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April 4 - 8, 2011--------News Archive

Simple Treatment Prevents Premature Births
Treating high-risk pregnant women with the hormone progesterone cut their rate of early delivery by 45 % and helped lower the risk of breathing complications in their babies.

Findings published online in the journal Ultrasound in Obstetrics and Gynecology offer a relatively simple way to prevent premature birth in women with a short cervix, a known cause of preterm birth.

"The study published today offers hope to women, families and children," Dr. Roberto Romero, chief of the perinatology research branch of the National Institutes of Health, said in a statement.

"Worldwide, more than 12 million premature babies - 500,000 of them in this country - are born each year, and the results are often tragic. Our clinical study clearly shows that it is possible to identify women at risk and reduce the rate of preterm delivery by nearly half, simply by treating women who have a short cervix with a natural hormone - progesterone," says Romero.

Babies born too early - before the 33rd week of pregnancy - have a higher risk of early death and long-term health and developmental problems.

In the United States, 12.8 percent of babies were born preterm in 2008, raising their risk of dying in their first year and having breathing difficulties, cerebral palsy, learning disabilities, blindness and deafness.

The study, done by researchers at the NIH and 44 medical centers around the world, looked at effects of giving progesterone to women with a short cervix, which is the part of the uterus that opens and shortens during labor.

Researchers suspect that women with a short cervix may not have enough of this hormone, and giving it during pregnancy in a gel form might help prolong their pregnancies.

The team studied 458 women with a short cervix who got either a vaginal gel containing progesterone or a placebo between the 19th and 23rd week of pregnancy.

Only 8.9 percent of women who got the gel delivered before the 33rd week of pregnancy, compared with 16.1 percent who were in the placebo group.

The treatment also helped babies. Only 3 percent of babies born to women treated with progesterone had respiratory distress syndrome compared with 7.6 percent of babies in the placebo group.

"We have for a long time known that short cervix is associated with an increased risk of preterm birth," said Dr. Ashley Roman of New York University's Langone Medical Center, who was not involved with the research.

Roman said other studies have shown that progesterone can cut the risk of premature birth in women with this problem. She said the NIH study is important because it shows that the treatment also reduces respiratory problems in newborn babies.

"Not only are fewer babies being delivered preterm, fewer babies have medical problems associated with prematurity," she said in a statement.

http://www.nih.gov/news/health/apr2011/nichd-06.htm

Babies Are Born Early Near Busy Road Intersections
Babies are born earlier when their mothers live near a concentration of freeways and main roads, reports a study of 970 mothers and their newborn babies in Logan City, a town south of Brisbane, Australia.

Senior research fellow and Associate Professor Adrian Barnett from Queensland University of Technology's (QUT) Institute of Health and Biomedical Innovation (IHBI) published the study in the online journal Environmental Health, showing that the more freeways and highways around a pregnant woman's home, the higher the likelihood of her baby being born prematurely.

"The most striking result was the reduction in gestation time of 4.4 per cent or almost two weeks associated with an increase in freeways within 400 metres of the women's home," said Professor Barnett, whose earlier study found a strong association between increased air pollution and small fetus size.

"Although the increased risks are relatively small, the public health implications are large because everyone living in an urban area gets exposed to air pollution. Pre-term and low-birth weight babies stay in hospital longer after birth, have an increased risk of death and are more likely to develop disabilities."

Professor Barnett said although air pollution levels in south-east Queensland were low compared with industrial cities, people's exposure to the chemical toxins in vehicle emissions was relatively high because of our outdoor lifestyle and open houses.

The study counted the number of roads around the mother's homes up to a 500 metre radius.

"We examined the distance between the home and busy roads to find the distance at which most of the negative effects on birth outcomes occurred because this has implications for local governments planning expansions or new roads," he said.

Most of the effects were within a 200-metre radius, but negative health effects were present up to 400 metres.

Professor Barnett said the study had also taken into account the effects of smoking levels and the socio-economic status of the mothers.

The effects of noise pollution were considered to be a possible contributing factor, but Professor Barnett said it was difficult to separate the effects of air and noise pollution.

"Vehicles braking and starting means that road junctions have some of the highest levels of noise and air pollution," he said.

"Disturbed sleep during pregnancy may cause extra stress and be a risk factor for adverse birth outcomes.

"This study points to the fact that pregnant women should reduce their exposure to traffic. A reduction in traffic emissions through improved vehicles or increased public transport use would have immediate health benefits by giving children a better start to life."

http://us.mobile.reuters.com/article/idUSTRE7354XR20110406?ca=rdt

New Gene Influencing Risk For Developing Epilepsy
Vanderbilt University researchers have identified a new gene that can influence a person's risk for developing epilepsy.

The findings, reported in the March 29 Proceedings of the National Academy of Sciences, could improve molecular diagnostic tools and point to novel therapeutic targets for epilepsy.

The gene, KCNV2, codes for a unique type of potassium channel, a protein that participates in the electrical activity of nerve cells. Disturbed electrical activity in the brain – and resulting

seizures – are hallmarks of epilepsy, a group of disorders that affects about 1 percent of the world's population.

A number of genetic mutations that cause inherited epilepsies have been identified. But the clinical severity of inherited epilepsies varies widely – from mild childhood seizures that resolve with age to severe lifelong seizures – even in individuals who have the same single-gene mutation, said Jennifer Kearney, Ph.D., assistant professor of Medicine in the Division of Genetic Medicine.

The gene, KCNV2, codes for a unique type of potassium channel, a protein that participates in the electrical activity of nerve cells. Disturbed electrical activity in the brain – and resulting seizures – are hallmarks of epilepsy, a group of disorders that affects about 1 percent of the world's population.

A number of genetic mutations that cause inherited epilepsies have been identified. But the clinical severity of inherited epilepsies varies widely – from mild childhood seizures that resolve with age to severe lifelong seizures – even in individuals who have the same single-gene mutation, said Jennifer Kearney, Ph.D., assistant professor of Medicine in the Division of Genetic Medicine.

The range of clinical severity "tells us that there are other factors that contribute," she said. "We think that susceptibility and resistance genes that are inherited in addition to the primary mutation are probably a major factor."

Identifying susceptibility and resistance genes may suggest new targets for drugs that fine-tune neuronal excitability, rather than dampening it completely as many current antiepileptic drugs do, Kearney said.

The investigators began to look for these types of "modifier" genes after they made a curious observation in a mouse model of epilepsy – that epilepsy severity depended on the genetic background strain of the mice.

They were studying mice with an epilepsy-causing gene mutation in a sodium channel, a protein that is important for neuronal excitability. The mice had spontaneous, progressive seizures and a reduced lifespan. But when the researchers "moved" the gene mutation into mice with a different genetic background (using breeding strategies), the epilepsy became less severe: the mice developed seizures later and had improved survival.

Using genetic strategies, the investigators zeroed in on two chromosome regions that influenced the difference in epilepsy severity in the two mouse strains. In one of these regions, the mouse Kcnv2 gene (the mouse equivalent of the human KCNV2 gene) appeared to be the strongest candidate gene, based on its potential for altering electrical activity in neurons.

The current report demonstrates that increased expression of the mouse Kcnv2 gene – not changes in its coding sequence – is associated with more severe epilepsy in the susceptible mouse strain. Increasing Kcnv2 expression in the resistant mouse strain caused these mice to develop more severe symptoms, supporting the gene's contribution as an epilepsy modifier.

The investigators then screened 209 pediatric epilepsy patients for variations in KCNV2 and found two different variations in two unrelated patients.

Colleagues in the laboratory of Alfred George Jr., M.D., director of the Division of Genetic Medicine, conducted electrophysiology studies in cells to examine how the two variations affected the function of the potassium channel. They found that both variations suppressed a type of potassium current that normally dampens excitability in neurons.

"The mutations make a neuron more excitable, so you could have longer periods of excitation and also repetitive excitation (that leads to seizures)," says Kearney.

The team plans to screen additional patients with epilepsy to assess the incidence of variations in KCNV2. They are also collaborating with Dave Weaver, Ph.D., director of the Vanderbilt High-Throughput Screening Facility, to find compounds that target the potassium channel and may be useful therapeutics for epilepsy.

Kearney said that understanding how genes such as KCNV2 modify the clinical severity of epilepsy is important for molecular diagnostics and genetic counseling. Patients may currently learn that they have an epilepsy-causing gene mutation, but because clinical severity varies, their prognosis may not be clear.

"We need to understand how all of these different gene interactions impact the final clinical disorder to improve risk assessment and disease management in epilepsy," Kearney said.

The National Institutes of Health supported the research.

http://www.eurekalert.org/pub_releases/2011-04/wfu-fps040411.php

Gene Linked To Autism's Social Dysfunction
With the help of two sets of brothers with autism, Johns Hopkins scientists have identified a gene associated with autism that appears to be linked very specifically to the severity of social interaction deficits.

The gene, GRIP1 (glutamate receptor interacting protein 1) acts as a blueprint, directing proteins at synapses - the specialized contact points between brain cells across which chemical signals flow.

It was identified more than a decade ago by Richard L. Huganir, Ph.D., professor and director of the Solomon H. Snyder Department of Neuroscience at the Johns Hopkins University School of Medicine, and a Howard Hughes Medical Institute investigator.

The new study tracked two versions of GRIP1 in the genomes of 480 people with autism, and was published March 22 in the Proceedings of the National Academy of Sciences, and lends support to a prevailing theory that autism spectrum disorders (ASD), molecularly speaking, reflect an imbalance between inhibitory and excitatory signaling at synapses.

“The GRIP1 variants we studied are not sufficient to cause autism by themselves, but appear to be contributing factors that can modify the severity of the disease,” says Tao Wang, M.D., Ph.D., assistant professor, McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine. “GRIP1 mutations seem to contribute to social interaction deficits in the patients we studied.”

The Johns Hopkins researchers examined a part of the genomes of 480 patients with autism and compared these with 480 people of similar ethnicity without the disorder. They analyzed about 50 genes known to make proteins involved in a brain-signaling pathway, ultimately focusing their investigation on GRIP1, a protein found at both inhibitory and excitatory synapses, according to Wang.

Initially, looking under a microscope at normal mouse neurons and neurons with a mutant version of GRIP1, the investigators marked the receptor proteins with green fluorescence, added a chemical that promotes their “disappearance” deep inside a cell and timed the rates at which they disappeared — leaving a cell unable to respond to signals from other cells. They also timed the reemergence of the protein back to the cell surface. With the GRIP1 mutant neurons, the receptors recycled to the surface twice as fast as in the normal neurons.

“If the receptors are recycling faster, the number of receptors on the surface is greater, so the cells are more sensitive to glutamate,” Huganir explains. “The quicker the recycling, the more receptors on the surface and the stronger the excitatory transmission.”

Even if just the excitatory synapses are affected, and the inhibitory ones don’t change, that alone affects the relative balance of signaling, Huganir says.

Next, using 10 mice genetically engineered to lack both normal and mutant GRIP proteins, researchers watched what happened when each animal was put into a box where it could choose between spending time with a mouse it hadn’t encountered before, or an inanimate object. They compared the behaviors of these mice with 10 normal mice put into the same social situation. Mice lacking both GRIP1 and GRIP2 spent twice as much time as wild-type (normal) mice interacting with other mice as they did with inanimate objects.

“These results support a role for GRIP1 in social behavior and implicate its variants in modulating autistic behavior,” says Wang.

Finally, the team looked at the behavioral analyses of individuals in two families, each with two autistic brothers, and correlated their scores on standard diagnostic tests that assessed social interaction with their genotypes for GRIP1 variants.

In one family, the brother with two copies of the GRIP1 mutant variety scored lower on social interaction tests than his brother who had only one copy of the GRIP1 variant. The boys’ mother, although not diagnosed as autistic, had a history of restricted interests, poor eye contact and repetitive behavior. Tests showed she also carried one copy of the variant.

In a second family, the autistic brother with one copy of the GRIP1 variant had lower social interaction scores than his autistic sibling without a GRIP1 variant.

Because the GRIP1 gene resides in synapses where other genes also implicated in autism have been found, this location is potentially important in terms of clinical relevance, says Huganir. The team plans to sequence hundreds more synaptic proteins in autistic patients to look for mutations and then follow up with functional analyses.

This study was supported in part by research grants from Autism Speaks Foundation and the National Institute of Child Health and Human Development.

Authors on the paper from Johns Hopkins, in addition to Huganir and Wang, are Rebeca Mejias, Abby Adamczyk, Victor Anggono, Tejasvi Niranjan, Gareth M. Thomas, Kamal Sharma, M. Daniele Fallin, Walter E. Kaufmann, Mikhail Pletnikov and David Valle.

Cindy Skinner, Charles E. Schwartz and Roger Stevenson, all of the Greenwood Genetic Center, are also authors on the paper.

Study Reveals How Eye Is Formed
Scientists at King’s College London have discovered specific cells responsible for ensuring that different parts of the eye come together during development.

Published in Nature Communications, these findings significantly enhance our understanding of how the different parts of the eye are organised into a functional organ, revealing clues as to the possible causes of congenital malformations that can lead to life-long visual problems. The study was funded jointly by the BBSRC, Wellcome Trust and Fight for Sight.

The eye of vertebrate animals contains many different parts making up a complex anatomy. At the back of the eye is the retina, containing neurons and photoreceptors which capture light and convert it into electrical pulses transmitted to the brain. It also has a pigmented epithelial layer of cells that help to nourish the retina. In the front of the eye, behind the cornea and iris, lies the lens, which focuses light onto the retina.

Arrangement of these different parts is critical for normal vision. During development the lens and the retina come from completely different tissues, the surface ectoderm and central nervous system, respectively, which raises the question "how do they align to form a functional eye"?

This study, carried out using chicken embryos, shows that neural crest cells, a migratory cell population in the embryo, play an important role in this process. They send out a signal, called TGF-ß, to the surface ectoderm, which activates the Wnt pathway.

Together both signals act to stop the lens being established in the wrong position and ensures that it only develops next to the future retina.

Dr Andrea Streit from the Department of Craniofacial Development in the Dental Institute at King’s, eplains:

‘Neural crest cells give rise to many tissues in the head, including bones and sensory neurons, however their role in organising the eye was previously unknown.

‘This finding opens up the exciting possibility that they not only integrate eye formation, but also different components of other sense organs and sensory circuits in the head.

‘Identifying the signals was a long journey, because of the complex interactions of the TGF-ß and Wnt pathways. But we are now in a position to ask more pointed questions about how different structures in the head are formed and how this relates to developmental abnormalities in humans.’















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