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Objective. Primary bladder tumors have a high degree of malignancy. To investigate the expression of human papillomavirus type 16 (HPV-16) in primary bladder tumors and the loss of cell differentiation and to explore the significance of HPV-16 detection, it is expected to be a disease. Treatment provides a theoretical basis. Methods. Fifty-seven patients with primary bladder tumors admitted to our hospital from January 2019 to January 2022 were selected as the research subjects, and they were divided into HPV-related groups according to the human papillomavirus (HPV) infection status ( n = 28 ) and HPV unrelated group ( n = 29 ). The general data of patients were collected, the expression of HPV-16 in bladder tissue samples was detected, and the correlation between pathological parameters and HPV-16 expression was analyzed. Results. Among HPV subtypes, HPV 16 subtype accounted for the highest proportion, followed by HPV-18 and HPV-6 subtypes; there was no significant difference in tumor stage (stage 1, stage a, stage 2a) between the HPV-related group and the HPV-unrelated group (stage 1, stage a, and stage 2a). P > 0.05 ); there was no significant difference in postoperative pathological expression (high expression and low expression) of patients ( P > 0.05 ); there was no statistical difference in age and gender between HPV-related and HPV-unrelated groups ( P > 0.05 ), HPV-related group and HPV-unrelated group compared daily regular drinking and smoking status, the difference was statistically significant ( P < 0.05 ); HPV-16 expression was not correlated with tumor differentiation degree and age of patients ( P > 0.05 ); the area under the curve (AUC) of HPV-16 for judging primary bladder tumor expression and cellular molecular deletion was 0.891, with a sensitivity of 83.94% and a specificity of 88.57%. Conclusion. HPV-16 is an upper, expressed in primary bladder tumors and will participate in the differentiation and loss of cells, which can provide effective guidance and basis for the diagnosis of primary bladder tumors, which is an important factor for judging the pathological stage and prognosis of patients and can provide a theoretical reference for the formulation of therapeutic measures.

To explore the causal relationship between maternal smoking around birth and childhood asthma using Mendelian randomization (MR). Using the data from large-scale genome-wide association studies, we selected independent genetic loci closely related to maternal smoking around birth and maternal diseases as instrumental variables and used MR methods. In this study, we considered the inverse variance weighted method (MR-IVW), weighted median method, and MR-Egger regression. We investigated the causal relationship between maternal smoking around birth and maternal diseases in childhood asthma using the odds ratio (OR) as an evaluation index. Multivariable MR (MVMR) included maternal history of Alzheimer's disease, illnesses of the mother: high blood pressure and illnesses of the mother: heart diseaseas covariates to address potential confounding. Sensitivity analyses were evaluated for weak instrument bias and pleiotropic effects. It was shown with the MR-IVW results that maternal smoking around birth increased the risk of childhood asthma by 1.5% (OR = 1.0150, 95% CI: 1.0018–1.0283). After the multivariable MR method was used to correct for relevant covariates, the association effect between maternal smoking around birth and childhood asthma was still statistically significant (P &lt; 0.05). Maternal smoking around birth increases the risk of childhood asthma.

To explore the causal relationship between DNA methylation, Golgi membrane protein, endoplasmic reticulum aminopeptidase, ADP-ribose pyrophosphatase, mitochondrialon abnormal spermatozoa by two-sample Mendelian randomization (TSMR) method.Genetic loci closely related to DNA methylation PhenoAge acceleration, Golgi membrane protein 1, endoplasmic reticulum aminopeptidase 1, endoplasmic reticulum aminopeptidase 2, ADP-ribose pyrophosphatase, mitochondrial were selected as instrumental variables, andTSMR was performed by the inverse variance weighted method, MREgger regression, and weighted median method respectively. Sensitivity analysis was conducted to evaluate the robustness of the MR results.IVW showed that the DNA methylation PhenoAge acceleration(OR = 1.12, 95% CI: 1.01–1.23), Golgi membrane protein 1(OR = 1.22, 95% CI: 1.04–1.44), and endoplasmic reticulum aminopeptidase 2(OR = 1.13, 95% CI: 1.04–1.24) were associated with an increased risk of abnormal spermatozoa. However, there was no evidence of the association between ADP-ribose pyrophosphatase, mitochondrial (IVW OR = 1.25, 95% CI: 0.95–1.63), endoplasmic reticulum aminopeptidase 1 (IVW OR = 1.01, 95% CI: 0.90–1.12) and abnormal spermatozoa. Sensitivity analysis detected little evidence of pleiotropy in the current study.There is a positive causal relationship between DNA methylation PhenoAge acceleration, Golgi membrane protein 1, and endoplasmic reticulum aminopeptidase 2 on abnormal spermatozoa.