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Articles by C. Zhang
Total Records ( 13 ) for C. Zhang
  J Yang , Y Park , H Zhang , X Xu , G. A Laine , K. C Dellsperger and C. Zhang

We hypothesized that the interaction between tumor necrosis factor- (TNF-)/nuclear factor-B (NF-B) via the activation of IKK-β may amplify one another, resulting in the evolution of vascular disease and insulin resistance associated with diabetes. To test this hypothesis, endothelium-dependent (ACh) and -independent (sodium nitroprusside) vasodilation of isolated, pressurized coronary arterioles from mLeprdb (heterozygote, normal), Leprdb (homozygote, diabetic), and Leprdb mice null for TNF- (dbTNF–/dbTNF–) were examined. Although the dilation of vessels to sodium nitroprusside was not different between Leprdb and mLeprdb mice, the dilation to ACh was reduced in Leprdb mice. The NF-B antagonist MG-132 or the IKK-β inhibitor sodium salicylate (NaSal) partially restored nitric oxide-mediated endothelium-dependent coronary arteriolar dilation in Leprdb mice, but the responses in mLeprdb mice were unaffected. The protein expression of IKK- and IKK-β were higher in Leprdb than in mLeprdb mice; the expression of IKK-β, but not the expression of IKK-, was attenuated by MG-132, the antioxidant apocynin, or the genetic deletion of TNF- in diabetic mice. Leprdb mice showed an increased insulin resistance, but NaSal improved insulin sensitivity. The protein expression of TNF- and NF-B and the protein modification of phosphorylated (p)-IKK-β and p-JNK were greater in Leprdb mice, but NaSal attenuated TNF-, NF-B, p-IKK-β, and p-JNK in Leprdb mice. The ratio of p-insulin receptor substrate (IRS)-1 at Ser307 to IRS-1 was elevated in Leprdb compared with mLeprdb mice; both NaSal and the JNK inhibitor SP-600125 reduced the p-IRS-1-to-IRS-1 ratio in Leprdb mice. MG-132 or the neutralization of TNF- reduced superoxide production in Leprdb mice. In conclusion, our results indicate that the interaction between NF-B and TNF- signaling induces the activation of IKK-β and amplifies oxidative stress, leading to endothelial dysfunction in type 2 diabetes.

  C. Yan , C. Zhang , Q.Y. Zhang , T.W. Liu and H. Huang
  The low-energy bombardment of Au (1 1 1) surface by noble metal atoms is studied with molecular dynamics (MD) simulations. With the incident-energy dependence of adatom yields, sputtering yields, and vacancy yields for different projectiles, we find that the implantation of projectiles in shallow layers below surface can be distinguished by subplantation (in the first and second layers) and implantation (deeper than the third layer). The transition from subplantation to implantation occurs at the incident energy of about 45eV for the low-energy bombardment of noble metal atoms on Au (1 1 1). The incident-energy dependence of defect yields is obviously different for the subplantation and implantation of projectiles. Based on our MD simulations, we discuss the influence of low-energy bombardment on film growth and the guide to the search for optimum deposition parameters.
  Juvenile cobias, Rachycentron canadum, were fed extruded diets containing toasted defatted soybean meal (SBM) or untoasted defatted SBM [white flakes (WF)] to study growth and feed conversion, and to study if SBM induces morphological changes in the gastrointestinal (GI) tract. Three diets were produced: a fish meal-based control diet (FM diet) with 558 g FM kg−1, and two diets with 335 g FM and either 285 g SBM kg−1 (SBM diet) or 285 g WF kg−1 (WF diet). The diets were extruded at approximately 120°C with 280 g kg−1 moisture. Triplicate groups of cobias (mean weight: 25.9 g) were fed the diets during 6 weeks. Feed intake of the FM and SBM diets were not significantly different, whereas the cumulative feed intake of cobias fed the WF diet was lower (P<0.05) than that of cobias fed the FM and SBM diets after the first 21-day period. Specific growth rate and feed conversion ratio were not significantly different between cobias fed the FM and SBM diets, but significantly poorer results were obtained in cobias fed the WF diet. No morphological differences in the GI tract could be attributed to the diets, and cobias fed soy did not develop enteritis in the distal intestine.
  Y Cheng , X Liu , J Yang , Y Lin , D. Z Xu , Q Lu , E. A Deitch , Y Huo , E. S Delphin and C. Zhang

Phenotypic modulation of vascular smooth muscle cells (VSMCs) plays a critical role in the pathogenesis of a variety of proliferative vascular diseases. Recently, we have found that microRNA (miRNA) miR-145 is the most abundant miRNA in normal vascular walls and in freshly isolated VSMCs; however, the role of miR-145 in VSMC phenotypic modulation and vascular diseases is currently unknown. Here we find that miR-145 is selectively expressed in VSMCs of the vascular wall and its expression is significantly downregulated in the vascular walls with neointimal lesion formation and in cultured dedifferentiated VSMCs. More importantly, both in cultured rat VSMCs in vitro and in balloon-injured rat carotid arteries in vivo, we demonstrate that the noncoding RNA miR-145 is a novel phenotypic marker and a novel phenotypic modulator of VSMCs. VSMC differentiation marker genes such as SM -actin, calponin, and SM-MHC are upregulated by premiR-145 or adenovirus expressing miR-145 (Ad-miR-145) but are downregulated by the miR-145 inhibitor 2'OMe-miR-145. We have further identified that miR-145-mediated phenotypic modulation of VSMCs is through its target gene KLF5 and its downstream signaling molecule, myocardin. Finally, restoration of miR-145 in balloon-injured arteries via Ad-miR-145 inhibits neointimal growth. We conclude that miR-145 is a novel VSMC phenotypic marker and modulator that is able of controlling vascular neointimal lesion formation. These novel findings may have extensive implications for the diagnosis and therapy of a variety of proliferative vascular diseases.

  H. Yang , Y. Wei , X. Gao , X. Xu , L. Fan , J. He , Y. Hu , X. Liu , X. Chen , Z. Yang and C. Zhang
  Aims  To determine the incidence of gestational diabetes mellitus (GDM) in China and to further identify population specific risk factors for GDM.

Methods  Following a universal GDM screening recommendation, 16 286 pregnant women who underwent a 50-g glucose challenge test from 18 cities in China were followed up through pregnancy. GDM was confirmed by oral glucose tolerance test according to American Diabetes Association criteria.

Results  The incidence of GDM was 4.3%. Previously reported risk factors for GDM, including advanced maternal age, pre-pregnancy obesity and family history of diabetes, were strongly associated with an elevated GDM risk. Moreover, after the adjustment for the above-mentioned risk factors, a history of recurrent vulvovaginal candidiasis, residency in south China and a history of spontaneous abortion were significantly associated with an increased GDM risk; adjusted odds ratio (OR) [95% confidence interval (95% CI)] were 1.97 (1.39, 2.80), 1.84 (1.59-2.13), and 1.46 (1.12, 1.91), respectively.

Conclusions  In this large study of GDM in Chinese women, advanced maternal age, pre-pregnancy overweight or obesity and family history of diabetes were confirmed to be risk factors. In addition, a history of recurrent vulvovaginal candidiasis or spontaneous abortion and residency in south China appeared to be novel risk factors in this population.

  J. Brite , E. J. Shiroma , K. Bowers , E. Yeung , S. K. Laughon , J. G. Grewal and C. Zhang


Gestational diabetes is a common pregnancy complication affecting races/ethnicities disproportionally. Adult height, an indicator of both genetic and early-life factors, is inconsistently associated with gestational diabetes risk. We examined the association and whether it varies by races in a nationally representative US cohort.


Analyses were conducted among 135 861 pregnancies in the Consortium on Safe Labor, 5567 of which were diagnosed with gestational diabetes based on medical records review. Generalized estimating equations were used to estimate odds ratios (95% confidence intervals) of gestational diabetes, controlling for other risk factors including body weight. Additionally, a meta-analysis of 15 761 pregnancies with gestational diabetes and 205 828 without gestational diabetes was conducted to estimate the pooled mean difference in height between those with gestational diabetes and control subjects.


Height was inversely associated with gestational diabetes risk across races/ethnicities, with the strongest association among Asians (P for interaction < 0.01). Comparing extreme quartiles (> 168 vs. < 157 cm), adjusted odds ratios (95% confidence intervals) were 0.18 (0.09-0.36) for Asians/Pacific Islanders, 0.33 (0.29-0.38) for non-Hispanic white women, 0.39 (0.31-0.51) for Hispanics and 0.59 (0.47-0.75) for non-Hispanic black women. Meta-analysis found women with gestational diabetes to be significantly shorter than others.


Taller women are at lower risk of developing gestational diabetes, with the magnitude of association varying significantly across races/ethnicities.

  C. Zhang , C.J. Lian , Z.J. Yang , S.C. Sun , S.S. Zhou and S.L. Niu
  The aim of this study was to investigate the effects of different dietary fatty source on fatty liver performance and liver nutritional components in the goose. The 450, 70 days old France Landaise geese were randomly divided into three groups after a pre-overfeeding week then the goose were given three carbohydrate-rich diet meals a day for 21 days of a carbohydrate-rich diet consisting of boiled and salted maize with 2% fat (goose fat, soybean oil and corn oil) and water added. On days 7 and 21, the circulating levels of Alanine Transarninase (ALT), Glutamic-oxalacetic Transaminase (AST), Triglyeride (TG), Low-Density Lipoprotein (LDL), High Density Lipoprotein (HDL), Total Protein (TP), Cholesterol (CHOL) were determined. On day 21, liver, abdominal adipose tissue and the left filet were removed. Water, crude protein, total lipids (ether extract) and fatty acid compositions were determined. The results showed that the lowest feed intake/liver weight was soybean oil group, highest was goose fat group but there was no significant statistical difference between them (p>0.05). While there was a significant statistical difference between soybean oil group, corn oil group and goose fat group in liver/body and liver/dressed (p<0.05). The soybean oil group had the highest level of phosphatides (lecithin and cephalin). The contents of linoleic acid in soybean oil group were significantly higher than the goose fat group and corn oil group (p<0.05). It was indicated that the effects of soybean oil on the goose made more effective fatty liver production and more PUFA deposited in livers it was good for farmer income and people health.
  X Zhang , Q Chen , J Feng , J Hou , F Yang , J Liu , Q Jiang and C. Zhang

Nedd1 is a new member of the -tubulin ring complex (TuRC) and targets the TuRC to the centrosomes for microtubule nucleation and spindle assembly in mitosis. Although its role is known, its functional regulation mechanism remains unclear. Here we report that the function of Nedd1 is regulated by Cdk1 and Plk1. During mitosis, Nedd1 is firstly phosphorylated at T550 by Cdk1, which creates a binding site for the polo-box domain of Plk1. Then, Nedd1 is further phosphorylated by Plk1 at four sites: T382, S397, S637 and S426. The sequential phosphorylation of Nedd1 by Cdk1 and Plk1 promotes its interaction with -tubulin for targeting the TuRC to the centrosome and is important for spindle formation. Knockdown of Plk1 by RNAi decreases Nedd1 phosphorylation and attenuates Nedd1 accumulation at the spindle pole and subsequent -tubulin recruitment at the spindle pole for microtubule nucleation. Taken together, we propose that the sequential phosphorylation...

  X Liu , Y Cheng , J Yang , T. J Krall , Y Huo and C. Zhang

It is well established that vascular smooth muscle cell (VSMC) apoptosis and proliferation are critical cellular events in a variety of human vascular diseases. However, the molecular mechanisms involved in controlling VSMC apoptosis and proliferation are still unclear. In the current study, we have found that programmed cell death 4 (PDCD4) is significantly downregulated in balloon-injured rat carotid arteries in vivo and in platelet-derived growth factor-stimulated VSMCs in vitro. Overexpression of PDCD4 via adenovirus (Ad-PDCD4) increases VSMC apoptosis in an apoptotic model induced by serum deprivation. In contrast, VSMC apoptosis is significantly decreased by knockdown of PDCD4 via its small interfering RNA. In the rat carotid arteries in vivo, VSMC apoptosis is increased by Ad-PDCD4. We have further identified that activator protein 1 is a downstream signaling molecule of PDCD4 that is associated with PDCD4-mediated effects on VSMC apoptosis. In addition, VSMC proliferation was inhibited by overexpression of PDCD4. The current study has identified, for the first time, that PDCD4 is an essential regulator of VSMC apoptosis and proliferation. The downregulation of PDCD4 expression in diseased vascular walls may be responsible for the imbalance of VSMC proliferation and apoptosis. The results indicate that PDCD4 may be a new therapeutic target in proliferative vascular diseases.

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