Maternal occupational exposure to solvents and gastroschisis in offspring-National Birth Defects Prevention Study 1997-2011

Objectives: The aim of this study was to assess the association between maternal occupational exposure to solvents and gastroschisis in offspring. Methods: We used data from the National Birth Defects Prevention Study, a large population-based case-control study of major birth defects conducted in 10 US states from 1997 to 2011. Infants with gastroschisis were ascertained by active birth defects surveillance systems. Control infants without major birth defects were selected from vital records or birth hospital records. Self-reported maternal occupational histories were collected by telephone interview. Industrial hygienists reviewed this information to estimate exposure to aromatic, chlorinated and petroleum-based solvents from 1 month before conception through the first trimester of pregnancy. Cumulative exposure to solvents was estimated for the same period accounting for estimated exposure intensity and frequency, job duration and hours worked per week. ORs and 95% CIs were estimated to assess the association between exposure to any solvents or solvent classes, and gastroschisis risk. Results: Among 879 cases and 7817 controls, the overall prevalence of periconceptional solvent exposure was 7.3% and 7.4%, respectively. Exposure to any solvent versus no exposure to solvents was not associated with gastroschisis after adjusting for maternal age (OR 1.00, 95% CI 0.75 to 1.32), nor was an association noted for solvent classes. There was no exposure-response relationship between estimated cumulative solvent exposure and gastroschisis after adjusting for maternal age. Conclusion: Our study found no association between maternal occupational solvent exposure and gastroschisis in offspring. Further research is needed to understand risk factors for gastroschisis

The take up of business support by minority ethnic enterprises: the experience of South Asian businesses in England

This research contributes to a greater understanding of minority ethnic business (MEB) needs and practices and helps identify the support needs of minority ethnic firms in relation to existing support provision. The aims are, therefore, to examine the take-up of support by minority ethnic enterprises focusing mainly on the South Asian community with some representation from the African-Caribbean and Korean communities. Fifty minority ethnic businesses across South West London were contacted and semi-structured interviews took place with the owner/owner managers. The findings suggest that policy makers need to appreciate the diversity of MEBs and policies aimed at these businesses should reflect that diversity

The randomised uterine septum transsection trial (TRUST) : Design and protocol

Peer reviewedPublisher PD

Septum resection in women with a septate uterus : a cohort study

© The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology.Peer reviewedPublisher PD

Corrigendum: Septum resection in women with a septate uterus:a cohort study

The authors of the above article would like to apologise for an error in one of the authors' names. W. Kuchenbecker should be W.K.H. Kuchenbecker, as above. The electronic version of this article has been updated at https:// doi.org/10.1093/humrep/dez284. The print version is correct. The Authors would like to assure readers that this does not affect any other content of the article.</p

The randomised uterine septum transsection trial (TRUST): Design and protocol

Background: A septate uterus is a uterine anomaly that may affect reproductive outcome, and is associated with an increased risk for miscarriage, subfertility and preterm birth. Resection of the septum is subject of debate. There is no convincing evidence concerning its effectiveness and safety. This study aims to assess whether hysteroscopic septum resection improves reproductive outcome in women with a septate uterus. Methods/design: A multi-centre randomised contr

Short-term patterns of pulsatile luteinizing hormone secretion do not differ between male-to-female transsexuals and heterosexual men

This study tested whether there is a difference in the pulsatile LH secretion between male-to-female transsexuals and eugonadal heterosexual men. The mean serum LH concentrations, the LH pulse frequency, and the LH pulse amplitude were compared between a group of eight male-to-female transsexuals and a group of 22 heterosexual men. Blood samples for LH determinations were collected every 10 min for seven hours. 17-β-estradiol and testosterone were measured at the beginning of each test. There were no significant differences between the heterosexual and transsexual group in LH pulse frequency (3.9±1.3 vs. 3.9±1.7), LH pulse amplitude (3.7±1.3 U/l vs. 3.0±0.5 U/l), mean serum LH concentration (5.2±1.4 U/l vs. 5.4±1.1 U/l), 17-β-estradiol (0.07±0.01 nmol/l vs. 0.08±0.02 nmol/l), or testosterone (22.9±3.7 nmol/l vs. 21.8±8.0 nmol/l). We conclude that the pulsatile release characteristics of LH do not allow a distinction between eugonadal heterosexual men and eugonadal male-to-female transsexuals

EFFECTS OF OPIATE RECEPTOR BLOCKADE ON GONADOTROPHIN SECRETION BEFORE AND AFTER ADMINISTRATION OF THE OESTROGEN RECEPTOR BLOCKER TAMOXIFEN IN EUGONADAL MEN

Both gonadal steroids and endogenous opioid peptides (EOPs) exert an inhibitory effect on gonadotrophin secretion. It is thought that the negative feedback action of the gonadal steroids, testosterone (T) and oestradiol (E2), on the gonadotrophin secretion is mediated by EOPs. To assess the effects of EOPs and oestrogen and their interrelationship on pulsatile LH secretion we studied two groups of eugonadal men. The subjects of the first group were tested on three different occasions, firstly under basal conditions, secondly during infusion of the opiate receptor blocker naloxone (NAL) (bolus 5 mg + 2.1 mg/h for 7 h), and finally during NAL infusion after 6 weeks administration of the oestrogen receptor blocker tamoxifen (10 mg twice daily). The subjects of the second group were studied before and after 6 weeks administration of tamoxifen. NAL infusion produced a significant increase in mean serum LH levels (4.8 ± SD 1.5 to 6.2 ± 1.8 U/l) and LH pulse frequency (3.7 ± 1.6 to 5.3 ± 1.2 pulses/7 h). No change was seen in mean LH pulse amplitudes (3.5 ± 1.5 vs 3.4 ± 1.0 U/l). After tamoxifen administration alone there was a significant increase in mean LH level (from 5.7 ± 1.3 to 10.1 ± 2.4 U/l), LH pulse amplitude (from 3.8 ± 0.9 to 4.6 ± 0.9 U/l) and LH pulse frequency (from 4.2 ± 1.5 to 5.8 ± 1.7 pulses/7 h). A significant rise in mean serum LH levels was observed during NAL infusion after previous tamoxifen administration in comparison to the infusion of NAL alone (from 6.2 ± 1.8 to 10.5 ± 6.2 U/l). LH pulse frequency (5.3 ± 1.2 vs 6.3 ± 1.3 pulses/7h) and amplitude (3.4 ± 1.0 vs 3.6 ± 1.5 U/l) however, did not change. Mean serum LH level and LH pulse frequency after opiate receptor and oestrogen receptor blockade together did not differ from the results obtained after oestrogen receptor blockade alone. NAL however was expected not only to block opioid‐mediated oestrogen action blockade on LH pulse frequency and mean serum LH levels after oestrogen receptor blockade could mean that the opioid inhibition depends on oestrogen rather than androgen action. If so there could be a parallel between the lack of effect of NAL infusion on gonadotrophin secretion in tamoxifen‐treated men and the same lack of effect in gonadectomized (Shoupe et al., 1985) and postmenopausal women (Reid et al., 1983; Melis et al., 1984; Caspar et al., 1985), in that a long‐term oestrogen deprivation reduces the opioid tone. The assumption that opioid inhibition is primarily dependent on oestrogen action conflicts, however, with a number of earlier studies on the relationship of androgens and EOPs. The feedback effect of the non‐aromatizable androgen dihydrotes‐tosterone can be blocked by NAL (Veldhuis et al, 1984) and androgen receptor blockade abolishes the LH response to NAL (Balzano et al., 1987). Another possible explanation is that androgen action was impeded after tamoxifen administration and for this reason blockade of androgen mediated opioid action by NAL infusion had no additional effect on the LH pulse frequency. In an earlier study we have found that antioestrogens probably interfere with androgen action on gonadotrophin secretion (Spijkstra et al., 1988). Such an effect was apparent in the group treated with tamoxifen alone in this study. While T levels had risen 60–80% following tamoxifen administration, this substantial rise was without a suppressing effect on LH pulse frequency, which had increased upon tamoxifen administration. The results obtained in this study therefore seem to be consistent with this assumption. However some caution is warranted when interpreting the results of the study in this way. Antioestrogens are known to bind to receptors other than E2 receptors (Sutherland et al., 1980), which raises the question if antioestrogens may exert effects other than their antioestrogenic or oestrogenic properties. Indeed studies with the antioestrogen clomiphene citrate both in vivo (Kerin et al., 1985) and in vitro (Miyake et al., 1983) provided indications in support of this assumption

Divergent effects of the antiestrogen tamoxifen and of estrogens on luteinzing hormone (lh) pulse frequency, but not on basal lh levels and lh pulse amplitude in men

We studied the role of estrogens on LH pulse modulation in men in two ways. Firstly, we compared LH pulse frequency and amplitude in 13 normal men before and after 6 weeks administration of the antiestrogen tamoxifen (10 mg twice daily). Secondly, we compared LH pulse frequency and amplitude between a group of 10 agonadal men not receiving sex steroid treatment and a group of 9 agonadal men (male to female transsexuals) continuously treated with 50 ng ethinyl estradiol/day. Tamoxifen administration to normal men resulted in a significant rise in the mean serum LH level from 5.7 ± 1.3 (± SD) to 10.1 ± 2.4 U/L, which was associated with significant increases in LH pulse frequency (from 4.2 ± 1.5 to 5.8 ± 1.7/7 h) and LH pulse amplitude (from 3.8 ± 0.9 to 4.6 ± 0.7 U/L). In the group of agonadal men the mean LH pulse frequency was 6.8 ± 1.5/7 h, while it was 5.9 ± 1.7/7 h in the estrogen-treated agonadal group (P = NS). The mean serum LH level and LH pulse amplitude were, however, significantly lower in the estrogen-treated agonadal men than in the agonadal men (14.7 ± 7.0 vs. 34.3 ± 8.6 and 4.1 ± 1.8 vs. 7.4 ± 1.8 U/L, respectively). We conclude that estrogens reduce basal LH levels and LH pulse amplitude. With regard to the modulation of LH pulse frequency our data provide contradictory results. While an antiestrogen increased LH pulse frequency in normal men, estrogen alone produced no change in LH pulse frequency in agonadal men. The study design in the agonadal men ignores the possible interaction of the two major testicular hormones (estradiol and testosterone) on gonadotropin secretion. Therefore, a possible explanation for this discrepancy in the effects of antiestrogen and estrogen could be an interaction between estrogens and androgens on gonadotropin secretion at the level of the LHRH pulse generator

Pulsatile luteinizing hormone release and ovarian steroid levels in female-to-male transsexuals compared to heterosexual women

It has been suggested that there is a difference in the interaction between sex steroids and gonadotropin secretion between transsexual and heterosexual women. In this study we tested whether there is a difference in the pulsatile release characteristics of luteinizing hormone (LH) and in ovarian steroid concentrations between 16 female-to-male (f-to-m) transsexuals and eight eugonadal heterosexual women during the early follicular phase of the menstrual cycle. Blood samples for LH determination were collected every 10 min for 7 hr in the transsexual group, and every 10 min for 6 hr in the heterosexual group. There were no significant differences between the transsexual and heterosexual group in mean serum LH concentration (6.9±2.4 U/l vs. 7.5±2.6 U/l), mean LH nadir interval (77±37 min vs. 70±16 min), and mean LH pulse amplitude (2.9±1.1 U/l vs. 3.0±1.1 U/l). Serum estrone, 17-β-estradiol, testosterone, progesterone and FSH concentrations also did not differ between the two groups. There also was not a higher prevalence of polycystic ovarian disease in our f-to-m transsexual group than in the general population