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Introduction Infertility affects over 186 million people globally, with about 1 in 7 couples in developed nations experiencing it. Causes include age-related fertility decline and environmental factors. Air pollution is a potential factor, but large-scale evidence is still lacking. This study examines the impact of several air pollutants on infertility in females aged 15 to 60, hypothesizing that air pollution increases infertility risks. Method We constructed a cohort in Taiwan between July 1, 2003, and December 31, 2013, using the National Health Insurance Research Database (NHIRD) of females aged 15 to 60. Concentrations of SO2, CO, O3, PM10, PM2.5, NOX, NO, NO2, THC, NMHC, and CH4 were estimated based on insurance registration. We calculated the HRs of exposure at a standard deviation increment for 10 years to determine the dose–response effect between air pollutants and infertility. Result Long-term exposure to SO2, CO, PM10, PM2.5, NOX, NO, NO2, THC, NMHC, and CH4 was associated with increased infertility in women of reproductive age. Each standard deviation increase in exposure to these pollutants was associated with a higher incidence of infertility by 13%, 116%, 35%, 77%, 80%, 66%, 76%, 116%, 52%, and 181%, respectively. Conversely, ozone exposure was associated with a 52% reduction in infertility risk. Conclusion This study demonstrates the significant impact of air pollution on female infertility, showing a clear dose–response relationship between exposure to various pollutants and infertility rates. These findings highlight the need for efforts to reduce air pollution and its effects on reproductive health. Further research is needed to understand the mechanisms and inform public health policies.

Purpose Results of previous studies have demonstrated that T-cell receptor cross-linking rapidly generates reactive oxygen species, which play essential signaling roles within mitochondria for the antigen-specific expansion of T-cells. However, oxidative stress also causes damage to cellular organelles. Thus, modulating ROS metabolism using antioxidants during naïve T-cell activation may promote the expansion and generation of functional T-cells. Notably, urothelial cancer is a sex-specific malignancy with high mortality rates worldwide. The present study aimed to evaluate the effects of various antioxidants on γδ T-cell proliferation, and the associated cytotoxicity against urothelial carcinoma cells (UCs). Methods Over a period of cell induction and expansion, peripheral blood mononuclear cells were cultured with or without different antioxidants, including N -acetyl cysteine (NAC), vitamin C and vitamin E. Subsequently, phenotypic characterization of γδ T-cells and their cytolytic effects against UCs were analyzed by flow cytometry and cell viability assays, respectively. Results and Conclusions The results revealed that NAC partially inhibited T-cell expansion in a dose-dependent manner. In addition, CD3 + /Vγ9 + levels and natural killer group 2D receptor expression were mildly reduced following treatment with a high dose of NAC, whereas CD3 + /CD56 + levels and CD314 expression in natural killer-like cells were moderately decreased following treatment with vitamin E. Particularly, the direct co-incubation of bladder cancer cells with γδ T-cells supplemented with antioxidants significantly enhanced bladder cancer cytolysis. Collectively, results of the present study revealed that co-administration of functional antioxidants during γδ T-cell expansion may enhance the quality and efficacy of adoptive T-cell therapies for cancer treatment.

Background and Objectives: This paper evaluates the efficacy and safety of ureteral access sheath (UAS) utilization in retrograde intrarenal surgery (RIRS). Materials and Methods: We searched PubMed, Embase, and the Cochrane Library up to 30 August 2023. The inclusion criteria comprised English-language original studies on RIRS with or without UAS in humans. The primary outcome was SFR, while the secondary outcomes included intraoperative and postoperative complications, the lengths of the operation and the hospitalization period, and the duration of the fluoroscopy. Subgroup analyses and a sensitivity analysis were performed. Publication bias was assessed using funnel plots and Egger’s regression tests. Dichotomous variables were analyzed using odds ratios (ORs) with 95% confidence intervals (CIs), while mean differences (MDs) were employed for continuous variables. Results: We included 22 studies in our analysis. These spanned 2001 to 2023, involving 12,993 patients and 13,293 procedures. No significant difference in SFR was observed between the UAS and non-UAS groups (OR = 0.90, 95% CI 0.63–1.30, p = 0.59). Intraoperative (OR = 1.13, 95% CI 0.75–1.69, p = 0.5) and postoperative complications (OR = 1.29, 95% CI 0.89–1.87, p = 0.18) did not significantly differ between the groups. UAS usage increased operation times (MD = 8.30, 95% CI 2.51–14.10, p = 0.005) and fluoroscopy times (MD = 5.73, 95% CI 4.55–6.90, p < 0.001). No publication bias was detected for any outcome. Conclusions: In RIRS, UAS usage did not significantly affect SFR, complications, or hospitalization time. However, it increased operation time and fluoroscopy time. Routine UAS usage is not supported, and decisions should be patient-specific. Further studies with larger sample sizes and standardized assessments are needed to refine UAS utilization in RIRS.

Background and objective Prostate cancer is a critical health issue, particularly in developed countries. Emerging evidence suggests that air pollution is associated with increased risk of prostate cancer. This study aimed to evaluate the impact of long-term exposure to seven specific air pollutants on prostate cancer risk in Taiwanese men and establish dose-response relationships to guide prevention strategies. Methods This retrospective cohort study analyzed the data of 425,916 men from Taiwan’s National Health Insurance Research Database (2000–2013). Seven pollutants (SO 2 , CO, PM 10 , PM 2.5 , NO x , NO, and NO 2 ) were assessed and Cox regression models were adjusted for confounders. Prostate cancer incidence was the primary outcome, with significance set at P  < 0.05. Key findings and limitations Increased exposure to air pollutants was associated with a 39–106% higher risk of prostate cancer per 1 standard deviation increase in pollutant levels. However, potential misclassification of exposure is a key limitation. Conclusions and clinical implications In over 400,000 Taiwanese men, higher levels of several air pollutants were associated with a greater likelihood of developing prostate cancer. These findings suggest that air pollution may be an important environmental factor in prostate cancer etiology. Further research is needed to confirm these associations before informing clinical practice or public health policy.

The COVID-19 pandemic prompted the rapid development of vaccines, including the ChAdOx1 nCov-19 (AstraZeneca) vaccine. While effective, adverse effects have been reported, including cutaneous manifestations. Kaposi sarcoma (KS), a vascular tumor linked to Kaposi sarcoma herpesvirus/human herpesvirus 8 (HHV-8), has seen increased detection during the pandemic. This study reports a case of classic cutaneous KS in a 79-year-old male following the first dose of the ChAdOx1 nCov-19 vaccine, without prior SARS-CoV-2 infection. The patient developed multiple reddish-blue papules on his legs and feet, confirmed as KS through histopathology. Treatment included radiotherapy and sequential chemotherapy with Doxorubicin. The potential reactivation of latent HHV-8 by the vaccine is explored through mechanisms involving the SARS-CoV-2 spike protein and adenovirus vector, which may induce immune responses and inflammatory pathways. Although establishing a direct causal link remains challenging, the case highlights the need for vigilance regarding KS reactivation post-vaccination. Further large-scale studies are warranted to elucidate the relationship between COVID-19 vaccines and latent virus reactivation, ensuring comprehensive safety assessments and informed public health decisions.

To enhance postoperative patient survival, particularly in older adults, understanding the predictors of mortality following hip fracture becomes paramount. Air pollution, a prominent global environmental issue, has been linked to heightened morbidity and mortality across a spectrum of diseases. Nevertheless, the precise impact of air pollution on hip fracture outcomes remains elusive. This retrospective study aims to comprehensively investigate the profound influence of a decade-long exposure to 12 diverse air pollutants on the risk of post-hip fracture mortality among older Taiwanese patients (older than 60 years). We hypothesized that enduring long-term exposure to air pollution would significantly elevate the 1-year mortality rate following hip fracture surgery. From Taiwan's National Health Insurance Research Database, we obtained the data of patients who underwent hip fracture surgery between July 1, 2003, and December 31, 2013. Using patients' insurance registration data, we estimated their cumulative exposure levels to sulfur dioxide (SO ), carbon dioxide (CO ), carbon monoxide (CO), ozone (O ), particulate matter having a size of <10 μm (PM ), particulate matter having a size of <2.5 μm (PM ), nitrogen oxides (NO ), nitrogen monoxide (NO), nitrogen dioxide (NO ), total hydrocarbons (THC), nonmethane hydrocarbons (NMHC), and methane (CH ). We quantified the dose-response relationship between these air pollutants and the risk of mortality by calculating hazard ratios associated with a 1 SD increase in exposure levels over a decade. Long-term exposure to SO , CO, PM , PM , NO , NO, NO , THC, NMHC, and CH demonstrated significant associations with heightened all-cause mortality risk within 1 year post hip fracture surgery among older adults. For older adults, each 1 SD increment in the average exposure levels of SO , CO, PM , PM , NO , NO, NO , THC, NMHC, and CH corresponded to a substantial escalation in mortality risk, with increments of 14%, 49%, 18%, 12%, 41%, 33%, 38%, 20%, 9%, and 26%, respectively. We further noted a 35% reduction in the hazard ratio for O exposure suggesting a potential protective effect, along with a trend of potentially protective effects of CO . This comprehensive nationwide retrospective study, grounded in a population-based approach, demonstrated that long-term exposure to specific air pollutants significantly increased the risk of all-cause mortality within 1 year after hip fracture surgery in older Taiwanese adults. A reduction in the levels of SO , CO, PM , PM , NO , NO, NO , THC, NMHC, and CH may reduce the risk of mortality after hip fracture surgery. This study provides robust evidence and highlights the substantial impact of air pollution on the outcomes of hip fractures.

Non-union occurring in structural bone grafting is a major problem in allograft transplantation because of impaired interaction between the host and graft tissue. Activated toll-like receptor (TLR) induces inflammatory cytokines and chemokines and triggers cell-mediated immune responses. The TLR-mediated signal pathway is important for mediating allograft rejection. We evaluated the effects of local knockdown of the TLR4 signaling pathway in a mouse segmental femoral graft model. Allografts were coated with freeze-dried lentiviral vectors that encoded TLR4 and myeloid differentiation primary response gene 88 (MyD88) short-hairpin RNA (shRNA), which were individually transplanted into the mice. They were assessed morphologically, radiographically, and histologically for tissue remodeling. Union occurred in autografted but not in allografted mice at the graft and host junctions after 4 weeks. TLR4 and MyD88 expression was up-regulated in allografted mice. TLR4 and MyD88 shRNAs inhibited TLR4 and MyD88 expression, which led to better union in the grafted sites. More regulatory T-cells in the draining lymph nodes suggested inflammation suppression. Local inhibition of TLR4 and MyD88 might reduce immune responses and ameliorate allograft rejection.

Psoriasis is an immune-mediated disorder which primarily affects skin and has systemic inflammatory involvement. Neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), systemic immune-inflammation index (SII), and monocyte-to-lymphocyte ratio (MLR) are novel complete blood count (CBC)-derived markers which can reflect systemic inflammation. This study aimed to systematically investigate the associations of NLR, PLR, SII, and MLR with psoriasis. This study was performed in compliance with the Preferred Reporting Items for Systematic Reviews and Meta-analyses statement. A comprehensive search of Pubmed, Embase, Scopus, and Google Scholar was conducted for relevant studies. Observational studies evaluating the correlations of NLR, PLR, SII, or MLR with psoriasis were included. The primary outcomes were the associations of these inflammatory markers with the presence and severity of psoriasis. The random-effect model was applied for meta-analysis. 36 studies comprising 4794 psoriasis patients and 55,121 individuals in total were included in the meta-analysis. All inflammatory markers were significantly increased in psoriasis groups compared to healthy controls (NLR: MD = 0.59, 95% CI: 0.47–0.7; PLR: MD = 15.53, 95% CI: 8.48–22.58; SII: MD = 111.58, 95% CI: 61.49-161.68; MLR: MD = 0.034, 95% CI: 0.021–0.048; all p < 0.001). Between-group mean differences in NLR and PLR were positively correlated with the mean scores of Psoriasis Area Severity Index (NLR: p = 0.041; PLR: p = 0.021). NLR, PLR, SII, and MLR are associated with the presence of psoriasis. NLR and PLR serve as significant indicators of psoriasis severity. These novel CBC-derived markers constitute potential targets in the screening and monitoring of psoriasis.

Background: Establishing animal models with metabolic disorders similar to human metabolic syndrome (MS) is important. In terms of eliciting a full array of MS, we have previously shown that Wistar rats are more responsive to sucrose water drinking than are C57BL/6J mice. This study was aimed at investigating the underlying molecular mechanism of sucrose water-induced MS in Wistar rats. Methods: Male Wistar rats were divided into 2 groups (n = 8 for each group) which were given plain water (C group) or 30% sucrose water (SW group) to drink ad libitum. After 20 weeks, the transcriptional levels and protein translocation of hepatic sterol regulatory element-binding protein-1c (SREBP-1c) and carbohydrate response element-binding protein (ChREBP) as well as the protein levels of protein tyrosine phosphatase-1B (PTP-1B) in insulin-responsive tissues (liver, muscle, and adipose tissue) were measured. Results: The sucrose water regimen successfully elicited visceral obesity, hypertriglyceridemia, insulin resistance, and high blood pressure. The upregulation of de novo lipogenesis in the liver of the sucrose water-treated rats was demonstrated by an increased activity of enzymes, mRNA levels of lipogenic proteins, and nuclear levels of SREBP-1c and ChREBP. Moreover, in the sucrose water-treated rats, protein levels of PTP-1B were significantly increased in liver and skeletal muscle but decreased in adipose tissue. Conclusion: The susceptibility of Wistar rats to sucrose water-induced MS is associated with the transactivation of SREBP-1c and ChREBP in the liver, and PTP-1B is involved in the upregulation of de novo lipogenesis in the liver and the pathology of systemic insulin resistance in rats with MS chronically induced by drinking sucrose water.

Left ventricular hypertrophy (LVH) is a hypertensive heart disease that significantly escalates the risk of clinical cardiovascular events. Its etiology potentially incorporates various clinical attributes such as gender, age, and renal function. From mechanistic perspective, the remodeling process of LVH can trigger increment in certain biomarkers, notably sST2 and NT‐proBNP. This multicenter, retrospective study aimed to construct an LVH risk assessment model and identify the risk factors. A total of 417 patients with essential hypertension (EH), including 214 males and 203 females aged 31–80 years, were enrolled in this study; of these, 161 (38.6%) were diagnosed with LVH. Based on variables demonstrating significant disparities between the LVH and Non‐LVH groups, three multivariate stepwise logistic regression models were constructed for risk assessment: the “Clinical characteristics” model, the “Biomarkers” model (each based on their respective variables), and the “Clinical characteristics + Biomarkers” model, which amalgamated both sets of variables. The results revealed that the “Clinical characteristics + Biomarkers” model surpassed the baseline models in performance (AUC values of the “Clinical characteristics + Biomarkers” model, the “Biomarkers” model, and the “Clinical characteristics” model were .83, .75, and .74, respectively; P  < .0001 for both comparisons). The optimized model suggested that being female (OR: 4.26, P  <.001), being overweight (OR: 1.88, p  = .02) or obese (OR: 2.36, p  = .02), duration of hypertension (OR: 1.04, P  = .04), grade III hypertension (OR: 2.12, P  < .001), and sST2 (log‐transformed, OR: 1.14, P  < .001) were risk factors, while eGFR acted as a protective factor (OR: .98, P  = .01). These findings suggest that the integration of clinical characteristics and biomarkers can enhance the performance of LVH risk assessment.