December 7th, 2009
The Reproductive Medicine Network (RMN) has today announced plans to launch a series of clinical trials and participants are needed.
The trials will focus on four areas: Female Infertility, Male Infertility, IVF (in vitro fertilization) and multiple gestations as a result of ovarian stimulation.
The RMN study for female infertility will address women with PCOS. It’s goal is to determine the efficacy of various medications designed to aid in conception and live birth outcomes.
The trials will include 750 female participants, 100 of which will visit the University of Michigan Hospital in Ann Arbor. (Interested Michigan-based women may contact Linda Vandell, 734-998-4973 email: vandelll@umich.edu.)
For further information on the study addressing infertile women, visit:
For additional information on the trials in general:
An interesting piece of information, the Reproductive Medicine Network was founded in 1989 and funded by the Eunice Kennedy Shriver Institute of Child Health and Human Development.
October 19th, 2009
If you wonder where the Federal Government’s $787 billion stimulus package is being spent, you’ll be pleased to hear that a $ 7.5 million grant has been designated for infertility research at the Yale School of Public Health. It was awarded through the National Institutes of Health (NIH).
Professor Heping Zhang’s Data Coordination Center team, which is part of the National Institute of Child Health and Human Development’s Reproductive Medicine Network, will focus on the drug Letrozole with a view to producing an increase in single births, which result in safer pregnancies.
The majority of fertility treatments currently available result in multiple pregnancies which boost the risk of premature births and birth defects. Nine-hundred infertile women will be recruited at seven sites throughout the U.S. for the two-year trial which will be followed by data analysis by the research team.
Two common fertility drugs, Clomid and gonadotrophins will also be used in the study.
To read more:
http://www.yaledailynews.com/news/scitech-news/2009/10/14/nih-awards-yale/
October 31st, 2008
Mark O. Goodarzi, MD, PhD, Michelle R. Jones, BSc, Yii-Der I. Chen, PhD and Ricardo Azziz, MD, MBA, MPH
Division of Endocrinology, Diabetes and Metabolism, Department of Medicine (M.O.G., M.R.J.), Department of Obstetrics and Gynecology (M.O.G., Y-D.I.C., R.A.), and Medical Genetics Institute (M.O.G., Y-D.I.C.), Cedars-Sinai Medical Center, Los Angeles, California 90048; and Departments of Medicine (M.O.G., Y-D.I.C., R.A.) and Obstetrics and Gynecology (R.A.), the David Geffen School of Medicine at UCLA, Los Angeles, California 90095
Diabetes Care
ABSTRACT
Objective: Insulin resistance has been reported in up to 70% of women with polycystic ovary syndrome (PCOS). Physiologic and genetic data currently implicate post-insulin receptor signaling defects in substrates such as GSK3β . The AKT2 gene was chosen as a candidate for PCOS because its product affects glucose metabolism and mitogenic signaling, interacts with GSK3β, and mediates cell survival in the ovary.
Research Design and Methods: Subjects were recruited from the reproductive endocrinology clinic at the University of Alabama at Birmingham; controls were recruited from the surrounding community. 287 White women with PCOS and 187 White controls were genotyped for 4 SNPs in AKT2. Genotyping took place at Cedars-Sinai Medical Center in Los Angeles. Single nucleotide polymorphisms (SNPs) and haplotypes were tested for association with PCOS risk and phenotypic markers of PCOS.
Results: Minor allele carriers of SNPs rs3730051 and rs8100018 had increased odds of PCOS (OR=2.2, p=0.004 and OR=2.4, p=0.001, respectively). The haplotype T-G-C-T was significantly associated with PCOS (OR=2.0, p=0.01). Carriers of the risk haplotypes for both AKT2 and GSK3B had a further increased odds of PCOS (OR=3.1, p=0.005).
Conclusions: These data suggest that polymorphisms in two components of the insulin signaling pathway, AKT2 and GSK3B, are associated with PCOS. Presence of multiple lesions in a single pathway may confer increased risk.
http://care.diabetesjournals.org/cgi/content/short/dc08-0532v1?rss=1
October 30th, 2008
Sathyapalan T, Kilpatrick ES, Coady AM, Atkin SL
Department of Diabetes and Endocrinology, University of Hull, Hull, UK; Department of Clinical Biochemistry, Hull Royal Infirmary, Hull, UK; Department of Obstetric Ultrasound, Hull & East Yorkshire Women’s & Children’s Hospital, Hull, UK.
Source J Clin Endocrinol Metab 2008 Oct 21.
Abstract Context: Polycystic ovary syndrome (PCOS) is associated with increased risk of cardiovascular morbidity whereas statins are proven to reduce cardiovascular mortality and morbidity through lipid lowering and perhaps through their pleotrophic effects. Statins can also reduce testosterone in vitro by inhibiting ovarian theca-interstitial cell proliferation, steroidogenesis and reducing inflammation in vivo.
Objective: To assess the effect of atorvastatin on inflammatory markers, insulin resistance and biochemical hyperandrogenemia in patients with PCOS.
Design: Randomised, double blind placebo controlled study.
Setting: Tertiary care setting in United Kingdom.
Patients: Forty medication naïve patients with PCOS and biochemical hyperandrogenaemia.
Methods: Patients were randomised to either atorvastatin 20mg daily or placebo.
Main outcome measures: The primary end point of the study was a change in the inflammatory marker hsCRP. The secondary end points were a change in insulin resistance and total testosterone.
Results: After 12 weeks of atorvastatin there was a significant reduction (mean+/-SEM) in total cholesterol (4.6+/-0.2 vs. 3.4+/-0.2 mmol/L,p<0.01), LDL cholesterol (2.9+/-0.2vs.1.8+/-0.2 mmol/L,p<0.01), triglycerides (1.34+/-0.08vs.1.08+/-0.13mmol/L,p<0.01), hsCRP (4.9+/-1.4vs.3.4+/-1.1mg/Lp=0.04), free androgen index (13.4+/-0.6vs.8.7+/-0.4 p<0.01), testosterone[4.1+/-0.2vs.2.9+/-0.1 nmol/Lp<0.01) and insulin resistance as measured by HOMA-IR(3.3+/-0.4vs.2.7+/-0.4). There was a significant increase in SHBG (31.1+/-1.0vs.35.3+/-1.2 nmol/L,p<0.01). There was a positive correlation between the reduction in HOMA-IR in the atorvastatin group with the reduction in triglycerides and the reduction of FAI. There was a significant deterioration of HOMA-IR in the placebo group (3.0+/-0.4vs.3.8+/-0.5).
Conclusions: This study suggests that atorvastatin is effective in reducing inflammation, biochemical hyperandrogenemia and metabolic parameters in patients with polycystic ovary syndrome after a 12 week period.
PubMed ID 18940877
