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1. Multiple-biomarkers provide powerful prediction of early acute renal allograft rejection by combination of serum fractalkine, IFN-γ and IP-10 | |||
Cui-Xiang Xu,Zhan-Kui Jin,Pu-Xun Tian | |||
Clinical Medicine 09 May 2018 | |||
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Abstract:Background/Aims: Biomarkers are urgently required for predicting rejection and for early anti-rejection treatment to prevent the functional impairment of the graft. We hypothesized that the combination of circulating fractalkine, IFN-γ and IP-10 might serve as effective biomarkers for predicting early acute rejection. Methods: We conducted a retrospective study of 87 subjects, who were classified into acute rejection group (ARG; n=38) and non-rejection group (NRG; n=49). Serum fractalkine, IFN-γ and IP-10 levels were measured by Luminex. Results: The levels of fractalkine on day 0, IP-10 on 4th day, fractalkine, IFN-γ and IP-10 on the 7th day in ARG was significantly higher than that in NRG. Kaplan-Meier survival analysis highlighted the higher-levels of fractalkine on day 0, 4th and 7th day, IFN-γ on day 0, 1st, 4th, and 7th day and IP-10 on the 4th and 7th day in rejection-free survival probability were significantly lower than low-levels. ROC analyses highlight the superiority of fractalkine on day 0, IP-10 on day 0, 4th and 7th day, and IFN-γ on day 0, 1st and 7th day in prediction of acute rejection. We found the combination of fractalkine on day 0, IP-10 on 7th day and IFN-γ on 7th day had the highest AUC (0.866) for predicting rejection with a sensitivity of 86.8% and a specificity of 89.8%. Conclusion: Our findings demonstrated a more powerful prediction of early acute renal allograft rejection by combination of multiple-biomarkers of fractalkine, IFN-γ and IP-10, and the results might help stratify the immunologic risk of acute allograft rejection in patients.????? | |||
TO cite this article:Cui-Xiang Xu,Zhan-Kui Jin,Pu-Xun Tian. Multiple-biomarkers provide powerful prediction of early acute renal allograft rejection by combination of serum fractalkine, IFN-γ and IP-10[OL].[ 9 May 2018] http://en.paper.edu.cn/en_releasepaper/content/4745000 |
2. Perspectives of traditional Chinese medicine in pancreas protection for acute pancreatitis | |||
LI Jun,ZHANG Shu,ZHOU Rui,ZHANG Jian,LI Zongfang | |||
Clinical Medicine 10 May 2017 | |||
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Abstract:Acute pancreatitis (AP) is one of the most common diseases. AP is associated with significant morbidity and mortality, but it lacks specific and effective therapies. Traditional Chinese medicine (TCM) is one of the most popular complementary and alternative medicine modalities worldwide for the treatment of AP. The current evidence from basic research and clinical studies has shown that TCM has good therapeutic effects on AP. This review summarizes the widely used formulas, single herbs and monomers that are used to treat AP and the potential underlying mechanisms of TCM. Because of the abundance, low cost, and safety of TCM as well as its ability to target various aspects of the pathogenesis, TCM provides potential clinical benefits and a new avenue with tremendous potential for the future treatment of AP. | |||
TO cite this article:LI Jun,ZHANG Shu,ZHOU Rui, et al. Perspectives of traditional Chinese medicine in pancreas protection for acute pancreatitis[J]. |
3. The roles of mitoferrin-2 in the process of arsenic trioxide-induced cell damage in human gliomas | |||
WANG Ligang | |||
Clinical Medicine 08 May 2017 | |||
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Abstract:Background: Among glioma treatment strategies, arsenic trioxide (As2O3) has shown efficacy as a therapeutic agent against human gliomas. However, the exact antitumor mechanism of action of As2O3 is still unclear. Mitochondria are considered to be the major source of intracellular reactive oxygen species (ROS), which are known to be associated with As2O3-induced cell damage. Therefore, we investigated whether mitoferrin-2, a mitochondrial iron uptake transporter, participates in As2O3-induced cell killing in human gliomas. Methods: Human glioma cell lines were used to explore the mechanism of As2O3's antitumor effects. First, expression of mitoferrin-2 was analyzed in glioma cells that were pretreated with As2O3. Changes in ROS production and apoptosis were assessed. Furthermore, cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). Results: In the present study we found that As2O3 induced ROS production and apoptosis in glioma cells. In addition, gene expression of mitoferrin-2, a mitochondrial iron uptake transporter, was increased 4 to 5 fold after exposure to As2O3 (5 μM) for 48 hours. Furthermore, apoptosis and cytotoxicity induced by As2O3 in glioma cells were decreased after silencing the mitoferrin-2 gene. Conclusions: Our findings indicated that mitoferrin-2 participates in mitochondrial ROS-dependent mechanisms underlying As2O3-mediated damage in glioma cells. | |||
TO cite this article:WANG Ligang. The roles of mitoferrin-2 in the process of arsenic trioxide-induced cell damage in human gliomas[OL].[ 8 May 2017] http://en.paper.edu.cn/en_releasepaper/content/4733708 |
4. 18F-FDG-PET-CT with little value in different diagnosis between pulmonary malignancy and amyloidosis | |||
LIU Minghui,SONG Zuoqing,LIU Renwang,LIU Jinghao,LIU Hongyu,CHEN Jun | |||
Clinical Medicine 05 May 2017 | |||
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Abstract:Pulmonary amyloidosis is rare and is often misdiagnosed due a lack of general awareness of the condition. The role of PET-CT in the differential diagnosis between pulmonary amyloidosis and lung malignant tumors is still unclear. Herein, we describe a 61-year-old Chinese woman who presented with a right lower lobe pulmonary nodule, and right hilar and mediastinal lymph nodes shadows. On PET-CT examination, the patient was found to have right lower lung malignant lesions with multiple right hilar and mediastinal lymph node metastases. She was diagnosed with nephrotic syndrome with a history of pathologic type of amyloidosis over the previous two months. After performing right thoracotomy, a histopathologic diagnosis of pulmonary amyloidosis was made. The patient has done well postoperatively, showing no local recurrence in the lung or deterioration of her condition in an over 3-year follow-up period. The pathology of nephrotic syndrome in patients with amyloidosis led to the diagnosis of systemic amyloidosis being made in this patient. From this case, combined with the domestic and international literature, we conclude that PET-CT is of little value for the different diagnosis between pulmonary amyloidosis and lung malignant tumors. | |||
TO cite this article:LIU Minghui,SONG Zuoqing,LIU Renwang, et al. 18F-FDG-PET-CT with little value in different diagnosis between pulmonary malignancy and amyloidosis[OL].[ 5 May 2017] http://en.paper.edu.cn/en_releasepaper/content/4730671 |
5. Mechanism of ginsenoside Rb1 regulation AQP4 expression to intervene the edema in spinal cord ischemia-reperfusion injury | |||
Huang fei | |||
Clinical Medicine 01 May 2017 | |||
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Abstract:Introduction Spinal Cord Ischemia-reperfusion Injury (SCII) is a common complication of spinal surgery and thoracic and abdominal surgery, lead to higher morbidity and mortality. Although the pathogenesis of SCII is not fully understood, the acute cytotoxic edema at the site of injury is the key cause of the SCII, and the degree of edema determines the prognosis of SCII. Therefore, avoiding spinal nerve cell edema is the key to the treatment of SCII. Methods The rat SCII model was established to elucidate whether ginsenoside Rb1 intervention could alleviate the edema of SCII in rats and further determine the effect of ginsenoside Rb1 on the expression and activity of AQP4. To establish the model of oxygen-glucose deprivation/reoxygenation(OGD/R)to simulate ischemia-reperfusion injury at the cellular level. The expression of AQP4 in OGD/R culture system was confirmed by RNA interference technique or rescue experiment. To determine the effect of ginsenoside Rb1 on the astrocytes edema in OGD/R cell culture conditions. Results In animal model, ginsenoside Rb1 could alleviate the edema of spinal cord and improve the neurological function by increasing the expression of AQP4. Further, at the cellular level, it can be concluded that ginsenoside Rb1 can reduce the astrocyte edema by increasing the expression of AQP4 and enhancing its function. Conclusion These findings demonstrate ginsenoside Rb1 can relieve spinal cord edema and improve neurological function by increasing AQP4 expression. | |||
TO cite this article:Huang fei. Mechanism of ginsenoside Rb1 regulation AQP4 expression to intervene the edema in spinal cord ischemia-reperfusion injury[OL].[ 1 May 2017] http://en.paper.edu.cn/en_releasepaper/content/4731386 |
6. Effects of Alprostadil on reducing plasmas D-dimer level and incidence of venous thromboembolism after radical prostatectomy: a randomized prospective cohort study | |||
YAN Yangye,XIE Tiancheng,XU Yunfei,LUO Ming | |||
Clinical Medicine 26 April 2017 | |||
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Abstract:Objectives: To investigate the effects of alprostadil on reducing plasma D-dimer level and incidence of venous thromboembolism after radical prostatectomy. Methods: This randomized prospective cohort study recruited 130 patients diagnosed with prostate cancer and received radical prostatectomy from September 2014 to January 2016 in Shanghai tenth People's Hospital. Patients were randomly assigned to an alprostadil group (n=65) and a control group (n=65). Alprostadil group received 10ug/d of alprostadil diluted in 10ml of normal saline through an intravenous injection over 5 min starting on operation day and continuing for 1 week after surgery. Plasma D-dimer levels were measured preoperatively, on the operation day and on 1st, 3rd, 5th, 7th days after surgery. All patients underwent Doppler ultrasonography evaluation of bilateral lower limbs on 7th day after surgery. The outcome of the study was analyzed using SPSS 20.0 software and via χ2 test and repeated measures analysis of variance. Results: Comparing to that in control group, the plasma D-dimer level was significantly decreased on the 7th day (p=0.000) after operation, and the incidence of venous thromboembolism was significant lower (3.1% vs. 15.4%, p=0.030) in alprostadil group. Conclusion: Systemic treatment of alprostadil for at least 1 week after radical prostatectomy contributes to the decreasing of plasma D-dimer level and incidence of venous thromboembolism.) | |||
TO cite this article:YAN Yangye,XIE Tiancheng,XU Yunfei, et al. Effects of Alprostadil on reducing plasmas D-dimer level and incidence of venous thromboembolism after radical prostatectomy: a randomized prospective cohort study[OL].[26 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4729881 |
7. Long-term survival after complete mesocolic excision versus non-complete mesocolic excision for colon cancer: a systemic review and meta-analysis | |||
GAO Zhidong | |||
Clinical Medicine 26 April 2017 | |||
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Abstract:Purpose The effect of complete mesocolic excision on survival is controversial. We did a meta-analysis to compare survival after complete mesocolic excision with non-complete mesocolic excision for patients with colon cancer. Methods We systematically searched Pubmed, ScienceDirect, Cochrane Library, and ClinicalTrials.gov to identify research comparing complete mesocolic excision with non-complete mesocolic excision for patients with colon cancer. The primary endpoint was survival. Results We identified 200 studies, 6 observational studies met selection criteria with a total of 4439 patients (2092 in complete mesocolic excision group, 2347 in non-complete mesocolic excision group). Complete mesocolic excision significantly increased 3-year survival rate and 5-year survival rate compared to non-complete mesocolic excision in patients with colon cancer (HR: 0.73, 95%CI: 0.55 - 0.90, p < 0.0001; HR: 0.40, 95%CI: 0.13 - 0.67, p = 0.034, respectively). For patients with node positive disease, complete mesocolic excision also increased 3-year survival rate (HR: 0.72, 95%CI: 0.52 - 0.92, p < 0.001). Conclusions Complete mesocolic excision was a more effective strategy compared with non-complete mesocolic excision in improving survival of colon cancer. | |||
TO cite this article:GAO Zhidong. Long-term survival after complete mesocolic excision versus non-complete mesocolic excision for colon cancer: a systemic review and meta-analysis[OL].[26 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4729706 |
8. Ex vivo flow perfusion maintains fat flap long-term viability: a novel model for large volume engineered tissue research | |||
An Yang,Nie Fangfei,Lidong | |||
Clinical Medicine 22 April 2017 | |||
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Abstract:Background Large volume muscle tissue engineering still remains a major challenge. An axial vascular pedicle and perfusion bioreactor are necessary for development and maintenance of large volume engineered muscle in order to provide circulation within the construct. We aimed to determine whether a novel model to investigate large volume engineered muscle flap from an existing rat groin fat ?ap was developed. Method A fat ?ap based on the super?cial inferior epigastric vascular pedicle in the rat was harvested and placed into a perfusion bioreactor. The ?aps were kept in the bioreactor for up to 7 weeks and meanwhile, transdifferentation of adipose to muscle tissue could have taken place. This system enables a myogenic differentiation medium ?ow through the bioreactor of a constant pH and a constant oxygen concentration. Assessment of viability was performed by immunofluorescence, histological staining, calcein based life/dead test and determination of RNA quantity and quality after 1, 3, 5 or 7 weeks. Result Immunofluorescence staining showed that smooth muscle around vessels were still intact without signs of necrosis, or atrophy. The visual assessment of viability by a calcein based life/dead test revealed a viability of the rat adipose tissue preserved in the bioreactor system with permanent perfusion. In this study, RNA samples from different experimental conditions were quanti?ed by photometry and intact rRNA bands of 18S and 28S were observed by gel electrophoresis, indicating that degradation of RNA was minimal. Conclusion This is the ?rst demonstration that ?ow perfusion maintains rat groin engineered muscle flap long-term viability in vitro and a large volume vascularized muscle could be engineered in a perfusion bioreactor. | |||
TO cite this article:An Yang,Nie Fangfei,Lidong. Ex vivo flow perfusion maintains fat flap long-term viability: a novel model for large volume engineered tissue research[OL].[22 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4726583 |
9. The effect of docetaxel induces apoptosis of prostate cancer cells through cofilin-1 and paxillin signal pathway | |||
XIAO Pan,ZHANG Huaiqiang | |||
Clinical Medicine 17 April 2017 | |||
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Abstract:Prostate cancer is a common multiple malignant tumor of male, whose mortality is the 2nd highest of all kinds of tumours in western countries, and the mortality of morbidity is 13% in the USA. The objective of this study was performed to investigate the anti-cancer effect of docetaxel induces apoptosis of prostate cancer through cofilin-1 and paxillin signal path. Treatment docetaxel (1-50 nM) disposed the human prostate cancer (LNCaP) cells for 24 h. Then cell growth and cytotoxicity were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5 -diphenyltetrazolium bromide assay (MTT) and Lactate dehydrogenase (LDH) assay, respectively. Docetaxel-induced cell death was analyzed using Flow cytometric and Caspase-3 assay, respectively. Real-time RT-PCR analysis was used to detect the expression of cofilin-1 gene and western blots was also used to probe the protein expression of paxillin. We found that supplement with docetaxel could inhibit cell growth, promoted cytotoxicity, activated apoptosis and increased caspase-3 activity in LNCaP cell. Interesting, administrate of docetaxel reduced the expression of cofilin-1 gene and the protein expression of paxillin in LNCaP cell. Meanwhile, knockdown of cofilin-1 advanced the anti-cancer effect of docetaxel against LNCaP cell through suppression of paxillin pathway. The present findings that the anti-cancer effect of docetaxel induces apoptosis of prostate cancer through suppression of cofilin-1 and paxillin signal path, and which will help to set a stage to the clinical treatment of prostate cancer. | |||
TO cite this article:XIAO Pan,ZHANG Huaiqiang. The effect of docetaxel induces apoptosis of prostate cancer cells through cofilin-1 and paxillin signal pathway[OL].[17 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4726257 |
10. Endogenous High-mobility Group Box 1 is Involved in the Progress of Benign Prostatic Hyperplasia by Promoting the Proliferation of Prostate Epithelial and Stromal Smooth Muscle Cells | |||
Nie Lihong,Zhao Ruining,Xu Xiaolin,Qin Kaiyue,Li Yajie | |||
Clinical Medicine 13 February 2017 | |||
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Abstract:Background: Our previous studies have demonstrated that chronic prostatic inflammation is involved in the pathogenesis and progression of benign prostatic hyperplasia (BPH), although its mechanisms are still unclear. High mobility group box 1 protein (HMGB1) is an important late inflammatory cytokine, which plays an important role in the initiation and amplication of the inflammation reaction. Additionally, HMGB1 induces tissue reorganization by promoting cell proliferation and migration. The present experiments were performed to determine the role of endogenous HMGB1 in the progress of BPH. Methods: Clinical information and tissue samples were obtained from 60 BPH patients. HMGB1 expression and distribution were analysed by RT-PCR, Western blotting and immunohistochemistry. Pearson correlation was analyzed to assess relationships among HMGB1 protein levels and each clinical parameters of BPH patients. In addition, Western blotting and ELISA were used to assay the endogenous production of HMGB1 in human prostate epithelial cells. The CCK8 assay and transwell migration assay were performed to examine the proliferation and migration of human prostate epithelial and stromal smooth muscle cells. Results: Prostatic inflammation increased HMGB1 expression in BPH patients, and HMGB1 protein could be secreted into the cytoplasm from nucleus of prostate epithelial cells subjected to prostatic inflammation. HMGB1 protein levels was positively correlated with prostate volume of BPH patients. In addition, LPS increased HMGB1 expression in prostate epithelial cells and led HMGB1 to be secreted into the extracellular space by prostate epithelial cells. Furthermore, HMGB1 promoted the proliferation of prostate epithelial and stromal smooth muscle cells and the migration of prostate stromal smooth muscle cells. Conclusions: the present study indicated that HMGB1 is involved in the progress of BPH and may represent a potential strategy to treat BPH. | |||
TO cite this article:Nie Lihong,Zhao Ruining,Xu Xiaolin, et al. Endogenous High-mobility Group Box 1 is Involved in the Progress of Benign Prostatic Hyperplasia by Promoting the Proliferation of Prostate Epithelial and Stromal Smooth Muscle Cells[OL].[13 February 2017] http://en.paper.edu.cn/en_releasepaper/content/4718958 |
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