[Objective]To study changes of ultrastructures and respiratory function of the spinal cord mitochondrial in experimental spinal cord injury.[Method]Forty-eight SCI models in adult SD rats were built based on modified Allen's method.Mitochondria was extracted from injuried spinal cord tissue by using modified Estabrook's method at 6h,12h and 24h after SCI.Then ultrastructural changes and respiratory function,including R3,R4,RCR,P/O were observed.[Result]Ultrastructure of mitochondria was damaged greatly.The results revealed that R3、RCR and P/O of injuried spinal cord mitochondria decreased significantly after injury compared to the normal control group(P

BACKGROUND: Pathogenesis and pathophysiological changes of chronic compressive cervical myelopathy havenotbeen completely clarified.OBJECTIVE: To establish an animal model of experimental chronic compressive cervical myelopathy for the exploration of the pathological and electrophysiological changes after chronic spinal compression.DESIGN: A randomized and controlled observatory study using experimental animals as subjects.SETTING: An Animal Experimental Center of a University and an Orthopaedic Laboratory of Affiliated Hospital of a Military Medical University MATERIALS: The study was conducted in the Animal Experimental Center of Nantong Medical University and the Orthopaedic Laboratory of Shanghai Changzheng Hospital from June 2002 to April 2003. Sixty 12-week healthy Chinese rabbits of either gender with a bodymass between 2.5 kg and 3.0 kg were randomly divided into control group( n = 6) and study group( n = 54).METHODS: Titanic metal screw was put into C5 vertebra through cervical anterior approach for progressive compression to establish chronic cervical myelopathy model.MAIN OUTCOME MEASURES:Principal consequences: ①histological examination ;②electrophysiological examination. Secondary consequence:neural function evaluation.RESULTS: Totally 48 rabbits entered into result analysis, in which 6 rabbits from control group and 42 rabbits from study group. Modified Tarlov's motor function evaluation was 3 in 31 rabbits with compression signs, and 4 in 11rabbits without compression signs. The latency of N1 wave in cortical somatosensory evoked potentials (CSEP) was (9.11 ± 1.61 ), ( 11.36 ± 2.17)and (17.55 ± 3.73) ms respectively in animals of control group, animals of study group without compression signs and animals of study group with compression signs. The lantency of CSEP N1 wave was significantly longer in animals of study group with compression signs than that of the animals in the control group and study group without compression signs (P＜0.05).CONCLUSION: This animal model can simulate clinical invasion process of chronic compressive cervical myelopathy. The severer the spinal compression is, the more often the compression signs appear, the longer the lantency of CSEP N1 wave is, and the more serious the spinal pathological damages are.

Objective To investigate immunogenicity and protection efficacy of the recombinant hypoxanthine-guanine-xanthine (HGXPRT) of Plasmodium falciparum expressed in Pichia pastoris. Methods 35 BALB/c mice were divided randomly into five groups: HGXPRT+ISA720 experiment group, HGXPRT+Freund experiment group, ISA720 adjuvant control group, Freund adjuvant control group, and blank control group. BALB/c mice were subcutaneously immunized three times with the HGXPRT protein formulated by either Freund or ISA720 adjuvants at a three weeks interval. Mice were bled via tail vein at 2 weeks after each immunization. Specific antibodies were detected by ELISA as well as IFAT using cultured parasites. The immunized mice were challenged with 105 P.yoelii 10 days after the third immunization and parasitemia was monitored daily by examining Giemsa-stained thin film. Results Strong immune response was induced by the HGXPRT antigen formulated with the adjuvant. Antibody titers of more than 1∶105 were detected after the third immunization while no specific antibody was detected in the mice immunized with adjuvants only. The antibodies against HGXPRT recognized the cultured parasite by IFAT. Four days after mice were challenged with P.yoelii, high parasitemia appeared in the two control groups, which were 24 h earlier than experiment groups. The mean parasitemia of HGXPRT+ISA720 experiment group(29.3%) was significantly lower than that of control groups (70.0%) (P

BACKGROUND:Exogenous basic fibroblast growth factor (bFGF) plays an important role in the ligament tissue healing process, and the use of transgenic methods to transfect exogenous genes into cells can promote the secretion of bFGF. OBJECTIVE:To observe phenotypic changes and the bFGF protein expression after bFGF recombinant adenovirus was used to transfect rabbit bone marrow mesenchymal stem cells (BMSCs). METHODS:Passage 2 BMSCs were divided into three groups:Ad.bFGF-eGFP group, Ad.eGFP group and control group. Under a phase contrast microscope we observed the changes in cellmorphology. The expression of bFGF protein in BMSCs was determined by enzyme-linked immunosorbent assay (ELISA). The proliferative curve was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). RESULTS AND CONCLUSION:The transfected cells showed a uniform phenotype of fibroblasts. MTT colorimetric assay revealed that more proliferative activity of transfected BMSCs was shown in the Ad.bFGF-eGFP group than in the Ad.eGFP group and control group. ELISA results showed that expression of bFGF protein was higher in the Ad.bFGF-eGFP group than in the Ad.eGFP group and control group (P<0.05). BFGF recombinant adenovirus can induce the differentiation of BMSCs into fibroblasts, increase proliferative ability and promote the expression of bFGF protein.