Higher waist circumference is associated with increased likelihood of female infertility: NHANES 2017-2020 results.

Background: Waist circumference can be used as an anthropometric measure to assess central obesity and is easier and more convenient than the waist-to-hip ratio in identifying the risk of obesity and medical problems. Most studies showing an association between obesity and infertility in women have used BMI to measure obesity. Our goal was to examine any potential association between waist circumference and infertility. Methods: This cross-sectional study, which formed part of the National Health and Nutrition Examination Survey (NHANES), comprised women ages 18 to 45 between 2017 and 2020. Participants without waist circumference data or information on infertility were removed from the study. The independent relationship between waist circumference and infertility was investigated using weighted binary logistic regression and subgroup analysis. Results: We investigated 1509 participants and discovered that the prevalence of infertility rose as the WC trisection rose. (tertile 1, 7.55%; tertile 2, 10.56%; tertile 3, 15.28%; trend < 0.001). Multivariate logistic regression showed that after total adjustment, higher WC levels were associated with an increased likelihood of infertility in women (OR1.02; 95% CI 1.01-1.03), and There was a 2% rise in the incidence of infertility for every unit (cm) increased WC. Subgroup analysis and interaction tests showed no significant dependence of the effects of marital status, diabetes, hypertension, and high cholesterol on the association between WC and infertility (p for all interaction tests > 0.05). The inflection point of the positive non-linear relationship between WC and infertility was 116.6 cm. Conclusion: Excessive waist circumference assessment may increase the probability of infertility, and more attention should be paid to the management of waist circumference should be given more attention.

[Ecological network construction and optimization in Foshan City, China]. / 佛山市生态网络构建及优化.

Under the background of rapid urbanization, the problem of fragmented habitat patches in economically developed areas is particularly prominent, where biodiversity is seriously threa-tened. Therefore, the construction of ecological network is an important measure to connect habitat patches and protect biological habitats. We extracted ecological source areas of Foshan City by using the connectivity index and morphological spatial pattern analysis (MSPA). Potential ecological corridors were identified based on InVEST model and minimal cumulative resistance (MCR). Combining the radiation channels extracted from hydrological analysis to build an ecological network in Foshan City. The ecological network was optimized by adding ecological source areas, stepping stones, and identifying fracture points. Finally, the network before and after optimization was evalua-ted from the aspects of both structure and function based on network analysis method and circuit theory. The results showed that ecological network in Foshan City was composed of 10 ecological source areas, 8 important corridors, 37 general corridors, and 11 radiation channels. After optimization, 7 new ecological source areas, 17 planning corridors, 13 stepping stones, and 80 fracture points were added. After optimization, the ecological network closure, the line rate index and the connection degree index were 0.59, 1.94, and 0.73, respectively. The maximum current density increased from 1.39 to 9.66 after optimization, indicating that the optimized ecological network structure was more perfect and highly connective.

Downregulation of lncRNA IGF2-AS-encoded peptide induces trophoblast - cycle arrest.

RESEARCH QUESTION: lncRNA IGF2-AS may be related to early pregnancy loss. Does lncRNA IGF2-AS affect trophoblast cell growth? The aim of the present study was to verify that lncRNA IGF2-AS encodes a polypeptide, IGF2-AS-168aa, and to study its role in the pathogenesis of trophoblasts. DESIGN: A small interfering RNA targeted to the IGF2-AS gene (si-IGF2-AS) was designed and transfected into JEG-3 and JAR cells for in-vitro gene silencing. Quantitative polymerase chain reaction and western blotting were used to determine lncRNA IGF2-AS levels in experimental cells. After IGF2-AS suppression, MTT assay was used to assess cell proliferation and apoptosis was determined by flow cytometry. Target gRNA IGF2-AS-gRNA was designed for knockout conducted the corresponding mRNA. HEK293T cells were transfected with the identified positive clone vectors. Finally, IGF2-AS-168aa was analysed by western blotting after the protein-coding region of the IGF2-AS gene was knocked out by CRISPR/Cas9 gene-editing technology. RESULTS: lncRNA IGF2-AS and IGF2-AS-168aa were significantly downregulated in JEG-3 and JAR cells transfected with si-IGF2-AS (lncRNA IGF2-AS: JAR: NC versus small interfering RNA (siRNA)-1: P = 0.019 NC versus siRNA-2: P = 0.013; JEG-3: NC versus siRNA-1: P = 0.001 NC versus siRNA-2: P = 0.004) (IGF2-AS-168aa: JAR: NC versus siRNA-1: P = 0.030 NC versus siRNA-2: P = 0.018; JEG-3: NC versus siRNA-1: P = 0.004 NC versus siRNA-2: P = 0.001). IGF2-AS gene was incapable of encoding IGF2-AS-168aa after the coding region was successfully knocked out in HEK293T cells. Flow cytometry and the MTT assay revealed that IGF2-AS gene silencing led to cell cycle block in the G1 phase, markedly decreasing cell proliferation and increasing apoptosis. CONCLUSION: The IGF2-AS gene encoded a peptide with a potential function in trophoblast cell cycle arrest.

Induction of apoptosis and ferroptosis by a tumor suppressing magnetic field through ROS-mediated DNA damage.

Magnetic field (MF) is being used in antitumor treatment; however, the underlying biological mechanisms remain unclear. In this study, the potency and mechanism of a previously published tumor suppressing MF exposure protocol were further investigated. This protocol, characterized as a 50 Hz electromagnetic field modulated by static MF with time-average intensity of 5.1 mT, when applied for 2 h daily for over 3 consecutive days, selectively inhibited the growth of a broad spectrum of tumor cell lines including lung cancer, gastric cancer, pancreatic cancer and nephroblastoma. The level of intracellular reactive oxygen species (ROS) increased shortly after field exposure and persisted. Subsequently, pronounced DNA damage and activation of DNA repair pathways were identified both in vitro and in vivo. Furthermore, use of free radical scavenger alleviated DNA damage and partially reduced cell death. Finally, this field was found to inhibit cell proliferation, and simultaneously induced two types of programmed cell death, apoptosis and ferroptosis. In conclusion, this tumor suppressing MF could determine cell fate through ROS-induced DNA damage, inducing oxidative stress and activation of the DNA damage repair pathways, eventually lead to apoptosis and ferroptosis, as well as inhibition of tumor growth.