[Sleep quality and sleep disturbances in Chinese pregnant women: a multicenter cross-sectional study].

Objective: This study aims to investigate the sleep quality of pregnant women in Xuhui District, Shanghai, and the related factors of sleep disturbances during pregnancy. Methods: From February 2019 to February 2021, we used online integrated sleep questionnaire (including PSQI, BQ, ESS, AIS) in Shanghai Jiao Tong University School of Medicine Affiliated Sixth People's Hospital, The International Peace Maternity and Child Health Hospitals of China Welfare Institution, and Shanghai Eighth People's Hospital, to investigate the sleep quality across pregnancy. We also collected maternal physical examination results, childbearing history, sociodemographic, and other clinical data. The prevalences and related factors of various sleep disturbances in pregnant women were analyzed, including insufficient/excessive nighttime sleep, low sleep efficiency, difficulty falling asleep, poor sleep quality, insomnia, daytime sleepiness, and high risk of sleep-disordered breathing (SDB). Results: This study includes 1 898 cases in the first trimester (T1), 3 099 cases in the second trimester (T2), and 1 539 cases in the third trimester (T3). Poor sleep quality (38.6%), daytime sleepiness (mild 41.9%, moderate 17.7%, severe 2.1%), and suspicious insomnia (32.3%) are most prevalent among women in T1 (P<0.01). In comparison, short sleep time (2.7%), long sleep time (8.6%), difficulty falling asleep (12.2%), poor sleep efficiency (35.4%), very poor sleep quality (6.7%), clinical insomnia (21.8%), and high-risk SDB (6.4%) are most prevalent among women in T3 (P<0.05). During pregnancy, late gestation (OR=1.016, 95%CI: 1.006-1.025) and multiple induced/drug abortions (OR=1.329, 95%CI: 1.043-1.692) are risk factors for poor sleep quality (PSQI>5), while multiple full-term deliveries (OR=0.800, 95%CI: 0.675-0.949) is its protective factor. Advanced maternal age (OR=0.976, 95%CI: 0.956-0.997), multiple full-term deliveries (OR=0.808, 95%CI: 0.680-0.959), late gestation (OR=0.983, 95%CI: 0.974-0.992) and hypertension (OR=0.572, 95%CI: 0.401-0.814) are protective factors for daytime sleepiness (ESS>6). The high-risk pregnancy category (OR=9.312, 95%CI: 1.156-74.978) is a risk factor for insomnia (AIS≥4), while multiple full-term deliveries (OR=0.815, 95%CI: 0.691-0.961) is its protective factor. High BMI (OR=1.334, 95%CI: 1.270-1.402) and hypertension (OR=4.427, 95%CI: 2.539-7.719) are risk factors for high-risk SDB in pregnant women. Conclusions: The prevalences of various sleep disturbances are high throughout pregnancy. Noticeably, symptoms of maternal SDB develop along with pregnancy. Different types of sleep disturbances are associated with different factors. Women of high-risk pregnancy category, in late gestation, with high BMI, hypertension, a history of induced/drug abortion, or without a history of full-term delivery can be at high risk of sleep disturbances during pregnancy.

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.

Melatonin Ameliorates Arsenite-Induced Neurotoxicity: Involvement of Autophagy and Mitochondria.

In the present study, the neuroprotective effect of melatonin on arsenite-induced neurotoxicity was investigated in rat primary cultured cortical neurons. Incubation of melatonin prevented arsenite-induced neuronal cell loss in a concentration-dependent manner. Furthermore, melatonin significantly attenuated arsenite-induced elevation in microtubule-associated protein light chain 3 (LC3)-II levels, a biomarker of autophagy. Our fluorescent staining assay showed that melatonin decreased arsenite-induced elevation of co-localized fluorescent puncta of monodansylcadaverine (a specific marker of autophagic vacuoles) and lysotracker red (a specific marker of lysosomes), indicating that melatonin is capable of inhibiting arsenite-induced autophagy and autolysosome formation. Because 3-methyladenine (an autophagic inhibitor) attenuated the arsenite-reduced α-synuclein levels (a protein essential for the neurite outgrowth and synaptic plasticity), melatonin via inhibiting autophagy attenuated the arsenite-reduced α-synuclein levels. At the same time, melatonin ameliorated the arsenite-induced reduction in growth associated protein 43 (a hallmark protein of neurite outgrowth) and discontinuous neurites of rat primary cultured cortical neurons. In addition, melatonin was found to prevent arsenite-induced decreases in cytochrome c oxidase levels (a biomarker of mitochondrial mass) and elevation in co-localized fluorescent puncta of autolysosomes and cytochrome c oxidase. Moreover, melatonin prevented arsenite-induced reduction in peroxisome proliferator-activated receptor gamma co-activator 1 α, a transcriptional co-activator of mitochondrial biosynthesis. Taken together, melatonin may exert its neuroprotective action via inhibiting arsenite-induced autophagy and enhancing mitochondrial biogenesis and thus restoring α-synuclein levels, neuronal integrity, and mitochondrial mass in rat primary cultured cortical neurons.

miR-506 acts as a tumor suppressor by directly targeting the hedgehog pathway transcription factor Gli3 in human cervical cancer.

Although significant advances have recently been made in the diagnosis and treatment of cervical carcinoma, the long-term survival rate for advanced cervical cancer remains low. Therefore, an urgent need exists to both uncover the molecular mechanisms and identify potential therapeutic targets for the treatment of cervical cancer. MicroRNAs (miRNAs) have important roles in cancer progression and could be used as either potential therapeutic agents or targets. miR-506 is a component of an X chromosome-linked miRNA cluster. The biological functions of miR-506 have not been well established. In this study, we found that miR-506 expression was downregulated in approximately 80% of the cervical cancer samples examined and inversely correlated with the expression of Ki-67, a marker of cell proliferation. Gain-of-function and loss-of-function studies in human cervical cancer, Caski and SiHa cells, demonstrated that miR-506 acts as a tumor suppressor by inhibiting cervical cancer growth in vitro and in vivo. Further studies showed that miR-506 induced cell cycle arrest at the G1/S transition, and enhanced apoptosis and chemosensitivity of cervical cancer cell. We subsequently identified Gli3, a hedgehog pathway transcription factor, as a direct target of miR-506 in cervical cancer. Furthermore, Gli3 silencing recapitulated the effects of miR-506, and reintroduction of Gli3 abrogated miR-506-induced cell growth arrest and apoptosis. Taken together, we conclude that miR-506 exerts its anti-proliferative function by directly targeting Gli3. This newly identified miR-506/Gli3 axis provides further insight into the pathogenesis of cervical cancer and indicates a potential novel therapeutic agent for the treatment of cervical cancer.

Suppression of RNA interference on expression of c-myc of SKOV3 ovarian carcinoma cell line.

AIM: To investigate suppression of RNA interference (RNAi) on expression of c-myc of SKOV3 ovarian carcinoma cell line. MATERIALS AND METHODS: The c-myc -siRNA was designed and synthesized, then transfected to SKOV3 ovarian carcinoma cell lines. The cell lines were divided into four groups, including the blank control group, the siRNA transfection group, the mock transfection group and the negative control group. The expression level of c-myc mRNA and protein were detected by RT-PCR and Western blotting, respectively. The growth and proliferation of SKOV3 ovarian carcinoma cell lines were observed with CCK-8 assay. RESULTS: After transfected with c-myc -siRNA, the expression level of c-myc mRNA and protein were down-regulated, the growth and proliferation of SKOV3 ovarian carcinoma cell line were inhibited in the siRNA transfection group. There were significant differences between the siRNA transfection group and the blank control group (p < 0.05). The silencing efficiency was 77.78%, the protein suppression rate was 67.78%, and the inhibition ratio was 56.35% by CCK-8 assay in siRNA transfection group. CONCLUSIONS: The down-regulation of c-myc expression of SKOV3 ovarian carcinoma cell line by c-myc -siRNA can lead to the suppression of cancer cell proliferation. The small interfering RNAs technique can inhibit the proliferation of carcinoma cell by oncogene silencing.

Role of HO-1 in the arsenite-induced neurotoxicity in primary cultured cortical neurons.

In the present study, the role of heme oxygenase (HO)-1 in sodium arsenite (arsenite)-induced neurotoxicity was investigated using primary cultured cortical neurons. Incubation with arsenite was found to cause cell death of primary cultured cortical neurons in concentration- and time-dependent manners. Furthermore, arsenite induced caspase 3 activation and decreased procaspase 12 levels, indicating that apoptosis is involved in the arsenite-induced neurotoxicity. The oxidative mechanism underlying arsenite-induced neurotoxicity was investigated. Western blot assay showed that arsenite significantly increased HO-1 levels, a redox-regulated protein. Co-incubation with glutathione (10 mM) attenuated arsenite-induced HO-1 elevation and caspase 3 activation, suggesting that oxidative stress is involved in the arsenite-induced neurotoxicity. The neurotoxic effects of inorganic arsenics were compared; arsenite was more potent than arsenate in inducing HO-1 expression and caspase 3 activation. Moreover, the cell viabilities of arsenite and arsenate were 60 ± 2 and 99 ± 2 % of control, respectively. HO-1 siRNA transfection was employed to prevent arsenite-induced HO-1 elevation. At the same time, arsenite-induced caspase 3 activation and neuronal death were attenuated in the HO-1 siRNA-transfected cells. Taken together, HO-1 appears to be neuroprotective in the arsenite-induced neurotoxicity in primary cultured cortical neurons. In addition to antioxidants, HO-1 elevation may be a neuroprotective strategy for arsenite-induced neurotoxicity.

Prediction of location of gestational sac for pregnancy of unknown location at first sight during exploratory surgery using the ratio of hCG in haemoperitoneum and venous serum.

OBJECTIVE: To evaluate a practical method to predict the location of gestational sacs for pregnancy of unknown location (PUL) during exploratory surgery. STUDY DESIGN: Sixty-nine cases of PUL with a positive pregnancy test and haemoperitoneum but unknown location of the gestational sac at first sight on exploratory surgery were analysed at the Department of Obstetrics and Gynaecology, Shanghai Jiaotong University. The level of hCG in the haemoperitoneum and venous serum were measured, and the ratio of hCG in haemoperitoneum and venous serum (Rp/v-hCG) was calculated. Rp/v-hCG<1.0 was taken to suggest an intrauterine gestational sac, and Rp/v-hCG>1.0 was taken to suggest an abdominal gestational sac. The sensitivity and specificity of Rp/v-hCG for predicting the location of the gestational sac were evaluated prospectively. RESULTS: Among 69 cases of PUL, 17 cases (17/69) were ultimately diagnosed as abdominal gestational sacs before 9 weeks of gestation, and 52 cases (52/69) were ultimately diagnosed as intrauterine gestational sacs. The diagnostic sensitivity and specificity of Rp/v-hCG at the time of exploratory surgery for predicting the location of the gestational sac were 94.1% and 100%, respectively (kappa=0.96; P=0.039). The rate of missed diagnosis was 5.9%. The location of the gestational sac was determined during the initial exploratory procedure for 15 cases (15/17) with an abdominal gestational sac (1 case of splenic pregnancy was diagnosed during secondary surgery) and 37 cases (37/52) with an intrauterine gestational sac. With the exception of gestational sacs located in the pouch of Douglas (52.9%, 9/17), the gestational sacs (47.1%, 8/17) located in the other places were difficult to find. CONCLUSIONS: Rp/v-hCG should be considered when exploratory surgery reveals no visible gestational sacs at first sight. If Rp/v-hCG is >1.0, more careful pelvic or abdominal exploration is required, rather than dilation and curettage, to locate abdominal gestational sacs.

Medical methods for cervical ripening before the removal of intrauterine devices in postmenopausal women: a systematic review.

In China, most women with intrauterine devices (IUDs) ask to have them removed following the menopause. As the cervix is stenotic after the menopause and most IUDs do not have a thread attached, various medical methods are used for cervical ripening prior to IUD removal. A systematic review of the relevant literature was conducted to compare different medical methods for cervical priming with no treatment, or with other methods, prior to IUD removal in postmenopausal women. Multiple electronic databases including the Cochrane Central Register of Controlled Trials, EMBASE, MEDLINE, the WHO Reproductive Health Library (2011) and the Chinese Biomedical Literature Database were searched systematically. Reference lists of articles published in English or Chinese between 1980 and 2011 were searched. All randomized controlled trials (RCTs) on IUD removal following the menopause using medical agents compared with no treatment, or with other treatments, were included. Outcomes were the ease of IUD removal, need for forced cervical dilatation, cervical width, procedure time, severe pain and any side-effects. Data were processed using RevMan 5 software. Thirty original RCTs were eligible for inclusion. Most medical agents such as oestrogens, mifepristone, misoprostol and methyl carboprost were highly effective for facilitating IUD removal, and reduced the need for further dilatation during the procedure. In particular, treatment with mifepristone or misoprostol prior to IUD removal was found to increase the width of the cervical canal and reduce the procedure time. Mifepristone was more effective than vaginal misoprostol for cervical dilatation, but it showed similar effectiveness to misoprostol and nilestriol in terms of the ease of IUD removal. Sublingual misoprostol was superior to oral misoprostol for facilitating IUD removal. A dose of misoprostol as low as 200µg was effective for cervical priming. For vaginal and oral misoprostol, the optimum times of application were 2-3h and 1 day prior to the procedure, respectively. All the prophylactic medical methods were able to alleviate pain during IUD removal, and vaginal misoprostol was more effective than nilestriol. Uterine injury was more common with no treatment and with nilestriol. Gastrointestinal side-effects such as nausea and diarrhoea were common with oral misoprostol and vaginal misoprostol, respectively. Therefore, mifepristone or sublingual misoprostol should be the medical treatments of choice. Oestrogen regimens might be alternatives when mifepristone or misoprostol are contraindicated, and there is a need for further study on combined regimens for cervical priming.

Quantitative Fourier transform IR photoacoustic spectroscopy of condensed phases.

Photoacoustic spectra of materials obtained using the Fourier transform technique require normalization to achieve correct relative peak heights over the spectral range studied. This paper discusses procedures for obtaining quantitative Fourier transform IR-photoacoustic spectroscopy spectra of solids and liquids. A normalization routine for absorption amplitudes is discussed and applied to experimental data obtained on polymeric samples.