Objective To seek a new method to identify viability of myocardium by adenosine stress echocardiography combined with quantitative tissue velocity imaging(QTVI)and tissue tracking(TT).Methods Fifteen healthy canines were selected to establish the models of acute myocardial infarction and reperfusion by ligating anterior descending branch of coronary artery for 90 minutes and then releasing the artery to get reperfusion.After reperfusion.peak velocity in systole(Vs),peak velocity in isovolumic contraction(VIVC)and the displacement in systole(Ds)were measured on anterior wall and anterior septum at baseline.The 2,3,5-triphenyl tetrazolium chloride(TTC)staining was set as a"gold standard"for defining the viable and non-viable groups.The sensitivity and specificity of assessing myocardial viability were determined with QTVI and TT.Comparison of variables between viable and non-viable group was made by using t test.One way analysis of variance and LSD-t test were used to estimate the significance of differences in different states.Results Compared with baseline,Vs,VIVC and Ds decreased significantly(P＜0.01)after reperfusion in both viable and non-viable group.After administration of adenosine,Vs and Ds increased(P＜0.05),but VIVC didn't change significantly compared with that before administration of adenosine in viable group(P＞0.05).Variables in non-viable group didn't change significantly after administration of adenosine(P＞0.05).By receiver operating characteristic(ROC)analysis for predicting myocardial viability,when a cutoff value of △Vs(%)rate was 17.9,the sensitivity and the specificity was 78.6%and 81.1%,respectively,and when the cutoff value of △Ds(%)rate was 18.4,the sensitivity and the specificity was 75.0%,83.6%,respectively.Combined △Vs(%)with △Ds(%),the sensitivity and specificity to prediction of myocardium viability could reach 94.6%and 68.0%,respectively.Conclusions When the viability of myocardium after myocardial infarction is assessed by using the method of adenosine stress echocardiography with QTVI and TT,the sensitivity and the specificity are greatly enhanced.

This study was aimed to verify the effects of staged sequential therapy on expressions of matrix metalloproteinase-9 (MMP-9) and its inhibitor TIMP-1 within lung tissues in asthmatic rats with the airway remodeling, by applying a series of tests such as the immunohistochemistry, western blot and real-time fluorescent quantitative PCR. SD rats were randomly divided into 7 groups, which were the asthmatic group (Group X), the normal group (Group Z), the No. 1 sequential therapy group (Group A1), the No. 2 sequential therapy group (Group A2), the No. 3 sequential therapy group (Group A3), the montelukast group (Group M), and the budesonide group (Group B). The asthmatic model was established in each group except Group Z, by sensitization with both ovalbumin (OVA) and aluminium hydroxide via injection at the 1st, 8th and 15th day in a 22-day duration, followed by OVA aerosol inhalation every other day for 8 weeks for asthma activation. At the 8th day after the asthmatic model was established, Group A1 was orally given Ma-Xing Er-Chen Tang (MXECT) during acute phase while given normal saline (NS) during catabasis and stable phase; Group A2 was given MXECT during acute phase, and given modified Jin-Shui Liu-Jun Jian (JSLJJ) during catabasis as well as given NS during stable phase; Group A3 was given MXECT during acute phase, and given modified JSLJJ during catabasis as well as given Liu-Wei Di-Huang (LWDH) Powders during stable phase;Group M was given salbutamol via aerosol inhalation after stimulation, while orally given montelukast during catabasis and stable phase; Group B was given salbutamol via aerosol inhalation after stimulation, while given inhaled budesonide during catabasis and stable phase; Group X was given NS. After the 7-week intervention, the immunohistochemistry, western blot and real-time quantitative PCR were applied to analyze the location and quantitative expression of MMP-9 and TIMP-1, so as to find out the biological mechanism on expressions of MMP-9 and TIMP-1 in lung tissues of asthmatic rats from molecular levels to gene levels. The results of immunohistochemistry, western blot and real-time fluorescent quantitative PCR showed as follows. Compared with Group Z, the contents of MMP-9 and TIMP-1 increased significantly within lung tissues in Group X. Compared with Group X, the contents of MMP-9 and TIMP-1 decreased within lung tissues of asthmatic rats in each treatment group. It was concluded that the expression of MMP-9 and TIMP-1 elevated during asthma. TCM staged sequential therapy can regulate the ratio between MMP-9 and its inhibitor so as to block the airway remodeling, by decreasing the expression of MMP-9 and its inhibitor within lung tissues in asthmatic rats. This is one of the important action mechanisms.

OBJECTIVE To study the changes in inflammatory factors caused by prostatitis.METHODS SD rats were castrated under sterile conditions.E2 0.25 mg· kg-1+ T 0.25,0.5 and 1.0 mg· kg-1 were given sc for 30 d,respectively.Serum samples were taken and levels of E2,T and dihydrotestosterone (DHT) were detected by ELISA.Pathological changes of prostate tissue were observed by HE staining.The expressions of tumor necrosis factor-alpha (TNF-α),cyclooxygenase-2 (COX-2) and macrophage inflammatory protein 1alpha (MIP-1α) in prostate were detected by immunohistochemistry.RESLULTS ELISA detection showed that E2 levels were significantly increased [(80±7) ng· L-1,P＜0.01] in E2 0.25 mg· kg-1 group and that T levels were significantly decreased [111 ±6 vs (111 ±5) nmol· L-1,P＜0.05]in E20.25 mg ·kg-1 and E2+T 0.25 mg·kg-1 groups compared with the sham-operated group.E2 was significantly increased [(80±7) ng· L-1,P＜0.01] in E20.25 mg· kg-1 groups compared with the castrated control.The sham and castrated control showed normal glandular epithelium without leukocyte infiltration.In E2 0.25 mg·kg-1 group,extensive infiltration of inflammatory cells was found in the glandular lumens,suggesting the occurrence of chronic prostatitis.In each E2+T groups,fewer inflammatory cells were noted in the stroma around glands.The expressions of TNF-m COX-2 and MIP-1α in sham group were negative or low,while those of castrated control and E2 0.25 mg· kg-1 groups were high,especially in E2 0.25 mg· kg-1 group.The expressions of TNF-α,COX-2 and MIP-1α in each E2+T group were significantly decreased.CONCLUSION Testosterone can inhibit prostatitis and the expression of inflammatory factors,such as TNF-α,COX-2 and MIP-1 α,in castrated SD rats initiated by estrogen.

ObjectiveTo investigate the correlation between polymorphism of interleukin(IL)-1β genes and risk and pathological characteristics of gastric cancer in human.MethodsFrom January to December 2010,200 cases of gastric cancer(patient group) and 200 cases of chronic superficial gastritis (control group) were collected.DNA was extracted and IL-1β gene -511,-31,-1473,+3954 site were detected by gene chip technology.The correlation between IL-1β gene -511,-31,-1473,+3954 site and risk and pathological characteristic of gastric cancer was observed.ResultsThe genotype frequency of IL-1β gene -511,-31,-1473,+3954 site was 48.75％(195/400),55.25％(221/400),53.25％(213/400),50.75％ (203/400) in patient group,47.25％ (189/400),53.00％ (212/400),52.50％ (210/400),52.50％ (210/400) in control group,and there was significant difference between two groups (P ＜0.05).While IL-1β gene -511,-31 site T allelic with the lower degree of differentiation of gastric cancer,IL-1 β gene -511,-1473 site T allelic with the early age of gastric cancer.ConclusionsIL-1β gene -511,-31,-1473,+3954 site genotype increase the risk of gastric cancer.IL-1β gene -511,-31 site T allelic are related with the degree of differentiation of gastric cancer.IL-1β gene -511,-1473 site T allelic are related with age of gastric cancer patient.

This paper reviewed the present nursing manager succession planning at home and abroad, covering the succession standard of nursing managers, the content and form of pre-job training, and the evaluation tool of management ability. These efforts aim to provide references for the construction of nursing management talents teams in China.

Objective To evaluate the effect of hydrogen peroxide (H2O2) on a senescence marker protein-30 (SMP30) and an autophagy-related protein microtubule-associated protein 1 light chain 3 type Ⅱ (LC3-Ⅱ) in normal human skin fibroblasts (NHSFs).Methods NHSFs were isolated from the foreskin of children,and subjected to culture in vitro.The second-to fourth-passage NHSFs were treated with 150 μmol/L H2O2 for 2 hours to establish a model for cellular senescence,while un-treated NHSFs served as control group.Senescence-associated β-galactosidase (SA-β-gal) staining was performed to determine the percentage of senescent cells,indirect immunofluorescence assay to determine the expression of the autophagy-related protein LC3,reverse transcription PCR (RT-PCR) to measure the mRNA expression of SMP30,and Western blot analysis to measure the protein expression of SMP30 and LC3.Results The percentage of senescent (SA-β-gal-positive) cells was significantly higher in the H2O2 group than in the control group (41.70％ ± 2.95％ vs.3.03％ ± 0.25％,t =22.59,P ＜ 0.05).Indirect immunofluorescence assay showed that the percentage of LC3-positive cells was significantly lower in the H2O2 group than in the control group (12.60％ ± 1.57％ vs.23.67％ ± 3.04％,t =5.61,P ＜ 0.05).As Western blot analysis showed,no significant difference in the expression of LC3-Ⅰ (LC3-Ⅰ/glyceraldehyde-3-phosphate dehydrogenase [GAPDH] ratio) was observed between the H2O2 group and control group (0.40 ± 0.02 vs.0.41 ± 0.04,P ＞ 0.05),while the H2O2 group showed significantly lower expression of LC3-Ⅱ (LC3-Ⅱ/GAPDH ratio:0.20 ± 0.02 vs.0.80 ± 0.03,t =29.69,P ＜ 0.05) and lower LC3-Ⅱ/LC3-Ⅰ ratio (0.51 ± 0.03 vs.1.98 ± 0.23,t =10.967,P ＜ 0.05) compared with the control group.Moreover,the mRNA and protein expression of SMP30 (SMP30/GAPDH ratio) was significantly lower in the H2O2 group than in the control group (mRNA:0.16 ± 0.01 vs.0.35 ± 0.01;protein:0.27 ± 0.02 vs.0.63 ± 0.02,both P ＜ 0.05).Conclusion H2O2 can decrease the expression of SMP30 and LC3-Ⅱ in NHSFs,and accelerate the senescence of NHSFs.

The mammalian central nervous system (CNS) is considered an immune privileged system as it is separated from the periphery by the blood brain barrier (BBB). Yet, immune functions have been postulated to heavily influence the functional state of the CNS, especially after injury or during neurodegeneration. There is controversy regarding whether adaptive immune responses are beneficial or detrimental to CNS injury repair. In this study, we utilized immunocompromised SCID mice and subjected them to spinal cord injury (SCI). We analyzed motor function, electrophysiology, histochemistry, and performed unbiased RNA-sequencing. SCID mice displayed improved CNS functional recovery compared to WT mice after SCI. Weighted gene-coexpression network analysis (WGCNA) of spinal cord transcriptomes revealed that SCID mice had reduced expression of immune function-related genes and heightened expression of neural transmission-related genes after SCI, which was confirmed by immunohistochemical analysis and was consistent with better functional recovery. Transcriptomic analyses also indicated heightened expression of neurotransmission-related genes before injury in SCID mice, suggesting that a steady state of immune-deficiency potentially led to CNS hyper-connectivity. Consequently, SCID mice without injury demonstrated worse performance in Morris water maze test. Taken together, not only reduced inflammation after injury but also dampened steady-state immune function without injury heightened the neurotransmission program, resulting in better or worse behavioral outcomes respectively. This study revealed the intricate relationship between immune and nervous systems, raising the possibility for therapeutic manipulation of neural function via immune modulation.