Obesity is caused by the imbalance between caloric intake and energy expenditure. It is also influenced by genetic factors. Many genes,such as ob gene, ? 3 receptor gene, ucp 1 gene, may involved in the prevalence of obesity. Pharmacologic treatments include anorexigenic agents, lipase inhibitor, ? 3 receptor agonists and many newer antiobesity drugs, which provide prospective ways in treating obesity.

Objective: To study the antitumor effect of Lycium barbarum polysaccharide (LBP X) and its immunity regulating effect on S 180 bearing mice. Methods: S 180 bearing mice were used as animal model. The effect of LBP X on tumor weight and immune function was observed. Results: LBP X could inhibit the growth of S 180 effectively and increase thymus index, the macrophage phagocytic function, anti SRBC antibody secreted by the spleen cells, lymphocyte proliferation and CTL activity and decrease LPO markedly in S 180 bearing mice. Conclusion: The mechanism of tumor inhibition by LBP X was due to enhance the immune function.

AIM: To examine whether lipoxin A_4 (LXA_4) induces apoptosis of rat renal interstitial fibroblasts and explore the mechanisms. METHODS: Rat renal interstitial fibroblasts (NRK-49F cells) were incubated in RPMI-1640 medium supplemented with 5% fetal calf serum and exposed to LXA_4 at the concentration of 10 nmol/L, 100 nmol/L or 1 ?mol/L for 24 hours. Prior to experiment, some cells were transfected with calpain 10 antisense oligodeoxynucleotide. Apoptosis of cells was recognized by double staining using fluorescent dye acridine orange and ethidium bromide, observed under laser scanning confocal microscopy and counted by flow cytometry following propidium iodide and annexin staining. Activity of caspase-3 was measured by colorimetric assay. The expression of calpain 10 mRNA was determined by RT-PCR. RESULTS: LXA_4 at the concentration of 100 nmol/L or 1 ?mol/L induced 9.83% or 33.82% apoptosis of cells, respectively. Treatment of cells with LXA_4 up-regulated the expression of calpain 10 mRNA and increased the activity of caspase-3. The transfection of the cells with calpain 10 antisense oligodeoxynucleotide inhibited the LXA_4-induced apoptosis, activity of caspase-3 and expression of calpain 10. CONCLUSION: LXA_4 at high concentration induceds apoptosis in rat renal interstitial fibroblasts via up-regulating of calpain 10 mRNA expression.

Objective To evaluate the effects of immobilization of flexor tendon with elastic rubber band after the repair in 58 cases with flexor tendon completely severed in Zone Ⅱ . Methods The severed flexor tendon was repaired with the modified Kessler method. The rubber band was linked to the end of the nail with silk thread. The forearm and hand joint were immobilized by dorsal plaster cast.The rubber band was fixed with short tube plaster at the lower part of forearm so as to keep the interphalangeal joints in flexion. 48 hours post operation, exercises were done to extend fingers initiatively and flex fingers passively with the help of the elastic rubber band. The practice lasted for 3 weeks. Results The patients were followed up for three to six months.The digital functions of flexion and extension were normal. Conclusion Using elastic rubber band to immobilize flexor tendon post operation proves to have a remarkable effect on the functional recovery.

Hypoglycemic effects of Yifusheng on hyperglycemia animals induced by alloxan or adrenaline were studied.The result showed that Yifusheng in the dosage of 0.25 g/kg and 0.125 g/kg could significantly decrease the content of plasma blood sugar(P

AIM: To find whether lipoxin A_4 (LXA_4) inhibits cell proliferation induced by TNF-? in rat mesangial cells, and to explore the molecular mechanisms of signal pathways of LXA_4 actions. METHODS: Cultured rat mesangial cells were growth-arrested and exposed to TNF-? with or without preincubation with LXA_4. Proliferation of mesangial cells was measured by MTT methods. Activities of STAT_3 were analyzed by electrophoretic mobility shift assay. Expression of cyclin E mRNA was assessed by RT-PCR. Cyclin E proteins were determined by Western blotting analysis. RESULTS: TNF-?-induced proliferation and increased mRNA and protein expression of cyclin E in mesangial cells were inhibited by LXA_4 in a dose-dependant manner. TNF-?-stimulation of the STAT_3-binding activities in mesangial cells was down-regulated by lipoxin A_4. CONCLUSION: Inhibitory effect of LXA_4 on TNF-?-induced mesangial cell proliferation is mediated by Jak_1/STAT_3 signal pathway.

Objective To study the apoptosis of multiple myeloma cell line KM-3 induced by NK cells. Methods WST-1 assay was used to detect the killing effect of KM-3 cells treated with NK cells at different effector(E):target(T) ratio. Flow cytometry was applied to analyze Annexin-V+/PI- apoptotic cells and the mitochondrial transmembrane potential. Results NK cells could significantly kill KM-3 cells in a dosand time-dependent manner (P <0.05). After KM-3 cells- were treated with NK cells for 48 hours, the Annexin-V+/PI- cells were increased obviously in dose-dependence (P <0.05). The Annexin-V+PI- cells were increased in time-dependence when treated with NK cells(E:T ratio at 10:1) (P<0.05). The mitochondrial transmembrane potential of KM-3 cells treated with NK cells were significantly decreased in dose-and time-dependence (P < 0.05). Conclusion NK cell can kill KM-3 cells and induce apoptosis in a dose-and time-dependence manner.

Purpose　The aim is to modify the pyrogenic pathol ogy mo del induced by injection of saccharomycetet water in rats,and to eliminate the t emperature decline period after injection of saccharomycete water sc.Metho ds　It was measured that the anus temperature of both two groups of rats (one group was injected of incubated saccharomycete water and the other inj ected unincubated saccharomycete water sc) 1,2,3,4,6,8 h after injection respect ively.Results　The anus temperature had no decline period and the temperature rose quickly in the group of injected with incubated saccharomyc ete water (in 34℃thermostasis water).There was significant difference(P＜0.05 or P＜0.01)between incubated group and unincubated group in temperature risin g by t-test.Conclusion　No temperature declining peri od was observed in the pyrogenic pathology model of rat, if those rats were trea ted with saccharomycete water which was incubated at 34℃for 0.5 h.

Objective: To explore the effect of LBP X on apoptosis of human leukemia HL 60 cells. Methods: The inhibitory effect of LBP X on growth of HL 60 cells was assayed by MTT method. The membrance fludity was determined with DPH fluorigenic labeling technique. HL 60 cells were stained with Hoechst 33 258 for nuclear morphology analysis. Agarose gel electrophoresis and flow cytometry were used to analyze apoptosis qualitatively and quantitatively. Results: 20-1 000mg/L LBP X inhibited the growth of HL 60 cells in dose dependent manner and the membrance fludity decreased. The nuclei of HL 60 cells treated with LBP X for 48 h shrinked, condensed and cleaved. Agarose gel electrophoresis of DNA from cells treated with LBP X revealed "DNA ladder". HL 60 cells exposed to LBP X showed apoptotic peaks. Conclusion: LBP X can induce apoptosis in human leukemia HL 60 cells.

Objective To examine whether lipoxin A4(LXA4) induces apoptosis of rat renal interstitial fibroblasts and explore the mechanism concerned.Methods Rat renal interstitial fibroblasts (NRK 49F cells)were incubated in RPMI 1640 medium supplemented with 5%fetal calf serum and exposed to LXA4 at the concentration of 10 nmol/L, 100 nmol/L or 1 ?mol/L for 24 hours. Prior to experiment,some NRK 49F cells were transfected with Smac antisense oligodeoxynucleotide. Apoptosis of NRK 49F cells was recognized by double staining using fluorescent dye acridine orange and ethidium bromide,and observed under laser scanning confocal microscopy and counted by flow cytometry following propidium iodide and annexin staining. Activity of caspase 3 was measured by colorimetric assay. The expression of Smac was determined by Western blotting analysis.Results LXA4 at the concentration of 100 nmol/L or 1 ?mol/L induced apoptosis of 9 83%or 33 82%of NRK 49F cells respectively, and reduced the cells of S and G2～M phase and increased the cells of G0～G1 phase in a dose dependent manner. Treatment of NRK 49F cells with LXA4 up regulated the expression of Smac protein and increased the activity of caspase 3. The transfection with Smac antisense oligodeoxynucleotide inhibited the LXA4 induced apoptosis and expression of Smac in NRK 49F cells. Conclusion LXA4 at high concentration can induce apoptosis of rat renal interstitial fibroblasts via the up regulation of Smac expression.