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A pioneering study opens roads for tailor-made antidepressants

In spite that the causes of depression have not still been fully identified, scientists acknowledge that genetic and environmental factors play a common role in the onset of this disorder. One of the environmental risk factors more often related to depression is exposure to threatening life events. On the other side, from a genetic point of view, the serotonin transporter gene, with a crucial role in communication between neurons, could predispose to depression.

An international group of scientists, headed by professors Jorge Cervilla Ballesteros and Blanca Gutiérrez Martínez, from the department of Legal Medicine, Toxicology and Psychiatry of the University of Granada, has recently published in the prestigious journal Molecular Psychiatry the pioneering study PREDICT-gene, confirming the relation between allele s in the serotonin transporter gene and exposure to threatening life events in the onset of depression. The study proves, for a population sample accounting for gender, age and family history of psychiatric disorders, that 24% of the Spanish population, comprising people with the s/s genotype, need minimal exposure to threatening life events, unlike individuals with s/l or l/l genotypes, thus confirming the relation between genetic and environmental factors in this mental disorder.

Tailor-made antidepressants

The most important consequence of research on interaction between genetic and environmental factors is that, in a foreseeable future, scientists will be able to produce measures to predict response to antidepressants taking into account each individual’s genotype, i. e. they will be able to design tailor-made drugs according to each person’s genetic configuration and their exposure to environmental factors.

The research group headed by professor Cervilla Ballesteros and Gutiérrez Martínez is currently working at the University of Granada to open roads for psycho-pharmaco-genetics, a field that will allow for individual treatments, tailor-made drugs, for each patient with depression, a disorder affecting one in every five Spaniards visiting the doctor’s.

This study is framed in the international project PREDICT and is funded by the European Union and the Spanish Ministry of Education and Science. One of its most important novelties is that it has been carried out through a very representative sample: a total of 737 people agreed to participate in the genetic tests, with ages ranging from 18 to 75, patients of nine primary care centres in the South of Spain. That is why this is the first representative population-based replication of earlier research, as until now research had been done into restricted population samples, comprising only women, adolescents, twins or people with affective disorders.

Contact: Professor Jorge Cervilla Ballesteros
jacb@ugr.es
34-663-075-835
Universidad de Granada

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August 6, 2007 Posted by | Alberta, Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Canada, Depression, France, General Psychiatry, Germany, Global, Global Health Vision, Global News, Health Canada, Music Video Pick Of The Day, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, Nova Scotia, Osaka, Ottawa, Prince Edward Island, Public Health, Quebec, RSS, RSS Feed, Spain, Toronto, UK, US, Virginia, Washington DC, Washington DC City Feed, World News | Leave a comment

European heat waves double in length since 1880

The most accurate measures of European daily temperatures ever indicate that the length of heat waves on the continent has doubled and the frequency of extremely hot days has nearly tripled in the past century. The new data shows that many previous assessments of daily summer temperature change underestimated heat wave events in western Europe by approximately 30 percent.

Paul Della-Marta and a team of researchers at the University of Bern in Switzerland compiled evidence from 54 high-quality recording locations from Sweden to Croatia and report that heat waves last an average of 3 days now—with some lasting up to 4.5 days—compared to an average of around 1.5 days in 1880. The results are published 3 August in the Journal of Geophysical Research-Atmospheres, a publication of the American Geophysical Union. The researchers suggest that their conclusions contribute to growing evidence that western Europe’s climate has become more extreme and confirm a previously hypothesized increase in the variance of daily summer temperatures since the 19th century.

The study adds evidence that heat waves, such as the devastating 2003 event in western Europe, are a likely sign of global warming; one that perhaps began as early as the 1950s, when their study showed some of the highest trends in summer mean temperature and summer temperature variance.

“These results add more evidence to the belief among climate scientists that western Europe will experience some of the highest environmental and social impacts of climate change and continue to experience devastating hot summers like the summer of 2003 more frequently in the future,” Della-Marta said.

The authors note that temperature records were likely overestimated in the past, when thermometers were not kept in modern Stevenson screens, which are instrument shelters used to protect temperature sensors from outside influences that could alter its readings. The researchers corrected for this warm bias and other biases in the variability of daily summer temperatures and show that nearly 40 percent of the changes in the frequency of hot days are likely to be caused by increases in summer temperatures’ variability. This finding demonstrates that even a small change in the variance of daily summer temperatures can radically enhance the number of extremely hot days.

“These findings provide observational support to climate modeling studies showing that European summer temperatures are particularly sensitive to global warming,” Della-Marta said. “Due to complex reactions between the summer atmosphere and the land, the variability of summer temperatures is expected to [continue to] increase substantially by 2100.”

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The research was supported by the European Environment and Sustainable Development Program, the Swiss National Science Foundation and the National Center for Excellence in Climate Research (NCCR Climate).

Contact: Jonathan Lifland
jlifland@agu.org
202-777-7535
American Geophysical Union

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August 3, 2007 Posted by | Alberta, Baltimore, Barcelona, Bethesda, Calgary, Canada, France, Germany, Global, Global Health Vision, Global News, Health Canada, Irvine, Italy, Japan, Medical Journals, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, Nova Scotia, Osaka, Ottawa, Pennsylvania, Prince Edward Island, Quebec, RSS, RSS Feed, Slovakia, Spain, Toronto, UK, University of Bern, US, Virginia, Washington DC, Washington DC City Feed | Leave a comment

Identifying the mechanism behind a genetic susceptibility to type 2 diabetes

Type 2 diabetes is reaching epidemic proportions in the developed world. Determining if and how certain genes predispose individuals to type 2 diabetes is likely to lead to the development of new treatment strategies for individuals with the disease.

In a study appearing in the August issue of the Journal of Clinical Investigation Valeriya Lyssenko and colleagues from Lund University in Sweden show that certain variants of the gene TCF7L2 make individuals more susceptible to type 2 diabetes. The susceptibility variants were associated with increased expression of TCF7L2 in pancreatic islet cells and decreased islet cell secretion of insulin. Consistent with this, ectopic overexpression of TCF7L2 in human islet cells decreased insulin secretion in response to exposure to glucose. This study identifies TCF7L2 type 2 diabetes susceptibility variants and provides a mechanism by which these genetic variants might cause susceptibility to the disease. As discussed by the authors and in the accompanying commentary by Andrew Hattersley from Peninsula Medical School in the United Kingdom, future studies are likely to investigate the potential for manipulating the signaling pathways controlled by TCF7L2 for the development of new therapeutics for type 2 diabetes.

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TITLE: Mechanisms by which common variants in the TCF7L2 gene increase risk of type 2 diabetes

AUTHOR CONTACT:
Valeriya Lyssenko
Lund University, University Hospital Malma, Malma, Sweden.
Phone: 46-40-391214; Fax: 46-40-391222; E-mail: Valeri.Lyssenko@med.lu.se.

View the PDF of this article at: https://www.the-jci.org/article.php?id=30706

ACCOMPANYING COMMENTARY
TITLE: Prime suspect: the TCF7L2 gene and type 2 diabetes risk

AUTHOR CONTACT:
Andrew T. Hattersley
Institute of Biomedical and Clinical Sciences, Peninsula Medical School, Exeter, United Kingdom.
Phone: 44-1392-406806; Fax: 44-1392-406767; E-mail: Andrew.Hattersley@pms.ac.uk.

View the PDF of this article at: https://www.the-jci.org/article.php?id=33077

Contact: Karen Honey
press_releases@the-jci.org
215-573-1850
Journal of Clinical Investigation

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August 2, 2007 Posted by | Alberta, Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Canada, Diabetes, France, Genes, Genetic, Genetic Link, Genetics, Genome, Genomic, Germany, Global, Global Health Vision, Global News, Health Canada, Human Genome, Irvine, Italy, Japan, Journal of Clinical Investigation, Medical Journals, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, Nova Scotia, Nunavut, Osaka, Ottawa, Pennsylvania, Prince Edward Island, Public Health, Quebec, Research, RSS, RSS Feed, Slovakia, Spain, Toronto, Type 2 Diabetes, US, Virginia, Washington DC, Washington DC City Feed, World News | Leave a comment

U-M researchers find family of ‘on switches’ that cause prostate cancer

Gene fusions trigger cancer growth, could impact treatment choices

ANN ARBOR, Mich. — Researchers at the University of Michigan Comprehensive Cancer Center have discovered how genes turn on the switch that leads to prostate cancer.

The team discovered that pieces of two chromosomes can trade places with each other and cause two genes to fuse together. The fused genes then override the “off” switch that keeps cells from growing uncontrollably, causing prostate cancer to develop.

By testing these gene fusions in mice and in cell cultures, the researchers showed that the fusions are what cause prostate cancer to develop. But it’s not just one set of genes that fuse. The researchers found that any one of several in a family of genes can become scrambled and fuse. Results of the study appear in the Aug. 2 issue of Nature.

“Each of these switches, or gene fusions, represent different molecular subtypes. This tells us there’s not just one type of prostate cancer. It’s a more complex disease and potentially needs to be treated differently in each patient,” says lead study author Arul Chinnaiyan, M.D., Ph.D., director of the Michigan Center for Translational Pathology, a new U-M center whose goal is to translate research into real world practice.

The gene fusion research is the centerpiece project of the new center. In the current study, researchers found one of several abnormal gene fusions in the prostate cancer tissue samples they tested. In 2005, the researchers identified a prostate-specific gene called TMPRSS2, which fuses with either ERG or ETV1, two genes known to be involved in several types of cancer.

The Nature paper reports on five additional genes that fuse with ERG or ETV1 to cause prostate cancer. Gene fusions were involved in 60 percent to 70 percent of the prostate cancer cell lines the researchers looked at. The genes involved are all controlled by a different mechanism. For example, four of the genes are regulated by androgen, a male sex hormone known to fuel prostate cancer. Androgen deprivation is a common therapy for prostate cancer.

Knowing which gene fusion is involved in an individual patient’s tumor could impact treatment options. If an androgen-regulated gene is involved, androgen therapy would be appropriate. But if the gene fusion involves a gene that represses androgen, the anti-androgen therapy could encourage the cancer’s growth. This may also explain why androgen treatment is not effective for some prostate cancers.

“Typing someone’s prostate cancer by gene fusion can affect the treatment given. We would not want to give androgen to someone whose prostate cancer gene fusion is not regulated by androgen,” says Chinnaiyan, who is the S.P. Hicks Collegiate Professor of Pathology at the U-M Medical School.

Rearrangements in chromosomes and fused genes are known to play a role in blood cell cancers like leukemia and lymphoma, and in Ewing’s sarcoma. A fused gene combination that plays a role in chronic myelogenous leukemia led researchers to develop the drug Gleevec, which has dramatically improved survival rates for that disease.

Chinnaiyan believes the prostate gene fusions will eventually lead to similar treatments for prostate cancer.

“More immediately, we hope to develop tests for diagnosis or prognosis. But long-term, we hope this will lead to better therapies to treat prostate cancer. The key challenge is to find a drug that would go after this gene fusion,” Chinnaiyan says.

The gene fusion technology has been licensed to San Diego-based Gen-Probe Inc., which is working on a screening tool to detect gene fusions in urine. The tool could one day supplement or replace the prostate specific antigen, or PSA, test currently used to screen for prostate cancer.

The idea of translating laboratory research findings into a test or treatment that will impact patients is central to the new Michigan Center for Translational Pathology. The center brings together experts in genomics, proteomics and bioinformatics to look at common patterns and potential targets in cancer and other diseases. This is the first center of its kind in the nation in that it is associated with one of 39 National Cancer Institute-designated “comprehensive” cancer centers, a premier medical school and a large health system with both clinicians and patients.

The center’s goal is to study the genes, proteins and other markers on cells to develop new diagnostic tests or screening tools as well as targeted treatments for cancer and other diseases, with the key being to translate these laboratory discoveries into clinical applications.

Chinnaiyan and his team have received numerous awards and honors, including the American Association for Cancer Research Team Science Award for their previously published work on gene fusions, and the Specialized Program of Research Excellence Outstanding Investigator award. The new Center for Translational Pathology supported in part by the Prostate Cancer Foundation, which has offered to match up to $1 million dollars in donations to support work related to developing therapies against prostate cancer gene fusions at the university.

“Mapping of the human genome was only the beginning. Equipped with the comprehensive analysis of the human genome, we can now systematically examine the blueprint of disease at the molecular level. This essential knowledge may lead to better diagnostic tests and promising new treatments for cancer, cardiovascular disease, diabetes and other illnesses,” Chinnaiyan says.

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For information about the Michigan Center for Translational Pathology, go to http://www.med.umich.edu/mctp.

About 218,890 men will be diagnosed with prostate cancer this year, and 27,050 will die from the disease, according to the American Cancer Society. The gene fusion work is not currently available for treatment or diagnosis, and no clinical trials are currently recruiting. For information about prostate cancer and currently available treatments, go to http://www.mcancer.org or call the U-M Cancer AnswerLine at 800-865-1125.

In addition to Chinnaiyan, U-M study authors were Scott Tomlins; Saravana Dhanasekaran, Ph.D.; Bharathi Laxman; Qi Cao; Beth Helgeson; Xuhong Cao; David Morris, M.D.; Anjana Menon; Xiaojun Jing; Bo Han; James Montie, M.D.; Kenneth Pienta, M.D.; Diane Roulston; Rajal Shah, M.D.; Sooryanarayana Varambally, Ph.D.; and Rohit Mehra, M.D. Mark Rubin, M.D., from Brigham and Women’s Hospital, Dana-Farber Cancer Institute and Harvard Medical School is also a study author.

Funding for the study came from the U.S. Department of Defense, the National Institutes of Health, the Early Detection Research Network, the Prostate Cancer Foundation and Gen-Probe Inc.

The University of Michigan has filed for a patent on the detection of gene fusions in prostate cancer, on which Tomlins, Mehra, Rubin and Chinnaiyan are co-inventors. The diagnostic field of use has been licensed to Gen-Probe Inc. Chinnaiyan also has a sponsored research agreement with Gen-Probe; however, GenProbe has had no role in the design or experimentation of this study, nor has it participated in the writing of the manuscript.

Reference: Nature, Vol. 448, No. 7153, Aug. 2, 2007

Contact: Nicole Fawcett
nfawcett@umich.edu
734-764-2220
University of Michigan Health System

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August 1, 2007 Posted by | acute lymphoblastic leukemia, Alberta, Baltimore, Barcelona, Bethesda, Calgary, Canada, Cancer, Cancer Biology, Cancer Biology and Therapy, Chemotherapy, Childhood Lukemia, France, Genes, Genetic, Genetic Link, Genetics, Genome, Genomic, Germany, Global, Global Health Vision, Global News, Health Canada, Human Genome, Irvine, Italy, Japan, journal Nature Genetics, Leukemia, Lung Cancer, Medical Journals, Nature Genetics, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, non-Hodgkin's lymphoma, Nova Scotia, Oncology, Osaka, Ottawa, Prince Edward Island, Public Health, Quebec, Research, RSS, RSS Feed, Slovakia, Spain, Toronto, UK, University of Michigan, US, Virginia, Washington DC, Washington DC City Feed, World News | 3 Comments

Flip of genetic switch causes cancers in mice to self-destruct, Stanford researchers find

STANFORD, Calif. – Killing cancerous tumors isn’t easy, as anyone who has suffered through chemotherapy can attest. But a new study in mice shows that switching off a single malfunctioning gene can halt the limitless division of tumor cells and turn them back to the path of their own planned obsolescence.

The surprising possibility that a cell’s own natural mechanism for ensuring its mortality could be used to vanquish tumors opens the door to a new approach to developing drugs to treat cancer patients, according to Dean Felsher, MD, PhD, associate professor of medicine (oncology) and of pathology at the Stanford University School of Medicine. Felsher is the senior author of the study to be published July 30 in the advance online version of the Proceedings of the National Academy of Sciences.

“Our research implies that by shutting off a critical cancer gene, tumor cells can realize that they are broken and restore this physiologic fail-safe program,” said Felsher.

Cancer can be notoriously resistant to medical treatment. Not only do cancer cells proliferate uncontrollably, they somehow circumvent the mechanism that causes normal cells to die when they get old or malfunction. That makes cancer cells effectively immortal unless doctors manage to squelch them.

The gene Felsher’s team studied produces a protein called Myc (pronounced “mick”), which promotes cell division. A mutation of the gene causes cells to overproduce the protein, prompting perpetual cell division and tumor growth. By turning off the mutated gene, the researchers found that not only did uncontrolled cell division cease, but the cells also reactivated a normal physiological mechanism, called senescence, which makes it possible for a cell to eventually die.

“What was unexpected was just the fact that cancer cells had retained the ability to undergo senescence at all,” said Felsher. Cancer researchers had long thought the senescence process had to be irreversibly disrupted for a tumor to develop.

The researchers worked with a series of mice engineered to have Myc-triggered cancers of either the liver, blood or bones, along with a specially constructed version of the Myc gene that they could switch off by feeding the mice antibiotics. When the mice dined on doses of the drugs, invariably, the tumors ceased growing and then diminished, with some disappearing over the course of just a few days.

Although Felsher’s lab had previously shown that mouse tumors diminished and disappeared when Myc was switched off, they hadn’t been sure how the process actually worked. Historically, most research involving genetic methods of battling cancer cells has focused on reactivating genes called tumor-suppressor genes, which are generally overcome by a proliferating cancer. No one had explored the idea that senescence might play a key role in diminishing tumors.

Felsher described senescence as acting like a fail-safe mechanism to stop cancer. When a cell detects a deleterious mutation, it launches the senescence process, resulting in the permanent loss of the cell’s ability to proliferate, thus halting any cancer.

“In order to become tumor cells, those cells have to overcome senescence,” said Chi-Hwa Wu, PhD, postdoctoral researcher in Felsher’s lab and first author of the study. Wu had the inspiration to explore whether the sudden diminishment they had observed in the tumors might be due to the reactivation of some latent remnant of the trigger for senescence.

Through a series of experiments looking at enzymes associated with the senescence process, as well as some molecular markers, Wu confirmed her suspicion. And not only was senescence occurring in cells that had been thought to be incapable of it, the process was reactivated in all the different tumors they studied.

Consider it a cell version of the Jekyll-and-Hyde transformation. “It’s sort of like Mr. Hyde realizing that there’s something wrong with him and then being able to put himself back into his normal state as Dr. Jekyll,” Felsher said.

In addition to the deepened understanding of how the process of senescence works, Felsher and Wu see a lot of potential for new approaches to treating cancer, beyond the traditional tactic of trying to kill cancer cells directly. “This work implies that maybe part of the strategy should involve figuring out how to get the cancer cells to just be allowed to do what they originally wanted to do anyway, which is to not be proliferating endlessly and growing uncontrolled,” said Felsher.

The next step for the team is to see how well the approach works in human cancer cells. “And we’re also trying to figure out what the mechanism is,” Felsher said. “What are the molecular mechanisms of this, so that we can figure out how to better treat cancer””

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Other authors on the research paper are Jan van Riggelen, PhD, postdoctoral researcher; Alper Yetil, graduate student in cancer biology; Alice Fan, MD, instructor in medicine (oncology), and medical student Pavan Bachireddy.

The study was funded by the National Cancer Institute, the National Institutes of Health, the Leukemia and Lymphoma Society, the Burroughs Wellcome Fund, the Damon Runyon Lilly Clinical Investigator Award, the Lymphoma Research Foundation and the Howard Hughes Medical Institute.

Stanford University Medical Center integrates research, medical education and patient care at its three institutions – Stanford University School of Medicine, Stanford Hospital & Clinics and Lucile Packard Children’s Hospital at Stanford. For more information, please visit the Web site of the medical center’s Office of Communication & Public Affairs at http://mednews.stanford.edu.

Contact: Lou Bergeron
louisb3@stanford.edu
650-723-3900
Stanford University Medical Center

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July 31, 2007 Posted by | acute lymphoblastic leukemia, Alberta, Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Canada, Cancer, Cancer Biology, Cancer Biology and Therapy, Childhood Lukemia, France, Genes, Genetic, Genetic Link, Genetics, Genome, Genomic, Germany, Global, Global Health Vision, Global News, Health Canada, Howard Hughes Medical Institute, Human Genome, Italy, Japan, Leukemia, Medical Journals, Molecular Biology, National Cancer Institute, National Institutes of Health, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, NIH, non-Hodgkin's lymphoma, Nova Scotia, Nunavut, Osaka, Ottawa, Prince Edward Island, Public Health, Quebec, Research, RSS, RSS Feed, Toronto, UK, US, Virginia, Washington DC, Washington DC City Feed, Wellcome Trust, World News | Leave a comment

Research links genetic mutations to lupus

WINSTON-SALEM, N.C. – A gene discovered by scientists at Wake Forest University School of Medicine has been linked to lupus and related autoimmune diseases. The finding, reported in the current issue of Nature Genetics, is the latest in a series of revelations that shed new light on what goes wrong in human cells to cause the diseases.

“This research is a huge leap toward understanding the cause of lupus and related autoimmune diseases,” said Fred Perrino, Ph.D., a co-author on the paper and a professor of biochemistry at Wake Forest. “There had been few clues before now.”

Perrino, who discovered the gene in 1998, said he suspected it was involved in human disease, but it took a group of researchers from around the world collaborating to put the puzzle together.

“We’ve known that lupus was a complex disease, but now we have a specific protein and a particular cellular process that appears to be one of the causes,” said Perrino. “We’re connecting the dots to understand the biology of what’s going on with the disease.”

In Nature Genetics, lead author Min Ae Lee-Kirsch, M.D., from the Technische Universität Dresden in Dresden, Germany, and colleagues report finding variations of the TREX1 gene discovered by Perrino in patients with systemic lupus erythematosus. The study involved 417 lupus patients from the United Kingdom and Germany. Mutations were found in nine patients with lupus and were absent in 1,712 people without lupus.

“Our data identify a stronger risk for developing lupus in patients that carry variants of the gene,” said Lee-Kirsch.

In recent years, the gene was also linked to Aicardi-Goutieres syndrome, a rare neurological disease that causes death in infants, and to chilblain lupus, an inherited disease associated with painful bluish-red skin lesions that occur during cold weather and usually improve in summer. The current research also links it to Sjogren’s syndrome, a form of lupus.

The diseases are all autoimmuine diseases, which means that the body makes antibodies against itself. In lupus, these antibodies cause pain and inflammation in various parts of the body, including the skin, joints, heart, lungs, blood, kidneys and brain. The disease is characterized by pain, heat, redness, swelling and loss of function.

Perrino began studying the protein made by the gene more than 14 years ago.

“We basically cracked open cells to locate the protein and find the gene,” said Perrino. “In the 14 years since, we’ve learned a lot about the protein and how it functions.”

The gene manufactures a protein, also known as TREX1, whose function is to “disassemble” or “unravel” DNA, the strand of genetic material that controls processes within cells. The “unraveling” occurs during the natural process of cells dying and being replaced by new cells. If a cell’s DNA isn’t degraded or unraveled during cell death, the body develops antibodies against it.

“If the TREX1 protein isn’t working to disassemble the DNA, you make antibodies to your own DNA and can end up with a disease like lupus,” said Perrino.

Perrino and colleagues at Wake Forest have been studying the gene and its protein since 1993. Thomas Hollis, Ph.D., an assistant professor of biochemistry at Wake Forest, is credited with solving the structure of both TREX1 and a similar protein, TREX2. Perrino has also developed a way to measure the function of the proteins.

In a study reported in April in the Journal of Biological Chemistry, Hollis and Perrino found that three variations of the gene reduced the activity of the protein by four- to 35,000-fold.

“Now that we have the structure, we can understand how it disassembles DNA and how mutations in the gene may affect that process,” said Hollis.

The researchers hope that understanding more about the gene’s mutations and the structure of the protein may lead to drug treatments to help ensure that mutant copies of the gene are inactive.

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Media Contacts: Karen Richardson, krchrdsn@wfubmc.edu; Shannon Koontz, shkoontz@wfubmc.edu; at 336-716-4587.

Wake Forest University Baptist Medical Center is an academic health system comprised of North Carolina Baptist Hospital and Wake Forest University Health Sciences, which operates the university’s School of Medicine. U.S. News & World Report ranks Wake Forest University School of Medicine 18th in primary care and 44th in research among the nation’s medical schools. It ranks 35th in research funding by the National Institutes of Health. Almost 150 members of the medical school faculty are listed in Best Doctors in America.

Contact: Karen Richardson
krchrdsn@wfubmc.edu
336-716-4453
Wake Forest University Baptist Medical Center

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July 29, 2007 Posted by | Alberta, Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Canada, Clinical Trials, France, Genes, Genetic, Genetic Link, Genetic Marker C allele of rs10505477, Genetics, Genome, Genomic, Global, Global Health Vision, Global News, Health Canada, Human Genome, Italy, Japan, Lupus, Nature Genetics, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, NIH, Nova Scotia, Nunavut, Osaka, Ottawa, Prince Edward Island, Public Health, Quebec, Research, RSS, RSS Feed, Slovakia, Spain, Toronto, UK, US, Virginia, Wake Forest University Baptist Medical Center, WASHINGTON, Washington DC, Washington DC City Feed, World Health Organisation, World News | 1 Comment

Children and young people show elevated leukaemia rates near nuclear facilities

Review covers 136 countries in US, Canada, UK, France, Germany, Japan and Spain

Leukaemia rates in children and young people are elevated near nuclear facilities, but no clear explanation exists to explain the rise, according to a research review published in the July issue of European Journal of Cancer Care.

Researchers at the Medical University of South Carolina carried out a sophisticated meta-analysis of 17 research papers covering 136 nuclear sites in the UK, Canada, France, the USA, Germany, Japan and Spain.

They found that death rates for children up to the age of nine were elevated by between five and 24 per cent, depending on their proximity to nuclear facilities, and by two to 18 per cent in children and young people up to the age of 25.

Incidence rates were increased by 14 to 21 per cent in zero to nine year olds and seven to ten percent in zero to 25 year-olds.

“Childhood leukaemia is a rare disease and nuclear sites are commonly found in rural areas, which means that sample sizes tend to be small” says lead author Dr Peter J Baker.

“The advantage of carrying out a meta-analysis is that it enables us to draw together a number of studies that have employed common methods and draw wider conclusions.”

Eight separate analyses were performed – including unadjusted, random and fixed effect models – and the figures they produced showed considerable consistency.

But the authors point out that dose-response studies they looked at – which describe how an organism is affected by different levels of exposure – did not show excess rates near nuclear facilities.

“Several difficulties arise when conducting dose-response studies in an epidemiological setting as they rely on a wide range of factors that are often hard to quantify” explains Dr Baker. “It is also possible that there are environmental issues involved that we don’t yet understand.

“If the amount of exposure were too low to cause the excess risk, we would expect leukaemia rates to remain consistent before and after the start-up of a nuclear facility. However, our meta-analysis, consistently showed elevated illness and death rates for children and young people living near nuclear facilities.”

The research review looked at studies carried out between 1984 and 1999, focusing on research that provided statistics for individual sites on children and young people aged from zero to 25.

Four studies covered the UK, with a further three covering just Scotland. Three covered France, two looked at Canada and there was one study each from the USA, Japan, Spain, the former East Germany and the former West Germany.

“Although our meta-analysis found consistently elevated rates of leukaemia near nuclear facilities, it is important to note that there are still many questions to be answered, not least about why these rates increase” concludes Dr Baker.

“Several hypotheses have been proposed to explain the excess of childhood leukaemia in the vicinity of nuclear facilities, including environmental exposure and parental exposure. Professor Kinlen from Oxford University has also put forward a hypothesis that viral transmission, caused by mixing populations in a new rural location, could be responsible.

“It is clear that further research is needed into this important subject.”

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Notes to editors

Meta-analysis of standardized incidence and mortality rates of childhood leukaemia in proximity to nuclear facilities. Baker PJ and Hoel D. European Journal of Cancer Care. 16, pages 355-363. July 2007.

The European Journal of Cancer Care provides a medium for communicating multi-professional cancer care across Europe and internationally. The Journal publishes peer-reviewed papers, reviews, reports, features and news, and provides a means of recording lively debate and an exchange of ideas. It is published six times a year by Blackwell Publishing.
Blackwell Publishing is the world’s leading society publisher, partnering with 665 medical, academic, and professional societies. Blackwell publishes over 800 journals and has over 6,000 books in print. The company employs over 1,000 staff members in offices in the US, UK, Australia, China, Singapore, Denmark, Germany and Japan and officially merged with John Wiley & Sons, Inc’s Scientific, Technical and Medical business in February 2007. Blackwell’s mission as an expert publisher is to create long-term partnerships with our clients that enhance learning, disseminate research, and improve the quality of professional practice. For more information on Blackwell Publishing, please visit http://www.blackwellpublishing.com or http://www.blackwell-synergy.com

Contact: Annette Whibley
wizard.media@virgin.net
Blackwell Publishing Ltd.

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July 18, 2007 Posted by | Alberta, Baltimore, Barcelona, Bethesda, Calgary, Canada, Cancer, Cancer Biology, Childhood Lukemia, European Journal of Cancer Care, France, Germany, Global, Global Health Vision, Global News, Health Canada, Japan, Leukemia, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, Nova Scotia, Nunavut, Osaka, Ottawa, Oxford University, Pennsylvania, Prince Edward Island, Quebec, RSS, RSS Feed, Slovakia, Spain, Toronto, UK, US, Virginia, WASHINGTON, Washington DC, Washington DC City Feed, World News | Leave a comment

Poor sleep associated with cognitive decline in elderly women

Disturbed sleep associated with decline in cognition over time; no link with total hours of sleep per night
Women who experienced cognitive decline over a 13 to 15 year period after age 65 were more likely to sleep poorly than women whose cognition did not decline, according to a study led by researchers at the San Francisco VA Medical Center (SFVAMC).

The women’s cognitive decline was associated with interrupted or fitful sleep. Total sleep time per night made no difference, says lead author Kristine Yaffe, MD, chief of geriatric psychiatry at SFVAMC and professor of psychiatry, neurology, epidemiology, and biostatistics at the University of California, San Francisco (UCSF).

“This indicates that it’s not how long you sleep, but how well you sleep,” she says.

The study appears in the July 17, 2007 issue of Neurology.

Yaffe speculates that there are three possible explanations for the association between cognitive decline and disturbed sleep. She says the first and most likely reason is that whatever neurodegenerative condition is starting to cause cognitive decline, such as Alzheimer’s disease, is also affecting areas of the brain that govern sleep.

“Sleep is very complex,” notes Yaffe. “It involves a coordinated series of neurologic functions that we don’t entirely understand. It’s not unlikely that early neurodegenerative disease could start having an effect on sleep centers as well.”

Another possibility is that someone who is becoming cognitively impaired is sleeping poorly “because they’re aware of their condition and they’re worried about it.”

Finally, Yaffe says that other factors entirely, such as brain inflammation or genetic changes, might cause both cognitive decline and sleep disturbance at the same time.

The researchers studied 2,474 women who were part of a larger ongoing prospective study of risk factors for osteoporosis that began in 1986. The mean age of the women was 68.9 years at the beginning of the study. Their cognitive health was measured at regular intervals over the course of the study using two standard cognitive tests: the Mini-Mental State Examination and the Trail Making Test, Part B, known as Trails B.

After 13 to 15 years in the study, the women were fitted with an actigraph, a small device worn on the wrist that measures movement and is known from previous studies to be highly accurate in differentiating sleep from wakefulness. The women wore the device for at least three consecutive 24-hour periods.

Women who performed progressively worse on both cognitive tests over time were significantly more likely to have difficulty falling asleep and staying asleep than women whose performance did not decline. Women who performed progressively worse on the Trails B test also napped significantly more during the day.

The association between cognitive decline and poor sleep remained even after the researchers adjusted for a host of other demographic factors such as age, education, depression, exercise, and health status.

“It’s been known for some time that people with cognitive problems often have sleep problems, but those studies have mostly been done on severely demented people in nursing homes,” observes Yaffe. “Ours was the first study to look at the relationship between sleep and cognition in healthy women dwelling in the community who did not have dementia to begin with.”

Yaffe offers several cautions concerning the results of the study. First, men and African-American women were excluded from the original osteoporosis study because both of those groups have low incidence of osteoporotic fractures. Additionally, sleep patterns were measured only once, “so it’s more of a snapshot.”

However, Yaffe says that the research group has received a grant from the National Institutes of Health to continue tracking sleep patterns and cognitive health over time in the same study cohort. “Hopefully, we’ll be able to tell if cognitive changes lead to sleep disturbances, or if the reverse is true, or if they have a common independent cause.”

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Co-authors of the paper were Terri Blackwell, MA, of the California Pacific Medical Center Research Institute (CPMCRI); Deborah E. Barnes, PhD, of SFVAMC and UCSF; Sonia Ancoli-Israel, PhD, of the University of California, San Diego and the VA San Diego Healthcare System; and Katie Stone, PhD, of CPMCRI, for the Study of Osteopororic Fractures Group.

The study was supported by grants from the National Institutes of Health and the National Institute on Aging.

SFVAMC has the largest medical research program in the national VA system, with more than 200 research scientists, all of whom are faculty members at UCSF.

UCSF is a leading university that advances health worldwide by conducting advanced biomedical research, educating graduate students in the life sciences and health professions, and providing complex patient care.

Contact: Steve Tokar
steve.tokar@ncire.org
415-221-4810 x5202
University of California – San Francisco

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July 16, 2007 Posted by | Alzheimers, Baltimore, Barcelona, Bethesda, Calgary, Global, Global Health Vision, Global News, Health Canada, Irvine, Italy, Japan, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, Nova Scotia, Osaka, Ottawa, Pennsylvania, Research, Research Australia, RSS, RSS Feed, Spain, Toronto, University of California, Virginia, Washington DC, Washington DC City Feed, World News | Leave a comment

One man’s junk may be a genomic treasure

Scientists have only recently begun to speculate that what’s referred to as “junk” DNA – the 96 percent of the human genome that doesn’t encode for proteins and previously seemed to have no useful purpose – is present in the genome for an important reason. But it wasn’t clear what the reason was. Now, researchers at the University of California, San Diego (UCSD) School of Medicine have discovered one important function of so-called junk DNA.

Genes, which make up about four percent of the genome, encode for proteins, “the building blocks of life.” An international collaboration of scientists led by Michael G. Rosenfeld, M.D., Howard Hughes Medical Investigator and UCSD professor of medicine, found that some of the remaining 96 percent of genomic material might be important in the formation of boundaries that help properly organize these building blocks. Their work will be published in the July 13 issue of the journal Science.

“Some of the ‘junk’ DNA might be considered ‘punctuation marks’ – commas and periods that help make sense of the coding portion of the genome,” said first author Victoria Lunyak, Ph.D., assistant research scientist at UCSD.

In mice, as in humans, only about 4 percent of the genome encodes for protein function; the remainder, or “junk” DNA, represents repetitive and non-coding sequences. The research team studied a repeated genomic sequence called SINE B2, which is located on the growth hormone gene locus, the gene related to the aging process and longevity. The scientists were surprised to find that SINE B2 sequence is critical to formation of the functional domain boundaries for this locus.

Functional domains are stretches of DNA within the genome that contain all the regulatory signals and other information necessary to activate or repress a particular gene. Each domain is an entity unto itself that is defined, or bracketed, by a boundary, much as words in a sentence are bracketed by punctuation marks. The researchers’ data suggest that repeated genomic sequences might be a widely used strategy used in mammals to organize functional domains.

“Without boundary elements, the coding portion of the genome is like a long, run-on sequence of words without punctuation,” said Rosenfeld.

Decoding the information written in “junk” DNA could open new areas of medical research, particularly in the area of gene therapy. Scientists may find that transferring encoding genes into a patient, without also transferring the surrounding genomic sequences which give structure or meaning to these genes, would render gene therapy ineffective.

Contributors to the paper include Lluis Montoliu, Rosa Roy and Angel Garcia-Díaz of the Department of Molecular and Cellular Biology, Centro Nacional de Biotecnología in Madrid, Spain; Christopher K. Glass, M.D., Ph.D., UCSD Department of Cellular and Molecular Medicine; Esperanza Núñez, Gratien G. Prefontaine, Bong-Gun Ju, Kenneth A. Ohgi, Kasey Hutt, Xiaoyan Zhu and Yun Yung, Howard Hughes Medical Institute, Department of Molecular Medicine, UCSD School of Medicine; and Thorsten Cramer, Division of Endocrinology, UCSD Department of Medicine.

The research was funded in part by the Howard Hughes Medical Institute and the National Institutes of Health.

Contact: Debra Kain
ddkain@ucsd.edu
619-543-6163
University of California – San Diego

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July 13, 2007 Posted by | Alberta, Baltimore, Barcelona, Bethesda, Biological Sciences, Calgary, Chile, DNA, Genes, Genetic, Genetics, Genome, Genomic, Global, Global Health Vision, Global News, Howard Hughes Medical Institute, Human Genome, Irvine, Italy, Japan, National Institutes of Health, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, NIH, Nova Scotia, Osaka, Ottawa, Pennsylvania, Prince Edward Island, Proteins, Quebec, Research, Research Australia, RSS, RSS Feed, Slovakia, Spain, Toronto, UCSD, University of California, Virginia, WASHINGTON, Washington DC, Washington DC City Feed, World News | Leave a comment

Adding folic acid to flour significantly reduces congenital malformations

This release is also available in French.

Quebec City, July 12, 2007 – Dr. Philippe De Wals of Université Laval’s Department of Social and Preventive Medicine today publishes a study clearly indicating that the addition of folic acid to flours has led to a 46% drop in the incidence of congenital neural tube deformation (mainly anencephaly and spina bifida) in Canada. Such deformations either result in the child’s death or in major health problems, including physical and learning disabilities. Dr. De Wals’s work as head of a team of a dozen Canadian researchers appears today in the New England Journal of Medicine.

The neural tube is the basis of the embryo’s nervous system. Poor development of the neural tube, which is sometimes due to a lack of folic acid, can result in major health problems. Folic acid is found in green vegetables, fruit, whole grains, and meat. However, even a balanced diet won’t supply enough folic acid for a pregnant mother and the child she is carrying. Before1998, Canadian medical authorities were already recommending that women in their child-bearing years consume vitamin supplements containing folic acid. “Canada decided to add folic acid to all flour produced in the country because formation of the neural tube in embryos is particularly intense during the first four weeks of pregnancy, which is before a lot of women even know they’re pregnant. Since half of Canadian pregnancies are unplanned and the human body can’t store folic acid, it is better to integrate folic acid into the food chain than to focus exclusively on taking vitamin supplements,” stated Dr. De Wals. Health Canada still recommends taking folic acid supplements to women in their child-bearing years.

Researchers Dr. Philippe De Wals and Fassiatou Tairou of Université Laval’s Faculty of Medicine compared the incidence of neural tube deformations before and after the introduction of folic acid–enriched flours for over 2 million births in Canada. Between 1993 and 1997, the incidence was 1.58 per 1,000 births. Between 2000 and 2002, the rate dropped 46% to 0.86. The biggest improvement occurred in the parts of Canada that had the highest rates of neural tube deformation before 1998—Newfoundland, Prince Edward Island, and Nova Scotia. In Québec, the drop was also pronounced, but closer to the Canadian average.

Currently, only Canada, the United States, and Chile require that folic acid be added to flour. The effectiveness of this practice, as demonstrated by Dr. De Wals’s team, could encourage other countries to follow suit. Every year, approximately 200,000 cases of spina bifida and anencephaly occur worldwide. Adding folic acid to food could reduce that number by half.

Contact: Martin Guay
martin.guay@dap.ulaval.ca
418-656-3952
Université Laval

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July 12, 2007 Posted by | Alberta, Baltimore, Barcelona, Bethesda, Bone Diseases, Calgary, Chile, Folic Acid, Global, Global Health Vision, Global News, Health Canada, Irvine, Italy, Japan, Medical Journals, Neurology, New England Journal of Medicine, Newfoundland, News, News Australia, News Canada, News Israel, News Italy, News Jerusalem, News Switzerland, News UK, News US, News USA, Nova Scotia, Nutritional Anthropology, Osaka, Ottawa, Pennsylvania, Prince Edward Island, Quebec, Research, Research Australia, RSS, RSS Feed, Slovakia, Spain, Spina Bifida, Toronto, Université Laval, Virginia, WASHINGTON, Washington DC, Washington DC City Feed, World News | 1 Comment