DataSheet_1_Mendelian randomization reveals the impact of diet on infertility in men and women.docx

BackgroundAlthough studies on the effects of diet on fertility has progressed, some cumulative evidence has piled against popular hypotheses. The aim of our study was to investigate the effects of 31 diets including 23 individual dietary intakes and 8 dietary habits on infertility in men and women.MethodsThe datas of diets and infertility were collected from genome-wide association studies (GWAS). Mendelian randomization (MR) methods were used to analyze causal relationships. Multivariate MR (MVMR) adjusted for the effects of other exposures on causality. And MR-Egger, Cochran’s Q, radial MR, and MR-PRESSO tests were employed to assess heterogeneity and horizontal pleiotropy.ResultsOur study found that coffee intake (OR, 3.6967; 95% CI, 1.0348 – 13.2065; P = 0.0442) and cooked vegetable intakes (OR, 54.7865; 95% CI, 2.9011 – 1030.5500; P = 0.0076) increased the risk of male infertility. For women, beer was a risk factor for infertility (OR, 4.0932; 95% CI, 1.8728 – 8.9461; P = 0.0004); but processed meat was negatively associated with infertility (OR, 0.5148; 95% CI, 0.2730 – 0.9705; P = 0.0401). MVMR demonstrated selenium as a protective factor against female infertility (OR, 7.4474e-12; 95% CI, 5.4780e-22 – 1.0125e-01; P = 0.0314).ConclusionWe found the causal relationships between four diets and infertility. We look forward to more high-quality epidemiologic studies to prove our conclusions.</p

DataSheet_1_Efficacy and toxicity of immune checkpoint inhibitors combination therapy for advanced renal cell carcinoma: a systematic review and network meta-analysis.docx

BackgroundAlthough immune checkpoint inhibitors (ICIs) show a significant overall survival advantage over standard advanced renal cell carcinoma (aRCC) therapies, tumor response to these agents remains poor. Some studies have shown that combination therapy including an ICI appears to be the best treatment; however, the overall benefit in terms of efficacy and toxicity still needs to be assessed. Thus, we performed a network meta-analysis to evaluate the differences in the efficacy of several combinations that include an ICI to provide a basis for clinical treatment selection.MethodsWe conducted a thorough search of PubMed, EMBASE, and the Cochrane Library for articles from January 2010 to June 2023. R 4.4.2 and STATA 16.0 were used to analyze data; hazard ratio (HR) and odds ratio (OR) with 95% confidence intervals (CI) were used to assess the results.ResultsAn indirect comparison showed that nivolumab plus cabozantinib and pembrolizumab plus lenvatinib were the most effective treatments for progression-free survival (PFS), with no significant differences between the two interventions (HR, 1.31; 95% CI, 0.96–1.78; P=0.08); rank probability showed that pembrolizumab plus lenvatinib had a 57.1% chance of being the preferred treatment. In the absence of indirect comparisons between pembrolizumab plus axitinib, nivolumab plus ipilimumab, avelumab plus axitinib, nivolumab plus cabozantinib, and pembrolizumab plus lenvatinib, pembrolizumab plus axitinib (40.2%) was the best treatment option for overall survival (OS). Compared to pembrolizumab plus lenvatinib, nivolumab plus ipilimumab (OR, 0.07; 95% CI, 0.01–0.65; P=0.02) and pembrolizumab plus axitinib (OR, 0.05; 95% CI, 0.00–0.78; PConclusionPembrolizumab plus lenvatinib and pembrolizumab plus axitinib resulted in the highest PFS and OS rates, respectively. Pembrolizumab plus axitinib may be the best option when AEs are a concern.Systematic review registrationhttps://inplasy.com/, identifier INPLASY202410078.</p

Effects of mCLCA3 antibody on OVA-induced airway inflammation.

<p>Histological examination of lung tissue by HE staining. (A) Control group; (B) Asthma group and (C) mCLCA3 antibody intervention group (magnification x400). (D) Quantitative analyses of airway inflammation in lung sections. Data are shown as mean ± SEM, n = 5. (*P<0.05, compared with the control group; ^#P<0.05, compared with the asthma group).</p

Effects of mCLCA3 antibody on muc5ac and cytokine levels in BALF.

<p>BALF was collected 24 h after the last OVA challenge. The muc5ac and cytokine levels were detected by ELISA. (A) The expression of muc5ac in BALF obtained from sensitized mice 24 h after the last PBS aerosol, OVA aerosol and OVA plus antibody intervention challenge. (B) The expression of IL-13 in BALF obtained from sensitized mice 24 h after the last PBS aerosol, OVA aerosol and OVA plus antibody intervention challenge. (C) The expression of IFN-γ in BALF obtained from sensitized mice 24 h after the last PBS aerosol, OVA aerosol and OVA plus antibody intervention challenge. Data are shown as mean± SEM, n = 5 (*P<0.05, compared with the control group; ^#P<0.05, compared with the asthma group).</p

Effects of mCLCA3 antibody on apoptosis-associated genes.

<p>(A) Bcl-2 and Bax expression in goblet cells was measured by immunohistochemistry (magnification x400). (B) Quantitative analyses of Bcl-2 and Bax expression levels in goblet cells. (C) The levels of Bcl-2 and Bax mRNA were detected by RT-PCR. (D) The expression of Bcl-2 and Bax in all groups of mice was analyzed by Western blotting. Bcl-2 and Bax expression levels were normalized with β-actin values and are expressed as fold changes compared to control. Data are shown as mean± SEM, n = 5 (*P<0.05, compared with the control group; ^#P<0.05, compared with the asthma group).</p

Effects of mCLCA3 antibody on OVA-induced goblet cell apoptosis.

<p>(A–C) Cell apoptosis was detected by TUNEL and AB staining. (A) The control group; (B) asthma group and (C) mCLCA3 antibody intervention group (magnification x400). (D) Quantitative analyses of goblet cell apoptosis in lung sections. Data are shown as mean± SEM, n = 5 (*P<0.05, compared with the control group; ^#P<0.05, compared with the asthma group).</p

Effects of mCLCA3 antibody on OVA-induced goblet cell hyperplasia and mCLCA3 expression.

<p>(A–C) Goblet cell hyperplasia was detected by PAS staining. (A) Control group; (B) Asthma group and (C) mCLCA3 antibody intervention group (magnification x400). (D-F) The expression of mCLCA3 in all groups was detected by immunohistochemistry. (D) Control group; (E) Asthma group and (F) mCLCA3 antibody intervention group (magnification x400). (G) Quantitative analyses of goblet cell hyperplasia in lung sections. (H) Quantitative analyses of mCLCA3 expression in lung sections. (I) The mRNA and protein level of mCLCA3 in PBS aerosol, OVA aerosol and OVA plus antibody intervention group. Data are shown as mean± SEM, n = 5 (*P<0.05, compared with the control group; ^#P<0.05, compared with the asthma group).</p