Mcdanielloft8331
Introduction The risk of contrast-induced nephropathy (CIN) as a common and important complication of coronary procedures may be influenced by the vascular access site. We compared the risks of CIN in diagnostic or interventional coronary management between patients treated via the transradial access (TRA) and those treated via the transfemoral access (TFA). Methods Patients undergoing invasive coronary catheterization or percutaneous coronary intervention (PCI) were enrolled. We excluded patients with congenital or structural heart disease and those with end-stage renal disease on dialysis. Based on the vascular access site used for invasive coronary catheterization, the patients were divided into 2 study groups the TFA and the TRA. CIN was defined as an absolute (≥0.5 mg/dL) or relative (>25%) increase in the baseline serum creatinine level within 48 hours following cardiac catheterization or PCI. Results Overall, 410 patients (mean age = 61.3 ± 10.8 years) underwent diagnostic or interventional coronary management 258 were treated via the TFA approach and 152 via the TRA approach. The patients treated via the TFA had a significantly higher incidence of postprocedural CIN (15.1% vs 6.6%; P= 0.01). The multivariate analysis showed that the TFA was the independent predictor of CIN (OR 2.37, 95% CI 1.11 to 5.10, and P= 0.027). Moreover, the BARC (Bleeding Academic Research Consortium) and Mehran scores were the other independent predictors of CIN in our study. Conclusion The risk of CIN was lower with the TRA, and the TFA was the independent predictor of CIN after the diagnostic or interventional coronary management. © 2020 The Author(s).Introduction The present study examined the effects of high cholesterol and high oxidized-cholesterol diets on the myocardial expression of TLR4 and pro-inflammatory cytokine in rats. Methods Male Wistar rats were allocated into 6 groups and fed with a normal diet, cholesterol, and oxidized-cholesterol rich diets with or without isoproterenol-induced myocardial infarction. TLR4 and MyD 88 expression and levels tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were measured in the heart and serum. Results Oxidized cholesterol-fed animals had higher serum levels of oxidized low-density lipoprotein (LDL) (263 ± 13 ng/dL) than the cholesterol-fed animals (98 ± 8 ng/dL; P less then 0.001). A high level of oxidized-LDL caused fibrotic cell formation and enhanced neutrophil infiltration in the absence of MI. Both cholesterol and oxidized-cholesterol upregulated TLR4 mRNA expression and increased TNF-α and IL-6 production in the hearts of rats with MI. In rats fed with oxidized-cholesterol the serum and myocardial levels of TNF-α (653 ± 42 pg/mL, 1375 ± 121 pg/100 mg, respectively) were higher than MI group (358±24 pg/mL, P less then 0.001 and 885 ± 56 pg/100 mg, P less then 0.01). A significant correlation was seen between TLR4 expression and infarct size. Conclusion These findings suggest that cardiac TLR4 is preferentially upregulated by oxidized cholesterol in rats. Oxidized cholesterol may have a critical role in cardiac toxicity in the absence of pathological conditions. © 2020 The Author(s).Introduction Cardiovascular system is highly sensitive to LPS-induced oxidative damage. This study aimed to show the inhibitory effect of bacterial Lipase on LPS-induced cardiomyoblasts toxicity. Methods Rat cardiomyoblasts H9C2 were classified into Control, LPS (cells received 0.1, 1 and 10 μg/mL LPS) and LPS+ Lipase groups. In LPS+Lipase group, different concentrations of lipopolysaccharide were pre-incubated with 5 mg/mL bacterial lipase at 37˚C overnight prior to cell treatment. After 72 hours, cell viability was assessed by MTT assay. The expression of key genes related to toll-like receptor signaling pathways was assessed by real-time PCR assay. DNA Damage inhibitor Percentage of fatty acids was evaluated in each group using gas chromatography assay. The levels of NO was also measured using the Griess reaction. Results Data showed H9C2 cells viability was decreased after exposure to LPS in a dose-dependent manner (P less then 0.05). Incubation of LPS with lipase increased cell survival rate and closed to near-to-control levels (P less then 0.05). Lipase had the potential to blunt the increased expression of IRAK and NF-κB in cells after exposure to the LPS. Compared to the LPS group, lipase attenuated the increased level of NO-induced by LPS (P less then 0.05). Gas chromatography analysis showed the reduction of saturated fatty acids in cells from LPS group while the activity of lipase prohibited impact of LPS on cell fatty acid composition. LPS decreased the ability of cardiomyoblasts to form colonies. Incubation of LPS with lipase enhanced clonogenic capacity. Conclusion Reduction in lipopolysaccharide-induced cytotoxicity is possibly related to lipase activity and reduction of modified lipopolysaccharide with toll-like receptor. © 2020 The Author(s).Introduction Limited data are available on the association of Dietary Inflammatory Index (DII) with metabolic syndrome (MetS) and its components. The present study was conducted to investigate the association of DII with MetS and its components among Iranian adults. Methods A total of 404 subjects, aged 18 years or older, were included in the current cross-sectional study. We used a validated and reliable 147-item food frequency questionnaire (FFQ) to assess dietary intakes. Fasting blood sample was obtained to quantify glycemic indicators and lipid profile. MetS was defined based on the guidelines of the National Cholesterol Education Program Adult Treatment Panel III (ATP III). Results Mean age of study participants was 38.20 ± 9.55 years. No significant association was found between DII and odds of MetS (odds ratio [OR] 0.92, 95% CI 0.48-1.76). In terms of MetS components, a significant positive association was seen between DII scores and reduced levels of high-density lipoprotein cholesterol (HDL-C) (OR 2.29, 95% CI 1.32-3.97); such that after controlling for energy intake, demographic variables and BMI, participants in the highest category of DII had 2.71 times greater odds for having reduced levels of HDL-C (OR 2.71, 95% CIs 1.34, 5.47). There was no other significant association between other components of MetS and DII scores either before or after adjusting for confounding variables. Conclusion We observed no significant association between DII and odds of MetS. However, higher score of DII was associated with lower levels of HDL. © 2020 The Author(s).