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Articles by Y Yan
Total Records ( 4 ) for Y Yan
  H Liu , S Li , Y Zhang , Y Yan and Y. Li

Glutamate decarboxylase 65 (GAD65) produces -aminobutyric acid, the main inhibitory neurotransmitter in adult mammalian brain. Previous experiments, performed in brain, showed that GAD65 gene possesses two TATA-less promoters, although the significance is unknown. Here, by rapid amplification of cDNA ends method, two distinct GAD65 mRNA isoforms transcribed from two independent clusters of transcription start sites were identified in post-natal rat testis. RT–PCR results revealed that the two mRNA isoforms had distinct expression patterns during post-natal testis maturation, suggesting that GAD65 gene expression was regulated by alternative promoters at the transcription level. By using GAD65-specific antibodies, western blotting analysis showed that the 58-kDa GAD65, N-terminal 69 amino acids truncated form of full-length GAD65 protein, was developmentally expressed during post-natal testis maturation, suggesting that GAD65 gene expression in testis may also be regulated by post-translational processing. Confocal immunofluorescence microscopy revealed that GAD65 protein was presented in Leydig cells of Day 1 testis, primary spermatocytes and spermatids of post-natal of Day 90 testis. The above results suggested that GAD65 gene expression is dynamically regulated at multiple levels during post-natal testis maturation.

  Z Zhu , Y Yan , Q Wang , J Qian and J. Ge

The serum proteins creatine kinase isoenzyme MB (CK-MB) and cardiac troponin T are classic biomarkers of cardiac ischemic damage in clinical practice, which can sensitively detect myocardial necrosis, while other two serum proteins, ischemia-modified albumin and N-terminal pro-B-type natriuretic peptide (NT-proBNP), have been recently identified as novel biomarkers of myocardial ischemia. In this study, the four biomarkers were detected in sera from 44 eligible patients with suspected coronary heart disease (CHD) before and after treadmill exercise test (TET), electrocardiogram (ECG) was measured during TET (TET-ECG) and invasive examination of coronary angiography (CAG), which is the ‘gold standard’ of CHD diagnosis, was also performed. For CAG, 25 patients were positive and 19 were negative, whereas for TET-ECG the numbers were 19 and 25, respectively. Among these four biomarkers, the NT-proBNP level in CAG positive group was much higher than those in CAG negative group both before and after TET, with statistical significance before TET (P = 0.008). Furthermore, according to receiver operating characteristic (ROC) curve, the serum biomarker NT-proBNP showed diagnostic effect of CHD and its cutoff value was 67 pg/ml, thus 30 of the patients in this study were NT-proBNP positive and 14 were negative. And it was found that NT-proBNP obviously enhanced the sensitivity of examinations whether analyzed alone or in combination with TET-ECG. More importantly, all the patients who were negative in both NT-proBNP and TET-ECG tests turned out to be CAG negative, which means that the combination of these two non-invasive examinations might take the place of invasive examination of CAG for CHD diagnosis. Further studies with more patients are warranted to validate the findings in this paper.

  M Hongbao , Y Yan and C. Shen

Background: Calcitonin gene-related peptide (CGRP) and substance P (SP) play counter-regulatory roles in coronary flow. This study is to assess whether effects of CGRP and SP are gender-specific. Methods: Langendorff-perfused hearts were used to compare coronary flow rates among 119 wild-type, -CGRP and SP receptor knockout mice under various perfusion pressures (20, 30, 40, 50 mmHg). Results: For mouse heart coronary flow rate, deletion of -CGRP gene resulted in significant reduction for both genders at all pressures; female CGRP knockout showed 15.3% reduction (P < .01); male CGRP knockout showed 13.8% reduction (P < .01); no significant difference between male and female CGRP knockout; female SP receptor knockout showed 13.9% increase (P < .01); female SP receptor knockout had a greater percentage decrease than male (P < .01). Conclusions: CGRP plays similar roles as a vasodilator in males and females. SP seems to act as a vasoconstrictor in females.

  D Zhang , X Jiang , P Fang , Y Yan , J Song , S Gupta , A. I Schafer , W Durante , W. D Kruger , X Yang and H. Wang

Background— Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular disease. Monocytes display inflammatory and resident subsets and commit to specific functions in atherogenesis. In this study, we examined the hypothesis that HHcy modulates monocyte heterogeneity and leads to atherosclerosis.

Methods and Results— We established a novel atherosclerosis-susceptible mouse model with both severe HHcy and hypercholesterolemia in which the mouse cystathionine β-synthase (CBS) and apolipoprotein E (apoE) genes are deficient and an inducible human CBS transgene is introduced to circumvent the neonatal lethality of the CBS deficiency (Tg-hCBS apoE–/– Cbs–/– mice). Severe HHcy accelerated atherosclerosis and inflammatory monocyte/macrophage accumulation in lesions and increased plasma tumor necrosis factor- and monocyte chemoattractant protein-1 levels in Tg-hCBS apoE–/– Cbs–/– mice fed a high-fat diet. Furthermore, we characterized monocyte heterogeneity in Tg-hCBS apoE–/– Cbs–/– mice and another severe HHcy mouse model (Tg-S466L Cbs–/–) with a disease-relevant mutation (Tg-S466L) that lacks hyperlipidemia. HHcy increased monocyte population and selective expansion of inflammatory Ly-6Chi and Ly-6Cmid monocyte subsets in blood, spleen, and bone marrow of Tg-S466L Cbs–/– and Tg-hCBS apoE–/– Cbs–/– mice. These changes were exacerbated in Tg-S466L Cbs–/– mice with aging. Addition of l-homocysteine (100 to 500 µmol/L), but not l-cysteine, maintained the Ly-6Chi subset and induced the Ly-6Cmid subset in cultured mouse primary splenocytes. Homocysteine-induced differentiation of the Ly-6Cmid subset was prevented by catalase plus superoxide dismutase and the NAD(P)H oxidase inhibitor apocynin.

Conclusion— HHcy promotes differentiation of inflammatory monocyte subsets and their accumulation in atherosclerotic lesions via NAD(P)H oxidase–mediated oxidant stress.

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