medicine and health

By Salynn Boyles
WebMD Health News

Reviewed by Brunilda Nazario, MD

Oct. 20, 2012 -- Babies conceived with the help of high-tech fertility treatments such as in vitro fertilization (IVF) have an increased risk for birth defects, a new study shows.

Compared to infants born to mothers who conceived without assisted reproduction, those born following treatments like IVF were 25% more likely to have birth defects.

Researchers say the actual or "absolute" risk remains low overall.

The study, which was presented today in New Orleans at a national conference of the American Academy of Pediatrics, is not the first to show a small increase in birth defects among babies conceived through assisted reproduction.

"We don't really understand why IVF raises the risk for birth defects," says researcher Lorraine Kelley-Quon, MD, of UCLA Medical Center. "But we have now seen many studies from all over the world that show this association."

In the new study, Kelley-Quon and colleagues from UCLA's Mattel Children's Hospital used a statewide birth database to compare the incidence of birth defects among babies conceived through high-tech reproduction such as IVF and those born to mothers who conceived naturally.

The two groups of women were matched for characteristics including age, race, and previous births.

The birth defect rate for babies born through IVF or other high-tech fertility treatments was 9% compared to 6.6% for those conceived naturally.

Malformations of the eye, heart defects, and defects of reproductive organs and the urinary system were all more common among babies conceived through high-tech treatments.

Fertility treatments such as artificial insemination, intrauterine insemination, and use of fertility-enhancing drugs were not associated with an increased birth defect risk.

The researchers did not have information on which assisted reproduction treatments the couples in the study had.

In vitro fertilization typically involves attempts to fertilize in a laboratory and a transfer of the embryo back into the womb.

Reproductive endocrinologist Nancy Klein, MD, of Seattle Reproductive Medicine, says more study is needed to confirm this finding.

She adds that while it does appear that babies born following assisted reproduction have a small increased risk for birth defects, it is still not clear if the procedures are to blame.

It may be that infertility itself is a risk factor for birth defects, she says.

Avner Hershlag, MD, who is chief of the Center for Human Reproduction at North Shore-LIJ Health Center in New York, says if IVF and other forms of assisted reproduction do raise the risk for birth defects, the risk is small.

"It is important to do the research to answer this question," he says. An estimated 5 million people were born using these techniques and the vast majority have no birth defects, he adds.

These findings were presented at a medical conference. They should be considered preliminary, as they have not yet undergone the "peer review" process, in which outside experts scrutinize the data prior to publication in a medical journal.

SOURCES: American Academy of Pediatrics National Conference and Exhibit, Oct. 20-23, 2012, New Orleans. Loraine I. Kelley Quon, MD, MSHS, Pediatric Surgery, Mattel Children's Hospital, David Geffen School of Medicine at UCLA, Los Angeles. Nancy Klein, MD, reproductive endocrinologist, Seattle Reproductive Medicine. Avner Hershlag, MD, chief of the Center for Human Reproduction, North Shore-LIJ Health Center, New York. News release, American Academy of Pediatrics. Davies, M.J. New England Journal of Medicine, May 14, 2012.

Protein discovery may lead to new treatment to prevent smoking relapse

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ScienceDaily (Oct. 22, 2012) — Scientists at the Centre for Addiction and Mental Health (CAMH) have identified a potential new approach to preventing smoking relapse, which occurs frequently in smokers who attempt to quit, despite current treatments.

"We have developed a protein peptide that may be a new type of highly targeted treatment to prevent smoking relapse," says Dr. Fang Liu, Senior Scientist in CAMH's Campbell Family Mental Health Research Institute and Professor in the Department of Psychiatry at the University of Toronto.

Dr. Liu and her team initially found that nicotine exposure can enhance binding between two types of brain receptors -- a nicotinic receptor and a glutamate receptor. They identified the sites where the two receptors bind together. With this information, they were able to generate a protein peptide to disrupt the binding of the two receptors.

Working with CAMH Senior Scientist Dr. Anh Dzung Le, the peptide was then tested in an animal model of relapse. As anticipated, it had the effect of reducing attempts to seek nicotine.

"These discoveries present an avenue to develop an anti-smoking medication that directly targets the relapse process by focusing on this brain target," says Dr. Liu, whose study was published online in the Journal of Experimental Medicine October 22. "We hope that it will lead to an alternative treatment for smokers who aren't succeeding with current smoking cessation medications." A year after treatment with current medications, only about 20 per cent of people remain abstinent, past research shows.

"As research continues, future steps are to determine how this discovery can be translated into a novel intervention for patients," says Dr. Liu. "We are optimistic that our findings will lead to new options for treatment for smoking, which is the leading preventable cause of disease, disability and premature death in our society."

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The above story is reprinted from materials provided by Centre for Addiction and Mental Health.
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Shupeng Li, ZhaoXia Li, Lin Pei, Anh D. Le, and Fang Liu. The a7nACh–NMDA receptor complex is involved in cue-induced reinstatement of nicotine seeking. Journal of Experimental Medicine, 2012 DOI: 10.1084/jem.20121270

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Electrical stimulation of the esophagus promising treatment for unresolved reflux symptoms

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ScienceDaily (Oct. 22, 2012) — Clinical evidence of the safety and effectiveness of electrical stimulation of a muscular valve in the esophagus demonstrates promising results in resolving symptoms of gastroesophageal reflux (GERD) and is being presented at the 77th Annual Scientific Meeting of the American College of Gastroenterology in Las Vegas, NV on October 22.

Three studies examined small numbers of patients who had a device implanted that uses low energy electrical pulses to strengthen a weak or dysfunctional lower esophageal sphincter (LES) which is the underlying cause of GERD or acid reflux. The LES is the ring shaped muscular valve that keeps the acidic contents of the stomach from the esophagus, or food tube.

Two studies by investigators Michael Crowell, Ph.D., FACG of Mayo Clinic Scottsdale and Edy Soffer, MD, FACG of the University of Southern California looked at various endpoints including esophageal acid exposure, improvement in GERD symptoms, and reduction of use of acid-suppressing medications known as proton pump inhibitors. In a study of 25 patients, the investigators found that 77 percent of patients reported either normalization or at least a 50 percent reduction in PPI use. At 12 months after the implant of the device, there was a statistically significant improvement in patients' scores on a scale measuring health-related quality of life for patients with GERD. The authors conclude, "Electrical stimulation of the lower esophageal sphincter is effective for treating patients with GERD over long-term year duration." The authors reported relationships with the Netherlands-based EndoStim BV which manufactures the device.

In a separate and unrelated study, Arjan Bredenoord, MD and colleagues at the University Medical Center Utrecht in Rotterdam, The Netherlands, presented a study at ACG of eleven patients with refractory GERD symptoms with devices implanted in the LES. They found that ten of the eleven patients (91 percent) were able to discontinue PPI medications. Overall, their research revealed a statistically significant improvement in patients' GERD symptoms, as well as a trend in improvement in their esophageal pH.

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Discoveries hold promise for treatment of Hepatitis B virus

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ScienceDaily (Oct. 22, 2012) — A University of Colorado Boulder-led team has discovered two prime targets of the Hepatitis B virus in liver cells, findings that could lead to treatment of liver disease in some of the 400 million people worldwide currently infected with the virus.

CU-Boulder Professor Ding Xue, who led the studies, said scientists have been looking for cellular targets of the Hepatitis B virus, or HBV, for more than three decades. Infections from HBV promote hepatitis (inflammation of the liver), cirrhosis (scarring of the liver) and liver cancer and can be transmitted through blood and bodily fluids, unprotected sex, unsterile needles and from infected mother to offspring during birth.

Xue said scientists have known for some time that HBV encodes a pathogenic, tumor-promoting protein known as HBx, but how it works has remained largely unknown. In two new studies, Xue and his colleagues showed that the "host targets" of HBx in human cells are two small cell proteins known as Bcl-2 and Bcl-xL, both of which are well-known cell death inhibitors but which have not previously been implicated in HBV infection.

HBx uses a particular "motif," a small string of protein building blocks known as amino acids that resemble those seen in some cell death-causing proteins, to interact with the Bcl-2 and Bcl-xL targets and stimulate an elevation of calcium in the host cell. The calcium elevation then triggers both viral HBV replication and cell death, said Xue.

When the researchers introduced gene mutations into the motif, HBx binding to the Bcl-2 and Bcl-xL proteins and viral replication were prevented. Similarly, when either Bcl-2 or Bcl-xL proteins were "knocked out" or weakened in human liver cells, HBx was less able to cause an increase in calcium and viral replication inside the infected cells.

"Our most important findings are the identification of the motif itself and the two HBx host targets," said Xue of CU-Boulder's molecular, cellular and developmental biology department. "Now we can start thinking about new drug targets to treat HBV."

Two papers on the subject led by Xue were published online Oct. 22 in the Proceedings of the National Academy of Sciences. In addition to major CU-Boulder co-authors Xin Geng, Brian Harry, Qinghua Zhou, Yan Qin and Amy Palmer, a group led by Professor Ning-Shao Xia from the National Institute of Diagnostics and Vaccine Development in Infectious Diseases at Xiamen University in China collaborated on one of the studies.

The World Health Organization estimated in July that about 600,000 people die annually from acute or chronic HBV infection, which is most predominant in Asia and Africa.

In one of the PNAS studies, the authors used a tiny roundworm known as C. elegans, a widely used animal model in biomedical research, to identify HBx host targets within the cell. Xue and his team showed that HBx can induce cell death in C. elegans through a protein known as CED-9, mimicking an early stage of liver infection by HBV.

Previous work had shown CED-9 in C. elegans is a homolog of the human Bcl-2 protein -- a different protein in a different animal that has a similar function. Despite the stark differences between roundworms and humans, scientists estimate 35 percent of C. elegans genes have human homologs.

"Our results suggest that C. elegans can serve as a good animal model for identifying crucial host factors and cell signaling pathways and aid in development of strategies to treat HBV-induced liver disorders," said Xue. "I think the use of C. elegans will galvanize the field of HBV study, which has been in search of a good animal model for three decades."

Simple animal models like fruit flies and roundworms have been critical for understanding fundamental biological processes such as aging, cell death and the regulation of gene expression. "Many would not have considered using C. elegans as a model to study HBV, but the genetic 'tools' of C. elegans are ideal for the identification of viral host targets, even though C. elegans is not a native host for the virus," said CU's Harry. Harry is pursuing both a Ph.D. degree in MCD Biology at CU-Boulder and an M.D. at the CU School of Medicine on the Anschutz Medical Campus in Aurora through the Medical Scientist Training Program.

"Both studies show that if you create two mutations in this small HBx motif, it takes away its ability to bind to Bcl-2 family proteins. This wipes out viral replication and host cell death caused by HBx expression," said Harry.

Xue said there currently is no effective treatment for chronic HBV carriers, although some people with chronic HBV are treated with interferon and anti-viral drugs. But such treatments are either unavailable or too expensive in developing countries where most of the HBV infections are occurring. "That's why these new findings could have profound clinical and pharmaceutical implications for the treatment of HBV patients," he said.

Harry said the Hepatitis B vaccine, which was developed in 1982, is administered around the world and has been shown to work well in preventing new infections. "The problem is that once you are infected, there is no effective way to remove the virus from the body," he said. "When the virus replicates in liver cells, it causes cycles of cellular damage, inflammation and tissue regeneration, resulting in the accumulation of genetic mutations and liver cancer."

HBV is 50 to 100 times more infectious than the HIV virus, according to WHO officials. In China and other parts of Asia, most people acquire HBV during childhood and 8 to 10 percent of the adult population is chronically infected. "Because of this, understanding how HBV and HBx cause pathogenesis can have dramatic clinical impact," said Xue.

Funding for the two PNAS studies was provided by the National Institutes of Health grants F30 NS070596 and R01 GM059083, GM079097, GM088241 and GM084027. Additional funding came from the China National Science Foundation and the Burroughs Wellcome Fund.

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The above story is reprinted from materials provided by University of Colorado at Boulder.
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Journal Reference:

Xin Geng, Brian L. Harry, Qinghua Zhou, Riley Robert Skeen-Gaar, Xiao Ge, Eui Seung Lee, Shohei Mitani, and Ding Xue. Hepatitis B virus X protein targets the Bcl-2 protein CED-9 to induce intracellular Ca2 increase and cell death in Caenorhabditis elegans. Proceedings of the National Academy of Sciences, 2012; DOI: 10.1073/pnas.1204652109

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Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

Sunday, October 21, 2012

New way to save blood from ravages of chemo treatment

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ScienceDaily (Oct. 18, 2012) — Chemotherapy kills blood cells as well as cancer cells, often with fatal results. Now Yale stem cell researchers have identified a method they hope one day will help cancer patients undergoing chemotherapy maintain a healthy blood supply, they report in the Oct. 18 issue of the journal Cell Reports.

The team, under the direction of Jun Lu, assistant professor of genetics at the Yale Stem Cell Center and Yale Cancer Center, studies how blood cells regenerate. Lu is particularly interested in roles played by tiny bits of genetic material called microRNAs in the production of blood and the function of blood stem and progenitor cells, which help determine the type of blood cell created. Chemotherapy kills these types of progenitor cells, making it difficult for blood to regenerate. While red blood cells can be replaced by transfusions, white blood cells and platelets often do not recover well, leaving cancer patients prone to infections and bleeding.

Using a novel technique to analyze simultaneously large numbers of microRNAs in living mice, the researchers identified several that are involved in blood formation. When they disabled one of these microRNAs, miR-150, they found that mice were able to more efficiently regenerate white cells and platelets depleted by chemotherapy. Mice without this microRNA showed no ill health effects. Conversely, mice with active miR-150 had difficulty generating new blood cells.

"We hope that finding specific microRNAs involved in blood formation will provide us ways not only to help cancer patients survive chemotherapy, but to make chemotherapy more efficient," Lu said.

Other Yale authors of the study include Brian D. Adams, Shangqin Guo, Haitao Bai, Yanwen Guo, Cynthia Megyola, Jijun Cheng and Kartoosh Heydari. Researchers from The Scripps Research Institute, Mount Sinai School of Medicine, and Shanghai First People's Hospital also contributed to the study.

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Brian D. Adams, Shangqin Guo, Haitao Bai, Yanwen Guo, Cynthia M. Megyola, Jijun Cheng, Kartoosh Heydari, Changchun Xiao, E. Premkumar Reddy, and Jun Lu. An In Vivo Functional Screen Uncovers miR-150-Mediated Regulation of Hematopoietic Injury Response. Cell Reports, 2012; DOI: 10.1016/j.celrep.2012.09.014

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Optimal treatment duration for MRSA-related pneumonia re-evaluated

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ScienceDaily (Oct. 19, 2012) — The national practice guideline for treating MRSA-related pneumonia is seven to 21 days. A Henry Ford Hospital study found that effective treatment can be done in half the time.

Researchers found that 40 percent of patients were treated for eight to 13 days on a therapy of the antibiotics vancomycin or linezolid, and had the highest survival rate.

The Henry Ford study is believed to be the first to evaluate the length of treatment for MRSA-related pneumonia.

The study is being presented October 19 at the annual Infectious Diseases Society of America meeting in San Diego.

"Based on our study, clinicians can effectively treat their patients within eight to 13 days, thus minimizing patients' exposure to antibiotics and their side effects," says Hadeel Zainah, M.D., a second-year Infectious Diseases fellow at Henry Ford and the study's lead author.

MRSA-related pneumonia is a respiratory illness that typically follows a bout of the flu. Symptoms include a cough, sore throat, head ache, shortness of breath, fever and chills.

In the retrospective study, researchers evaluated the medical charts of 115 patients hospitalized with MRSA pneumonia. Patients received either vancomycin or linezolid, or both.

Of the 115 patients, 32 died after 28 days.

Other findings:

• 27 percent of patients were treated for 14-20 days.

• 13.9 percent of patients were treated for more than 20 days.

• These treatment durations had lower survival rates than the eight to 13 days.

Researchers did not evaluate whether the treatment duration affected length of stay or whether one antibiotic fared better than the other.

The study was funded by Henry Ford Hospital.

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