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Chongqing, China

Zhu B.,Chongqing University | Zhou X.,Southwest Hospital
Chinese Journal of Lung Cancer

PI3K/AKT signal pathway is an important intracellular signal transduction pathway. It plays important roles in cell apoptosis and survival by affecting the activity of downstream effector molecules, and it is closely associated with the development and progression of human tumors. Recent researches of PI3K/AKT indicate that this pathway plays important roles in tumor cells proliferation, blood vessel neogenesis, tumor metastasis and resistance to chemotherapy and radiotherapy. The profound research of PI3K/AKT is beneficial to the prevention of tumor and to the finding of potential targets for new drugs. This article reviewed the composition, function and regulation of PI3K/AKT signal pathway, and its effect in metastasis and drug resistance of lung cancer. Source

Zhou X.,Arizona State University | Zhou X.,Chonqing University | Ye J.,Arizona State University | Feng Y.,Southwest Hospital
IEEE Transactions on Biomedical Engineering

Tuberculosis (TB) is a major global health concern, causing nearly ten million new cases and over one million deaths every year. The early detection of possible epidemic is the first and important defense line against TB. However, traditional surveillance approaches, e.g., U.S. Centers for Disease Control and Prevention (CDC), publish the TB morbidity surveillance results on a quarterly basis, with months of reporting lag. Moreover, in some developing countries, where most infections occur, there may not be enough medical resources to build traditional surveillance systems. To improve early detection of TB outbreaks, we developed a syndromic approach to estimate the actual number of TB cases using Google search volume. Specifically, the search volume of 19 TB-related terms, obtained from January 2004 to April 2009, were examined for surveillance purpose. Contemporary TB surveillance data were extracted from the CDCs reports to build and evaluate the syndromic system. We estimate the actual TB occurrences using a nonstationary dynamic system. Respective models are built to monitor both national-level and state-level TB activities. The surveillance results of the syndromic system can be updated every day, which is 12 weeks ahead of CDCs reports. © 2011 IEEE. Source

Yang B.,Chongqing Medical University | Guo H.,Chongqing Medical University | Zhang Y.,Chongqing Medical University | Chen L.,Southwest Hospital | And 2 more authors.

Chondrogenic differentiation of mesenchymal stem cells (MSCs) is accurately regulated by essential transcription factors and signaling cascades. However, the precise mechanisms involved in this process still remain to be defined. MicroRNAs (miRNAs) regulate various biological processes by binding target mRNA to attenuate protein synthesis. To investigate the mechanisms for miRNAs-mediated regulation of chondrogenic differentiation, we identified that miR-145 was decreased during transforming growth factor beta 3 (TGF-β3)-induced chondrogenic differentiation of murine MSCs. Subsequently, dual-luciferase reporter gene assay data demonstrated that miR-145 targets a putative binding site in the 3′-UTR of SRY-related high mobility group-Box gene 9 (Sox9) gene, the key transcription factor for chondrogenesis. In addition, over-expression of miR-145 decreased expression of Sox9 only at protein levels and miR-145 inhibition significantly elevated Sox9 protein levels. Furthermore, over-expression of miR-145 decreased mRNA levels for three chondrogenic marker genes, type II collagen (Col2a1), aggrecan (Agc1), cartilage oligomeric matrix protein (COMP), type IX collagen (Col9a2) and type XI collagen (Col11a1) in C3H10T1/2 cells induced by TGF-β3, whereas anti-miR-145 inhibitor increased the expression of these chondrogenic marker genes. Thus, our studies demonstrated that miR-145 is a key negative regulator of chondrogenic differentiation by directly targeting Sox9 at early stage of chondrogenic differentiation. © 2011 Yang et al. Source

Huang G.,Chongqing Medical University | Wen Q.,Affiliated Hospital of Guiyang Medical College | Zhao Y.,Southwest Hospital | Gao Q.,Chongqing Medical University | Bai Y.,Chongqing Medical University

CD274, one of two co-stimulatory ligands for programmed death 1 and widely expressed in the mononuclear phagocyte system (MPS), may co-stimulate T cells and regulates inflammatory responses. However, changes in CD274 gene expression and the underlying molecular mechanism are poorly understood during inflammatory responses. Therefore, delineation of the complex mechanisms regulating CD274 expression is critical to understand this immunoregulatory system during inflammatory responses. The purpose of this study was to assess the molecular mechanisms regulating CD274 expression in an in vitro monocyte model of inflammatory response. Firstly, CD274 expression levels in human primary monocytes after lipopolysaccharide (LPS) treatment were observed and correlated with NF-κB activation. Secondly, based on the distribution of putative NF-κB binding sites, 5′ truncated human CD274 promoter reporters were constructed, transfected into U937 cells and critical promoter regions for basal (nt -570 to +94) and LPS-induced (nt -1735 to -570) transcription were identified by dual luciferase assays. Finally, a key NF-κB binding site (nt -610 to -601) for LPS-inducible CD274 transcriptional activity was characterized by point mutation analysis and chromatin immunoprecipitation analysis assays (ChIP). Thus, the present study establishes a molecular basis to understand the mechanisms governing CD274 expression in certain infections and inflammatory disorders. © 2013 Huang et al. Source

Ming L.,Southwest Hospital
Journal of Spinal Cord Medicine

Background/Objective: Spinal intramedullary tuberculoma is rare, accounting for 2/100,000 of cases of tuberculosis and only 2% of all cases of tuberculosis of the central nervous system. Diagnostic imaging is essential to improving diagnosis and management of this disease. Methods: The clinical profile, radiological data, and histological slides of 2 cases of intramedullary tuberculomas confirmed by pathologic examinations were reviewed. Results: In 2 cases, magnetic resonance imaging (MRI) showed thickening of the spinal cord and oval lesions with a low T1-weighted image signal and a typical "target sign" T2-weighted image signal. After gadopentetate dimeglumine administration, the lesion's rim shape was enhanced, showing uneven wall thickness and sharp margins. Conclusions: MRI findings of spinal intramedullary tuberculoma were specific, and accurate diagnosis could be obtained. MRI is the optimal measure because it shows location, size, and number of lesions and the presence of degeneration and necrosis. © 2010 by the American Paraplegia Society. Source

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