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Articles by G Zhao
Total Records ( 5 ) for G Zhao
  K Dong , Q Li , C Liu , Y Zhang , G Zhao and X. Guo
 

Motility and chemotaxis systems are critical for the virulence of leptospires. There were multiple copies of putative chemotaxis homologs located at leptospires large chromosome. CheB1 and CheB3 from Leptospira interrogans strain Lai are predicted to have a global CheB-like domain, but CheB2 is predicted to have a C-terminal effector domain only. In order to verify the function of three putative cheB genes, they were cloned into pQE31 vector and then expressed, respectively, in wild-type Escherichia coli strain RP437 and cheB defective strain RP4972. The results of swarming assays and the predicted ternary structures of CheB1 and CheB3 of L. interrogans strain Lai suggested that the absence of an N-terminal regulatory domain may be one of the reasons for the failure of CheB2 to complement an E. coli cheB mutant. Furthermore, CheB2 links solely to CheR1 and CheR3 in the interaction network of leptospires. Taken together, these results indicated that CheB2 may not function alone, and under certain physiological conditions, it may require CheB3 and CheR1 to function. The existence of multiple copies of chemotaxis gene homologs suggested that L. interrogans strain Lai might have a more complex chemosensory pathway.

  G Zhao and Y. Guan
 

DNA polymerases amplify DNA fragments through primer extension reactions. However, polymerization behavior of short primers in the primer extension process has not been systematically explored. In this study, we examined the minimal primer length required for primer extension, and the effect of primer length, mismatches and other conditions on DNA polymerization using a non-radioactive method. Under the condition we conducted, the shortest primers polymerized by Klenow fragment (KF) and Taq DNA polymerase in our experiments were respectively heptamer and octamer. The extension efficiency was also affected by the up-stream overhanging structure of the primer–template complex. We hypothesized a simple model to interpret these observations based on the polymerase structures. Furthermore, it was found that the longer the primer, the more efficient is the primer extension. These polymerization behavior of short primers lay foundation about DNA polymerization mechanism and development of novel nucleic acid detection assays.

  E. S Ford , C Li , G Zhao , W. S Pearson and S. Capewell
 

Background— Cohorts consistently show that individuals with low levels of cardiovascular risk factors experience low rates of subsequent cardiovascular events. Our objective was to examine the prevalence and trends in low risk factor burden for cardiovascular disease among adults in the US population.

Methods and Results— We used data from adults 25 to 74 years of age who participated in 4 national surveys. We created an index of low risk from the following variables: not currently smoking, total cholesterol <5.17 mmol/L (<200 mg/dL) and not using cholesterol-lowering medications, systolic blood pressure <120 mm Hg and diastolic blood pressure <80 mm Hg and not using antihypertensive medications, body mass index <25 kg/m2, and not having been previously diagnosed with diabetes mellitus. The age-adjusted prevalence of low risk factor burden increased from 4.4% during 1971 to 1975 to 10.5% during 1988 to 1994 before decreasing to 7.5% during 1999 to 2004 (P for nonlinear trend <0.001). The patterns were similar for men and women, although the prevalence among women exceeded that among men in each survey (P<0.001 for each survey). In addition, whites had a significantly higher prevalence of low risk factor burden than blacks during each survey except during 1976 to 1980 (1971 to 1975, 1988 to 1994, 1999 to 2004: P<0.001; 1976 to 1980: P=0.154). Furthermore, a larger percentage of whites had a low risk factor burden than Mexican Americans during 1988 to 1994 (P<0.001) and 1999 to 2004 (P=0.001).

Conclusions— The prevalence of low risk factor burden for cardiovascular disease is low. The progress that had been made during the 1970s and 1980s reversed in recent decades.

  J. P Bannister , A Adebiyi , G Zhao , D Narayanan , C. M Thomas , J. Y Feng and J. H. Jaggar
 

Rationale: Voltage-dependent L-type (CaV1.2) Ca2+ channels are a heteromeric complex formed from pore-forming 1 and auxiliary 2 and β subunits. CaV1.2 channels are the principal Ca2+ influx pathway in arterial myocytes and regulate multiple physiological functions, including contraction. The macromolecular composition of arterial myocyte CaV1.2 channels remains poorly understood, with no studies having examined the molecular identity or physiological functions of 2 subunits.

Objective: We investigated the functional significance of 2 subunits in myocytes of resistance-size (100 to 200 µm diameter) cerebral arteries.

Methods and Results: 2-1 was the only 2 isoform expressed in cerebral artery myocytes. Pregabalin, an 2-1/-2 ligand, and an 2-1 antibody, inhibited CaV1.2 currents in isolated myocytes. Acute pregabalin application reversibly dilated pressurized arteries. Using a novel application of surface biotinylation, data indicated that >95% of CaV1.2 1 and 2-1 subunits were present in the arterial myocyte plasma membrane. 2-1 knockdown using short hairpin RNA reduced plasma membrane-localized CaV1.2 1 subunits, caused a corresponding elevation in cytosolic CaV1.2 1 subunits, decreased intracellular Ca2+ concentration, inhibited pressure-induced vasoconstriction ("myogenic tone"), and attenuated pregabalin-induced vasodilation. Prolonged (24-hour) pregabalin exposure did not alter total 2-1 or CaV1.2 1 proteins but decreased plasma membrane expression of each subunit, which reduced myogenic tone.

Conclusions: 2-1 is essential for plasma membrane expression of arterial myocyte CaV1.2 1 subunits. 2-1 targeting can block CaV1.2 channels directly and inhibit surface expression of CaV1.2 1 subunits, leading to vasodilation. These data identify 2-1 as a novel molecular target in arterial myocytes, the manipulation of which regulates contractility.

  X Fang , X Li , B Stanton , Y Hong , L Zhang , G Zhao , J Zhao , X Lin and D. Lin
 

Objective To assess the relationship between parental HIV/AIDS and psychosocial adjustment of children in rural central China. Methods Participants included 296 double AIDS orphans (children who had lost both their parents to AIDS), 459 single orphans (children who had lost one parent to AIDS), 466 vulnerable children who lived with HIV-infected parents, and 404 comparison children who did not experience HIV/AIDS-related illness and death in their families. The measures included depressive symptoms, loneliness, self-esteem, future expectations, hopefulness about the future, and perceived control over the future. Results AIDS orphans and vulnerable children consistently demonstrated poorer psychosocial adjustment than comparison children in the same community. The level of psychosocial adjustment was similar between single orphans and double orphans, but differed by care arrangement among double orphans. Conclusion The findings underscore the urgency and importance of culturally and developmentally appropriate intervention efforts targeting psychosocial problems among children affected by AIDS and call for more exploration of risk and resilience factors, both individual and contextual, affecting the psychosocial wellbeing of these children.

 
 
 
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