Renal ischemia-reperfusion injury (RIRI) as a pathological process induces remote organ injury such as lung complications and it is regulated in a hormone-dependent manner. This study investigates the effect of estrogen on RIR-induced pulmonary injury in ovariectomized (OV) rats. A total of 60 female Wistar rats were divided into six groups: (i) intact sham, (ii) OV sham, (iii) OV sham + estradiol valerate (E), (iv) intact ischemia, (v) OV ischemia, and (vi) OV ischemia + E. Bilateral ischemia was performed for 45 min in all groups except sham. Before the ischemia, OV groups received an intramuscular (i.m.) injection of E. After reperfusion, blood samples were collected for serum analysis and kidney and lung tissue were separated for pathological experiment and malondialdehyde (MDA) and nitrite measurement. The left lung was weighed to measure pulmonary edema. Estrogen deficiency caused a greater increase in blood urea nitrogen and creatinine levels during IRI. Ischemia reduced nitrite of serum and lung tissue. The increased level of MDA during ischemia, returned to normal levels via estrogen injection. The severity of renal and lung damage in ischemic groups increased significantly, and estrogen improved this injury. Estrogen as an antioxidant agent can reduce oxidative stress and may improve renal function and ameliorating lung damage caused by RIR.

The results of the WHI, which reported a doubling of the risk of Alzheimer\'s disease (AD) and a decline in cognitive function in women who were given menopause hormone therapy (MHT), have raised concerns on the deleterious impact of MHT on the central nervous system. Such as for the cardiovascular system, the very late age of initiation of treatment and the nature of the molecules have led to conclusions that cannot be extended to women in their fifties, at the onset of their menopause which is the usual age of MHT initiation. The molecules, which are used in France, 17-beta estradiol and natural progesterone (or its isomer, dydrogesterone) are very different from the equine conjugated estrogens and medroxyprogesterone acetate used in the WHI. It can now be stated that if MHT is started within the window of opportunity (i.e. before the age of 60 or within the first 10years after the beginning of menopause) no deleterious effect on cognition is observed. Moreover, cognition remains relatively stable at the beginning of menopause since the cognitive reserve as well as the different compensation circuits allow compensation for estrogen deficiency. This does not in any way prejudge a possible positive effect of MHT on AD, which is very difficult to demonstrate, as the age of onset of this dementia is very late, 20 or 30years after the initiation of treatment.

During their lives, women go through three different phases during which sex hormones play a fundamental role in contributing to specific cardiovascular and coronary risks. To evaluate this risk, we must take into account these various phases with their associated cardiovascular risk factors, and this during three key steps: contraception, pregnancy and menopause. Arterial risk linked to estrogen combined with progestin contraception, depends on the dosage of estrogen. The main cardiovascular risk factor responsible for increasing the risk of myocardial infarction is tobacco, especially after 35 years of age, contraindicating estrogen combined with progestin contraception at the benefit of progestin. Spontaneous dissections and coronary emboli are the most common coronary lesions linked with oestroprogestative contraception. Acute myocardial infarction during pregnancy occurs mostly in the peripartum or postpartum period; and is often caused by spontaneous coronary dissection lesions. Fertility treatment is not associated with an increased risk of developing cardiovascular disease later in life. Hormone therapy during menopause does not increase coronary risk in the first 10 years after menopause and may even have a protective effect, by sustaining arterial integrity. The transdermal route is to be preferred for its metabolic effect. Hormonal treatment during menopause is nonetheless contraindicated in the case of proven coronary disease and uncontrolled cardiovascular risk factors.

OBJECTIVE: Exposure to diethylstilbestrol (DES) in utero is associated with adverse health effects, including genital anomalies in women and men, and cancers in women. Animal studies showed birth defects and tumors in the offspring of DES exposed mice, revealing transgenerational transmission of DES effects. In humans, birth defects, such as hypospadias were observed in children of prenatally exposed women. The aim of this research was to further assess the health effects in children of prenatally exposed women.
METHODS: In a retrospective cohort study, the reports of women exposed to DES in utero on their 4409 children were compared with those of unexposed women on their 6203 children. Comparisons used odd ratios (OR) between children of exposed and unexposed women and standardized incidence rate (SIR) with the general population. These cohorts were recruited on a voluntary basis to answer questionnaires.
RESULTS: There was a global increase of defects in children born to exposed women when compared with those born to unexposed (OR 2.29, 95% CI: 1.80-2.79, P<0.001) and with the general population (SIR 2.39, 95% CI: 2.11-2.68). Increased defects were observed in male genital tract, esophagus, lip or palate, musculoskeletal and circulatory systems. For female genital tract anomalies, there was no significant increase. However, this cohort being relatively young, further follow-up is needed. An increase of cerebral palsy was revealed. The incidence of cancers was not increased, in particular for breast, uterus and ovary.
CONCLUSIONS: Our results confirmed a transgenerational transmission of defects in male genital tract. With caution due to possible bias associated with this method, our data suggest an increase of defects for esophagus, lip or palate, musculoskeletal and circulatory system in children of exposed women.

The mechanisms involved in human pregnancy maintenance and parturition are highly complex and involve mother, fetus and placenta. The \"final common pathway\" to delivery is composed by inflammatory and endocrine interactive paths that tip the balance in favor of coordinated uterine contractility and cervical dilation. These mechanisms involve a shift from progesterone to estrogen dominance, CRH action, increased sensitivity to oxytocin, gap junction formation, and increased prostaglandins activity. Complementary changes in the cervix involve a decrease in progesterone dominance and the actions of prostaglandins and relaxin, via connective tissue alterations, leading to cervical softening and dilation. Neuronal, hormonal, inflammatory and immune pathways participate in initiation of labor and the utero-placental unit plays a major role in the synthesis and release of parturition mediators.

In addition to protein hormones, steroids measurement constitutes the basis of modern endocrinology. Immunoassays have shown their limits in this field. In contrast, mass spectrometry shows an excellent sensitivity and specificity that make it the method of choice for steroids assays. The recent introduction of UHPLC-MS is a major advance which reinforces this position. In fact, mass spectrometry provides a lot of advantages such as determination of certain steroids in saliva, diagnosis of enzyme deficiencies, or measurement of molecules previously inaccessible like aldosterone. However, standardization is still needed to ensure good comparability of results between laboratories. In the future, mass spectrometry should not replace the immunoassays but rather complement it.

This review aims to discuss how endogenous and exogenous testosterone exposures in men and estrogens/progesterone exposures in women interact with sleep regulation. In young men, testosterone secretion peaks during sleep and is linked to sleep architecture. Animal and human studies support the notion that sleep loss suppresses testosterone secretion. Testosterone levels decline slowly throughout the aging process, but relatively few studies investigate its impact on age-related sleep modifications. Results suggest that poorer sleep quality is associated with lower testosterone concentrations and that sleep loss may have a more prominent effect on testosterone levels in older individuals. In women, sex steroid levels are characterized by a marked monthly cycle and reproductive milestones such as pregnancy and menopause. Animal models indicate that estrogens and progesterone influence sleep. Most studies do not show any clear effects of the menstrual cycle on sleep, but sample sizes are too low, and research designs often inhibit definitive conclusions. The effects of hormonal contraceptives on sleep are currently unknown. Pregnancy and the postpartum period are associated with increased sleep disturbances, but their relation to the hormonal milieu still needs to be determined. Finally, studies suggest that menopausal transition and the hormonal changes associated with it are linked to lower subjective sleep quality, but results concerning objective sleep measures are less conclusive. More research is necessary to unravel the effects of vasomotor symptoms on sleep. Hormone therapy seems to induce positive effects on sleep, but key concerns are still unresolved, including the long-term effects and efficacy of different hormonal regimens.