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Articles by Y. Chen
Total Records ( 7 ) for Y. Chen
  Y. Chen , S.L. Yang , W.D. Deng and H.M. Mao
  In order to investigate the molecular mechanism of black-traits in the black-bone sheep, differential mRNA fingerprinting by prerential coding sequences amplification method was used to analyze the differential gene expression in live, heart, pancrease and lumbar muscle between the black-bone sheep and the Lanping native sheep, respectively. Seventy-one expressive sequence tags were obtained between the black-bone sheep and the Lanping native sheep. The results showed that the black-trait of black-bone sheep was controlled by major genes, as well as minor genes based on many differential expressive fragments. and also showed among positive expressive sequence tags in the black-bone sheep, one EST had high similarity (99%) to gluttathion-s-transferase of human (GSTs).
  X Hu , X Xu , G Zhu , D Atzler , M Kimoto , J Chen , E Schwedhelm , N Luneburg , R. H Boger , P Zhang and Y. Chen

Background— Asymmetrical methylarginines inhibit NO synthase activity and thereby decrease NO production. Dimethylarginine dimethylaminohydrolase 1 (DDAH1) degrades asymmetrical methylarginines. We previously demonstrated that in the heart DDAH1 is predominantly expressed in vascular endothelial cells. Because an earlier study showed that mice with global DDAH1 deficiency experienced embryonic lethality, we speculated that a mouse strain with selective vascular endothelial DDAH1 deficiency (endo-DDAH1–/–) would largely abolish tissue DDAH1 expression in many tissues but possibly avoid embryonic lethality.

Methods and Results— By using the LoxP/Cre approach, we generated the endo-DDAH1–/– mice. The endo-DDAH1–/– mice had no apparent defect in growth or development compared with wild-type littermates. DDAH1 expression was greatly reduced in kidney, lung, brain, and liver, indicating that in these organs DDAH1 is distributed mainly in vascular endothelial cells. The endo-DDAH1–/– mice showed a significant increase of asymmetric dimethylarginine concentration in plasma (1.41 µmol/L in the endo-DDAH1–/– versus 0.69 µmol/L in the control mice), kidney, lung, and liver, which was associated with significantly increased systolic blood pressure (132 mm Hg versus 113 mm Hg in wild-type). The endo-DDAH1–/– mice also exhibited significantly attenuated acetylcholine-induced NO production and vessel relaxation in isolated aortic rings.

Conclusions— Our study demonstrates that DDAH1 is highly expressed in vascular endothelium and that endothelial DDAH1 plays an important role in regulating blood pressure. In the context that asymmetric methylarginines are broadly produced by many type of cells, the strong DDAH1 expression in vascular endothelium demonstrates for the first time that vascular endothelium can be an important site to actively dispose of toxic biochemical molecules produced by other types of cells.

  F. Bragg , L. Li , M. Smith , Y. Guo , Y. Chen , I. Millwood , Z. Bian , R. Walters , J. Chen , L. Yang , R. Collins , R. Peto , Y. Lu , B. Yu , X. Xie , Y. Lei , G. Luo and Z. Chen


To examine the relationship of self-reported diabetes, and of random blood glucose levels among individuals without known diabetes, with the prevalence of cardiovascular disease in Chinese adults.


We examined cross-sectional data from the China Kadoorie Biobank of 0.5 million people aged 30-79 years recruited from 10 diverse regions of China in the period 2004-2008. Logistic regression was used to estimate the odds ratios of prevalent cardiovascular disease associated with self-reported diabetes, and with measured random blood glucose levels among participants with no history of diabetes, adjusting simultaneously for age, sex, area, education, smoking, alcohol, blood pressure and physical activity.


A total of 3.2% of participants had self-reported diabetes (men 2.9%; women 3.3%) and 2.8% had screen-detected diabetes (men 2.6%; women 2.8%), i.e. they had no self-reported history of diabetes but a blood glucose level suggestive of a diagnosis of diabetes. Compared with individuals without a history of diabetes, the odds ratios associated with self-reported diabetes were 2.18 (95% CI 2.06-2.30) and 1.88 (95% CI 1.75-2.01) for prevalent ischaemic heart disease and stroke/transient ischaemic attack, respectively. Among participants without self-reported diabetes there was a positive association between random blood glucose and ischaemic heart disease and stroke/transient ischaemic attack prevalence (P for trend <0.0001). Below the diabetic threshold (<11.1 mmol/l) each additional 1 mmol/l of random blood glucose was associated with 4% (95% CI 2-5%) and 5% (95% CI 3-7%) higher odds of prevalent ischaemic heart disease and stroke/transient ischaemic attack, respectively.


In this adult Chinese population, self-reported diabetes was associated with a doubling of the odds of prevalent cardiovascular disease. Below the threshold for diabetes there was still a modest, positive association between random blood glucose and prevalent cardiovascular disease.

  D Li , P Chen , A Shi , E Shakiba , R Gergerich and Y. Chen

Seven strains (G1 to G7) of soybean mosaic virus (SMV) and 3 resistance loci (Rsv1, Rsv3, and Rsv4) have been identified in soybean. The interaction of SMV strains and host resistance genes results in resistant (symptomless), susceptible (mosaic), or necrotic (leaf and stem necrosis) reactions. The necrotic reaction may be gene dosage dependent and influenced by temperature. Using a set of soybean isolines and hybrids containing homozygous or heterozygous alleles of rsv, Rsv1, Rsv1-n, Rsv3, or Rsv4, this study has explored the relationship of SMV-induced symptoms and resistance gene dosage at different temperatures. Results showed that SMV-inoculated plants carrying Rsv3 or Rsv4 were symptomless at both homozygous and heterozygous states at all temperature regimes. Threshold temperatures for symptoms changing from stem tip necrosis (STN) to mosaic were 30, 33, and 33 °C in G7-inoculated homozygous genotypes V94-3971(Rsv1) and PI 96983 (Rsv1) and G1-inoculated V262 (Rsv1-n), respectively. However, at the heterozygous state, threshold temperature was 30 °C in G7-inoculated V94-3971 x Essex F1 for the symptom change from STN to mosaic, 31 °C in G7-inoculated Essex x PI 96983 F1 from STN to mixture of necrosis and mosaic (N-M), and 32 °C in G1-inoculated V262 x Essex F1 from N-M to mosaic. Incomplete necrosis was observed in the heterozygous state in G1-inoculated V262 x Essex F1 and G7-inoculated PI 96983 x Essex F1 where necrotic and mosaic symptoms were mixed. High temperature (37 °C) tends to mask the expression of mosaic symptoms in both homozygous and heterozygous plants. STN expression in response to temperature was affected by resistance gene, gene dosage, host genetic background, and specific SMV strains. Thus, Rsv3 and Rsv4 are a better choice as source of genetic resistance for breeding SMV-resistant cultivars.

  L Xiao , C Feng and Y. Chen

Glucocorticoid (GC) has been shown to affect the neuronal survival/death through a genomic mechanism, but whether or not it does through a nongenomic mechanism is unknown. Using a previously identified GR-deficient primary hippocampal neuron culture, we show here that a 15-min coexposure of N-methyl-d-aspartate (NMDA) with corticosterone at a stress-induced level significantly enhances neuronal death compared to NMDA alone. This enhancing effect of GC can be mimicked by the BSA-conjugated corticosterone, which is plasma membrane impermeable and cannot be blocked by RU38486 spironolactone. Furthermore, using a calcium-imaging technique, we found that B could increase both the percentage of neurons showing a significant increment of intracellular free calcium ([Ca2+]i) due to NMDA stimulation and the amplitude of [Ca2+]i increment in the individual responsive cells. Interestingly, this boosting effect of GC on [Ca2+]i increment could be blocked by the NMDA receptor subunit 2A (NR2A)-specific antagonist [(R)-[(S)-1-(4-bromo-phenyl)-ethylamino]-(2,3-dioxo-1,2,3,4-tetrahydro-quinoxalin-5-yl)-methyl]-phosphonic acid (NVP-AAM077) but not by the NMDA receptor subunit 2B (NR2B)-specific antagonist Ro25-6981. Moreover, we also found that GC can dramatically attenuate the NMDA-induced activation of ERK1/2 without affecting that of p38; and that the NMDA-induced ERK1/2 activation and its attenuation by GC both can be occluded by the NVP-AAM077 but not by Ro25-6981. Consistently, the enhancing effect of GC on NMDA neurotoxicity can also be blocked by NVP-AAM077 and the ERK1/2 inhibitor PD98059 but not by Ro25-6981 and p38 inhibitor SB203580. Indeed, the NMDA neurotoxicity itself can be blocked by Ro25-6981 or SB203580, whereas it is increased by NVP-AAM077 and PD98059. Therefore, it is probable that NMDA triggers a prodeath signaling through the NR2B-p38 MAPK pathway, and a prosurvival signaling through the NR2A-ERK1/2 MAPK pathway, whereas the latter was negatively regulated by rapid GC action. Taken together, the present data suggest a nongenomic action by GC that enhances NMDA neurotoxicity through facilitating [Ca2+]i increment and attenuating the NR2A-ERK1/2-mediated neuroprotective signaling, implicating a novel pathway underlying the regulatory effect of GC on neuronal survival/death.

  K.S. Kang , Y. Chen , K.J. Han , K.H. Yoo and J. Kim
  Polymer conductivity is key factor to improve the performance of the electronic and photonic devices. Poly(3,4-ethylenedioxythiophene):poly(4-styrenesulfonate) (PEDOT:PSS) films were soaked into 0.03, 0.14, 0.41, and 1.13 M concentrations of HCl–methanol solution for 10, 20, 30, 40, 50, 60, and 70 min. The resulting films were investigated using Fourier transform infrared (FTIR) spectrometry, conductivity measurements, and field emission scanning electron microscopy. The characteristic FTIR absorption peaks of poly(4-styrenesulfonate) (PSS) of the films decreased as the soaking time increased. While PSS absorption peaks appeared in the HCl–methanol soaking solution and increased with the soaking time. The conductivity of PEDOT:PSS film was approximately 1.20 × 10− 6 S/cm before soaking in the HCl–methanol solution. The conductivity of PEDOT:PSS was enhanced nearly three orders of magnitude after soaking the films into the HCl–methanol solvent. The surface of PEDOT:PSS film was initially very smooth. However, numerous humps appeared on the surface of the films after soaking PEDOT:PSS film into the HCl–methanol solution for 10, 20, and 30 min. The number of humps was reduced and disappeared thereafter.
  R. Iv , Q. He , H.P. Wang , J. Jin , Y. Chen and J.H. Chen

Background: We sought investigate the relationship between serum level of sCD30 and recipient/graft survival rates, rejection types, as well as other prognostic factors among Chinese kidney transplant patients.

Materials and methods: We performed enzyme-linked immunosorbent assays of serum sCD30 levels in duplicate among retrospective cohort of 707 renal transplant patients.

Results: The incidences of rejection increased in relation to the pretransplant sCD30 level. The reversal rates of rejection were 100%, 90.6%, and 78.6% for the low, intermediate, and high sCD30 groups. This observation suggested that high levels of sCD30 and pretransplant panel-reactive antibody (PRA)-positive patients are risk factors for acute rejection with odds ratios of 6.862 and 1.756. High sCD30 was an independent risk factor for functional graft survival. The 5-year graft survival rates were 99.39% ± 6.1%, 93.11% ± 1.93%, and 82.07% ± 3.97% among the low, intermediate, and high sCD30 groups, while the 5-year recipient survival rates were 89.25% ± 2.41%, 91.82% ± 1.64%, and 88.85% ± 2.36%, respectively. Increased sCD30 levels were observed among patients who were PRA-positive, cytomegalovirus antigens or antibodies positive, on long-term dialysis, and ≤ 20 years old.

Conclusions: Pretransplant sCD30 serum levels reflect immune status.
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