Objective To observe the changes in the expression of renal tissue TNF-α , NF-κB and the interrelation to renal cell apoptosis, and their influences of Inula Britannica(an inhibitor of inflammatory signal pathway) in exhausted swimming rats, and to investigate the role of inflammatory signal pathway. Methods Forty-eight male Wistar rats were randomly divided into three groups: control group (CN, n=8), exhaustive swimming group (ES, n=24) and Inula Britannica group (IB, n=16). The rats of CN were quiet without swimming. The rats of ES swam to exhaustion and were sacrificed at immediately (ESI, n=8), 6 hour (ES 6 h, n=8) and 24 hour (ES 24 h, n=8) after exhanstiing swimming. The rats of IB group took orally Inula Britannica at the dose of 25 ml/kg body weight at 24 h before swimming and then swam to exhaustive state. The rats of IB group were sacrificed at 6 hour (IB 6 h, n=8) and 24 hour (IB 24 h, n=8) after exhaustiing swimming. The renal cell apoptosis was measured by the method of terminal-deoxynucleotidyl transferase mediated d-UTP nick end labeling (TUNEL). The expression of TNF-α in renal tissue was examined by immunohistochemistry. The changes of NF-κB in renal tissue were measured by flow cytometry and immunnhistochemistry. The interrelation between TNF-α and NF-κB was analyzed by Pearson method, and the interrelation between TNF-α, NF-κB and renal tissue cell apoptosis was analyzed by Spearman method. Resulls The number of renal tissue apoptotic cells was increased progressively from ESI to ES 24 h rats (P <0.05). Immunohistochemistry staining showed that the positive expressions of renal tissue TNF-α and NF-κB were increased progressively at 0 h (0.136±0.009, 0.129±0.011), 6 h (0.171±0.011, 0.166± 0.009) and 24 h (0.229±0.008, 0.218±0.019) after exhaustiing swimming in ES compared with control group (0.109±0.010, 0.095±0.010) ( all P<0.05). The similar changes of renal tissue NF-κB was also revcalved by flow cytometry. The expression of TNF-α was positively correldted with NF-κB (r=0.955, P<0.01 ), and renal cell apoptosis was also positively correlated with TNF-α and NF-κB (r =0.953, r=0.939, P<0.01) in ES rats. Pretreatment with Inula Britannica, inhibited the up-regulation of expressions of renal tissue TNF-α (6 h:0.142±0.012, 24 h:0.130±0.010) and NF-κB (6 h:0.138±0.010, 24 h:0.136±0.011 ) induced by exhausting swimming. Conclusion Overtraining can induce the up-regulating expressions of renal tissue TNF-α and NF-κB, and Inula Britannica can partly counter the above changes in exhaustied swimming rats, which may be one important mechanisms of overtraining-induced renal tissue cell apoptosis and the anti- apoptosis effect of Inula Britannica.

Inflammatory breast carcinoma (IBC) is a particularly local advanced breast cancer,which has characters of high invasion,high metastasis and high human mortality.Because of high malignancy and rapid development,extensive body metastasis often happens in early stage and the prognosis is very poor.Currently,the therapy strategy of operation,chemotherapy combined with radiotherapy is used to treat IBC.However,the effect is always very limited.Now,the advances in researches of molecular biology and cancer immunology bring hope.Some recent progresses of therapy in IBC are reviewed in the article.

Objective To study the expressions of apoptosis related genes Bcl-2 and Bax proteins in rat's renal tissue and the relationship between the ratio of Bcl-2/Bax and renal cell apoptosis induced by overtraining,and observe the effect of anisodamine on the expression of genes Bcl-2 and Bax in exhausted rats.Methods The animal model of acute kidney injury induced by exhausting swimming was reproduced.Forty eight male Wistar rats were randomly assigned into sedentary control group(CN,n=8),exhausting swimming group(immediate,6 hours and 24 hours after exhausting swimming,ESI,ES6h and ES24h,8 each),Anisodamine group(6 hours and 24 hours after exhausting swimming,AD6h and AD24h,8 each).The expressions of Bcl-2 and Bax were detected by immunohistochemical staining and image analyzer.The correlation between the ratio of Bcl-2/Bax and renal cell apoptosis was analyzed.Results The analysis showed that the expression of Bax increased,and of Bcl-2 decreased,the ratio of Bax/Bcl-2 increased remarkably in ESI group compared with CN group(P

Objective To explore stimulative of posttraumatic growth(PTG) of head-injured patients associated with limb movement disorder,in order to provide reference for psychological nursing intervention.Methods Phenomenological methodology was used in the study.A semi-structured interview was conducted on seven head-injured patients with limb movement disorder recruited by purposive sampling method.Data were analyzed by Colaizzi's analysis procedure.Results Through interview,the following four themes were summarized:positive state of mind and coping style of patients; patients' high level of self-efficacy; social support; high quality of medical services.Conclusions In order to promote PTG of head-injured associated with limb movement disorder patients,nurses should strive to adjust the patient mentality and coping strategies,improve their self-efficacy levels,help patients get support from the community,at the same time should also focus on quality of medical services.

Objective To observe the expression changes of renal tissue Bax,Bcl-2 and caspase-3,to wxamine the correlation between the ratio of Bax to Bcl-2,caspase-3 and renal tubular cells apoptosis,and to investigate the role of caspase-related signal pathway.Methods Forty-eight male Wistar rats were randomly divided into three groups: control (CN,n=8),exhaustive swimming (ES,n=24) and inula britannica (IB,n=16) group.The rats of CN were quiet without swimming.The rats of ES swam to exhaustive state and were sacrificed at immediately(ESI),6 hour (ES 6 h) and 24 hour (ES 24 h) after exhaustive swimming respectively.The rats of IB took orally inala britannica at the dose of 25 ml/kg body weight at 24 h before swimming and then swam to exhaustive state.The rats of IB group were sacrificed at 6 hour (IB 6 h) and 24 hour (IB 24 h)after exhaustive swimming.The animal model of overtraining-induced acute kidney injury was developed by exhaustive swimming.The renal cell apoptosis was measured by the method of TUNEL.The expressions of Bax,Bcl-2,caspase-3 in renal tissue were observed by immunohistochemistry.The expression of caspase-3 protein was examined by Western blotting.The correlation between the ratio of Bax to Bcl-2 and caspase-3 was analysed by Pearson method,and the correlation between the ratio of Bax to Bcl-2,caspase-3 and renal tubular cell apoptosis was analysed by Spearman method.Results The number of renal tubular apeptotic cells was increased progressively in ESI to ES 24 h rats by TUNEL (P＜0.05).Immunohistochemistry staining showed that the ratio of Bax to Bcl-2 and caspase-3 in renal tubular cells were increased progressively at 0 h,6 h and 24 h after exhaustive swimming compared with control group (P＜0.05).The change of renal tissue caspase-3 was also revealved by Western blotting analysis.The ratio of Bax to Bcl-2 and caspase-3 in renal tubular cell was correlated positively (r=0.865,P＜0.05),The ratio of Bax to Bcl-2,and caspase-3 was also correlated positively to renal tubular cell apoptosis (r=0.674,r=0.837,P＜0.05) in ES rats.Pretreatment with inula britannica inhibited the up-regulation of the ratio of Bax to Bcl-2,caspase-3 and cell apoptosis in renal tubular cell induced by exhaustive swimming.Conclusion Overtraining can induce renal tubular cells apoptosis through activating caspase-related signal pathway by impairing the balance of Bax and Bcl-2,which may be one of the important molecular mechanisms of overtraining-induceed renal tubular cells apoptosis.

Objective To explore the effect of intrahepatic injection of liposome-mediated VEGF plasmid on ischemia-reper-fusion liver injury and its mechanism. Methods Rabbits were randomly divided into normal group, ischemia-reperfusion group and recombinant VEGF therapy group( liposome-mediated transfer of VEGF plasmid into liver via portal vein 20 min before ischemia of liver). The model of liver ischemia-reperfusion injury was established. Liver function and the activity of SOD.XO in blood were determined at the 0,2nd,6th,12th,and 24th h after operation. RT-PCR technique was applied to detect the expression level of Fas mRNA in liver tissues of every group,and flow cytometry was used to measure cell apoptosis rate at the 6th h after operation. At the 24th h after operation,all rabbits were killed and liver tissues of ischemia were taken to make pathological sections for observing the morphology and microstructure under the light microscopy and electron microscopy. ResuJts The level of ALT in recombinant VEGF therapy group was markedly reduced as compared with ischemia-reperfusion group at the 6th,12th,and 24th h after operation( P<0. 05). The activity of SOD in recombinant VEGF therapy group was significantly higher than in ischemia-reperfusion group at the 6th, 12th,and 24th h after operation. The activity of XO in recombinant VEGF therapy group was significantly lower than that in ischemia-reperfusion group at the 6th,12th,and 24th h after operation(P< 0. 05 or P<0. 01). In addition,there was significant difference in the expression of Fas mRNA and cell apoptosis rate between recombinant VEGF therapy group and ischemia-reperfusion group(P<0. 01). The injury of hepatocytes in recombinant VEGF therapy group was significantly alleviated as compared with that in ischemia-reperfusion group under the light microscopy and e-lectron microscopy. Conclusion Liposome-mediated transfer of VEGF plasmid into liver before ischemia of liver can obviously protect hepatocytes by increasing anti-oxidative ability, decreasing the expression of Fas mRNA, and finally inhibiting hepato-cyte apoptosis.

Objective To investigate the relationship of apolipoprotein E ?4 allele to early cognitive dysfunction after cardiac surgery and to identify the predictors of cognitive decline after cardiac operation. Methods Two hundred and thirty patients aged over 18 yr undergoing coronary artery bypass grafting (CABG) were studied. They were capable of completing the preoperative cognitive function tests in terms of the education they had received. Patients with neurological or mental disease and those with serious hepato-renal or cardiac dysfunction were excluded. Cognitive function was evaluated using a battery of nine neuro-psychologieal tests before operation, at one week and 3 months after operation. Cognitive decline was defined as ≥20% decrement in 20% or more of the completed tests. The changes in the Z-based scores were used to evaluate the severity of cognitive decline. Logistic regression and multiple linear regression were used to determine the relationship of ApoE genotype to cognitive decline and identify the predictors of postoperative cognitive decline ( POCD) after cardiac operation. Results The incidence of cognitive decline was as high as 51.9 % and 21.0% at 1 week and 3 months after operation respectively. The ?4 allele was present in 7.4 % , ?3 allele in 86.1 % and ?2 allele in 6.5 % of the 230 patients. The cognitive decline was not significantly associated with the presence or absence of the ?4 allele. The ?4 allele was associated with poor baseline performance. Age, the use of cardiopulmonary bypass (CPB), duration of endotracheal intubation were predictors of cognitive impairment after cardiac operation. There was positive correlation between the neuro-psychological test scores at 1 week and 3 months after operation. Conclusion The results suggest that age, the use of CPB and duration of endotracheal intubation are the predictors of POCD. The ?4 allele is not associated with POCD after cardiac operation. The cognitive dysfunction at 3 months after operation is positively correlated with the level of cognitive decline at 1 week after operation.

To investigate the cardioprotective effect of percutaneous transluminal myocardial laser revascularization (PTMR) and its mechanism, in the ischemia/reperfusion (I/R) model of in vivo porcine heart, the effect of PTMR on myocardial infarct size (IS) was observed using TTC method,and expression of heat shock protein (HSP) 70 and 86 in myocardium was detected with Western blotting. It was found that PTMR significantly limited the myocardial IS induced by I/R (32%?3% vs 56%?7% in control group, P

On the model of isoprenaline (ISO)-perinjured rat heart, the protctive effect of ischemic preconditioning (IPC) on ischemia reperfusion (I/R) damage was observed.It was found that compared with alone I/R group,IPC ameliorated I/R-induced reduced reduction of coronary blood flow (CBF) (8. 8 + 0. 6 vs 6. 6 + 0. 4mL/min,P

Objective To determine the ESBLs of Klebsiella pneumoniae and ESBL typing by molecular genetic procedures. Methods MIC test and ESBLs confirmation test were taken by agar dilution method in 80 strains of Klebsiella pneumoniae isolated in Beijing area from July 1999 to December 1999. To the 20 ESBLs positive conjugates isoelectric focusing was given. And nucleotide sequencing was analysed to conjugate strain CK23. Results 28 (35%) of the 80 strains of Klebsiella pneumoniae produced ESBLs. In the 28 strains, 20 were successfully done with conjugation of resistant plasmid. Isoelectric focusing results revealed that 13 (65%) of the 20 strains produced an ESBLs protein with a pI of 8.8 with or without additional pI 7.6 and pI 5.4. These ? lactamases were all inhibited by clavulanite acid. The strains with pI=8.8 protein were highly resistant to cefotaxime and ceftriaxone but were susceptible or intermediate to ceftazidime. We picked CK23 strain out from 13 conjugates for gene cloning by the primers designed for bla CTX M and nucleotide sequencing. The results showed that the ESBLs gene in CK23 was CTX M, highly similar to CTX M 3 but had 3 amino acids, which were Glu39Gly, Leu122Pro, Asp278His. Conclusions 28 (35%) of the 80 strains of Klebsiella pneumoniae produced ESBLs. Resistant plasmid successfully conjugated in 20 of the 28 ESBLs producing strains. 13 of the 20 (65%) conjugates pruduced a pI =8.8 ESBLs,which was CTX M ESBLs,with only 3 amino acids different from CTX M 3. This paper indicated that a type of CTX M ESBLs existed in Klebsiella pneumoniae in Beijing, which specifically confers resistance to cefotaxime.