to regenerate skeletal muscle since they allow allogenic transplantation, can be produced in large quantities, and, as compared to adult myoblasts, present more embryonic-like features and more proliferative capacity in vitro, which indicates a potential for more self-renewal and regenerative capacity in vivo. Different approaches have been described to make myogenic progenitors either by gene overexpression or by directed differentiation through culture conditions, and several myopathies have already been modeled using iPSC-MP. However, even though results in animal models have shown improvement from previous work with isolated adult myoblasts, major challenges regarding host response have to be addressed and clinically relevant transplantation protocols are lacking. Despite these challenges we are closer than we think to bringing iPSC-MP towards clinical use for treating human muscle disease and sporting injuries.

Roca, I.; Requena, J.; Edel, M.J.; Alvarez-Palomo, A.B. Myogenic Precursors from iPS Cells for Skeletal Muscle Cell Replacement Therapy. J. Clin. Med. 2015, 4, 243-259.

Roca I, Requena J, Edel MJ, Alvarez-Palomo AB. Myogenic Precursors from iPS Cells for Skeletal Muscle Cell Replacement Therapy. Journal of Clinical Medicine. 2015; 4(2):243-259.

Roca, Isart; Requena, Jordi; Edel, Michael J.; Alvarez-Palomo, Ana B. 2015. "Myogenic Precursors from iPS Cells for Skeletal Muscle Cell Replacement Therapy." J. Clin. Med. 4, no. 2: 243-259.

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JCM | Free Full-Text | Myogenic Precursors from iPS Cells ...

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GERMANTOWN, Md. (TheStreet) -- Neuralstem (CUR - Get Report) is providing an overly optimistic picture about its surgical stem-cell therapy for amyotrophic lateral sclerosis (ALS), the degenerative and fatal nerve disease.

Instead of disclosing the results from all 15 ALS patients enrolled in Neuralstem's phase II study of NSI-566, the company decided to only release a comparison between the patients who responded and those who didn't respond. Of course, the seven responders in the study showed more stabilization or improvements in muscle function compared with the eight patients deemed non-responders.

The scientific term for this conclusion is, "Duh."

When you work backwards and do some simple math on the muscle performance of all 15 ALS patients in the Neuralstem study, the results aren't very encouraging. Neuralstem chose to stay mum on this more customary analysis.

Neuralstem shares are down 14% to $3.21 in Thursday trading.

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Neuralstem Stock Plunges After Latest Study on ALS Drug

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Mutations in the methyl CpG binding protein 2 gene (MECP2) are the cause of the devastating childhood neurological disorder Rett Syndrome. Despite intense efforts spanning several decades the precise function of MECP2 has been difficult to pin down. Research primarily funded by the Rett Syndrome Research Trust (RSRT) and the National Institutes of Neurological Disease and Stroke (NINDS), and published today in the journal Nature reveals important information that could lead to new treatment approaches. The study, led by Michael Greenberg, Ph.D., Chairman of the Department of Neurobiology at Harvard University, shows that MECP2 dampens the expression of long genes.

In the early 1990s, Adrian Bird of the University of Edinburgh discovered the MeCP2 protein and proposed that it functions as a repressor of downstream genes. Since then, much effort has been focused on identifying these genes in the hopes that they could potentially become drug development targets. However, the results from numerous labs over the past 15 years have yielded long lists of genes with very little overlap, making it difficult to come to a consensus as to how mutations in MeCP2 lead to neurological dysfunction.

Today's publication sheds new and important light on this puzzle. Researchers Harrison Gabel and Benyam Kinde of the Greenberg lab set out to analyze various gene expression datasets in search of a common theme. This led them to an intriguing finding: the genes disrupted in Rett Syndrome are exceedingly long. The median size gene is about 20,000 nucleotides long, but about 10% of genes are greater than 100,000 nucleotides in length and some extend for more than one million nucleotides. It is the genes that are longer than 100,000 nucleotides that are the most affected in Rett Syndrome.

All of our cells contain the same genes. What differentiates a liver cell from a heart cell from a brain cell are the particular genes that are either silenced or active and the degree of activation, also known as expression.

The researchers in the Greenberg lab found that across all analyzed datasets, and in studies of different mouse brain regions, in the absence of MECP2 the expression of long genes is increased. Furthermore, they found that the longer a gene was, the more it increased. While the increase in expression is modest - only about 3 to 10% - it applies to thousands of genes and therefore might have a significant impact on the function of the brain.

The scientists gathered additional data in support of the gene length hypothesis. They found that in the biological mirror image of Rett, the MECP2 Duplication Syndrome, long genes are under expressed. They next analyzed long gene expression in mice of different ages. Although pre-symptomatic mice showed detectable overexpression, the effect was more dramatic in symptomatic mice. The researchers also found that the degree of increased long gene expression correlates with disease severity: mice with more severe Rett-like symptoms displayed more overexpression. Finally they looked at gene expression in autopsied brains of individuals with Rett. Just as in the mice models they found that long genes were overexpressed.

Greenberg's lab also found that the disruption of long gene expression appears to be a distinctive signature of Rett Syndrome and related disorders. "When we analyzed gene expression data from other neurological disorders that do not have similarities to Rett Syndrome, we did not see the same effects on very long genes," said Gabel.

The data from the Greenberg lab converge to suggest that Rett Syndrome may result from a relatively subtle yet widespread overexpression of long genes with functions important for the brain while the Duplication Syndrome could be due to under expression of these same genes.

"Interestingly, we found that while all cell types in the body use short and medium length genes, there is more expression of long genes in the brain than elsewhere in the body. This fact could help explain why Rett is mostly a neurological disease," says Kinde.

Last year the labs of Mark Zylka and Ben Philpot at the University of North Carolina at Chapel Hill discovered that a class of drugs called topoisomerase inhibitors reduces the expression of long genes. This begged the question of whether these drugs could be helpful in Rett Syndrome. Indeed the Greenberg lab found that adding low doses of the drug topotecan to cultured cells lacking MeCP2 normalized levels of long genes. Testing of the drug in mouse models of Rett is now underway.

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Length matters

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Stanford Course - Genetic Engineering Biotechnology
The co-evolution of genetic engineering and biotechnology in the last 30+ years has allowed for groundbreaking findings in molecular biology that have revolu...

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IMAGE:Cyberpsychology, Behavior, and Social Networking is an authoritative peer-reviewed journal published monthly online with Open Access options and in print that explores the psychological and social issues surrounding... view more

Credit: Mary Ann Liebert, Inc., publishers

New Rochelle, NY, March 11, 2015--Social network sites such as Facebook play an important role in maintaining relationships, including romantic relationships, whether individuals are involved in a geographically close or long-distance romantic relationship. A new study that compares the relative importance of social networks and explores the role they play in helping to maintain a close-by versus a long-distance romantic relationship is published in Cyberpsychology, Behavior, and Social Networking, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Cyberpsychology, Behavior, and Social Networking website until April 11, 2015.

In the article "The Use of Social Network Sites for Relationship Maintenance in Long-Distance and Geographically-Close Romantic Relationships," coauthors Cherrie Joy Billedo, Peter Kerkhof, and Catrin Finkenauer, VU University Amsterdam and University of the Philippines, describe differences in the intensity of use and the types of uses of social network sites between the two groups studied. They report how use of social network sites allows individuals to access information about, and monitor the activities of, romantic partners, and how that can be used to gauge a partner's involvement in the relationship and loyalty, with potentially positive or detrimental effects.

"Social network sites are used more frequently by those in long-distance relationships," says Editor-in-Chief Brenda K. Wiederhold, PhD, MBA, BCB, BCN, Interactive Media Institute, San Diego, California and Virtual Reality Medical Institute, Brussels, Belgium. "As long-distance relationships become more common, and continue to succeed, it becomes increasingly valuable to understand the role that technology plays in strengthening or damaging a romantic relationship."

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About the Journal

Cyberpsychology, Behavior, and Social Networking is an authoritative peer-reviewed journal published monthly online with Open Access options and in print that explores the psychological and social issues surrounding the Internet and interactive technologies, plus cybertherapy and rehabilitation. Complete tables of content and a sample issue may be viewed on the Cyberpsychology, Behavior, and Social Networking website.

About the Publisher

Mary Ann Liebert, Inc., publishers is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including Games for Health Journal, Telemedicine and e-Health, and Journal of Child and Adolescent Psychopharmacology. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN), was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 80 journals, books, and newsmagazines is available on the Mary Ann Liebert, Inc., publishers website.

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Are social networks helpful or harmful in long-distance romantic relationships?

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SALT LAKE CITY, March 12, 2015 /PRNewswire-USNewswire/ -- The ACMG Foundation for Genetic and Genomic Medicine and genetics professionals from around the world will be on hand to present bicycles to 19 local Salt Lake City-area children from the Shriners Hospitals for Children in Salt Lake City and Wasatch Adaptive Sports of Snowbird, Utah as part of the ACMG's 2015 Annual Clinical Genetics Meeting and Conference in the Salt Palace Convention Center, Exhibit Hall ABC, Friday, March 27 at 10:30 a.m.

The annual ACMG Foundation Day of Caring is sponsored by the ACMG Foundation for Genetic and Genomic Medicine, a prominent non-profit genetics foundation based in Bethesda, Maryland.

"It's supporters like the ACMG Foundation that help set Shriners Hospitals for Children apart, and for that we're truly grateful," said Dawn Wright, Public Relations Manager at Shriners Hospitals for Children, Salt Lake City said. "We go to great lengths to enrich our patients' lives beyond their medical care and equipment and encourage them to live life without limits."

"We would like to thank the ACMG Foundation and their supporters for providing bikes and helmets to children with special needs in our community. We strongly believe in the promotion of independence and well-being through recreation and are excited to see the dream of owning a bike become a reality for our families" said Peter Mandler, Executive Director of Wasatch Adaptive Sports, which is based out of Snowbird, Utah.

"The medical genetics community is dedicated to improving the lives of children and adults with genetic conditions," said Bruce R. Korf, MD, PhD, FACMG, President of the ACMG Foundation. "We are delighted that we can play a role in helping children with genetic conditions in the Salt Lake City area. What better way to demonstrate caring than by supporting children with a special surprise that helps them have some of the same experiences that their peers have."

The ACMG Foundation for Genetic and Genomic Medicine, whose theme is Better Health Through Genetics, supports education, research and a variety of other programs to translate genetic research into better health for all individuals.

The ACMG Foundation 2015 Day of Caring is supported by PerkinElmer, Shire, members of the American College of Medical Genetics and the ACMG Foundation for Genetic and Genomic Medicine.

The ACMG Foundation for Genetic and Genomic Medicine, a 501(c)(3) nonprofit organization, is a community of supporters and contributors who understand the importance of medical genetics in healthcare. Established in 1992, the ACMG Foundation for Genetic and Genomic Medicine supports the American College of Medical Genetics and Genomics; mission to "translate genes into health" by raising funds to attract the next generation of medical geneticists and genetic counselors, to sponsor important research, to promote information about medical genetics, and much more.

To learn more about the important mission and projects of the ACMG Foundation for Genetic and Genomic Medicine and how you too can support this great cause, please visit http://www.acmgfoundation.org or contact us at acmgf@acmgfoundation.org or 301/718-2014.

Media Alert Kathy Beal kbeal@acmg.net 301-238-4582

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Pioneering DNA research set to offer hope to millions of people could also help secure more jobs for Newcastle, health secretary Jeremy Hunt has told the Chronicle.

Mr Hunt was in the city to meet scientists and Tyneside families who have been involved with genetic testing that has been labelled as significant as the development of the internet by Prime Minister David Cameron.

In a medical breakthrough, North East scientists taking part in an unprecedented genome sequencing project have, for the first time in the UK, diagnosed rare diseases in two families after mapping their genes.

The technique, developed at Newcastle University, uses an individuals genetic blueprint to enable doctors to personalise medical care.

It means the Tyneside patients involved can now receive specialised treatment for their conditions, as well as helping prevent future generations who share their DNA from suffering a life of uncertainty.

Mr Hunt was introduced to the families taking part in the 100,000 Genomes Project at the Institute of Genetic Medicine at Newcastle University.

He said: This is historic, a huge amount of hard work into this. Its a very proud day for Newcastle and a very proud day for the NHS.

If you said in 1990 that the world was going to change because of this thing called the internet, people would have looked at you sceptically. David Cameron believes that genetic research is going to have that kind of impact on humanity.

The fact that Newcastle is at the centre of this genetic breakthrough adds to the sense of buzz here and hopefully will secure more jobs.

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Health secretary praises Newcastle scientists for 'historic' DNA breakthrough

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IMAGE: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... view more

Credit: Mary Ann Liebert, Inc., publishers

New Rochelle, NY, March 12, 2015-- After giving birth, a woman's estrogen levels drop to lower than usual levels, and while they return to the normal range relatively quickly among women who are not breastfeeding, this hypoestrogenic state may continue in lactating women and cause menopause-like symptoms. The results of a new study comparing vaginal dryness, hot flashes, and mood changes in women who are or are not breastfeeding 3 and 6 weeks after giving birth are reported 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 until April 12, 2015.

The article "Application of the Estrogen Threshold Hypothesis to the Physiologic Hypoestrogenemia of Lactation" provides evidence of the impact of breastfeeding on symptoms related to low estrogen levels during the postpartum period. Whereas lactating women showed no differences in the prevalence of hot flashes than non-breastfeeding women, they were significantly more likely to have vaginal dryness, report coauthors Sanjay Agarwal, MD, (University of California, San Diego School of Medicine), Julie Kim, MD (Cedars-Sinai Medical Center, Los Angeles, CA), Lisa Korst, MD, PhD (Childbirth Research Associates, North Hollywood, CA), and Claude Hughes, MD, PhD (Quintiles, Inc., Morrisville, NC).

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"The changes in vaginal lubrication secondary to low estrogen levels that can affect breastfeeding mothers may lead to discomfort on sexual intercourse," says Arthur I. Eidelman, MD, Editor-in-Chief of Breastfeeding Medicine. "Physicians should be aware of this problem, which may too often be minimized, and provide appropriate treatment, such as vaginal estrogen cream."

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.

About the Publisher

Mary Ann Liebert, Inc., publishers is a privately held, fully integrated media company known for establishing authoritative peer-reviewed journals in many promising areas of science and biomedical research, including Journal of Women's Health, Childhood Obesity, and Pediatric Allergy, Immunology, and Pulmonology. Its biotechnology trade magazine, Genetic Engineering & Biotechnology News (GEN) was the first in its field and is today the industry's most widely read publication worldwide. A complete list of the firm's 80 journals, books, and newsmagazines is available on the Mary Ann Liebert, Inc., publishers website.

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Can breastfeeding women have menopause-like symptoms?

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Sin city genetics
Getting ready to go into a three gallon pot.

By: (RMC)rockymountaincultivators

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Sin city genetics - Video

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SizeGenetics Review - Does Size Genetics Work?
http://www.sizegeneticspeniextender.com/ -- Click Link To Left For Full SizeGenetics Review! SizeGenetics Review - Does Size Genetics Work?

By: MrSizeGeneticsz

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SizeGenetics Review - Does Size Genetics Work? - Video

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In a study published in The Lancet on March 10, researchers from Brigham and Women's Hospital (BWH) report that patients with a genetic sensitivity to warfarin -- the most widely used anticoagulant for preventing blood clots -- have higher rates of bleeding during the first several months of treatment and benefited from treatment with a different anticoagulant drug. The analyses from the TIMI Study Group, suggest that using genetics to identify patients who are most at risk of bleeding, and tailoring treatment accordingly, could offer important safety benefits, particularly in the first 90 days of treatment.

"We were able to look at patients from around the world who were being treated with warfarin and found that certain genetic variants make a difference for an individual's risk for bleeding," said Jessica L. Mega, MD, MPH, a cardiologist at BWH, senior investigator in the TIMI Study Group and lead author of the paper. "For these patients who are sensitive or highly sensitive responders based on genetics, we observed a higher risk of bleeding in the first several months with warfarin, and consequently, a big reduction in bleeding when treated with the drug edoxaban instead of warfarin."

Warfarin has been in clinical use for 60 years and genetics has been thought to influence an individual's sensitivity to the drug. The FDA label for warfarin notes that genetic variants in two genes -- CYP2C9 and VKORC1 -- can assist in determining the right warfarin dosage for an individual. But a conclusive link between variation in these two genes and bleeding has been debated. By leveraging data from their ENGAGE AF-TIMI 48 trial -- an international, randomized, double-blind trial in which patients with atrial fibrillation received either a higher dose of edoxaban, a lower dose of edoxaban or warfarin to prevent blood clots from forming in the heart and leading to stroke -- the TIMI investigators were able to observe important connections between genetic differences and patient outcomes. The trial represents the largest study of this kind to date and included nearly three years of follow-up with participants.

In ENGAGE-TIMI 48, patients were randomly assigned treatment and followed over time. The research team divided 14,000 study participants into three categories based on genetic makeup: normal responders, sensitive responders or highly sensitive responders. During the first 90 days, sensitive and highly sensitive responders who received warfarin experienced significantly higher rates of bleeding compared to normal responders. As a result, during this early time period, edoxaban was more effective than warfarin at reducing bleeding in sensitive and highly sensitive responders.

"These findings demonstrate the power of genetics in personalizing medicine and tailoring specific therapies for our patients," said Marc S. Sabatine, MD, MPH, a cardiologist at BWH, Chairman of the TIMI Study Group and senior author of the paper.

Warfarin remains the most common anticoagulant in part due to economics and availability, but several novel oral anticoagulants (NOACs), including dabigatran, rivaroxaban and apixaban, have entered the market. Edoxaban, a Xa inhibitor, received FDA approval for stroke prevention in atrial fibrillation earlier this year based on the results of the ENGAGE AF-TIMI 48 trial.

Story Source:

The above story is based on materials provided by Brigham and Women's Hospital. Note: Materials may be edited for content and length.

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Conclusive link between genetics, clinical response to warfarin uncovered

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A multi-year, ongoing study suggests that a new kind of gene therapy for hemophilia B could be safe and effective for human patients. Published in the journal Science Translational Medicine, the research showed that a reprogrammed retrovirus could successfully transfer new factor IX (clotting) genes into animals with hemophilia B to dramatically decrease spontaneous bleeding. Thus far, the new therapy has proven safe.

"The result was stunning," said Timothy Nichols, MD, director of the Francis Owen Blood Research Laboratory at the University of North Carolina School of Medicine and co-senior author of the paper. "Just a small amount of new factor IX necessary for proper clotting produced a major reduction in bleeding events. It was extraordinarily powerful."

The idea behind gene therapy is that doctors could give hemophilia patients a one-time dose of new clotting genes instead of a lifetime of multiple injections of recombinant factor IX that until very recently had to be given several times a week. A new FDA-approved hemophilia treatment lasts longer than a few days but patients still require injections at least once or twice a month indefinitely.

This new gene therapy approach, like other gene therapy approaches, would involve a single injection and could potentially save money while providing a long-term solution to a life-long condition. A major potential advantage of this new gene therapy approach is that it uses lentiviral vectors, to which most people do not have antibodies that would reject the vectors and make the therapy less effective.

In human clinical studies, approximately 40 percent of the potential participants screened for a different kind of viral vector -- called adeno-associated viral vectors -- have antibodies that preclude them from entering AAV trials for hemophilia gene therapy treatment. This means that more people could potentially benefit from the lentivirus gene therapy approach.

Hemophilia is a bleeding disorder in which people lack a clotting factor, which means they bleed much more easily than people without the disease. Often, people with hemophilia bleed spontaneously into joints, which can be extremely painful and crippling. Spontaneous bleeds into soft tissues are also common and can be fatal if not treated promptly. Hemophilia A affects about one in 5,000 male births. These patients do not produce enough factor VIII in the liver. This leads to an inability to clot. Hemophilia B affects about one in 35,000 births; these patients lack factor IX.

This new method was spearheaded by Luigi Naldini, PhD, director of the San Raffaele Telethon Institute for Gene Therapy and co-senior author on the Science Translational Medicine paper.

For this study, Naldini and Nichols developed a way to use a lentivirus, which is a large retrovirus, to deliver factor IX genes to the livers of three dogs that have naturally occurring hemophilia. The researchers removed the genes involved in viral replication. "Essentially, this molecular engineering rendered the virus inert," Nichols said. "It had the ability to get into the body but not cause disease." This process turned the virus into a vector -- simply a vehicle to carry genetic cargo.

Unlike some other viral vectors that have been used for gene therapy experiments, the lentiviral vector is so large that it can carry a lot of payload -- namely, the factor IX genes that people with hemophilia B lack. (This approach could also be used for hemophilia A where the FVIII gene is considerably larger.)

These viral vectors were then injected directly into the liver or intravenously. After more than three years, the three dogs in the study experienced zero or one serious bleeding event each year. Before the therapy, the dogs experienced an average of five spontaneous bleeding events that required clinical treatment. Importantly, the researchers detected no harmful effects.

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New gene therapy for hemophilia shows potential as safe treatment

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Using mutant protein, CHOP hematologist safely removes unwanted antibodies, reverses hemophilia in dog model of bleeding disease

Using gene therapy to produce a mutant human protein with unusually high blood-clotting power, scientists have successfully treated dogs with the bleeding disorder hemophilia, without triggering an unwanted immune response. In addition, the "turbocharged" clotting factor protein eliminated pre-existing antibodies that often weaken conventional treatments for people with hemophilia.

"Our findings may provide a new approach to gene therapy for hemophilia and perhaps other genetic diseases that have similar complications from inhibiting antibodies," said the study leader, Valder R. Arruda, M.D., Ph.D., a hematology researcher at The Children's Hospital of Philadelphia (CHOP).

Arruda and colleagues published their animal study results in the print edition of Blood on March 5.

Hemophilia is an inherited bleeding disorder that famously affected European royal families descended from Queen Victoria. Most commonly occurring in two types, hemophilia A and hemophilia B, the disease impairs the blood's ability to clot, sometimes fatally. When not fatal, severe hemophilia causes painful, often disabling internal bleeding and joint damage.

Doctors treat hemophilia with frequent intravenous infusions of blood clotting proteins called clotting factors, but these treatments are expensive and time-consuming. Moreover, some patients develop inhibiting antibodies that negate the effectiveness of the infusions.

For more than two decades, many research teams, including at CHOP, have investigated gene therapy strategies that deliver DNA sequences carrying genetic code to produce clotting factor in patients. However, this approach has been frustrated by the body's immune response against vectors--the non-disease-causing viruses used to carry the DNA. Those responses, which defeated initial benefits seen in experimental human gene therapy, were dose-dependent: higher amounts of vectors caused more powerful immune responses.

Arruda and colleagues therefore investigated gene therapy that used lower dosages of vector (adeno-associated viral-8 vector, or AAV-8 vector) to produce a more potent clotting factor--a variant protein called FIX-Padua.

Arruda was part of a scientific team in 2009 that discovered FIX-Padua in a young Italian man who had thrombosis, excessive clotting that can dangerously obstruct blood vessels. A mutation produced the mutant clotting factor, called FIX-Padua, named after the patient's city of residence. This was the first mutation in the factor IX gene found to cause thrombosis. All previously discovered FIX mutations lead to hemophilia, the opposite of thrombosis.

FIX-Padua is hyperfunctional--it clots blood 8 to 12 times more strongly than normal, wild-type factor IX. In the current study, the researchers thus needed to strike a balance--to relieve severe hemophilia in dogs, by using a dose strong enough to allow clotting, but not enough to cause thrombosis or stimulate immune reactions. "Our ultimate goal is to translate this approach to humans," said Arruda, "by adapting this variant protein found in one patient to benefit other patients with the opposite disease."

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Study bolsters 'turbocharged' protein as a promising tool in hemophilia gene therapy

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5 through 7 spinal cord injury
Kendall first Walmart trip 5 months post injury.

By: Christie Embry Martin

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5 through 7 spinal cord injury - Video

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Lindsey Caldwell

Heart disease is the leading cause of death among Americans. Recently the bio-tech industry has been exploding with cardiac research like last week's heart attack preventing nanobots. New research by the team at the University of California, Berkley has created working human heart cells on a tiny chip designed to test the efficacy of new drugs in clinical trials. This heart-on-a-chip is officially known as a cardiac microphysiological system, or MPS. Using this heart-on-a-chip, scientists can measure the potential cardiac damage of a drug before it reaches expensive human trials.

Drug trials can take years, and to mitigate risk these drugs undergo testing in non-human subjects. Animals are often used in place of humans, but animal models can be problematic. Specifically, they are less effective at predicting cardiotoxicity, wherein a drug damages the heart. This is important because one-third of drugs withdrawn from testing are pulled due to cardiotoxic effects.

Drugs that are first tested in animal models can succeed to future testing stages without setting off alarms. After successful early stages more time and money is invested and the drugs progress to human trials, only to be stopped in their tracks because they are found to be toxic to human hearts.

The cells on this tiny MPS chip are human heart cells that were created from pluripotent stem cells. These cells react to drugs the same way as a human heart inside a living person. By creating a portable, low-risk, and accurate drug testing environment, scientists may be able to advance clinical trials of new drugs and bring them to market sooner.

Here is a video by the UC Berkley research team of their heart cells actually beating.

Source: Berkeley

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Heart-on-a-chip tests drugs cardiotoxicity with its real heartbeat

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