Predictive role of neutrophil-to-lymphocyte ratio in metabolic syndrome: Meta-analysis of 70,937 individuals.

Objective: Neutrophil-to-lymphocyte ratio (NLR) has been shown to be an independent predictor for cardiovascular diseases and metabolic diseases. The role of NLR in metabolic syndrome (MS) has also been explored albeit with conflicting results. The objective of this study was to assess the predictive role of NLR in MS.

Rosiglitazone reduces diabetes angiopathy by inhibiting mitochondrial dysfunction dependent on regulating HSP22 expression.

The effects of rosiglitazone (RSG) in patients with type 2 diabetes mellitus (T2DM) remain controversial. Here, we first used network pharmacology to identify the common targets of RSG in the treatment of diabetes angiopathy (DA). Enrichment analysis found that the common genes were involved in the inflammatory response, leukocyte cell-cell adhesion, mitochondrion organization and oxidative stress.

HIF-1α mediates the protective effect of plasma extracellular particles induced by remote ischaemic preconditioning on oxidative stress injury in human umbilical vein endothelial cells.

Remote ischaemic preconditioning (RIPC) is considered to alleviate myocardial ischaemia/reperfusion (I/R) injury. The present study explored whether blood plasma particulate matter, which is termed extracellular particles (EPs), and is released from cells during RIPC, could reduce HO-induced damage in human umbilical vein endothelial cells (HUVECs). Firstly, EPs were derived from volunteers who did or did not undergo RIPC.

Pim-2 kinase inhibits inflammation by suppressing the mTORC1 pathway in atherosclerosis.

Background: Inflammatory immunity theory has raised considerable concern in the pathogenesis of atherosclerosis. Proviral integration site of murine 2 (Pim-2) kinases functions in apoptosis pathways and the anti-inflammatory response. Here, we investigated whether Pim-2 kinase inhibits atherosclerotic inflammation by suppressing the mTORC1 pathway.

Plasma exosomes induce inflammatory immune response in patients with acute myocardial infarction.

Exosomes are a kind of nanoscale extracellular vesicles with diameters of 30-100 nm and act as intracellular communication vehicles to influence cellular activities. Emerging pieces of evidence have indicated that exosomes play important roles in inflammation. However, the biological roles of plasma exosomes in acute myocardial infarction (AMI) patients have remained largely unexplored.

LncRNA GAS5 inhibits NLRP3 inflammasome activation-mediated pyroptosis in diabetic cardiomyopathy by targeting miR-34b-3p/AHR.

Long noncoding RNA GAS5 is down-regulated in cardiomyocytes in diabetic cardiomyopathy (DCM). Here, we studied the involvement of GAS5 in DCM by analyzing its expression in DCM mouse model and cardiac muscle cell line (HL-1 cells). Compared with normal mice, GAS5 was severely down-regulated in heart tissues of DCM mice.

NSD2 silencing alleviates pulmonary arterial hypertension by inhibiting trehalose metabolism and autophagy.

Nuclear receptor binding SET domain 2 (NSD2)-mediated metabolic reprogramming has been demonstrated to regulate oncogenesis via catalyzing the methylation of histones. The present study aimed to investigate the role of NSD2-mediated metabolic abnormality in pulmonary arterial hypertension (PAH). Monocrotaline (MCT)-induced PAH rat model was established and infected with adeno-associated virus carrying short hairpin RNA (shRNA) targeting NSD2.

FoxO4 promotes myocardial ischemia-reperfusion injury: the role of oxidative stress-induced apoptosis.

Myocardial cell apoptosis is the main pathophysiological process underlying ischemia-reperfusion (I/R) injury. FoxO4, which was initially identified as a tumor suppressor that limits cell proliferation and induces apoptosis, plays diverse roles in cardiovascular diseases. However, its contribution to myocardial I/R injury remains unclear.

Plasma exosomes induced by remote ischaemic preconditioning attenuate myocardial ischaemia/reperfusion injury by transferring miR-24.

Remote ischaemic preconditioning (RIPC) is well known to protect the myocardium against ischaemia/reperfusion injury (IRI). Exosomes are small extracellular vesicles that have become the key mediators of intercellular communication. Various studies have confirmed that circulating exosomes mediate RIPC.

A novel fibroblast growth factor-1 ligand with reduced heparin binding protects the heart against ischemia-reperfusion injury in the presence of heparin co-administration.

Aims: Fibroblast growth factor 1 (FGF1), a heparin/heparan sulfate-binding growth factor, is a potent cardioprotective agent against myocardial infarction (MI). The impact of heparin, the standard of care for MI patients entering the emergency room, on cardioprotective effects of FGF1 is unknown, however.

Methods And Results: To address this, a rat model of MI was employed to compare cardioprotective potentials (lower infarct size and improve post-ischemic function) of native FGF1 and an engineered FGF1 (FGF1ΔHBS) with reduced heparin-binding affinity when given at the onset of reperfusion in the absence or presence of heparin.

Pim-2 protects H9c2 cardiomyocytes from hypoxia/reoxygenation-induced apoptosis via downregulation of Bim expression.

We know that silencing Bim, a pro-apoptosis protein, significantly attenuates glucose and oxygen-deprived induced apoptosis in cardiomyocytes. However, the mechanisms underlying the regulation of the Bim activation in the heart have remained unknown. Pim-2 is one of three Pim serine/threonine kinase family members thought to be involved in cell survival and proliferation.

Pathogenesis, diagnosis and treatment of cerebral fat embolism.

In this study, we analyzed two cases of pure cerebral fat embolism and reviewed related literatures to explore the pathogenesis, clinical manifestations, diagnosis and treatment of cerebral fat embolism, improve the treatment efficiency and reduce the misdiagnosis rate. In our cases, patients fully returned to consciousness at the different times with good prognosis, normal vital signs and without obvious sequelae. For patients with the limb fractures, who developed coma without chest distress, dyspnea or other pulmonary symptoms 12 or 24 h post injury, cerebral fat embolism should be highly suspected, except for those with intracranial lesions, such as delayed traumatic intracerebral hemorrhage, etc.

Rapamycin protects cardiomyocytes against anoxia/reoxygenation injury by inducing autophagy through the PI3k/Akt pathway.

The purpose of this study was to investigate the potential cardioprotection roles of Rapamycin in anoxia/reoxygenation (A/R) injury of cardiomyocytes through inducing autophagy, and the involvement of PI3k/Akt pathway. We employed simulated A/R of neonatal rat ventricular myocytes (NRVM) as an in vitro model of ischemial/reperfusion (I/R) injury to the heart. NRVM were pretreated with four different concentrations of Rapamycin (20, 50, 100, 150 μmol/L), and pretreated with 10 mmol/L 3-methyladenine (3MA) for inhibiting autophagy during A/R.

BH3-only protein Bim is upregulated and mediates the apoptosis of cardiomyocytes under glucose and oxygen-deprivation conditions.

Bim is a potent pro-apoptotic BH3-only Bcl-2 member. However, the expression of Bim and its role in cardiac injury induced by ischemia remain unclear. H9c2 cells were subjected to a glucose and oxygen-deprived (GOD) condition in vitro, mimicking ischemia environment in vivo.

How to interpret epicardial adipose tissue as a cause of coronary artery disease: a meta-analysis.

Background: Experimental and clinical studies have suggested that epicardial adipose tissue (EAT) may cause coronary artery disease (CAD). A meta-analysis was conducted to investigate the relationship between EAT and CAD.

Methods: A systematic literature search of Cochrane, Medline, Pubmed, Elsevier, Springerlink, Ovid, and Embase from their respective inceptions to August 2011 was conducted using specific search terms such as 'epicardial adipose tissue' and 'epicardial fat'.