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Liu Z.-H.,Shenyang Medical College | Wang M.-H.,The Affiliated Hospital of Chengde Medical College | Ren H.-J.,Shenyang Medical College | Qu W.,Shenyang Medical College | And 6 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2014

Interleukin 7/Interleukin 7 receptor (IL-7/IL-7R) signaling induces the upregulation of cyclin D1 to promote cell proliferation in lung cancer, but its role in preventing the apoptosis of non-small cell lung cancer (NSCLC) cell lines remains unknown. To study the role of IL-7 in lung cancer cell apoptosis, normal HBE cells as well as A549 and H1299 NSCLC cells were examined using flow cytometry. The results showed that the activation of IL-7R by its specific ligand, exogenous interleukin-7, was associated with a significant decline in apoptotic cells. Western blot and real-time PCR assays indicated that the activation of IL-7/IL-7R significantly upregulated anti-apoptotic bcl-2 and downregulated pro-apoptotic bax and p53 at both protein and mRNA levels. The knockdown of IL-7R through small interfering RNAs significantly attenuated these effects of exogenous IL-7. However, there was no significant anti-apoptotic effect in H1299 (p53-) cells. Furthermore, the inhibition of p53 significantly abolished the effects of IL-7/IL-7R on lung cancer cell apoptosis. These results strongly suggest that IL-7/IL-7R prevents apoptosis by upregulating the expression of bcl-2 and by downregulating the expression of bax, potentially via the p53 pathway in A549 and HBE cells. Source


Xu H.,The Affiliated Hospital of Chengde Medical College
Zhonghua nan ke xue = National journal of andrology | Year: 2012

To observe the effects of nicotine on endogenous carbon monoxide (CO) concentration and nitric oxide synthase (NOS) activity in the corpus cavernosum of adult male rats, and explore the possible mechanism of cigarette smoking affecting erectile dysfunction. Forty adult male rats were equally divided into three treatment groups to receive subcutaneous injection of nicotine at 0.5 mg/kg pre d for 1, 2 and 3 months, and a control group to receive saline only. After treatment, the corpus cavernosum was harvested for detection of CO concentration by modified two-wavelength spectrophotometry and NOS activity by improved Griess measurement. CO concentration and NOS activity were decreased by 9.05 and 13.37%, respectively, after 1 month of nicotine injection (P < 0.01), 16.47 and 22.5% after 2 months (P < 0.01), and 22.99 and 31.74% after 3 months (P < 0.01), as compared with (13.664 +/- 0.404) umol/mg prot and (9.721 +/- 0.470) U/mg prot in the control group. Nicotine can reduce endogenous CO concentration and NOS activity in the corpus cavernosum of adult male rats, which suggests the involvement of endogenous CO and NOS in the pathophysiological process of smoking-induced erectile dysfunction . Source


Tan X.,Capital Medical University | Tan X.,The Affiliated Hospital of Chengde Medical College | Jie Y.,Capital Medical University | Zhang Y.,Capital Medical University | And 3 more authors.
Experimental Eye Research | Year: 2014

Anti-Tim-1 monoclonal antibody (mAb) RMT1-10 is effective in promoting allograft survival through blocking Tim-1. However, its role in corneal transplantation is unclear. This study aims to evaluate the effect of RMT1-10 on high-risk corneal transplantation. BALB/c mice were transplanted with corneal grafts from C57BL/6 mice and intraperitoneally injected with RMT1-10 or isotype IgG. The transparency of corneal graft was evaluated by slit lamp biomicroscopy. Flow cytometry was used to determine the phenotype of CD4+ T cells, including CD154, Tim-3, CD25 and Foxp3, and to analyze the proliferation capacity of CD4+ T cells and the suppressive capacity of T regulatory (Treg) cells. The levels of interferon-gamma (IFN-γ), IL-4 and transforming growth factor-beta1 (TGF-β1) were investigated by intracellular staining and/or ELISA assay. The delayed-type hypersensitivity (DTH) response was evaluated by ear swelling assay. RMT1-10 therapy delayed the onset of rejection and significantly prolonged the survival of corneal allograft. In RMT1-10 treated mice, percentages of CD4+CD154+ cells and CD4+Tim-3+ cells were significantly decreased while the frequency of CD4+CD25+Foxp3+ Treg cells was significantly up-regulated, compared with those of isotype IgG treated mice. And, invitro proliferation of CD4+ T cells was significantly inhibited by RMT1-10. In addition, percentage of intracellular expression of IFN-γ and IL-4 in CD4+ T cells isolated from RMT1-10 treated mice was significantly reduced. After co-culturing with RMT1-10 invitro, CD4+ T cells produced significantly decreased levels of IFN-γ and IL-4 and significantly increased levels of TGF-β1. Furthermore, RMT1-10 inhibited DTH response of recipient mice and enhanced the suppressive capacity of Treg cells isolated from RMT1-10 treated mice. Our data indicate that Tim-1 blockade with RMT1-10 could suppress immunological rejection and prolong the survival of corneal allograft through regulating T cell responses. © 2014 Elsevier Ltd. Source


Liu C.,Hangzhou Normal University | Liu C.,Ohio State University | Bai Y.,Ohio State University | Xu X.,Ohio State University | And 10 more authors.
Particle and Fibre Toxicology | Year: 2014

Background: Prior experimental and epidemiologic data support a link between exposure to fine ambient particulate matter (<2.5 μm in aerodynamic diameter, PM2.5) and development of insulin resistance/Type II diabetes mellitus. This study was designed to investigate whether inhalational exposure of concentrated PM2.5 in a genetically susceptible animal model would result in abnormalities in energy metabolism and exacerbation of peripheral glycemic control. Methods: KKay mice, which are susceptible to Type II DM, were assigned to either concentrated ambient PM2.5 or filtered air (FA) for 5-8 weeks via a whole body exposure system. Glucose tolerance, insulin sensitivity, oxygen consumption and heat production were evaluated. At euthanasia, blood, spleen and visceral adipose tissue were collected to measure inflammatory cells using flow cytometry. Standard immnunohistochemical methods, western blotting and quantitative PCR were used to assess targets of interest. Results: PM2.5 exposure influenced energy metabolism including O2 consumption, CO2 production, respiratory exchange ratio and thermogenesis. These changes were accompanied by worsened insulin resistance, visceral adiposity and inflammation in spleen and visceral adipose depots. Plasma adiponectin were decreased in response to PM2.5 exposure while leptin levels increased. PM2.5 exposure resulted in a significant increase in expression of inflammatory genes and decreased UCP1 expression in brown adipose tissue and activated p38 and ERK pathways in the liver of the KKay mice. Conclusions: Concentrated ambient PM2.5 exposure impairs energy metabolism, concomitant with abnormalities in glucose homeostasis, increased inflammation in insulin responsive organs, brown adipose inflammation and results in imbalance in circulating leptin/adiponectin levels in a genetically susceptible diabetic model. These results provide additional insights into the mechanisms surrounding air pollution mediated susceptibility to Type II DM. © 2014 Liu et al.; licensee BioMed Central Ltd. Source


Liu J.L.,The Affiliated Hospital of Chengde Medical College | Gao W.,Chinese Peoples Liberation Army | Kang Q.M.,The Affiliated Hospital of Chengde Medical College | Zhang X.J.,The Affiliated Hospital of Chengde Medical College | Yang S.G.,The Affiliated Hospital of Chengde Medical College
PLoS ONE | Year: 2013

Objective:The prognostic significance of survivin for the survival of patients with gastric cancer remains controversial. Thus, the objective of this study was to conduct a systematic review of the literature evaluating survivin expression in gastric cancer as a prognostic indicator.Methods:Relevant literature was searched using PubMed, EMBASE, and Chinese biomedicine databases. A meta-analysis of the association between survivin expression and overall survival in patients with gastric cancer was performed. Studies were pooled and summary hazard ratios (HRs) were calculated. Subgroup analyses were also conducted.Results:Final analysis of 1365 patients from 16 eligible studies was performed. Combined HR suggested that survivin expression had an unfavorable impact on survival of gastric cancer patients (HR=1.39, 95% CI: 1.16-1.68). The unfavorable impact also appeared significant when stratified according to the studies categorized by patients' ethnicity, detection methods, type of sample, and HR estimate. The combined HR in the English literature showed an inverse effect on survival (HR=1.40, 95% CI: 1.13-1.75), while HR in the non-English literature did not (HR=1.38, 95% CI: 0.93-2.05). When stratified according to the location of survivin expression, combined HR showed that expression in cytoplasm was significantly associated with poor prognosis of gastric cancer patients (HR=1.46, 95% CI: 1.12-1.90). While expression in nucleus was not significantly associated with poor prognosis (HR=1.29, 95% CI: 0.72-2.31), the heterogeneity was highly significant (chi-squared=11.5, I2=74%, p=0.009).Conclusions:This study showed that survivin expression was associated with a poor prognosis in patients with gastric cancer. Cytoplasmic expression of survivin may be regarded as a prognostic factor for gastric cancer patients. In contrast, survivin expression in nucleus did not have a significant impact on patients' overall survival. © 2013 Liu et al. Source

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