Objective To assess the risk of acute myocardial infarction (AMI) and analyze its out‐come by studying the abnormal ECG presentations in AMI patients .Methods The clinical data and ECG presentations of 381 AMI patients were retrospectively analyzed .The abnrmal ECG presentations and the mortalty were comparatively analyzed in AMI patients with multiple lead pathological Q wave ,elevated ST‐segment ,atrial fibrillation (AF) ,bundle branch conduction block ,cardiogenic shock ,and heart failure .Results T he incidence of cardiogenic shock ,heart fail‐ure and the mortality were significantly higher in patients with multiple lead pathological Q wave than in those without multiple lead pathological Q wave (58 .1% vs 21 .4% ,54 .3% vs 23.2% , 40.0% vs 6 .5% ,P<0 .05) and in patients with abnormal presentations such as elevated ST‐seg‐ment and AF than in those without abnormal ECG presentations (P<0 .05 ,P<0 .01) .Conclusion Abnormal ECG presentations ,such as multiple lead pathological Q wave ,can be used as the evi‐dence for the risk and outcome of AMI .

This experiment, using cultured bovine pulmonary artery endothelial cells (BPAEC), was undertaken to investigate roles of endogenous ONOO- in lipopolysaccharide (LPS)-caused injury to endothelial cells. The fluorescent intensity of nitrotyrosine (NT), a marker of ONOO- generation, in BPAEC represented content of endogenous ONOO- generation. The fluorescent intensity of NT and number of NT positive cells were detected with flow cytometry, and the percentage of NT positive cells was calculated. Results were as follows. (1) LPS (1 mg/L, 5 mg/L and 10 mg/L) caused marked increase in fluorescent intensity of NT in a dose dependent manner. The number and percentage of NT positive cells were markedly increased (P＜0.05). Aminoguanidine (AG), a selective inhibitor of inducible nitric oxide synthase, inhibited the increase in fluorescent intensity of NT in BPAEC induced by LPS. However, the number and percentage of NT positive cells had tendency to reduce. (2) LPS caused the enhancement of MDA content and activity of LDH in cultured supernatant (P＜0.01). AG reversed the enhancement of MDA content induced by LPS (P＜0.01). In contrast, AG had marginal effect on activity of LDH. (3) LPS induced the increase in apoptotic rate in BPAEC in a dose dependent manner. Some BPAEC stained with fluorescent probe ethidium bromide showed morphological features of apoptosis with chromatin condensation and nuclear fragmentation. AG reduced the apoptotic rate and number of apoptotic cells, both of which were still higher than those of vehicle group (P＜0.05). (4) LPS inhibited mitochondrial respiration. Effect of LPS on mitochondrial membrane potential (ΔΨ) depended on the doses of LPS. 1 mg/L LPS led to a little increase in ΔΨ, while 5 mg/L and 10 mg/L LPS significantly reduced ΔΨ. In conclusion, LPS caused injury to cultured BPAEC and increased production of ONOO-. Cytotoxicity of LPS may be mediated by endogenous ONOO-.

In this study we found: 1\, There was endogenous ONOO- formation in lungs in the early stage of endotoxic shock. Exogenous ONOO- led to increase in microvascular permeability, severe lung pathological changes and enhanced MDA content. 2\, It was, for the first time, found that responses of isolated pulmonary artery preincubated with ONOO- showed abnormal manifestations. (1) Low dose of ONOO- let to the inhibition of endothelial dependent relaxation, but enhacement of contractile response, both of which were similar to changes of reactivity in isolated pulmonary artery induced by LPS. (2) High dose of ONOO- reduced contractile response to PE and relaxation to SNP. 3\, ONOO- had direct effect for relaxation of precontracted isolated pulmonary artery. The relaxing action of ONOO- was weak and was negtively regulated by endothelial cells, supporting the notion that ONOO- may be involved in pulmonary hypertension in the early stage of endotoxic shock. 4\, It was, for the first time, found that LPS-induced increase in endogenous ONOO- generation in BPAEC and that endogenous ONOO- mediated injury to BPAEC induced by LPS, which may be a novel mechanism for endotoxin-elicited damage to endothelial cells. 5\, Exposure of pulmonary artery to LPS led to reduction in endothelial dependent relaxation but enhancement in contractile response, both of which were reversed by concomitant exposure to CCK and LPS. 6\, CCK protected cultured BPAEC against the detrimental effects of LPS such as lipoperoxide damages and cellular apoptosis as well as LPS-induced endogenous ONOO- formation. The underlying mechanism of CCK for cytoprotection may be mediated by its receptors and related to its reduced ability of endothelia to generate ONOO- induced by LPS.

Our previous experiments confirmed that endothelial derived ONOO- mediated injury to cultured BPAEC induced by LPS, and that CCK protected endothelial functions against the detrimental effect of LPS in vitro. In the present study, using cultured BPAEC, we investigated effect of CCK on LPS-induced generation of ONOO- in BPAEC and on injury to BPAEC induced by LPS. Results were as follows.(1)CCK inhibited increase in endothelial generation of ONOO- induced by LPS, for fluorescent intensity of NT in BPAEC reduced from (6.55±0.30) AU of LPS group to (4.37±0.08) AU (P＜0.01), the latter being still higher than (3.27±0.15) AU of vehicle group (P＜0.01). In contrast, the number and percentage of NT positive cells reduced a little. Proglumide, a nonspecific inhibitor of CCK receptors, might in part reverse the effect of CCK. (2)CCK markedly reduced MDA content in supernatant in LPS group (P＜0.01), which was completely reversed by proglumide(P＜0.01). Activities of LDH in supernatant in LPS, LPS+CCK group were (85.30±8.66) U/L and (71.33±4.07) U/L, respectively. Proglumide elicited increase in activity of LDH ［(81.00±6.35) U/L］. However, effect of CCK or proglumide was not significant in the alterations of activity of LDH. (3)CCK significantly inhibited increase in apoptotic rate in BPAEC induced by LPS, from 13.50%±0.60% of LPS group to 5.35%±0.25%(P＜0.001), the latter being completely reversed by proglumide with apoptotic rate of 11.45%±0.65%(P＜0.05).These results further confirmed that CCK afforded the cyoprotection for the mitigation lipoperoxide damage and inhibition of apoptosis in BPAEC induced by LPS. The cytoprotection of CCK may be mediated by CCK receptors and related to the reductive ability of endothelia to generate ONOO- induced by LPS.

Conditions for the preparation of apricot kernel oil emulsion were studied. The experimental results showed that with the use of S15 Emulphor as the main emulsifier,at a temperature of 40~60℃,and agitated for three times at a speed of 1000~1200r/min,the resulted oil in water apricot kernel oil emulsion had a satisfactory stability,with disperse phase particle size of ≤10?m and easily absorbable by human body.

Objective To investigate the values of serum vascular endothelial growth factor (VEGF) ,carcinoembryonic antigen (CEA) ,carbohydrate antigen 19-9 (CA19-9) and ferritin (SF) determination in assessing the efficacy of chemotherapy in patients with advanced gastric cancer .Methods Wedetermined the concentrations of serum VEGF ,CEA ,CA19-9 and SF for 85 patients with advanced gastric cancer ,before and after 1 cycles of chemotherapy and evaluated the the effect of chemotherapy after 2 cycle of chemotherapy .Results In effective group ,serum concentrations of VEGF ,CEA ,CA19-9 and SF significantly decreased after chem-otherapy cycle(P< 0 .05) ,serum VEGF and CEA concentrations significantly increased in progress group (P< 0 .05) ,serum VEGF ,CEA ,CA19-9 and SF concentrations in stable group and serum CA19-9 and SF concentrations in progress group did not change significantly(P> 0 .05) ,compared with those before chemotherapy cycle .Multiple regression analysis showed that serum CEA ,VEGF ,CA19-9 concentration changes correlated with chemotherapy efficiency ,while serum SF didn′t(t=1 .58 ,P=0 .119) . Conclusion Serum CEA ,VEGF ,CA19-9 concentration changes associated with gastric cancer chemotherapy efficiency ,which help predict the efficiency of chemotherapy .

Objective To study the possible role of cytokines interleukin-1beta(IL-1?),interleukin-6(IL-6),interleukin-8(IL-8),tumor necrosis factor alpha(TNF-?)and granulocyte macrophage colony stimulating factor(GM-CSF)in the pathogenesis of vitiligo.Methods The serum levels of IL-?,IL-6,IL-8,TNF-?,and GM-CSF were measured in50patients with vitiligo and20healthy volunteers with radioimmunoassay.Results The serum level of IL-6and GM-CSF in focal type and generalized type of vitiligo,and the serum level of IL-1?in generalized type were significantly higher than those in normal controls.In segmental type of vitiligo,the serum levels of all the cytokines tested were not significantly different from those in normal controls.The GM-CSF levels in focal type and generalized type,and the IL-6level in generalized type of the progressive stage were significantly higher than those in the stable stage.Conclusion IL-6and GM-CSF may be involved in the autoimmune mechanism of non-segmental type of vitiligo.

Objective To investigate the combined detection of serum vascular endothelial growth factor (VEGF),squamous cell carcinoma antigen (SCC-Ag)and cytokeratin 19 fragment (CYFRA21-1)value in assessing the efficacy of chemotherapy in patients with advanced squamous cell carcinoma of the lung.Methods 60 cases of lung squamous cell carcinoma patients in January 2011 between June 2013 to be admitted to hospital were treated with gemcitabine plus cisplatin or carboplatin chemotherapy.Detected the levels of serum VEGF,SCC-Ag and CYFRA21-1 expression in 60 cases before and after 1 cycle of chemotherapy in patients using ELISA and immunoradiometric assay,and evaluated the efficacy evaluation with reference to RECIST criteria after 2 cycle of chemotherapy.Results Effective group serum VEGF and CYFRA21-1 levels were 413± 114 pg/ml and 14.7±9.6 ng/ml;serum VEGF and CYFRA21-1 levels after one cycle of chemotherapy were 272±131 pg/ml and 10.8±7.1 ng/ml,which decreased after chemotherapy (P<0.01).Progress group serum VEGF and CYFRA21-1 levels were 472±207 pg/ml and 18.9±17.6 ng/ml;serum VEGF and CYFRA21-1 levels after one cycle of chemotherapy were 537±219 pg/ml and 21.5±20.2 ng/ml,which increased after chemotherapy (P<0.01).Stable group serum VEGF CYFRA21-1 levels and were 419±246 pg/ml and 17.0±12.9 ng/ml;serum VEGF and CYFRA21-1 levels after one cycle of chemotherapy were 421±252 pg/ml and 16.8±11.7 ng/ml,which had no changes before and after treatment (P>0.05). Serum SCC-Ag levels before and after each treatment group difference was not statistically significant (P>0.05).Multiple regression analysis showed that serum VEGF,CYFRA2 1-1 levels and the efficacy of lung squamous were related changed (t=5.86,P<0.001;t=2.26,P=0.027),and there was no significant correlation between SCC-Ag levels changes and the effect of chemotherapy (t=1.52,P=0.133).Conclusion Serum VEGF and CYFRA21-1 expression level changes associat-ed with squamous cell carcinoma of the lung chemotherapy effect,which can advance understanding of the effect of chemo-therapy,combined with advanced squamous cell carcinoma detection of serum VEGF and chemotherapy assessment CY-FRA2 1-1 has a certain reference value.

Objective To translate the Venous Leg Ulcer Quality of life Questionnaire (VLU-QoL) into Chinese and evaluate the reliability and validity of Chinese version.Methods VLU-QoL was translated into Chinese according to the standards setted by ISPOR.Totally 232 patients with venous leg ulcer were recruited and investigated by the Chinese version of VLU-QoL.Results The Chinese version of VLU-QoL comprised 34 items,Cronbach α was 0.940,inter-rater reliability was 0.841;test-retest reliability was 0.825.I-CVI was 0.83-1.00,S-CVI/Ave was 0.955;Criterion-related validity were 0.714 and 0.541;factor analysis got 3 factors,which explained 54.367％ of the total variance.Conclusions The Chinese version of VLU-QoL has been proved to be reliable and valid.It can be used as a valid tool for the measurement of quality of life for patients with venous leg ulcer.

Objective To explore the prognostic factor by analyzing clinical characters, pathologic features and treatment methods of thymic carcinoma. Methods From January 2000 to Deceber 2011, 71 patients received re-section of thymic carcinoma. They were analyzed retrospectively based on Masaoka stage(stageII 7,stageIII 33, stageIV 31). The clinical factors included histological classification, Masaoka stage, treatment and prognosis. Sur-vival rate was calculated and the survival curve was plotted by Kaplan-Meimer and Log-Rank method, Multi-analy-sis was carried out by COX regression. Results For these patients, the median survival time was 57. 2 months, the 5-year survival rate was 47. 9%. 25 patients received complete resection with 5-years survival rate 68%, 46 patients received partial resection with 5-years survival rate 36. 9%. 41 patients whose lump size was greater than or equal to 8 cm with 5-years survival rate 53. 6%, 40% with lower than 8 cm. Histology Masaoka staging with 5-years survival rate was stage II(57. 1%) , stage III(69. 7%) and stage IV(29. 0%) , respectively. Defferent his-tological type with 5-years survival rate squamous carcinoma(55. 1%) , adenocarcinoma (14. 3%) ,small cell car-cinoma ( 28. 6%) , adenosquamous carcinoma ( 33. 3%) , and carcinoid ( 100%) , respectively. The operation method, the maximum diameter, mass Masaoka stage and different pathology types for survival were statistically dif-ferent (P<0. 05). Preoperative treatment, postoperative radiotherapy and differentiation degree of survival had no statistical difference. Conclusion Surgical method, lump size, masaoka stage and histological type are the impor-tant factors affecting prognosis. Adjuvant radiotherapy maybe is not the poor prognosis factor of thymic tumors. Sur-gical method and lump size are the significant independent prognostic factors in patients with thymic tumors.