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Articles by X Zhao
Total Records ( 15 ) for X Zhao
  X Gong , W Ye , H Zhou , X Ren , Z Li , W Zhou , J Wu , Y Gong , Q Ouyang , X Zhao and X. Zhang
 

Acetylcholinesterase (AChE) expression may be induced during apoptosis in various cell types. Here, we used the C-terminal of AChE to screen the human fetal brain library and found that it interacted with Ran-binding protein in the microtubule-organizing center (RanBPM). This interaction was further confirmed by coimmunoprecipitation analysis. In HEK293T cells, RanBPM and AChE were heterogeneously expressed in the cisplatin-untreated cytoplasmic extracts and in the cisplatin-treated cytoplasmic or nuclear extracts. Our previous studies performed using morphologic methods have shown that AChE translocates from the cytoplasm to the nucleus during apoptosis. Taken together, these results suggest that RanBPM is an AChE-interacting protein that is translocated from the cytoplasm into the nucleus during apoptosis, similar to the translocation observed in case of AChE.

  S Yu , B Zheng , X Zhao and Y. Feng
 

A bioinformatic screening of the genome of the thermophilic bacterium Fervidobacterium nodosum Rt17-B1 for ester-hydrolyzing enzymes revealed a putative bacterial esterase (FNE) encoded by Fond_1301 with typical GDSL family motifs. To confirm its putative esterase function, the FNE gene was cloned, functionally expressed in Escherichia coli, and purified to homogeneity. Recombinant FNE exhibited the highest esterase activity of 14,000 U/mg with p-nitrophenyl acetate (pNPC2) as substrate. The catalytic efficiency (kcat/Km) toward p-nitrophenyl acetate (C2) was approximately 120-fold higher than toward p-nitrophenyl butyrate (C4). No significant esterase activity was observed for the substrates with a chain length ≥C8. The monomeric enzyme has a molecular mass of 27.5 kDa and exhibits optimal activity around 75°C, at pH 8.5. Its thermostability is relatively high with a half-life of 80 min at 70°C, but less stable compared with some other hyperthermophilic esterases. A structural model was constructed using acetylesterase from Aspergillus aculeatus as a template. The structure showed an /β-hydrolase fold and indicated the presence of a typical catalytic triad consisting of a serine, aspartate, and histidine, which was verified by site-directed mutagenesis. Sequence analysis showed that FNE was only distantly related to other esterases. A comparison of the conserved motifs shared with GDSL proteins revealed that FNE could be grouped into GDSL family and was further classified as SGNH hydrolase.

  W Sun , X Gao , X Zhao , D Cui and Q. Xia
 

The study was undertaken to examine the effects of C-peptide on glomerular volume (VGLOM), mesangial matrix synthesis, and degradation in streptozotocin (STZ)-diabetic rats with poor or moderate glycemic control. Series 1 (poor glycemic control) included groups of healthy rats, hyperglycemic rats, diabetic insulin-treated rats and diabetic C-peptide-treated rats. Series 2 (moderate glycemic control) included groups of healthy rats, diabetic insulin-treated rats, diabetic insulin- and C-peptide-treated rats. After 8 weeks, the left kidney was excised for evaluation of VGLOM and mesangial matrix area via light microscopy. Mesangial cells were cultured for 48 h and type IV collagen expression and matrix metalloproteinase (MMP)-2 expression were measured by ELISA and RT–PCR. The results indicated that in Series 1, C-peptide administration suppressed the diabetes-induced increase in the VGLOM and the mesangial matrix area. In Series 2, C-peptide administration resulted in a similar decrease in the VGLOM and a greater decrease in the mesangial matrix area when compared with insulin therapy alone. Moreover, C-peptide (300 nM) completely inhibited the glucose-induced increase of the collagen IV mRNA expression and protein concentration in mesangial cells cultured in 30 mM glucose medium. MMP-2 mRNA expression was not influenced by C-peptide. In conclusion, C-peptide administration to STZ-diabetic rats for 8 weeks results in the inhibition of diabetes-induced expansion of the mesangial matrix. This effect is independent of the level of glycemic control and results from the inhibition of diabetes-induced excessive formation of mesangial type IV collagen.

  X Zhao , S Chandarana , M Husein , J Rogers and D. L. MacRae
 

Objectives  To establish and compare the distance and angle from the limen nasi to the sphenoid ostium in pediatric patients with normal sinonasal anatomy vs pediatric patients with cystic fibrosis (CF).

Design  Retrospective review of computed tomographic images.

Setting  Tertiary university-based medical center.

Participants  Patients (newborn to age 20 years) with normal sinonasal anatomy (n = 117) or CF (n = 15).

Main Outcome Measures  We used a fourth-degree polynomial to curve-fit the distance to the sphenoid ostium vs age for patients with normal sinonasal anatomy, producing a coefficient of determination (R2) of 82%. With this regression curve, we produced a normative distance equation and a normative distance graph using age to predict the distance (95% confidence interval). We validated the normative distance curve fit among 30 new pediatric patients.

Results  No significant difference in the distance to the sphenoid ostium was found between healthy patients and patients with CF. There was no correlation between age and angle in either patient group. The mean (SD) angle was statistically different between healthy patients (37.5° [7.5°]) and patients with CF (41.4° [7.4°]).

Conclusions  Using a normative distance graph and the mean angle, surgeons performing pediatric endoscopic sinus surgery can predict the distance to the sphenoid ostium for healthy patients and for patients with CF. These findings may decrease complications of endoscopic sinus surgery among the pediatric population.

  X Zhao and P. Li
 

A Web-based database is developed to provide psycholinguists with a large-scale phonological representation system for all Mandarin Chinese monosyllables. The construction of the system is based on the slot-based phonological pattern generator (PatPho), with an adequate consideration of the language-specific features of the Chinese phonology. Users can retrieve the relevant phonological representations through an interactive query system on the Web. The query outcomes can be saved in a number of formats, such as Excel spreadsheets, for further analyses. This representation system can be used for a variety of purposes—in particular, connectionist language modeling and, more generally, the study of Chinese phonology.

  C. J Fabian , B. F Kimler , C. M Zalles , J. R Klemp , B. K Petroff , Q. J Khan , P Sharma , K. D. R Setchell , X Zhao , T. A Phillips , T Metheny , J. R Hughes , H. W Yeh and K. A. Johnson
 

Preclinical and correlative studies suggest reduced breast cancer with higher lignan intake or blood levels. We conducted a pilot study of modulation of risk biomarkers for breast cancer in premenopausal women after administration of the plant lignan secoisolariciresinol given as the diglycoside (SDG). Eligibility criteria included regular menstrual cycles, no oral contraceptives, a >3-fold increase in 5-year risk, and baseline Ki-67 of ≥2% in areas of hyperplasia in breast tissue sampled by random periareolar fine-needle aspiration (RPFNA) during the follicular phase of the menstrual cycle. SDG (50 mg/d) was given for 12 months, followed by repeat RPFNA. The primary end point was change in Ki-67. Secondary end points included change in cytomorphology, mammographic breast density, serum bioavailable estradiol and testosterone insulin-like growth factor-I and IGF-binding protein-3, and plasma lignan levels. Forty-five of 49 eligible women completed the study with excellent compliance (median = 96%) and few serious side effects (4% grade 3). Median plasma enterolactone increased ~9-fold, and total lignans increased 16-fold. Thirty-six (80%) of the 45 evaluable subjects showed a decrease in Ki-67, from a median of 4% (range, 2-16.8%) to 2% (range, 0-15.2%; P < 0.001, Wilcoxon signed rank test). A decrease from baseline in the proportion of women with atypical cytology (P = 0.035) was also observed. Based on favorable risk biomarker modulation and lack of adverse events, we are initiating a randomized trial of SDG versus placebo in premenopausal women. Cancer Prev Res; 3(10); 1342–50. ©2010 AACR.

  X Zhao , C Graves , S. J Ames , D. E Fisher and R. A. Spanjaard
 

Retinoic acid (RA) induces growth arrest and differentiation of S91 murine melanoma cells and serves as a valuable model for this disease. RA acts through activation of RA receptors (RAR), which are members of the nuclear receptor superfamily of ligand-inducible transcription factors. Interestingly, differentiation is mediated by RAR, but not by RAR or RARβ, suggesting that RAR possesses unique and uncharacterized molecular properties. To address this question, DNA microarrays in combination with RAR isoform-specific agonists were employed to identify novel RAR target genes that may play a role in this process. Here, we identified and validated carbohydrate sulfotransferase 10 (CHST10) as a novel RAR target gene in S91 cells. The RAR-inducible CHST10 promoter was obtained, and two atypical, independently functioning RA response elements were identified in a 425 bp region. Surprisingly, this fragment is bound by RAR, but not by RAR or RARβ, thus providing a mechanism for the observed RAR-specific regulation. CHST10 is a sulfotransferase that forms HNK-1 glycan on neural cell adhesion proteins and glycolipids, and HNK-1 is thought to modulate cell adhesion and possibly metastasis. We show that CHST10 is also regulated by RAR in a significant subset of human melanoma cells, and three-dimensional cell culture migration assays suggest that CHST10 functions as a suppressor of invasiveness, but not proliferation, in these cells. Induction of CHST10 by RAR-activating retinoids may present a novel therapeutic strategy to inhibit invasiveness in a subset of melanoma patients. [Cancer Res 2009;69(12):5218–25]

  N. M Brown , C. A Belles , S. L Lindley , L. D Zimmer Nechemias , X Zhao , D. P Witte , M. O Kim and K. D. R. Setchell
 

We describe for the first time the chemopreventive effects of S-(–)equol and R-(+)equol, diastereoisomers with contrasting affinities for estrogen receptors (ERs). S-(–)equol, a ligand for ERβ, is an intestinally derived metabolite formed by many humans and by rodents consuming diets containing soy isoflavones. Whether the well-documented chemopreventive effect of a soy diet could be explained by equol's action was unclear because neither diastereoisomers had been tested in animal models of chemoprevention. Sprague–Dawley rats (n = 40–41 per group) were fed a soy-free AIN-93G diet or an AIN-93G diet supplemented with 250 mg/kg of S-(–)equol or R-(+)equol beginning day 35. On day 50, mammary tumors were induced by dimethylbenz[a]anthracene and thereafter, animals were palpated for number and location of tumors. On day 190, animals were killed and mammary tumors were removed and verified by histology, and the degree of invasiveness and differentiation was determined. S-(–)equol and R-(+)equol plasma concentrations measured on days 35, 100 and 190 by tandem mass spectrometry confirmed diet compliance and no biotransformation of either diastereoisomer. In this model, S-(–)equol had no chemopreventive action, nor was it stimulatory. In contrast, R-(+)equol compared with Controls reduced palpable tumors (P = 0.002), resulted in 43% fewer tumors (P = 0.004), increased tumor latency (88.5 versus 66 days, P = 0.003), and tumors were less invasive but showed no difference in pattern grade or mitosis. Both enantiomers had no effect on absolute uterine weight but caused a significant reduction in body weight gain. In conclusion, the novel finding that the unnatural enantiomer, R-(+)equol, was potently chemopreventive warrants investigation of its potential for breast cancer prevention and treatment.

  S Zhang , J Lu , X Zhao , W Wu , H Wang , Q Wu , X Chen , W Fan , H Chen , F Wang , Z Hu , L Jin , Q Wei , H Shen , W Huang and D. Lu
 

Checkpoint kinase (CHEK) 2, a tumor suppressor gene, plays an essential role in the DNA damage checkpoint response cascade. We first investigated two polymorphisms in the proximal promoter of the CHEK2 gene and evaluated their associations with the risk of lung cancer in a case–control study using 500 incident lung cancer cases and 517 cancer-free controls. We found that CHEK2 rs2236141 –48 G > A was significantly associated with lung cancer risk (P = 0.0018). Similar results were obtained in a follow-up replication study in 575 lung cancer patients and 589 controls (P = 0.042). Quantitative polymerase chain reaction showed that individuals with the G allele had lower levels of CHEK2 transcripts in peripheral blood mononuclear cells and normal lung tissues. The –48 G->A variant eliminated a methylation site and thereby relieve the transcriptional repression of CHEK2. Therefore, this polymorphism affected downstream transcription through genetic and epigenetic modifications. Luciferase reporter assays demonstrated that the major G allele significantly attenuated reporter gene expression when methylated. Electrophoretic Mobility shift assays and surface plasmon resonance revealed that the methylated G allele increased transcription factor accessibility. We used in vivo chromatin immunoprecipitation to confirm that the relevant transcription factor was Sp1. Using lung tissue heterozygous for the G/A single-nucleotide polymorphism, we found that Sp1 acted as a repressor and had a stronger binding affinity for the G allele. These results support our hypothesis that the CHEK2 rs2236141 variant modifies lung cancer susceptibility in the Chinese population by affecting CHEK2 expression.

  G. C Fonarow , M. J Reeves , E. E Smith , J. L Saver , X Zhao , D. W Olson , A. F Hernandez , E. D Peterson , L. H Schwamm and on behalf of the GWTG Stroke Steering Committee and Investigators
 

Background— Stroke results in substantial death and disability. To address this burden, Get With The Guideline (GWTG)-Stroke was developed to facilitate the measurement, tracking, and improvement in quality of care and outcomes for acute stroke and transient ischemic attack (TIA) patients in the United States.

Methods and Results— We analyzed the characteristics, performance measures, and in-hospital outcomes in the first 1 000 000 acute ischemic stroke, intracerebral hemorrhage, subarachnoid hemorrhage, and TIA admissions from 1392 hospitals that participated in the GWTG-Stroke Program 2003 to 2009. Patients were 53.5% women, 73.3% white, and with mean age of 70.1±14.9 years. There were 601 599 (60.2%) ischemic strokes, 108 671 (10.9%) intracerebral hemorrhages, 34 945 (3.5%) subarachnoid hemorrhages, 26 977 (2.7%) strokes not classified, and 227 788 (22.8%) TIAs. Performance measures showed small to moderate differences by cerebrovascular event type. In-hospital mortality rate was highest among intracerebral hemorrhage (25.0%) and subarachnoid hemorrhage (20.4%), and intermediate in ischemic stroke (5.5%) patients and lowest among TIA patients (0.3%). Significant improvements over time from 2003 to 2009 in quality of care were observed: all-or-none measure, 44.0% versus 84.3% (+40.3%, P<0.0001). After adjustment for patient and hospital variables, the cumulative adjusted odds ratio for the all-or-none measure over the 6 years was 9.4 (95% confidence interval, 8.3 to 10.6, P<0.0001). Temporal improvements in length of stay and risk-adjusted in-hospital mortality rate (for ischemic stroke and TIA) were also observed.

Conclusions— With more than 1 million patients enrolled, GWTG-Stroke represents an integrated stroke and TIA registry that supports national surveillance, innovative research, and sustained quality improvement efforts facilitating evidence-based stroke/TIA care.

  Y. T Shen , F. I Malik , X Zhao , C Depre , S. K Dhar , P Abarzua , D. J Morgans and S. F. Vatner
  Background—

Therapy for chronic systolic heart failure (sHF) has improved over the past 2 decades, but the armamentarium of drugs is limited and consequently sHF remains a leading cause of death and disability. In this investigation, we examined the effects of a novel cardiac myosin activator, omecamtiv mecarbil (formerly CK-1827452) in 2 different models of heart failure.

Methods and Results—

Two different models of sHF were used: (1) pacing-induced sHF after myocardial infarction (MI-sHF) and (2) pacing-induced sHF after 1 year of chronic pressure overload left ventricular hypertrophy (LVH-sHF). Omecamtiv mecarbil increased systolic function in sHF dogs, chronically instrumented to measure LV pressure, wall thickness, and cardiac output. Omecamtiv mecarbil, infused for 24 hours, induced a sustained increase without desensitization (P<0.05) in wall thickening (25±6.2%), stroke volume (44±6.5%) and cardiac output (22±2.8%), and decreased heart rate (15±3.0%). The major differences between the effect of omecamtiv mecarbil on cardiac function and the effect induced by a catecholamine, for example, dobutamine, is that omecamtiv mecarbil did not increase LV dP/dt but rather increased LV systolic ejection time by 26±2.9% in sHF. Another key difference is that myocardial O2 consumption (MVO2), which increases with catecholamines, was not significantly affected by omecamtiv mecarbil.

Conclusions—

These results demonstrate that chronic infusion of the cardiac myosin activator, omecamtiv mecarbil, improves LV function in sHF without the limitations of progressive desensitization and increased MVO2. This unique profile may provide a new therapeutic approach for patients with sHF.

  B Jin , X Zhao , Z Long , F Qi and S. Yu
 

The adoption of radio frequency identification (RFID) tags and devices facilitates the observation and monitoring of event patterns, while highly temporal restrained RFID data further make events complicated. Although the existing Pub/Sub systems can help distributed applications monitor and disseminate interesting events, they are unable to express RFID-related events directly. Extending a system for new RFID requirements not only needs a lot of work, but also provides no performance guarantees. It is, therefore, necessary to design and implement an effective and efficient Pub/Sub system in order to capture and disseminate RFID-related events. This paper presents a composite subscription specification for RFID-related application scenarios. It enables the subscription of predicates for RFID code as well as various complex events. Moreover, this paper proposes the algorithms for RFID-code subscription matching and complex events detection which have been implemented in our Pub/Sub system, OncePubSub. Also, experiments were conducted to quantify the performance and overhead of the above algorithms. Performance evaluation results indicate that OncePubSub is more efficient than SIENA- and JESS-based systems.

  H. A North , X Zhao , S. M Kolk , M. A Clifford , D. M Ziskind and M. J. Donoghue
  Hilary A. North, Xiumei Zhao, Sharon M. Kolk, Meredith A. Clifford, Daniela M. Ziskind, and Maria J. Donoghue

Eph receptors are widely expressed during cerebral cortical development, yet a role for Eph signaling in the generation of cells during corticogenesis has not been shown. Cortical progenitor cells selectively express one receptor, EphA4, and reducing EphA4 signaling in cultured progenitors suppressed proliferation, decreasing cell number. In vivo, EphA4-/- cortex had a reduced area, fewer cells and less cell division compared with control cortex. To understand the effects of EphA4 signaling in corticogenesis, EphA4-mediated signaling was selectively depressed or elevated in cortical progenitors in vivo. Compared with control cells, cells with reduced EphA4 signaling were rare and mitotically inactive. Conversely, overexpression of EphA4 maintained cells in their progenitor states at the expense of subsequent maturation, enlarging the progenitor pool. These results support a role for EphA4 in the autonomous promotion of cell proliferation during corticogenesis. Although most ephrins were undetectable in cortical progenitors, ephrin B1 was highly expressed. Our analyses demonstrate that EphA4 and ephrin B1 bind to each other, thereby initiating signaling. Furthermore, overexpression of...

  K. E Szulwach , X Li , R. D Smrt , Y Li , Y Luo , L Lin , N. J Santistevan , W Li , X Zhao and P. Jin
 

The microRNA miR-137 represses expression of Ezh2, a histone methyltransferase, which in turn alters the epigenetic architecture of chromatin that is important for regulation of miR-137 levels.

  J Das , G Ren , L Zhang , A. I Roberts , X Zhao , A. L.M Bothwell , L Van Kaer , Y Shi and G. Das
 

Interleukin (IL)-17–producing T helper (Th17) cells play a critical role in the pathophysiology of several autoimmune disorders. The differentiation of Th17 cells requires the simultaneous presence of an unusual combination of cytokines: IL-6, a proinflammatory cytokine, and transforming growth factor (TGF) β, an antiinflammatory cytokine. However, the molecular mechanisms by which TGF-β exerts its effects on Th17 cell differentiation remain elusive. We report that TGF-β does not directly promote Th17 cell differentiation but instead acts indirectly by blocking expression of the transcription factors signal transducer and activator of transcription (STAT) 4 and GATA-3, thus preventing Th1 and Th2 cell differentiation. In contrast, TGF-β had no effect on the expression of retinoic acid receptor–related orphan nuclear receptor t, a Th17-specific transcription factor. Interestingly, in Stat-6–/–T-bet–/– mice, which are unable to generate Th1 and Th2 cells, IL-6 alone was sufficient to induce robust differentiation of Th17 cells, whereas TGF-β had no effect, suggesting that TGF-β is dispensable for Th17 cell development. Consequently, BALB/c Stat-6–/–T-bet–/– mice, but not wild-type BALB/c mice, were highly susceptible to the development of experimental autoimmune encephalomyelitis, which could be blocked by anti–IL-17 antibodies but not by anti–TGF-β antibodies. Collectively, these data provide evidence that TGF-β is not directly required for the molecular orchestration of Th17 cell differentiation.

 
 
 
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