Shou-Yan Zhang

Objective: To investigate the association between gamma-glutamyl transferase (GGT) and type 2 diabetes mellitus (T2DM) risk. Methods: This was a secondary analysis based on a publicly available DRYAD dataset that included 15 444 study participants that received medical examinations at a single centre in Japan between 2004 and 2015. Crude, minimally-adjusted and fully-adjusted regression models were used to evaluate the relationship between GGT levels and T2DM risk. Results: The study participants (mean ± SD age of 43.72 ± 8.90 years; 8415 of 15 444 [54.49%] were male) were followed-up for a median of 1968 days (5.39 years). After adjusting for potential covariates, a non-linear relationship between the baseline GGT level and T2DM incidence was observed. The inflection point for T2DM risk was 10 IU/l GGT; below this point, the T2DM incidence increased by 1.18-fold per unit change in GGT. Above this point, the association between GGT and the incidence rate of T2DM became nonsignificant. Conclusion: Baseline GGT exhibited a non-linear association with T2DM incidence. Elevated GGT levels should be incorporated into routine screening for individuals at high risk of T2DM, allowing for early intervention targeting GGT to potentially reduce T2DM-related morbidity.

Objective: Qishen Yiqi Drop Pill (QSYQ) has been recognized as a potential protective agent for various cardiovascular diseases. However, the effect of QSYQ in cardiac complications associated with diabetes is not clear currently. In this study, we investigate whether QSYQ could exert cardiac protective effects against high glucose‐induced injuries in cardiac H9c2 cells.Methods: H9c2 cells were exposed to 24 hours of high glucose in presence or absence of QSYQ and LY294002. Cell cytotoxicity, apoptosis, reactive oxygen species (ROS) generation, mitochondrial membrane potential and mitochondrial permeability transition pore (mPTP) opening were determined. Levels of bax, bcl‐2, p53, cleaved caspase‐3, PI3K and Akt were evaluated by Western blot.Results: Our data indicated that QSYQ significantly increased the cell viability and decreased cytotoxicity. By analysing the apoptotic rate as well as the expression levels of cytoapoptosis‐related factors including cleaved caspase‐3, bax, bcl‐2, and p53, we found that QSYQ could remarkably suppress apoptosis of cardiomyoblasts caused by high glucose. In addition, it also showed that QSYQ reduced the generation of ROS. We further found that QSYQ treatment could inhibit the loss of mitochondrial membrane potential and mPTP opening. Moreover, Western blot analysis showed enhanced phosphorylation of PI3K/Akt. The specific inhibitor of PI3K, LY294002 not only inhibited QSYQ induced PI3K/Akt signalling pathway activation, but alleviated its protective effects.Conclusions: In summary, these findings demonstrated that QSYQ effectively protected H9c2 cells against the series injuries due to high glucose at least partially by activating the PI3K/Akt signalling pathway.

The clinical use of doxorubicin (DOX) is limited by its toxic effect. However, there is no specific drug that can prevent DOX‐related cardiac injury. C1qTNF‐related protein‐6 (CTRP6) is a newly identified adiponectin paralog with many protective functions on metabolism and cardiovascular diseases. However, little is known about the effect of CTRP6 on DOX‐induced cardiac injury. The present study aimed to investigate whether CTRP6 could protect against DOX‐related cardiotoxicity. To induce acute cardiotoxicity, the mice were intraperitoneally injected with a single dose of DOX (15 mg/kg). Cardiomyocyte‐specific CTRP6 overexpression was achieved using an adenoassociated virus system at 4 weeks before DOX injection. The data in our study demonstrated that CTRP6 messenger RNA and protein expression were decreased in DOX‐treated hearts. CTRP6 attenuated cardiac atrophy induced by DOX injection and inhibited cardiac apoptosis and improved cardiac function in vivo. CTRP6 also promoted the activation of protein kinase B (AKT/PKB) signaling pathway in DOX‐treated mice. CTRP6 prevented cardiomyocytes from DOX‐induced apoptosis and activated the AKT pathway in vitro. CTRP6 lost its protection against DOX‐induced cardiac injury in mice with AKT inhibition. In conclusion, CTRP6 protected the heart from DOX‐cardiotoxicity and improves cardiac function via activation of the AKT signaling pathway.

Objective: Mental health condition of medical professionals in China is under-recognized. The current study aimed to determine the prevalence of depression and anxiety among healthcare professionals and explore the potential influence factors. Method: The study employed a cross-sectional design. All employees were surveyed in the first week of September 2017. General information included gender, age, workload, workplace violence, sleep quality and so on. Depression and anxiety were evaluated using PHQ-9 and GAD-7, respectively. SPSS 22.0 was used for data analysis. Logistic regression was conducted to explore risk factors contributed to metal health. Results: A total of 1,950 questionnaires were delivered, and 1,864 were returned with a response rate of 95.6%. The prevalence of depression and anxiety were 24.1% and 28.9%. As for workload, the average number of beds in charge per month is 65.97±95.58 beds, among which internal medicine department and surgical department endure more workloads. Though workers in ER and ICU manage fewer beds, they bear the longest nonstop working length in the previous month (19.18±10.82 h). There were 78.0% had suffered WPV in the preceding year. Staffs in ER and ICU are at higher risk to physical violence, especially doctors. Regarding to sleep quality, only 9.2% participants reported that they sleep well. Logistic regression indicated that workplace violence and sleep quality were independent risk factors for both anxiety and depression. Conclusion: The current study revealed the devastating conditions of mental disorders in medical workers and associated factors. Effective interventions are necessary to improve this situation.

Combined value of red blood cell distribution width and global registry of acute coronary events risk score on predicting longterm major adverse cardiac events in STEMI patients undergoing primary PCI Combined value of red blood cell distribution width and global registry of acute coronary events risk score on predicting long-term major adverse cardiac events in STEMI patients undergoing primary PCI

Association between matrix metalloproteinase 9 C-1562T polymorphism and the risk of coronary artery disease: an update systematic review and meta-analysis Association between matrix metalloproteinase 9 C-1562T polymorphism and the risk of coronary artery disease: an update systematic review and meta-analysis

Irisin, a newly identified hormone, is critical to modulating body metabolism, thermogenesis and reducing oxidative stresses. However, whether irisin protects the heart against myocardial ischemia and reperfusion (I/R) injury remains unknown. In this study, we determine the effect of irisin on myocardial I/R injury in the Langendorff perfused heart and cultured myocytes. Adult C57/BL6 mice were treated with irisin (100 mg/kg) or vehicle for 30 min to elicit preconditioning. The isolated hearts were subjected to 30 min ischemia followed by 30 min reperfusion. Left ventricular function was measured and infarction size were determined using by tetrazolium staining. Western blot was employed to determine myocardial SOD‐1, active‐caspase 3, annexin V, p38, and phospho‐p38. H9c2 cardiomyoblasts were exposed to hypoxia and reoxygenation for assessment of the effects of irisin on mitochondrial respiration and mitochondrial permeability transition pore (mPTP). Irisin treatment produced remarkable improvements in ventricular functional recovery, as evident by the increase in RPP and attenuation in LVEDP. As compared to the vehicle treatment, irisin resulted in a marked reduction of myocardial infarct size. Notably, irisin treatment increased SOD‐1 and p38 phosphorylation, but suppressed levels of active‐caspase 3, cleaved PARP, and annexin V. In cardiomyoblasts exposed to hypoxia/reoxygenation, irisin treatment significantly attenuated hypoxia/reoxygenation (H/R), as indicated by the reduction of lactate dehydrogenase (LDH) leakage and apoptotic cardiomyocytes. Furthermore, irisin treatments suppressed the opening of mPTP, mitochondrial swelling, and protected mitochondria function. Our results indicate that irisin serves as a novel approach to eliciting cardioprotection, which is associated with the improvement of mitochondrial function.