Seyed Sobhan Bahreiny

Pentraxin 3 (PTX3) is an immunomodulatory molecule involved in inflammation and ovarian physiology. However, its circulating levels in polycystic ovary syndrome (PCOS) remain uncertain due to inconsistent findings. This meta-analysis aimed to clarify the association between PTX3 levels and PCOS. A systematic search of PubMed, Embase, Scopus, Web of Science, CNKI, and Google Scholar was conducted up to April 2025 without language restrictions. Observational studies comparing circulating PTX3 levels between patients with PCOS and healthy controls were included. Effect sizes were calculated as standardized mean differences (SMDs) with 95% confidence intervals (CIs) using a random-effects model. Nineteen studies (25 datasets) involving 1,230 women with PCOS and 1,179 controls were included. Pooled analysis showed significantly higher PTX3 levels in PCOS compared with controls (SMD = 0.993; 95% CI: 0.076 to 1.909; p = 0.034). In subgroup analysis by BMI, the most pronounced elevation in PTX3 concentrations was observed in women with a BMI between 25 and 30 kg/m² (SMD = 2.102; p = 0.008). Meta-regression analysis also identified age (β = 0.37, p = 0.026) as a positive and luteinizing hormone levels (β = − 0.33, p = 0.028) as a negative moderator of PTX3 concentrations. The observed increase in PTX3 concentrations in PCOS supports its role as a candidate biomarker for disease identification and monitoring. Future studies should clarify its relationship with infertility status, explore its role across different PCOS phenotypes, and address methodological heterogeneity to refine its clinical utility. The online version contains supplementary material available at 10.1186/s13048-026-02091-0.

Background and Aims: Atherosclerosis (AS), a major cause of cardiovascular mortality, involves chronic inflammation mediated by transcription factors such as NF‐κB, PPARs, and AP‐2α. Beyond its antiplatelet role, aspirin exerts anti‐inflammatory effects that may influence these molecular pathways. This review systematically evaluates aspirin's modulatory effects on these transcription factors in AS. Methods: Relevant English‐language studies (1980–2025) were retrieved from PubMed, ScienceDirect, and Google Scholar using keywords related to aspirin, atherosclerosis, and inflammation‐related transcription factors. Results: Aspirin inhibits NF‐κB activation, reduces proinflammatory cytokine production, and enhances PPAR and AP‐2α signaling, contributing to anti‐inflammatory and plaque‐stabilizing effects. Clinical findings (e.g., ARRIVE, ASPREE) show variable cardiovascular outcomes, likely reflecting dose‐ and population‐dependent responses. Conclusion: Aspirin modulates key inflammatory transcription factors in AS, offering potential benefits beyond platelet inhibition. Further studies should clarify AP‐2α's mechanistic role and explore aspirin‐based combination strategies tailored to patient‐specific inflammatory profiles.

Female infertility is a critical global health concern, with a rising prevalence and significant psychosocial consequences. This study aimed to investigate the association between Systemic Inflammatory Response Index (SIRI) and female infertility. This cross-sectional study enrolled 3059 reproductive-aged women (18-45 years) to examine the association between SIRI and female infertility using data from the National Health and Nutrition Examination Survey (NHANES) spanning from 2015 to 2020. Multivariable logistic regression generalized additive models (GAM), restricted cubic splines (RCS), and threshold effect analyses were leveraged. Machine learning approaches were also utilized to validate predictive performance and identify key features. Elevated SIRI was independently associated with increased odds of infertility. In the fully adjusted logistic model, each unit increase in SIRI corresponded to a 34% increase in infertility risk (OR 1.34, p = 0.001). Women in the highest SIRI quartile had more than double the odds of infertility compared to those in the lowest quartile (OR 2.08, p < 0.001), with a significant dose-response trend (p trend < 0.001). GAM and RCS models confirmed a monotonic and curvilinear association, respectively. Threshold analysis revealed a critical inflection point at SIRI = 1.66. Machine learning validation identified SIRI as one of the most influential predictors, with XGBoost achieving the highest (AUC = 0.866). These findings support the role of chronic systemic inflammation in female infertility and highlight SIRI as a valuable biomarker for risk prediction and clinical assessment.

Background: Methotrexate (MTX) is a highly employed chemotherapeutic and immunosuppressive agent, but its clinical application is often restricted by dose-dependent hepatotoxicity. Objectives: This study investigates the hepatoprotective potential of arbutin (ARB), a natural β-glucoside of hydroquinone, against MTX-induced liver damage. Methods: The experimental design involved 40 male Wistar rats, randomly allocated to five groups of 8 animals: (1) a control group receiving normal saline; (2) an MTX-only group administered an intraperitoneal MTX injection (20 mg/kg) on day 9; and (3 - 5) three MTX + ARB co-treatment groups receiving oral ARB at 25, 50, and 100 mg/kg over 10 continuous days, with MTX administered. Hepatic injury markers (ALT, AST, ALP), oxidative stress [malondialdehyde (MDA), nitric oxide (NO)], antioxidants [cellular glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), GPx], and TNF-α and IL-1β pro-inflammatory cytokines were analyzed in liver tissue. Additionally, histopathological alterations, including hepatocellular necrosis, inflammatory infiltration, and sinusoidal congestion, were examined to assess tissue-level damage. Results: The findings showed that MTX exposure caused significant liver toxicity, indicated by higher serum ALP, ALT, and AST levels, decreased antioxidant enzyme activity, and increased pro-inflammatory cytokine production. Notably, ARB co-treatment, especially at 50 and 100 mg/kg doses, effectively counteracted these detrimental effects. Histopathological analysis confirmed that ARB mitigated MTX-induced liver damage, including necrosis, inflammation, and sinusoidal congestion. Conclusions: Arbutin demonstrates strong hepatoprotective effects against MTX-related toxicity by reducing inflammation, oxidative stress, and liver injury. The results suggest its potential as an adjunct therapeutic option for MTX treatment.

The Body Roundness Index (BRI) has recently been proposed as an effective metric for assessing obesity-related health risks, but its association with femal

Background: Vascular endothelial growth factor‐A (VEGF‐A), In combination with other pro‐angiogenic factors, plays a pivotal role in angiogenesis and the pathogenesis of acute lymphoblastic leukemia (ALL).Aims: This meta‐analysis aims to evaluate the diagnostic value of VEGF‐A and its prognostic relevance in the outcome of patients with ALL.Methods and Results: A comprehensive literature search was conducted up to January 2025 across multiple databases. Standardized mean differences (SMDs) with 95% confidence intervals (CIs) were pooled using a random‐effects model to quantify effect sizes. Subgroup analyses and meta‐regression were employed to explore heterogeneity sources. Data extracted from 15 studies encompassing 674 patients with ALL demonstrated a significant correlation between elevated VEGF‐A levels and unfavorable prognosis (SMD: 0.878; 95% CI: 0.276–1.479; p = 0.004). Notably, increased VEGF‐A levels were particularly evident in pediatric patients older than 8 years (SMD: 0.758; 95% CI: 0.178–1.338; p = 0.010).Conclusion: The results indicate that heightened VEGF‐A expression is associated with poorer clinical outcomes in ALL, supporting its utility as a diagnostic and prognostic biomarker in this patient population.

Pentraxin 3 (PTX3), a novel biomarker of vascular inflammation and endothelial dysfunction, has been identified as a potential predictor of diabetic retinopathy (DR). This meta-analysis aimed to assess the association between circulating PTX3 levels and both the presence and severity of DR in patients with diabetes. A systematic literature search was conducted across PubMed, Web of Science, Embase, Scopus, and Google Scholar up to January 2025. Observational studies comparing PTX3 levels between patients with and without DR, as well as proliferative (PDR) and non-proliferative (NPDR) stages, were considered. Standardized mean differences (SMD) with 95% confidence intervals (CI) were calculated using random effects models. A total of 15 studies comprising 1,339 patients with diabetes were included in this meta-analysis. The pooled analysis demonstrated significantly higher PTX3 levels in the DR group than in the non-DR controls (SMD = 1.232; 95% CI: 0.747, 1.718; p < 0.001). Subgroup analyses also indicated significantly elevated PTX3 levels in both NPDR (SMD = 0.928; 95% CI: 0.35, 1.50; p = 0.002) and PDR groups (SMD = 1.99; 95% CI: 0.83, 3.15; p = 0.001) compared to non-DR patients. Comparison of PTX3 levels between PDR and NPDR stages, suggested a possible increase in PDR patients (SMD = 0.635; 95% CI: -0.03, 1.30; p = 0.064). Meta-regression analysis identified HbA1c, BMI, and region as significant moderators of PTX3 levels. The significant elevation of PTX3 in both NPDR and PDR underscores its potential as a biomarker for DR diagnosis and monitoring in clinical settings.

Insulin sensitivity, resistance, and pancreatic beta-cell function play key roles in metabolic and reproductive health. Despite the known role of glucose-insulin homeostasis in female reproductive health, the association and regression modeling of estimated glucose disposal rate (eGDR), homeostatic model assessment of insulin resistance (HOMA-IR), beta-cell function (HOMA-β), and insulin disposition index (Insulin-DI) with female infertility remain unclear. This cross-sectional study aimed to assess the associations between insulin-related indices and female infertility. This study examined data from 2832 women aged 18–45 years who participated in the National Health and Nutrition Examination Survey (NHANES) 2017–2023 cycles. To evaluate the associations between four insulin-related indices and infertility, multivariable logistic regression, generalized additive models, and threshold effect analyses were applied, while controlling for relevant sociodemographic, lifestyle, and metabolic confounders. Furthermore, integrated meta-analysis across models, distributional analysis, subgroup and interaction analyses were conducted to explore potential effect modifications. eGDR showed a strong inverse association with infertility across all models (OR range: 0.636–0.85, p < 0.001), with a significant nonlinear pattern (p = 0.003) and a threshold at 4.59. HOMA-IR was positively associated in unadjusted models (OR = 1.147, p < 0.001) but lost significance after full adjustment. HOMA-β showed a weak positive association (OR = 1.003, p = 0.0227), while Insulin-DI was inversely related to infertility only in unadjusted models. Subgroup analyses revealed significant effect modifications by BMI and age, especially for eGDR and HOMA-IR. Reduced insulin sensitivity, as indicated by lower eGDR, is strongly linked to higher infertility risk. HOMA-IR and Insulin-DI also show threshold-based nonlinear associations. Graphical abstract Illustrating the Insulin-Related Indices and Female Infertility: Biological Mechanisms and Prognostic Implications