Objective: To investigate the current status and influencing factors of sleep disorders among pregnant women, so as to provide insights into health management during pregnancy. Methods: Pregnant women who underwent prenatal checkups at Hangzhou Obstetrics and Gynecology Hospital from January to October 2023 were selected as subjects, and general data including age, pregnancy period and exercise were collected through questionnaire surveys. Sleep quality, pregnancy stress, anxiety and depression were evaluated using Pittsburgh Sleep Quality Index, Pregnancy Stress Rating Scale, Pregnancy-related Anxiety Scale and Edinburgh Postnatal Depression Scale, respectively. Factors affecting sleep disorders among pregnant women were analyzed using a multivariable logistic regression model. Results: A total of 386 pregnant women was surveyed, with a mean age of (30.28±4.65) years, including 20.47% in the first trimester, 47.93% in the second trimester and 31.61% in the third trimester. Women with anxiety and depression accounted for 14.51% and 21.76%, respectively. Pregnancy stress was mainly moderate, accounting for 51.04%. There were 106 pregnant women with sleep disorders, accounting for 27.46%. Mutivariable logistic regression analysis showed that age (≥35 years, OR=1.656, 95%CI: 1.094-2.503), pregnancy period (third pregnancy, OR=2.097, 95%CI: 1.213-3.621), regular exercise in the past 6 months (OR=0.376, 95%CI: 0.210-0.670), anxiety (OR=2.794, 95%CI: 1.545-5.048), depression (OR=3.501, 95%CI: 1.877-6.529) and pregnancy stress (moderate, OR=1.355, 95%CI: 1.018-1.801; severe, OR=2.538, 95%CI: 1.417-4.540) were the factors affecting sleep disorders among pregnant women. Conclusions Sleep disorders of pregnant women is influenced by age, pregnancy period, pregnancy stress, anxiety, depression and exercise. It is necessary to identify high-risk individuals with sleep disorders early, and to provide psychological intervention and prenatal health guidance.

Objective To observe the therapeutic effect of NF-κB gene short hairpin RNA (shRNA) on endometriosis and identify the function of NF-κB on the maintenance and development of endometriosis in Macaca fascicularis.Methods The Macaca fascicularis model of endometriosis was developed,which divided into experimental group,negative control group and simple model group.The high specificity adenovirus vector mediated shRNA targeting NF-κB gene and negative control shRNA adenovirus with no-load NF-κB gene were synthesised.The experimental group injected the adenovirus which carried the NF-κB shRNA into the endometriosis lesions under laparoscopy surgery,the negative control group with no-load shRNA adenovirus and the simple models group injected with normal saline.Four weeks later after the injection,an observed operation was performed through laparoscopy and some lesions were collected.The CD34 immunohistochemistry of these lesions were done to detect the microvessel density,then the variation of the microvessel density among each group were observed.The expression of the NF-κB and proliferating cell nuclear antigen (PCNA) were detected through western blot.Results First,the Macaca fascicularis model of endometriosis was successful developed,and the experimental group has an evident atrophy in ectopic lesions compared with the previous.The lesions' microvessel density in experimental group decreased evidently compared with the negative control group and simple model group (0.002 0±0.000 3 versus 0.021 9±0.002 6 versus 0.024 5±0.003 3),and the differences was statistically significant (P＜0.01).The expression of PCNA (0.37±0.17 versus 0.57±0.26 versus 0.57±0.28) and NF-κB (0.338 ± 0.174 versus 0.678 ± 0.021 versus 0.645 ±0.098) in experiment group was lower than the negative control group and simple model group,the differences were statistically significant (all P＜0.01).Conclusion Through targeting suppressed the NF-κB gene expression by NF-κB shRNA,we can inhibit the development of endometriosis through reducing the ability of angiogenesis and cell proliferation of ectopic endometrial cells.

OBJECTIVETo study the effect of interleukin-1β (IL-1β) on the expressions activin A, follistatin, and cripto in cultured human endometrial stromal cells (HESCs) form patients with endometriosis.

METHODSCultured HESCs were stimulated with 250, 500, and 750pg/ml IL-1β, and the mRNA and protein expressions of activin A, follistatin, and cripto were assayed using real-time reverse transcriptase-polymerase chain reaction and enzyme-linked immunosorbent assay.

RESULTSIL-1β treatment caused significant dose-dependent increments of the mRNA and protein expressions of activin A and follistatin and of the mRNA expression of cripto in cultured HESCs.

CONCLUSIONIL-1β can affect the expressions of activin A, follistatin and cripto in HESCs from patients with endometriosis.

Activins ; metabolism ; Cells, Cultured ; Endometriosis ; metabolism ; Endometrium ; cytology ; Female ; Humans ; Interleukin-1beta ; pharmacology ; Stromal Cells ; drug effects ; metabolism

OBJECTIVETo assess the effect of a high specific adenovirus vector-mediated shRNA targeting nuclear factor-κB (NF-κB) on cell proliferation of the endometrium of Macaca fascicularis.

METHODSThe adenoviral vector NF-κB-p65-shRNA and the empty vector were separately trasnfected in cultured endometrial cells of Macaca fascicularis. The changes in the expression of the target gene protein and apoptotic proteins, cell proliferation, and cell cycle distribution were observed after the transfection.

RESULTSCompared with the control cells, infection of the endometrial cells with the NF-κB-p65-shRNA adenovirus significantly increased the expression levels of apoptotic proteins, promoted apoptosis of the endometrial cells, and reduced the cells in division?stage.

CONCLUSIONSNF-κB-p65 shRNA adenovirus can effectively promote apoptosis of endometrial cells and inhibit the proliferation of endometrial cells of Macaca fascicularis.

Adenoviridae ; Animals ; Apoptosis ; Cell Proliferation ; Cells, Cultured ; Endometrium ; cytology ; Female ; Genetic Vectors ; Macaca fascicularis ; RNA, Small Interfering ; genetics ; Transcription Factor RelA ; genetics ; Transfection