Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
Articles by W Xu
Total Records ( 8 ) for W Xu
  Y Wu , W Xu , G Huang , S Gong , J Li , Y Qin and X. Li

Arabinogalactan proteins (AGPs) are a large family of highly glycosylated of hydroxyproline-rich glycoproteins that play important roles in plant growth, development, and signal transduction. A cDNA encoding a putative classical AGP named GhH6L was isolated from cotton fiber cDNA libraries, and the deduced protein contains 17 copies of repetitive motif of X–Y–proline–proline–proline (where X is serine or alanine and Y is threonine or serine). Northern blotting analysis and quantitative RT–PCR results showed that it was preferentially expressed in 10 days post-anthesis (dpa) fibers and was also developmentally regulated. A promoter fragment was isolated from cotton (Gossypium hirsutum) by genome walking PCR. Expression of β-glucuronidase (GUS) gene under the GhH6L promoter was examined in the transgenic Arabidopsis plants; only petiole and pedicel were stained, no staining was detected in other tissues. Subcellular localization indicated that GhH6L was localized to the plasma membrane and in the cytoplasm. These data further our understanding of GhH6L as well as shed light on functional insight to GhH6L in cotton.

  Y Min , W Xu , D Liu , S Shen , Y Lu , L Zhang and H. Wang

Dendritic cells (DCs) are important for the initiation of the adaptive immune response against Mycobacterium tuberculosis. Autophagy is an innate and adaptive defense mechanism and important for the control of M. tuberculosis. However, the role of autophagy in the adaptive immune response against M. tuberculosis remains to be determined. In the present study, we studied the effects of autophagy on the maturation of DCs infected with Bacillus Calmette–Guérin (BCG). The phenotype and function of the DCs were assessed by measuring the expression of CD86 and HLA-DR and the secretion of IL-10 and IL-6. Autophagy was evaluated by the change in LC3II, a molecular marker for autophagy. Following stimulation of autophagy, DCs that were matured in the presence of BCG showed enhanced expression of CD86 and HLA-DR and increased IL-6 production. The expression of LC3II was increased after the stimulation of autophagy. These results demonstrated that autophagy might result in the increased maturation of BCG-infected DCs, suggesting that autophagy could contribute to an enhanced adaptive immune response against M. tuberculosis.

  M Chen , X Qiu , W Xu , L Wang , J Zhao and X. Li

Test case generation based on design specifications is an important part of testing processes. In this paper, Unified Modeling Language activity diagrams are used as design specifications. By setting up several test adequacy criteria with respect to activity diagrams, an automatic approach is presented to generate test cases for Java programs. Instead of directly deriving test cases from activity diagrams, this approach selects test cases from a set of randomly generated ones according to a given test adequacy criterion. In the approach, we first instrument a Java program under testing according to its activity diagram model, and randomly generate abundant test cases for the program. Then, by running the instrumented program we obtain the corresponding program execution traces. Finally, by matching these traces with the behavior of the activity diagram, a reduced set of test cases are selected according to the given test adequacy criterion. This approach can also be used to check the consistency between the program execution traces and the behavior of activity diagrams.

  Q Sun , M Hang , W Xu , W Mao , X Hang , M Li and J. Zhang

This Phase II study was conducted to evaluate the effects of irinotecan plus capecitabine in patients with advanced gastric cancer (AGC) who had received a first-line therapy of 5-fluorouracil/platinum regimen.


Patients received capecitabine 1000 mg/m2 b.i.d. on days 1–14 followed by a 7-day rest period, and irinotecan 100 mg/m2 was administered through a 90 min intravenous infusion on days 1 and 8, based on a 3-week cycle.


Forty-six (95.8%) of the 48 patients were assessable for response. Thirteen cases of partial response were confirmed, response rate of 27.1% (95% CI, 14.5–39.7%). The median follow-up period was 25.2 months. The median time to progression and overall survival for all patients were 4.1 months (95% CI, 3.4–4.8 months) and 7.6 months (95% CI, 5.1–10.1 months). Grade 3 diarrhea and hand-foot syndrome occurred in eight (17.4%) and two (4.3%) patients, respectively. The most common Grade 3/4 hematological adverse event was neutropenia in four (8.7%) patients. There were no treatment-related deaths during this study.


Irinotecan plus capecitabine was a relatively active and tolerable regimen as a second-line chemotherapy for AGC. Further investigation of this regimen is warranted, including the addition of new biological agents such as bevacizumab or cetuximab to improve the salvage regimen.

  J Zheng , G Wang , G. Y Yang , D Wang , X Luo , C Chen , Z Zhang , Q Li , W Xu , Z Li and D. Wang

This Phase II study was conducted to evaluate the activity and feasibility of a regimen of nedaplatin and 5-fluorouracil as induction chemotherapy, followed by intensity-modulated radiotherapy concurrent with chemotherapy in patients with locoregionally advanced nasopharyngeal carcinoma.


Patients received neoadjuvant chemotherapy comprised two cycles of 5-fluorouracil at 700 mg/m2/day administered on days 1–4 as continuous intravenous infusion and nedaplatin (100 mg/m2 administered i.v. over 2 h) given after the administration of 5-fluorouracil on day 1, repeated every 3 weeks, followed by intensity-modulated radiotherapy concurrent with nedaplatin. During intensity-modulated radiotherapy, nedaplatin was administered at a dose of 100 mg/m2 intravenous infusion on days 1, 22 and 43, given ~60 min before radiation.


Fifty-nine (95.8%) of the 60 patients were assessable for response. Thirty-eight cases of complete response and 14 cases of partial response were confirmed after completion of chemoradiation, with the objective response rate of 86.7% (95% CI, 78.1–95.3%). The median follow-up period was 48 months (range, 30–62 months). The 3-year progression-free survival and overall survival were 75.0% (95% CI, 63.0–87.0%) and 85.5% (95% CI, 75.9–95.1%). No patient showed Grade 3 or higher renal dysfunction. The most commonly observed late effect was xerostomia, but the severity diminished over time, and the detectable xerostomia at 24 months was 10.2%. There were no treatment-related deaths during this study.


Neoadjuvant chemotherapy with nedaplatin and 5-fluorouracil followed by concomitant nedaplatin and intensity-modulated radiotherapy is an effective and safe treatment for Southern China patients affected by locoregionally advanced nasopharyngeal carcinoma.

  Y Li , W Pan , W Xu , N He , X Chen , H Liu , L Darryl Quarles , H Zhou and Z. Xiao

Cleidocranial dysplasia (CCD) is an autosomal dominant bone disease in humans caused by haploinsufficiency of the RUNX2 gene. The RUNX2 has two major isoforms derived from P1 and P2 promoters. Over 90 mutations of RUNX2 have been reported associated with CCD. In our study, DNA samples of nine individuals from three unrelated CCD families were collected and screened for all exons of RUNX2 and 2 kb of P1 and P2 promoters. We identified two point mutations in the RUNX2 gene in Case 1, including a nonsense mutation (c.577C>T) that has been reported previously and a silent substitution (c.240G>A). In vitro studies demonstrated that c.577C>T mutation led to truncated RUNX2 protein production and diminished stimulating effects on mouse osteocalcin promoter activity when compared with full-length Runx2-II and Runx2-I isoforms. These results confirm that loss of function RUNX2 mutation (c.577C>T) in Case 1 family is responsible for its CCD phenotype.

  W Xu , L Yi , Y Feng , L Chen and J. Liu

Pancreatic phospholipase A2 (phospholipase A2 group 1B, G1B) belongs to the superfamily of secreted phospholipase A2 (PLA2) enzymes. G1B has been proposed to be a potential target for diseases such as hypertension, obesity, and diabetes. Human pancreatic prophospholipase A2 (pro-hG1B) is activated by cleavage of the first seven-residue propeptide (phospholipase A2 propeptide, PROP). However, questions still remain on the mode of action for pro-hG1B. In this work, we expressed pro-hG1B in Pichia pastoris and determined the crystal structure at 1.55-Å resolution. The x-ray structure demonstrates that pro-hG1B forms a trimer. In addition, PROP occupies the catalytic cavity and can be self-cleaved at 37 °C. A new membrane-bound surface and activation mechanism are proposed based on the trimeric model of pro-hG1B. We also propose a new autoproteolytic mechanism for pro-hG1B by the reaction triad Asp49-Arg0-Ser(-2) that is similar to the serine protease catalytic triad.

  C. S Brandt , M Baratin , E. C Yi , J Kennedy , Z Gao , B Fox , B Haldeman , C. D Ostrander , T Kaifu , C Chabannon , A Moretta , R West , W Xu , E Vivier and S. D. Levin

Cancer development is often associated with the lack of specific and efficient recognition of tumor cells by the immune system. Natural killer (NK) cells are lymphocytes of the innate immune system that participate in the elimination of tumors. We report the identification of a tumor cell surface molecule that binds NKp30, a human receptor which triggers antitumor NK cell cytotoxicity and cytokine secretion. This previously unannotated gene belongs to the B7 family and, hence, was designated B7-H6. B7-H6 triggers NKp30-mediated activation of human NK cells. B7-H6 was not detected in normal human tissues but was expressed on human tumor cells, emphasizing that the expression of stress-induced self-molecules associated with cell transformation serves as a mode of cell recognition in innate immunity.

Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility