Li Z.-S.,State Key Laboratory of Tumor Biology |
Wei M.-Q.,Xi Jing Hospital |
Fu X.,State Key Laboratory of Tumor Biology |
Cheng H.,State Key Laboratory of Tumor Biology |
Li Q.,State Key Laboratory of Tumor Biology
Neuropathology | Year: 2011
Both chordoma and Rathke's cleft cyst are relatively rare diseases in the central nervous system. In this paper we report the first case of a chordoma coexisting with a Rathke's cleft cyst. A 49-year-old man presented with a 19-month history of distending pain, movement dysfunction and diplopia of the left eye. The preoperative diagnosis was consistent with chordoma with cystic change. Final pathological diagnosis of chordoma coexisting with Rathke's cleft cyst was made according to histological and immunohistochemical studies and the clinical and radiological features are discussed. Considering the close relationship between the notochordal tissue and Rathke's pouch during early embryogenic development, a possible mechanism is also discussed with the literature review. © 2010 Japanese Society of Neuropathology.
Chen Z.,Liao Cheng Hospital |
Li W.,Liao Cheng Hospital |
Ning Y.,Liao Cheng Hospital |
Liu T.,Liao Cheng Hospital |
And 2 more authors.
Experimental and Molecular Pathology | Year: 2014
Objective: The aim of the present work was to investigate the mechanism of transforming growth factor (TGF)-β1 and Sloan-Kettering Institute (Ski) in the pathogenesis of hypertrophic scars (HS). Background: Wound healing is an inherent process, but the aberrant wound healing of skin injury may lead to HS. There has been growing evidence suggesting a role for TGF-β1 and Ski in the pathogenesis of fibrosis. Material and methods: The MTT assay was used to detect the cell proliferation induced by TGF-β1. The Ski gene was transduced into cells with an adenovirus, and then the function of Ski in cell proliferation and differentiation was observed. Ski mRNA levels were measured by RT-PCR. Western blotting was used to detect the protein expression of α-SMA, E-cadherin, Meox1, Meox2, Zeb1 and Zeb2. Results: TGF-β1 can promote human skin fibroblast (HSF) cell proliferation in a time-dependent manner, but the promoting effect could be suppressed by Ski. TGF-β1 also induces the formation of the myofibroblast phenotype and the effect of TGF-β1 could be diminished by Ski. Also, Ski modulates the cardiac myofibroblast phenotype and function through suppression of Zeb2 by up-regulating the expression of Meox2. Conclusions: Ski diminishes the myofibroblast phenotype induced by TGF-β1 through the suppression of Zeb2 by up-regulating the expression of Meox2. © 2014 Elsevier Inc.
Jie Q.,Xi Jing Hospital |
Hu Y.,Xi Jing Hospital |
Yang L.,Xi Jing Hospital |
Yang L.,University of Hong Kong |
And 4 more authors.
Journal of Pediatric Orthopaedics Part B | Year: 2010
This study investigated the repair effects of fat and fibrin graft interposition through a proximal tibia transphyseal injury model and assessed the effectiveness of treatment to physeal injury with the fibrin. In this study, a unilateral growth plate injury was created in the right proximal tibia of 28 rats without any graft interposition; all left tibias were left untouched. In the other group of 28 rats, a bilateral physeal injury was made with the left tibia filled with autogenously adipose tissue and the right tibia filled with fibrin. To compare the malformed extents induced by different interventions, the length and the metaphyseal-diaphyseal angle of the tibia of three injured groups were examined. Further studies on bone density analysis and histological change were used to compare the bony bridge formation under different interventions. Results showed that the deformity angle and medial length of the tibia were significantly different between the grafted groups and nongrafted group at 4, 16, and 24 weeks postoperative (P<0.01). Results also showed no significant difference between fibrin-graft and fat-graft groups (P>0.05). Furthermore, the bone mineralization density of bony bridge induced by injury was significantly different between the grafted group and nongrafted group at 4, 16, and 24 weeks postoperative (P<0.01). Histological findings showed that bony repair after physeal injury was inhibited by both fibrin and fat interventions. We concluded that fibrin could be a substitute of adipose tissue in preventing the deformities induced by epiphyseal injury. Similar to autogenous fat, fibrin was found to alleviate limb shortness and prevent angular malformation by forming a scar instead of a bony bridge. The use of fibrin can help us to develop effective and compound intervention grafts to prevent skeletal deformity and regenerate normal cartilage tissue in the future. © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.
Ai T.,Xian Jiaotong University |
Wang Z.,Sengong Hospital |
Zhang M.,Xian Jiaotong University |
Zhang L.,Xian Jiaotong University |
And 3 more authors.
International Journal of Biological Markers | Year: 2012
Aim: To guide clinicians in selecting treatment options for patients with non-small cell lung cancer (NSCLC), it is desirable to have reliable markers predicting clinical outcome. This study analyzed the correlation between signal transducer and activator of transcription 3 (STAT3) and cyclin D1 in NSCLC and their association with clinicopathological features and survival.Methods: We investigated 65 specimens of NSCLC tissues by immunohistochemistry using STAT3 and cyclin D1 antibodies. First we determined the correlation between STAT3 and cyclin D1 expression and the clinicopathological features of the tumor. Then we assessed the prognostic relevance of STAT3 and cyclin D1.Results: A significant correlation was found between high levels of STAT3 expression and the degree of tumor differentiation. Additionally, a significant positive correlation was found between the expression of STAT3 and cyclin D1 (r=0.405, p=0.001). The overexpression of STAT3 and the presence of metastasis were significantly associated with shorter overall survival in univariate analysis (p=0.028 and p=0.036, respectively). Multivariate analysis confirmed that STAT3 expression was an independent prognostic factor (p=0.001).Conclusions: STAT3 might be correlated with tumor differentiation, and its elevated expression may be an adverse prognostic indicator for patients with NSCLC. Activation of the STAT3/cyclin D1 signaling pathway may be attributed to the malignant transformation of NSCLC and may represent a possible target for therapy. © 2012 Wichtig Editore - ISSN 0393-6155.
Li R.,Xi Jing Hospital |
Xu M.,Xi Jing Hospital |
Wang X.,Xi Jing Hospital |
Wang Y.,Philadelphia University |
And 8 more authors.
Journal of Molecular and Cellular Cardiology | Year: 2010
Deficiency of adiponectin (APN), an adipocyte-derived vascular protective molecule, contributes to diabetic vascular injury. The current study determined whether obesity/hyperlipidemia may alter the vascular response to APN, and investigated the involved mechanisms and pathologic significance. Adult male Sprague-Dawley rats were fed a regular or high-fat diet (HF) for 4-16. weeks. Circulating APN levels, aortic pAMPK/AMPK, peNOS/eNOS, and APN receptor expression levels were determined. Compared to time-matched animals fed control diet, plasma APN levels in HF-diet animals were significantly increased at 8. weeks, and rapidly declined thereafter. Despite unchanged or elevated circulating APN levels, phosphorylated AMPK and eNOS in vascular tissue were significantly reduced at all observed time points. Recombinant full-length APN (rAPN)-induced AMPK/eNOS phosphorylation and vasodilatation were significantly reduced in 16-week obese/hyperlipidemic aortic segments. Vascular APN receptor 1 (AdipoR1) and receptor 2 (AdipoR2) expression were significantly reduced 16. weeks after HF-diet. Pre-incubation of rAPN with obese/hyperlipidemic plasma, but not with normal plasma, significantly reduced its AMPK and eNOS activation effect, and blunted its protective effect against TNFα-induced HUVEC apoptosis. This study demonstrated for the first time that obesity/hyperlipidemia reduces vascular responsiveness to APN. Modification/inactivation of APN by unidentified factors present in obese/hyperlipidemic plasma, decreased vascular AdipoR1/R2 expression, and reduced circulating APN levels contribute to reduced vascular responsiveness to APN at different stages of the obese condition. Reduced APN bioactivity allows unmitigated TNFα pro-apoptotic and pro-inflammatory actions, contributing to vascular injury in obesity/hyperlipidemia. © 2010 Elsevier Ltd.