Atrial fibrillation (AF) is a prevalent cardiac arrhythmia affecting millions of individuals worldwide and posing significant challenges to healthcare systems. The growing body of research has uncovered sex-related differences in AF pathophysiology, including the role of fatty acid-binding protein 4 (FABP4) and leptin as potential biomarkers. FABP4 and leptin, key adipokines involved in cardiovascular health, have been linked to inflammation, oxidative stress, and endothelial dysfunction, all of which may contribute to AF development. These adipokines exhibit sex-specific differences in their concentrations, with females generally showing higher FABP4 levels and males displaying distinct leptin profiles. Furthermore, hormonal influences, particularly estrogen, and testosterone, play significant roles in shaping AF risk and atrial remodeling. Estrogen is associated with cardioprotective effects, while testosterone may exert proarrhythmic effects. Understanding these sex-specific mechanisms could lead to more tailored and effective clinical management of AF. The future of AF research holds promise for precision medicine, novel therapeutic targets, artificial intelligence integration, and personalized care approaches. Emphasizing patient-centered care, telemedicine, and multidisciplinary collaboration can further enhance AF management and improve patient outcomes. In conclusion, recognizing and addressing sex-related factors in AF pathophysiology offer opportunities for gender-responsive interventions and advancements in AF management. Implementing these insights may pave the way for targeted therapies and improved quality of life for individuals affected by AF.

OBJECTIVES: This study was performed to identify the distribution of undiagnosed isolated hypertension subtypes and their correlates amongst adults aged 35 years and older in Bangladesh using data from the Bangladesh Demography and Health Survey 2011. METHODS: Out of a total of 17,964 selected households, 7,880 were included in the final analysis for this study. Systolic and diastolic blood pressure (BP) were measured 3× at 10-minute intervals. Hypertension subtypes were defined for individuals not under antihypertensive treatment as systolic-diastolic hypertension (SDH): systolic BP (SBP) ≥ 140 mm Hg and diastolic BP (DBP) ≥ 90 mm Hg; isolated diastolic hypertension (IDH): SBP < 140 mm Hg and DBP ≥ 90 mm Hg, and isolated systolic hypertension (ISH): SBP ≥140 mm Hg and DBP < 90 mm Hg. RESULTS: The predominant hypertension subtypes were SDH and IDH [5.2%; 95% confidence interval (CI): 4.7–5.1] followed by ISH (3.8%; 95% CI: 3.4–4.2). Multiple logistic regression showed that age and gender were significant predictors of ISH. SDH was associated with females [odds ratio (OR): 1.8; 95% CI: 1.3–2.6], the older age group (OR-7.4; 95% CI: 4.3–12.7), and overweight or obese individuals (OR: 1.6; 95% CI: 1.1–2.4). Non-manual work (OR: 1.5; 95% CI: 1.0–2.0]) and being overweight or obese (OR: 1.9; 95% CI: 1.4–2.8) were factors associated with IDH. CONCLUSION: ISH, IDH and SDH represent salient subtypes of hypertension in Bangladesh. To identify preventive intervention for averting adverse cardiovascular events, further research is needed.
Adult ; Bangladesh ; Blood Pressure ; Demography ; Family Characteristics ; Female ; Health Surveys ; Humans ; Hypertension ; Logistic Models ; Overweight

Objective: To verify possible associations between polymorphisms of glutathione S-transferase Mu (GSTM1), glutathione S-transferase θ (GSTT1) and glutathione S-transferase Pi (GSTP1) genes and susceptibility to lung cancer. Methods: A total of 106 lung cancer patients and 116 controls were enrolled in a case-control study. The GSTM1 and GSTT1 were analyzed using PCR while GSTP1 was analyzed using PCR-restriction fragment length polymorphism. Risk of lung cancer was estimated as odds ratio at 95% confidence interval using unconditional logistic regression models adjusting for age, sex, and tobacco use. Results: GSTM1 null and GSTT1 null genotypes did not show a significant risk for developing lung cancer. A significantly elevated lung cancer risk was associated with GSTP1 heterozygous, mutant and combined heterozygous+mutant variants of rs1695. When classified by tobacco consumption status, no association with risk of lung cancer was found in case of tobacco smokers and nonsmokers carrying null and present genotypes of GSTM1 and GSTT1. There is a three-fold (approximately) increase in the risk of lung cancer in case of both heterozygous (AG) and heterozygous+mutant homozygous (AG+GG) genotypes whereas there is an eightfold increase in risk of lung cancer in cases of GG with respect to AA genotype in smokers. Conclusions: Carrying the GSTM1 and GSTT1 null genotype is not a risk factor for lung cancer and GSTP1Ile105Val is associated with elevated risk of lung cancer.

Previously, we proposed a new perspective of triptolide (TP)-associated hepatotoxicity: liver hypersensitivity upon lipopolysaccharide (LPS) stimulation. However, the mechanisms for TP/LPS-induced hepatotoxicity remained elusive. The present study aimed to clarify the role of LPS in TP/LPS-induced hepatotoxicity and the mechanism by which TP induces liver hypersensitivity upon LPS stimulation. TNF- inhibitor, etanercept, was injected intraperitoneally into mice to investigate whether induction of TNF- by LPS participated in the liver injury induced by TP/LPS co-treatment. Mice and hepatocytes pretreated with TP were stimulated with recombinant TNF- to assess the function of TNF- in TP/LPS co-treatment. Additionally, time-dependent NF-B activation and NF-B-mediated pro-survival signals were measured and . Finally, overexpression of cellular FLICE-inhibitory protein (FLIP), the most potent NF-B-mediated pro-survival protein, was measured and to assess its function in TP/LPS-induced hepatotoxicity. Etanercept counteracted the toxic reactions induced by TP/LPS. TP-treatment sensitized mice and hepatocytes to TNF-, revealing the role of TNF- in TP/LPS-induced hepatotoxicity. Mechanistic studies revealed that TP inhibited NF-B dependent pro-survival signals, especially FLIP, induced by LPS/TNF-. Moreover, overexpression of FLIP alleviated TP/LPS-induced hepatotoxicity and TP/TNF--induced apoptosis . Mice and hepatocytes treated with TP were sensitive to TNF-, which was released from LPS-stimulated immune cells. These and other results show that the TP-induced inhibition of NF-B-dependent transcriptional activity and FLIP production are responsible for liver hypersensitivity.