Long non-coding RNA (lncRNA) myocardial infarction-associated transcript (MIAT) has been widely-demonstrated to function as diagnostic markers for acute myocardial infarction (MI). This study was designed to explore the modulatory role of MIAT and its underlying molecular mechanism in MI. Firstly, MI mouse model was developed via ligation of the descending branch of the left coronary artery, and cell model was established through exposure to hypoxic conditions . Online prediction indicated that MIAT could bind to microRNA-10a-5p (miR-10a-5p), while miR-10a-5p was highlighted to bind to early growth response gene-2 (EGR2). MIAT and EGR2 were subsequently determined to be highly-expressed, whereas miR-10a-5p was found to be poorly-expressed in cardiomyocytes exposed to hypoxia as well as in MI mice using RT-qPCR and Western blot assay. The binding relationships between MIAT and miR-10a-5p, and between miR-10a-5p and EGR2 were further confirmed by dual-luciferase reporter and RNA immunoprecipitation assays. The results of in vitro and in vivo experimentation also suggested that overexpression of miR-10a-5p or silencing of MIAT and EGR2 reduced cardiomyocyte apoptosis and increased ATP content, thus alleviating the impairment of cardiac function following MI. In a word, inhibition of MIAT protects against cardiac dysfunction induced by MI through the crosstalk with miR-10a-5p/EGR2.

To investigate the dose-response relationship between cumulative dust exposure (CDE) and cumulative abnormal rate of pulmonary function in coal mixture workers. Three hundred and twenty eight coal mixture workers (exposed group) and 169 nondust-exposed workers (control group) were recruited. Basic information data were collected and pulmonary function tests were performed. Pulmonary function was compared between the two groups after comparing smoking behaviors. Pulmonary function indices [forced vital capacity in 1 second after full inspiration (FVC)%, forced expiratory volume (FEV)1%, and FEV1/FVC%] were compared among groups stratified by service length (exposure duration). The relationship between CDE dose and cumulative abnormal rate of pulmonary function in coal mixture workers was analyzed. Abnormal rate of pulmonary function in the exposed group (35.1%) was significantly higher than the control group (10.1%; p < 0.001); FVC%, FEV1%, and FEV1/FVC% in the exposed group decreased significantly compared with the control group (all p < 0.05). Differences in FVC%, FEV1%, and FEV1/FVC% among coal mixture workers stratified by exposure duration in the exposed group were statistically significant (all p < 0.05). The discernible increase in the cumulative abnormal rate was observed, from ≥ 1000 mg/m(3)·years group to ≥ 1700 mg/m(3)·years group. Correlation analysis revealed a positive correlation between the CDE dose and the cumulative abnormal rate of pulmonary function. Higher abnormal pulmonary function rate was found among coal mixture workers, characterized by decreased pulmonary function indices. Our results suggested a positive relationship between CDE dose and cumulative abnormal pulmonary function rate, and a rapid increase in cumulative abnormal rate within a certain range of CDE dose. A lower limit value of 1000 mg/m(3)·years has reference significance.

The objective of this study was to investigate the association between serum resistin levels and acute cerebral infarction (ACI). PubMed, SpringerLink, Wiley, EBSCO, Ovid, Web of Science, Wanfang, China National Knowledge Infrastructure, and VIP databases (last updated search in October 2014) were exhaustively searched, and data from the eligible studies were extracted and analyzed to assess the association between serum resistin levels and ACI. STATA software (version 12.0, Stata Corporation, College Station, TX, USA) was utilized for data analysis. Ten studies including 1829 ACI patients and 1557 healthy controls were eligible for inclusion in the meta-analysis. Our major result revealed that ACI patients exhibited higher serum resistin levels compared with healthy controls. Asubgroup analysis based on ethnicity showed a significant association between serum resistin levels and ACI in Asians, but surprisingly not in Caucasians. The results of our meta-analysis suggest that serum resistin levels are associated with an increased risk of ACI.

We explored the role of TNFR/TNF-α signalingin apoptosis among alveolar macrophages (AM) and its relevance to the development of coal workers’ pneumoconiosis (CWP). Purified alveolar macrophages (AMs) were prepared from bronchoalveolar lavage fluid harvested from 366 CWP patients and 120 healthy subjects enrolled inthe study. The purified AMs were then divided into control, SOD, anti-TNFR, TNFR and NFkB inhibitor groups and analyzed for apoptosis usingflow cytometry (sub-diploid peak) and western blotting (Bcl-2, Caspase-3 and Caspase-8 expression). We found thatAM apoptosis washigher amongCWP patients than thehealthycontrols. Expression ofBcl-2, Caspase-3 and Caspase-8 was higher inAMs from CWP patientsthan in those from the controlsand correlated with increased AM apoptosis. Univariate and multivariate analyses suggested that CWP grade, initial exposure time, exposure time inyears, and CWP onset agewereall associated with altered levels of Bcl-2, Caspase-3 and Caspase-8. Inhibition of TNFR/TNF-α signaling usinganti-TNFR antibody, SOD or NFkB inhibitionreduced AM apoptosisand decreased Bcl-2, Caspase-3 and Caspase-8 expression. These data suggestinhibition of a TNFR/TNF-α signaling pathway is a potentiallyeffective means ofalleviating CWP by inhibiting AM apoptosis.