It is well known that many genetic factors are involved in the occurrence and progression of atrioventricular block (AV block) and atrial fibrillation (AF). However, the genetic variants discovered so far have only explained parts of these processes. More genes and variants remain to be identified.
View Article and Find Full Text PDFLysophosphatidic acid (LPA), as a phospholipid signal molecule, participates in the regulation of various biological functions. Our previous study demonstrated that LPA induces cardiomyocyte hypertrophy ; however, the functional role of LPA in the post-infarct heart remains unknown. Growing evidence has demonstrated that autophagy is involved in regulation of cardiac hypertrophy.
View Article and Find Full Text PDFBackground/aims: The alterations in myocyte autophagy after myocardial infarction (MI) and the underlying mechanisms have not been fully understood. In this study, we investigated the temporal changes of myocyte autophagy in the remote non-infarcted myocardium in rabbits after MI and the relationships between alterations of myocyte autophagy and left ventricular (LV) remodeling and myocardial oxidative stress.
Methods: Rabbits were assigned to MI or sham operation.
Caffeoylxanthiazonoside (CYT) is an active constituent isolated from the fruit of the L plant. The aim of the present study was to investigate the cardioprotective effects of oral administration of CYT on chronic heart failure (CHF) and its underlying mechanisms. A rat model of CHF was first established, and cardiac function indices, including the heart/body weight index, left heart/body weight index, fractional shortening (FS), ejection fraction (EF), cardiac output (CO) and heart rate (HR), were subsequently determined by cardiac ultrasound.
View Article and Find Full Text PDFBackground: While depression and certain cardiac biomarkers are associated with acute myocardial infarction (AMI), the relationship between them remains largely unexplored. We examined the association between depressive symptoms and biomarkers in patients with AMI.
Methods: We performed a cross-sectional study using data from 103 patients with AMI between March 2013 and September 2014.
Objective: To explore the levels of autoantibodies against AT1-receptor (AT1-AA) in hypertensive patients with acute coronary syndrome (ACS) and observe the in vitro effects of AT1-AA on resting tension of isolated anterior descending artery of vascular ring in male Wistar rats.
Methods: All patients were recruited from June 2007 to August 2008. There were hypertensive patients with ACS (n = 120), those with simple hypertension (n = 253) and those with simple ACS (n = 115).
Nicotinamide adenine dinucleotide 3-phosphate (NADPH) oxidase activity and endoplasmic reticulum (ER) stress are increased after myocardial infarction (MI). In this study, we proposed to test whether activation of the NADPH oxidase in the remote non-infarcted myocardium mediates ER stress and left ventricular (LV) remodeling after MI. Rabbits with MI or sham operation were randomly assigned to orally receive an NADPH oxidase inhibitor apocynin or placebo for 30 days.
View Article and Find Full Text PDFZhonghua Xin Xue Guan Bing Za Zhi
May 2014
Objective: To explore the effect of the autoantibody against the β3-adrenoceptor on rats with experimental heart failure.
Method: The peptide corresponding to the sequence of β3 adrenoceptor was synthesized to actively immunize the rats, ELISA was used to detect the serum level of autoantibody against the β3-adrenoceptor (β3AA). Total IgGs were extracted from the serum containing β3AA in immunized rats.
OBJECTIVE: To summarize the reconstruction exp erience of the electrical injuries in emergency. METHODS: All 309 wounds in 105 patients who suffered from elect rical injuries were reviewed during a 10 year period from Jan. 1st 1986 to Dec.
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