Marshall Islands sues nine nuclear powers in international court

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THE HAGUE , Netherlands, April 24 (UPI) -- The Republic of the Marshall Islands, a small island nation in the Pacific Ocean, filed a lawsuit in the International Court of Justice in The Hague, Netherlands, accusing nine nuclear powers of flagrant denial of human justice.

While not seeking compensation, it noted the harm it allegedly suffered because of the nuclear arms race. The suit contends nuclear powers are not abiding by Article VI of the Non-Proliferation Treaty requiring nations to pursue negotiations in good faith, leading to the cessation of the nuclear arms race. The lawsuit explains the nuclear nations actions in modernizing their nuclear arsenals while avoiding disarmament negotiations.

The Marshall Islands was a nuclear testing site for the United States in the 1940s and 1950s.

Our people have suffered the catastrophic and irreparable damage of these weapons, and we vow to fight so that no one else on Earth will ever again experience these atrocities, said Marshall Islands Foreign Secretary Tony de Brum.

The suit said the United States, Russia, the United Kingdom, France and China continuously violate customary international law in failing to disarm. The four other nuclear powers -- Israel, India, Pakistan and North Korea -- are not bound by the treaty but are bound by international law.

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Marshall Islands sues nine nuclear powers in international court

Pacific Island Nation Sues U.S., Others For Violating Nuclear Treaty

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hide captionThe second atomic bomb test at Bikini Atoll on July 25, 1946. The Marshall Islands, where Bikini is located, is suing the U.S. for what it calls a violation of the Nuclear Non-Proliferation Treaty.

The second atomic bomb test at Bikini Atoll on July 25, 1946. The Marshall Islands, where Bikini is located, is suing the U.S. for what it calls a violation of the Nuclear Non-Proliferation Treaty.

The Marshall Islands, the Pacific chain where the U.S. carried out dozens of nuclear tests in the late 1940s and 1950s, has filed suit in the Hague against Washington and the governments of eight other countries it says have not lived up to the Nuclear Non-Proliferation Treaty.

The Guardian says that in the "unprecedented legal action," brought before the International Court of Justice on Thursday, "the Republic of the Marshall Islands accuses the nuclear weapons states of a 'flagrant denial of human justice.' It argues it is justified in taking the action because of the harm it suffered as a result of the nuclear arms race."

Besides the U.S., the Marshall Islands is also suing Russia, China, France and the U.K., which have all signed the Non-Proliferation Treaty, or NPT, as well as four other countries that have never signed India, Pakistan, North Korea and Israel, which has never acknowledged possessing nuclear weapons.

In court documents, the Marshall Islands argues that the 1958 NPT, which did not come into force until 1970, amounts to a compact between nuclear haves and have-nots. Non-weapons states essentially agreed not to try to acquire nuclear weapons in exchange for weapons states moving toward disarmament, the Marshalls says.

According to the Guardian:

"Although the size of the arsenals are sharply down from the height of the cold war, the Marshall Islands' legal case notes there remain more than 17,000 warheads in existence, 16,000 of them owned by Russia and the US enough to destroy all life on the planet."

The Marshalls were the site of 66 nuclear tests from 1946 to 1958, including the first thermonuclear weapon in 1952 and, two years later, the highest-yielding test ever conducted by the U.S., code-named Castle Bravo, which was equivalent to 1,000 Hiroshima bombs.

Although islanders were relocated from Bikini and Eniwetok atolls ground zero for the majority of the tests three other Marshall atolls underwent emergency evacuations in 1954 after they were unexpectedly exposed to radioactive fallout. The Marshallese say they've suffered serious health issues ever since.

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Pacific Island Nation Sues U.S., Others For Violating Nuclear Treaty

Mount Sinai Researchers Identify Genetic Alterations in Shared Biological Pathways as Major Risk Factor for Autism …

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Newswise (NEW YORK April 24) A substantial proportion of risk for developing autism spectrum disorders (ASD), resides in genes that are part of specific, interconnected biological pathways, according to researchers from the Icahn School of Medicine at Mount Sinai, who conducted a broad study of almost 2,500 families in the United States and throughout the world. The study, titled Convergence of Genes and Cellular Pathways Dysregulated in Autism Spectrum Disorders, was first published online in The American Journal of Human Genetics on April 24.

ASD affects about one percent of the population in the United States and is characterized by impairments in social interaction and communication, as well as by repetitive and restricted behaviors. ASD ranges from mild to severe levels of impairment, with cognitive function among individuals from above average to intellectual disability.

Previously, ASD has been shown to be highly inheritable, and genomic studies have revealed that that there are various sources of risk for ASD, including large abnormalities in whole chromosomes, deletions or duplications in sections of DNA called copy number variants (CNVs), and even changes of single nucleotides (SNVs) within a gene; genes contain instructions to produce proteins that have various functions in the cell.

The researchers reported numerous CNVs affecting genes, and found that these genes are part of similar cellular pathways involved in brain development, synapse function and chromatin regulation. Individuals with ASD carried more of these CNVs than individuals in the control group, and some of them were inherited while others were only present in offspring with ASD.

An earlier study, results of which were first published in 2010, highlighted a subset of these findings within a cohort of approximately 1,000 families in the U.S. and Europe; this larger study has expanded that cohort to nearly 2,500 families, each comprising trios of two parents and one child. By further aggregating CNVs and SNVs (the latter identified in other studies), Mount Sinai researchers discovered many additional genes and pathways involved in ASD.

We hope that these new findings will help group individuals with ASD based upon their genetic causes and lead to earlier diagnosis, and smarter, more focused therapies and interventions for autism spectrum disorders, said first author Dalila Pinto, PhD, Assistant Professor of Psychiatry, and Genetics and Genomic Sciences at the Icahn School of Medicine at Mount Sinai. Dr. Pinto is a Seaver Foundation Faculty Fellow, and a member of the Mindich Child Health & Development Institute, the Icahn Institute for Genomics and Multiscale Biology, and the Friedman Brain Institute at the Icahn School of Medicine at Mount Sinai; other Mount Sinai researchers on this study include Mafalda Barbosa, Graduate Student in Psychiatry; Xiao Xu, PhD, Postdoctoral Fellow in Psychiatry; Alexander Kolevzon, MD, Clinical Director of the Seaver Autism Center and Associate Professor of Psychiatry and Pediatrics; and Joseph D. Buxbaum, PhD, Director of the Seaver Autism Center, Vice Chair for Research in Psychiatry, and Professor of Psychiatry, Neuroscience, and Genetics and Genomic Sciences.

This study was jointly supported through the main funders of the International Autism Genome Project: Autism Speaks, the Health Research Board (Ireland), the Hillbrand Foundations, the Genome Canada, the Ontario Genomics Institute, and the Canadian Institutes of Health Research.

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Mount Sinai Researchers Identify Genetic Alterations in Shared Biological Pathways as Major Risk Factor for Autism ...

The National CLAS Standards in Health and Health Care: A Tool for Tribal Communities – Video

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The National CLAS Standards in Health and Health Care: A Tool for Tribal Communities
Miscommunication in health and medical contexts can have tragic consequences. Standards for culturally and linguistically appropriate services (CLAS) address...

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The National CLAS Standards in Health and Health Care: A Tool for Tribal Communities - Video

How Health Coaches Can Help Reverse the Health Care Crisis – Video

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How Health Coaches Can Help Reverse the Health Care Crisis
This video is owned by the Institute for Integrative Nutrition, from which I #39;m happily a current student! 🙂 Wanted to share a bit of how we Health Coaches can help you not only to live a healthier...

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Kuster: Health Care Law Gaining Fans As It Unfolds

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Hanover U.S. Rep. Annie Kuster, D-N.H., said Thursday she continues to support the Affordable Care Act and that more Americans are coming to appreciate the health-care law as they gain coverage or see its benefits.

Peoples perspectives are changing, Kuster said in an interview after an appearance at Dartmouth College.

The first-term Democrat said almost 100,000 New Hampshire residents are benefiting from the ACA through expanded Medicaid and private plans offered via the states exchange and young people under 26 staying on their parents plans.

The new health care law promises to be a central issue in the November elections, and President Obama last week said Democrats should forcefully defend and be proud of the fact....were helping because of something we did.

A Gallup poll released two weeks ago found 54 percent of Americans disapprove of the law, while 43 percent approve, the latter number increasing since last November.

Nationally, approximately 8 million Americans have signed up for private health care coverage through the new marketplaces and an additional 3 million gained coverage under Medicaid expansion.

Kuster said that rather than repealing the law, as many Republican lawmakers have advocated, her goal is to ease the transition and to not leave people with their lives disrupted. For example, she said she hopes to ensure that people are not punished with fines and fees for failing to sign up in a timely manner.

Efforts to smooth the laws adoption in New Hampshire are not all legislative fixes, she said.

Instead, improvements are likely to come from competition within the private sector as more companies join the states exchange, she said.

Kuster was in Hanover Thursday to meet with area businesswomen and Tuck School of Business at Dartmouth faculty and students as part of an ongoing Womens Economic Agenda tour of the state.

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Health Care Workers Must Out LGBT Ugandans, According to New Guidelines

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The recently revised draft guidelines for Ugandan health workers who may encounter LGBT people essentially requires those health care workers to out LGBT Ugandans.

The latest revision of draft guidelines for Ugandan health care workers who may encounter LGBT people set a dangerous precedent that essentially requires those health care providers to report anyone who admits to being gay.

Signed by Uganda's director general of health services, the April revision of the "Draft Guidelines for Health Workers Regarding Health Services for Homosexuals," makes Ugandan health workers the "frontline enforcers of the newly passed Anti-Homosexuality Act," according to BuzzFeed, which obtained a copy of the draft policy.

"The purpose of these guidelines is to clarify to health workers how to handle clients and patients involved in homosexual activities," reads the draft, "but not to promote acts of homosexuality."

After claiming that LGBT Ugandans have a fundamental right to medical care and privacy surrounding that care, the guidelines note a health care worker may "break confidentiality" when the person seeking care is a minor, when someone has been "sodomized," if the patient has a "compromised" mental status, or is guilty of "aggravated homosexuality" as defined by the Anti-Homosexuality Act.

According to the draconian law, signed by Ugandan president Yoweri Museveni in February, "aggravated homosexuality" is defined as any repeated instances of same-sex sexual contact including such behavior in private, between consenting adults any such instance where at least one person is HIV-positive or if one partner is a minor, mentally disabled, or under the influence of drugs or alcohol.

Although the latest revision strikes a clause seen in last month's version that required LGBT Ugandans to inform the health worker treating them that they are LGBT, this iteration of the guidelines clamp down on organizations that may treat LGBT people, citing a provision in the law that prohibits "aiding or abetting" homosexuality.

In a clause that appears to allude to the recent raid by Ugandan police on a U.S.-funded HIV clinic that saw at least one clinic employee arrested for "recruiting" young men into homosexuality, the guidelines note, "It is the sole responsibility of the researcher, investigator, health worker or his/her facility to ensure no acts of promotion or recruitment of subjects into acts of homosexuality as stipulated by the anti Homosexuality Act, 2014 occur. In the event of promotion or recruitment, they shall be held accountable."

BuzzFeed also notes that the guidelines are signed by Jane Ruth Aceng, the health services general director, who also served as the lead author of the so-called scientific report that convinced President Museveni that homosexuality was not an innate characteristicbut rather a socially acquired ill that could be cured. Indeed, the guidelines' foreword notes that state officials are "well aware that homosexuality is not a medical disorder nor an abonormality [sic], [but that] those involved in the practice may present with direct/inderect [sic] consequences that require medical care/treatment." Nowhere in the forward or the draft guidelines are such treatments clearly enumerated, meaning it's entirely possible that such "treatment" may include efforts to "convert" gay people, or, as is more common in the cases of lesbians in homophobic African nations, such treatment may involve so-called corrective rape.

Just two days ago, the World Bank released a report explaining that it would consider granting a thus-far-withheld $90 million health care loan to the Ugandan government if the government can prove that LGBT people and the health workers who treat them will be safe from penalty under the wide-reaching law.

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New genetic brain disorder in humans discovered

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A newly identified genetic disorder associated with degeneration of the central and peripheral nervous systems in humans, along with the genetic cause, is reported in the April 24, 2014 issue of Cell.

The findings were generated by two independent but collaborative scientific teams, one based primarily at Baylor College of Medicine and the Austrian Academy of Sciences, the other at the University of California, San Diego School of Medicine, the Academic Medical Center (AMC) in the Netherlands and the Yale University School of Medicine.

By performing DNA sequencing of more than 4,000 families affected by neurological problems, the two research teams independently discovered that a disease marked by reduced brain size and sensory and motor defects is caused by a mutation in a gene called CLP1, which is known to regulate tRNA metabolism in cells. Insights into this rare disorder, the researchers said, may have important implications for the future treatment of more common neurological conditions.

"What we found particularly striking, when considering the two studies together, is that this is not a condition that we would have been able to separate from other similar disorders based purely on patient symptoms or clinical features," said Joseph G. Gleeson, MD, Howard Hughes Medical Institute investigator, professor in the UC San Diego departments of Neurosciences and Pediatrics and at Rady Children's Hospital-San Diego, a research affiliate of UC San Diego. "Once we had the gene spotted in these total of seven families, then we could see the common features. It is the opposite way that doctors have defined diseases, but represents a transformation in the way that medicine is practiced."

Each child tested was affected by undiagnosed neurological problems. All of the children were discovered to carry a mutation in the CLP1 gene and displayed the same symptoms, such as brain malformations, intellectual disabilities, seizures and sensory and motor defects. A similar pattern emerged in both studies, one led by Gleeson, with Murat Gunel, MD, of the Yale University School of Medicine and Frank Baas, PhD, of the Academic Medical Center in the Netherlands, and the other by Josef Penninger and Javier Martinez of the Austrian Academy of Sciences, teamed with James R. Lupski, MD, PhD, of the Baylor College of Medicine.

"Knowing fundamental pathways that regulate the degeneration of neurons should allow us to define new pathways that, when modulated, might help us to protect motor neurons from dying, such as in Lou Gehrig's disease," said Penninger, scientific director of the Institute of Molecular Biotechnology of the Austrian Academy of Sciences.

The CLP1 protein plays an important role in generating mature, functional molecules called transfer RNAs (tRNAs), which shuttle amino acids to cellular subunits called ribosomes for assembly into proteins. Mutations affecting molecules involved in producing tRNAs have been implicated in human neurological disorders, such as pontocerebellar hypoplasia (PCH), a currently incurable neurodegenerative disease affecting children. Although CLP1 mutations have been linked to neuronal death and motor defects in mice, the role of CLP1 in human disease was not known until now.

These scientists performed DNA sequencing on children with neurological problems. Seven out of the more than 4,000 families studied shared an identical CLP1 mutation, which was associated with motor defects, speech impairments, seizures, brain atrophy and neuronal death.

Bass at the AMC said the neurological condition represents a new form of PCH. "Identification of yet another genetic cause for this neurodegenerative disorder will allow for better genetic testing and counseling to families with an affected child," he said.

In a published paper last year, Gleeson and colleagues identified a different gene mutation for a particularly severe form of PCH, and reported early evidence that a nutritional supplement might one day be able to prevent or reverse the condition.

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New genetic brain disorder in humans discovered

Genetic alterations in shared biological pathways as major risk factor for ASD

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24-Apr-2014

Contact: Sid Dinsay sid.dinsay@mountsinai.org 212-241-9200 The Mount Sinai Hospital / Mount Sinai School of Medicine

A substantial proportion of risk for developing autism spectrum disorders (ASD), resides in genes that are part of specific, interconnected biological pathways, according to researchers from the Icahn School of Medicine at Mount Sinai, who conducted a broad study of almost 2,500 families in the United States and throughout the world. The study, titled "Convergence of Genes and Cellular Pathways Dysregulated in Autism Spectrum Disorders," was first published online in the American Journal of Human Genetics on April 24.

ASD affects about one percent of the population in the United States and is characterized by impairments in social interaction and communication, as well as by repetitive and restricted behaviors. ASD ranges from mild to severe levels of impairment, with cognitive function among individuals from above average to intellectual disability.

Previously, ASD has been shown to be highly inheritable, and genomic studies have revealed that that there are various sources of risk for ASD, including large abnormalities in whole chromosomes, deletions or duplications in sections of DNA called copy number variants (CNVs), and even changes of single nucleotides (SNVs) within a gene; genes contain instructions to produce proteins that have various functions in the cell.

The researchers reported numerous CNVs affecting genes, and found that these genes are part of similar cellular pathways involved in brain development, synapse function and chromatin regulation. Individuals with ASD carried more of these CNVs than individuals in the control group, and some of them were inherited while others were only present in offspring with ASD.

An earlier study, results of which were first published in 2010, highlighted a subset of these findings within a cohort of approximately 1,000 families in the U.S. and Europe; this larger study has expanded that cohort to nearly 2,500 families, each comprising "trios" of two parents and one child. By further aggregating CNVs and SNVs (the latter identified in other studies), Mount Sinai researchers discovered many additional genes and pathways involved in ASD.

"We hope that these new findings will help group individuals with ASD based upon their genetic causes and lead to earlier diagnosis, and smarter, more focused therapies and interventions for autism spectrum disorders," said first author Dalila Pinto, PhD, Assistant Professor of Psychiatry, and Genetics and Genomic Sciences at the Icahn School of Medicine at Mount Sinai. Dr. Pinto is a Seaver Foundation Faculty Fellow, and a member of the Mindich Child Health & Development Institute, the Icahn Institute for Genomics and Multiscale Biology, and the Friedman Brain Institute at the Icahn School of Medicine at Mount Sinai; other Mount Sinai researchers on this study include Mafalda Barbosa, Graduate Student in Psychiatry; Xiao Xu, PhD, Postdoctoral Fellow in Psychiatry; Alexander Kolevzon, MD, Clinical Director of the Seaver Autism Center and Associate Professor of Psychiatry and Pediatrics; and Joseph D. Buxbaum, PhD, Director of the Seaver Autism Center, Vice Chair for Research in Psychiatry, and Professor of Psychiatry, Neuroscience, and Genetics and Genomic Sciences.

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Genetic alterations in shared biological pathways as major risk factor for ASD

Researchers discover that two defective copies of a single gene cause rare brain disorder

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CHICAGO (Reuters) - International teams of researchers using advanced gene sequencing technology have uncovered a single genetic mutation responsible for a rare brain disorder that may have stricken families in Turkey for some 400 years.

The discovery of this genetic disorder, reported in two papers in the journal Cell, demonstrates the growing power of new tools to uncover the causes of diseases that previously stumped doctors.

Besides bringing relief to affected families, who can now go through prenatal genetic testing in order to have children without the disorder, the discovery helps lend insight into more common neurodegenerative disorders, such as ALS, also known as Lou Gehrig's disease, the researchers said.

The reports come from two independent teams of scientists, one led by researchers at Baylor College of Medicine and the Austrian Academy of Sciences, and the other by Yale University, the University of California, San Diego, and the Academic Medical Center in the Netherlands.

Both focused on families in Eastern Turkey where marriage between close relatives, such as first cousins, is common. Geneticists call these consanguineous marriages.

In this population, the researchers focused specifically on families whose children had unexplained neurological disorders that likely resulted from genetic defects.

Both teams identified a new neurological disorder arising from a single genetic variant called CLP1. Children born with this disorder inherit two defective copies of this gene, which plays a critical role in the health of nerve cells.

Babies with the disorder have small and malformed brains, they develop progressive muscle weakness, they do not speak and they are increasingly prone to seizures.

Dr Ender Karaca, a post-doctoral associate in the department of molecular and human genetics at Baylor, first encountered the disorder in 2006 and 2007 during his residency training as a clinical geneticist in Turkey.

"We followed them for years," said Karaca, a lead author on one of the papers. Karaca said he and his colleagues performed some basic genetic tests on the families but to no avail.

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Researchers discover that two defective copies of a single gene cause rare brain disorder

Scientists Build a Custom Chromosome

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BALTIMORE, MD. Scientists have built a custom chromosome -- a package of genetic material assembled entirely from synthetic DNA. This engineered chromosome belongs to yeast, but experts say it can help them understand how genes work in humans as well. And it could help make these tiny living factories better at producing everything from medicines to biofuels. Students were key to the project In a lab at Johns Hopkins University, students stitched together machine-made strands of DNA, the chemical that carries the genetic blueprints of life. Their goal: to assemble all 6,000 genes in the genome of yeast. "So, in every single well there should have hopefully been something, said Macintosh Cornwell, a student at Johns Hopkins. Cornwell, a junior, is looking for signs his last stitching reaction worked. So, overall, we had pretty moderate success across the board, he said. Johns Hopkins geneticist Jef Boeke leads the class. He said yeast does familiar jobs, like turning grapes into wine, but they also do more than that. We have yeast that are used not just to make alcohol and bread, but also all kinds of chemicals, medicines, vaccines and fuels. And I think were going to see more and more of this in the future, said Boeke. And with genetic engineering, Boeke said, scientists could help yeast do those jobs better. Plus, these one-celled creatures share about a third of their genes with us. Studying their genes can teach us a lot about ourselves. Like us, yeast cells keep their genetic material in bundles of DNA known as chromosomes. Think of each chromosome as a book of genetic instructions, Boeke said. The book would be made up of chapters, the chapters would be made up of paragraphs and words and, ultimately letters, explained Boeke. And each gene is a word made up of letters of DNA, the chemical chain that forms the iconic twisted ladder shape. Boekes class has strung together all the words in one genetic book so far -- one chromosome out of yeasts 16. They engineered the new chromosome to let researchers shuffle genes around like a deck of cards. Some will have winning decks at making biofuels and some at making some other useful product, he said. Researchers say they are careful to consider the ethical implications of re-writing the code of life, but Boeke adds that his students are learning the basic tools of modern biology and getting excited about the possibilities. We could teach them how to do something at once very practical but at the same time amazing and unique, said Boeke. Cornwell said its helped him prepare for a career in science. The range of skills you learn and the amount of experience you get in such a small time period, its invaluable, really, said Cornwell. He and his class are on the cutting edge of this new world of biology.

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GEN Publishing introduces 'Clinical OMICs' digital publication

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PUBLIC RELEASE DATE:

24-Apr-2014

Contact: Tamlyn Oliver toliver@clinicalomics.com 914-740-2199 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, April 24, 2014GEN Publishing recently introduced Clinical OMICs a semi-monthly digital publication focusing on the application of OMICs technologies in clinical settings. These advanced techniques, such as next-gen sequencing, are beginning to transform medical care just as they revolutionized basic life science research over the past decade-and-a-half.

"GEN's editors and reporters have written about the research use of pharmacogenomics, genomics, metabolomics, transcriptomics, etc. etc. for years," said John Sterling, editor-in-chief of Genetic Engineering & Biotechnology News (GEN). "The rapid advance of OMICs technologies has reached the point where we are convinced that the time is now for a new publication that shows how these diagnostic methodologies are dramatically impacting clinical practice."

Clinical OMICs is directed at clinical lab directors and managers, oncologists, infectious disease specialists, and cardiologists. Intended to serve as a resource for the development and standardization of best OMICs practices, Clinical OMICs provides critical information and insights on the trend toward personalized medicine.

The premier issue contains articles on translating OMICs into cancer biology and medicine, how payers are grappling with reimbursement issues, a profile of Lawrence Brody, who is overseeing NHGRI's new division of genomics and society, the move of next-gen sequencing systems into the clinic, and a case study of a genomics test for coronary artery disease. Late-breaking clinical OMICs news, OMICs-related clinical APPS, and new products are also featured.

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Clinical OMICs is brought to you by GEN Publishing, the parent company of Genetic Engineering & Biotechnology News.

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Genetic code of the deadly tsetse fly unraveled

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19 hours ago Side view of a pregnant tsetse fly. Credit: Geoffrey M. Attardo

Mining the genome of the disease-transmitting tsetse fly, researchers have revealed the genetic adaptions that allow it to have such unique biology and transmit disease to both humans and animals.

The tsetse fly spreads the parasitic diseases human African trypanosomiasis, known as sleeping sickness, and Nagana that infect humans and animals respectively.

Throughout sub-Saharan Africa, 70 million people are currently at risk of deadly infection. Human African trypanosomiasis is on the World Health Organization's (WHO) list of neglected tropical diseases and since 2013 has become a target for eradication. Understanding the tsetse fly and interfering with its ability to transmit the disease is an essential arm of the campaign.

This disease-spreading fly has developed unique and unusual biological methods to source and infect its prey. Its advanced sensory system allows different tsetse fly species to track down potential hosts either through smell or by sight. This study lays out a list of parts responsible for the key processes and opens new doors to design prevention strategies to reduce the number of deaths and illness associated with human African trypanosomiasis and other diseases spread by the tsetse fly.

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"Tsetse flies carry a potentially deadly disease and impose an enormous economic burden on countries that can least afford it by forcing farmers to rear less productive but more trypanosome-resistant cattle." says Dr Matthew Berriman, co-senior author from the Wellcome Trust Sanger Institute. "Our study will accelerate research aimed at exploiting the unusual biology of the tsetse fly. The more we understand, the better able we are to identify weaknesses, and use them to control the tsetse fly in regions where human African trypanosomiasis is endemic."

The team, composed of 146 scientists from 78 research institutes across 18 countries, analysed the genome of the tsetse fly and its 12,000 genes that control protein activity. The project, which has taken 10 years to complete, will provide the tsetse research community with a free-to-access resource that will accelerate the development of improved tsetse-control strategies in this neglected area of research.

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The tsetse fly is related to the fruit fly a favoured subject of biologists for more than 100 years but its genome is twice as large. Within the genome are genes responsible for its unusual biology. The reproductive biology of the tsetse fly is particularly unconventional: unlike most insects that lay eggs, it gives birth to live young that have developed to a large size by feeding on specialised glands in the mother.

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Genetic code of the deadly tsetse fly unraveled

Gene Therapy May Enhance Cochlear Implants, Animal Study Finds

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By Steven Reinberg HealthDay Reporter

WEDNESDAY, April 23, 2014 (HealthDay News) -- Australian researchers say that gene therapy may one day improve the hearing of people with cochlear implants, allowing them to appreciate music and hear in noisy environments.

In experiments with deaf guinea pigs, senior study author Gary Housley and colleagues found that inserting genes in the area of the cochlear implant and passing an electric charge through the implant stimulated the growth of cochlear cells.

"Our study found a [new] way to provide safe localized delivery of a gene to the cochlea, using the cochlear implant device itself. The gene acts as a nerve growth factor, which stimulates repair of the cochlear nerve," said Housley, a professor and director of the Translational Neuroscience Facility at the University of New South Wales, in Sydney.

The cochlear implant is surgically placed in the cochlea, in the inner ear. The implant works by using a line of small electrodes within the cochlea to selectively stimulate cochlear nerve fibers at different positions and enhancing different sounds, or frequencies, Housley explained.

"In the cochlea of a person with good hearing, sound vibrations are encoded by sensory cells, called 'hair cells,' which stimulate the cochlear nerve fibers," he said. "With hearing loss, the hair cells are lost, and without them the cochlear nerve fibers die and retract into the bone within the core of the cochlea."

This makes the job of the cochlear implant difficult as the amount of electrical current needed to stimulate the nerves is quite high, Housley added.

The gene therapy, which makes the cells close to the electrode produce the nerve growth factor, causes the nerve fibers to grow out to those cells -- and therefore to the electrodes, he explained. This means that much less current is needed, so more selective groups of nerve fibers can be stimulated.

"In the future, people with cochlear implants may get this gene therapy at the time of their implant, and the computer system -- which is part of the cochlea implant that converts sound to electrical pulses along the array of electrodes -- should be able to provide a better sound perception," Housley said.

Scientists note, however, that research with animals often fails to provide similar results in humans.

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Gene Therapy May Enhance Cochlear Implants, Animal Study Finds

Cochlear Implant Also Uses Gene Therapy to Improve Hearing

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The electrodes in a cochlear implant can be used to direct gene therapy and regrow neurons.

Growth factor: The cochlear nerve regenerates after gene therapy (top) versus the untreated cochlea from the same animal (bottom).

Researchers have demonstrated a new way to restore lost hearing: with a cochlear implant that helps the auditory nerve regenerate by delivering gene therapy.

The researchers behind the work are investigating whether electrode-triggered gene therapy could improve other machine-body connectionsfor example, the deep-brain stimulation probes that are used to treat Parkinsons disease, or retinal prosthetics.

More than 300,000 people worldwide have cochlear implants. The devices are implanted in patients who are profoundly deaf, having lost most or all of the ears hair cells, which detect sound waves through mechanical vibrations, and convert those vibrations into electrical signals that are picked up by neurons in the auditory nerve and passed along to the brain. Cochlear implants use up to 22 platinum electrodes to stimulate the auditory nerve; the devices make a tremendous difference for people but they restore only a fraction of normal hearing.

Cochlear implants are very effective for picking up speech, but they struggle to reproduce pitch, spectral range, and dynamics, says Gary Housley, a neuroscientist at the University of New South Wales in Sydney, Australia, who led development of the new implant.

Cyborg cavy: An Xray image shows the cochlear implant in the left ear of a guinea pig.

When the ears hair cells degrade and die, the associated neurons also degrade and shrink back into the cochlea. So theres a physical gap between these atrophied neurons and the electrodes in the cochlear implant. Improving the interface between nerves and electrodes should make it possible to use weaker electrical stimulation, opening up the possibility of stimulating multiple parts of the auditory nerve at once, using more electrodes, and improving the overall quality of sound.

Peptides called neurotrophins can encourage regeneration of the neurons in the auditory nerve. Housley used a common process, called electroporation, to cause pores to open up in cells, allowing DNA to get inside. It usually requires high voltages, and it hasnt found much clinical use, but Housley wanted to see whether the small, distributed electrodes of the cochlear implant could be used to achieve the effect.

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Cochlear Implant Also Uses Gene Therapy to Improve Hearing