Poor sleep in middle-aged women is not associated with menopause per se.

Whether sleep problems of menopausal women are associated with vasomotor symptoms and/or changes in estrogen levels associated with menopause or age-related changes in sleep architecture is unclear. This study aimed to determine if poor sleep in middle-aged women is correlated with menopause. This study recruited women seeking care for the first time at the menopause outpatient department of our hospital. Inclusion criteria were an age ≥40 years, not taking any medications for menopausal symptoms, and no sleeping problems or depression. Patients were assessed with the Pittsburgh Sleep Quality Index (PSQI), modified Kupperman Index (KI), and Menopause Rating Scale (MRS). A PSQI score of <7 indicated no sleep disorder and ≥7 indicated a sleep disorder. Blood specimens were analyzed for follicle-stimulating hormone and estradiol levels. A total of 244 women were included in the study; 103 (42.2%) were identified as having a sleep disorder and 141 as not having one. In addition, 156 (64%) women were postmenopausal and 88 (36%) were not menopausal. Follicle-stimulating hormone and estradiol levels were similar between the groups. Patients with a sleep disorder had a significantly higher total modified KI score and total MRS score (both, P<0.001) compared with those without a sleep disorder. Correlations of the PSQI total score with the KI and MRS were similar in menopausal and non-menopausal women. These results do not support that menopause per se specifically contributes to sleep problems.

Poor sleep in middle-aged women is not associated with menopause per se

Whether sleep problems of menopausal women are associated with vasomotor symptoms and/or changes in estrogen levels associated with menopause or age-related changes in sleep architecture is unclear. This study aimed to determine if poor sleep in middle-aged women is correlated with menopause. This study recruited women seeking care for the first time at the menopause outpatient department of our hospital. Inclusion criteria were an age ≥40 years, not taking any medications for menopausal symptoms, and no sleeping problems or depression. Patients were assessed with the Pittsburgh Sleep Quality Index (PSQI), modified Kupperman Index (KI), and Menopause Rating Scale (MRS). A PSQI score of <7 indicated no sleep disorder and ≥7 indicated a sleep disorder. Blood specimens were analyzed for follicle-stimulating hormone and estradiol levels. A total of 244 women were included in the study; 103 (42.2%) were identified as having a sleep disorder and 141 as not having one. In addition, 156 (64%) women were postmenopausal and 88 (36%) were not menopausal. Follicle-stimulating hormone and estradiol levels were similar between the groups. Patients with a sleep disorder had a significantly higher total modified KI score and total MRS score (both, P<0.001) compared with those without a sleep disorder. Correlations of the PSQI total score with the KI and MRS were similar in menopausal and non-menopausal women. These results do not support that menopause per se specifically contributes to sleep problems.

The cost-effectiveness analysis of laparoscopic treatment of ectopic pregnancy: a single-center review of a five-year experience.

PURPOSE: The aim of this study was to investigate the cost-effectiveness of laparoscopic treatment for ectopic pregnancy by comparing the medical expenses and time of hospitalization of laparoscopic and open surgery for ectopic pregnancy in partial area of Shanghai, China. MATERIALS AND METHODS: Clinical data of 762 cases with ectopic pregnancy undergoing surgical treatment (307 cases for laparoscopic surgery and 455 cases for open surgery) were analyzed retrospectively. The clinical information including the medical expenses and time of hospitalization was compared. The patients were divided into three groups according to the treatments of different lesions (lesions resection, conservative laparotomy, and exploration group) and were analyzed. RESULTS: The total hospitalization expenses and the top three single costs including surgery, exams, and medicine expenses were higher in laparoscopic group than in open surgery group. There was no significant difference between the two groups on the total time of hospitalization. The hospital days of preoperation were higher but the postoperative hospital days were lower in laparoscopic group than in open surgery group. Compared with the open surgery treatment, the hospitalization expenses of laparoscopic treatment for ectopic pregnancy increased. There was no significant difference on the total hospitalization days. CONCLUSION: The preoperative waiting period of inpatients increased and the post-operative hospital days reduced in laparoscopic group.

Selective regulation of osteoblastic OPG and RANKL by dehydroepiandrosterone through activation of the estrogen receptor ß-mediated MAPK signaling pathway.

The aim of the work was to investigate the differential regulation by dehydroepiandrosterone (DHEA) of the osteoblastic production via the estrogen receptor beta (ER ß)-mediated signaling pathway. Having developed hMG63-ER ß cells and hMG63-shER ß cells, we analyzed the regulation by DHEA of human osteoblastic viability, the receptor activator of nuclear factor kappa-B ligand (RANKL), osteoprotegerin (OPG), and the differential expression of ER ß, ER α, or p-ERK1/2 (extracellular signal-regulated kinase) in hMG63, hMG63-shER ß, and hMG63-ER ß cells pretreated with or without U0126, flutamide, and ICI 182780, followed by DHEA culture. When the level of ER ß was high, DHEA (10 - 7 mol/l) could effectively amplify the proliferation and inhibit the etoposide-induced apoptosis of hMG63 cells (p<0.01 and p<0.05, respectively), which was blocked by U0126. When the expression of ER ß was silenced, DHEA could not significantly improve the viability of hMG63. In the presence of ER ß, DHEA activated the pERK1/2-MAPK signaling pathway but not p38 and JNK. Besides, the regulation of p-ERK1/2 upon DHEA treatment was mainly modulated by ER ß instead of androgen receptor and ER α. The secretion of OPG was declined following the silence of ER ß (p<0.05). RANKL and ER α, however, were unaffected by culture with or without DHEA and U0126, regardless of the ER ß level. DHEA seems to act selectively on osteoblasts via the dominant ER ß receptor, which mediates amplified cell viability through the MAPK signaling pathway involving pERK1/2 and upregulates the production of OPG rather than RANKL.

[Over-expression of a polyketide synthase (PKS) module of a giant polyene antibiotic gene cluster in E. coli by double induction].

A 2,671 bp DNA carrying a type I PKS module with KS and AT domains from Streptomyces sp. FR-008 was cloned in-frame into the BamHI site immediately downstream of the PT7 promoter of the E. coli expression vector pET-15b, no considerable expression under IPTG induction was detected. The same PKS gene cloned downstream of the tandem PRPL promoters of pBV220 also yielded no over-expression under 42 degrees C induction. This gene was, however, over-expressed when it was cloned downstream of the tandem PRPT7 or PRPLPT7 promoters. In the case of the tandem PRPLPT7 promoters, the over-expression was dependent on the 42 degrees C plus IPTG double induction. While in the case of the tandem PRPT7 promoters, over-expression could be achieved when the gene was induced by IPTG or 42 degrees C individually or by IPTG and 42 degrees C double induction. Based on these experiences an expression vector pHZ330 containing the tandem PRPT7 promoters was constructed. In addition, the PKS protein expressed in E. coli was injected into rabbits to generate PKS-specific antibodies. Western blotting experiment indicated that these antibodies were PKS-specific which could be used either for the study of the PKS gene cluster or for the detection of the heterologous expression of Streptomyces sp. FR-008 PKS genes.