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Xiao-liang Xu

Publications and source records attributed to Xiao-liang Xu.

5 recordsLinked to original sources

[Expression and identification of HCV core protein in human hepatocytes].

AIM: To construct the recombinant plasmid of HCV core protein, and to express and identify it in normal human hepatocyte HL-7702. METHODS: HCV core gene was cloned by using PCR from plasmid pBRTM/HCV1-3011 which included the full length of HCV gene. The core segment with expression plasmid pcDNA3.1(-) was recombined to construct eukaryotic expression plasmid pcDNA3.1(-)/core, which was then transfected into human hepatocytes by using poly-cation. The expression of core protein was detected by immunochemical staining and Western blot. RESULTS: The length and sequence of the cloned core segment were correct. The transfected HL-7702 cells expressed the core protein. CONCLUSION: The eukaryotic expression plasmid pcDNA3.1(-)/core including HCV core gene is successfully constructed. The effective expression of HCV core protein in human hepatocytes is useful for further development of HCV core antigen.

Blotting, Western↗

Ectopic bone formation of human bone morphogenetic protein-2 gene transfected goat bone marrow-derived mesenchymal stem cells in nude mice.

OBJECTIVE: To evaluate the osteogenic potential of bone morphogenetic protein (BMP)-2 gene transfected goat bone marrow-derived mesenchymal stem cells (MSCs). METHODS: Goat bone marrow-derived MSCs were transfected by Adv-human bone morphogenetic protein (hBMP)-2 gene (Group 1), Adv-beta gal transfected MSCs (Group 2) and uninfected MSCs (Group 3). Western blot analysis, alkaline phosphatase staining, Von Kossa staining and transmission electron microscopy were adopted to determine the phenotype of MSCs. Then the cells were injected into thigh muscles of the nude mice. Radiographical and histological evaluations were performed at different intervals. RESULTS: Only Adv-hBMP-2 transfected MSCs produced hBMP-2. These cells were positive for alkaline phosphatase staining at the 12th day and were positive for Von Kossa staining at the 16th day after gene transfer. Electron microscopic observation showed that there were more rough endoplasmic reticulum, mitochondria and lysosomes in Adv-hBMP-2 transfected MSCs compared to MSCs of other two groups. At the 3rd and 6th weeks after cell injection, ectopic bones were observed in muscles of nude mice of Group 1. Only fibrous tissue or a little bone was found in other two groups. CONCLUSIONS: BMP-2 gene transfected MSCs can differentiate into osteoblasts in vitro and induce bone formation in vivo.

Animals↗

A UML profile for framework modeling.

The current standard Unified Modeling Language(UML) could not model framework flexibility and extendability adequately due to lack of appropriate constructs to distinguish framework hot-spots from kernel elements. A new UML profile that may customize UML for framework modeling was presented using the extension mechanisms of UML, providing a group of UML extensions to meet the needs of framework modeling. In this profile, the extended class diagrams and sequence diagrams were defined to straightforwardly identify the hot-spots and describe their instantiation restrictions. A transformation model based on design patterns was also put forward, such that the profile based framework design diagrams could be automatically mapped to the corresponding implementation diagrams. It was proved that the presented profile makes framework modeling more straightforwardly and therefore easier to understand and instantiate.

Algorithms↗

[BMP-2 gene modified tissue-engineered bone repairing segmental tibial bone defects in goats].

OBJECTIVE: To evaluate the effectiveness of the tissue-engineered bone substitute loaded with adenovirus mediated human bone morphogenetic protein-2 gene (Adv-hBMP-2) transfected bone marrow derived mesenchymal stem cells (BMSC) in the repair of diaphyseal segmental bone defect of large animal. METHODS: The right tibial bone defects (2.6 cm) model of 26 goats were established and divided into 5 groups: I. Adv-hBMP-2 transfected BMSC/calcined bone (CB) group (n = 9); II. adenovirus-beta-galactosidase (Adv-betagal) gene transfected BMSC/CB group (n = 6); III. untransfected BMSC/CB group (n = 6); IV. single CB group (n = 3); VI. untreated group (n = 2). The above tissue-engineered bone substitutes were implanted in the bone defects respectively except group VI. Roentgenography, histomorphometrical analysis and biomechanical measurement were studied at various times. RESULTS: X-ray: at 4 - 8th weeks after implantation, more bony callus was found in the bone defects of group I. The complete healing rates of group I, II, III, IV, and V were 5/8, 1/5, 0/5, 0/2, 0/1 respectively at 26th week after implantation. Histomorphometrical analysis showed much more new bony callus including cortical bone formed in group I than those of other groups. The compression strength of the implanted bone substitute of group I is significantly higher than those of group II and III. CONCLUSION: The tissue-engineered bone substitute loaded with human BMP-2 gene transfected BMSC can repair diaphyseal segmental bone defect of large animal (goat).

Animals↗

[The role of Smads and related transcription factors in the signal transduction of bone morphogenetic protein inducing bone formation].

OBJECTIVE: To clarify the mechanisms of the signal transduction of bone morphogenetic proteins (BMPs) inducing bone formation and to provide theoretical basis for basic and applying research of BMPs. METHOD: We looked up the literature of the role of Smads and related transcription factors in the signal transduction of BMPs inducing bone formation. RESULTS: The signal transduction processes of BMPs included: 1. BMPs combined with type II and type I receptors; 2. the type I receptor phosphorylated Smads; and 3. Smads entered the cell nucleus, interacted with transcription factors and influenced the transcription of related proteins. Smads could be divided into receptor-regulated Smads (R-Smads: Smad1, Smad2, Smad3, Smad5, Smad8 and Smad9), common-mediator Smad (co-Smad: Smad4), and inhibitory Smads (I-Smads: Smad6 and Smad7). Smad1, Smad5, Smad8, and probable Smad9 were involved in the signal transduction of BMPs. Multiple kinases, such as focal adhesion kinase (FAK), Ras-extracellular signal-regulated kinase (ERK), phosphatidylinositol 3-kinase (PI3K), and Akt serine/threonine kinase were related to Smads signal transduction. Smad1 and Smad5 related with transcription factors included core binding factor A1 (CBFA1), smad-interacting protein 1 (SIP1), ornithine decarboxylase antizyme (OAZ), activating protein-1 (AP-1), xenopus ventralizing homeobox protein-2 (Xvent-2), sandostatin (Ski), antiproliferative proteins (Tob), and homeodomain-containing transcriptian factor-8 (Hoxc-8), et al. CBFA1 could interact with Smad1, Smad2, Smad3, and Smad5, so it was involved in TGF-beta and BMP-2 signal transduction, and played an important role in the bone formation. Cleidocranial dysplasia (CCD) was thought to be caused by heterozygous mutations in CBFA1. The CBFA1 knockout mice showed no osteogenesis and had maturational disturbance of chondrocytes. CONCLUSION: Smads and related transcription factors, especially Smad1, Smad5, Smad8 and CBFA1, play an important role in the signal transduction of BMPs inducing bone formation.

Animals↗