Clinical Value and Mechanism Exploration of Serum miR-379 in Obesity-Polycystic Ovary Syndrome.

Objective: As a common endocrine and metabolic disorder, polycystic ovary syndrome (PCOS) is mostly associated with an obese phenotype. The present research focuses on the clinical significance of miR-379 in obesity-PCOS and attempts to elucidate its potential mechanisms. Methods: Healthy individuals (n = 46), obesity-PCOS (n = 92), and non-obesity PCOS (n = 31) subjects were enrolled. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to examine the level of serum miR-379. The receiver operating characteristic (ROC) curve and logistic regressions were applied to reveal the diagnostic significance. Dual luciferase reporters were performed to validate the targeting relationships. And cell count kit (CCK-8) assay was used to detect cell proliferation. Results: Serum miR-379 was highly expressed in PCOS patients (P < 0.05), in especially obesity-PCOS patients. Higher miR-379 was associated with greater body mass index (BMI), higher bioavailable testosterone (bT), and greater insulin resistance (IR). Additionally, miR-379 was an independent risk factor for the development of obesity-PCOS. The sensitivity of miR-379 in identifying patients with obesity-PCOS from healthy or non-obesity-PCSO patients was 81.52% and 72.83%, and the specificity was 86.96% and 80.65%. Semaphorin 3 A (SEMA3A) was identified as a target of miR-379 and was reduced in the patients with obesity PCOS (P < 0.05). Inhibition of miR-375 reduced KGN proliferation, but this reduction was partially restored by silencing of SEMA3A (P < 0.05). Conclusion: Elevated miR-379 assists the diagnosis of obesity-PCOS and regulates the proliferation of KGN by targeting SEMA3A engaged in disease development.

Immune Cells in the Spleen of Mice Mediate the Inflammatory Response Induced by Mannheimia haemolytica A2 Serotype.

(1) Background: Mannheimia haemolytica (M. haemolytica) is an opportunistic pathogen and is mainly associated with respiratory diseases in cattle, sheep, and goats. (2) Methods: In this study, a mouse infection model was established using a M. haemolytica strain isolated from goats. Histopathological observations were conducted on various organs of the mice, and bacterial load determination and RNA-seq analysis were specifically performed on the spleens of the mice. (3) Results: The findings of this study suggest that chemokines, potentially present in the spleen of mice following a M. haemolytica challenge, may induce the migration of leukocytes to the spleen and suppress the release of pro-inflammatory factors through a negative feedback regulation mechanism. Additionally, an interesting observation was made regarding the potential of hematopoietic stem/progenitor cells congregating in the spleen to differentiate into immune cells, which could potentially collaborate with leukocytes in their efforts to counteract M. haemolytica invasion. (4) Conclusions: This study revealed the immune regulation mechanism induced by M. haemolytica in the mouse spleen, providing valuable insights into host-pathogen interactions and offering a theoretical basis for the prevention, control, and treatment of mannheimiosis.

Effect of maternal oxygen supplementation for parturient undergoing elective cesarean section by high-flow nasal oxygen compared with room air on fetal acidemia: study protocol for a randomized controlled trial.

BACKGROUND: Maternal oxygen supplementation is usually used as an intrauterine resuscitation technique to prevent fetal hypoxia and acidemia during delivery. However, there has been a great deal of controversy regarding the effects of prophylactic maternal oxygen during cesarean section, during which the incidence of fetal acidemia seems to be higher compared with that during labor. High-flow nasal oxygen (HFNO) can improve oxygenation better in patients with high-flow oxygen airflow. The purpose of this study is to determine whether maternal oxygen supplementation with HFNO has a positive effect on fetal acidemia during cesarean section through umbilical arterial blood gas analysis. METHOD: This prospective, single-center, randomized, double-blinded trial will enroll 120 patients undergoing cesarean section. Participants will be randomly assigned to the HFNO group or air group at a 1:1 ratio. For parturients in the HFNO group, the flow rate is 40L/min, and the oxygen is heated to 37℃ with humidity 100% oxygen concentration through the Optiflow high-flow nasal oxygen system. And for the air group, the flow rate is 2 L/min with an air pattern through the same device. The primary outcome was umbilical artery (UA) lactate. Secondary outcomes include UA pH, PO2, PCO2, BE, the incidence of pH < 7.20 and pH < 7.10, Apgar scores at 1 and 5 min, and neonatal adverse outcomes. DISCUSSION: Our study is the first trial investigating whether maternal oxygen supplementation with HFNO can reduce the umbilical artery lactate levels and the incidence of fetal acidemia in cesarean section under combined spinal-epidural anesthesia. TRIAL REGISTRATION: ClinicalTrials.gov NCT05921955. Registered on 27 June 2023.

Sheep and goat pathogen database: a pathogen data integration and analysis database of sheep and goat infectious diseases.

The prevalence of infectious diseases in sheep and goats has a significant impact on the development of the sheep and goat industry and public health security. The identification and analysis of pathogens are crucial for infectious disease research; however, existing databases pay little attention to sheep and goat diseases, and pathogen data are relatively scattered. Therefore, the effective integration, analysis and visualization of these data will help us conduct in-depth research on sheep and goat infectious diseases and promote the formulation of disease prevention and control strategies. This article considered the pathogens of 44 infectious diseases in sheep and goats as the main research objects and collected and downloaded relevant scientific literature, pathogen genomes, pathogen transcriptomes, pathogen occurrence records, and other data. The C# programming language and an SQL Server database were used to construct and realize the functions of the Sheep and Goat Pathogen Database (SGPD) within a B/S architecture based on the ASP.NET platform. The SGPD mainly provides an integrated platform for sheep and goat pathogen data retrieval, auxiliary analysis, and user upload, including several functionalities: (1) a Disease Introduction module that queries basic information regarding the 44 recorded sheep and goat infectious diseases, such as epidemiology, clinical characteristics, diagnostic criteria, and prevention and control measures; (2) an Omics Information module that allows users to query and download the genome and transcriptome data related to the pathogens of sheep and goat infectious disease, and provide sequence alignment functionality; (3) a Pathogen Structure module that enables users to view electron micrographs of pathogen structure and tissue sections related to sheep and goat disease from publicly published research; (4) a Literature Search module based on the "Pathogen Dictionary" search strategy that facilitates searches for published research related to pathogens of infectious disease; (5) a Science Popularization module that allows users to view popular science materials related to sheep and goat infectious diseases; and (6) a Public Health module that allows users to query the risk factors of zoonotic disease transmission and the corresponding related literature, and realize the visualization of pathogen distribution. The SGPD is a specialized sheep and goat pathogen information database that provides comprehensive resources and technical support for sheep and goat infectious disease research, prevention, and control.

Overexpression of Nuclear Enriched Autosomal Transcript 1 Facilitates Cell Proliferation, Migration Invasion, and Suppresses Apoptosis in Endometrial Cancer by Targeting MicroRNA-202-3p/T Cell Immunoglobulin and Mucin Domain 4 Axis.

Background: Endometrial cancer (EC) is an intractable gynecological cancer with increasing incidence and mortality worldwide. Accumulating studies indicated that long noncoding RNA nuclear enriched autosomal transcript 1 (NEAT1) was a novel oncogene implicated in a variety of cancers. However, whether NEAT1 could accelerate cell growth in EC is unclear. Materials and Methods: NEAT1, microRNA (miR)-202-3p, and T cell immunoglobulin and mucin domain 4 (TIMD4) levels were detected by quantitative real-time polymerase chain reaction. Cell proliferation and apoptosis were examined by cell counting kit-8 and flow cytometry. Transwell assay was employed for the evaluation of cell migration and invasion. The relationship between miR-202-3p and NEAT1 or TIMD4 was determined by luciferase reporter system. TIMD4 protein expression was assessed by Western blot assay. Results: NEAT1 was upregulated, whereas miR-202-3p was downregulated in EC tumors and cells. Depletion of NEAT1 restrained EC cell proliferation, migration, invasion, and improved apoptosis. MiR-202-3p was targeted by NEAT1 and could bind to TIMD4. Subsequently, it is observed that miR-202-3p inhibitor neutralized NEAT1 silencing mediated suppression on EC cell progression. Meanwhile, TIMD4 rescued miR-202-3p induced inhibition on cell progression in EC. Furthermore, it was obvious that NEAT1 facilitated TIMD4 expression by absorbing miR-202-3p in EC. Conclusions: Upregulation of NEAT1 accelerated EC cell progression through sponging miR-202-3p to facilitate TIMD4 expression, providing potential novel treatment method for EC.

[Imbalance between Th1 and Th2 cells in cord blood is influenced by maternal allergic rhinitis and associated with atopic dermatitis during the first two years of life].

OBJECTIVE: To investigate the influence of maternal atopy on cord blood effector T cells and to identify these biologic markers as predictors of atopic dermatitis (AD). METHODS: Seventy mother-infant pairs were recruited in this prospective birth cohort study. Suspected factors for allergy, including maternal allergic history, total serum IgE, and maternal age at birth, were collected. Mother peripheral blood samples and cord blood were obtained and assayed for the percentage of interferon-γ (IFN-γ) and interleukin 4 (IL-4) producing T cells(Th1 and Th2 respectively) using flow cytometry. Their offspring at the age of 2 years old were evaluated by their dermatologist whether they had AD. Statistical analysis was performed using multiple logistic regression models and receiver-operating characteristic curve was employed to predict atopic dermatitis. RESULTS: Twenty-one allergic and 49 nonallergic mothers were recruited in this study. During the first two years of life, 15.7% children (n = 11) developed a physician-diagnosed AD (all children were the only child in the family). In group with maternal allergic rhinitis, a significantly increased percentage of Th2 was observed in peripheral blood of mother (7.10[1.18;16.1]% vs. 0.37[0.25;0.72]%, U = 10.0, P < 0.05) and cord blood of newborns (1.02[0.57;1.34]% vs. 0.21[0.15;0.42]%, U = 127.5, P < 0.05), respectively. Maternal atopic history did not affect the percentage of Th1 cells in cord blood (0.69[0.40;1.12]% vs.0.50[0.31;0.66]%, U = 361.0, P > 0.05). Children with reduced Th1/Th2 ratio in cord blood had a higher risk to develop AD (OR = 1.72, P = 0.001) . The model including Th1/Th2, maternal allergy, maternal age at birth and maternal total IgE showed high ability to discriminate children with and without AD. AUC was 0.907 (95% CI: 0.804-1.011, P < 0.001). CONCLUSIONS: Elevated IL-4⁺CD4⁺ T cells in cord blood were of relevance with maternal allergic history. Imbalance between Th1 cell and Th2 cell at birth are associated with maternal allergy and promoted subsequent AD development.

T cell subsets in cord blood are influenced by maternal allergy and associated with atopic dermatitis.

BACKGROUND: This study aimed to investigate the influence of maternal allergy on cord blood regulatory and effector T cells and to evaluate their role as a predictor of atopic dermatitis (AD) during the first 2 yr of life. METHODS: Seventy mother-infant pairs were recruited in this prospective birth cohort study (21 allergic and 49 non-allergic mothers). Cord blood samples were collected and assayed for the percentage of regulatory T cells (Treg), interferon-γ (IFN-γ), and interleukin-4 (IL-4) producing T cells (Th1 and Th2, respectively) using flow cytometry. Experiments were undertaken to assess the function of cord blood CD4(+) CD25(+) CD127(-) Treg cells by cell proliferation and cytokine responses. Their offspring at the age of 2 yr old were evaluated by dermatologists to determine whether they had AD. RESULTS: During the first 2 yr of life, 15.7% of the children developed a physician-diagnosed AD. A significantly increased percentage of Th2 cell was observed in cord blood of newborns with maternal allergy. Treg/Th2 ratio significantly decreased among the offspring of allergic mothers. Treg cell-associated suppression of Th2 response was attenuated in Der p1-stimulated CD4(+) CD25(-) T cells from the offspring of allergic mothers. Children with reduced Th1/Th2 (p = 0.001, OR = 0.37) and Treg/Th2 (p = 0.001, OR = 0.47) ratio in cord blood had a higher risk of developing AD. CONCLUSION: Maternal allergic status is associated with increased percentage of IL-4(+) CD4(+) T cells and a reduced Treg/Th2 ratio in cord blood at their children's birth, which may predispose to an increased risk for developing AD.

[Expression of cyclin D1 and p16 protein in vulvar white lesion].

OBJECTIVE: To investigate the relationship between cell cycle protein (cyclin D1 and p16) expression and vulvar white lesion. METHODS: Biopsies from 34 cases with vulvar white lesion, including 12 cases with lichen sclerosus (LS), 18 with squamous hyperplasia (SH) and 4 SH accompanied with LS, were examined for protein expression of cyclin D1 and p16 using immunohistochemical techniques. Normal vulvar tissues from 11 patients with other benign gynecologic diseases were used as control. RESULTS: Fifty-six percent of patients with vulvar white lesion were immunopositive for cyclin D1 protein, which was significantly higher than that of control group (9%, P < 0.05); but there was no significant difference between LS (58%) and SH patients (50%, P > 0.05) in expression of cyclin D1 protein. Immunopositive expression of p16 protein in patients was 6%, with no significant difference from the control group (0, P > 0.05). CONCLUSIONS: Cyclin D1 and p16 are important factors modulating cell cycle. The interrupt of balance between these two factors derived from abnormal expression of cyclin D1 may be one of the causes of vulvar white lesion.