DataSheet_1_Fibroblast growth factor 21 and prognosis of patients with cardiovascular disease: A meta-analysis.docx

BackgroundThe role of fibroblast growth factor 21 (FGF21) in predicting the long-term prognosis of patients with cardiovascular disease (CVD) remains unknown.MethodsA comprehensive search in PubMed, Embase, and the Cochrane Library was performed to identify studies reporting the association between FGF21 and prognosis among patients with CVD. A meta-analysis was performed, with patients stratified by coronary artery disease (CAD) or heart failure (HF). The endpoint of CAD or HF was major adverse cardiovascular events defined by each study and a composite of death or HF readmission, respectively. The I2 method and linear regression test of funnel plot asymmetry were used to test heterogeneity (I2 > 50% indicates substantial heterogeneity) and publication bias (asymmetry P ResultsA total of 807 records were retrieved, and nine studies were finally included. Higher FGF21 levels were significantly associated with the risk of major adverse cardiovascular events in patients with CAD (multivariate hazard ratio [HR]: 1.77, 95% confidence interval [CI]: 1.40–2.23, P 2 = 0%, fixed-effect model). Increased FGF21 levels were also associated with the risk of all-cause death among patients with CAD (multivariate HR: 2.67, 95% CI: 1.25–5.72, P 2 = 64%, random-effect model). No association was found between FGF21 and the endpoint among patients with HF (HR: 1.57, 95% CI: 0.99–2.48, P > 0.05, random-effect model), but a large heterogeneity (I2 = 95%) and potential publication bias (Asymmetry P ConclusionIncreased FGF21 levels were independently associated with poor prognosis of CAD, whereas the role of FGF21 in predicting clinical outcomes of HF requires further investigation.</p

In vitro proliferation assays using human VSMCs(A) and ECs(B), stimulated with PDGF at 50 ng/ml and ECGF at 50 ng/ml, respectively.

<p>**P<0.01 and *P<0.05, the cell counts of the BMS group vs. those of the CREGES and SES groups.</p

Nanoporous CREG-Eluting Stent Attenuates In-Stent Neointimal Formation in Porcine Coronary Arteries

<div><p>Background</p><p>The goal of this study was to evaluate the efficacy of a nanoporous CREG-eluting stent (CREGES) in inhibiting neointimal formation in a porcine coronary model.</p> <p>Methods</p><p>In vitro proliferation assays were performed using isolated human endothelial and smooth muscle cells to investigate the cell-specific pharmacokinetic effects of CREG and sirolimus. We implanted CREGES, control sirolimus-eluting stents (SES) or bare metal stents (BMS) into pig coronary arteries. Histology and immunohistochemistry were performed to assess the efficacy of CREGES in inhibiting neointimal formation.</p> <p>Results</p><p>CREG and sirolimus inhibited in vitro vascular smooth muscle cell proliferation to a similar degree. Interestingly, human endothelial cell proliferation was only significantly inhibited by sirolimus and was increased by CREG. CREGES attenuated neointimal formation after 4 weeks in porcine coronary model compared with BMS. No differences were found in the injury and inflammation scores among the groups. Scanning electron microscopy and CD31 staining by immunohistochemistry demonstrated an accelerated reendothelialization in the CREGES group compared with the SES or BMS control groups.</p> <p>Conclusions</p><p>The current study suggests that CREGES reduces neointimal formation, promotes reendothelialization in porcine coronary stent model.</p> </div

Morphometric analysis in 4 weeks.

*<p>P <0.05 vs. BMS.</p

The coronary arteries of pigs implanted with BMS, SES, or CREGES.

<p>The coronary arteries were harvested 4 weeks after stent implantation, paraformaldehyde-fixed, paraffin-embedded, and stained with HE. The upper panel shows representative arteries from the BMS (a) and SES (b), and CREGES(c) groups. The middle panel shows high-magnification images of the arteries in the corresponding groups. The lower panel shows representative coronary angiographic images immediately after (d, f), and 4 weeks after stent implantation (e, g) in the BMS, SES, and CREGES groups. The white arrow indicates the site implanted. The implantation of BMS induced significant neointima formation. In contrast, the CREGES and SES significantly reduced neointima formation.</p

The proportion of CREG protein remaining bound to the stent.

<p>Each data point represents the mean value obtained from 12 wire segments (error bars denote ±1 SD).</p

MOESM1 of Association between insulin receptor substrate-1 polymorphisms and high platelet reactivity with clopidogrel therapy in coronary artery disease patients with type 2 diabetes mellitus

Additional file 1: Figure S1. Flow diagram of the study cohorts. Table S1. Primers, PCR product lengths, and reaction conditions of selected tagSNPs. Table S2. Information on genotyped SNPs of IRS-1. Table S3. Genotypes and allele frequencies of IRS-1 polymorphisms according to platelet activity in non-DM patients. Table S4. Linkage disequilibrium measurements between SNP pairs of eight tag SNPs of the IRS-1 gene. Table S5. Genotypes and allele frequencies of IRS-1 polymorphisms in DM and non-DM patients. Table S6. Baseline demographic data and clinical characteristics according to the rs13431554

CREGES accelerate reendothelialization.

<p>SEM images (a:BMS, b:DES, c:CREGES,40X) from the porcine coronary arteries 5 day after the stents implanted. The coronary arteries were collected 2 and 4 weeks after the stent implantation. Paraffin-embedded sections were immunostained with an anti-CD31 antibody to reveal the endothelium (the brown layer covering the neointima). CREGES implantation promoted reendothelialization of the injured coronary artery to a greater extent than BMS or SES implantation at 2 weeks. Representative images of stained sections in the (e) BMS, (f) SES, and (g) CREGES groups at 2 weeks and in the (i) BMS, (j) SES, and (k) CREGES groups at 4 weeks. Negative control (d,h).</p

Representative photomicrographs of a-SMC actin (a, b, c), CD68(d, e, f) and Ki67 (g, h, i) in the BMS, SES, and CREGES groups.

<p>Cell replication (Ki67) occurred less frequently around the SES and CREGES struts compared with the BMS struts.</p

Endothelialization analysis at 5days, 2 weeks and 4 weeks.

*<p>P <0.05 vs.CREGES.</p