Sun B.-L.,Key Laboratory of Cerebral Microcirculation in Universities of Shandong |
Xie F.-M.,Affiliated Hospital of Taishan Medical College |
Yang M.-F.,Key Laboratory of Cerebral Microcirculation in Universities of Shandong |
Cao M.-Z.,Shanxian Central Hospital |
And 5 more authors.
Acta Neurochirurgica, Supplementum | Year: 2011
Substances and fluid in the brain and subarachnoid spaces may be drained into extracranial lymphatics. This study aimed to investigate the possible role of cerebral lymphatic drainage in the process of cerebral injury following subarachnoid hemorrhage (SAH). Wistar rats were divided into non-SAH, SAH, and SAH plus cervical lymphatic blockage (SAH + CLB) groups. Autologous arterial hemolysate was injected into rats' cisterna magna to induce SAH. At time of 24 and 72 h after SAH, the rats were sacrificed for serum lactate dehydrogenase (LDH) activity, brain tissue superoxide dismutase (SOD) activity, and brain tissue malonaldehyde (MDA) content detection. It was found that serum LDH activity increased in rats of SAH group comparing with non-SAH group. SAH also resulted in decreased brain tissue SOD activity and increased brain tissue MDA content. In rats of SAH + CLB group, the increase of serum LDH activity was to a lager extent. Meanwhile, brain tissue SOD activity decreased and MDA content increased to a lager extent, as compared with SAH group. It was concluded that blockage of cerebral lymphatic drainage deteriorates cerebral oxidative injury after SAH, indicating cerebral lymphatic drainage may exert intrinsic protective effects against cerebral injury following SAH. © Springer-Verlag/Wien 2011. Source
Red blood cell distribution width levels correlate with liver fibrosis and inflammation a noninvasive serum marker panel to predict the severity of fibrosis and inflammation in patients with hepatitis b
Ou Q.-S.,Fujian Medical University |
Liu C.,Fujian Medical University |
Lin J.-P.,Fujian Medical University |
Chen H.-J.,Fujian Medical University |
And 4 more authors.
Medicine (United States) | Year: 2015
We aimed to study whether red blood cell distribution width (RDW) could be one of the variables determining the extent of liver fibrosis and inflammation in patients with biopsy-proven hepatitis B. A total of 446 hepatitis B virus-infected patients who underwent liver biopsy were divided into 2 groups: absent or mild and moderate-severe according to the severity of liver fibrosis and inflammation. The independent variables that determine the severity of liver fibrosis and inflammation were explored. RDW values increased with progressive liver fibrosis and inflammation. After adjustments for other potent predictors, liver fibrosis (moderate-severe) was independently associated with RDW, platelet, and albumin (odds ratio1.121, 0.987, and 0.941, respectively), whereas increased odds ratios of significant inflammation were found for RDW, alanine aminotransferase, albumin, and PLT (odds ratio1.146, 1.003, 0.927, and 0.990, respectively). The sensitivity and specificity of model A were 70.0% and 62.9% for detection of significant liver fibrosis [area under the receiver-operating characteristic curve (AUC)0.713, P<0.001]. The sensitivity and specificity of model B were 66.1% and 79.4% for predicting advanced liver inflammation (AUC0.765, P<0.001). Compared with preexisting indicators, model A achieved the highest AUC, whereas model B showed a higher AUC than RDW to platelet ratio (0.670, P<0.001) and FIB-4 (0.740, P0.32). RDWmay provide a useful clinical value for predicting liver fibrosis and necroinflammation in hepatitis B-infected patients with other markers. © 2015 Wolters Kluwer Health, Inc. All rights reserved. Source
Gao W.,Central Hospital of Jinan |
Bing X.,Central Hospital of Jinan |
Bing X.,Clinical College |
Li M.,Clinical College |
And 4 more authors.
Medical Oncology | Year: 2013
c-Met plays an important role in colorectal tumorigenesis and disease progression and thus is believed to be an attractive inhibitory target for receptor molecular therapeutic. SU11274 was identified as a small molecule, ATP competitive inhibitor of the catalytic activity of the c-Met kinase. Our study had investigated the relationship between the high expression of c-Met and colorectal carcinoma and the effect of c-Met inhibitor SU11274 in colorectal carcinoma in vitro and vivo. Immunohistochemistry was used to detect the expression of c-Met in 60 patients with colorectal cancer and 20 patients with benign adenoma and surrounding normal colon tissues. The effect of SU11274 on human colorectal carcinoma LoVo cells was detected by Western blot and MTT. And the influence of SU11274 on cell cycle was determined by flow cytometry. In addition, LoVo cell-transplanted tumor growth and expression of c-Met in nude mice was examined for inhibition of SU11274 in vivo. We found c-Met had high expression and was closely related to lymph node metastasis and TNM stage in colorectal carcinoma tissues. SU11274 significantly suppressed the phosphorylation of c-Met as well as the survival and proliferation of LoVo cell lines. G1-phase arrest was also induced by SU11274. SU11274 apparently restrained the growth of the xenograft tumor in nude mice. Our data suggest developing therapies that specifically inhibit the activation of c-Met may represent a novel therapeutic modality for patients with colorectal carcinoma expressing high levels of c-Met. © 2013 Springer Science+Business Media New York. Source