Beyond The Abstract – The Effect Of Age On Outcomes Of Sling Surgery For Urinary Incontinence

UroToday – This study demonstrates the need for caution when performing slings on older women with stress incontinence. We found that older women were not only more likely to fail surgery and require another procedure for stress incontinence, but also were more likely to experience emptying difficulty and new urge incontinence after a sling. These findings suggest a need for thorough pre-operative counseling of older women undergoing sling surgery, as their risk of surgical morbidity is higher than for younger women.

Jennifer Anger, MD, MPH, as part of Beyond the Abstract on UroToday. This initiative offers a method of publishing for the professional urology community. Authors are given an opportunity to expand on the circumstances, limitations etc… of their research by referencing the published abstract.

Link to Full Abstract

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Copyright © 2007 – UroToday
Reproduced for blog with permission of UroToday.

E. Coli Bacteria Migrating Between Humans, Chimps In Ugandan Park

Scientists from the University of Illinois at Champaign-Urbana have found that people employed in chimpanzee-focused research and tourism in a park in western Uganda are exchanging gastrointestinal bacteria – specifically Escherichia coli – with local chimpanzee populations. And some of the E. coli strains migrating to chimps are resistant to antibiotics used by humans in Uganda.

Their study will appear in the April 2007 issue of Biological Conservation and is available now on the journal’s Web site.

Other studies have found bacterial exchanges between humans and non-human primates – particularly in areas where the animals are known to frequent garbage piles near human settlements. But this is the first study to document the exchange of E. coli between humans and chimps in a protected wildlife area. It is also the first to find antibiotic-resistant strains in chimpanzees in Africa.

“Antibiotic resistance has traditionally been associated with two factors: indiscriminate and over-prescription of antibiotics by physicians in the developed world and the inclusion of antibiotics in animal feed in the developed world,” said Tony L. Goldberg, a professor of veterinary pathobiology and the principal investigator of the study. The new findings, Goldberg said, show that over-the-counter sales of antibiotics for human consumption can also have an impact on wildlife.

The research team, which included researchers from Makerere University in Kampala, Uganda, and McGill University in Montreal, examined two of 10 known communities of chimpanzees living in Kibale National Park, Uganda. One of the two chimp groups has been the focus of two decades of research by international teams of scientists. The other is regularly visited by employees of a local tourism venture.

Goldberg’s team compared strains of E. coli in the chimps to those of the Ugandans employed in research and tourism in the park.

The team also analyzed samples from people living in a village 5 kilometers from the research site and 25 kilometers from the tourism station. People in the village had no known contact with the chimps.

The team collected 250 E. coli isolates from 25 humans and 23 chimpanzees. Of these, 89 unique genotypes (strains) of E. coli were found.

The E. coli strains from the chimps were more like those of the humans working in the park than like humans living in the village.

“This expands our notion of the situations in which people and chimps can exchange microbes,” Goldberg said. “Habitat overlap, even without direct contact between people and primates, is sufficient for the exchange to occur.”

The further finding that humans had transferred some antibiotic resistant strains to chimps “was the smoking gun,” Goldberg said. More than 81 percent of the humans and 4.4 percent of the chimps studied were found to harbor at least one E. coli isolate that was clinically resistant to an antibiotic. Antibiotics are used frequently in human populations in this region of Uganda, Goldberg said, but antibiotics have never been used in local wildlife, so the antibiotic-resistant bacteria in chimps clearly originated in humans.

Goldberg said it was not clear whether the exchange of bacteria was the result of direct or indirect (environmental) association between the chimps and humans working in the park. Both make use of local streams and other environmental features.

Regardless of the route of transmission, it places both at risk, Goldberg said.

“We’re as concerned about potential effects on human health as on animal health,” he said.

He noted that the exchange of microbes between non-human primates and humans is not new. Two deadly viruses, HIV and Ebola, are believed to be linked to chimpanzees and other non-human primates. Human diseases also pass to monkeys and apes, with equally dire consequences: Pneumonia, respiratory disease, scabies and a polio-like virus have caused epidemic mortality in chimpanzees in some African locales.


This study was funded by the Morris Animal Foundation.

Contact: Diana Yates

University of Illinois at Urbana-Champaign

The Effect Of Obesity-Related Gene Can Be Blunted By High Levels Of Physical Activity, Study Suggests

High levels of physical activity can help to counteract a gene that normally causes people to gain weight, according to a new study by researchers at the University of Maryland School of Medicine. They analyzed gene variants and activity levels of the Old Order Amish in Lancaster County, Pa., and found that the obesity-related FTO gene had no effect on individuals who were the most physically active.

“Our results strongly suggest that the increased risk of obesity due to genetic susceptibility can be blunted through physical activity,” the authors conclude. “These findings emphasize the important role of physical activity in public health efforts to combat obesity, particularly in genetically susceptible individuals.” The results of the study are being published in the Sept. 8, 2008, issue of the Archives of Internal Medicine.

Soren Snitker, M.D., Ph.D., the senior author and an assistant professor of medicine and pediatrics at the University of Maryland School of Medicine, says, “Our study shows that a high level of physical activity can ‘level the playing field,’ equalizing the risk of obesity between those who have copies of the FTO gene variant and those who don’t.”

The FTO gene recently has been linked to obesity and increased body mass index, or BMI, in several large-scale studies. More than half of all people of European descent have one or two copies of a variation of this gene, British scientists reported last year. Individuals with two copies of the gene variant are on average 7 pounds heavier and 67 percent more likely to be obese than those who don’t have it.

University of Maryland researchers found this same link between variations of the FTO gene and increased risk of obesity in their study of 704 Amish men and women. But, in examining the gene in this unique group of people with a similar genetic background and active lifestyle, the researchers also found that high levels of physical activity helped to counteract the gene’s effects.

“Having multiple copies of FTO gene variants had no effect on body weight for people who were the most physically active, regardless of whether they were men or women. But in less active people, the association between the gene and increased BMI was significant,” says Evadnie Rampersaud, Ph.D., the lead author and a former postdoctoral fellow at the University of Maryland School of Medicine who is now at the University of Miami Institute for Human Genomics. “This provides evidence that the negative effects of the FTO variants on increasing body weight can be moderated by physical activity.”

Dr. Snitker, of the University of Maryland School of Medicine, says the FTO gene is likely only one of a number of genes linked to obesity and notes that the effect of these genes may have changed over time.

“Some of the genes shown to cause obesity in our modern environment may not have had this effect a few centuries ago when most people’s lives were similar to that of present-day Amish farmers,” he says. He adds that environmental and lifestyle factors, such as a high-fat diet and lack of exercise, also may serve as triggers for obesity in genetically susceptible people.

“We are just starting to unravel these complex interactions between genomics and environment. It’s really a new age of discovery,” Dr. Snitker says. “One day, we hope to be able to provide a personally optimized prescription to prevent or treat obesity in people based on their individual genetic makeup.”

In this study, which was funded by the National Institutes of Health (NIH), the researchers examined dozens of variations in the FTO gene. They gauged the participants’ physical activity level with the help of a device worn on the hip called an accelerometer, which measures body movement. “We were able to get objective measurements of physical activity over seven consecutive 24-hour periods using this device, and that is a real strength of our study,” says Dr. Rampersaud.

Participants were classified as having “high activity” or “low activity” levels. The more active people used 900 more kilocalories, or units of energy, a day, which translates into three to four hours of moderately intensive activity, such as brisk walking, housecleaning or gardening.

Despite an active lifestyle, 54 percent of the men in the study were considered overweight (BMI over 25) and 10.1 percent were obese (BMI over 30). Sixty-three percent of the women were overweight, and 30 percent were considered obese. The mean BMI was slightly higher in women (27.8) than in men (25.7).

These figures are in line with previous University of Maryland studies that showed that the Amish are as obese as other Caucasians in the United States. The earlier research also found that the Amish have half the incidence of Type 2 diabetes as well as favorable cholesterol levels, despite a diet high in fat and cholesterol, although the reasons for this remain unclear.

The Old Order Amish are considered ideal for genetic research because they are a genetically homogenous people who trace their ancestry back 14 generations to a small group that came to Pennsylvania from Europe in the mid-1700s. They don’t drive cars or have electricity in their homes, eschewing many of the trappings of modern life. Most Amish men are farmers or work in physically demanding occupations such as blacksmithing or carpentry. Women are homemakers who work without the aid of modern appliances and often care for many children.


University of Maryland School of Medicine researchers, led by Alan R. Shuldiner, M.D., have conducted more than a dozen studies of the Amish in Lancaster County, Pa. since 1993, looking at various medical problems, such as diabetes, obesity, osteoporosis and high blood pressure. The latest research is an offshoot of a larger NIH-funded study, the Heredity and Phenotype Intervention (HAPI) Heart Study, examining how genes and lifestyle factors influence the Amish people’s risk of developing cardiovascular disease.

Among the co-authors of the FTO gene study are Dr. Shuldiner, who is a professor of medicine, head of the Division of Endocrinology, Diabetes and Nutrition, and director of the Program in Genetics and Genomic Medicine at the School of Medicine; Toni I. Pollin, Ph.D., an assistant professor of medicine; and Braxton D. Mitchell, Ph.D., a professor of medicine.

Source: Karen Warmkessel

University of Maryland Medical Center

Defining The Signaling Mechanism And Relevance Of H2 Relaxin In Prostate Cancer Progression

UroToday – The objectives of this study were to elucidate the mechanism(s) by which H2 relaxin promotes prostate cancer progression, and to determine the distribution and level of expression of H2 relaxin in prostate cancer patient samples. The identification of novel pathways that promote androgen-independent growth of prostate cancer cells is critical for the development of successful new therapies to treat CaP. They have identified H2 relaxin as a facilitator of androgen independent prostate cancer (AI CaP) H2 relaxin treatment allows for the AI growth of LNCaP, and can facilitate androgen receptor (AR)-dependent transactivation of the PSA promoter.

PKA and cAMP activity were assessed in LNCaP cells treated with recombinant human (rh) H2 relaxin. B-catenin and GSK-B expression were assessed by Western blot analysis. Immunoprecipitation and immunocytochemistry were used to determine whether rh H2 relaxin induced binding of B-catenin to AR and subsequent translocation of the AR/B-catenin complex to the nucleus. H2 relaxin levels were assessed using by ELISA, immunocytochemistry and RT-PCR analysis. Sixty patient samples have been analyzed to date.

Their data demonstrate that H2 relaxin is able to activate the cAMP/PKA pathway and the GSK-B/B-catenin/AR pathway. cAMP activity peaked at 10 minutes following treatment with rh H2 relaxin, while PKA activity peaked at 15 minutes post-treatment. H2 relaxin treatment increased phosphorylation of GSK-B and elevated B-catenin levels. Immunoprecipitation and immunocytochemistry studies demonstrated that H2 relaxin promoted the interaction of B-catenin and AR, and the translocation of this complex to the nucleus. Analysis of H2 relaxin levels in patient samples revealed that H2 relaxin is elevated in ~50% of prostate cancer patients.
They conclude that H2 relaxin is able to activate the cAMP/PKA pathway in LNCaP promoting an interaction between B-catenin and AR that results in translocation of the B-catenin/AR complex to the nucleus.

Presented by Ruth L Vinall and associates from the University of California, Davis
From the 2007 annual meeting of the AUA

Reported by UroToday Contributing Editor Christopher P. Evans, MD, FACS

UroToday – the only urology website with original content global urology key opinion leaders actively engaged in clinical practice.

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Copyright © 2007 – UroToday
Reproduced for blog with permission of UroToday.

Preschool-Age Children Who Slept Less Were More Likely To Be Hyperactive And Inattentive; Possible Association With ADHD

Short sleep duration may contribute to the development or worsening of hyperactivity and inattention during early childhood, suggests a research abstract that will be presented Tuesday, June 14, in Minneapolis, Minn., at SLEEP 2011, the 25th Anniversary Meeting of the Associated Professional Sleep Societies LLC (APSS).

Results show that less sleep in preschool-age children significantly predicted worse parent-reported hyperactivity and inattention at kindergarten. In contrast, hyperactivity and inattention at preschool did not predict sleep duration at kindergarten. The sample consisted of approximately 6,860 children, and analyses controlled for gender, ethnicity and family income.

“Children who were reported to sleep less in preschool were rated by their parents as more hyperactive and less attentive compared to their peers at kindergarten,” said lead author Erika Gaylor, PhD, senior researcher for SRI International, an independent, nonprofit research institute in Menlo Park, Calif. “These findings suggest that some children who are not getting adequate sleep may be at risk for developing behavioral problems manifested by hyperactivity, impulsivity, and problems sitting still and paying attention.”

According to the authors, attention-deficit/hyperactivity disorder is not generally diagnosed until the school-age years. However, the onset of developmentally inappropriate inattention, hyperactivity and impulsivity is often much younger. Sleep problems, particularly difficulty falling asleep and staying asleep, are frequently reported in children and adolescents with ADHD. However, the direction of causation, if any, has been difficult to determine. Longitudinal studies may provide a window into the direction of this complex relationship.

The analyses used data from the preschool and kindergarten waves of the Early Childhood Longitudinal Study – Birth Cohort. The dataset includes a contemporary, representative sample of children and their families living in the U.S. and followed longitudinally from birth through kindergarten entry. Total nighttime sleep duration was calculated using parent-reported bedtimes and wake times, which were obtained via interview at both time points. Parents also rated their children’s behavior on brief measures of attention/task persistence and hyperactivity/impulsivity.

Last year at SLEEP 2010, Gaylor reported that having a regular bedtime was the most consistent predictor of positive developmental outcomes at 4 years of age. Having an earlier bedtime also was predictive of higher scores for most developmental measures.

Emilee McStay

American Academy of Sleep Medicine

New CU-Boulder Study Shows Diversity Decreases Chances Of Parasitic Disease

A new University of Colorado at Boulder study showing that American toads who pal around with gray tree frogs reduce their chances of parasitic infections known to cause limb malformations has strong implications for the benefits of biodiversity on emerging wildlife diseases.

The experiments showed that when the toad tadpoles were raised in tanks with the parasitic trematodes — tiny worms whose larvae burrow into tadpole limb regions and disrupt normal leg development — 40 percent of the emerging frogs became deformed, said CU-Boulder Assistant Professor Pieter Johnson. But when the toad tadpoles were joined in the tanks with gray tree frog tadpoles, parasitic infections in the toads dropped by almost half, said Johnson, lead author of the study.

The study showed tree frog tadpoles acted as “sponges” for the trematode parasites, which were subsequently killed by the immune systems of frog tadpoles, said Johnson. As a result, fewer parasites were available to infect and cause malformations in the toads. Both the gray tree frog and American toad are broadly distributed in the Midwest and eastern United States and often occur in the same wetlands, he said.

“This is one of the first experimental studies to definitively show that an increase in diversity of host species actually can reduce parasite transmission and disease,” said Johnson of CU-Boulder’s ecology and evolutionary biology department. Published in the October issue of Ecology Letters, the study has implications for the declining global diversity of wildlife species that are susceptible to parasitic infections, said Johnson.

Other research has shown that a decrease in diversity in mammal host species for ticks carrying Lyme disease increases the risk of Lyme disease in humans, Johnson said. Similar relationships between wildlife diversity and disease prevalence have been suggested by other researchers to influence other vector-borne diseases, including West Nile virus, tick-borne encephalitis and bubonic plague, he said.

“In the absence of parasites, the toads and frogs are pure competitors,” Johnson said. “But when trematode parasitism is present in the ecosystem, the adage ‘the enemy of my enemy is my friend’ comes into play for the toads, which are essentially shielded from infections by the tree frogs.” Co-authors on the Ecology Letters study included Richard Hartson from the University of Wisconsin-Madison and Donald Larson and Daniel Sutherland from the University of Wisconsin-La Crosse.

The researchers also ran experiments involving American toad tadpoles coupled with green frog tadpoles, and others involving American toads, eastern tree frogs and green frogs together in the same tanks, said Johnson. In the tanks containing toad tadpoles and green frog tadpoles, the toad tadpoles had similarly high infection rates to those shown when they were the only tadpoles in the tanks.

But when all three tadpole types were raised together, the toad tadpoles were once again buffered from the parasites by the “dilution effect” provided by tree frogs. “Thus, the important determinant of parasite transmission was not total host diversity but the specific composition of the host community,” wrote the authors.

The trematode has a complex life cycle involving snails, amphibians and predators. Host snails release parasite larvae into the water, infecting amphibians and causing deformations. Deformed toads and frogs rarely survive long in the wild because of their susceptibility to predators like wading birds, which ingest them and later defecate into wetlands, releasing trematodes to infect other snails and completing the life cycle.

As few as 12 trematode larvae, known as cercariae, can kill or deform a single tadpole by forming cysts in its developing limbs, causing missing limbs, extra limbs and other severe malformations, Johnson said. A 2007 CU-Boulder study led by Johnson showed high levels of nutrients like nitrogen and phosphorus used in farming and ranching activities fuel trematode infections in North American amphibians by hiking the abundance and reproduction of the snail species that hosts trematodes.

Deformed frogs first gained international attention in the mid-1990s when a group of Minnesota schoolchildren discovered a pond where more than half of the leopard frogs had missing or extra limbs, he said. Since then, reports of deformed amphibians have become widespread in the United States, leading to speculation they were being caused by factors like pesticides, increased ultraviolet radiation or parasitic infection.

A recent study of more than 6,000 species of amphibians worldwide concluded that 32 percent were threatened and 43 percent were declining in population because of causes like habitat loss, pollution and emerging diseases.


The new study was funded primarily by the National Science Foundation.

Johnson was recently awarded a five-year, $875,000 David and Lucille Packard Fellowship to support his studies of emerging diseases in changing environments. For more information on Johnson’s research visit the Web here.

Pieter Johnson
University of Colorado at Boulder

New Direction For Development Of Psychotropic Drugs Suggested By Researchers

Leading brain and behavior researchers have called for a new direction to develop innovative psychotropic drugs to treat mental illness at the annual meeting of the American College of Neuropsychopharmacology. The panel of academic, industry and government representatives concluded that several factors have impeded the development of novel treatments for mental illness including: incomplete understanding of the impact of mental illness on the brain; continued skepticism of results from animal models for certain disorders; an outdated paradigm of treatment and the industry preference toward so-called “me-too” drugs.

“We need to do better when treating major mental illness, and right now that means we need groundbreaking new research that will result in new medications that are both more effective and have fewer side effects than drugs currently on the market,” noted Dennis Charney, MD, Dean of Academic and Scientific Affairs for Mount Sinai School of Medicine and Professor, Department of Psychiatry, Neuroscience and Pharmacology & Biochemistry.

The findings come in the wake of considerable debate in the academic and clinical communities as to whether newer drugs (particularly anti-psychotic medications) represent significant improvement over treatments that have been available for nearly half a century, as well as a greater recognition of the disease burden resulting from mental illness. Currently, mental disorders cause more disability than any class of illness in Americans 15 – 44 years, and the suicide rate in that age group is higher than annual mortality from homicide, AIDS and most cancers.

“There is near universal agreement that we’ve had only modest progress in developing drugs for schizophrenia and affective disorders in the past several decades. This panel discussion is part of a broader effort to determine why new drug development has been such a historically inefficient process,” explained Dr. Bryan Roth, Professor of Pharmacology at UNC Chapel Hill and Director of the NIMH Psychoactive Drug Screening Program at the National Institutes of Health. Affective disorders include bipolar, depressive and anxiety disorders.

The group, reviewing over a decade of psychotropic drug-development research from industry, government and academia, identified several factors that have contributed to the slow progress in developing new treatments.

Review of past clinical research highlighted that a “single disease model” of schizophrenia and mood disorders has prevailed. Increasingly, clinicians and researchers have begun to understand that a combination of several key symptom modalities may need to be addressed separately. “Some early studies are suggesting that we are looking at the wrong targets for mood disorders. Until we have treatments that make it into the clinical setting, we won’t fully know the usefulness of single target treatments,” added Husseini Manji, MD, FRCPC, Chief, NIMH Laboratory of Molecular Pathophysiology.

The most promising new direction for CNS (central nervous system) drug development appears to be focusing on treatments that act on more than one molecular target. “We typically have used the ‘silver bullet’ approach (currently the prevailing practice in industry) designed to hit one molecular target at a time. This analysis shows that drugs with more complex action (or utilizing more than one drug at a time) have a greater potential for positive treatment outcomes,” concluded Roth.

This shift may be most noticeable when addressing schizophrenia, a disease in which psychosis has long prevailed as the dominant symptom. Now, notes Carpenter, additional attention is being paid to other important symptoms that may have a greater impact on long-term functionality, including cognitive impairment and depression in people with schizophrenia.

Because of limitations in animal models of complex psychiatric disorders like schizophrenia, investigators were often not discouraged by negative results in key tests, particularly if other data seemed encouraging. Roth was surprised by his own findings: “When reviewing this data, we found that animal models were actually quite good at predicting results in human subjects.”

However, the overall effectiveness of animal models for mood disorders is still unknown. “Some of these novel molecular targets may be much better than existing ones, but we won’t know anything for sure until we have large scale clinical trials,” said Manji.

Evaluating decades of research that failed to yield its intended results has provided investigators with insights on how to do better, the researchers believe. Several panel participants expressed the belief that past theories and practices that have been standard practice in new drug development for several decades must change, and new paradigms of mental illness should be embraced to guide future medication development and treatment practice.

“One of the primary reasons we have encountered such difficulty in developing treatments for schizophrenia and mood disorders is a lack of understanding of the diseases themselves,” explained William Carpenter, MD, Director of the Maryland Psychiatric Research Center and Professor of Psychiatry at the University of Maryland School of Medicine. “We now have a better understanding of the complex nature of these illnesses, which affect multiple targets in the brain.”

“What is different now is that we have the power of molecular biology combined with improved animal models to identify targets for the development of novel treatments for mood disorders and schizophrenia,” noted Charney.


ACNP held its Annual Meeting December 3 – 7, 2006, in Hollywood, FL.

ACNP, founded in 1961, is a professional organization of more than 700 leading scientists, including three Nobel Laureates. The mission of ACNP is to further research and education in neuropsychopharmacology and related fields in the following ways: promoting the interaction of a broad range of scientific disciplines of brain and behavior in order to advance the understanding of prevention and treatment of disease of the nervous system including psychiatric, neurological, behavioral and addictive disorders; encouraging scientists to enter research careers in fields related to these disorders and their treatment; and ensuring the dissemination of relevant scientific advances. A non-profit organization, ACNP receives revenues from a variety of sources including membership dues, publication sales, registration fees, and pharmaceutical industry grants.

Contact: Sharon Reis


3 Legendary Physician-Scientists To Be Honoured By LA BioMed

The Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed) will honor three of its legendary physician-scientists for their internationally recognized contributions to medicine at its fifth annual Legends dinner celebration May 1 at Trump National Golf Club.

Dominic DeCristofaro, M.D., Grant B. Hieshima, M.D., and Jerrold Turner, M.D., are the three Legends to be honored at the dinner event. All three are alumni of LA BioMed, one of the nation’s largest independent not-for-profit biomedical research institutes.

“After 56 years of discovery, cures, commitment and lives saved, LA BioMed will take one night to honor those who helped the institute achieve so much over the last half century,” said LA BioMed President and CEO Kenneth P. Trevett J.D. “Drs. DeCristofaro, Hieshima and Turner are outstanding examples of the dedicated physician-scientists at LA BioMed, and each of them has contributed greatly to the advancement of science and medicine, as well as to the betterment of this campus.”

Legends Event Chairman Joel Kopple, M.D. is planning a memorable evening that will feature Olympic Champion Rafer Johnson as the master of ceremonies. Johnson is a world record-setting decathlete who won the silver medal at the 1956 Olympics and the gold medal at the 1960 Olympics. After retiring from the sport, he became a sportscaster, an actor, a community leader and a philanthropist.

The winner of the Liu Young Investigator Award, sponsored by Institute Board member Patty Liu, also will be announced during the dinner. Kevin Bruhn, Ph.D., Agnes Chen, M.D., and Stanislav L. Karsten, Ph.D., are the nominees for the $10,000 award that seeks to nurture excellence and provide support for an outstanding young scientist conducting research on LA BioMed’s campus.

Details on the 2008 Legends

Dr. DeCristofaro

Dr. DeCristofaro is a renowned cardiologist who chose that specialty after watching his older brother, Nick, struggle with rheumatic heart disease. Dr. DeCristofaro earned a bachelor’s degree in chemistry at the University of Illinois at Urbana-Champaign and his medical degree from Chicago Medical School. After completing his internship in internal medicine at Los Angeles County-USC Medical Center, Dr. DeCristofaro came to Harbor-UCLA Medical Center where he pursued research as a resident, earning fellowships from the National Institutes of Health and the American Heart Association (AHA).

Upon completion of his research fellowships, he entered private practice in Long Beach and became director of the cardiac catheterization lab at St. Mary Medical Center. He also helped establish a cardiology training program with support from AHA, the St. Mary Medical Center Foundation and the medical group to which he belongs, Cardiovascular Associates.

During the almost 40 years since then, Dr. DeCristofaro’s name is synonymous with heart care at St. Mary’s. He has served in numerous capacities, including chief of staff, chair of the Department of Medicine and as a member of the Board of Directors. He has co-authored numerous publications and invited presentations on diagnosis and treatment of heart disease. He also continues to practice cardiology part-time at St. Mary’s.

Dr. DeCristofaro served as president and chairman of the LA BioMed Board of Directors when the institute was known as the Research and Education Institute. He also served as president of the California AHA affiliate. He chaired the annual meeting for the California Heart Association, and he served the AHA national organization as the chairman of the Southwest Regional Research Review and Advisory Committee. He and his wife have been active fundraisers and volunteers for AHA, and the organization recognized his service in 1998 by awarding Dr. DeCristofaro its prestigious Heart of Gold Award.

Dr. DeCristofaro is now a UCLA clinical professor of medicine, honorary status. He and his wife, Marge, live in Rolling Hills, their home for the past 30 years.

Dr. Hieshima

Dr. Hieshima was born in 1942 at the Santa Anita Racetrack Assembly Center, a gathering spot for Japanese-American internees before they were shipped off to relocation camps during World War II. He attended UCLA and received his medical education at Tulane University, where he graduated in 1969 with honors.

His postgraduate training at Harbor-UCLA Medical Center began in surgery and then changed to radiology. In 1973, he completed a residency in diagnostic radiology and subsequently obtained subspecialty training in neuroradiology and nuclear medicine.

Appointed assistant professor of radiology at Harbor-UCLA Medical Center in 1974, he worked to evolve new techniques in the management of vascular trauma. After moving to the UCLA Center for Health Sciences in 1983, he became a professor of radiology and helped to pioneer new therapies for aneurysms and vasospasm.

The University of California, San Francisco (UCSF) recruited him in 1986 to be a professor of radiology and neurological surgery. There, he directed the neurovascular section devoted to multi-disciplinary evaluation and treatment of arteriovenous fistulas, malformations, aneurysms and stroke. In 1996, Dr. Hieshima was named director of the Neuroscience Institute at St. Joseph’s Medical Center in Orange County, California.

Dr. Hieshima is recognized nationally and internationally as one of the premier figures in the field of interventional neuroradiology, a minimally invasive approach using imaging techniques to detect and treat vascular diseases of the central nervous system. Dr. Hieshima has trained more than 100 fellows in diagnostic and interventional neuroradiology. He has more than 150 scientific publications and 60 book chapters. He also has lectured at more than 400 medical conferences.

He has been involved in more than 20 grants and research awards to study new techniques for the treatment of intracranial aneurysms, arteriovenous malformations, cerebrovascular thrombolysis and angioplasty.

In 1997, he was honored by the Joint Section of Cerebrovascular Surgery with a Lifetime Achievement Award. In 1999, he received the Luessenhop Award as well as the exclusive Gold Medal from the American Society of Neuroradiology.

He is retired and lives with his wife, Donna, in Huntington Beach.

Dr. Turner

Dr. Turner first became interested in tropical diseases when he was in junior high school. As a medical student at UCLA, he worked with the faculty of the Division of Parasitology in the Department of Infectious Diseases. His summer parasitology research project in Guatemala was interrupted when he acquired paralytic poliomyelitis, an acute onset of paralysis.

After weeks in a Guatemalan hospital, he was transferred to the student health section of the UCLA Medical Center for rehabilitation. A year later, he joined the Class of 1958 for his senior year of medical school.

After an internal medicine internship at the UCLA Medical Center, Turner rejoined the Division of Parasitology as a faculty member and began his academic teaching career. He studied tropical medicine in Puerto Rico, Haiti, Mexico, South Africa, Kenya and Egypt. He also obtained a diploma in tropical medicine and hygiene from the London School of Hygiene and Tropical Medicine.

Dr. Turner returned to clinical internal medicine by joining the residency program at Harbor-UCLA Medical Center in 1964. He taught parasitology at UCLA until retirement, earning four “Golden Apple Teaching Awards” and an “Exceptional Quality Teaching Award” from the medical students. He also taught parasitology at the University of California, Irvine College of Medicine.

Dr. Turner served in several administrative roles at Harbor-UCLA Medical Center. He’s also received numerous honors and awards, including the Silver Knight of Management Award, Harbor-UCLA Medical Center, from the National Management Association in 1982; the Distinguished Service Award from the UCLA Medical Alumni Association in 1988, and the Distinguished Service and Leadership Award from the Harbor-UCLA Medical Center’s Department of Medicine in 1991 and 1997.

He was a co-director of the Parasitic Disease Diagnostic Laboratory at LA BioMed, when it was still known as the Research and Education Institute. For four years, this laboratory examined all specimens collected by the Los Angeles County Health Department for parasitic disease diagnosis. In 1984, Dr. Turner opened Turner Parasitology, a private laboratory for diagnostic parasitology.

Dr. Turner also served as the chief of the Section of Parasitic Diseases in the Division of Infectious Disease, Department of Medicine, Harbor-UCLA Medical Center from 1973 until his retirement. Dr. Turner and his wife, Ellen, live across the street from UCLA in Westwood.


The event begins with a reception at 6:30 p.m., followed by a dinner and ceremony at 7:30 p.m.

About LA BioMed

Founded 56 years ago, LA BioMed conducts biomedical research, trains young scientists and provides community services, including childhood immunization, nutrition assistance and anti-gang violence programs. The institute’s researchers conduct studies in such areas as cardio-vascular disease, emerging infections, cancer, diabetes, kidney disease, dermatology, reproductive health, vaccine development, respiratory disorders, inherited illnesses and neonatology.

LA BioMed is an independent research institute that is academically affiliated with the David Geffen School of Medicine at the University of California, Los Angeles. The institute is located on the campus of Harbor-UCLA Medical Center near Torrance. Please visit our website at www.LABioMed

Source: Laura Mecoy

Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed)

Refractive Errors Significantly Affect Adults In United States

Approximately half of all adults in the United States aged 20 and older
have refraction errors in their eyes that result in less than 20/20
vision, according to an article released on August 11, 2008 in the Archives
of Ophthalmology, one of the JAMA/Archives journals.

When the eye does not properly focus light on the retina, it results in
nearsightedness, farsightedness, or astigmatism. These refractive
errors account for nearly 80% of vision impairment in residents older
than 12 in the United States. Providing eye care to this population,
including glasses and contact lenses, costs and estimated $3.8 to $7.2
billion US dollars per year.

To investigate the prevalence of refractive error in the U.S. public,
Susan Vitale, Ph.D., M.H.S., and colleagues at the National Eye
Institute, part of the National Institutes of Health in Bethesda,
analyzed data taken as part of the National Health and Nutrition
Examination Survey (NHANES) conducted by the Centers for Disease
Control and Prevention (CDC). In this survey, a nationally
representative sample was selected and noted for demographic
characteristics, and a vision test was administered.

A total 12,010 participants over age 20 performed the survey between
1999 and 2004 with complete data. Approximately half of these adults
had one type of refractive error, including 3.6% who were farsighted,
33.1% who were nearsighted, and 36.2% who had astigmatism. Refractive
error of any kind increased with age, from the youngest age group from
20-39 years (46.3%) to those 40 through 59 (50.6%) to the oldest group
aged 60 or older (62.7%).

Comparing age and sex yielded additional results. Nearsightedness was
less common in those older than 60, but this age group was more likely
to have farsightedness and astigmatism than others. Additionally, in
this older age group, men were more likely to have refractive error
than women (66.8% versus 59.2%). Among 20 to 39 year olds, women were
more likely to be nearsighted than men (39.9% versus 32.6%).

When analyzing ethnicity, Mexican-Americans were less likely to have
refractive errors than non-Hispanic whites or non-Hispanic blacks.

The authors conclude that refractive error is a highly prevalent
condition among the American public. “Refractive error is, therefore,
the most common condition affecting the ocular health of the U.S.
population, involving young adults, middle-aged persons and older
adults of all ethnicities,” they say. “Accurate, current estimates of
the prevalence of refractive error are essential for projecting vision
care needs and planning for provision of vision care services to the
many people affected.”

Prevalence of Refractive Error in the United States, 1999-2004
Susan Vitale, PhD, MHS; Leon Ellwein, PhD; Mary Frances Cotch, PhD;
Frederick L. Ferris III, MD; Robert Sperduto, MD
Arch Ophthalmol. 2008;126(8):1111-1119.
Here For Abstract

Anna Sophia McKenney

Lancet Article Highlights Hope In The Tuberculosis Drug Development Pipeline

According to a paper published today in the Lancet, there is unprecedented progress in the development of the global tuberculosis (TB) drug pipeline with 10 drug candidates currently in clinical development. The paper was a team of renowned international experts led by Zhenkun Ma, Ph.D., Chief Scientific Officer for the TB Alliance, a not-for-profit organization accelerating the discovery and development of new TB drugs. The article, published as part of the Lancet’s Series on Tuberculosis, also highlights the significant funding and other challenges associated with the pursuit of life-saving treatment for the nearly 2 million people who die each year from TB.

Of the 10 compounds in clinical development, three TB drugs are being co-developed by the TB Alliance and its partners. These clinical candidates are basic building blocks for a new generation of novel TB drug regimens that have the potential to greatly reduce the global TB burden by shortening the duration of the current treatment regimen, which currently takes six to 30 months. Results of a recent modeling study in a WHO region suggest that new and improved TB drugs, vaccines, and diagnostics could reduce the global incidence of TB by 71% by 2050. In 2008, there were more than 9 million new cases of TB.

“A decade ago, there were essentially no drugs being developed to treat TB, so there has been tremendous progress in this area,” said Dr. Ma, lead author of the paper “Global Tuberculosis Drug Development Pipeline: The Need and the Reality.” “Still, the global TB drug pipeline must continue to be strengthened to ensure we can deliver the tools to help stop the devastation TB wreaks on patients, families, and countries around the world.”

Dr. Ma notes that access to increased and sustainable funding to bring the next generation of TB treatments to patients is a key challenge to unleashing the hope in the drug pipeline. According to MГ©decins Sans FrontiГЁres, currently, there is a 75 percent funding shortfall to support the necessary TB drug research and development.

“While we’re headed in the right direction, this draws much needed attention to the challenges that lie ahead,” said Dr. Stefan Kaufmann, Director, Department of Immunology at the Max Planck Institute for Infection Biology. “Only together and with a global commitment can we support the development of new TB regimens and dramatically reduce the mortality of TB and its economic impacts.”

Multi-drug combinations are needed to treat drug-sensitive and drug-resistant disease. Until recently, only one new TB drug in a regimen has been tested at a time. However, with the availability of drug candidates, the Critical Path to TB Regimens (CPTR) initiative was recently launched, which is intended to enable several new TB drugs to be tested simultaneously, in combination. This is expected to lead to a dramatic reduction in the time that it takes to develop an innovative TB drug regimen.

TB kills nearly two million people every year, and is second only to HIV/AIDS in mortality among infectious diseases. However, 94% of TB cases and 98% of deaths occur in the developing world, and therefore there is very little market incentive for the private sector to invest in TB drug development.

Critical Path to TB Drug Regimens Initiative

With support from public and private partners, promising compounds will be tested through the Critical Path to TB Drug Regimens (CPTR), an initiative created by the TB Alliance, the Critical Path Institute, and the Bill & Melinda Gates Foundation. CPTR is a new collaboration that aims to speed the development of truly novel combination treatments for tuberculosis by testing individual TB drug candidates from different companies together-and replace an almost 50-year-old drug regimen.

Global Alliance for TB Drug Development (TB Alliance)