Methods
We linked a census of treatment with assisted reproductive technology in South Australia to a registry of births and terminations with a gestation period of at least 20 weeks or a birth weight of at least 400 g and registries of birth defects (including Selleck Bucladesine cerebral palsy and terminations for defects at any gestational period). We compared risks of birth defects (diagnosed before a child’s fifth birthday) among pregnancies in women who received treatment with assisted reproductive technology,
spontaneous pregnancies (i.e., without assisted conception) in women who had a previous birth with assisted conception, pregnancies in women with a record of infertility but no treatment with assisted reproductive technology, and pregnancies in women with no record of infertility.
Results
Of
the 308,974 births, 6163 resulted from assisted conception. The unadjusted odds ratio for any birth defect in pregnancies involving MX69 research buy assisted conception (513 defects, 8.3%) as compared with pregnancies not involving assisted conception (17,546 defects, 5.8%) was 1.47 (95% confidence interval [CI], 1.33 to 1.62); the multivariate-adjusted odds ratio was 1.28 (95% CI, 1.16 to 1.41). The corresponding odds ratios with in vitro fertilization (IVF) (165 birth defects, 7.2%) were 1.26 ( 95% CI, 1.07 to 1.48) and 1.07 (95% CI, 0.90 to 1.26), and the odds ratios with intracytoplasmic sperm injection (ICSI) (139 defects, 9.9%) were 1.77 (95% CI, 1.47 to 2.12) and 1.57 (95% CI, 1.30 to 1.90). A history
BX-795 solubility dmso of infertility, either with or without assisted conception, was also significantly associated with birth defects.
Conclusions
The increased risk of birth defects associated with IVF was no longer significant after adjustment for parental factors. The risk of birth defects associated with ICSI remained increased after multivariate adjustment, although the possibility of residual confounding cannot be excluded.”
“Myocardial ischemia followed by ischemia/reperfusion (I/R) induces irreversible damage to cardiac muscle. Medical treatment that effectively prevents I/R injury would alleviate the consequent development of cardiac remodeling and failure. Mechanisms that extend life span often make organisms resistant to stress, and an accumulation of such mechanisms may prevent aging and susceptibility to age-associated diseases. Sirtuins are a group of molecules involved in longevity and stress resistance. Stimulation of silent information regulator I (Sirt1), the mammalian ortholog of yeast Sir2 and a member of the sirtuin family, extends the life span of mice fed a high-fat diet and retards aging in the heart. Recent evidence suggests that stimulation of Sirt1 mimics ischemic preconditioning and protects the heart from I/R injury, suggesting an intriguing possibility of using longevity factors to treat cardiac disease. Here, we discuss the cardioprotective effects of Sirt1 and possible underlying mechanisms.