BACKGROUND: Nerve tissue-engineered scaffolds must have axial y aligned structures, that can promote oriented growth of new axons, to guarantee the effective repair and regeneration of damaged nerves. OBJECTIVE: To investigate the effect of heparin sulfate/col agen nerve tissue-engineered scaffolds on peripheral nerve injury repair. METHODS: Heparin sulfate/col agen nerve tissue-engineered scaffolds were prepared, and its internal structure and porosity was observed and measured. Then rat Schwann cel s were seeded on the scaffolds to observe cel adhesion. Afterwards, 32 rats undergoing removal of left sciatic nerve were randomly divided into two groups (n=16 per group), and the rats were implanted by heparin sulfate/col agen nerve tissue-ergineered scaffolds as experimentd group, and the rats were implanted by autdogous sciatic nerve as control group. At 16 weeks after implantation, diameter, thickness of myelin sheath as wel as density of myelinated nerve fiber, the percentage of neural tissue and electrophysiology was detected, respectively. RESULTS AND CONCLUSION: The tissue-engineered scaffolds whose porosity was 91% were composed of microtubules arranging paral el y along the axial direction, and the microtubule diameter was 180 μm; the scaffolds had good biocompatibility with the Schwann cel s. In addition, at 16 weeks after implantation, no significant differences were found in myelin sheath thickness, myelinated nerve fiber density, as wel as conduction velocity and latency of motor and sensory nerves between two groups;compared with the control group, diameter of myelinated nerve fiber, percentage of neural tissue and amplitude of motor and sensory nerves in the experimental group were significantly decreased (P < 0.05). To conclude, the heparin sulfate/col agen nerve tissue-engineered scaffold can effectively repair peripheral nerve injury, but its effect is weaker than that of autologous nerve repair.

Objective: To screen for differentially expressed genes associated with the development and progression of human growth hormone adenoma, so as to lay a foundation for future study. Methods: The whole genome oligonucleotide microarray (Affymetrix 133 plus 2.0) was used to examine gene profiles of 8 growth homone adenoma samples and 2 normal pooled pituitary samples. Differentially expressed genes were subjected to bioinformatics analysis. Real-time qPCR was used to verify the microarray result of a randomly selected candidate gene. Results: A total of 187 up-regulated genes and 899 down-regulated genes associated with growth hormone adenoma were screened out, with their functions mainly associated with molecular binding, apoptosis/tumor, metabolism, signal transduction, cell cycle, and transportation activities. Conclusion: Microarray technology can be used for preliminary screen of growth hormone adenoma associated genes. The development and progression of growth homone adenoma are complex processes involving multiple genes, molecules, and pathways.

AIM: To study the action of NF-?B p65 in tubule-interstitium in rats with active Heymann nephritis(AHN). METHODS: Twenty female Wistar rats in 6-8 weeks of age were divided into two groups. The nephritis was induced with Fx1A/CFA by subcutaneous injection and with CFA as control. After rats were killed, the activation of NF-?B p65 in renal tissue was observed by immune histochemistry. RESULTS: The lesion score of renal interstitium and activation of NF-?B p65 of renal tubule in rats with AHN was higher than those of control group(P

Wnt/β-catenin signaling pathway plays an important role in the proliferation, growth, invasion, and metastasis of human cancers. Moreover, β-catenin/T-cell factor 4 (TCF4) interaction regulates the transcription of the key oncogenes in Wnt/β-catenin signaling pathway. Therefore, β-catenin/TCF4 interaction would be a promising therapeutic target for the development of highly selective anticancer agents. At present, most ongoing small-molecule inhibitors targeting β-catenin/TCF4 interaction, including PKF222-815, iCRT3/5/14, LF3, and sanguinarine, have been developed in preclinical studies for human cancer therapeutics. In this review, we summarized the research advances of up-to date inhibitors targeting β-catenin/TCF4 interaction, including the molecular structure and cellular functions of β-catenin in canonical Wnt signaling pathway. This review holds a hopeful avenue for the development of novel and highly selective Wnt inhibitors targeting β-catenin/TCF4 interaction for future anticancer strategy.

Animals ; Anti-HIV Agents ; pharmacology ; HIV ; drug effects ; genetics ; physiology ; HIV Infections ; drug therapy ; immunology ; virology ; Humans ; Mucous Membrane ; immunology ; virology ; Virus Replication ; drug effects

Apoptosis ; Down-Regulation ; Electron Transport Complex IV ; chemistry ; genetics ; metabolism ; Humans ; Mitochondria ; metabolism ; Mutation ; Neoplasms ; genetics ; metabolism ; pathology

Animals ; Central Nervous System ; radiation effects ; Humans ; Mice ; Microwaves ; Rats

Aim To establish and evaluate the simple and effective animal model of rheumatoid arthritis in SD rats induced by heat-killed mycobacterium tuberculosis H37Ra(Mtb).Methods SD rats were immunized s.c.at the base of the tail with Mtb(1 mg/rat) in mineral oil,and then body weight,blood routine,clinical signs of arthritis were observed regularly.And also hind paw volume in SD rats with AA was tested.Meanwhile,T-lymphocyte subset was determined by flow cytometry in peripheral blood,the level of TNF-?in serum and IL-1 and IL-6 and vascular endothe-lial growth factor(VEGF) in joint tissue were tested by ELISA.The ankle pathological change and radiographic evidence of the hind paws of SD rats were observed to evaluate the AA model effects and availability in SD rats.Results When compared with normal control rats,the total number of white blood cells,platelets and monocytes in peripheral blood and ratio of CD4/CD8 was markedly raised after immunization with Mtb.But body weight of model rats was significantly low from day 14 to 28 after injection of Mtb.The inflammatory arthritic lesions such as edema and erythema in the paws appeared after 9～10 d.The peak of inflammation was 14～16 d.The level of TNF-?in serum and IL-1,IL-6 and VEGF in joint tissue was significantly higher in SD rats with Mtb than that in normal control rats at d 28.The histopathological examination revealed cellular infiltration,synovial and cartilage hyperplasia in ankle joints of SD rats.Conclusions The model induced by Mtb in SD rats is more similar in clinical characterization of rheumatoid arthritis in human being.It is a more efficient and simpler manipulative procedure for screening of new anti-arthritis drugs and experimental studying of anti-rheumatoid arthritis.

Objective To study the protection and mechanism of co-administration of vitamin E with coenzyme Q10(CoQ10) to valproate-associated hepatotoxicity in infantal rats.Methods The rat models were established by oral administration of valproic acid(VPA) in ablactation(21 days) Wistar rats,at doses of 500 mg/(kg?d) during 30 days,other groups received the same amount of VPA with phemobarbitone(PB) and co-administration with vitamin E and CoQ10.The changes of liver cell morphology and the blood coagulation test,as well as the contents of succinic dehydrogenase(SDH),cytochrome oxidase(CCO),cytochrome,the levels of glutothione(GSH) and malondial dehyde(MDA) in rat liver mitochondria were detected by chromatometry,HPLC,Oil-Red-O staining and electron microscope,respectively.Results 1.Average content of cytochrome aa3 in liver mitochondria of infantal rats were reduced by 58.80% and(61.80%) because of administration of VPA and VPA added with PB.The protection against the loss of cytochrome aa3 by coadministration of VitE and CoQ10 was obvious.As for activities of SDH and CCO,which affected by VPA and VPA added with PB in rats,were significantly lowered compared with control group(P