Objective To determine the incidence of thrombogenic events during the prostate operation period in patients discontinuing aspirin.Methods Among a retrospective cohort of 342 patients admitted in our institution for benign prostatic hyperplasia (or prostate cancer),combined with acute coronary syndrome (or stroke),we studied 4 patients who had not been taking aspirin before thrombogenic vascular event.Data on age,sex,vascular disease risk factors,and clinical outcome were collected.Results The 4 patients' mean age was 78.8±5.9 years.Each patient had at least two following risk factors:atrial fibrillation,old cerebral infarction and type 2 diabetes.80％ patients had a clinical history of hypertension.2 of the 4 patients stopped aspirin before a surgical procedure and developed acute ischemic stroke and acute myocardial infarction,separately.The other two patients developed acute ischemic stroke without aspirin prescription.The median time between admission and thrombogenic events was 15.5± 10.5 days.All patients were not given finasteride on admission.Conclusions This study should alert clinicians to know the risk of aspirin withdrawl perioperatively in patients at high risk of cardiovascular and cerebrovascular diseases.

Adult ; Calcinosis ; Heart Aneurysm ; pathology ; Heart Ventricles ; Humans ; Male ; Thrombosis ; pathology

The pharmacological mechaisms of Panax notoginseng saponins on nervous system diseases (Alzheimer's disease, Parkinson's disease, ischermic cerebral apoplexy and depressive disorder) , including panax notoginseng saponins, protoparaxotriol saponins, panasadiol saponins, ginsenoside Rg1, ginsenoside Rb1, ginsenoside Re and notoginsenoside R1 were summarized to analyze the study hotspots and potential advantages (such as estrogen-like effect) of notoginsenoside's pharmacological actions, provide reference for further pharmacological studies and new ideas for clinical treatment of nervous system diseases and drug studies and development.
Animals ; Drugs, Chinese Herbal ; administration & dosage ; Gene Expression ; drug effects ; Humans ; Nervous System Diseases ; drug therapy ; genetics ; metabolism ; Panax notoginseng ; chemistry ; Saponins ; administration & dosage

Objective To observe the apoptosis of Th1 and Th2 cells in C57BL/6 mice chronically infected with Schistosoma japonicum.Methods The apoptotic Th1 and Th2 cells in spleen and lymph node from C57BL/6 mice infected with Schistosoma japonicum for 13 weeks were examined by three-color and indirect flow cytometery with staining surface molecule and intracellular cytokines.Results Compared with the normal mice,the proportion of apoptotic Th1 and Th2 cells of 13-week post-infection was significantly high,and the apoptotic Th1 cells increased more than apoptotic Th2 cells in the infected C57BL/6 mice,and the Th1 cells were more susceptible to apoptosis than Th2 cells.Conclusions Unequal susceptibility to apoptosis in Th1 and Th2 cells may be one of the reasons leading to Th2 polarization on mice chronically infected with Schistosoma japonicum,which provides the new proof of Th polarization.

Objective To evaluate the effects of two different dosage of rosuvastatin on endothelial dysfunction in diabetic rats. Methods The 24 diabetic rats were randomly divided into three groups (n=8,each): diabetic control group, 20 mg rosuvastatin daily (RV 20 mg group) and 10mg rosuvastatin daily for 8 weeks (RV 10 mg group) and normal control group (SD group). The levels of blood glucose, lipid, nitric oxide(NO) and endothelin-1 (ET-1) were measured before and 8 weeks after treatment. Results The levels of blood glucose were higher in all diabetic rats groups than in SD group before experiment (P＜0. 01). Compared with diabetic rats control group, blood glucose was slightly lower in RV 10 mg group and RV 20 mg group at 8 weeks (P＞0. 05). The plasma NO level was significantly lower in diabetic rats control group than in SD group (P＜0. 05).After 8 weeks, plasma NO levels were significantly higher in RV 20 mg and RV 10 mg groups than in diabetic rats control group (P＜0. 01 or P＜0. 05). The plasma levels of ET-1 was significantly higher in diabetic rats control group than in SD group (P＜0. 01). After 8 weeks, plasma ET-1 levels were significantly lower in RV 20 mg and RV 10 mg group than in diabetic rats control group (P＜0. 01).Meanwhile, the plasma lipids were lower in RV 20 mg and RV 10 mg group than in diabetic control group (P＜0. 05 or P＜0. 01). Conclusions Rosuvastatin can adjust blood lipids and significantly improve endothelial function in diabetic rats by increasing plasma NO level and decreasing plasma ET-1 level.

Objective To investigate the effect of gradient heat stress on phagocytosis of hepatic Kupffer cells (KCs) in vitro in rats. Methods Rat Kupffer cells were isolated in vitro and the temperature for gradient heat stress was set at 37, 39, 41 and 43℃. After thermal stimulation, cell injury was detected by PI and Hochest33342 staining. CCK-8 assay was used to investigate difference in cellular proliferation rate over 24h between the groups. Flow cytometry was used to investigate the influence of heat stress on the phagocytosis of KCs. Results Compared to the normal control group, cells in each heat stress group exhibited varying degrees of damage, especially cells in 43℃ group. The ratio of damage cells increased with the increase of heat stress severity (P<0.05). Proliferation assay indicated that the proliferation rate of cells in each heat stress group was significantly decreased in comparison with normal control group 6h after heat stress (P<0.05). After 12h recovery, decrease in proliferation rate was observed only in 43℃ group (P<0.001), and no difference in the rate of proliferation could be observed between the heat stress groups and normal control group after 24h recovery. Flow cytometry showed, that the phagocytosis of KCs decreased in heat stress groups compared with control group, especially in 43℃ group (P<0.05). This phenomenon disappeared after 24h recovery. Conclusion Heat stress can inhibit the phagocytosis of rat liver KCs through its cytotoxic effect on KCs, and subsequently inhibits its proliferative ability. Further investigation of the effect of heat stress on KCs may help understand the pathogenesis of heat stress.

Bioimprinting is a new developed technique to improve the characteristics of enzymes.Bioimprinting by lauric acid was conducted to improve the esterification activity of lipase PS in sol-gel immobilization process with methyltrimethoxysila(MTMS) and tetramethoxysila(TMOS) as the precursors.Results generated by checking the esterification activity and scanning electron microscope showed that bioimprinting can enhance the specific activity and thermal stability of lipase PS.The bioimprinting system was optimized by orthogonal experiment,and the optimal condition for lipase bioimprinting is water/silane molar ration(R) 12,polyethylene glycol(PEG) 120?l,and lauric acid 0.15 mmol.Compared with the free enzyme and the non-imprinted enzymes,the specific activity of imprinted enzymes has been improved 44.3 fold and 2.4 fold,respectively.Imprinted lipase show better thermal stability,and the relative activity is 58% after incubated in 80 ℃ for 0.5 h,while no activity was detected for the free enzyme.

Objective To investigation the expressions of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and its receptors in non-small cell lung cancer (NSCLC) and their clinical significances.Methods The serum expression levels of TRAIL in 79 cases of NSCLC and 80 cases of normal subjects were detected by enzyme-linked immunosorbent assay (ELISA).The expressions of TRAIL-R2 and TRAIL-R4 in 42 cases of NSCLC and matched normal tissues were detected by immunohistochemistry.The relationships among TRAIL,TRAIL-R2,TRAIL-R4 and clinicopathologic features of NSCLC were analyzed.Results The expression of TRAIL in NSCLC patients was lower than that in normal human [(994.3 ±293.0)ng/ml vs.(1 141.7 ±266.1)ng/ml,t =3.29,P =0.00].The expression of TRAIL was closely correlated with clinical stage (F =2.28,P =0.00) and differentiated degree (t =5.76,P =0.00).The positive expression rate of TRAIL-R2 in NSCLC was 73.8％ (31/42),significantly lower than that in the normal tissue 100.0％ (42/42) (x2 =3.88,P =0.05).The expression of TRAIL-R2 was closely correlated with clinical stage (x2 =27.89,P=0.00) and differentiated degree (x:=9.50,P =0.00).The positive expression rate of TRAIL-R4 in NSCLC was 81.0％ (34/42),significantly higher than that in the normal tissue 50.0％ (21/42) (x2 =7.34,P =0.01).The expression of TRAIL-R4 was also closely correlated with clinical stage (x2 =17.82,P =0.00) and differentiated degree (x2 =4.47,P =0.03).There was a negative correlation between the expression of TRAIL-R2 and TRAIL-R4 in NSCLC (r =-0.67,P=0.01).Conclusion The decrease of TRAIL and TRAIL-R2 and increase of TRAIL-R4 expression may promote the occurrence and development of NSCLC,and they may provide targets for clinical treatment of NSCLC.

Aim To observe the analgesic effect of doxorubicin ( DOX) on chronic sciatic nerve constric-tion injury (CCI) rat model, and analyze the underly-ing mechanism from the ultrastructure of sciatic nerve ganglion and the expressions of some apoptotic pro-teins.Methods A total of 60 SD rats were randomly divided into four groups: sham operation group ( Sham ) , CCI model group ( Model ) , sham operation+DOX 5 mg· kg -1 group ( Sham+DOX) , CCI mod-el +DOX 5 mg· kg -1 group (Model+DOX).DOX was given by caudal vein injection after model estab-lishment .Sham group and model group were given the same amount of saline . The mechanical withdrawal threshold and thermal withdrawal latency were deter-mined by behavioral test .The ultrastructural changes of L4-5 DRG were examined by light microscopy and scanning electron microscopy , respectively .The pro-tein expression levels of Bax , Bcl-2 , PKCɑ, PKCδand PKCε in DRG tissues were determined by Western blot.Results The fluorescence of DOX was found in DRG after DOX was given intravenously .In compari-son with sham group , the thermal and mechanical pain thresholds had no obvious changes in sham +DOX group, while the thresholds were decreased obviously seven days after surgery in model group .In comparison with model group , the pain thresholds in model +DOX group increased significantly , which lasted for the en-tire observation time of six days .The ultra-structure of tissues was damaged obviously in both sham +DOX group and model+DOX group.The protein expression of Bax/Bcl-2 increased, while the expressions of PKCδand PKCεdecreased with DOX injection .Conclusions DOX can retrograde and reach the DRG tissues after intravenous administration . The attenuation effect of DOX on neuropathic pain is related to the apoptosis in-duced by the down-regulation of PKCδ and PKCε in DRG cells.

ObjectiveTo investigate the temporal features of renal injury in rats with severe heat stroke (SHS) and their relationship with inflammatory response.Methods Fifty-six male Wistar rats were randomly divided into normal control group and SHS for 0, 2, 6, 24, 48, 72 hours group (SHS-0, 2, 6, 24, 48, 72 h groups), with 8 rats in each group. Rats were placed in an artificial climate chamber [temperature (39.5±0.2)℃, humidity (60±5)%] to induce SHS model, and the criterion for successful model reproduction was the onset of lowering peak systolic blood pressure (SBP). Then the rats were transferred to room temperature (23.0±0.2)℃ after successful reproduction of the model. The rats of normal control group were kept in room temperature of (23.0±0.2)℃. Heart blood and renal tissue samples were harvested, and the levels of serum creatinine (SCr) and blood urea nitrogen (BUN) were determined by automatic biochemistry analyzer. The levels of myeloperoxidase (MPO), tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) in renal tissue specimens were determined by enzyme linked immunosorbent assay (ELISA). The changes in histopathology in kidney were observed with light microscopy, and Paller scores were used to assess the degree of renal injury.Results Compared with normal control group, the levels of SCr and BUN in serum, and MPO, TNF-α and IL-6 in the renal tissue homogenate were significantly increased in SHS-6 h group [SCr (μmol/L): 174.0±27.0 vs.68.0±11.3, BUN (mmol/L): 12.6±2.3 vs. 4.3±1.2, MPO: (203.0±38.0)% vs. (100.0±1.4)%, TNF-α: (121.0±16.0)% vs. (100.0±1.4)%, IL-6: (118.0±19.0)% vs. (100.0±1.3)%, allP< 0.05], and they peaked at 24 hours [SCr (μmol/L): 489.0±96.0 vs. 68.0±11.3, BUN (mmol/L): 19.3±5.7 vs. 4.3±1.2, MPO: (511.0±41.0)% vs. (100.0± 1.4)%, TNF-α: (399.0±47.0)% vs. (100.0±1.4)%, IL-6: (473.0±56.0)% vs. (100.0±1.3)%, allP< 0.01], then declined to the normal levels at 72 hours. Under light microscopy, tissue edema and necrosis of renal tubules were found, and leukocyte infiltration was found to be most profuse at 24 hours, then they returned to normal levels at 72 hours. Paller scores in SHS-6 h group were significantly higher than those of the normal control group (75.45±9.70 vs. 14.23±3.26,P< 0.01), and it peaked at 24 hours (186.00±14.25 vs. 14.23±3.26,P< 0.01), followed by a gradual lowering, back to normal level at 72 hours.ConclusionThe results suggest that progressive renal damage occurred in the rats with SHS within 24 hours, and it was accompanied with elevated levels of MPO, TNF-α and IL-6 in the kidney homogenate, suggesting that inhibition of neutrophil activation and the release of IL-6, TNF-α may protect the SHS associated renal injury.