He E.,China Institute of Technology |
Guan H.,Shenzhen Second Hospital |
Chen Y.,Laboratory of Biochemistry and Molecular Biology Research |
Chen Z.H.,Health Center |
And 9 more authors.
Nucleosides, Nucleotides and Nucleic Acids | Year: 2010
Thymidine kinase 1 (TK1) is converting thymidine to thymidine monophosphate, and is related to DNA replication and cell proliferation. The use of the TK1 protein levels as a proliferation marker in malignancies is here summarized. TK1 protein in serum (STK1p) and TK1 expression in tissues were determined by a chemoluminescent dot blot assay and by immunohistochemistry staining, respectively. The expression of TK1 in tumor tissues correlated to pathological stages and clinical grades of carcinomas (ca) of esophagus, lung and in premalignancy of breast ductal ca. STK1p could monitor the out-come of tumor therapy by being correlated to remission [breast ca, non-Hodgkin's lymphoma], relapse [breast ca] and to survival [non-Hodgkin's lymphoma] of patients. In a health screening study of 12,641 persons, STK1p seemed to predict the risk of development of neoplasia related diseases at early stage. Copyright © 2010 Taylor and Francis Group, LLC.
Wu G.,411 Hospital of PLA |
Wu H.-B.,Tongji University |
Jiang H.,411 Hospital of PLA
Yaoxue Xuebao | Year: 2014
Hyperuricemia mice model was established with uricase inhibitor (potassium oxonate) and uric acids in serum were observed. Polydatin (5, 10, 20 mg·kg-1) and benzbromarone (16.7 mg·kg-1) were given ig for 7 d in mice. Kidney tissues were used to detect gene contents of urate anion transporter 1 (URAT1), organic anion transporter 1 (OAT1) and organic anion transporter 3 (OAT3) by real-time-PCR. The results showed that polydatin and benzbromarone can significantly reduce uric acid in blood of hyperuricemia mice (P<0.05), compared with the model group. URAT1, OAT1 and OAT3 contents of the kidney in hyperuricemia mice changed significantly (P < 0.05), compared with the blank group. Polydatin can significantly inhibit the changing trends in these genes induced by potassium oxonate in a dose-dependent manner, the difference was significant (P<0.05), compared with the model group. Those indicated that polysatin could reduce the level of the serum uric acid through promoting uric acid excretion.
Liu F.,Shanghai University |
Wang G.-Y.,411 Hospital of PLA |
Li Z.-S.,Shanghai University
BMC Gastroenterology | Year: 2015
Background: Endoscopic sphincterotomy (ES) is a therapeutic technique developed as an advanced application of endoscopic retrograde cholangiopancreatography (ERCP). An important adverse event associated with this procedure is hemorrhage, which may sometimes be uncontrollable. We sought to examine whether cap-assisted hemoclip application is effective in controlling ES-induced hemorrhage. Methods: In this prospective study, we investigated the outcomes in 10 patients who had uncontrolled ES-induced hemorrhage and were treated by cap-assisted application of hemoclip with a forward-viewing endoscope. Results: Nine of the 10 investigated patients were successfully treated using the cap-assisted hemoclip technique with forward-viewing endoscope, yielding a success rate of 90 %. The patient with hemorrhage non-responsive to hemoclipping required catheter embolization of the bleeding artery after its identification by digital subtraction angiography. One of the 10 patients developed mild pancreatitis after the procedure, but was successfully managed conservatively. Conclusions: Cap-assisted hemoclip application with a forward-viewing endoscope appears to be an effective therapeutic modality for achieving hemostasis in cases of ES-induced hemorrhage, without the occurrence of any severe adverse events; we believe that this method should be considered as an option in the management of ES-induced hemorrhage. © 2015 Liu et al.
Wang W.,Shanghai University |
Zhao W.,Shanghai University |
Liu Z.,Xuzhou Medical College |
Xia J.,411 Hospital of PLA |
And 2 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2015
Objective: To investigate the influences of trigeminal neuropathic pain on the cerebral blood flow in a ET-1 focal cerebral ischemia model. Methods: Male Sprague-Dawley (SD) rats (220-260 g) were randomly divided into a model group (trigeminal neuralgia, TN group) and a sham operation group (sham group). The TN group received bilateral infraorbital nerve chronic constriction surgery, and the sham group only underwent exposure of the infraorbital nerve. The mechanical pain threshold of the rats was continuously monitored for 30 days post surgery. On postoperative day 30, the animals were anesthetized, and 3 μL (120 pM/μL) ET-1 was injected into the surroundings of the middle cerebral artery (MCA) to establish a cerebral focal ischemia-reperfusion injury model in rats. The changes in cerebral blood flow of these two groups were monitored 30 min after the injection of ET-1. Results: The mechanic pain threshold values between rats in the two groups were not significantly different (P>0.05). The threshold value in the TN group on postoperative day 9 significantly decreased compared with that before surgery (P<0.01). Between postoperative days 9 and 30, the pain threshold values in the TN group were significantly lower than those in the sham group (P<0.01). From postoperative day 10, the mean arterial pressure in the TN group significantly increased compared with that before surgery (P<0.05), and the blood pressure (BP) in the TN group was higher than that in the sham group between postoperative days 10 and 30 (P<0.05). After 75 min of ET-1 microinjection, the cerebral blood flow in the rat frontal cortex exhibited reperfusion, and the cerebral blood flow in the TN group was significantly higher than that in the sham group (P<0.05). In addition, the content of calcitonin gene-related peptide (CGRP) in the blood of rats in the TN group was significantly higher than that in the sham group (P<0.05). Conclusions: Trigeminal neuropathic pain may increase the mean arterial pressure and the content of CGRP in the plasma of rats, thus increasing the cerebral blood flow in the frontal cortex of the ET-1 ischemia-reperfusion model. © 2015 E-Century Publishing Corporation. All rights reserved.
Wang M.,411 Hospital of PLA |
Deng X.,411 Hospital of PLA |
Ying Q.,411 Hospital of PLA |
Jin T.,411 Hospital of PLA |
And 2 more authors.
Biochemical and Biophysical Research Communications | Year: 2015
MicroRNA-224 is overexpressed in various malignant tumors with poor prognosis, which plays a critical role in biological processes including cell proliferation, apoptosis and several developmental and physiological progressions. However, the potential association between miR-224 and clinical outcome in patients with meningiomas remains unknown. Here, we investigate miR-224 expression and biological functions in meningiomas. MiR-224 expression was measured by Northern blot analysis and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) in meningioma and normal brain tissues. Kaplan-Meier analysis and Cox regression analysis were used to exam its correlation with clinicopathological features and prognostic value. The biological effects of miR-224 on the cell proliferation and apoptosis in meningioma cells were examined by MTT assay and apoptosis assay. We found the expression levels of miR-224 were significantly higher in meningioma tissues than that in normal brain, positively correlated with advanced pathological grade. Kaplan-Meier analysis indicated that meningioma patients with low miR-224 expression exhibited significantly prolonged overall and recurrence-free survival. Furthermore, we demonstrated that ERG2 was an identical candidate target gene of MiR-224 in vitro. Our results indicated that downregulation of miR-224 suppressed cell growth and resulted in the enhancement of cell apoptosis through activation of the ERG2-BAK-induced apoptosis pathway. Our findings imply the miR-224 expression could predict the overall survival and recurrence-free survival of patients with meningioma and it might be a promising therapeutic target for treating malignant meningiomas. © 2015 Elsevier Inc.