The aim of the present study was to determine the effects of the short-term application of pantoprazole on the co-treatment of acute ST-segment elevation myocardial infarction (STEMI) with aspirin and clopidogrel. A total of 207 acute patients showing primary symptoms of STEMI, who received successful emergent percutaneous coronary intervention treatment during hospitalization were randomly divided into two groups. In the test group proton pump inhibitors (PPIs), the patients were treated with a combination of aspirin and clopidogrel and pantoprazole, while those in the control group were treated only with aspirin and clopidogrel. Gastrointestinal bleeding events and major adverse cardiac events (MACEs) were observed in the two groups. Gastrointestinal bleeding events of the two groups mostly occurred within the first week of hospitalization, although the incidence in the PPIs group was significantly higher than that in the control group (p<0.05). However, no significant difference was observed for the incidence of MACEs between the two groups (p>0.05). In conclusion, the results of the present study have shown that the short-term application of pantoprazole combined with aspirin and clopidogrel does not increase the incidence of MACEs in patients with acute STEMI, reduces the risk of gastrointestinal bleeding, and is thus worth promoting clinically, particularly for high-risk groups.

BackgroundIntegrin linked kinase (ILK), as an important component of mechanical stretch sensor, can initiate cellular signaling response in the heart when cardiac preload increases. Previous work demonstrated increased ILK expression could induce angiogenesis to improved heart function after MI. However the patholo-physiological role of ILK in cardiac remodeling after MI is not clear.Method and ResultsHearts were induced to cardiac remodeling by infarction and studied in Sprague-Dawley rats. Until 4 weeks after infarction, ILK expression was increased in non-ischemic tissue in parallel with myocytes hypertrophy and compensatory cardiac function. 8 weeks later, when decompensation of heart function occurred, ILK level returned to baseline. Followed ILK alternation, vascular endothelial growth factor (VEGF) expression and phosphorylation of endothelial nitric oxide synthase (eNOS) was significantly decreased 8 weeks after MI. Histology study also showed significantly microvessel decreased and myocytes loss 8 weeks paralleled with ILK down-regualtion. While ILK expression was maintained by gene delivery, tissue angiogenesis and cardiac function was preserved during cardiac remodeling.ConclusionTemporally up-regulation of ILK level in non-ischemic myocytes by increased external load is associated with beneficial angiogenesis to maintain infarction-induced cardiac hypertrophy. When ILK expression returns to normal, this cardiac adaptive response for infarction is weaken. Understanding the ILK related mechanism of cardiac maladaptation leads to a new strategy for treatment of heart failure after infarction.

Qianlie Xiaozheng decoction (QLXZD), a traditional Chinese medicinal formula, has been used clinically to treat advanced prostate cancer (PCa) for more than 10 years. However, experimental evidence supporting its efficacy is lacking. Here, we investigated the anticancer properties and molecular mechanism of QLXZD in vitro in a human PCa cell line (PC3) and in vivo using PC3 xenografts in nude mice. We confirmed the antineoplastic activity of QLXZD by analyzing cell viability and tumor volume growth, which decreased significantly compared to that of the controls. Autophagy following QLXZD treatment was detected morphologically using transmission electron microscopy and was confirmed by measuring the expression of autophagy markers (LC3-II and p62) using fluorescence analysis, flow cytometry, and western blotting. Increasing autophagic flux induced by QLXZD was monitored via pmCherry-GFP-LC3 fluorescence analysis. QLXZD-induced autophagic cell death was alleviated by the autophagy inhibitors, 3-methyl adenine and hydroxychloroquine. We evaluated the total expression and phosphorylation levels of proteins involved in the Akt/mTOR pathway regulating autophagy. Phosphorylation of Akt, mTOR, and p70S6K, but not total protein levels, decreased following treatment. This is the first study to demonstrate the autophagy-related mechanistic pathways utilized during QLXZD-mediated antitumor activity both in vitro and in vivo. These findings support the clinical use of QLXZD for PCa treatment.

Aims Identification and intervention of left ventricular hypertrophy (LVH) in essential hypertension (EH) are important for the prevention of adverse cardiovascular events. However, effective methods for diagnosing LVH are still lacking. This study aimed to explore the relationship between soluble ST2 (sST2) and LVH in EH patients to identify a potential specific biomarker for hypertensive LVH. Methods and results This study included 97 EH patients. Based on the criteria for LVH, participants were divided into the LVH group ( n = 52) and the non‐LVH group ( n = 45). The level of serum sST2 was detected by enzyme‐linked immunosorbent assay. Pearson correlation analysis, logistic regression analysis, and receiver operating characteristic (ROC) curve analysis were used to investigate the potential of sST2 as a biomarker of LVH in EH patients. Compared with the non‐LVH group, the sST2 level was elevated in EH patients with LVH ( P < 0.001). Pearson correlation analysis indicated that the sST2 level was positively correlated with the left ventricular mass index in EH patients ( r = 0.454, P < 0.001). Logistic regression analysis showed that the odds ratio (OR) value of LVH was 2.990, suggesting that sST2 is an independent risk factor for LVH in EH patients [OR = 2.990, 95% confidence interval (CI), 1.650–5.419; P < 0.001]. The area under the ROC curve was 0.767 (95% CI, 0.669–0.866; P < 0.001), with a sensitivity of 0.808 and specificity of 0.689, indicating the possibility of considering sST2 as a biomarker for diagnosing LVH. Conclusions Up‐regulation of sST2 is strongly related to LVH in EH patients, is an independent risk factor for hypertensive LVH, and can be used as a biomarker for the diagnosis of LVH.