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Background: Previous studies have shown that changes in the microbial community of the female urogenital tract are associated with Human papillomavirus (HPV) infection. However, research on this association was mostly focused on a single site, and there are currently few joint studies on HPV infection and multiple sites in the female urogenital tract. Methods: We selected 102 healthy women from Yunnan Province as the research object, collected cervical exfoliation fluid, vaginal, urethral, and rectal swabs for microbial community analysis, and measured bacterial load, and related cytokine content. The link between HPV, microbiota, and inflammation was comprehensively evaluated using bioinformatics methods. Findings: The impact of HPV infection on the microbial composition of different parts varies. We have identified several signature bacterial genera that respond to HPV infection in several detection sites, such as Corynebacterium, Lactobacillus, Campylobacter, and Cutibacterium have been detected in multiple sites, reflecting their potential significance in cross body sites HPV infection responses. There was a solid microbial interaction network between the cervix, vagina, and urethra. The interrelationships between inflammatory factors and different bacterial genera might also affect the immune system's response to HPV infection. Interpretation: It might be an effective strategy to prevent and treat HPV infection by simultaneously understanding the correlation between the microbial changes in multiple parts of the female urogenital tract and rectum and HPV infection, and controlling the microbial network related to HPV infection in different parts. [ABSTRACT FROM AUTHOR]

In this paper, the preconditioned generalized accelerated overrelaxation (GAOR) methods for solving weighted linear least squares problems are considered. Two new preconditioners are proposed and the convergence rates of the new preconditioned GAOR methods are studied. Comparison results show that the convergence rates of the new preconditioned GAOR methods are better than those of the preconditioned GAOR methods in the previous literatures whenever these methods are convergent. A numerical example is given to confirm our theoretical results. [ABSTRACT FROM AUTHOR]

Background and Aim: Cohort studies have linked metabolic syndrome (MetS) to gastrointestinal (GI) cancer risk. We aimed to evaluate the associations between MetS, its components, and combinations of MetS components with eight GI cancers risk. Methods: We conducted a systematic search of prospective cohort studies and performed a meta‐analysis. Subgroup analyses regarding diagnostic criteria, sex, cancer sites, histological subtypes, ethnic groups, and studies adjusted for alcohol consumption were carried out. Mendelian randomization (MR) was employed to evaluate the causality between 17 MetS‐related traits and eight GI cancers among Europeans and Asians separately. Results: Meta‐analyses of 31 prospective studies indicated that MetS was significantly associated with an increased risk of colorectal cancer (CRC) (RR [95% CI] = 1.13 [1.12–1.15]), esophageal cancer (EC) (RR [95% CI] = 1.17 [1.03–1.32]), gallbladder cancer (GBC) (RR [95% CI] = 1.37[1.10–1.71]), liver cancer (LC) (RR [95% CI] = 1.46 [1.29–1.64]), and pancreatic cancer (PaC) (RR [95% CI] = 1.25 [1.20–1.30]), but not gastric cancer (GC) (RR [95% CI] = 1.11 [0.96–1.28]). Regarding the associations between MetS components and GI cancers risk, the following associations showed statistical significance: obesity‐CRC/LC/EC/, hypertriglyceridemia‐LC/PaC, reduced high‐density lipoprotein (HDL)‐CRC/LC/GC/PaC, hyperglycemia‐CRC/LC/PaC, and hypertension‐CRC/LC/EC/PaC. Sex‐specific associations were observed between individual MetS components on GI cancers risk. Among the top three common combinations in both sexes, obesity + HTN + hyperglycemia had the strongest association with CRC risk (RR [95% CI] = 1.54 [1.49–1.61] for males and 1.27 [1.21–1.33] for females). MR analyses revealed causality in 16 exposure–outcome pairs: waist‐to‐hip ratio/BMI/HbA1c‐CRC; BMI/childhood obesity/waist circumference/T2DM/glucose‐EC; BMI/waist circumference/cholesterol‐LC; cholesterol/childhood obesity/waist circumference/HbA1c‐PaC; and HbA1c‐GBC. These results were robust against sensitivity analyses. Conclusions: Since MetS is reversible, lifestyle changes or medical interventions targeting MetS patients might be potential prevention strategies for GI cancers. [ABSTRACT FROM AUTHOR]

The comorbidities between gastroesophageal reflux disease (GERD) and various neurodegenerative and psychiatric disorders have been widely reported. However, the genetic correlations, causal relationships, and underlying mechanisms linking GERD to these disorders remain largely unknown. Here, we conducted a bidirectional Mendelian randomization (MR) analysis to determine the causality between GERD and 6 neurodegenerative and psychiatric disorders. Sensitivity analyses and multivariable MR were performed to test the robustness of our findings. Linkage disequilibrium score regression was used to assess the genetic correlation between these diseases as affected by heredity. Multiple bioinformatics tools combining two machine learning algorithms were applied to further investigate the potential mechanisms underlying these diseases. We found that genetically predicted GERD significantly increased the risk of Alzheimer's disease, major depressive disorder, and anxiety disorders. There might be a bidirectional relationship between GERD and insomnia. GERD has varying degrees of genetic correlations with AD, ALS, anxiety disorders, insomnia, and depressive disorder. Bioinformatics analyses revealed the hub shared genes and the common pathways between GERD and 6 neurodegenerative and psychiatric disorders. Our findings demonstrated the complex nature of the genetic architecture across these diseases and clarified their causality, highlighting that treatments for the cure or remission of GERD may serve as potential strategies for preventing and managing neurodegenerative and psychiatric disorders. [ABSTRACT FROM AUTHOR]