Objective To investigate the cognitive behavioral characteristic longitudinally of the patients after subcortical infarction engaged in feature and binding working memory tasks.Methods The behavioral performances were recorded from 28 patients after subcortical infarction at the 1 st week (W1),3 rd moth (M3) and 6th month (M6) while performing color,location,and color-location binding delayed match-to-sample working memory task.25 healthy volunteers(controls) were investigated once using the same task protocol during the study period.Computer recorded the behavior reaction time and accuracy.Single factor variant analysis of repeated measurement was adopted.Results The accuracy of three memory tasks of M3 ((64.92 ± 5.47) ％ ; (92.88 ± 2.98) ％ ;(82.35 ±7.44)％) was improved than that of W1 ((61.06 ±7.78)％; (90.59 ±2.95)％; (77.06 ±5.58) ％) and the difference had statistically significant (P ＜ 0.05).But the reaction time of M3 ((868.31 ±118.91)ms; (833.37 ± 120.99) ms; (918.72 ± 101.28) ms) was shortened than that of W1 ((914.02 ±110.53) ms; (859.89 ± 139.94) ms; (1150.17 ± 92.02) ms) and the difference also had statistically significant (P ＜ 0.05).In the location-memory task,the correct rate of M6 ((93.91 ± 2.86) ％) was improved than that of M3 ((92.88 ± 2.98) ％) and the reaction time of M6 ((813.24 ± 119.54) ms) was shortened than M3 ((833.37 ±120.99) ms).M6 and M3 to be compared in the color memory task,the correct rate ((64.50 ± 4.49) ％ ; (64.92 ± 5.47) ％) and the reaction time ((866.47 ± 123.87) ms; (868.31 ± 118.91) ms) had no significant difference (P ＜ 0.05).But in the color-location binding task,the correct rate of M6 ((78.49 ± 7.85) ％) and M3 ((82.35 ± 7.44)％) to be compared had significant decreased nearly the level ((77.06 ± 5.58)％) of the stroke beginning.All behavioral performances of patients were worse than that of control subjects except the compare result of location-memory task in M6((93.91 ± 2.86) ％ ; (813.24 ± 119.54) ms).Conclusion Feature memory and binding memory had been damaged in different degrees in the patient after subcortical infarction.The binding memory had the secondary damage what might be related to the secondary nerve fiber degeneration after infarction.

Objective To study the probability of transferring the regulatory T cells induced by TGF-β1 to prolong the allograft survival and the mechanisms involved.Methods According to the different culture conditions.three experimental groups were established:control group(T cells from C57 BL/6 mice cultured with II-2),MLR group(T cells from C57BL/6 mice activated by alloantigen)and TGF-βgroup(T cells from C57BL/6 mice activated by alloantigen and cultured with 5.0 ng/ml TGF-β1).After the culture,the ratio of CI4+CD25+T and the Foxq3 expression were measured by FACS and RT-PCR,respectively.On 9th day,the pathologic analysis was performed and the ratios of TH1,TH2 and Treg and the proliferation of lymphocytes were measured.Results The ratio of CD4+CD25+T in TGF-β group was higher than that in control group and MLR group(P<0.05),and Foxp3 was expressed in CD4+CD25+T cell from TGF-βgroup.After transferring ofthe cells,the allografi survival time in TGF-β group was prolonged and its mean survival time(MST)was(22.8±1.9)d,which was longer than that in MLR group and control group (P0.05),lower than that of control group(P<0.05). And the ratio of CD4+CD25+T in TGF-β group was higher than that in control and MLR group obviously(P

AIM: Previous studies performed with XBP-01 in vitro indicated that XBP-01 could inhibit vascular smooth muscle cells from being transformed into foam cell and could eliminate the atherosclerotic plaque in C57 BL/6J mouse. This experiment is to investigate its mechanism of eliminating plaques in vitro. METHODS: The cultured porcine artery smooth muscle cells incubated with XBP-01 of 0.1 mg/L for 24 hours after preincubated with oxidized low density lipoprotein of 15 mg/L for 72 hours in vitro. The samples were analyzed by fluorescence microscope?confocal microscope system and flow cytometry. RESULTS: Apoptosis was triggered by being incubated with oxidized low density lipoprotein and this process was accelerated additionally by being incubated with XBP-01. CONCLUSION: XBP-01 can be effective in eliminating atherosclerotic plaque by accelerating the process in which oxidized low density lipoprotein induced smooth muscle cell apoptosis

AIM:To observe the effects of adipose differentiation-related protein ( adipophilin) on the expres-sion of inflammatory factors in RAW264.7 macrophage and to clarify the related mechanism.METHODS:The cell models with high expression and low expression of adipophilin were constructed by transfecting PA317 packaging cells with stable high or low expression adipophilin retroviral vectors into the RAW264.7 cells.The concentrations of IL-6, MCP-1 and TNF-αin the cell culture medium were detected by ELISA.The protein levels of AP-1, p-AP-1, ERK1/2 and p-ERK1/2 were measured by Western blot.The protein levels of adipophilin, p-ERK1/2 and p-AP-1 and the releases of the inflamma-tory factors in the RAW264.7 cells treated with or without ERK1/2 inhibitor PD98059 or AP-1 inhibitor curcumin were de-termined.RESULTS:The RAW264.7 cells with high expression of adipophilin had higher levels of IL-6, MCP-1 and TNF-α, and higher protein levels of p-AP-1 and p-ERK1/2 than those in the cells with low expression of adipophilin. ERK1/2 inhibitor had no significant effect on the expression of adipophilin, but the protein expression of ERK1/2 and AP-1 was significantly inhibited (P<0.05).The administration of AP-1 inhibitor curcumin had no significant effect on the protein expression of adipophilin and ERK1/2, but the protein expression of AP-1 was significantly inhibited (P<0.05). At the same time, the releases of inflammatory factors IL-6, MCP-1 and TNF-αwere significantly decreased.CONCLU-SION:Adipophilin may regulate the expression of inflammatory factors through ERK1/2-AP-1 pathway in RAW264.7 mac-rophages.

Objective To investigate the effects and mechanism of evodiamine on the proliferation and apoptosis of osteosarcoma MG-63 cells.Methods MG-63 cells were cultured with evodiamine for 24 hours,and the cell proliferation was evaluated by methyl thiazolyl tetrazolium (MTT) assay.Cell cycle arrest,apoptosis and intracellular Ca2+ accumulation were evaluated by flow cytometry.BALB/C mice model of osteosarcoma was established to investigate the tumor inhibitory effect of evodiamine on human osteosarcoma.Wnt/β-catenin signaling protein expressions in osteosarcoma cells were detected by Western blotting.Results As concentration of evodiamine increasing (0.25 μmol/L,0.5 μmol/L,1.0 μmol/L,2.0 μmol/L and 4.0 μmol/L),the inhibition rate of MG-63 ceils increased [(4.18 ± 1.26)％,(15.49 ± 2.26)％,(40.55 ± 6.57)％,(49.87 ±7.69)％ and (60.42 ±8.29)％].The difference was statistically significant between 2.0 μmol/L group and the control group (t =-2.66,P ＜ 0.05).MG-63 cells were cultured with 2.0 μmol/L evodiamine for 24 hours,and the apoptotic rate was (64.67 ± 8.63) ％,the proportion of S phase cells was (85.33 ± 9.31)％,the fluorescence of Ca2+ was 97.33 ± 21.31.The corresponding data of the control group were (4.94 ± 0.81) ％,(43.67 ± 8.92) ％ and 28.67 ± 8.92,the differences were statistically significant (t =-11.90,P ＜ 0.05;t =-7.22,P ＜ 0.05;t =-6.65,P ＜ 0.05).On mice model,the tumor weight of evodiamine group and the control group was (2.15 ±0.35)g and (4.29 ±0.49)g respectively,the difference was statistically significant (t =7.95,P ＜ 0.05).Comparing with the control group (1.00 ± 0.00),evodiamine decreased the expression of β-catenin protein (0.72 ± 0.36) and increased the expressions of Bax (1.15± 0.27) and Caspase-3 (1.46 ± 0.18) protein,and the differences were statistically significant (t =-3.05,P ＜ 0.05;t =-6.42,P ＜ 0.05;t =-5.85,P ＜ 0.05).Conclusion Evodiamine inhibits proliferation and induces apoptosis of human osteosarcoma MG-63 cells by blocking Wnt/β-catenin signaling.

Magnesium stents have gained increasing interest as an ideal stent of future intervention. In order to study the deformation behavior of magnesium alloy stents in the interventional treatment, the finite element method was used to analysis the effects of different crimp and expansion dimensions on the mechanical properties (maximum stress, radial recoil rate, longitudinal shortening rate and radial strength). The results showed that crimping and expanding have a minimal influence on the stent radial strength. When the expansion size is same, the maximum equivalent stress and recoil rate decrease with the crimp size. When the crimp size is same, in contrast with the radial recoil rate, the maximum equivalent stress and longitudinal shortening rate increase with the expansion size. In addition the paper verified the radial strength-radial displacement curve obtained by FEM. Results are basically consistent, indicating the finite element method can efficiently provide researchers with reliable, high-quality design.
Alloys ; Finite Element Analysis ; Magnesium ; Stents

AIM: Based on the finding of adipophilin expression with the increase in cellular cholesterol, the aim of the present study was to look for the active site of adipophilin in cellular cholesteryl metabolism. METHODS: Mouse peritoneal macrophages were incubated with 80 mg/L Ox-LDL (Ox-LDL group) or 80 mg/L Ox-LDL plus 1 mmol/L adipophilin antisense oligonucleotides (Ox-LDL+antisense group), respectively. At the various time points, the incubated cell samples were observed with adipophilin immunofluorescence staining, flow cytometric analysis and cellular cholesterol analysis. RESULTS: The Ox-LDL+antisense group cells contained significantly lower cholesteryl ester (19.9?1.9) mg/g (protein) than that of cells in Ox-LDL group (46.6?3.4) mg/g (protein) at 4 days. From 12 h, expression of adipophilin in Ox-LDL group increased more quickly than that of the cells in Ox-LDL+antisense group. At day 4, the level of adipophilin expression in Ox-LDL group was significantly higher than that in Ox-LDL+antisense group. During the observation, the amount of Ox-r[CL-3H] LDL taking up increased gradually in both groups, however, from day 1 the taking up amount in Ox-LDL+antisense group was less than that in Ox-LDL group. There was a statistical difference between the two groups from day 2 to day 4. From 6 h to day 2, the relative ACAT activity increased in both groups. The relative ACAT activity kept unchanged from day 2 to day 4 in the two groups. At day 2, the relative ACAT activity in Ox-LDL+antisense group was significantly lower than that in Ox-LDL group. Correlative analysis between activity of ACAT and adipophilin expression showed than R2 were 0.6176 and 0.8212 (P

AIM: To investigate the relationship betw een ADRP and the development of atherosclerosis. METHODS: Antisense oligodeoxynucleotide of mouse ADRP was constr ucted. The mouse peritoneum macrophages were cultured with Ox-LDL or Ox-LDL plus the antisense fragment. The cellular cholesterol was measured and the expressio n of ADRP was observed with RT-PCR and western blotting. New Zealand white rabbi ts were fed with high cholesterol chow for 12 weeks. The levels of serum lipid a nd cholesterol content of aortic wall were investigated. The areas of fatty stre ak of the aortas was measured after staining with Sudan Ⅳ. The aortic, and live r specimens with HE and immunohistochemistry staining were observed under light microscopes. RESULTS: Antisense oligodeoxynucleotides of mouse ADRP decreased cellular cholesterol ester, induced cellular lipid droplets and the expression of ADRP. The expression of ADRP was induced by high-cholesterol-diet feeding in rabbit atherosclerotic lesions. The fatty streak of the aorta with immunohistoch emistry staining was strongly positive for ADRP in animals fed with high cholest erol chow, and the liver was negative with or without high cholesterol chow. CONCLUSIONS: The expression of ADRP in vessel walls is related t o the atherosclerosis, and has a potential role in lipid accumulation in macroph ages and pathogenesis of atherosclerosis.

To observe the effects of diabetogenic (high fat high sucrose, lacking choleserol) diet on atherogenesis in New Zealand white rabbits. Two groups of New Zealand white rabbits received regular rabbit chow (the normal control), or high fat high sucrose diet for 4 months. The levels of plasma total cholesterol, HDL cholesterol, triglycerides, insulin, and glucose were investigated, the areas of fatty streak of the aortae were measured after staining with Sodan IV, and the aortic, coronary specimens were observed with light and electron microscopies. The plasma glucose, triglycerides, and total cholesterol were increased significantly by high fat high sucrose feeding. At the end of 4 months, the early charateristics of atherosclerosis were present in the animals' vascular specimens. Our findings suggest that high fat high sucrose feeding can induce hyperglycemia, hypertriglyceridemia and atherosclerosis in New Zealand white rabbits, and this could be a potential animal model for studying the mechanisms of diabetes-accelerated atherosclerosis. This study raised a question: What is the mechanism by which high fat high sucrose feeding induces atherosclerosis?. The related hypothesis was given in this article.

Objective To prepare recombinant adenovirus pAd-gal-9 containing murine galectin-9 and explore galectin-9's pro-apoptotic effect on T lymphocytes. Methods The recombinant adenovirus plas-mid pAd/CMV/V5-DEST-gal-9 was prepared by conventional molecular cloning and LR reaction. The pAd/ CMV/V5-DEST-gal-9 linearlized by Pac I was transfected into 293A cells with Lipofectin 2000. Eight days after transfection, the 293A cells were subjected to freeze/thraw circle for three times and the supernatant was collected after centrifugation. Higer titer pAd-gal-9 was produced by large-scale infection of 293A cells with the supernatant containing pAd-gal-9. The supernatant was condensed to get purified pAd-gal-9 by CsCl density gradient centrifugation. After titer determination with gradient dilution of harvested pAd-gal-9 infec-tion in 293A-seeded 96-wells, pAd-gal-9 was used to infect the CHO cell line. Immunohistological assay, Western blot and flow cytometry were employed to ascertain the subcellular location expression of galectin-9. We added solid-phase transgenic CHO cells or freshly-cultured supernatant to medium containing activated T cells to detect the pro-apoptotic effect of galectin-9. Results The pAd-gal-9 was prepared successful. Im-munohistochemical staining of CHO infected with pAd-gal-9 confirmed that galectin-9 was expressed in the cytosol. Intercellular staining indicated that mean fluorescence intensity of galectin-9 was significantly higher in pAd-gal-9-infected CHO group than control group. Supernatant from pAd-gal-9-infected CHO promoted the apoptosis of T cells. The percent of apoptotic T cells was higher than the Tim-3 positive T cells. Conclu-sion CHO infected with pAd-gal-9 can secret galectin-9 to promote the apoptosis of activated T cells via Tim-3-independent mechanisms.