Male infertility is a multifactorial disorder that affects approximately 10% of couples at childbearing age, with substantial clinical and social impact. The main regulating enzymes in folate and homocysteine metabolism are methylenetetrahydrofolate reductase (MTHFR) and cystathionine β-synthase (CBS). In our previous study, we showed that a mutation C677T in the gene, MTHFR is a risk factor for idiopathic male infertility in the Indian population. To assess that a common polymorphism in the cystathionine β-synthase (CBS) gene (844ins68) is acting as susceptibility factor for male infertility or not, we investigated this variant in 120 idiopathic male infertile patients and 200 fertile male controls. No significant association was observed (OR = 0.8348, 95% CI: 0.1578 to 4.4164, ² = 0.040, P > .05); therefore we conclude that this common 844ins68 variant is a neutral insertion variant for idiopathic male infertility in the Indian population.

Several in vitro models that attempt to replicate the intraperitoneal environment have been developed to study the pathogenesis of endometriosis. The chicken chorioallantotic membrane has been used, but it has not been well characterized and may introduce some species specific variables. In vitro models using human tissues include amniotic membrane, human peritoneal explants, and cell culture monolayers. These models have been used to qualitatively, quantitatively, and temporally assess attachment of endometrial cells to peritoneal mesothelial and subsequent transmesothelial invasion. These models have also been used to assess the role of cytokines in the development of the early endometriotic lesion. Two- and three dimensional invasion chamber models have been utilized to assess endometrial cell interactions with peritoneal mesothelial cells and the extracellular matrix. Invasion models are also useful to evaluate novel therapeutic approaches. This review will focus on the above models to assist reproductive scientists interested in the pathogenesis of endometriosis.

Antenatal glucocorticoids are used to mature lung function in fetuses at risk for preterm delivery, but they also suppress cortisol synthesis in both pregnant women and their fetuses. We recently discovered in pregnant rabbits that even though exogenous betamethasone is not a mineralocorticoid, it also suppresses production of aldosterone. Lower aldosterone levels were linked to reduced P450 side chain cleavage (P450scc) messenger RNA levels in the rabbit maternal and fetal adrenal cortex. To establish whether this occurs in humans, we assayed aldosterone levels in women and newborns treated with antenatal betamethasone for preterm labor. In mothers treated with betamethasone, maternal cortisol depression after 48 hours was accompanied by aldosterone depression. Both pregnant women and their newborns treated with betamethasone showed depressed aldosterone levels in a 1- to 3-day period after the first betamethasone dose. We conclude that suppression of aldosterone biosynthesis is a side effect of antenatal steroids that has been largely overlooked, but may be clinically relevant at a time when the newborn is learning to control plasma electrolytes and blood volume.