BACKGROUND:Now a correspondingly stable project was performed in the rehabilitative treatment for patients with chronic heart failure in China,but it was difficult to be carried out on the wide range because of difficulties in adjusting movement capacity,lower compliance and so on,especially for the elder patients or those with severe chronic heart failure.The movement project will be required with the advantages of good compliance,moderatemovementcapacityandreproducibilityin clinic.OBJECTIVE:To investigate the change of exercise tolerance and cardiac function after the intervention in movement training in patients with chronic heart failure.DESIGN: Randomized and controlled observation.PARTICIPANTS:Seventy inpatients with stable chronic heart failure were chosen from the Department of Gerontology in Wuhan Union Hospital of Hubei Province from August 2002 to October 2003.All patients agreed to this test. Functional class of New York Heart Association (NYHA)was (2.69±0.13).Chronic heart failure duration of all patients was over six months. Seventy patients were randomly divided into movement group(n=34) and control group(n=36).In the movement group with 19 males and 15 females,functional class was(2.68±0.12).In the control group,there were 19 males and 17females.METHODS:Thepatientsinthemovementgroupunderwentthree weeks of movement training (bicycle ergometer,treadmill walking and walking on foot). The patients in the control group underwent three weeks of activity restriction. All patients received the 6-minute walking test under the condition of the same rating of perceived exertion before and after the test. Totally 5 mL of venous blood was drawn without eating anything in the morning before and after the test.The levels of interleukin-6 and norepinephrine were evaluated and left ventricle ejection fraction was observed and determined.MAIN OUTCOME MEASURES:Comparison of walking distance,interleukin-6,norepinephrine,l.eftventricleejectionfractionandcardiac functional class before and after the intervention in all patients.RESULTS:Seventy patients with chronic heart failure were involved in the statistical analysis at last. After the intervention,walking distance covered during 6minutes and left ventricle ejection fraction in the movement group were obviously longer and higher than those before the intervention and in the control group [(385±30)m,(43±5)％;(324±35)m,(39±6)％;(292±30)m,(35±4)％,P＜ 0.05].After the intervention,the levels of plasma interleukin-6 and norepinephrine and cardiac functional class in the movement group were lower than those in the control group and before the intervention[(0.86±0.25) pmol/L,(2.05±0.48) nmol/L,(1.89±0.11);(1.00±0.25)pmol/L,(2.21 ±0.47)nmol/L, (2.45 ±0.12);(1.12±0.23) pmol/L,(2.46 ±0.53) nmol/L,(2.68±0.12),P＜ 0.05-0.01].CONCLUSION:Theprojectof movementtrainingdesignedinour study can improve exercise tolerance and ameliorate cardiac function in patients with chronic heart failure. This project has the advantage of better compliance designed according to oneself.

Objective To investigate the effect of skeletal muscle training on exercise tolerance in patients with chronic heart failure(CHF). MethodsSeventy patients with CHF were divided into group A( n =34),undergoing 3 weeks of exercise training(bicycle ergometer, treadmill walking and walking on foot),and group B( n =36), undergoing 3 weeks of activity restriction. Before and after exercise training and after activity restriction, 6 minutes of walking test was performed and levels of interleukin-6(IL-6), norepinephrine(NE) and left ventricle ejection fraction(LVEF) were evaluated. ResultsAfter exercise training in group A, the maximum distance walked was (385?30.12)m. The levels of LVEF, plasma IL-6 and NE were (43?5.23)%,(0.86?0.25)pmol/L and (2.05? 0.48 )nmol/L,respectively. All the above parameters were significantly ameliorated when compared with group B ( P 0.05). ConclusionThe skeletal muscle training could improve exercises tolerance and ameliorate cardiac function in patients with chronic heart failure,which was beneficial for the rehabilitative treatment.

Objective To explore the effects of physical training on serum activity of some peripheral inflammatory markers associated with endothelial dysfunction, such as granulocyte macrophage-colony stimulating factor (GM-CSF), macrophage chemoattractant protein-1 (MCP-1), soluble intercellular adhesion molecule-1(sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) in patients with chronic heart failure. Methods Forty-eight patients were enrolled and randomly divided into two groups: a training group and a rest group. The patients of both groups were both given conventional internal medicine therapy, and the patients of the training group were given physical training in addition. The serum levels of GM-CSF, MCP-1, sICAM-1 and sVCAM-1 in patients of the two groups were determined with stable chronic heart failure before and after 12 weeks of programmed physical training. At the same time, the motor functional status of chronic heart failure patients was evaluated by using the 6-minute walking test. Results It was shown that the physical training produced a significant reduction in serum GM-CSF, MCP-1, sICAM-1 and sVCAM-1 as well as a significant improvement in performance of the 6-minute walking test. Conclusion The physical training could significantly alleviate the inflammation reaction and improve the motor function of patients with chronic heart failure.

Objective To investigate the neuralprotective effect of Rho kinase inhibitor fasudil hydrochloride in cerebral ischemia/reperfusion injury in rats.Methods The SD rats were randomly divided into four groups:the sham group,the ischemia/reperfusion group,the fasudil hydrochloride group and the physiological saline group.Fasudil hydrochloride were injected intraperitoneally 30 minutes before ischemia.And the physiological saline group were treated with the intraperitoneal injection of the same volume of saline.The phosphorylation and protein expression of GluR6 at 6 hours during reperfusion were detected using immunoprecipitation and immunoblotting analysis to examine the effect of Fasudil hydrochloride.Furthermore,TUNEL staining was used to examine the apoptosis of neurons in rat hippocampal CA1 regions after 3 days reperfusion.Results 1.Immunoprecipitation and immunoblotting analysis were used to analyze the phosphorylation of GluR6 in serine site.The results showed that the GluR6 serine phosphorylation level increased significantly at 6h of reperfusion compared with the sham group (P＜0.05).Fasudil hydrochloride group could inhibit the increased phosphorylation of GluR6 at 6h of reperfusion compared with the ischemia/reperfusion group and saline group,respectively (P ＜ 0.05).2.TUNEL staining was used to examine the apoptosis of neurons in 3 days after reperfusion in CA1 regions of hippocampus.The results indicated that significant numbers of TUNEL positive cells (40.20 ± 2.77) were observed 3 days after ischemia/reperfusion.The numbers of viable neurons per 1 mm length of CA1 pyramidal cells were quantitatively analyzed.Fasudil hydrochloride markedly decreased the neuronal loss compared with the ischemia/reperfusion group (19.80 ± 2.86) (P＜0.05).Conclusion Fasudil hydrochloride can inhibit induced phosphorylation of GluR6 by the ischemia/reperfusion.Fasudil hydrochloride can reduce the neurons apoptosis in hippocampal CA1 regions,and perform a neuralprotective effect on ischemia/reperfusion injury in rats.

Objective To investigate the effects of the FKBP51 · PHLPP · AKT signal module on the phosphorylation of Akt and hippocampal neuronal injury after the cerebral ischemia / reperfusion induced neuronal death in rat hippocampus.Methods Transient(15 min)brain ischemia was induced by the four-vessel occlusion in Sprague-Dawley rats.6 rats were used in each group.The antisense oligodeoxynucletides(AS ODN)of PHLPP2 (PH domain and leucine rich repeat protein phosphatases) was used to suppress the assembly of FKBP51 · PHLPP · Akt signal module by intracerebroventricular infusion once per day for 3 days before ischemia.After 6 hours reperfusion,interactions of PHLPP2 and FKBP51 (FK506 binding protein 5) with Akt were detected by immunoprecipitation (IP) and the phosphorylation of Akt was detected by western blot (IB).After 5 days reperfusion,rats were perfusion-fixed with paraformaldehyde and Hematoxylin-Eosin staining was used to examine the survival number of CA1 pyramidal cells of hippocampus.Results Compared to PHLPP2 MS ODN group(1.24±0.24,1.68±0.11,0.58±0.01),PHLPP2 AS ODN suppressed the assembly of the FKBP51 · PHLPP · Akt signaling module(1.06±0.01,1.04±0.13),and increased the phosphorylation of Akt(0.76±0.02) (P＜0.05).Furthermore,compared to PHLPP2 MS ODN group (20.1±2.5),the number of surviving neurons significantly increased in PHLPP2 AS ODN group(88.3±2.7)(P＜0.05).Conclusion The increasing assembly of FKBP51 · PHLPP · Akt signal module can damage CA1 pyramidal cells of hippocampus by inhibiting the phosphorylation level of Akt.

Objective To investigate effect of FK506 binding protein 51 (FKBP51) on the c-JunN-terminal kinase (JNK) pathway in cerebral ischemia-reperfusion injury.Methods Transient global cerebral ischemia rat models were made by four-vessel method.Healthy male SD (Sprague Dawley) rats were randomly divided into:sham group,ischemia/reperfusion group (I/R group),FKBP51 antisense oligonucleotide group (FKBP51 ASODN group),FKBP51 missense oligonucleotide group (FKBP51 MSODN group),and solvent control group (TE group).The effect of FKBP51 ASODN on expression of FKBP51 protein and JNK was detected,and c-Jun phosphorylation was detected by Western blot.Results (1) FKBP51 protein expression in the FKBP51 ASODN group was reduced.The change of FKBP51 protein expression between the FKBP51 ASODN and sham groups was statistically significant (P ＜ 0.05).(2) The expression differences of total JNK protein between all the groups were not statistically significant (P ＞ 0.05).The expression of p-JNK in sham group was significantly less than the other groups (P ＜ 0.05).The expressions of p-JNK in I/R 3d,TE,and FKBP51 MSODN groups were higher relative to Sham group; however,the differences among those three groups were not statistically significant (P ＞ 0.05).The expression of p-JNK in FKBP51 ASODN group was significantly less than FKBP51 MSODN group (P ＜ 0.05).(3) The expression differences of total c-Jun protein among all groups were not statistically significant (P ＞ 0.05).The expression of p-c-Jun in sham group was significantly less than the other groups (P ＜ O.05).The expressions of p-c-Jun in I/R 6 h,TE,and FKBP51 MSODN groups were higher relative to the sham group; however,the differences among those three groups were not statistically significant (P ＞ 0.05).The expressions of p-c-Jun in FKBP51 ASODN group was significantly less than FKBP51 MSODN group (P ＜ 0.05).Conclusions FKBP51 might activate JNK signaling pathway in cerebral ischemia-reperfusion injury.

Objective To explore the effect of FKBP51 acting on Caspase-3 and hippocampal CA1 area neu-ronal necrosis in cerebral ischemia reperfusion injury of rat.Methods SD rats were randomly divided into Sham group,ischemia reperfusion group ( I/R group ) , TE buffer group ( TE group ) , FKBP51 antisense oligonucleotide group (FKBP51 ASODN group) and FKBP51 missense oligonucleotide group (FKBP51 MSODN group).Transient global cerebral ischemia rats models were made by four-vessel method.We used Western blot to detect the expression of FKBP51,the effect of FKBP51 ASODN to FKBP51 expression and Caspase-3 activity;while we used HE staining technique to detect FKBP51 ASODN effect to rat hippocampal CA1 area neuronal necrosis.Results (1) In Sham group and I/R group (0min,15min,30min,1h,3h,6h,1d,3d),FKBP51 expressed,and the difference among the groups was no statistical significance (F=0.64,P>0.05).(2)The expression of FKBP51 in FKBP51 ASODN group was obviously reduced, and the difference was statistically significant compared with Sham group ( t =8.21, P <0.05).(3)The expression of Cleaved-Caspase-3 in Sham group obviously declined than the other groups,the differ-ence between them was statistically significant (F=12.31,P<0.05);The expression of FKBP51 in FKBP51 ASODN group was decreasing compared with FKBP51 MSODN group,and the difference was statistical significance(t=9.71, P<0.05).(4)HE staining showed:the number of Sham group (186.3 ±2.5) hippocampal CA1 pyramidal cells was most.The cells arranged densely,and nucleoli were large and round,the difference was statistically significant com-pared with the other groups (χ2 =81.91,P<0.05);The hippocampal CA1 pyramidal cells of I/R group (15.4 ± 2.6),TE group (18.5 ±2.2) and FKBP51 MSODN group (17.5 ±1.8) were almost completely disappeared,only left a few residual cells,a great quantity of denaturated cells which presented karyopykosis,tinctorialed endochylema, ruptured of membrane and released cell content;the hippocampal CA1 pyramidal cells FKBP51 ASODN group (92.8 ±2.6) survival increased significantly compared with other group,the difference was statistically significant (χ2 =52.36,P<0.05).Conclusion In cerebral ischemia reperfusion injury,FKBP51 can enhance the activation of Caspase-3 (Cleaved-Caspase-3) expression and inhibit the survival of the neurons.

Objective To investigate diagnostic and prognostic significance of protein C in acute leukemia with disseminated intravaseular coagnlation(DIC). Methods APTT, P-T, D-Dimer, Fbg, antithrombin (AT) and protein C(PC) were determinated in plasma of 44 DIC patients with acute leukemia and 30 normal controls. Results PC was markedly lower in disseminated intravaseular coagulation with acute leukemia group(67.03±36.98) than that of control group (99.53±45.20), and significantly correlation DIC score( r = -0.57,P＜0.01). PC of abnormality rate in DIC group was 86.36 %. APTT, PT, D-Dimer, Fbg were significantly increased and AT was decreased during the progress of DIC in relation to values observed in the control group. Conclusion DIC is related to the disorder of coagulation and fibfinolysis system. PC is a sensitive index to diagnose and prognose DIC in acute leukemia.

Objective To investigate the effect of Rho kinase inhibitor fasudil on taxed lineage kinase 3 (MLK3), c-Jun NH2-terminal kinase (JNK) phosphorylation, caspase-3expression, and neuronal injury in hippocampal CA1 region follwong cerebral ischemic rep erfusion in rats. Methods A total of 72 Sprague-Dawley rats were randomly divided into sham operation, ischemia-reperfusion, normal saline, and fasudil groups. A global cerebral ischemic model was prepared by four-vessel ligation. The levels of MLK3 and JNK phosphorylation, and caspase-3 expression were detected by Western blot analysis. Cresy1 violet staining was used to detect the numbers of survival neurons in hippocampal CA1 region. Results When 6 hours after ischemia-reperfusion, the level of MLK3 phosphorylation in the fasudil group (1.13 ± 0. 03)was significantly lower than that in the normal saline group (2. 08 ± 0. 01 ,P = 0. 000 3), while the levels of MLK3 was no significant difference. When 3 hours after ischemia-reperfusion, the level of JNK phosphorylation in the fasudil group (1.27 ±0. 02)was significantly lower than that in the normal saline group (2.09 ±0. 01, P=0. 000 2), while the levels of JNK was no significant difference. When 6 hours after ischemia-reperfusion, the expression level of caspase-3in the fasudil group (1.28 ± 0. 02) was significantly lower than that in the normal saline group (2. 10 ± 0. 01, P = 0. 000 6). When 5 days after ischemia-reperfusion, the pyramidal cells in hippocampal CA1 region almost completely disappeared in the ischemia-reperfusion group, and only a few cells left (9. 8 ±2. 1). The numbers of survival pyramidal cell (8. 28 ± 3.2) in hippocampal CA1 region in the fasudil group was significantly more than that in the normal saline group (11.8 ± 1.6, P ＜0. 05). Conclusions Fasudil may significantly inhibit the ischemia-reperfusion-induced phosphorylation of MLK3 and JNK, as well as the expression of caspase-3, and thus reduce neuronal injury in hippocampal CA1 region.

Objective To observed the clinical effect of vidarabine and interferonα-2b aerosol inhalation in the treatment of children with infantile herpangina.Methods 58 children with infantile herpangina were divided ran-domly into the observation group and control group,29 cases in each group.All children were given theroutine nursing and general supportive therapy.The patients in the control group were treated by ribavirin and those in the observation group treated by vidarabine and interferon aerosol inhalation.The fever clearance time,the disappearance time of her-pes,the days of hospitalization and cases of adverse reaction was observed and recorded.Results The cooling time, bleb disappear time and hospital stay of the observation group were lower than those of the control group,the difference were statistically significant(P <0.05).Comparation of the clinical effects of the two groups showed that the test group were significantly better than those in the control group(P <0.05).The total effective rate in the observation group was 96.6%,which was higher than 75.9% in the control group(χ2 =5.22,P <0.05).No obvious adverse e-vents took place in both groups.Conclusion Vidarabine and interferon aerosol inhalation in treating infantile herpan-gina takes a good effect,no obviously adverse reaction and is worth being widely applied in clinic.