AIM:To observe the effects of fasudil on inflammatory reaction in cerebral ischemia/reperfusion rats.METHODS:Focal cerebral ischemia/reperfusion model in rats was made by transient occlusion of middle cerebral artery for 1.5 h followed by 24 h reperfusion.Fasudil was injected intraperitoneally before operation and 12 h after operation.The neurological function was scored and the infarct volume was measured after operation.The water content of brain was measured with dry-wet weight;The myeloperoxidase(MPO)activity was determined by spectrophotometer;The permeability of the blood brain barrier was evaluated by measurement of the Evans Blue(EB)content in the brain with spectrophotometer;The brain content of IL-8 was evaluated with ELISA;The level of NF-?B p65 mRNA expression was determined by RT-PCR;The expressions of ICAM-1,VCAM-1 and NF-?B p65 protein were observed by immunohistochemistry;The MCP-1 and the expression of NF-?B p65 protein in the nuclear extracts were detected by western blotting.RESULTS:Fasudil improved the neurological function,decreased the infarct size,reduced the permeability of blood brain barrier and brain water content,inhibited the MPO activity,decreased the content of IL-8 and the protein expressions of ICAM-1,VCAM-1 and MCP-1 in brain tissue,inhibited the expressions of NF-?B p65 mRNA and protein and reduced the content of NF-?B p65 protein in the nuclear extracts significantly(P

Objective To investigate the effects of pre-ischemic administration of L-NAME on brain protective effects of simvastatin against focal cerebral ischemic/reperfusion injury in rats. Methods ① Animals were subjected to transient 2-hour middle cerebral artery occlusion(MCAO)with the use of the intraluminal filament method previously described by Zea Longa. ② 54 male rats were treated with simvastatin or vehicle by gavage two weeks before MCAO, and L-NAME was injected into laterar ventricle of rats 45 minutes before MCAO. After neurological deficit was assessed at 22 hours of reperfusion, rats were killed, and the brains were rapidly removed. The coronal sections of the brains were prepared and stained with 2% TTC, and the infarct volumes were determined. Another 54 male rats were performed as description above except that the brain tissues were made into homogenate at 22 hours of reperfusion, and the contents of lactic acid(LA) and MDA, and the activities of superoxide dismutase(SOD) in the brain tissues were also measured. Results Administration of simvastatin significantly reduced the size of brain infarct, improved neurological deficits, decreased the contents of LA and MDA and increased the activities of SOD, but L-NAME could abrogate these effects. Conclutions L-NAME could abrogate the protection of simvastatin against ischemic/reperfusion injury,which may be by inhibiting the expression and activity of endothelial NO synthase(eNOS) up-regulated by simvastatin.

Aim To Study the inhibition mechanism of edelfosine on cytokinesis in Schizosaccharomyces pombe. Methods To observe the inhibition of cytokinesis and growth, the experiments of inhibition of cyto-kinesis and parallel growth were carried out. To explore the inhibition mechanism of edelfosine, the experiment of retransfection of yeast genes was carried out. Results Edelfosine inhibited the cytokinesis of S.pombe in low dosage and cell growth in high dosage. The mid2△、spm1△ and pmp1△ strains were resistant to edelfosine in high dosage. However, these strains retrieved the sensitive to edelfosine in high dosage by retransfected the relevant genes, respectively. A reciprocal action, which was the Mid2p induced the phosphorylated Spm1, while the Pmp1 dephosphorylated Spm1, existed among the Spm1、Mid2 and Pmp1 in S.pombe treated with edelfosine. Conclusion The inhibition of edelfosine on cytokinesis and cell growth due to the effect of Spm1、Mid2 and Pmp1.

Some immune responses induced by atherosclerosis may aggravate the state of the illness by inducing persistent arterial inflammation, whereas others may inhibit arterial inflammation and atherosclerosis.Thus, the prevention and treatment of atherosclerosis may be achieved by the method of immunomodulation, by which selectively suppress proatherogenic immune responses or activate antiatherogenic ones.

Aim To investigate the effects of fasudil on neuronal apoptosis after cerebral ischemia/reperfusion(I/R) injury in rats.Method Focal cerebral ischemia/reperfusion model in rats was made by transient occlusion of the middle cerebral artery for 90 minutes followed by 24 h reperfusion.The number of neural apoptotic cells was measured by the method of TUNEL staining;Bcl-2,Bax,Caspase-3 protein expressions were observed by immunohistochemical staining;the expression of phospho-MYPT and phospho-Akt protein was determined by Western blot.Result Compared with the MCAO group,fasudil could decrease the number of neural apoptotic cells,upregulate the expression of Bcl-2 and phospho-Akt protein and inhibit the expression of Bax,Caspase-3 and phospho-MYPT protein significantly(P

Objective To evaluate the efficacy and safety of mNGF to peripheral neuropathy induced by n-bexane. Methods 54 cases were treated with mNGF (18 μg i. m qd.) and the period of treatment is 56 days. 15 severe cases treated with two periods of treatment. Subjects received symptoms and signs of nerve system and activi-ties of daily living (ADL) scale were examined before and every 14 days after treated, The efficacy of mNGF was as-sessed by score increase of each index before and after treatment himself. To evaluate the safety, subjects received Is-boratory examinations before and every 28 days after treated, recorded adverse events everyday. Results During the trial, The indexes had improved remarkably in two weeks after the treatment , There were highly significant differ-ences in score increase after 4 ～ 8 weeks of treatment(P < 0. 01). It indicated that treatmented with mNGF was effec-tive. There were no severe adverse events (SAE) found among 54 trial subjects. There were no evident abnormalities in laboratory examinations before and after treatment. Pains of the injected sites are the main ADR, the incidence was 68.5% (37/54). Conclusion The results of the research indicated that mNGF clinical application could be consid-ered as safe and effective.

Objective:To explore the clinical value on application of laparoscopic ultrasonography (Lap US) in the adnexal operation. Methods:Eleven patients including 7 cases of tubal pregnancy, 3 cases of teratoma of ovary and 1 case of endometrial cyst of ovary were examined by LapUS, then operated with laparoscopy.Results:The results showed that the modality presented is a big progress over the traditional operative management for adnexal diseas. Conclusions:It is a good approach for micro-surgery in the adnexal operation by laparoscopy.

Aim To investigate whether ischemic postconditioning could induce ischemic tolerance to focal cerebral reperfusion injury and comparison with ischemic preconditioning. Methods A reversible middle cerebral artery occlusion (MCAO)was used in this study. Fifty male Sprague-dawley rats were randomized into five groups(n=10): sham-operated group,MCAO group,preconditioning group, postconditioning group and nimodipin group . The neurological function was scored and the infarct volume was measured after operation. The grouping,experimental methods and procedures of another fifty rats were as above except that ipsilateral brain of infarction was dissected and made into homogenate,then the contents of MDA,SOD,GSH and LA were quantitatively measured. Results The postconditioning and preconditioning improved the neurological function,reduced the cerebral infarction volumes and cerebral swelling significantly compared with those of the MCAO group. Contents of LA and MDA were lower, while the activity of SOD in the brain tissues were higher in preconditioning group and postconditioning group than those of the MCAO group. Conclusion Postconditioning could induce brain tolerance, and increase the antioxidant activity, which might be an important mechanism of induction of brain tolerance.

Objective:To explore the mechanism of cardiac function decreasing in patients with ankylosing spondylitis based on Keap1-Nrf2-ARE signaling pathway .Methods:Experiment group included 140 ankylosing spondylitis ( AS) patients and control group included 60 healthy individuals .Echocardiography ( UCG) was used to detect cardiac function parameters .Enzyme-linked immunosor-bent assay(ELISA) was adopted to determine serum proteins ,oxidative stress indicators and cytokines .Erythrocyte sedimentation and plasma C reactive protein ,immunoglobulin were detected with Westergren method and Hitachi 7060 automatic biochemical analyzer re-spectively.Results:(1)Compared with the normal control group , character of AS group in active stage:cardiac function parameters(E peak,EF,E/A),antioxidant indicators(SOD,CAT,TAOC),cytokines(IL-4,IL-10)decreased (P<0.01 or P<0.05 all).A peak, Keap1,Nrf2,oxidation index(ROS,RNS,MDA),cytokines(IL-1,TNF-α),inflammatory indicators(ESR,CRP)increased(P<0.01 or P<0.05 all).(2)Compared with the normal control group, character of AS group in stable stage: cardiac function parameters(E peak,E/A),Keap1,antioxidant indicators(SOD,CAT,TAOC),cytokines(IL-4,IL-10)decreased (P<0.01 or P<0.05 all).A peak, Nrf2,oxidation index(ROS,RNS,MDA),cytokines(TNF-α),inflammatory indicators(ESR,CRP) increased(P<0.01 or P<0.05 all).(3)Compared with AS group in stable stage , character of AS group in active stage:cardiac function parameters(E peak,EF,E/A),antioxidant indicators(SOD,TAOC),cytokines(IL-10)decreased (P<0.01 or P<0.05 all).Keap1,Nrf2,oxidation index(ROS, RNS,MDA),cytokines(IL-1β,TNF-α),inflammatory indicators(ESR,CRP),clinical evaluation indicators (VAS,BASDAI,BASFI, BASMI,BAS-G)increased(P<0.01 or P<0.05 all).(4)Compared with AS patients with normal Keap1 or Nrf2 of peripheral blood, A peak increased while E peak and E/A decreased in AS patients with abnormal Keap1 or Nrf2 of peripheral blood (P<0.01 or P<0.05).(5)Spearman correlation analysis showed:AS parameters of cardiac function in patients with E peak and antioxidant indicators (SOD,CAT,TAOC),cytokines(IL-4,IL-10)showed significant positive correlation.E peak and Keap1, Nrf2,oxidation index(ROS, RNS,MDA),cytokines(IL-1β,TNF-α),inflammatory indicators(ESR,CRP),clinical evaluation indicators (VAS,BASDAI,BASFI, BASMI,BAS-G),IgG,course of the disease were significantly negatively correlated .A peak and Nrf2,oxidation index ( ROS,RNS, MDA) ,cytokines ( IL-1β,TNF-α) ,clinical evaluation indicators , Palpitation showed significant positive correlation .A peak and antiox-idant indicators(SOD,CAT,TAOC),cytokines(IL-4,IL-10)were significantly negatively correlated .E/A and Keap1,antioxidant indi-cators(SOD,CAT,TAOC),cytokines(IL-4,IL-10)showed significant positive correlation.E/A and oxidation index(ROS,RNS, MDA) ,cytokines ( TNF-α) ,cxcinical evaluation indicators ,course of the disease were significantly negatively correlated .EF and course of the disease were significantly negatively correlated .FS and Keap1 showed significant negative correlation .Conclusion:Cardiac func-tion decreasing in patients with ankylosing spondylitis is 33.56%.The characteristic performance is that E peak , E/A decreased while A peak increased.E peak,E/A and antioxidant indicators ,anti-inflammatory cytokines show significant positive correlation .E peak,E/A and Keap1,oxidation index,pro-inflammatory cytokines,inflammatory indicators are significantly negatively correlated .A peak and Keap1,oxidation index ,pro-inflammatory cytokines show significant positive correlation .A peak and antioxidant indicators ,anti-inflam-matory cytokines are significantly negatively correlated .The rising of Keap1 expression cause activate the Keap 1-Nrf2-ARE signaling pathway .After the signaling pathway is activated ,the body's antioxidant ability decreased , pro-inflammatory cytokines imbalanced , in-flammation index increased .When the body is long be in unbalance condition , the number of abnormal immune complex deposition in-creased.In the end,the result is that AS is caused and cardiac function is decreased .

Objective To investigate the changes of CD4+CD25+ regulatory T (Treg) cells in elderly patients with septic shock, and to evaluate the effects of the changes on 28-day mortality rate.Methods The 75 consecutive elderly patients with septic shock were recruited from December 2006to December 2008, and the general states and clinical characteristics of them were analyzed. The CD4+ CD25+ FoxP3 regulatory T cells and human leucocyte antigen DR (HLA-DR) were measured by flow cytometer at the 1st, 4th and 7-10th day of septic shock after being diagnosed. Results The patients were at an average age of (69.2±7.5) years, and the 28-day mortality rate was 53.3%.There were no significant differences in the percentage of CD4 + CD25+ FoxP3/CD4+T cells between the survivors and the non-survivors at the 1st day (1.76 % ±0.31% vs. 1.68 %±0.24 %, P＞0.05)and the 4th day (1.94%±0.32% vs. 1.82% ±0.28%, P＞0.05). However, compared with the survivors, non-survivors had a higher percentage of CD4+ CD25+ FoxP3/CD4+ T cells (2.65%±0.28% vs. 1.79%±0.27%, P＜0.01) at the 7-10th day of septic shock after being diagnosed.Furthermore, from the 4th day to the 7-10th day, the expressions of monocyte HLA-DR in the nonsurvivors were significantly lower than in the survivors (P＜0. 01), and they were inversely correlated with the percentage of CD4+ CD25+ FoxP3/CD4+ T cells at the 4th day (r=-0.39, P=0.023) and the 7-10th day (r= -0. 58, P＜0. 01) respectively. The multiple logistic regression analysis showed that the percentages of CD4+ CD25+ FoxP3/CD4+ T cells (OR = 3.47, 95% CI: 1.33-10.0) and HLA-DR (OR= 0. 27, 95% CI: 0.14-0.73) were independent predictors of 28-day mortality rate.Conclusions Persistent higher percentage of CD4+ CD25+ Treg cells in the elderly patients with septic shock indicates that the patients are under the states of immunosuppression and have a higher risk ofmortality in intensive care unit at admission.