Objective Animal models have suggested that anogenital distance (AGD) at birth reflects androgen levels during in utero development and predicts adult AGD. A recent study showed an association between perineal length and androgen levels in men, suggesting that serum testosterone levels in adulthood will depend on factors involved during the fetal period. The aim of this study is to assess the relationship between AGD measures and reproductive hormone levels in women.Design Cross-sectional study conducted between February and November 2011.Setting University-affiliated fertility clinics.Population 100 young college students.Methods Physical and gynaecological examinations were conducted on university students. All participants provided a blood sample for determination of reproductive hormones and completed an epidemiological questionnaire on lifestyles and gynaecological history. We used multiple linear regression analysis to examine the associations between perineal length measurements [anus-fourchette (AGD AF ) and anus-clitoris (AGD AC )] and reproductive hormone levels.Main outcome measures Anogenital distance measurements and reproductive hormone levels.Results In the multiple linear regression analyses, AGD AF was positively associated with serum testosterone levels. Serum testosterone increased 0.06 ng/ml (95%CI 0.01, 0.10; P = 0.02) for each 1-cm increase in AGD AF . None of the measurements was associated with other reproductive hormones.Conclusions Anogenital distance may predict normal reproductive development in women, and may be a new tool of potential clinical interest to evaluate ovarian function. Our results suggest that serum testosterone levels in adulthood may depend on factors operating in the prenatal period.Keywords Androgens, anogenital distance, prenatal exposure, women.Please cite this paper as: Mira-Escolano MP, Mendiola J, M ınguez-Alarc on L, Melgarejo M, Cutillas-Tol ın A, Roca M, L opez-Esp ın JJ, Noguera-Velasco JA, Torres-Cantero AM. Longer anogenital distance is associated with higher testosterone levels in women: a cross-sectional study.

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Background In several observational and clinical studies, the association between serum cholesterol levels and cancer is still unsettled although serum total cholesterol has been associated with increased mortality from cancer. Moreover, the importance of abnormal levels of serum lipid components as the main features of dyslipidemia and the risk of individual cancers is unclear. The prevalence of dyslipidemia is increasing worldwide but, the precise aetiology of the link between risk of cancer and the behaviour of lipid profile, prior diagnosis, has yet to be determinated. Low levels of high-density lipoprotein cholesterol (HDL) at baseline of many of the studies analyzed has to be taken into account, and continued low levels of HDL without explanation should be considered by clinicians.

The nucleotide-binding domain and leucine-rich repeat-containing receptor with a pyrin domain 3 (NLRP3) inflammasome is a sensor for different types of infections and alterations of homeostatic parameters, including abnormally high levels of the extracellular nucleotide ATP or crystallization of different metabolites. All NLRP3 activators trigger a similar intracellular pathway, where a decrease in intracellular K+ concentration and permeabilization of plasma membrane are key steps. Cationic amphipathic antimicrobial peptides and peptide toxins permeabilize the plasma membrane. In fact, some of them have been described to activate the NLRP3 inflammasome. Among them, the bee venom antimicrobial toxin peptide melittin is known to elicit an inflammatory reaction via the NLRP3 inflammasome in response to bee venom. Our study found that melittin induces canonical NLRP3 inflammasome activation by plasma membrane permeabilization and a reduction in the intracellular K+ concentration. Following melittin treatment, the apoptosis-associated speck-like protein, an adaptor protein with a caspase recruitment domain (ASC), was necessary to activate caspase-1 and induce IL-1β release. However, cell death induced by melittin prevented the formation of large ASC aggregates, amplification of caspase-1 activation, IL-18 release and execution of pyroptosis. Therefore, melittin-induced activation of the NLRP3 inflammasome results in an attenuated inflammasome response that does not result in caspase-1 dependent cell death.

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