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Purpose: Studies have demonstrated that hormonal imbalance, such as elevated level of estrogen or reduced level of progesterone, was the main inducing factor of uterine leiomyoma (UL) development and some cancers. UL has been reported to be associated with several cancers in observational studies. However, the causal associations between UL and cancers remain unclear. Methods: A two-sample Mendelian randomization (MR) analysis was conducted to investigate the causal associations between UL and 16 site-specific cancers using the public databases. Four methods, namely, the inverse variance weighting (IVW), MR-Egger, weighted median, and weighted mode, were applied in our MR analysis. Sensitivity tests were also performed to evaluate the robustness of these causal associations. Results: The IVW analysis indicated that genetically predicted UL increased the risk of low malignant potential ovarian cancer [odds ratio (OR) = 1.22, 95% confidence interval (CI): 1.06-1.40, p = 0.004], serous ovarian cancer (OR = 1.29, 95% CI: 1.10-1.52, p = 0.002), invasive mucinous ovarian cancer (OR = 1.24, 95% CI: 1.08-1.44, p = 0.003), clear cell ovarian cancer (OR = 1.25, 95% CI: 1.03-1.51, p = 0.023), breast cancer (OR = 1.07, 95% CI: 1.02-1.11, p = 0.002), and brain tumor (OR = 1.23, 95% CI: 1.06-1.42, p = 0.007). Conversely, genetically predicted UL reduced the risk of gastric cancer (OR = 0.91, 95% CI: 0.85-0.98, p = 0.008). The causal effects were consistent in the sensitivity analysis. Conclusions: Our results demonstrated that UL exhibits a causal relationship with high risk of several cancers. We suggest reinforcing the cancer screening in UL patients to enable the early detection of cancers. [ABSTRACT FROM AUTHOR]

Background: The causal relationship between juvenile idiopathic arthritis (JIA) and primary ovarian failure (POF) remains uncertain. To elucidate this relationship, we employed a two-sample Mendelian randomization analysis. Methods: The single nucleotide polymorphisms (SNPs) associated with JIA were obtained from a previously published genome-wide association study (GWAS), while the pooled data for POF originated from the FinnGen consortium. The study populations consisted exclusively of individuals of European descent. In our Mendelian randomization analysis, we performed inverse-variance weighted analysis, weighted-median analysis, weighted-mode analysis and Mendelian randomization-Egger regression analysis, supplemented by sensitivity analyses to validate the accuracy and robustness of the findings. Results: The IVW (OR = 1.23, 95% CI 1.06-1.43; P = 0.007) and weighted median (OR = 1.25, 95% CI 1.06-1.47; P = 0.009), along with sensitivity analysis validation, provide compelling evidence of a significant causal association between JIA and POF. Conclusion: The study revealed a significant causal association between genetically predicted JIA and POF, indicating that JIA significantly elevates the risk of developing POF. Therefore, it is recommended to implement screening for premature ovarian failure in women diagnosed with JIA. [ABSTRACT FROM AUTHOR]

The human microbiota influences physiology, disease, and metabolic reproduction. The origin of uterine bacteria is controversial. The main assumption is that the germs enter the uterine cavity from the vagina through the cervical canal, bloodstream, fallopian tubes, and gynecological surgical channels. Understanding the microbiota at various anatomical sites is critical to the female reproductive system and pregnancy. Today's study focuses on the role of uterine bacteria in pregnancy and embryo implantation. According to our findings, the uterine microbiome influences embryo implantation and pregnancy outcome. Pregnancy is a natural, evolutionarily selected approach to human reproduction. During pregnancy, the microbiota of the reproductive tract changes, facilitating the maintenance of pregnancy, and the human immune system undergoes a series of changes that recognize and adapt to the non-self. From the beginning of pregnancy, a non-self fetus must establish a placenta of embryonic origin to protect itself and promote growth; the VMB tends to be more stable and lactobacillusdominated in late gestation than in early gestation. Any material that disrupts this connection, such as microbial changes, is associated with a higher risk of poor health and poor pregnancy outcomes in women (eclampsia). The presence of any material that disrupts this connection, such as microbial changes, is associated with a higher risk of poor health and poor pregnancy outcomes (preeclampsia, preterm birth, gestational diabetes, etc.). In this work, we review the last decade of relevant research to improve our understanding of the mechanisms by which the microbiota of the female reproductive tract influences female reproductive health. This work discusses the mechanisms associated with the reproductive tract microbiota and pregnancy immunity, aswell as the impact of an abnormal microbiota on adverse pregnancy outcomes. Emphasis is placed on the characteristics and sources of the female vaginal, uterine, and placental microbiota and the importance of a well-stabilized local human microbiota and immune system for embryo implantation, placental development, fetal growth, and pregnancy outcome. [ABSTRACT FROM AUTHOR]

Candida albicans (C. albicans) is the most common causative agent of invasive fungal infections in hospitals. The body defends against and eliminates C. albicans infection by various mechanisms of immune response, and the latter mechanism of immune evasion is a major challenge in the clinical management of C. albicans infection. The role of macrophages in combating C. albicans infection has only recently been recognized, but the mechanisms remain to be elucidated. This review focuses on the interaction between C. albicans and macrophages (macrophages), which causes the body to generate an immune response or C. albicans immune escape, and then regulates the body's immune microenvironment, to explore the effect of C. albicans virulence resistance vs. macrophage killing and clarify the role and mechanism of C. albicans pathogenesis. In general, a thorough understanding of the molecular principles driving antifungal drug resistance is essential for the development of innovative treatments that can counteract both existing and emerging fungal threats. [ABSTRACT FROM AUTHOR]

The vaginal microbiota, the host endocrine system, the vaginal anatomy, and the local mucosal immunity comprise the vaginal microbiota, which interacts with each other to maintain the balance of the vaginal microbiota, which maintains female reproductive health. Puberty, menstruation, pregnancy, and menopause are four phases women go through during their reproductive and post-reproductive years. Vaginal microbiota composition and abundance are heavily influenced by estrogen and progesterone, which start at puberty and continue during the reproductive years in a dynamic balance with some fluctuations. Estrogen promotes proliferation of vaginal epithelial cells and increases glycogen storage, while progesterone lyses vaginal epithelial cells, facilitating the release of glycogen to maintain normal pH. This review summarizes the latest national and international evidence on the composition and distribution of vaginal microecology in women during different physiological and pathological periods and proposes a hormonedriven microbial diversity hypothesis to explain the temporal patterns of vaginal microbial diversity during the female reproductive cycle and menopause. A relatively balanced vaginal microecological system has a positive effect on the maintenance of female health. An imbalance in the ratio of flora can lead to susceptibility to infections or reproductive complications. The study of human microecology and its role in the development and progression of human disease is essential for the prevention, diagnosis, and treatment of related obstetric and gynecologic conditions. [ABSTRACT FROM AUTHOR]

Placenta-specific 8 (PLAC8) is closely associated with the proliferation, apoptosis and autophagy of several tumor cells. However, the expression and function of PLAC8 in oral squamous cell carcinoma (OSCC) remain unknown. Therefore, the present study investigated the function and mechanism of PLAC8 in OSCC. Reverse transcription-quantitative PCR and western blot analyses were performed to quantify the expression of PLAC8 in OSCC cell lines. The function of PLAC8 in OSCC was investigated via transfection, the Transwell and Cell Counting Kit-8 assays, immunofluorescence staining and western blotting. The results demonstrated that PLAC8 exspression was downregulated in OSCC cell lines. PLAC8 inhibited the cell proliferation in OSCC. In addition, PLAC8 restrained invasion and epithelialmesenchymal transition of OSCC cells. Furthermore, β-catenin helped to repress PLAC8 expression by regulating the Wnt/β- catenin and PI3K/Akt/GSK3β signaling pathways in OSCC cells. Collectively, the results of the present study suggest that PLAC8 acts as a tumor suppressor in OSCC by downregulating β-catenin. [ABSTRACT FROM AUTHOR]

We attempted to analyze the effects of miR-1-3p and CCL2 on the proliferation, migration, and invasion of bladder cancer cells. A total of 18 pairs of bladder cancer tissues with corresponding adjacent tissues and the 6 cases of normal tissues were collected. The expressions of miR-1-3p and CCL2 in the cancer tissues were evaluated using quantitative real-time polymerase chain reaction and western blot. The relationship between miR-1-3p and CCL2 was assessed using luciferase reporter assay. The UM-UC-3 bladder cancer cells were transfected with CCL2 small interfering RNA and miR-1-3p mimics. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, colony formation assay, wound healing assay, Transwell assay, and the flow cytometry test were used to detect the proliferation, migration, invasion, and apoptosis of bladder cancer cells. Bladder cancer tissues had lower levels of miR-1-3p but higher levels of CCL2 than normal tissues (p < 0.05). The transfection of miR-1-3p mimics and CCL2 small interfering RNA remarkably suppressed cell proliferation and invasion and promoted apoptosis of cells (p < 0.05). Results of the luciferase reporter gene assay demonstrated that miR-1-3p targeted CCL2. MiR-1-3p suppresses the proliferation and invasion of urinary bladder cancer cells by targeting CCL2. [ABSTRACT FROM AUTHOR]