Developing and implementing successful interventions often depend upon effectively addressing ethnicity and social class factors, as these influence sexual behavior and its risks. Sexual attitudes differ across cultures. In most cultures, there are strong standards regarding sexual behavior which differ for men and women. Cultural differences also affect the extent to which early sexual behavior is considered acceptable.

Guidelines for Prevention, I

Factors influencing the decline in stroke mortality: A statement for healthcare professionals from the American Heart Association/American Stroke Association

A beginner's guide to permanent left bundle branch pacing.

The incidence and prevalence of diabetes mellitus is rapidly increasing worldwide at an alarming rate. Type 2 diabetes mellitus (T2DM) is the most prevalent form of diabetes, accounting for approximately 90–95% of the total diabetes cases worldwide. Besides affecting the ability of body to use glucose, it is associated with micro-vascular and macro-vascular complications. Augmented atherosclerosis is documented to be the key factor leading to vascular complications in T2DM patients. The metabolic milieu of T2DM, including insulin resistance, hyperglycemia and release of excess free fatty acids, along with other metabolic abnormalities affects vascular wall by a series of events including endothelial dysfunction, platelet hyperactivity, oxidative stress and low-grade inflammation. Activation of these events further enhances vasoconstriction and promotes thrombus formation, ultimately resulting in the development of atherosclerosis. All these evidences are supported by the clinical trials reporting the importance of endothelial dysfunction and platelet hyperactivity in the pathogenesis of atherosclerotic vascular complications. In this review, an attempt has been made to comprehensively compile updated information available in context of endothelial and platelet dysfunction in T2DM.

/pdf/endothelial-dysfunction-and-platelet-hyperactivity-in-type-2-3vbes9ziat.pdf

Endothelial dysfunction and platelet hyperactivity in type 2 diabetes mellitus: molecular insights and therapeutic strategies.

Mitochondrial fission and selective mitochondrial autophagy (mitophagy) form an essential axis of mitochondrial quality control that plays a critical role in the development of cardiac ischemia-reperfusion (IR) injury. However, the precise upstream molecular mechanism of fission/mitophagy remains unclear. Dual-specificity protein phosphatase1 (DUSP1) regulates cardiac metabolism, but its physiological contribution in the reperfused heart, particularly its influence on mitochondrial homeostasis, is unknown. Here, we demonstrated that cardiac DUSP1 was downregulated following acute cardiac IR injury. In vivo, compared to wild-type mice, DUSP1 transgenic mice (DUSP1TG mice) demonstrated a smaller infarcted area and the improved myocardial function. In vitro, the IR-induced DUSP1 deficiency promoted the activation of JNK which upregulated the expression of the mitochondrial fission factor (Mff). A higher expression level of Mff was associated with elevated mitochondrial fission and mitochondrial apoptosis. Additionally, the loss of DUSP1 also amplified the Bnip3 phosphorylated activation via JNK, leading to the activation of mitophagy. Increased mitophagy overtly consumed mitochondrial mass resulting into the mitochondrial metabolism disorder. However, the reintroduction of DUSP1 blunted Mff/Bnip3 activation and therefore alleviated the fatal mitochondrial fission/mitophagy by inactivating the JNK pathway, providing a survival advantage to myocardial tissue following IR stress. The results of our study suggest that DUSP1 and its downstream JNK pathway are therapeutic targets for conferring protection against IR injury by repressing Mff-mediated mitochondrial fission and Bnip3-required mitophagy.

DUSP1 alleviates cardiac ischemia/reperfusion injury by suppressing the Mff-required mitochondrial fission and Bnip3-related mitophagy via the JNK pathways.

Berberine alleviates cardiac ischemia/reperfusion injury by inhibiting excessive autophagy in cardiomyocytes.

MicroRNAs and autophagy play critical roles in cardiac hypoxia/reoxygenation (H/R)-induced injury. Here, we investigated the function of miR-21 in regulating autophagy and identified the potential molecular mechanisms involved. To determine the role of miR-21 in regulating autophagy, H9c2 cells were divided into the following six groups: control group, H/R group, (miR-21+ H/R) group, (miR-21-negative control + H/R) group, (BEZ235+ H/R) group and (miR-21+ BEZ235+ H/R) group. The cells underwent hypoxia for 1 hr and reoxygenation for 3 hrs. Cell count kit-8 was used to evaluate cell function and apoptosis was analysed by Western blotting. Western blotting and transmission electron microscopy were used to investigate autophagy. We found that miR-21 expression was down-regulated, and autophagy was remarkably increased in H9c2 cells during H/R injury. Overexpression of miR-21 with a miR-21 precursor significantly inhibited autophagic activity and decreased apoptosis, accompanied by the activation of the AKT/mTOR pathway. In addition, treatment with BEZ235, a novel dual Akt/mTOR inhibitor, resulted in a significant increase in autophagy and apoptosis. However, we found that miR-21-mediated inhibition of apoptosis and autophagy was partly independent of Akt/mTOR activation, as demonstrated in cells treated with both miR-21 and BEZ235. We showed that miR-21 could inhibit H/R-induced autophagy and apoptosis, which may be at least partially mediated by the Akt/mTOR signalling pathway.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1111/jcmm.12990

MicroRNA-21 protects against cardiac hypoxia/reoxygenation injury by inhibiting excessive autophagy in H9c2 cells via the Akt/mTOR pathway.

Primary percutaneous coronary intervention, or thombolytic therapy, provides effective myocardial blood reconstruction in patients with acute myocardial infarction to reduce acute myocardial ischemic injury. However, reperfusion can itself induce cardiomyocyte death, termed myocardial reperfusion injury (I/R). Hypoxia/reoxygenation (H/R) induces apoptosis and excessive autophagy among cardiomyocytes, leading to cell death. The present study investigated the effect of curcumin, a natural extract from Curcuma longa, on these two cellular processes in H9c2 myocytes. The levels of cellular apoptosis and autophagy were found to be upregulated in the H9c2 myocytes during H/R and were correlated with a reduced rate of cell survival. However, curcumin significantly suppressed the levels of H/R‑induced apoptosis (expression of annexin V) and autophagy (LC3B‑II/LC3B‑I ratio) in the H9c2 myocytes and promoted cell survival. Additionally, the expression of B‑cell lymphoma 2 (Bcl‑2) was significantly downregulated and the expression levels of Bcl‑2‑associated X protein, beclin‑1, Bcl‑2/adenovirus E1B 19 kDa interacting protein 3 (BNIP3) and silent information regulation 1 (SIRT1) were significantly upregulated in myocytes following H/R injury. These effects on the expression of these proteins were reversed by curcumin treatment. These findings suggested that the protective effect of curcumin against H/R injury in the H9c2 myocytes was through the inhibition of apoptosis and autophagy by inducing the expression of Bcl‑2 and inhibiting the expression levels of Bax, beclin‑1, BNIP3 and SIRT1. Therefore, curcumin may offer a promising therapeutic approach for the treatment of cardiomyocyte injury resulting from I/R.

/pdf/curcumin-inhibits-autophagy-and-apoptosis-in-hypoxia-1y7dhxdk2w.pdf

Curcumin inhibits autophagy and apoptosis in hypoxia/reoxygenation-induced myocytes.

AIMS High and unstable capture thresholds affect the success rate of permanent His-bundle pacing (HBP). We aimed to introduce the modified techniques during different periods and the corresponding success rate of HBP implantation. METHODS AND RESULTS Patients from a single centre who had intrinsic QRS < 120 ms and HBP attempts were included in the study. The success rate and pacing parameters were described for three periods based on procedural modifications, i.e. Stage 1 using the conventional HBP procedure (August 2012 to May 2013), Stage 2 with addition of the dual-lead method (June 2013 to October 2014), and Stage 3 with the further addition of stability assessment during fixation (November 2014 to October 2016). The patients with successful permanent HBP were followed. A total of 310 patients were included with the average age of 70.3 ± 10.7 years. The success rate of acute HBP was 84.85%, 98.3%, and 99.20% during Stages 1-3, respectively (P < 0.001). The permanent HBP implantation rates increased from 77.3% during Stage 1 to 85.7% during Stage 2 and 89.6% during Stage 3 (P = 0.07). The acute His-bundle capture threshold reduced from 1.30 ± 0.7 V/0.5 ms during Stage 1 to 1.11 ± 0.6 V/0.5 ms during Stage 2 and further to 0.85 ± 0.51 V/0.5 ms during Stage 3 (P < 0.001). At the 12-month follow-up, the mean change in the HBP threshold decreased from 0.60 ± 0.59 V/0.5 ms during Stage 1 to 0.33 ± 0.39 V/0.5 ms during Stage 3 (P = 0.002). CONCLUSION The HBP implantation success rate, pacing threshold, and its stability during follow-up were improved by using the dual-lead method and stability assessment techniques.

Pacing parameters and success rates of permanent His-bundle pacing in patients with narrow QRS: a single-centre experience.

Aims: The aim of this study was to examine endothelial dysfunction and inflammation in hypertension and prediabetes by studying adhesion molecules and inflammatory factors Methods and Results: This study included 133 outpatients Participants were categorized into three groups based on the presence or absence of hypertension and prediabetes: control subjects without prediabetes and hypertension (N group, n = 39); patients with hypertension only (H group, n = 34); and patients with hypertension and prediabetes (HD group, n = 60) Hypertension was diagnosed according to JNC7 criteria Prediabetes was defined according to 2010 American Diabetes Association criteria Plasma was isolated from overnight fasting blood samples for enzyme-linked immunosorbent assay (ELISA) analysis of concentrations of intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor-α (TNF-α), P-selectin, and interleukin-6 (IL-6) as indicators of endothelial function and inflammation We found that the H and HD groups showed sig

Peiren Shan

Papers

Berberine alleviates cardiac ischemia/reperfusion injury by inhibiting excessive autophagy in cardiomyocytes.

MicroRNA-21 protects against cardiac hypoxia/reoxygenation injury by inhibiting excessive autophagy in H9c2 cells via the Akt/mTOR pathway.

Curcumin inhibits autophagy and apoptosis in hypoxia/reoxygenation-induced myocytes.

Pacing parameters and success rates of permanent His-bundle pacing in patients with narrow QRS: a single-centre experience.

Serum Markers of Endothelial Dysfunction and Inflammation Increase in Hypertension with Prediabetes Mellitus