Effect of coronary collateral circulation on the prognosis of elderly patients with acute ST-segment elevation myocardial infarction treated with underwent primary percutaneous coronary intervention.

Investigate the effect of coronary collateral circulation (CCC) on the prognosis of elderly patients with acute ST-segment elevation myocardial infarction (STEMI) and acute total occlusion (ATO) of a single epicardial coronary artery.Three hundred forty-six advanced-age patients (age ≥60 years) with STEMI and ATO who underwent primary percutaneous coronary intervention (PCI) were enrolled in this study. According to the Rentrop grades, the patients were assigned to the poor CCC group (Rentrop grade 0-1) and good CCC group (Rentrop grade 2-3).Multivariate logistic regression analysis revealed that poor coronary collateral circulation was an independent factor for Killip class ≥2 (odds ratio [OR]: -1.559; 95% confidence interval [CI]: 1.346-2.378; P = .013), the use of an intra-aortic balloon pump (IABP) (OR: -1.302; 95% CI: 0.092-0.805; P = .019), and myocardial blush grade (MBG) 3 (OR: 1.516; 95% CI: 2.148-9.655; P < .001). We completed a 12-month follow-up, during which 52 patients (15.0%) were lost to follow-up and 19 patients (5.5%) died. Univariate analysis (Kaplan-Meier and log-rank tests) suggested that poor CCC had a significant effect on all-cause mortality (P = .046), while multivariate analysis (Cox regression analysis) indicated that CCC had no statistically significant effect on all-cause mortality (P = .089) after the exclusion of other confounding factors. After excluding the influence of other confounding factors, this study showed that the mortality rate increased by 26.9% within 1 year for every 1-hour increment of time of onset. The mortality rate in patients with Killip class ≥2 was 8.287 times higher than that in patients with Killip class 0 to 1. The mortality rate in patients over 75 years was 8.25 times higher than that in patients aged 60 to 75 years. The mortality rate in patients with myocardial blush grade 3 (MBG 3) was 5.7% higher than that in patients with MBG 0-2.The conditions of CCC in the acute phase had no significant direct effect on all-cause mortality in patients, but those with good CCC had a higher rate of MBG 3 after primary PCI and a lower rate of Killip ≥2.

Protein arginine methyltranferase-1 induces ER stress and epithelial-mesenchymal transition in renal tubular epithelial cells and contributes to diabetic nephropathy.

BACKGROUND: In this study, we examined the association of PRMT1 with ER stress and epithelial-mesenchymal transition (EMT), two critical pathogenic mechanisms leading to DN development, in proximal tubular epithelial cells (PTECs). METHODS: The level of PRMT1 was compared between the serum from DN patients and healthy individuals by ELISA, and between renal tissues of DN mice and normal mice using RT-qPCR and immunohistochemistry. Using high-glucose-treated PTEC cell line, HK2 cells as the model system, the significance of PRMT1 in ER stress and EMT was assessed by shRNA targeting PRMT1 (sh-PRMT1) and/or by overexpressing PRMT1. Mechanistic studies focused on three major pathways controlling ER stress: protein kinase R-like ER kinase (PERK), inositol requiring-1α (IRE1α), and activating transcription factor 6 (ATF6). RESULTS: PRMT1 was up-regulated in the serum of DN patients and renal tissues of DN mice. High glucose administration induced elevation of PRMT1 expression in HK2 cells in vitro, accompanied with ER stress and EMT activation. PRMT1 knockdown attenuated high glucose-induced ER stress and apoptosis by inactivating PERK and ATF6, but not IRE1α. PRMT1 activated ATF6 by recruiting H4R3me2as to the promoter. Furthermore, PRMT1-induced ER stress was concomitant with the activation of an EMT-like state. Specifically, inhibition of ATF6, but not PERK blocked PRMT1-induced EMT in high-glucose-treatment HK2 cells. CONCLUSIONS: By activating ER stress, PRMT1 essentially regulates the apoptosis and EMT of PTECs in response to diabetic milieu. Thus, targeting PRMT1 may alleviate both tissue injury and renal fibrosis, and thus benefit the treatment of DN.

Triglyceride to HDL-cholesterol ratio as an independent risk factor for the poor development of coronary collateral circulation in elderly patients with ST-segment elevation myocardial infarction and acute total occlusion.

To determine the prognostic role of triglyceride (TG) to high-density lipoprotein cholesterol (HDL) ratio for poorly developed coronary collateral circulation (CCC) in elderly patients with ST-segment elevation myocardial infarction (STEMI) and acute total occlusion (ATO).As a retrospective case-control study, elderly patients (age ≥60 years) with both STEMI and ATO (n = 346) were classified as having either poorly- or well-developed CCC (Rentrop grades 0-1 and 2-3, respectively). The ratio of TG/HDL was calculated according to the detected levels of TG and HDL. The difference of TG/HDL ratio in those 2 groups was compared by Student t test, and multivariate logistic regression analysis indicating occurrence of poorly developed CCC was performed. Receiver operator characteristic curve (ROC) analysis of TG/HDL ratio which determine the optimal cut-off value of TG/HDL ratio was applied.The TG/HDL ratio was significantly higher in patients with poorly developed CCC than in those with well-developed CCC (2.88 ±â€Š2.52 vs 1.81 ±â€Š1.18, P < .001). In multivariate logistic regression analysis, higher TG/HDL ratio (OR 1.789, 95% CI 1 . 346-2.378, P < .001) and the presence of left circumflex branch of coronary artery (LCX) occlusion (OR6.235, 95% CI 2.220-17.510, P = .001) were emerged as independent positive predictors of poor development of CCC, whereas presence of right coronary artery (RCA) occlusion (OR 0.474, 95% CI 0.265-0.850, P = .002) and onset time (OR 0.693, 95% CI 0.620-0.775, P < .001) were found as negative indicators. The optimal cut-off value of TG/HDL ratio was found as 1.58 in ROC analysis, which yielded an area under the curve value of 0.716 (95% CI 0.654-0.778, P < .001) and demonstrated a sensitivity of 80.9% and a specificity of 59.3% for prediction of poorly developed CCC.TG/HDL ratio is an independent risk factor for predicting poor development of CCC in elderly patients with STEMI and ATO.

Mechanism and clinical significance of cyclooxygenase-2 expression in gastric cancer.

AIM: To determine the correlation between methylation status of 5' CpG island of cyclooxygenase-2 (COX-2) gene and protein expression in gastric cancer tissues for distinguishing the molecular characters of gastric cancers. METHODS: Methylation status of 5' CpG island of COX-2 gene was studied by PCR amplification after HpaII and Hha I restrictive enzyme digestion; COX-2 expression was evaluated by immunohistochemical method. RESULTS: Hpa II and HhaI site were all methylated in 12 normal gastric mucosa tissues, whereas they were demethylated in 77.27% (34/44) and 84.09% (37/44) gastric cancer tissues, respectively. Expression of COX-2 was detected in 68.18% (30/44) gastric cancer tissues, but no expression was found in normal gastric mucosa tissues. In gastric cancer tissues, COX-2 expression was correlated significantly with HpaII site demethylation (29/30 vs 5/14, P<0.001 and HhaI site demethylation (28/30 vs 9/14, P<0.05). CONCLUSION: The demethylation of 5' CpG island of gene is necessary for COX-2 expression in human gastric cancer. The expression status of COX-2 may provide theoretical basis for COX-2 targeting gastric cancer treatments.

Synthesis, molecular docking, and biofilm formation inhibitory activity of 5-substituted 3,4-dihalo-5h-furan-2-one derivatives on Pseudomonas aeruginosa.

Pseudomonas aeruginosa (P. aeruginosa) colonize on most wounds and live as biofilm, which causes antibiotic resistance and wounds unhealed. To investigate the effects of 5-substituted 3,4-dihalo-5H-furan-2-one compounds on biofilm formation of P. aeruginosa, a set of 5-(aryl-1'-hydroxy-methyl)- or 5-(aryl-2-methylene)-3,4-dihalo-5H-furan-2-one compounds were designed and synthesized. Their inhibitory activities on biofilm formation of P. aeruginosa were studied by MIC assay, quantitative analysis of biofilm inhibition, and observation of biofilm formation with SEM. It was found that compounds 2i, 3f, 3i showed remarkable effects of biofilm formation inhibition on P. aeruginosa. Furthermore, molecular docking was performed to identify the key structural features of these compounds with the binding site of LasR receptor.