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Articles by Y. Jin
Total Records ( 5 ) for Y. Jin
  B Huang , W Qin , B Zhao , Y Shi , C Yao , J Li , H Xiao and Y. Jin

MicroRNAs (miRNAs), which are a newly identified class of small single-stranded non-coding RNAs, regulate their target genes via post-transcriptional pathway. It has been proved that miRNAs play important roles in many biological processes. To better understand miRNA function on type 2 diabetes, we used an oligonucleotide microarray to monitor miRNA expression profiles of Goto–Kakizaki (GK) and Wistar rats' skeletal muscle. It was found that seven miRNAs were down-expressed and two miRNAs were over-expressed in the muscle of GK rats. Among them, miR-24 showed the most prominent change. p38 MAPK, which is a direct target of miR-24, also showed expression difference. All the data give a clue that miR-24 might be associated with diabetes through down-regulation of p38 MAPK.

  W Qin , B Zhao , Y Shi , C Yao , L Jin and Y. Jin

MicroRNAs (miRNAs) are a type of small non-coding RNAs that regulate cognate mRNA expressions at the post-transcriptional stage. Although several miRNAs are known to be involved in various biological processes, including developmental timing, patterning, embryogenesis, differentiation and organogenesis, growth control, and apoptosis, many target genes and the functions of most miRNAs are still unclear. Since there is only a partial complementarity between miRNAs and their targets in animal cells, it is difficult to identify the specific target genes for a given miRNA and elucidate its function. In this study, we confirmed that bone morphogenetic protein receptor II (BMPRII) is a direct target of miR-21, and also showed that the protein level of BMPRII correlates inversely with the amount of miR-21 in PC3 and Lncap cells. These findings suggest that miR-21 may have a potential role in regulating the malignancy and metastatic abilities of prostate cancer cells and in self-renewal of stem cells by regulating the expression of BMPRII.

  Y Xie , M Wu , R Song , J Ma , Y Shi , W Qin and Y. Jin

Regulatory T (Treg) cells are a subpopulation of T cells that not only prevent autoimmunity, but also control a wide range of T cell-dependent immune responses. Glucocorticoid treatment (dexamethasone, or Dex) has been reported to amplify IL-2-mediated selective in vivo expansion of Treg cells. We simultaneously administered Dex and IL-2 to the donor in a murine allogeneic lymphocyte transplantation model to expand functional suppressive CD4+CD25+FOXP3+ T cells in the graft and to raise the regulatory T cell/effector T cell (Treg/Teff) ratio to prevent graft-versus-host disease (GVHD). After combined treatment of the donor with Dex (5 mg/kg/day) and IL-2 (300,000 IU/mouse/day) for 3 days, grafts were subjected to flow cytometric analysis, and transplantation was carried out from male C57BL/6 mice to female BALB/c mice aged 8–12 weeks. Results showed that short-term simultaneous administration of Dex and IL-2 markedly expanded functional suppressive CD4+CD25+FOXP3+ T cells in the murine spleen. In this murine allogeneic transplantation model, the grafts from donors with Dex and IL-2 pre-treatment led to a longer survival time for the recipients than for the control group (median survival time > 60 day vs. 12 day, P = 0.0002). The ratio of Treg/Teff also increased remarkably (0.43 ± 0.15 vs. 0.14 ± 0.01, P = 0.01). This study demonstrated that co-stimulation with Dex and IL-2 selectively expanded functional CD4+CD25+FOXP3+ T cells in vivo, and that grafts from donors pre-treated with Dex and IL-2 led to longer survival time and greater suppression of GVHD after allogeneic transplantation. Thus, GVHD can be suppressed by the specific expansion of regulatory T cells with Dex and IL-2 in graft donors.

  W Cao , C Xu , G Lou , J Jiang , S Zhao , M Geng , W Xi , H Li and Y. Jin

The aim of this study was to assess the efficacy and toxicity of the combination of paclitaxel and nedaplatin as a first-line chemotherapy for patients with advanced esophageal cancer.


Patients with advanced esophageal cancer received 175 mg/m2 of paclitaxel over a 3 h infusion, followed by nedaplatin 80 mg/m2 in a 1 h infusion on day 1 every 3 weeks until the documented disease progression, unacceptable toxicity or patient's refusal.


Between March 2005 and December 2007, 48 patients entered in the study. Forty-six (95.8%) of the 48 patients were assessable for response. The overall response rate was 41.7% (95% CI, 27.8–55.7%) with 2 complete responses and 18 partial responses. The median follow-up period was 20.5 months (range, 12.5–27.2 months). The median overall time to progression and overall survival (OS) were 6.1 months (95% CI, 4.8–7.4 months) and 11.5 months (95% CI, 9.1–13.9 months), respectively. The estimate of OS at 12 and 24 months was 43.8% (95% CI, 29.7–77.8%) and 10.4% (95% CI, 1.8–19.1%), respectively. Most patients experienced anemia, during their course of therapy with 6 (13.0%) patients for grade 3/4 anemia, and grade 1 or 2 anemia was detected in 23 (50%) patients. Grade 3 leucopenia, neutropenia and thrombocytopenia were documented in 8 (17.4%), 9 (17.4%) and 2 (4.3%) patients, respectively. Grade 3 nausea and vomiting were detected in 3 (6.5%) and 2 (4.3%) patients, respectively. Two patients (4.3%) were hospitalized because of treatment-related complications. The treatment was well tolerated and no toxic death occurred.


Combination of paclitaxel and nedaplatin is a tolerated treatment modality with promising activity in previously untreated advanced esophageal cancer.

  Y. Zhang , H.X. Zheng , Z.D. Zhang , Y. Jin , F. Yang , J.J. He , W.J. Cao , D.H. Sun and L. Lv
  Field isolates of Foot-and-Mouth Disease Virus (FMDV) were found to use four αυ integrins (αυβ1, αυβ3, αυβ6 and αυβ8) as cellular receptors. Researchers established a stable Chinese Hamster Ovary clone K1 (CHO-K1) cell line expressing the murine αυβ1 heterodimer (designated as CHO-K1-αυβ1) using a highly efficient lentiviral-based gene transfer technology to deliver murine αυ, Internal Ribosome Entry Site (IRES) and β1 genes into cell chromosomes and the inserted genes were then transcribed from a Cytomegalovirus (CMV) promoter. αυβ1 expression was stringently regulated by Doxycycline (Dox) and was found to be stable. CHO-K1-αυβ1 cells were susceptible to FMDV type Asia l/HN/2006. The plaque assay revealed that the virus produced bigger and more plaques in CHO-K1-αυβ1 cells (1.05x104 PFU mL-1) than in CHO-K1 cells. When sodium heparin (1 and 2 mg mL-1) was used as the inhibitor, the number of plaques in CHO-K1 cells were significantly decreased (4.0x103-35 and 20 PFU mL-1), supported by time-course of replication and proliferation. The number and size of plaques on CHO-K1-αυβ1 cells showed no obvious change, indicating that the αυβ1 heterodimer expressed on CHO-K1-αυβ1 can be used as an FMDV receptor.
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