Methamphetamine study suggests increased risk for HIV transmission

WINSTON-SALEM, N.C. – New findings that one in 20 North Carolina men who have sex with men (MSM) reported using crystal methamphetamine during the previous month suggests increased risk for spreading HIV and other sexually transmitted diseases (STD), according to researchers from Wake Forest University School of Medicine and colleagues.

The rate of methamphetamine use among 1,189 MSM was 30 times higher than levels reported in the general U.S. population over the same period. Methampehtamine, or “meth,” is a highly addictive stimulant that has been found to impair judgment, decrease inhibition, increase impulsivity and enhance sexual sensitivity – which can all increase the potential for transmitting HIV.

The study’s authors found that participants who reported using methamphetamines were more likely to report inconsistent condom use during anal sex within the past three months, a history of STD infection, being HIV-positive and using medications designed to treat erectile dysfunction.

“Until now, there has been little data on meth use in the Southeast,” said lead author Scott D. Rhodes, Ph.D. M.P.H., associate professor in the Department of Social Sciences and Health Policy. “Our findings, including that meth users were more likely to be HIV-positive, suggest that prevention, intervention and treatment efforts are urgently needed.”

Rhodes noted that some of the men reported having sex with both men and women, which means the risk of HIV extends to both sexes.

The study’s results will be published on Aug. 20 in AIDS Patient Care and STDs, a leading AIDS journal that provides the latest research for clinicians and researchers. It is among the first to document meth use among MSM in the South, which carries a disproportionate HIV, AIDS, and STD burden, with 46 percent of newly identified cases.

“The findings underscore the need for further research and intervention,” said Rhodes. “The HIV/AIDS epidemic is clearly not over. We must develop innovative intervention approaches designed to reach communities at highest risk. Men who have sex with men, whether or not they identify themselves as gay, who use drugs like methamphetamines are clearly at higher risk. Yet currently nothing is being done in the Southeast.”

Participants were recruited in 2005 in five gay bars and in five geographically defined internet chat rooms in central North Carolina (primarily rural/suburban areas) and were asked to complete a brief assessment of drug use and other risk behaviors. Of the 1,189 MSM, two-thirds self-identified as black or other minorities, and 25 percent as bisexual. The mean age was 29 years.

In addition to being more inclined to risky sexual behaviors, the study participants who said they used methamphetamines were also more likely to report having higher education and health insurance coverage.

“Because users of methamphetamines were more likely to have higher educational levels and report having health insurance, we must change the way we think about meth users and develop sophisticated prevention strategies that are appropriate for these types of users,” noted Rhodes. “In addition, the link between meth use and the use of drugs for sexual dysfunction among a young population deserves attention. Meth use in combination with one of these medications may be having an even more profound impact on the HIV and STD disease epidemics in the South.”

Rhodes is also affiliated with the Maya Angelou Research Center on Minority Health at Wake Forest. In 2006, Rhodes won the New Investigator Award in Clinical Sciences at Wake Forest.

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The study’s co-authors include Emily Knipper and Aimee M. Wilkin, M.D., M.P.H., both with Wake Forest, Kenneth C. Hergenrather, Ph.D., M.S.Ed., M.R.C., of George Washington University, Leland J. Yee, Ph.D., M.P.H., of the University of Pittsburgh, and Morrow R. Omli, M.A.Ed., of the University of Florida.

Media Contacts: Karen Richardson, krchrdsn@wfubmc.edu, or Shannon Koontz, shkoontz@wfubmc.edu, 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 family medicine, 20th in geriatrics, 25th in primary care and 41st 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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Low vitamin D levels may be common in otherwise healthy children

Many otherwise healthy children and adolescents have low vitamin D levels, which may put them at risk for bone diseases such as rickets. African American children, children above age nine and with low dietary vitamin D intake were the most likely to have low levels of vitamin D in their blood, according to researchers from The Children’s Hospital of Philadelphia.

A study in the current issue of the American Journal of Clinical Nutrition measured blood levels of vitamin D in 382 healthy children between six years and 21 years of age living in the northeastern U.S. Researchers assessed dietary and supplemental vitamin D intake, as well as body mass, and found that more than half of the children had low blood levels of vitamin D. Of the subjects, 55 percent of the children had inadequate vitamin D blood levels and 68 percent overall had low blood levels of the vitamin in the wintertime.

“The best indicator of a person’s vitamin D status is the blood level of a vitamin D compound called 25-hydroxyvitamin D,” said Babette Zemel, Ph.D., a nutritional anthropologist at Children’s Hospital and primary investigator of this study. “Vitamin D deficiency remains an under-recognized problem overall, and is not well studied in children.”

Vitamin D is crucial for musculoskeletal health. The primary dietary source of the vitamin is fortified milk, but the best way to increase vitamin D levels is from exposure to sunshine. Severe deficits in vitamin D may lead to muscle weakness, defective bone mineralization and rickets. In addition to musculoskeletal effects, vitamin D is important for immune function, and low blood levels of the vitamin may contribute to diseases such as hypertension, cancer, multiple sclerosis and type 1 diabetes. Decreased blood levels of vitamin D have also been linked to obesity.

Further study is needed to determine the appropriate blood levels of vitamin D in children, said Dr. Zemel, who added that a review of the current recommendations for vitamin D intake is needed.

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Grants from the National Institutes of Health and several private sources supported this study.

Dr. Zemel’s co-authors were Mary B. Leonard, M.D. and Virginia A. Stallings, M.D., of The Children’s Hospital of Philadelphia and University of Pennsylvania School of Medicine, as well as Francis L. Weng and Justine Shults, also of the University of Pennsylvania School of Medicine.

About The Children’s Hospital of Philadelphia: The Children’s Hospital of Philadelphia was founded in 1855 as the nation’s first pediatric hospital. Through its long-standing commitment to providing exceptional patient care, training new generations of pediatric healthcare professionals and pioneering major research initiatives, Children’s Hospital has fostered many discoveries that have benefited children worldwide. Its pediatric research program is among the largest in the country, ranking third in National Institutes of Health funding. In addition, its unique family-centered care and public service programs have brought the 430-bed hospital recognition as a leading advocate for children and adolescents. For more information, visit http://www.chop.edu.

Contact: Joey Marie McCool
McCool@email.chop.edu
267-426-6070
Children’s Hospital of Philadelphia

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New Risk Factors Discovered for Alzheimer’s Disease

Pittsburgh, Pa. – July 06, 2007 – A recent study in Journal of Neuroimaging suggests that cognitively normal adults exhibiting atrophy of their temporal lobe or damage to blood vessels in the brain are more likely to develop Alzheimer’s disease. Older adults showing signs of both conditions were seven-times more likely to develop Alzheimer’s than their peers.

“Alzheimer’s disease, a highly debilitating and ultimately fatal neurological disease, is already associated with other risk factors such as poor cognitive scores, education or health conditions,” says study author Caterina Rosano. “This study, because it focused on healthy, cognitively normal adults, shows that there other risk factors we need to consider.”

MRI images of participants’ brains were examined to identify poor brain circulation, damaged blood vessels and/or atrophy of the medial temporal lobe. Subjects showing any one or a combination of these symptoms were more likely to develop Alzheimer’s in the following years.

“Similarly to heart disease, brain blood vessel damage is more likely to occur in patients with high blood pressure, high cholesterol or diabetes,” says Rosano. “Since we know that prevention of these conditions can lower risk of heart attack and stroke, it is likely that it would also lower the risk of developing Alzheimer’s.”

This study is published in Journal of Neuroimaging. Media wishing to receive a PDF of this article may contact medicalnews@bos.blackwellpublishing.net.

Dr. Caterina Rosano is a physician neuroepidemiologist and assistant professor of epidemiology with the Center for Aging and Population Health at the University of Pittsburgh. She is currently developing a model to predict the incidence of cognitive and physical functional limitations in older adults. She can be reached for questions at rosanoc@edc.pitt.edu .

Journal of Neuroimaging addresses the full spectrum of human nervous system disease including stroke, neoplasia, degenerative and demyelinating disease, epilepsy, infectious disease, toxic-metabolic disease, psychoses, dementias, heredo-familial disease and trauma. Each issue offers original clinical articles, case reports, articles on advances in experimental research, technology updates, and neuroimaging CPCs. For more information, please visit http://www.blackwellpublishing.com/jon.

Wiley-Blackwell was formed in February 2007 as a result of the merger between Blackwell Publishing Ltd. and John Wiley & Sons, Inc.’s Scientific, Technical, and Medical business. Together, the companies have created a global publishing business with deep strength in every major academic and professional field. Wiley-Blackwell publishes approximately 1,250 scholarly peer-reviewed journals and an extensive collection of books with global appeal. For more information on Wiley-Blackwell, please visit http://www.blackwellpublishing.com or http://interscience.wiley.com.

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Type 1 diabetes and heart disease — Heavier may mean healthier

Contact: Michele D. Baum
BaumMD@upmc.edu
412-647-3555
University of Pittsburgh Schools of the Health Sciences

Pittsburgh scientists find more fat equals less coronary artery calcification
CHICAGO, June 23 — Researchers at the University of Pittsburgh Schools of the Health Sciences studying links between an early sign of heart disease called coronary artery calcification and body fat have found that, paradoxically, more fat may have some advantages, at least for people – particularly women – who have type 1 diabetes. Cardiovascular complications, including heart disease, are a leading cause of death for people with diabetes, who tend to suffer cardiovascular disease decades earlier than non-diabetics.

“Gaining weight may reflect good or better treatment with insulin therapy, which may partly explain why participants who gained weight over time had lower mortality rates,” said Trevor Orchard, M.D., professor of epidemiology at the University of Pittsburgh Graduate School of Public Health (GSPH), who is presenting the findings during the 67th annual meeting of the American Diabetes Association. Scientific sessions take place June 22-26 at the McCormick Place Convention Center, Chicago.

For this particular report, Dr. Orchard and his colleagues focused on 315 patients with type 1 diabetes participating in the Pittsburgh Epidemiology of Diabetes Complications Study, an 18-year prospective study of childhood onset type 1 diabetes, which began in 1986. As part of the study, the patients recently received a special computed tomography scan (CT) to assess coronary artery calcification.

The participants’ mean age was 42, and mean duration of diabetes was 34 years. In addition to the CT scan, patients were evaluated for fat underneath the skin and in the abdominal region, body mass index (BMI) and waist circumference. Although investigators noted a positive association for all measures of fatness and having any coronary artery calcification, in the two-thirds of patients who had calcification, the relationship reversed so that people with more fat had less severe calcification.

This association also varied by gender. Women with less fat under the skin had more evidence of coronary artery calcification than those with more fat. Thinner men also had more evidence of coronary artery calcification than men with a higher BMI.

“What it comes down to is a kind of double-edged relationship,” said Baqiyyah Conway, M.P.H., lead author of the abstract, adding that these associations of less severe artery calcification with greater fat persisted even when controlling for standard cardiovascular disease risk factors such as increased levels of LDL, or bad cholesterol, triglycerides, high blood pressure and lower levels of HDL, or good cholesterol. Controlling for kidney disease, another common complication of diabetes, weakened the association in men but not in women.

“This is not a firm recommendation to people with type 1 diabetes to put on weight, but it does raise the possibility that weight recommendations in type 1 diabetes may be somewhat different than those for the general population, and emphasizes the complex relationship between body fat and cardiovascular risk in diabetes,” said Dr. Orchard, who also is professor of medicine and pediatrics at the University of Pittsburgh School of Medicine.

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CONTACT: Amy Dugas, DugasAK@upmc.edu
PHONE: (412) 647-3555

EMBARGOED FOR RELEASE UNTIL 5 P.M., EDT, SATURDAY, JUNE 23

In addition to Dr. Orchard and Ms. Conway, other authors are Rachel G. Miller, M.S.; Tina Costacou, Ph.D.; and Daniel Edmundowicz, M.D., all of the University of Pittsburgh Schools of the Health Sciences.

Founded in 1948 and fully accredited by the Council on Education for Public Health, GSPH is world-renowned for contributions that have influenced public health practices and medical care for millions of people. One of the top-ranked schools of public health in the United States, GSPH was the first fully-accredited school of public health in the Commonwealth of Pennsylvania, with alumni who are among the leaders in their fields of public health. A member of the Association of Schools of Public Health, GSPH currently ranks third among schools of public health in NIH funding received. The only school of public health in the nation with a chair in minority health, GSPH is a leader in research related to women’s health, HIV/AIDS and human genetics, among others. For more information about GSPH, visit the GSPH Web site at http://www.publichealth.pitt.edu.

Note to editors: This presentation is abstract No. 0129-OR, scheduled for 5 p.m., EDT, Saturday, June 23.

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University of Pittsburgh scientists find new contributor to aggressive cancers

Contact: Jim Swyers
SwyersJP@upmc.edu
412-647-3555
University of Pittsburgh Schools of the Health Sciences

PITTSBURGH, June 6 — Mutations in the cell adhesion molecule known as integrin alpha 7 (integrin á7) lead to unchecked tumor cell proliferation and a significantly higher incidence in cancer spread, or metastasis, in several cancer cell lines, report researchers at the University of Pittsburgh School of Medicine in a study being published today in the Journal of the National Cancer Institute. These findings suggest that integrin á7 represents an important new target for cancer therapy and prevention.

Integrin á7 belongs to a major class of cell membrane proteins that play a role in the attachment of a cell to the extracellular matrix (ECM), which is the material that holds cells within a particular type of tissue together. Integrins also help cells attach to one another and are involved in transmitting chemical signals between cells and the ECM.

In this study, the researchers, led by Jianhua Luo, M.D., Ph.D., associate professor in the division of molecular and cellular pathology, University of Pittsburgh School of Medicine, examined whether this gene is mutated in specimens of various human cancers as well as whether the level of integrin á7 expression is associated with clinical relapse of human cancers. They also investigated whether integrin á7 has tumor suppressor activity.

To determine whether mutations in integrin á7 contribute to cancer, Dr. Luo and his collaborators sequenced the integrin á7 genes from 66 human cancer specimens and cell lines representing a number of different kinds of cancer, including cancer of the prostate, liver, brain (glioblastoma) and muscle (leiomyosarcoma).

They found mutations in the integrin á7 gene, particularly those that resulted in an abnormally shortened protein product, or truncation, in 16 of 28 prostate cancers. They also found truncation-inducing mutations in five of 24 liver cancer samples, five of six glioblastomas, and one of four leiomyosarcomas.

Integrin á7 mutations also were associated with a significant increase in the recurrence of cancer among patients. Nine of 13 prostate cancer patients with integrin á7 mutations experienced a recurrence of their cancer after radical prostatectomy versus only one of eight prostate cancer patients without such mutations. There were five recurrences among eight hepatocellular carcinoma patients with integrin á7 mutations versus only one recurrence of cancer among 16 patients without such mutations.

To examine the effect of alterations in the level of integrin á7 on tumor formation, the researchers assessed the ability of cancer cells to form colonies in a standard growth medium after increasing or decreasing the level of normal integrin á7 in the cell lines. In this experiment, control cancer cells formed large colonies with up to 100 cells each. Cancer cells with normal levels of integrin á7 expression formed fewer and smaller colonies. When the investigators decreased the level of integrin á7 in two cancer cells lines using siRNAs, or silencing RNAs, both cell lines formed more colonies and grew better than corresponding control cell lines.

“When we increased levels of normal integrin á7 in cancer cells, they grew at a much slower rate. This suggests that this protein is a fairly potent tumor suppressor,” said Dr. Luo.

Dr. Luo and his coworkers then investigated the role of integrin á7 in metastasis by examining the relationship between the level of integrin á7 expression and cell migration by increasing the expression of normal integrin á7 in three cell lines. The migration rate was significantly reduced in all of the cells compared to those in which the expression of integrin á7 remained deficient, suggesting that the level of normal integrin á7 expression is inversely associated with tumor cell migration.

Finally, to investigate whether normal integrin á7 possesses tumor suppressor activity, the researchers implanted human cancer cells into immune deficient mice. Some mice received tumor cells in which levels of integrin á7 were increased, others received tumor cells in which the levels of normal integrin á7 were decreased. Six weeks after mice were implanted with cancer cells in which levels of normal integrin á7 were deficient, they had tumors with an average volume about four times as large as mice with implanted cancer cells in which normal integrin á7 levels were increased. Similarly, the researchers found no visible metastasis in mice with tumors in which levels of normal integrin á7 had been increased. On the other hand, they did find evidence of metastasis in three of 12 mice with one type of tumor deficient in normal integrin á7 and in four of the 12 mice with another type of tumor deficient in normal integrin á7. Furthermore, the six-week survival of mice bearing tumors with increased levels of normal integrin á7 was higher than that of mice bearing tumors in which normal integrin á7 had not been experimentally increased. Thus, increasing the level of normal integrin á7 in tumors was associated with decreased tumor growth and metastasis in this animal model.

According to Dr. Luo and his coworkers, these findings suggest that not only is integrin á7 an important tumor suppressor, but it is potentially a critical new target for cancer treatment.

“Our study shows rather definitively that when we experimentally decreased the level of integrin á7 protein or the protein was naturally mutated in cells, those cells lost their inhibitory signals for both cell migration and proliferation. This suggests that the loss of integrin á7 activity may lead to unchecked tumor cell proliferation and a significantly increased risk of tumor metastasis. More importantly, it suggests that if we can somehow restore normal integrin á7 levels in tumor cells in vivo, we may be able to reduce the risk of them spreading to other sites, which would be a significant achievement in cancer therapy,” explained Dr. Luo.

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CONTACT: Clare Collins, CollCX@upmc.edu
PHONE: (412) 647-3555

This work was supported by grants from the National Cancer Institute, the development fund from the department of urology, University of Pittsburgh School of Medicine, and the John Rangos Foundation for Enhancement of Research in Pathology.

In addition to Dr. Luo, others involved in the study include George K. Michalopoulos, M.D., Ph.D., Baoguo Ren, M.D., Yan P. Yu, M.D., and Chuanyue Wu, Ph.D., department of pathology, University of Pittsburgh School of Medicine; George C. Tseng, Ph.D., department of biostatistics, University of Pittsburgh Graduate School of Pubic Health; and Ka Chen, Uma N. Rao, M.D., and Joel Nelson, M.D., department of urology, University of Pittsburgh School of Medicine.

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University of Pittsburgh discovers genetic ‘shut down’ trigger in healthy immune cells

Contact: Michele Baum
baummd@upmc.edu
412-647-3555
University of Pittsburgh Schools of the Health Sciences

Discovery could have significant implications for targeting cancer, infection treatments
PITTSBURGH, May 9 — A fundamental genetic mechanism that shuts down an important gene in healthy immune system cells has been discovered that could one day lead to new therapies against infections, leukemia and other cancers. Results of a University of Pittsburgh School of Medicine study on the mechanism, called a somatic stop-codon mutation, are being reported today in the online journal PLoS ONE, published by the Public Library of Science.

“This kind of loss-of-function mutation can be very dangerous, and it is the first such mutation that has been identified in normal immune cells in blood,” said Bora E. Baysal, M.D., Ph.D., assistant professor of obstetrics, gynecology and reproductive sciences at the University of Pittsburgh School of Medicine. “We did control experiments for two years to make sure it was real and not a technical error.”

Dr. Baysal and his colleagues tested 180 samples, including blood from healthy individuals and other material from those with childhood leukemia, looking at specific portions of DNA in immune cells known as monocytes, natural killer cells and lymphocytes. These cells are key to the body’s immune response against infection and disease. The investigators found somatic stop-codon mutations in an average of 5.8 percent of crucial portions of genetic material that deliver instructions from DNA, called messenger RNA, in normal blood samples and in a quarter of leukemia samples.

“DNA is the blueprint for all living cells. It carries the genetic code for most biological functions and is passed virtually unchanged from generation to generation,” said Dr. Baysal, who also is an associate investigator at the university-affiliated Magee-Womens Research Institute. “Harmful alterations in the code – mutations – can produce genetic disorders and play an important role in the development of cancer. Normal cells such as monocytes, lymphocytes and natural killer cells have many mechanisms to recognize and repair mutations, but a stop-codon mutation is a kind of permanent “off” switch that has escaped DNA repair,” he added.

“We believe there is a good biological reason for this. It may allow the cells to survive in a low-oxygen environment, such as where there is cancer or infection,” said Dr. Baysal. “It is part of the process for immune cells to ‘armor up’ for battle against cancer cells and other diseases.”

Earlier research on the mutated gene suggests the stop-codon mutation might be part of the programmed adaptive response to oxygen deprivation. This mutation and its location is “unusual because it predicts loss-of-function, it targets a classical tumor-suppressor gene, and it occurs in (peripheral blood mononuclear cells),” Dr. Baysal wrote, adding that the mutation is present at much higher levels in messenger RNA compared to DNA.

“This may give us a tool to modify the immune cells’ survival in a low oxygen environment, which could help the cells to survive and fight infections and tumors,” said Dr. Baysal, calling the mutated gene a potential “therapeutic target.”

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CONTACT: Jim Swyers, SwyersJP@upmc.edu
PHONE: (412) 647-3555
FAX: (412) 624-3184

The study was funded by the National Cancer Institute.

For copies of the paper, visit http://www.plosone.org/home.action.

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