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At least 1,243 records · Page 69Linked to original sources
PubMed2002

Local cytokines in endometrial tissue: the role of interleukin-8 in the pathogenesis of endometriosis.

Endometriosis, defined by the presence of viable endometrial tissue outside the uterine cavity, is among the most common gynecologic disorders affecting women of reproductive age. Endometriosis is associated with an inflammatory peritoneal environment, where multiple cytokines and growth factors are found at elevated levels. Interleukin-8 (IL-8) is a cytokine that induces chemotaxis of neutrophils and is a potent angiogenic agent. In addition, IL-8 was recently found to stimulate proliferation of various cells. We have observed that IL-8 is elevated in the peritoneal fluid of women with endometriosis and the levels correlate with the severity of the disease. We hypothesized that IL-8 may play a role in the growth and maintenance of ectopic endometrial tissue not only by chemoattracting and stimulating leukocytes to secrete growth factors and cytokines, but also by directly affecting endometrial cell proliferation. We found that IL-8 mRNA and protein levels in the endometrium were significantly higher during early proliferative and late secretory phases than during the mid-cycle. IL-8 receptors A and B are also expressed in the endometrium mostly localized in the stroma. Interestingly, IL-8 receptor expression is higher in the eutopic endometrium of women with endometriosis compared to the endometrium of women without endometriosis. Endometrial cells in culture proliferate significantly when treated with IL-8, which is inhibited by anti-IL-8 neutralizing antibody. More convincingly, IL-8 antisense oligonucleotide treatment decreases IL-8 production by endometrial cells as well as cell proliferation when compared to non-sense oligonucleotide treatment. The addition of IL-8 reverses the inhibitory effect of IL-8 antisense oligonucleotides on cell proliferation. These findings suggest that IL-8 may act as an autocrine growth factor in the endometrium. We have also studied the effect of endometrial cell adhesion on IL-8 expression and observed that IL-8 stimulates the adhesion of endometrial cells to fibronectin. Treatment of the cells with anti-IL-8 neutralizing antibody inhibited partially the cell adhesion. Thus, IL-8 may also be relevant for stimulating the attachment of endometrial implants in the pathogenesis of endometriosis. In addition, adherence of endometrial cells induced further IL-8 expression by an integrin-dependent mechanism. In summary, IL-8 may act as an autocrine growth factor in the endometrium and may also play a role in the pathogenesis of endometriosis by promoting the vicious circle of endometrial cell attachment, cell growth, and further secretion of this cytokine.

Cell Adhesion↗
PubMed2004

Stress and dysmenorrhoea: a population based prospective study.

BACKGROUND: Dysmenorrhoea is the most common gynaecological disorder in women of reproductive age. Despite the association between stress and pregnancy outcomes, few studies have examined the possible link between stress and dysmenorrhoea. AIMS AND METHODS: Using a population based cohort of Chinese women, the independent effect of women's perceived stress in the preceding menstrual cycle on the incidence of dysmenorrhoea in the subsequent cycle was investigated prospectively. The analysis included 1160 prospectively observed menstrual cycles from 388 healthy, nulliparous, newly married women who intended to conceive. The perception of stress and the occurrence of dysmenorrhoea in each menstrual cycle were determined from daily diaries recorded by the women. RESULTS: After adjustment for important covariates, the risk of dysmenorrhoea was more than twice as great among women with high stress compared to those with low stress in the preceding cycle (OR = 2.4; 95% CI 1.4 to 4.3). The risk of dysmenorrhoea was greatest among women with both high stress and a history of dysmenorrhoea compared to women with low stress and no history of dysmenorrhoea (OR = 10.4, 95% CI 4.9 to 22.3). Stress in the follicular phase of the preceding cycles had a stronger association with dysmenorrhoea than stress in the luteal phase of the preceding cycles. CONCLUSION: This study shows a significant association between stress and the incidence of dysmenorrhoea, which is even stronger among women with a history of dysmenorrhoea.

Adult↗
PubMed1985

Adenohypophyseal response to hypophysiotropic hormones in male obese Zucker rats.

Description of the recessive, homozygote obese Zucker rat (fafa) includes disorders of growth and reproduction. The aim of this study was to compare responsiveness of adenohypophyseal cells, obtained from male fafa rats and from their lean siblings, to growth hormone-releasing factor (GRF) and to luteinizing hormone-releasing hormone (LHRH). Pituitary cells were cultured for 4 days and were then challenged with either GRF-29 (the NH2-terminal 29 amino acid GRF peptide that expresses full biological activity of its parent 44 amino acid molecule) or [D-Trp6]LHRH (LHRH-A, an LHRH agonist). Medium was assayed for growth hormone (GH), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) by radioimmunoassay. Dose-response curves were compared using the computer program ALLFIT. The median effective GRF-29 concentration (EC50) computed for hypophyseal cells cultured from lean animals (0.30 +/- 0.01 fM; means +/- SE of 4 experiments) was less (P less than 0.01) than that calculated for cells obtained from fafa rats (15.8 +/- 6.7 fM). In contrast, cells derived from lean littermates required a larger (EC50) concentration of LHRH-A than did gonadotrophs cultured from obese rats [58.2 +/- 1.2 vs. 10.7 +/- 1.2 pM (P less than 0.01) and 59.4 +/- 10.4 vs. 15.7 +/- 7.6 pM (P less than 0.05)] to secrete LH and FSH, respectively. Our data describe an attenuated pituitary response to GRF-29 and an enhanced response to LHRH-A in the fafa.

Animals↗
PubMedDate not supplied

Interactions of persistent environmental organohalogens with the thyroid hormone system: mechanisms and possible consequences for animal and human health.

Several classes of environmental contaminants have been claimed or suggested to possess endocrine-disrupting potency, which may result in reproductive problems and developmental disorders. In this paper the focus is on the multiple and interactive mechanisms of interference of persistent polyhalogenated aromatic hydrocarbons (PHAHs) and their metabolites with the thyroid hormone system. Evidence suggests that pure congeners or mixtures of PHAHs directly interfere with the thyroid gland; with thyroid hormone metabolizing enzymes, such as uridine-diphosphate-glucuronyl transferases (UGTs), iodothyronine deiodinases (IDs), and sulfotransferases (SULTs) in liver and brain; and with the plasma transport system of thyroid hormones in experimental animals and their offspring. Changes in thyroid hormone levels in conjunction with high PHAH exposure was also observed in captive as well as free ranging wildlife species and in humans. Maternal exposure to PHAHs during pregnancy resulted in a considerable fetal transfer of hydroxylated PHAHs, which are known to compete with thyroxine (T4) for plasma transthyretin (TTR) binding sites, and thus may be transported to the fetus with those carrier proteins that normally mediate the delivery of T4 to the fetus. Concomitant changes in thyroid hormone concentrations in plasma and in brain tissue were observed in fetal and neonatal stages of development, when sufficient thyroid hormone levels are essential for normal brain development. Alterations in structural and functional neurochemical parameters, such as glial fibrillary acidic protein (GFAP), synaptophysin, calcineurin, and serotonergic neurotransmitters, were observed in the same offspring up to postnatal day 90. In addition, some changes in locomotor and cognitive indices of behavior were observed in rat offspring, following in utero and lactational exposure to PHAHs. Alterations in thyroid hormone levels and subtle changes in neurobehavioral performance were also observed in human infants exposed in utero and through lactation to relatively high levels of PHAHs. Overall these studies indicate that persistent PHAHs can disrupt the thyroid hormone system at a multitude of interaction sites, which may have a profound impact on normal brain development in experimental animals, wildlife species, and human infants.

Animals↗
PubMed2001

Photoperiodism in humans and other primates: evidence and implications.

Most of the anatomical and molecular substrates of the system that encodes changes in photoperiod in the duration of melatonin secretion, and the receptor molecules that read this signal, have been shown to be conserved in monkeys and humans, and the functions of this system appear to be intact from the level of the retina to the level of the melatonin-duration signal of change of season. While photoperiodic seasonal breeding has been shown to occur in monkeys, it remains unclear whether photoperiod and mediation of photoperiod's effects by melatonin influence human reproduction. Epidemiological evidence suggests that inhibition of fertility by heat in men in summer contributes to seasonal variation in human reproduction at lower latitudes and that stimulation of fertility by lengthening of the photoperiod in spring contributes to the variation at higher latitudes. Parallels between the seasonality of human reproduction and seasonal affective disorder suggest that they may be governed by common biological processes. Historical and experimental evidence indicates that human responses to seasonal changes in the natural photoperiod may have been more robust prior to the Industrial Revolution and that subsequently they have been increasingly suppressed by alterations of the physical environment.

Animals↗
PubMed2005

The effects of a low-carbohydrate, ketogenic diet on the polycystic ovary syndrome: a pilot study.

BACKGROUND: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder affecting women of reproductive age and is associated with obesity, hyperinsulinemia, and insulin resistance. Because low carbohydrate diets have been shown to reduce insulin resistance, this pilot study investigated the six-month metabolic and endocrine effects of a low-carbohydrate, ketogenic diet (LCKD) on overweight and obese women with PCOS. RESULTS: Eleven women with a body mass index >27 kg/m2 and a clinical diagnosis of PCOS were recruited from the community. They were instructed to limit their carbohydrate intake to 20 grams or less per day for 24 weeks. Participants returned every two weeks to an outpatient research clinic for measurements and reinforcement of dietary instruction. In the 5 women who completed the study, there were significant reductions from baseline to 24 weeks in body weight (-12%), percent free testosterone (-22%), LH/FSH ratio (-36%), and fasting insulin (-54%). There were non-significant decreases in insulin, glucose, testosterone, HgbA1c, triglyceride, and perceived body hair. Two women became pregnant despite previous infertility problems. CONCLUSION: In this pilot study, a LCKD led to significant improvement in weight, percent free testosterone, LH/FSH ratio, and fasting insulin in women with obesity and PCOS over a 24 week period.

Journal Article↗
PubMed2003

Differential expression of two estrogen receptor beta isoforms in the human fetal testis during the second trimester of pregnancy.

Testicular cancer is more common in individuals with disorders of the male reproductive tract. It has been suggested that inappropriate exposure to estrogens during fetal life may have an impact on maturation of testicular germ cells that are the cells of origin of the majority of testis cancers. The aim of the present study was to establish whether human fetal germ cells (gonocytes) are a potential target of estrogen action. To address this issue, we used RT-PCR and immunohistochemistry to examine the pattern of expression of estrogen receptors (ER alpha, ER beta, and ER beta 2 variant) in human fetal testes at 12-19 wk gestation. ER alpha, mRNA, and protein were not detected in any of the fetal testes. In contrast, using an antibody directed against the hinge domain of ER beta expression was detected in multiple testicular nuclei. RT-PCR with primers specific for full-length wild-type ER beta (ER beta 1) or the ER beta 2 variant formed by splicing of an alternative eighth exon, was performed on whole-tissue extracts and materials recovered by laser capture and revealed that mRNAs for both isoforms were expressed. Immunohistochemistry with isotype-specific monoclonal antibodies showed that ER beta 1 was low/undetectable in gonocytes, whereas these cells expressed the highest levels of ER beta 2, compared with other testicular cell types. Both ER beta 1 and ER beta 2 were detected in some but not all Sertoli cells, peritubular cells, and other interstitial cells including those tentatively identified as Leydig cells. Our immunohistochemical results demonstrate that during the second trimester, some but not all somatic cells within the human fetal testis express wild-type ER beta (ER beta 1) protein and/or the variant isoform of ER beta (ER beta 2) that lacks amino acids essential for binding of estradiol. ER beta 2 protein was readily detectable in fetal gonocytes, whereas ER beta 1 was not. We did not detect expression of ER alpha. The expression of ER beta 2, a variant proposed act as a dominant negative receptor, might prevent estrogen action in gonocytes. We suggest that during this period of fetal life, estrogenic ligands are most likely to act on somatic cells that contain ER beta 1 protein.

Estrogen Receptor alpha↗
PubMed2005

Heritability of polycystic ovary syndrome in a Dutch twin-family study.

BACKGROUND: Polycystic ovary syndrome (PCOS) is one of the most common endocrine disorders among women of reproductive age. There is evidence for a genetic component in PCOS based on familial clustering of cases. OBJECTIVE: In the present study, the heritability of PCOS was estimated. DESIGN/PARTICIPANTS: Data from 1332 monozygotic twins (genetically identical) and 1873 dizygotic twins/singleton sisters of twins (who share on average 50% of their segregating genes) registered with The Netherlands Twin Register were used. PCOS was defined as less than nine menstrual cycles and acne or hirsutism in agreement with the 2003 Rotterdam consensus. RESULTS: Results point to a strong contribution of familial factors to PCOS. The resemblance in monozygotic twin sisters (tetrachoric correlation 0.71) for PCOS was about twice as large as in dizygotic twin and other sisters (tetrachoric correlation 0.38). Univariate analyses point to strong contributions of genetic factors to the variance in PCOS. Next, a trivariate genetic analysis of oligomenorrhea, acne, and hirsutism was carried out. This analysis confirmed that the familial component in PCOS is due to genetic factors. CONCLUSIONS: This study demonstrated a large influence of genetic factors to the pathogenesis of PCOS, justifying the search for susceptibility genes.

Adult↗
PubMed2001

Insulin resistance in polycystic ovary syndrome: progress and paradoxes.

Over the past 20 years, it has been clearly documented that 1) polycystic ovary syndrome (PCOS) has major metabolic sequelae related to insulin resistance and 2) insulin resistance plays an important role in the pathogenesis of the reproductive abnormalities of the disorder. Women with PCOS are at significantly increased risk of developing type 2 diabetes mellitus (DM). Studies in isolated adipocytes and in cultured skin fibroblasts from PCOS women have demonstrated intrinsic postbinding defects in insulin-mediated glucose metabolism. In fibroblasts, the mitogenic pathway of insulin action is intact, consistent with a selective defect in insulin signaling. While PCOS skeletal muscle is resistant to insulin in vivo, cultured muscle cells have normal insulin sensitivity, consistent with a major role of extrinsic factors in producing insulin resistance in this tissue. Excessive serine phosphorylation of the insulin receptor or downstream signaling proteins may be involved in the pathogenesis of insulin resistance in PCOS. The putative serine kinase is extrinsic to the insulin receptor but its identity is unknown. The explanations for tissue-specific and signaling pathway-specific differences in insulin action in PCOS are unknown but may involve differential roles of insulin receptor substrate (IRS)-1 and IRS-2 in insulin signal transduction.

Adipocytes↗
PubMed1995

A variety of environmentally persistent chemicals, including some phthalate plasticizers, are weakly estrogenic.

Sewage, a complex mixture of organic and inorganic chemicals, is considered to be a major source of environmental pollution. A random screen of 20 organic man-made chemicals present in liquid effluents revealed that half appeared able to interact with the estradiol receptor. This was demonstrated by their ability to inhibit binding of 17 beta-estradiol to the fish estrogen receptor. Further studies, using mammalian estrogen screens in vitro, revealed that the two phthalate esters butylbenzyl phthalate (BBP) and di-n-butylphthalate (DBP) and a food antioxidant, butylated hydroxyanisole (BHA) were estrogenic; however, they were all less estrogenic than the environmental estrogen octylphenol. Phthalate esters, used in the production of various plastics (including PVC), are among the most common industrial chemicals. Their ubiquity in the environment and tendency to bioconcentrate in animal fat are well known. Neither BBP nor DBP were able to act as antagonists, indicating that, in the presence of endogenous estrogens, their overall effect would be cumulative. Recently, it has been suggested that environmental estrogens may be etiological agents in several human diseases, including disorders of the male reproductive tract and breast and testicular cancers. The current finding that some phthalate compounds and some food additives are weakly estrogenic in vitro, needs to be supported by further studies on their effects in vivo before any conclusions can be made regarding their possible role in the development of these conditions.

Animals↗
PubMed2003

Health issues of migrant and seasonal farmworkers.

This paper describes the socioeconomic conditions under which the 3 to 5 million migrant and seasonal farmworkers in the United States live. Health consequences resulting from occupational hazards and from poverty, substandard living conditions, migrancy, language and cultural barriers, and impaired access to health care are described. Specific problems include infectious diseases, chemical- and pesticide-related illnesses, dermatitis, heat stress, respiratory conditions, musculoskeletal disorders and traumatic injuries, reproductive health problems, dental diseases, cancer, poor child health, inadequate preventive care, and social and mental health problems. By increasing awareness among health care professionals of the plight of migrant and seasonal farmworkers, the authors hope to encourage development of a stronger public health infrastructure and to improve the health status of these individuals.

Agricultural Workers' Diseases↗