Neutrophil-to-lymphocyte ratio (NLR) has been reported to serve as a prognostic marker in inflammatory diseases. The purpose of this study was to evaluate the association of NLR at admission with in-hospital mortality in patients with sepsis presenting to emergency department. This was a secondary analysis based on a single-center, retrospective, cohort study. Patients with sepsis admitted to an academic emergency department between January 2010 and January 2015 were enrolled. NLR of patients was analyzed from the hospital's electronic health record (EHR) system. A total of 174 adult patients, of which 80 (46.0%) died in hospital. The primary outcome was in-hospital mortality. Secondary outcome was 28-day mortality. Contrary to previous studies, a larger NLR was found to have less odds of in-hospital mortality, as well as the presence of bacteremia. Patients who has severe/shock or had a history of chronic heart failure (CHF) had larger odds of death during hospital. Multivariate logistic regression analysis indicated that low NLR was an independent predictor of in-hospital mortality (OR = –0.98; 95% CI –0.96 to –0.99; P = .022). However, no correlation was found between the NLR and 28-day hospital mortality in patients with sepsis (P = .988). As a predictor of in-hospital survival, the area under curve (AUC) of the NLR was 0.622 (95%CI 0.54–0.71; P = .006) and the cut-off value was 9.11 with 0.551 sensitivity and 0.707 specificity. NLR at admission was an independent predictor of in-hospital mortality of sepsis patients.

This study aims to investigate the relationship between the triglyceride glucose (TyG) index and peripheral artery disease (PAD). A total of 3125 participants with completed TyG and ankle brachial pressure index (ABPI) records were enrolled from the National Health and Nutrition Examination Survey (NHANES) cycle of 1999–2004. The TyG index was calculated as ln [triglycerides (mg/dL) × glucose (mg/dL)/2], and the presence of PAD was defined as ABPI ≤.9. The participants were 59.9 ± 12.9 years old and 51.5% (1608) were male. The prevalence of PAD was 7.2% (225). Compared with the reference lowest quartile of TyG index, the highest quartile was associated with 1.27-fold increased (odds ratio [OR] 2.27, 95% confidence interval [CI] 1.53-3.41; P < .001) risk of PAD. After adjusting for sociodemographic, lifestyles, and cardiometabolic factors, the multivariate-adjusted OR and 95% CI were 1.74 (1.02–3.01; P = .044) in participants within the highest quartile. Subgroup analysis showed that the association between TyG index and the risk of PAD was still consistent across subgroups. In conclusion, higher TyG index was significantly associated with the higher risk of PAD, which could be a marker of PAD.

Previous studies showed that miR-124 had a protective role by reducing oxidant stress and preventing cell apoptosis and autophagy. However, its role in doxorubicin-induced cardiomyopathy was less known. In our study, we confirmed increased ROS and decreased expression of miR-124 in doxorubicin-treated heart tissues and primary cardiomyocytes. The oxidative stress and cell apoptosis were alleviated by overexpressing miR-124, characterized by decreased activity of MDA and increased activity of SOD. While inhibiting miR-124 generated opposed effects. Mechanistically, our bioinformatic prediction and luciferase assay confirmed that miR-124 inhibited the expression of p66Shc, a proapoptotic signaling pathway. Our results suggested that miR-124 was hopeful to become a therapeutic target in doxorubicin-related cardiomyopathy.

Objectives: The relationship between lipid levels and arterial stiffness remains controversial. Therefore, we aimed to determine the relationship between lipid profiles and brachial–ankle pulse wave velocity (baPWV) as an indicator of arterial stiffness. Methods: A total of 909 participants aged 24 to 84 years were stratified into four baPWV quartiles in our study. Serum lipids, baPWV, and other variables of the participants were measured. Univariable and multivariable linear regression analyses were used to examine the relationships between lipid parameters and baPWV. Results: The highest baPWV quartile group had higher aspartate transaminase, alanine aminotransferase, plasma glucose, total cholesterol, triglyceride (TG), and low-density lipoprotein cholesterol levels and maximum ankle–brachial index, and lower high-density lipoprotein cholesterol levels and estimated glomerular filtration rate. Univariate regression analysis showed that total cholesterol, TG, and low-density lipoprotein cholesterol levels were positively related and high-density lipoprotein cholesterol levels were negatively related to baPWV. After adjusting for age, body mass index, smoking status, aspartate transaminase, alanine aminotransferase, plasma glucose, and estimated glomerular filtration rate, only TG levels were correlated with baPWV (β = 0.075). Conclusions: Four lipid variates are associated with arterial stiffness, and TG levels are positively related to arterial stiffness, independent of cardiovascular risks and liver function.

Background: The cardiotoxicity of isoniazid on zebrafish embryos and its underlying mechanism is unclear.Methods: Here, we exposed zebrafish embryos at 4 h post-fertilization to different levels of isoniazid and recorded the morphology and number of malformed and dead embryos under the microscope.Results: The high concentration of isoniazid group showed more malformed and dead embryos than the low concentration of isoniazid group and control group. The morphology of the heart and its alteration were visualized using transgenic zebrafish (cmlc2: GFP) and confirmed by in situ hybridization. The negative effects of isoniazid on the developing heart were characterized by lower heart rate and more heart looping disorders. Mechanistically, PCR showed decreased expression of heart-specific transcription factors when exposed to isoniazid. Oxidative stress was induced by isoniazid in cardiomyocytes, mediated by decreased activities of catalase and superoxide dismutase, which were rescued by scavengers of reactive oxygen species.Conclusion: In conclusion, this study demonstrated that isoniazid led to heart looping disturbance by the downregulation of cardiac-specific transcription factors and induction of cardiomyocyte apoptosis.