Zhang Z.,Beijing University First Hospital |
He F.,First Renmin Hospital |
Shi Y.,Renmin Hospital
Rheumatology International | Year: 2013
For the purpose of investigating Behcet's disease in China, all the patients diagnosed as Behcet's disease in our hospital during the past 2 years were recruited into the study. The clinical and laboratory data of the patients were recorded and further analyzed; 334 patients were included with 195 males and 139 females. The mean age at onset was 35.8 ± 11.1 years. The most frequent initial manifestations were oral aphthae and genital ulceration. The common manifestations observed throughout the disease course were oral aphthae, genital ulceration and various cutaneous lesions. Besides these, many organs/systems including joint, eye, vessel, gastrointestine, nervous system, cardiovascular system, and pulmonary system were also involved in 28.4, 26.1, 17.4, 16.8, 9.6, 8.1, and 4.8 % of our patients, respectively. Involvement of ocular and vascular was more common in males than in females. Behcet' disease most frequently affects the Chinese patients aged 30-39 and displays a wide clinical spectrum with varieties of severe internal organ involvement. The disease is more common and severe in males than in females in Chinese populations. © 2012 Springer-Verlag.
PubMed | Yan'an University, Nuclear Industry 215 Hospital, Central Hospital, Renmin Hospital and Fengcheng Hospital
Type: Journal Article | Journal: Biochemical and biophysical research communications | Year: 2016
Recently, long noncoding RNAs (lncRNAs) have been shown to have critical regulatory roles in human cancer biology. LncRNA CCAT2 is a novel identified lncRNA that was previously reported to be up-regulated in different cancers, however, its role in prostate cancer remains unclear. The aim of this study was to investigate the expression and role of lncRNA CCAT2 in prostate cancer. The expression levels of lncRNA CCAT2 in PCa tissues and cell lines (DU145 and 22RV1) were evaluated by quantitative real-time PCR (qRT-PCR), and its association with prognosis of patients was analyzed by statistical analysis. Furthermore, the effect of CCAT2 on proliferation, migration, and invasion was studied in PCa cells. We found that the expression level of CCAT2 was higher in PCa tissues and cells compared to adjacent non-tumor tissues and normal prostate stromal immortalized cells WPMY-1. Kaplan-Meier survival analysis revealed that patients with high CCAT2 expression level had poorer overall survival and progression-free survival than those with low CCAT2 expression. Furthermore, multivariate analysis showed that the status of CCAT2 expression was an independent prognostic indicator for this disease. We also found that knockdown of CCAT2 could inhibit cell growth, migration, and invasion invitro. In addition, knockdown of CCAT2 stimulated epithelial-mesenchymal transition (EMT) through abrogating N-cadherin, vimentin expression and intensifing the expression levels of E-cadherin. In conclusion, our data suggested that lncRNA CCAT2 was a novel molecule involved in PCa progression, which provided a potential prognostic biomarker and therapeutic target for new therapies in patients with prostate cancer.
Xia Z.-y.,Renmin Hospital |
Gao J.,Renmin Hospital |
Ancharaz A.K.,Renmin Hospital |
Liu K.-x.,Sun Yat Sen University |
And 2 more authors.
Injury | Year: 2010
Objective: The emergence of ischaemic post-conditioning (IPO) provides a potential method for experimentally and clinically attenuating various types of organ injuries. There has been little work, however, examining its effects in the setting of lung ischaemia reperfusion (IR). The stress protein, haeme oxygenase-1 (HO-1), has been found to exert a potent, protective role in a variety of lung injury models. In this study, we hypothesised that the induction of HO-1 by IPO plays a protective role against the deleterious effects of IR in the lung. Methods: Anaesthetised and mechanically ventilated adult Sprague-Dawley rats were randomly assigned to one of the following groups (n = 8 each): the sham-operated control group, the IR group (40 min of left-lung ischaemia and 105 min of reperfusion), the IPO group (three successive cycles of 30-s reperfusion per 30-s occlusion before restoring full perfusion) and the ZnPPIX + IPO group (ZnPPIX, an inhibitor of HO-1, was injected intra-peritoneally at 20 mg kg-1 24 h prior to the experiment and the rest of the procedures were similar to that of the IPO group). Lung injury was assessed by arterial blood gas analysis, wet-to-dry lung weight ratio and tissue histological changes. The extent of lipid peroxidation was determined by measuring plasma levels of malondialdehyde (MDA) production. Expression of HO-1 was determined by immunohistochemistry. Results: Lung IR resulted in a significant reduction of PaO2 (data in IR, P < 0.05 vs. data in sham) and increase of lung wet-to-dry weight ratio, accompanied with increased MDA production and severe lung pathological morphological changes as well as a compensatory increase in HO-1 protein expression, as compared with sham (All P < 0.05). IPO markedly attenuated all the above pathological changes seen in the IR group and further increased HO-1 expression. Treatment with ZnPPIX abolished all the protective effects of post-conditioning. Conclusion: It may be concluded that IPO protects IR-induced lung injury via induction of HO-1. © 2009 Elsevier Ltd. All rights reserved.
PubMed | Jilin University, Jilin Medical College and Renmin Hospital
Type: Journal Article | Journal: Oncology letters | Year: 2016
The function of calcium efflux from the endoplasmic reticulum (ER) in cisplatin-induced apoptosis is not fully understood in cancer cells. The present study used western blot analysis, flow cytometry, immunofluorescence and 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide assay to investigate calcium signaling in human cervical cancer cells exposed to cisplatin. In the present study, treatment with cisplatin increased free Ca
Liu W.-K.,Xi'an University of Science and Technology |
Jiang X.-Y.,Renmin Hospital |
Zhang Z.-X.,Xi'an University of Science and Technology
Onkologie | Year: 2010
Background: Endometrial cancer is the 4th most common gynecological cancer. The expression of prostate stem cell antigen (PSCA), piwi-like 1 (PIWIL1), and T-box 2 (TBX2) in endometrial cancer remains to be elucidated. Material and Methods: The expression of PSCA, PIWIL1, and TBX2 was examined using the streptavidin-peroxidase method in 64 endometrial endometrioid adenocarcinoma (EAC) and paired normal endometrium (NE) samples from the Shaanxi Province in Ch na. Results: Positive expression rates of PSCA, PIWIL1, and TBX2 were 75% (48/64), 25% (16/64), and 56% (36/64), respectively in EACs, but 5% (3/64), 6% (4/64), and 2% (1/64), respectively in NEs. The difference was statistically significant (p < 0.05). PSCA was positively correlated with TBX2 (p = 0.003) but not PIWIL1 (p = 0.188). PIWIL1 was positively correlated with TBX2 (p = 0.003). PSCA was positively correlated with age, tumor grade, and lymph node metastasis (p < 0.05). TBX2 had an association with lymph node metastasis (p = 0.014). PIWIL1 was not associated with clinicopathological features (p > 0.05). Conclusions: We report the first analysis of PSCA, PIWIL1, and TBX2 expression in EAC. Our findings suggest that PSCA and TBX2 might be candidate targets for cancer therapy, and have helped us further understand the carcinogenesis of endometrial cancer. Copyright © 2010 S. Karger AG, Basel.
Geng S.,Wuhan University |
Geng S.,Renmin Hospital |
Gao Y.-D.,Wuhan University |
Yang J.,Wuhan University |
And 3 more authors.
International Immunopharmacology | Year: 2012
Store-operated calcium entry (SOCE) is the main Ca 2 + influx pathway of dendritic cells (DCs). DCs primed with histamine facilitate Th2 immune response via different types of histamine receptors. Histamine induces DCs to release Ca 2 + from internal store. Therefore, we wonder that whether histamine could activate SOCE in DCs through its receptors, and what's the functional relevance of the Ca 2 + influx through SOCE induced by histamine in Th 2 response. We certificate that histamine induced a transient Ca 2 + release followed by pronounced Ca 2 + influx after re-addition of external Ca 2 + which could be inhibited by SOCE blockers SKF-96365 and BTP-2. Moreover, the percentages of DCs that showed an obvious Ca 2 + release response to histamine were decreased in the presence of histamine 1 (H1) receptor antagonist pyridylethylamine (Pyr) or histamine 4 (H4) receptor antagonist JNJ7777120 (JNJ). Histamine up-regulated the mRNA expression of STIM1 in DCs, one of the two major proteins of SOCE channel. SOCE blocker BTP-2 and histamine receptor antagonists JNJ and Pyr inhibited the increase of CD86 induced by histamine on DCs. Histamine increased the level of IL-10 and decreased the level of IL-12p70 secreted by DCs. SOC blockers SKF and BTP-2 inhibited the level of both IL-10 and IL-12p70 secreted by DCs. Pretreatment of SOC blockers and H1, H4 receptor antagonists with DCs inhibited the Th2 polarization of T helper cells induced by histamine in mixed lymphocyte responses (MLR). We demonstrated that SOCE was involved in histamine-induced maturation and Th 2 response of DCs which was through histamine 1 and 4 receptor. © 2011 Elsevier B.V. All rights reserved.
Zhao Y.,Wuhan University |
Zhao Y.,Renmin Hospital |
Yang J.,Wuhan University |
Yang J.,Renmin Hospital |
And 4 more authors.
International Archives of Allergy and Immunology | Year: 2010
Background: Allergic asthma is an inflammatory disease regulated by the T helper (Th) cells. The Th1/Th2 imbalance has been well documented in the pathogenesis of allergic asthma. Recently, Th17 cells have been found to participate in the development of allergic asthma in animals. However, whether Th17 immunity contributes to the systemic immune responses in allergic asthmatic patients is unclear. Methods: Peripheral blood mononuclear cells were isolated from allergic asthmatics (n = 29) and healthy controls (n = 12). The frequencies of Th1, Th2 and Th17 cells were analyzed by flow cytometry. The related cytokine (IFN-γ, IL-4, IL-17, IL-22, IL-23 and IL-25) concentrations in plasma and culture supernatants were measured by enzyme-linked immunosorbent assay and Luminex. The level of retinoic acid-related orphan receptor γt (RORγt), a key transcription factor controlling Th17 differentiation, was examined by real-time quantitative polymerase chain reaction. Results: The percentages of Th2 and Th17 cells as well as the concentrations of Th2- and Th17-related cytokines were higher in allergic asthmatics than those in healthy controls; some patients were even treated with inhaled glucocorticoid. The percentages of Th17 cells as well as the plasma concentrations of IL-17 and IL-22 tended to increase with the severity of the disease, while the IL-25 level was elevated in mild patients. A parallel elevation of IL-17 and IL-23 concentrations and an increase in RORγt level were found in allergic asthmatics. Conclusion: Our results suggest that besides predominant Th2 immunity, abnormal Th17 immunity may be also involved in the pathogenesis of allergic asthma. Copyright © 2009 S. Karger AG.
Liu W.-K.,Xi'an Jiaotong University |
Jiang X.-Y.,Renmin Hospital |
Zhang M.-P.,Xi'an Jiaotong University |
Zhang Z.-X.,Xi'an Jiaotong University
European Journal of Gastroenterology and Hepatology | Year: 2010
Objectives: This study aimed to investigate the relationship between human papillomavirus type 16 (HPV16) and expression of cyclooxygenase-2 (COX-2), P53 in esophageal squamous cell carcinoma (ESCC), which has not yet been elucidated. Methods HPV16 was detected by amplifying the HPV16 E6 gene by the PCR method, and the expression of COX-2, P53 protein in 69 ESCCs and 32 normal esophageal mucosa (NEM) from Shaanxi Province was examined by the streptavidin-peroxidase method. Estimation of overall survival by HPV16, COX-2, and P53 was calculated with the Kaplan-Meier method and analyzed with the log-rank test. Results The infection rate of HPV16 in ESCCs (35 of 69, 50.7%) was significantly higher than that in NEMs (two of 32, 6.25%) (P< 0.01). The expression rate of COX-2 in ESCCs (44 of 69, 63.8%) was higher than that in NEMs (two of 32, 6.25%) (P< 0.01). The expression intensity of COX-2 expression had statistical difference in histological grade (R = 0.4453, P = 0.0019), tumor stage (R = 0.438, P = 0.000), and metastasis (R = 0.417, P = 0.002). P53 expression rate was 49.3% (34 of 69) in ESCC and 18.8% (six of 32) in NEMs. The expression rate of P53 proteins in ESCC was statistically higher than that in N67EMs (P = 0.0037). The infection of HPV16 had inverse correlation with the overexpression of COX-2 in ESCCs (R = -0.321, P = 0.008). The HPV16 DNA in ESCC had no statistical correlation with P53 protein (R = -0.014, P = 0.9055) and the elevated expression of COX-2 had positive correlation with P53 protein in ESCC (R = 0.441, P = 0.000). No statistical correlation was observed between the infection of HPV16 and clinicopathological features in ESCCs including sex, age, tumor stage, and lymph node metastasis, respectively (P>0.05). The COX-2 had no statistical correlation with sex and age (P>0.05), but had association with tumor stage and lymph node metastasis, respectively (P< 0.05). The expression of P53 protein had significant association with lymph node metastasis (P = 0.0005), but not with sex, age, and tumor stage, respectively (P>0.05). The overexpression of COX-2, infection of HPV16, and P53 protein in ESCC were not correlated with survival during the 5-year follow-up period (P>0.05). Conclusion: We first concluded that the increased expression of COX-2 had inverse correlation with HPV16 in ESCC. COX-2, HPV16, and P53 had no significant effect on the survival of patients with ESCC. These observations might help us to further understand the significant association between HPV16 and other molecules involved in the carcinogenesis and progression of ESCC. © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Interleukin-2 inhibits polarization to T helper type 1 cells and prevents mouse acute graft-versus-host disease through up-regulating suppressors of cytokine signalling-3 expression of naive CD4+ T cells
Zhao J.,Fudan University |
Zhao J.,Renmin Hospital |
Zhang T.,Fudan University |
Zhang T.,Qingdao Municipal Hospital |
And 2 more authors.
Clinical and Experimental Immunology | Year: 2010
T helper type 1 (Th1)-type polarization plays a critical role in the pathophysiology of acute graft-versus-host disease (aGVHD). The differentiation of T cells into this subtype is dictated by the nature of the donor naive CD4+ T cell-host antigen presenting cell (APC) interaction. Suppressors of cytokine signalling (SOCS) are a family of molecules that act as negative regulators for cytokine signalling, which regulate the negative cytokine signalling pathway through inhibiting the cytokine-induced Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. Studies have shown that SOCS proteins are key physiological regulators of both innate and adaptive immunity. These molecules are essential for T cell development and differentiation. SOCS-3 can inhibit polarization to Th1 and contribute to polarization to Th2. In this study, we found that interleukin (IL)-2 pre-incubation of C57BL/6 naive CD4+ T cells could up-regulate the expression of SOCS-3. Naive CD4+ T cells constitutively expressed low levels of SOCS-3 mRNA. SOCS-3 mRNA began to rise after 4 h, and reached peak level at 6 h. At 8 h it began to decrease. High expression of SOCS-3 mRNA induced by IL-2 could inhibit the proliferation of naive CD4 + T cells following stimulation with allogeneic antigen. IL-2-induced high SOCS-3 expression in naive CD4+ T cells could inhibit polarization to Th1 with stimulation of allogeneic antigens. We have demonstrated that IL-2-induced high SOCS-3 expression in naive CD4+ T cells could reduce the incidence of aGVHD between major histocompatibility complex (MHC) completely mismatched donor and host when high SOCS3 expression of CD4+T cells encounter allogeneic antigen in time. These results show that IL-2-induced high SOCS-3 expression can inhibit aGVHD through inhibiting proliferation and polarization to Th1 with the stimulation of allogeneic antigen. © 2010 British Society for Immunology.
Chen F.-C.,Hubei University of Medicine |
Shi X.-Y.,Hubei University of Medicine |
Li P.,Hubei University of Medicine |
Yang J.-G.,Hubei University of Medicine |
And 2 more authors.
Medicine (United States) | Year: 2015
Tropisetron is an adjuvant for butorphanol used in intravenous patientcontrolled analgesia (PCA) and has been reported to provide superior pain control. It is efficacious in reducing the incidence of postoperative nausea and vomiting. However, this admixture is not available commercially and stability data applicable to hospital practice are limited. This study aimed to describe the drug compounding and evaluates the long-term (up to 14 days) stability of butorphanol and tropisetron in 0.9% sodium chloride injection for PCA use. In this study, commercial solutions of butorphanol tartrate and tropisetron hydrochloride were combined and further diluted with 0.9% sodium chloride injection to final concentrations of butorphanol tartrate 0.08 mg/mL and tropisetron hydrochloride 0.05 mg/mL. The polyolefin bags and glass bottles were stored at 4°C and 25°C for up to 14 days. The drug stabilities were determined by visual inspection, pH measurement, and high-pressure liquid chromatography assay of drug concentrations. The data obtained for admixtures prepared and stored at temperatures of 25°C and 4°C show the drugs have maintained at least 98% of the initial concentration. All solutions remained clear and colorless over the 14-day period, and the pH value did not change significantly. The results indicate that admixtures of butorphanol tartrate 0.08 mg/mL and tropisetron hydrochloride 0.05 mg/mL in 0.9% sodium chloride injection solution were stable for 14 days when stored in polyolefin bags or glass bottles at 4°C and 25°C and protected from light. The infusion is feasible for manufacturing in pharmacy aseptic units and can be stored for up to 14 days for routine use in PCA infusions. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.