Aim: To study the synthesis and anti-platelet aggregation activities of ferulic acidic esters so as to search for novel antithrombus agents. Methods: Based on prodrug strategy and combination principles, monoesters were first synthesized by reaction of ferulic acid with alcohols, and then the monoesters were coupled with aspirin to afford bis-esters. The target compounds were assayed for anti-platelet aggregation activities in vitro. Results: Sixteen target compounds and eight sideproducts including 15 new compounds were synthesized and their struc-tures were determined by IR, MS and ~1H NMR. The results demonstrated that some tested compounds exhibited potential anti-platelet aggregation activities. Conclusion: The bis-esters of ferulic esters coupling with aspirin with 4 to 5 carbons in side chain might be used as lead compounds for further study in searching for novel antithrom-bus agents.

Objective: To establish an anti-tumor drug sensitivity test by micocapsulated tumor cells in vivo and in vitro.Methods: Alginate-polylysine-alginate(APA) microcapsule technique was used to encapsulate tongue cancer Tca8113 cells. MTT method was used to detect the cytotoxic effect of methotrexate(MTX)and fluorouracil (FU) on encapsulated cells, then IC 50 was calculated. Encapsulated cells were also seeded into the abdominal cavities of adult Kunming mice and FU was injected through tail vein. After two weeks, microcapsules were recollected and histological examination was performed . Results: Encapsulated tumor cells derived from tongue could survive and proliferate in clusters. MTX and FU inhibited the cell growth in a dose-dependant way. IC 50 of MTX and FU was 200 ?mol/L and 0.85 mg/ml respectively. Necrosis of the cells in microcapsules and fibrotic encapsulation of microcapsules were observed in the in vivo tests. There was no significant difference between treatment group and control group. Conclusion: Microcapsulted tumor cells may be used in the anti-tumor drugs sensitive experiment in vitro.

Objective To assess the feasibility of interventional techniques in the establishment of animal model of superior mesenteric vein-portal vein (SMV-PV) thrombosis. Methods Nine miniature pigs were involved in the study including one for preliminary experiment. After general anesthesia, a balloon catheter was placed in the main trunk of PV to block the portal flow and then thrombin or autologous blood clot was injected to the SMV. Venography was performed to confirm the thrombosis 30 minutes later. Changes in the imaging before and after the thrombosis were observed. Pigs died during the experiment were anatomized to analyze the causes, and pathological examination was performed when necessary. Results The model of SMV-PV thrombosis was successfully established in all the pigs. One pig died of diffuse intravascular coagulation 10 minutes after model establishment in the preliminary experiment. Two pigs died of hepatorrhexis and over dose of anesthetics respec-tively 3 hours after model establishment, and the rest 6 pigs were fed for 14 days. Conclusion Interventional techniques are effective in the establishment of SMV-PV thrombosis model.

AIM: To observe the change of insulin receptor in rabbit kidney with acute ischemic-reperfusion injury. METHODS: 15 Japanese white rabbits were allocated randomly into control group, ischemic-reperfusion group(IR group). IR group received clamping for 1 h followed by 2 h or 48 h of reperfusion. At 2 h or 48 h after reperfusion, glucose and insulin in serum were determined. Insulin receptor in renal tissue was analyzed by radioligand binging assay(BAD). RESULTS: The level of serum glucose increased after 2 h reperfusion in 2 groups, but in IR group the value increased much more higher than those in control groups(P

Objective To investigate the protective effect and mechanism of Astragaloside Ⅳ (AS-Ⅳ) on hypoxia/re-oxygenation induced by RAW264.7 murine macrophages.Methods The hypoxia/re- oxygenation induced RAW264.7 murine macrophages served as a model of I/R injury. The cells were divided into the control group, the model group, and the AS-Ⅳ group. The cell morphological changes of each group were observed directly under inverted microscope. Inducible nitric oxide synthase (iNOS), cluster of differentiation 206 (CD206), and peroxisome proliferator activated receptor-γ (PPAR-γ) were separately examined by RT-PCR, Western blot analysis and immunofluorescence staining.Results Compared with the model group, the numbers of cell in AS-Ⅳ group significantly increased , and the cell physiological status were much better. Compared with the model group, the iNOS immunofluorescence semi quantitative (0.62 ± 0.02 vs. 1.32 ± 0.09), the expression of mRNA (1.51 ± 0.07 vs. 3.46 ± 0.39), and protein (2.30 ± 0.14 vs. 5.16 ± 0.49) significantly reduced in AS-Ⅳ group (P<0.01). The CD206 immunofluorescence semi quantitative (1.01 ± 0.03 vs.0.61 ± 0.01), the expression of mRNA (0.91 ± 0.03 vs.0.51 ± 0.01), and protein (0.61 ± 0.04 vs.0.19 ± 0.01) significantly reduced in AS-Ⅳ group (P<0.01). Compared with the model group, the PPAR-γ immunofluorescence semi quantitative (0.60 ± 0.14 vs. 0.34 ± 0.03), mRNA (2.00 ± 0.14 vs.1.04 ± 0.03), andprotein (0.67 ± 0.05 vs.0.19 ± 0.01) significantly increased (P<0.01). Conclusions The AS-Ⅳ could attenuate ischemia-reperfusion injury by altering macrophages phenotype through upregulation PPAR-γ.

Objective:To study the function of transcription factor 4 (TCF4) and to prepare TCF4 polyclonal antibody.Methods:pET-41/TCF4 was transformed into E.coli BL21(DE3) and induced by IPTG.The purified GST-TCF4 fusion protein was applied to immunize rabbit to produce antiserum. The specificity of the affinity of purified anti-TCF4 antibody was examined by Western blotting analysis of the eukaryotic expressed products of TCF4. Dig-labeled probe and antibody against TCF4 were used to examine the expression of TCF4 in Saos-2 cells under mechanical stretch. Results:Western blotting showed that the antibody could bind to TCF4 specifically. The expression of TCF4 mRNA and protein were significantly increased in Saos-2 cells under mechanical stretch. Conclusion: TCF4 antibody has been prepared successfully.

Objective To investigate the expression of NF-κBp65 in hippocampus after the XST intervention therapy in the SD rats with global cerebral I/R injury and testify the protective effect of XST after global cerebral I/R injury.Methods 72 healthy SD rats were randomly divided into 3 groups,sham operation(SO) group ( n =24),I/R group( n =24) and XST group( n =24).The model of acute global cerebral ischemia/reperfusion (including:I/R and XST group) injury was produced by means of simple Pulsinelli- brierley's four arteries occlusion method.H.E.staining was performed to detect the number of surviving neurons and TUNEL was used to detect the rate of neurons apoptosis.The expression activation of NF-κB p65 in hippocampus comu-ammonis ( CA1 ) region were examined by immunohistochemical method (SABC).Results The survival pyramidal neurons in the XST group continued to increase,and it was significantly more than the I/R group at each time-point after reperfusion[ (99.23 ±4.22)/mm vs (75.83 ±7.17 )/mm,(80.93 ± 5.36)/mm vs (51.50 ± 8.26 )/mm,(103.24 ± 5.48 )/mm vs (35.67 ± 13.17 )/mm,( 126.22 ± 7.54 )/mm vs (9.83 ± 4.71 )/mm ],the differences were statistically significant ( P ＜0.01 ).The apoptosis rate of pyramidal cell in the XST group at each time-point were more significantly reduced than the I/R group [ ( 8.82 ± 2.71 ) ％ vs ( 22.58 ± 4.68 ) ％.( 19.15 ± 6.23 ) ％ vs (42.68 ± 3.04 ) ％,( 11.82 ± 2.87 ) ％ vs ( 55.51 ± 6.81 ) ％,( 8.44 ± 3.23 ) ％ vs ( 71.69 ± 7.71 ) ％ ],the differences were statistically significant ( P ＜0.01 ).The positive neurons of NF-κBp65 expression in the XST group at different time-points were significantly less than the L/R group[ ( 13.20 ±2.50) vs ( 18.00 ± 1.87),(8.20 ±5.31) vs (41.60±3.65),(6.70±3.36) vs (55.30±5.10),(7.10±3.57) vs (72.80 ±4.71)],the differences were statistically significant ( P ＜ 0.05,P ＜ 0.01 ).Conclusions After global cerebral ischemia/reperfusion,XST could protect the brain from global cerebral ischemia/reperfusion injury by holding up the expression of NF- kappaB p65,and inhibiting neuronal apoptosis,and increasing the number of surviving neurons.Thus,the results of this experiment could provide a powerful and weighty objective indication for XST being used during cerebral resuscitation.

Objective To study the main clinical characters of recurrent sarcoidosis.Methods Sarcoidosis recurrence were defined as presenting activity through imaging or histology after having self-relief or treated relief.There were 12 patients who consistent to the standard in all sarcoidosis patients from 2004 to 2008 in our hospital.Results All patients but one were male.The time of recurrent to the remission was from 4 to 38 months.10 patients received oral steroid therapy.Recurrences often occurred in drug reducing or 6 months after drug withdrawal.There were 2 patients with recurrence time greater than 3 years after remission.Three patients presented new organ damages in recurrence.Conclusions The recurrence of sarcoidosis mostly occurred in the course of drug reduction or in the early stage of drug withdrawal and the recurrence time were hardly over 3 years after remission.The sarcoidosis patients must receive long time follow-up and the program of oral steroid therapy must be standardized.

Objective To determine the role and mechanism of peroxisome proliferator activated receptors (PPAR) α in a mouse model of D-galactosamine/lipopolysaccharide (D-GalN/LPS)-induced acute liver failure(ALF).Methods Firstly,C57BL/6 mice were randomly divided into control group(n =8),ALF 2h group(n =8),ALF 4h group (n =8),ALF 6h group (n =8).Secondly C57BL/6 mice were randomly divided into control group(n =8),ALF group(n =8),WY14643 group(n =8).To induce ALF,the mice were injected intraperitoneally with D-GalN (700 mg/kg) and LPS (10 μg/kg).WY14643 (6 mg/kg),the selective agonist of PPAR α,was administered via tail vein two hours prior to D-GalN/LPS exposure.Two,four,and six hours after D-GalN/LPS treatment in the first study,mice were anesthetized and blood was collected,6h after D-GalN/LPS treatment in the second study,blood was collected.The liver tissue was harvested for histology and mRNA extraction.Serum levels of ALT and AST were measured to evaluate the hepatic damage.Inflammatory cytokines (TNFα,IL-1β,IL-6) and chemokines (CXCL-1,CXCL-10) were detected by real-time quantitative PCR.Differential protein expression of p-NF-κBp65,p-JNK,p-ERK,p-p38 in inflammatory pathways was detected by Western blotting.Significance of inter-group differences was assessed by one-way ANOVA,and pairwise comparison was performed by the least significant difference test.Results The gene and protein expression of PPAR α were gradually reduced during the development of ALF.Compared with the model group,the liver architecture was better preserved almost with normal morphology in WY14643-treated mice.Serum ALT and AST levels in WY14643-treated group were significantly lower [ALT:(555 ±62)U/L vs (2 898 ±822) U/L,P ＜0.05; AST:(791 ±58) U/L vs (3 013 ±997)U/L,P ＜ 0.05].The expression of proinflammatory cytokines and chemokines was significantly suppressed during the activation of PPAR α.In the second study,the levels of gene expression of proinflammatory cytokines and chemokines were detected in control group,ALF group and WY14643 group respectively as followings:TNFα (0.161 ± 0.085,7.996 ± 1.068,3.346 ± 0.94,P ＜ 0.05),IL-1β(0.041 ±0.002,3.657 ±0.904,0.176±0.089,P＜0.01),IL-6 (0.018 ±0.008,1.762 ±0.589,0.163±0.0487,P ＜0.05),CXCL-1 (0.063 ±0.008,7.881 ±0.966,2.737 ±0.864,P ＜0.01),CXCL-10 (0.054 ±0.005,5.671 ±0.948,2.578 ±0.804,P ＜0.05).Conclusion Our findings first demonstrate that PPARα protects liver from injury in an ALF mouse model by suppressing inflammatory response,indicating PPARα as a potential new therapeutic target for ALF.

Clinical death of patients often results in such strong psychological stress as anxiety,fear and depression among the family members.Behavior problems incurred by such negative feelings often lead medical disputes.Early psychological intervention upon death to the families can not only protect their mental health but also effectively prevent medical disputes from happening.An analysis of the psychological response and characteristics of such families presents the principles and practice for psychological counseling.Discussions in this regard may inspire hospital administrators in how to prevent medical disputes so incurred.