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Articles by Z Yang
Total Records ( 13 ) for Z Yang
  T Zhang , X Xu , L Shen , Y Feng , Z Yang , Y Shen , J Wang , W Jin and X. Wang
 

Overexpression of foreign proteins in Escherichia coli often leads to the formation of inclusion bodies (IBs), which becomes the major bottleneck in the preparation of recombinant proteins and their applications. In the present study, 36 proteins from IBs were refolded using a simple refolding method. Refolding yields of these proteins were defined as the percentage of soluble proteins following dilution refolding in the amount of denatured proteins in the samples before diluting into refolding buffer. Furthermore, a mathematical model was deduced to evaluate the role of biochemical properties in the protein refolding. Our results indicated that under the experimental conditions, isoelectric point of proteins might be mostly contributing to the high efficacy of protein refolding since the increment of one unit resulted in a decrease of 14.83% in the refolding yield. Other important mediators were components of protein secondary structure and the molecular weight (R2 = 0.98, P = 0.000, F-test). Six proteins with low efficiency in the protein refolding possessed relatively low isoelectric points. Furthermore, refolding yields of six additional proteins from IBs were predicted and further validated by refolding the proteins under the same conditions. Therefore, the model of protein refolding developed here could be used to predict the refolding yields of proteins from IBs through a simple method. Our study will be suggestive to optimize the methods for protein refolding from IBs according to their intrinsic properties.

  L Hyman , A Heijl , M. C Leske , B Bengtsson , Z Yang and for the Early Manifest Glaucoma Trial Group
 

Objectives  To characterize intraocular pressure (IOP) changes during 6 years of follow-up among patients with early, newly diagnosed glaucoma randomized to no initial treatment in the Early Manifest Glaucoma Trial (control group) and to evaluate factors associated with IOP changes in this group.

Methods  Early Manifest Glaucoma Trial control patients, aged 50 to 80 years at baseline, were followed up for 6 years or to the time of progression, when treatment could be initiated. After baseline, patients were followed up every 3 months with comprehensive ophthalmologic examinations, including Goldmann applanation tonometry. Change in IOP over 6 years was assessed by linear regression analyses.

Results  At baseline, the median IOP of this cohort (N = 118) was 20.8 mm Hg and was higher for the 15 patients with exfoliation glaucoma (24.0 mm Hg vs 20.0 mm Hg for others; P = .005). In patients without exfoliation glaucoma, IOP remained stable during follow-up (median IOP change of –0.01 mm Hg/y; interquartile range, 0.85 mm Hg/y). In comparison, patients with exfoliation glaucoma showed a significantly larger median change of 0.96 mm Hg/y (interquartile range, 3.11 mm Hg/y) (P = .004). In the overall cohort, the only factor related to IOP change was exfoliation glaucoma (P < .001). Among patients without exfoliation glaucoma, no factors were associated with IOP change.

Conclusions  In patients with early glaucoma, IOP remained stable without treatment during a 6-year period, regardless of baseline IOP, except for patients with exfoliation glaucoma, where IOP increased by almost 1 mm Hg annually. No factors, aside from exfoliation glaucoma, were related to longitudinal changes in IOP. These new natural history data may be useful in guiding management decisions for glaucoma treatment, particularly in patients with early disease or with exfoliation glaucoma.

  J Ju , S. C Picinich , Z Yang , Y Zhao , N Suh , A. N Kong and C. S. Yang
 

The cancer-preventive activity of vitamin E has been studied. Whereas some epidemiological studies have suggested a protective effect of vitamin E against cancer formation, many large-scale intervention studies with -tocopherol (usually large doses) have not demonstrated a cancer-preventive effect. Studies on -tocopherol in animal models also have not demonstrated robust cancer prevention effects. One possible explanation for the lack of demonstrable cancer-preventive effects is that high doses of -tocopherol decrease the blood and tissue levels of -tocopherols. It has been suggested that -tocopherol, due to its strong anti-inflammatory and other activities, may be the more effective form of vitamin E in cancer prevention. Our recent results have demonstrated that a -tocopherol-rich mixture of tocopherols inhibits colon, prostate, mammary and lung tumorigenesis in animal models, suggesting that this mixture may have a high potential for applications in the prevention of human cancer. In this review, we discuss biochemical properties of tocopherols, results of possible cancer-preventive effects in humans and animal models and possible mechanisms involved in the inhibition of carcinogenesis. Based on this information, we propose that a -tocopherol-rich mixture of tocopherols is a very promising cancer-preventive agent and warrants extensive future research.

  G. X Li , Y. K Chen , Z Hou , H Xiao , H Jin , G Lu , M. J Lee , B Liu , F Guan , Z Yang , A Yu and C. S. Yang
 

(–)-Epigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, has been shown to inhibit tumorigenesis and cancer cell growth in animal models. Nevertheless, the dose–response relationship of the inhibitory activity in vivo has not been systematically characterized. The present studies were conducted to address these issues, as well as the involvement of reactive oxygen species (ROS), in the inhibitory action of EGCG in vivo and in vitro. We characterized the inhibitory actions of EGCG against human lung cancer H1299 cells in culture and in xenograft tumors. The growth of tumors was dose dependently inhibited by EGCG at doses of 0.1, 0.3 and 0.5% in the diet. Tumor cell apoptosis and oxidative DNA damage, assessed by the formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) and phosphorylated histone 2A variant X (-H2AX), were dose dependently increased by EGCG treatment. However, the levels of 8-OHdG and -H2AX were not changed by the EGCG treatment in host organs. In culture, the growth of viable H1299 cells was dose dependently reduced by EGCG; the estimated concentration that causes 50% inhibition (IC50) (20 µM) was much higher than the IC50 (0.15 µM) observed in vivo. The action of EGCG was mostly abolished by the presence of superoxide dismutase (SOD) and catalase, which decompose the ROS formed in the culture medium. Treatment with EGCG also caused the generation of intracellular ROS and mitochondrial ROS. Although EGCG is generally considered to be an antioxidant, the present study demonstrates the pro-oxidative activities of EGCG in vivo and in vitro in the described experimental system.

  C.E Chadjichristos , K.E.L Scheckenbach , T.A.B van Veen , M.Z Richani Sarieddine , C de Wit , Z Yang , I Roth , M Bacchetta , H Viswambharan , B Foglia , T Dudez , M.J.A van Kempen , F.E.J Coenjaerts , L Miquerol , U Deutsch , H.J Jongsma , M Chanson and B.R. Kwak
 

Background— Endothelial dysfunction is the initiating event of atherosclerosis. The expression of connexin40 (Cx40), an endothelial gap junction protein, is decreased during atherogenesis. In the present report, we sought to determine whether Cx40 contributes to the development of the disease.

Methods and Results— Mice with ubiquitous deletion of Cx40 are hypertensive, a risk factor for atherosclerosis. Consequently, we generated atherosclerosis-susceptible mice with endothelial-specific deletion of Cx40 (Cx40del mice). Cx40del mice were indeed not hypertensive. The progression of atherosclerosis was increased in Cx40del mice after 5 and 10 weeks of a high-cholesterol diet, and spontaneous lesions were observed in the aortic sinuses of young mice without such a diet. These lesions showed monocyte infiltration into the intima, increased expression of vascular cell adhesion molecule-1, and decreased expression of the ecto-enzyme CD73 in the endothelium. The proinflammatory phenotype of Cx40del mice was confirmed in another model of induced leukocyte recruitment from the lung microcirculation. Endothelial CD73 is known to induce antiadhesion signaling via the production of adenosine. We found that reducing Cx40 expression in vitro with small interfering RNA or antisense decreased CD73 expression and activity and increased leukocyte adhesion to mouse endothelial cells. These effects were reversed by an adenosine receptor agonist.

Conclusions— Cx40-mediated gap junctional communication contributes to a quiescent nonactivated endothelium by propagating adenosine-evoked antiinflammatory signals between endothelial cells. Alteration in this mechanism by targeting Cx40 promotes leukocyte adhesion to the endothelium, thus accelerating atherosclerosis.

  Z Yang , B. H Funke , L. H Cripe , G. W Vick , D Mancini Dinardo , L. S Pena , R. J Kanter , B Wong , B. H Westerfield , J. J Varela , Y Fan , J. A Towbin and M. Vatta
 

Background— Danon disease is an X-linked dominant disorder characterized by the clinical triad of hypertrophic cardiomyopathy, skeletal myopathy, and variable mental retardation. Pathologically, autophagic vacuoles are noted in both skeletal and cardiac muscle. It exhibits an X-linked dominant mode of inheritance, and male carriers are severely affected, whereas female carriers develop milder and later-onset cardiac symptoms. Danon disease has been associated with mutations in the lysosome-associated membrane glycoprotein 2 (LAMP2) gene located at Xq24, typically resulting in splicing defects or protein truncation affecting the LAMP2. Because of its rarity, the full spectrum of genetic mutation resulting in Danon disease has not been elucidated.

Methods and Results— We analyzed 3 male cases with clinical and pathological findings consistent with Danon disease. Comprehensive mutational analysis failed to yield detectable products for selected LAMP2 exons, and genomic DNA deletion was suspected. Genomic junction fragment polymerase chain reaction analysis in case 1 identified a novel Alu-mediated 34-kb microdeletion encompassing the entire 5'-untranslated region and exon 1 of LAMP2. In case 2 and 3, junctional polymerase chain reaction and Southern blot analyses mapped the breakpoint to an MIRb and (TA)n simple repeats present in intron 3, which determined a 64-kb and a 58-kb deletion, respectively, thereby ablating exons 4 to 10. Western blot analysis confirmed the absence of LAMP2 in protein extract from lymphocytes of index case 2.

Conclusion— This article is the first report of Danon disease caused by microdeletions at Xq24, which functionally ablate LAMP2. The microdeletion mechanism appears to involve 1 Alu-mediated unequal recombination and 2 chromosomal breakage points involving TA-rich repeat sequences.

  J Dong , Y Li , Z Yang and J. Luo
 

Background and objectives: To explore the correlation between dietary sodium intake and cardiovascular and overall mortality, and then determine whether this correlation can be explained by protein and energy intake paralleled with sodium intake in dialysis patients.

Design, setting, participants, & measurements: This single-center retrospective cohort study enrolled 305 incident patients who started peritoneal dialysis in our unit from July 2002 to February 2007. All patients were followed until death or until being censored in February 2008. Demographic data were collected at baseline. Biochemical, dietary, and nutrition data were examined at baseline and thereafter at regular intervals to calculate the average values throughout the study.

Results: Participants with the highest average sodium intake were more likely to be younger, male, and overweight. Patients in the high tertile of average sodium intake had higher albumin, prealbumin, and lean body mass levels, and more nutrient intakes paralleling with sodium intake. Low average sodium intake independently predicted the increased risk for overall and cardiovascular death after adjusting for recognized confounders. Further adjustment for dietary protein, energy, and other nutrient intakes individually had minimal impact on the association between average sodium intake and overall death, with hazard ratios varying between 0.35 and 0.44, and cardiovascular death, with hazard ratios varying between 0.06 and 0.11.

Conclusions: This study revealed that low dietary sodium intake independently predicts the high overall and cardiovascular mortality in dialysis patients. This correlation could not be entirely explained by deficient protein and energy intake.

  A Liu , A. D Patterson , Z Yang , X Zhang , W Liu , F Qiu , H Sun , K. W Krausz , J. R Idle , F. J Gonzalez and R. Dai
 

Fenofibrate, widely used for the treatment of dyslipidemia, activates the nuclear receptor, peroxisome proliferator-activated receptor . However, liver toxicity, including liver cancer, occurs in rodents treated with fibrate drugs. Marked species differences occur in response to fibrate drugs, especially between rodents and humans, the latter of which are resistant to fibrate-induced cancer. Fenofibrate metabolism, which also shows species differences, has not been fully determined in humans and surrogate primates. In the present study, the metabolism of fenofibrate was investigated in cynomolgus monkeys by ultraperformance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-QTOFMS)-based metabolomics. Urine samples were collected before and after oral doses of fenofibrate. The samples were analyzed in both positive-ion and negative-ion modes by UPLC-QTOFMS, and after data deconvolution, the resulting data matrices were subjected to multivariate data analysis. Pattern recognition was performed on the retention time, mass/charge ratio, and other metabolite-related variables. Synthesized or purchased authentic compounds were used for metabolite identification and structure elucidation by liquid chromatographytandem mass spectrometry. Several metabolites were identified, including fenofibric acid, reduced fenofibric acid, fenofibric acid ester glucuronide, reduced fenofibric acid ester glucuronide, and compound X. Another two metabolites (compound B and compound AR), not previously reported in other species, were characterized in cynomolgus monkeys. More importantly, previously unknown metabolites, fenofibric acid taurine conjugate and reduced fenofibric acid taurine conjugate were identified, revealing a previously unrecognized conjugation pathway for fenofibrate.

  A Liu , A. D Patterson , Z Yang , X Zhang , W Liu , F Qiu , H Sun , K. W Krausz , J. R Idle , F. J Gonzalez and R. Dai
 

Fenofibrate, widely used for the treatment of dyslipidemia, activates the nuclear receptor, peroxisome proliferator-activated receptor . However, liver toxicity, including liver cancer, occurs in rodents treated with fibrate drugs. Marked species differences occur in response to fibrate drugs, especially between rodents and humans, the latter of which are resistant to fibrate-induced cancer. Fenofibrate metabolism, which also shows species differences, has not been fully determined in humans and surrogate primates. In the present study, the metabolism of fenofibrate was investigated in cynomolgus monkeys by ultraperformance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-QTOFMS)-based metabolomics. Urine samples were collected before and after oral doses of fenofibrate. The samples were analyzed in both positive-ion and negative-ion modes by UPLC-QTOFMS, and after data deconvolution, the resulting data matrices were subjected to multivariate data analysis. Pattern recognition was performed on the retention time, mass/charge ratio, and other metabolite-related variables. Synthesized or purchased authentic compounds were used for metabolite identification and structure elucidation by liquid chromatographytandem mass spectrometry. Several metabolites were identified, including fenofibric acid, reduced fenofibric acid, fenofibric acid ester glucuronide, reduced fenofibric acid ester glucuronide, and compound X. Another two metabolites (compound B and compound AR), not previously reported in other species, were characterized in cynomolgus monkeys. More importantly, previously unknown metabolites, fenofibric acid taurine conjugate and reduced fenofibric acid taurine conjugate were identified, revealing a previously unrecognized conjugation pathway for fenofibrate.

  X Wang , W Song , Z Yang , Y Wang , Z Tang and C. Xu
 

The endosperm in plants is a major source of human nutrition and industrial raw material. The genetic study of endosperm poses a great challenge due to its complex genetic composition and unique physical and developmental properties. In this note, we shall revisit 2 classic mating designs—North Carolina Design III (NCIII) and triple test cross (TTC)—and demonstrate their efficiency in detecting quantitative trait loci underlying endosperm traits.

  X. O Zhu , Z Yang , C. M Guo , X. T Ni , J. N Li , Y. C Ge , L Myatt and K. Sun
 

Human amnion fibroblasts produce abundant prostaglandins toward the end of gestation, which is one of the major events leading to parturition. In marked contrast to its well-described antiinflammatory effect, glucocorticoids have been shown to up-regulate cyclooxygenase-2 (COX-2) expression in human amnion fibroblasts. The mechanisms underlying this paradoxical induction of COX-2 by glucocorticoids have not been resolved. Using cultured human amnion fibroblasts, we found that the induction of COX-2 mRNA expression by cortisol was a glucocorticoid receptor (GR)-dependent process requiring ongoing transcription. Upon transfection of a COX-2 promoter-driven reporter gene into the amnion fibroblasts, cortisol stimulated the COX-2 promoter activity. This was abolished by mutagenesis of a cAMP response element (CRE) at –53 to approximately –59bp as well as by cotransfection of a plasmid expressing dominant-negative CRE-binding protein (CREB). The phosphorylation level of CREB-1 was significantly increased by cortisol treatment of the amnion fibroblasts, whereas the effect was attenuated either by the protein kinase A inhibitor H89 or the p38 -MAPK inhibitor SB203580. The induction of the COX-2 promoter activity and the phosphorylation of CREB-1 were also blocked by the GR antagonist RU486. Chromatin immunoprecipitation (ChIP) assay revealed that the binding of CREB-1 to the CRE of the COX-2 promoter was increased by cortisol treatment of the amnion fibroblasts. In conclusion, cortisol, via binding to GR, stimulated COX-2 expression by increasing phosphorylated CREB-1 binding to the CRE of the COX-2 gene. Cortisol may phosphorylate CREB-1 by activating either protein kinase A or p38-MAPK in the amnion fibroblasts.

  Y Wei , Y Ge , F Zhou , H Chen , C Cui , D Liu , Z Yang , G Wu , J Gu and J. Jiang
 

ATF5, a member of ATF/CREB family of b-ZIP transcription factors, is highly expressed in a wide variety of neoplasms and regulates cell differentiation, cell survival and apoptosis. However, the mechanism of human ATF5 transcriptional regulation has not been clarified. Here, we identified the transcription start site of the ATF5 gene, cloned its 5'-flanking region and identified the region –105 to +3 relative to the transcription start site as that having promoter activity. This region contained potential binding sites for several transcription factors, including EBF1, Sp1 and E2F1. EBF1 transcription factor binds to the ATF5 promoter and regulates the ATF5 transcription in an EBF-binding site independent manner. Thus, our studies not only provided molecular basis of ATF5 transcriptional regulation, but also identified ATF5 as a target gene of EBF1 transcription factor.

  Z Yang , A. E Kenny , D. A Brito and C. L. Rieder
 

Mitosis happens faster in Taxol-treated cells because Taxol-stabilized kinetochores get through the checkpoint faster.

 
 
 
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