Predictive value of inflammation-based Glasgow prognostic score for the prognosis in patients with ST-segment elevation myocardial infarction / 中国胸心血管外科临床杂志

@#Objective    To analyze prognostic ability of inflammation-based Glasgow prognostic score (GPS) in patients with ST-segment elevation myocardial infarction (STEMI). Methods    We retrospectively analyzed the clinical data of 289 patients with STEMI admitted to the Department of Emergency in West China Hospital from April 2015 to January 2016. All study subjects were divided into three groups: a group of GPS 0 (190 patients including 150 males and 40 females aged 62.63±12.98 years), a group of GPS 1 (78 patients including 58 males and 20 females aged 66.57±15.25 years), and a group of GPS 2 (21 patients including 16 males and 5 females aged 70.95±9.58 years). Cox regression analysis was conducted to analyze the independent risk factors of predicting long-term mortality of patients with STEMI. Results    There was a statistical difference in long-term mortality (9.5% vs. 23.1% vs. 61.9%, P<0.001) and in-hospital mortality (3.7% vs. 7.7% vs. 23.8%, P<0.001) among the three groups. The Global Registry of Acute Coronary Events (GRACE) scores and Gensini scores increased in patients with higher GPS scores, and the differences were statistically different (P<0.001). Multivariable Cox regression analysis showed that the GPS was independently associated with STEMI long-term all-cause mortality (1 vs. 0, HR: 2.212, P=0.037; 2 vs. 0, HR: 8.286, P<0.001). Conclusion    GPS score is helpful in predicting the long-term and in-hospital prognosis of STEMI patients, and thus may guide clinical precise intervention by early risk stratification.

Research progress of epigenetic regulation of vascular diseases / 中国胸心血管外科临床杂志

@#Epigenetics refers to heritable changes in gene expression independent of DNA nucleotide sequence itself, and the main mechanisms include DNA methylation, histone modifications, noncoding RNAs, and so on. Vascular disease is a chronic disease regulated by the interaction between environmental and genetic factors. In recent years, more and more studies have confirmed that epigenetic regulation plays an important role in the occurrence and development of vascular diseases. This article reviews recent advances in epigenetics in vascular disease.

The Effect of PCDH15 Gene Variations on the Risk of Noise-induced Hearing Loss in a Chinese Population / 生物医学与环境科学（英文）

Noise-induced hearing loss (NIHL) is a complex disease caused by interactions between environmental and genetic factors. This study investigated whether genetic variability in protocadherin related 15 (PCDH15) underlies an increased susceptibility to the development of NIHL in a Chinese population. The results showed that compared with the TT genotype of rs11004085, CT/CC genotypes were associated with an increased risk of NIHL [adjusted odds ratio (OR) = 2.64; 95% confidence interval (CI): 1.14-6.11, P = 0.024]. Additionally, significant interactions between the rs11004085 and rs978842 genetic variations and noise exposure were observed in the high-level exposure groups (P < 0.05). Furthermore, the risk haplotype TAGCC was observed when combined with higher levels of noise exposure (P < 0.05). Thus, our study confirms that genetic variations in PCDH15 modify the susceptibility to NIHL development in humans.

Association of leptin levels with pathogenetic risk of coronary heart disease and stroke: a meta-analysis / Associação entre as concentrações de leptina e o risco patogenético de doença arterial coronariana e acidente vascular cerebral: uma metanálise

Objective This meta-analysis aimed to investigate the association of leptin levels with pathogenetic risk of CHD and stroke. Materials and methods Studies were identified in the PubMed, Embase, and Springer link database without language restriction. Odds ratios (ORs) and corresponding 95% confidence intervals (95% CIs) were used as effect indexes. The association of leptin levels with pathogenetic risk of CHD and stroke, as well as the risk variation of CHD with each additional one unit of leptin level were examined via meta-analysis. The publication bias was assessed via Egger’s linear regression test. Results Eight nested case-control studies consisting of 1,980 patients and 11,567 controls were included for current meta-analysis. ORs (95% CIs) of association of leptin levels with CHD and stroke was 1.90 (1.06, 3.43), and 2.14 (1.48, 3.08), respectively. In addition, significant result was obtained regarding the risk variation of CHD with each additional one unit of leptin level (OR =1.04, 95% CI =1.00‐1.08, P=0.044). There was no significant publication bias as suggested by Egger test outcomes. Conclusion There was a significant association of leptin with pathogenetic risk of CHD and stroke, and raised leptin levels could significantly increase the pathogenetic risk of CHD. .

Objetivo O objetivo desta metanálise foi investigar a associação entre os níveis de leptina e o risco patogenético de doença arterial coronariana e acidente vascular cerebral. Materiais e métodos Foram identificados estudos nas bases de dados PubMed, Embase e Springer Link sem restrição quanto à língua. A razão de chances (OR) e os intervalos de confiança de 95% correspondentes (95% CI) foram usados como índices de efeitos. A associação entre os níveis de leptina e o risco patogenético de doença arterial coronariana e acidente vascular cerebral com cada unidade adicional na concentração de leptina foi analisada por meio de metanálise. O viés da publicação foi avaliado por meio do teste de regressão linear de Egger. Resultados Oito estudos com caso controle aninhado envolvendo 1.980 pacientes e 11.567 controles foram incluídos na metanálise. As ORs (95% CIs) da associação entre as concentrações de leptina e a doença arterial coronariana e o acidente vascular cerebral foram de 1,90 (1,06; 3,43) e 2,14 (1,48; 3,08), respectivamente. Além disso, foram obtidos resultados significativos com a variação de risco para a doença arterial coronariana a cada unidade adicional na concentração de leptina (OR =1,04; 95% CI =1,00‐1,08; P=0,044). Não houve viés de publicação significativo sugerido pelos desfechos no teste de Egger. Conclusão Há associação significativa entre a leptina e o risco patogenético de doença arterial coronariana e acidente vascular cerebral, e concentrações aumentadas de leptina podem elevar significativamente o risco patogenético de doença arterial coronariana. .

Upregulated DJ-1 Promotes Renal Tubular EMT by Suppressing Cytoplasmic PTEN Expression and Akt Activation / 华中科技大学学报（医学）（英德文版）

Recently,phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is suggested as a new agent in the fighting against fibrogenesis.In tumor,DJ-1 is identified as a negative regulator of PTEN.But the expression of DJ-1 and the regulation of PTEN in fibrosis are unclear.Renal fibrosis was induced in 5/6 subtotal nephrectomy rat model.Human proximal tubular epithelial cells (HKC) were treated with transforming growth factor-beta 1 (TGF-β1),or transfected with DJ-1 or PTEN.Confocal microscope was used to investigate the localization of DJ-1 and PTEN.The selective phosphoinositide-3 kinase (PI3K) inhibitor,LY294002,was administered to inhibit PI3K pathway.The DJ-1 and PTEN expression,markers of epithelial-mesenchymal transition (EMT) and Akt phosphorylation were measured by RT-PCR,Western blotting or immunocytochemistry.In vitro,after HKC cells were stimulated with 10 ng/mL TGF-β1 for 72 h,the expression of DJ-1 was increased,and that of PTEN was decreased.In vivo,the same results were identified in 5/6-nephrectomized rats.In normal HKC cells,most of DJ-1 protein localized in cytoplasm,and little in nucleus.TGF-β1 upregulated DJ-1 expression in both cytoplasma and nuclei.In contrary,TGF-β1 emptied cytoplasmic PTEN protein into nucleus.Overexpression of D J-1 decreased the expression of PTEN,promoted the activation of Akt and the expression of vimentin,and also led to the loss of cytoplasmic PTEN.Contrarily,overexpression of PTEN protected HKC cells from TGF-β1-induced EMT.In conclusion,DJ-1 is upregulated in renal fibrosis and DJ-1 mediates EMT by suppressing cytoplasmic PTEN expression and Akt activation.

Role of Protein Kinase Cin Advanced Glycation End Products-induced Epithelial-Mesenchymal Transition in Renal Proximal Tubular Epithelial Cells / 华中科技大学学报（医学）（英德文版）

d by AGE-BSA may be mediated via the activation of PKC signal transduction pathway.