Evaluation of acute myocardial infarction patients with mid-range ejection fraction after emergency percutaneous coronary intervention.

BACKGROUND: There is currently no classification for acute myocardial infarction (AMI) according to left ventricular ejection fraction (LVEF). We aimed to perform a retrospective analysis of patients undergoing emergency percutaneous coronary intervention (PCI), comparing the clinical characteristics, in-hospital acute heart failure and all-cause death events of AMI patients with mid-range ejection fraction (mrEF), preserved ejection fraction (pEF) and reduced ejection fraction (rEF). MATERIAL AND METHODS: Totally 1270 patients were stratified according to their LVEF immediately after emergency PCI into pEF group (LVEF 50% or higher), mrEF group (LVEF 40%-49%) and rEF group (LVEF <40%). Kaplan-Meier curves and log rank tests were used to assess the effects of mrEF, rEF and pEF on the occurrence of acute heart failure and all-cause death during hospitalisation. The Cox proportional hazards model was used for multivariate correction. RESULTS: Compared with mrEF, rEF was an independent risk factor for acute heart failure events during hospitalisation (HR 5.01, 95% CI 3.53 to 7.11, p<0.001), and it was also an independent risk factor for all-cause mortality during hospitalisation (HR 7.05, 95% CI 4.12 to 12.1, p<0.001); Compared with mrEF, pEF was an independent protective factor for acute heart failure during hospitalisation (HR 0.49, 95% CI 0.30 to 0.82, p=0.01), and it was also an independent protective factor for all-cause death during hospitalisation (HR 0.33, 95% CI 0.11 to 0.96, p=0.04). CONCLUSIONS: mrEF patients with AMI undergoing emergency PCI share many similarities with pEF patients in terms of clinical features, but the prognosis is significantly worse than that of pEF patients, suggesting that we need to pay attention to the management of mrEF patients with AMI.

Association between MASP-2 gene polymorphism and risk of infection diseases: A meta-analysis.

BACKGROUND: The role of MASP-2 is vital in the process of complement activation by the lectin pathway. It is generally considered that the functional activation of MASP-2 contribute to the infection disease development process. AIMS: To analyze the association between MASP-2 functional gene (rs72550870) polymorphism and the infection disease risk by a meta-analysis. METHOD: Relevant case-control studies were identified by searching Cochrane Library, PubMed, Emabase, DOAJ, CAB Abstracts, CSA, CINAHL, EBSCO, Scopus, Global Health, Index Copernicus, CA, China National Knowledge Infrastructure (CNKI) databases up to 10th January 2016. The data were extracted and the methodological quality of studies were evaluated. The STATA 12.0 software was used to perform statistical analysis. RESULTS: 9 studies were included. There was no significant association between masp-2 gene (p.D120G, rs72550870) polymorphism and the risk of infection disease under the allele model (G vs. A: OR = 0.89, 95%CI = 0.66-1.21)(P = 0.445>0.05) and the recessive model (AG + GG vs.AA: OR = 0.88, 95%CI = 0.65-1.20) (P = 0.428>0.05). CONCLUSION: This is the first comprehensive meta-analysis indicates that the MASP-2 functional gene (rs72550870) polymorphism is not associated with the infection diseases, and the key functional gene polymorphism of rs72550870 did not increase susceptibility to the infection diseases. Similarly, there were no obvious difference in subgroup analysis based on geographical areas and pathogenic microorganisms.

Exploring the Communal Pathogenesis, Ferroptosis Mechanism, and Potential Therapeutic Targets of Dilated Cardiomyopathy and Hypertrophic Cardiomyopathy via a Microarray Data Analysis.

Background: Cardiomyopathies are a heterogeneous group of heart diseases that can gradually cause severe heart failure. In particular, dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM) are the two main types of cardiomyopathies, yet the independent and communal biological mechanisms of both remain far from elucidated. Meanwhile, ferroptosis is a non-apoptotic form of cell death that has been proven to be associated with cardiomyopathies, but the concrete nature of the interaction remains unclear. Hence, this study explored the pathogenesis and ferroptosis mechanism of HCM and DCM via a bioinformatics analysis. Methods: Six datasets were downloaded from the Gene Expression Omnibus (GEO) database based on the study inclusion/exclusion criteria. After screening the differentially expressed genes (DEGs) and hub genes of HCM and DCM, subsequent analyses, including functional annotation, co-expression, validation, and transcription factors (TF)-mRNA-microRNA (miRNA) regulatory network construction, were performed. In addition, ferroptosis-related DEGs were also identified and verified in HCM and DCM. Results: We found 171 independent DEGs of HCM mainly enriched in the regulation of ERK1 and ERK2 cascade, while 171 independent DEGs of DCM were significantly involved in cell adhesion. Meanwhile, 32 communal DEGs (26 upregulated genes and 6 downregulated genes) and 3 hub genes [periostin (POSTN), insulin-like growth factor-binding protein-5 (IGFBP5), and fibromodulin (FMOD)] were determined to be shared between HCM and DCM and the functional annotation of these genes highlighted the important position of growth hormone in HCM and DCM. Moreover, we identified activating transcription factor 3 (ATF3), lysophosphatidylcholine acyltransferase 3 (LPCAT3), and solute carrier family 1 member 5 (SLC1A5) as ferroptosis-related genes in HCM and STAT3 as a ferroptosis-related gene in DCM. Conclusion: The identified independent and communal DEGs contribute to uncover a potentially distinct and common mechanism of HCM and DCM and ferroptosis-related genes could provide us with a novel direction for exploration. In addition, 3 hub genes could be potential biomarkers or therapeutic targets in patients with cardiomyopathy.

The effect of remote health intervention based on internet or mobile communication network on hypertension patients: Protocol for a systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: To systematically review the impact of remote health interventions based on an internet or mobile communication network on patients with hypertension and to provide a theoretical basis for hypertension patients with the implementation of remote health interventions. METHODS: Data were retrieved from a total of 4 Chinese databases and 3 foreign databases. The Chinese databases included: China National Knowledge Infrastructure (CNKI), WanFang Data, Chinese Biomedical Database (SinoMed), and Chongqing Chinese Science and Technology Journey database (VIP). The foreign language databases included PubMed, The Cochrane Library, and EMbase, and the date range for the search was from the date the database became active to December 1, 2018. After screening and extracting the materials and evaluating the risk of bias in each study (conducted by 2 researchers), the quality of the selected literature was evaluated by Review Manager (RevMan) [Computer program]. Version 5.3. Copenhagen: The Nordic Cochrane Centre, The Cochrane Collaboration, 2014, and the statistical analysis was applied by Stata 12.0 software. RESULT: This study will provide high-quality evidence-based medicine research evidence for remote health interventions on hypertensive patients based on the Internet and mobile communication network using systematic evaluation and meta-analysis methods. CONCLUSION: This systematic review will provide a scientific conclusion as to whether the remote health intervention model based on an internet or mobile communication network can better control blood pressure and improve patient compliance than the traditional nursing intervention model for hypertensive patients. ETHICS AND DISSEMINATION: This protocol for a systematic review and meta-analysis of randomized controlled trials does not require ethical approval and the results of this paper will be published in an open form in internationally influential academic journals. PROTOCOL AND REGISTRATION: A protocol had been registered in PROSPERO CRD42019122404.

Anti-parasitic effects of water-soluble alkaloid fractions from ethanolic extracts of Sophora moorcroftiana seeds in Caenorhabditis elegans.

Parasite infections of humans and animals remain a major global health problem, with limited choice of drugs being available to the treatment of parasitosis in the clinic. Sophora moorcroftiana (S. moorcroftiana) is a shrub that grows in Tibet Plateau of China. Decoction of the seeds has been used as a traditional Tibetan medicine to treat parasitosis for years. But the anti-parasitic effects of water-soluble fractions in the seeds need further investigation. In the present study, the water-soluble alkaloid fractions (E2) were obtained from S. moorcroftiana seeds by refluxing extraction with 60% ethanol and low polarity fraction (E2-a) and high polarity fraction (E2-b) were subsequently isolated from E2 using column chromatography. As a parasite model, Caenorhabditis elegans (C. elegans) were treated with different fractions and their survivals were recorded. The results showed that that E2-a induced a lower survival rate in C. elegans than E2-b and E2. The protoscoleces of Echinococcus granulosus (E. granulosus) were cultured in the presence of E2-a. Compared with E2-b and E2, protoscoleces exhibited decreased survival rate following E2-a treatment. Furtherly, the effects of E2-a on the behavior, brood size, and lifespan of the worms were investigated. Body bend frequencies of the worms treated with the high concentration of E2-a were reduced by two-thirds compared with the control group (P < 0.01). Compared with non-E2-a-treated group, exposure of nematodes to E2-a led to a decrease in head thrashes and pharyngeal pumps frequency (P < 0.01). E2-a treatment resulted in a significantly lower brood size (P < 0.01). Additional E2-a treatment induced a significantly shortened lifespan, compared with the control (P < 0.05). These findings indicated that water-soluble fraction E2-a from S. moorcroftiana seeds was a potential helminthic agent.

Protective effects of drag-reducing polymers on ischemic reperfusion injury of isolated rat heart.

Drag-reducing polymers (DRPs) are blood-soluble macromolecules that can increase blood flow and reduce vascular resistance. The purpose of the present study was to observe the effect of DRPs on ischemic reperfusion (I/R) injury of isolated rat hearts. Experiments were performed on isolated rat hearts subjected to 30 min of ischemia followed by 90 min of reperfusion in Langendorff preparations. Adult Wistar rats were divided into the following five groups: control group, I/R group, group III (I/R and 2×10(-7)  g/ml PEO reperfusion), group IV (I/R and 1×10(-6)  g/ml PEO reperfusion), and group V (I/R and 5×10(-6)  g/ml PEO reperfusion). Left ventricular end-diastolic pressure (LVEDP), left ventricular systolic pressure (LVSP), maximum rate of ventricular pressure increase and decrease ( ± dp/dtmax), heart rate (HR) and coronary flow were measured. Lactate dehydrogenase (LDH) and creatine kinase (CK) activity and coronary flow, myocardial infarction size and cardiomyocytes apoptosis were also assayed. Our results showed that PEO decreased LVEDP and increased LVSP, ± dP/dtmax in group IV and group V compared with the I/R group (all P <  0.05). The coronary flow significantly increased and the activities of LDH and CK in the coronary flow significantly decreased in group IV and group V compared with those in the I/R group (all P <  0.05). Cell apoptosis and myocardial infarction size were reduced in group IV and group V compared with the I/R group (all P <  0.05). Collectively, these results suggested that DRPs had a protective effect on cardiac I/R injury of isolated rat hearts and it may offer a new potential approach for the treatment of acute ischemic heart diseases.

[Correlation among serum MBL, MASP-2, HsCRP and C3 levels in rheumatoid arthritis].

OBJECTIVE: To investigate the correlation among serum levels of manning-binding lectin (MBL), MBL-associated serine proteases-2 (MASP-2), complement C3 and high-sensitive C reactive protein (HsCRP) in patients with rheumatoid arthritis (RA). METHODS: Fasting venous blood were collected from 50 RA patients (25 in active stage and 25 in remission) and 40 healthy subjects for detecting serum levels of MBL, MASP-2, complement C3 and HsCRP using enzyme-linked immunosorbent assay (ELISA) and immune turbidity assay. RESULTS: The serum levels of MBL and MASP-2 were significantly lower and HsCRP level was significantly higher in patients with RA (in both acute stage and remission) than in the healthy control group (P<0.05), but complement C3 level was similar between the RA patients and control group. Bivariate Pearson correlation analysis showed that in RA patients, MBL was positively correlated with MASP-2 level (r=0.550, P=0.001) and negatively with HsCRP (r=-0.323, P=0.022) but not correlated with C3 (r=-0.022, P=0.882); MASP-2 was negatively correlated with HsCRP (r=0.453, P=0.453) and was not correlated with C3 (r=0.049, P=0.738). ROC curve analysis revealed the largest area under curve (AUC) of HsCRP (0.844, P=0.001) and smaller AUCs of MBL (0.025, P=0.001) and MASP-2 (0.266, P=0.001). HsCRP had a much higher sensitivity (84%) than MBL (10%) and MASP-2 (40%) in the diagnosis of RA. CONCLUSION: In RA patients, MBL and MASP-2 are negatively correlated with HsCRP level. Serum MBL and MASP-2 levels decrease with the progression of joint injury in RA patients, suggesting their involvement in the pathological process of RA; but due to their low sensitivity, they are not appropriate indicators for evaluating the disease activity of RA.