Objective To investigate the liver repair effects of Pim-3 gene in rat with fulminant hepatic failure (FHF). Methods Thirty-two rats were divided into four groups (eight for each group). Three groups of rats were pretreated with Ringer's solution, vector plasmid or Pim-3 gene recombinant plasmid respectively and, one day later, received intraperitoneal injections with lipopolysacchride (LPS) and D-galactosamine (D-GalN). The fourth group served as normal control.Eight hours after the LPS/D-GalN injection, the liver tissues and blood samples were collected. The contents of serum transaminase was tested by automatic blood biochemistry meter. The morphological changes were observed by light microscopy using hematoxylin and eosin (HE) staining. Tumor necrosis factor (TNF)-α and interleukin (IL)-1β gene expression was detected by reverse transcriptionpolymerase chain reaction(RT-PCR). The serum levels of TNF-α and IL-1β were measured by enzyme linked immunosorbent assay (ELISA), and cell apoptosis by TdT-mediated dUTP nick end labeling (TUNEL) assay. Comparisons between groups were done by analysis of variance. ResultsThe over expressions of Pim-3 gene and reporter gene, green fluorescent protein (GFP) were induced by injection with recombinant plasmid solution.In comparison with the rats retreated with Ringer' s solution or vector plasmid, those pretreated with recombinant plasmid had a lower mortality and lower serum transaminase levels. The injection of recombinant plasmid significantly reduced hemorrhage, necrosis and inflammatory infiltration in the liver. Liver apoptotic index (AI) was dramatically lower in rats treated with recombinant vectors compared to the rats treated with Ringer's solution or vector plasmids [(10. 2±6.9)％ vs (83. 1±12.6) ％ and (79.9±13.4) ％ respectively, P＜0. 01]. In addition, the expression of exogenous Pim-3 gene remarkable inhibited the transcriptions and expressions of TNF-α and IL-1β. ConclusionsPim-3 gene can protect rats from LPS/D-GalN-induced FHF possibly by inhibiting expressions and secretions of inflammatory cytokines, such as TNF-α and IL-13, in liver tissues.

BACKGROUND:Previous animal experiments have demonstrated that mandibular advancement can cause the remodeling of temporomandibular joint tissue of young SD rats. This is mainly characterized by accelerated growth rate of the condyle tissue and secondary growth of mandible. But the ultrastructural remodeling of condylar chondrocytes remains poorly understood. OBJECTIVE:To observe the histological and ultrastructural variations of reconstructed condylar cartilage of young rats under the effect of continuous mandibular advancement. METHODS:SD rats aged 4 weeks were randomly divided into control and experimental groups. Rats in the experimental group were subjected to mandibular advancement for 24 hours and sacrificed at 3, 7, 14, 21 and 30 days of intervention. Condylar cartilage samples were harvested and their histological and ultrastructural changes were observed under optical microscope and transmission electron microscope. RESULTS AND CONCLUSION:After 14 days of intervention, the thickness of condylar cartilage in the experimental group increased first and then became thin in the period of observation. The cartilage thickness variations in the postmedian condylar were significant (P < 0.01). After 7 days of intervention, the ultrastructure of condylar chondrocytes was reconstructed, including intracelular karyopyknosis, rough endoplasmic reticulum compartment sweling, smaler even absent lipid droplets, less and irregular microfilaments around the nucleus, broadened and increased extracelular matrix and the emergence of large gaps. These results demonstrate that under continuous mandibular advancement, the rat condylar cartilage wil become thick or thin with the endurance time, and chondrocyte matrix synthesis ability wil be significantly enhanced.

In this study, the peripheral blood mononuclear cells of healthy adult were acquired and inducted by vascular endothelial growth factor, et cetera. The differentiated endothelial cells were observed and identified as EPCs by the double positive staining of fluorescent labeled acetylated-LDL and lectin, seeded on the polyurethane small-diameter artificial vessels, treated by shear stress of 15 dyn/cm2, and observed by scanning electronic microscopy. As a result, the peripheral blood mononuclear cells differentiated into EPCs. They were positively stained by labeled acetylated-LDL and lectin. Under observation of scanning electronic microscope, the unseeded polyurethane small-diameter artificial vessel being suited for the growth and spreading of the cells; the cell lineage on surface of artificial vessels of stationary group being arrayed in chaos, and that of shear stress group being arrayed in direction. Therefore, the peripheral cells can differentiate into EPCs, and EPCs can be used as novel source cells for the accelerated endothelialization of small diameter artificial vessel. Shear stress contributes to the mechanic moulding of cell lineage on the surface of artificial vessel.
Bioartificial Organs ; Biocompatible Materials ; Blood Vessel Prosthesis ; Cell Adhesion ; Cell Differentiation ; Cells, Cultured ; Endothelial Cells ; cytology ; Humans ; Leukocytes, Mononuclear ; cytology ; Polyurethanes ; chemistry ; Prosthesis Design ; Shear Strength ; Stem Cells ; cytology ; Stress, Mechanical