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1Effect of cholecystokinin on cytokines during endotoxic shock in rats显示文摘AIM To study the effect of cholecystokinin-octapeptide (CCK-8) on systemic hypotension and cytokine production in lipopolysaccharide (LPS)-induced endotoxic shock (ES) rats.``METHODS The changes of blood pressure were observed using physiological record instrument in four groups of rats: LPS (8 mg. kg-1, iv) induced ES; CCK-8 (40 μg.kg- 1 iv) pretreatment 10 min before LPS (8 mg. kg- 1);CCK-8 (40 μg.kg-1, iv) or normal saline (control) groups.Differences in tissue and circulating specificity of the proinflammatory cytokines (TNF-a, IL-l3 and IL-6) were assayed with ELISA kits.``RESULTS CCK-8 reversed LPS-induced decrease of mean artery blood pressure (MABP) in rats. Compared with control, LPS elevated the serum level of IL-6 significantly (3567_-687 ng.L-1 vs 128_+22 ng.L-1, P<0.01), while contents of TNF-a and IL- lβ elevated significantly (277 _± 86ng.L-1 vs not detectable and 43 ± 9 ng.L-1 vs notdetectable, P<0.01) but less extent than IL-6, CCK-8significantly inhibited the LPS-induced increase in serum TNF-a, IL-lβ and IL-6. LPS elevated spleen and lung content of IL-Iβ significantly (5184 ± 85 ng.L-1 vs 1047 ±21 ng.L-1 and 4050 ± 614 ng.L-1 vs not detectable,P<0,01). while levels of TNF-a and IL-6 also rosesignificantly but in less extent than IL-lβ. CCK-8 inhibited the LPS-induced increase of the cytokines in spleen and lung. in the heart, CCK-8 significantly inhibited LPS.induced increase of TNF-a (864 ± 123 ng. L-1 in CCK-8 +LPS group vs 1599_-227 ng-L-1 in LPS group, P<0.01),and IL-lβ (282 ± 93 ng-L-1 in CCK-8 + LPS group vs 621 ±145 ng.L-1 in LPS group, P<0.01).``CONCLUSION CCK-8 reverses ES, which may be relatedto its inhibitory effect on the overproduction of cytokines.Yi-Ling Ling~1 Ai-Hong Meng~1 Xiao-Yun Zhao~1 Bao-En Shan~2 Jun-Lan Zhang~1 Xiao-Peng Zhang~3 1 Department of Pathophysiology,Hebei Medical University,Shijiazhuang 050017,Hebei Province,China2 Research Center of Fourth Hospital,Hebei Medical University,Shijiazhuang 050000,Hebei Province,China3 Department of Chest Surgery of Hebei Provincial People’s Hospital,Shijiazhuang 050000,Hebei Province,China 2001World Journal of Gastroenterology2001,7,5:31
2Effect of cholecystokinin octapeptide on tumor necrosis factor α transcription and nuclear factor-κB activity induced by lipopolysaccharide in rat pulmonary interstitial macrophages显示文摘AIM: To elucidate the anti-inflammatory mechanism ofan intestinal neuropeptide, sulfated cholecystokininoctapeptide (sCCK-8), the effects of sCCK-8 onlipopolysaccharide (LPS)-induced tumor necrosis factorpulmonary interstitial macrophages (PIMs) werestudied.METHODS: PIMs from rat were stimulated with LPS(:1mg @ L-1) in the presence or absence of sCCK-8 (10-8-:10-6mol@ L-1) or/and CCK receptor antagonistproglumide (2 mg @ L-1). The expression of TNF-α mRNAwas assayed by reverse transcription polymerase chainreaction (RT-PCR) at 3h of the stimulation, and nuclearelectrophoretic mobility shift assay (EMSA) at 1 h ofat 30 min of the stimulation was detected by Westernblot.RESULTS: sCCK-8, at concentrations from 10-8 mol @ L-1to 10-6 mol @ L-1 obviously inhibited LPS-induced TNF-αdependent manner, P<0.05, P<0.01. Stimulation PIMsP<0.01, which was elevated by sCCK-8, P<0.05. Thewere attenuated by CCK receptor antagonistproglumide, P<0.01.CONCLUSION: sCCK-8 inhibits LPS-induced TNF-α mRNAwhich is mediated through CCK receptors and inhibitinginflammatory mechanisms of sCCK-8.Bin Cong Shu-Jin Li Yi-Ling Ling Department of Pathophysiology,Hebei Medical University,Shijiazhuang 050017,Hebei Province,China Yu-Xia Yao Molecular Biological Laboratory,Hebei Medical University,Shijiazhuang 050017,Hebei Province,China Gui-jun Zhu Department of chest surgey,The Fourth Hospital,Hebei Medical University,Shijiazhuang 050017,Hebei Province,China 2002World Journal of Gastroenterology2002,8,4:31
3CCK-8 inhibits expression of TNF-α in the spleen of endotoxic shock rats and sigual transduction mechanism of p38 MAPK显示文摘AIM:To study the effect of sulfated cholecystokinin-octapeptide(CCK-8)on systemic hypotension,gene andprotein expression of TNF-α in spleen of lipopolysaccharide(LPS)-induced endotoxic shock(ES)rats,and furtherinvestigate the signal transduction mechanism of p38mitogen-activated protein kinase(MAPK).METHODS:The changes of blood pressure were observedusing physiological record instrument in four groups of rats:LPS(S mg·kg^(-1),iv),CCK-8(40μg·kg^(-1),iv)pretreatment10 rain before LPS(8 mg·kg^(-1)),CCK-8(40μg·kg^(-1),iv)ornormal saline(control)group.The content of TNF-αinspleen was assayed 2 h after LPS administration usingELISA kit and the expression of TNF-α mRNA was examined30 min,2 h and 6 h after LPS administration by reversetranscribed polymerase chain reaction(RT-PCR).Activationof p3S MAPK was detected with Western blot 30 min afterLPS administration.RESULTS:CCK-8 reversed LPS-induced decrease of meanarterial pressure(MAP)in rats.The content of TNF-α inspleen was(282±30)ng·L^(-1)in control group,while itincreased to(941±149)ng·L^(-1)in LPS group,P<0.01.CCK-8 significantly inhibited the LPS-induced increase ofTNF-α content in spleen.It decreased to(462±87)ng·L^(-1)inCCK-8+LPS group,P<0.01.The expression of TNF-αmRNA 30 min and 2 h after treatment was stronger in LPSgroup,while it was lowered after CCK-8 pretreatment.Thep38 MAPK expression increased significantly in LPS group(5.84 times of control)and CCK-8 increased the activationof p38 MAPK in ES rats(10.74 times of control).CONCLUSION:CCK-8 reverses the decrease of MAP in ESrats and has inhibitory effect on the gene and proteinexpression of TNF-α in spleen,and p38 MAPK may beinvolved in its signal transduction mechanisms.Ai-Hong Meng Yi-Ling Ling Xiao-Yun Zhao Jun-Lan Zhang Department of Pathophysiology,Hebei Medical University,Shijiazhuang 050017,Hebei Province,China Xiao-Peng Zhang Department of Chest Sugery of Hebei Provincial People’s Hospital,Shijiazhuang 050000,China 2002World Journal of Gastroenterology2002,8,1:19
4Overexpression of cyclin Y in non-small cell lung cancer is associated with cancer cell proliferation显示文摘Cyclin Y (CCNY) is a key cell cycle regulator that acts as a growth factor sensor to integrate extracellular signals with the cell cycle machinery. The expression status of CCNY in lung cancer and its clinical significance remain unknown. The data indicates that CCNY may be deregulated in non-small cell lung cancer, where it may act to promote cell proliferation. These studies suggest that CCNY may be a candidate biomarker of NSCLC and a possible therapeutic target for lung cancer treatment.YUE WenTao1, ZHAO XiaoTing1, ZHANG LiNa1, LIU ZhiDong2, MA Li1, JIA WenYun1, QIAN Zhe1, ZHANG ChunYan1, WANG Yue1, YANG XueHui1 & XU ShaoFa2 1 Department of Cellular Biology, Beijing Chest Hospital, Capital Medical University, Beijing, 101149, China 2 Department of Thoracic Surgery, Beijing Chest Hospital, Capital Medical University, Beijing, 101149, China 2010Science China(Life Sciences)2010,53,4:10
5低剂量环索奈德与固定剂量丙酸氟替卡松沙美特罗联合制剂对支气管哮喘长期控制效果的比较显示文摘研究背景:轻度持续性支气管哮喘(简称哮喘)约占哮喘患者的70%,对于轻度哮喘选择最好的一线治疗十分重要。我们比较了以环索奈德和丙酸氟替卡松/沙美特罗联合制剂作为轻度哮喘的一线治疗的效果。方法:纳入12~75岁轻度持续性哮喘患者1432例进行随机、Dirkje SP Paul MO Soren P. Chest 刘国梁 2011中华结核和呼吸杂志2011,34,9:5
6The Relationships between cyclin D1 Expression and Prognosis of Non-small Cell Lung Cancer显示文摘Background and objective cyclin D1 is a member of the cyclin family,and it has been proven that it plaied an important role in tumorigenesis,invasion and metastasis.We performed a retrospective study on the cyclin D1 expression in non-small cell lung cancer (NSCLC) according to the clinical characteristics.Methods One hundred fifteen postsurgical NSCLC patients were investigated.Immunohistochemistry was used to evaluate the cyclin D1 expression.Results Overall survival was significantly lower in patients with cyclin D1-high expression of tumors than those with cyclin D1 low expression of tumors (χ2=5.132,P=0.023).In early stage patients (stage I,II),the overall survival was significantly lower in patients with cyclin D1-high expression of tumors than those with cyclin D1-low expression of tumors (χ2=6.863,P=0.009).cyclin D1 status (hazard ratio=0.630;P=0.035),differentiation (hazard ratio=0.399;P<0.001),and pTNM (hazard ratio=1.576;P<0.001) to be independent prognostic factors for NSCLC patients.Specifically,the cyclin D1 status (hazard ratio=0.188;P=0.008) was a significant prognostic factor for patients with stage I NSCLCs.Conclusion cyclin D1 expression is an independent prognosis factor for postoperative patient in stage I,II NSCLCs.Jiping ZHU1,Like YU1,Ping ZHAN2,Yong SONG2,Qin WANG3 1Department of Respiratory Medicine,Nanjing Chest Hospital,Nanjing 210029,China 2Department of Respiratory Medicine,Jinling Hospital,Nanjing University School of Medicine,Nanjing 210001,China 3Department of Respiratory Medicine,81 Hospital of PLA,Nanjing 210002,China 2010中国肺癌杂志2010,13,8:3
7Definition for sepsis and organ failure and guideline for the use of innovative therapies in sepsis显示文摘Menbers of the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference 1992Crit Care Med1992,20,:2
8Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis显示文摘AMERICAN COLLEGE OF CHEST PHYSICIAN/SOCIETY OF CRITICAL CARE MEDICINE CONSENSUS 1992Crit Care Med1992,20,:1
9Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis显示文摘American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference 1992Crit Care Med1992,20,6:1
10Definitions for sepsis and organ faiture and guidelines in sepsis 显示文摘American College of Chest Physicians/Society of Critical Care Medi- cine Consensics Conference Committee ACCP/SCCM Consensus Committee 1992Crit Care Med1992,20,:1
11American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference:Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis显示文摘Members of the American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference Committee 1992Crit Care Med1992,20,:1
12A double- blind pla-cebo- controlled clinical trial of three anti-tuberculosis chemo-prophylaxis regimens in patients with silicosis in Hong Kong显示文摘Hong Kong Chest Service Tuberculosis Research Centre Ma-dras British Medical Research Council 1992Am Rev Respir Dis1992,145,:1
13Evidence - based guidelines for weaning and discontinuing ventilator support 显示文摘A Collective Task Force Facilitated By the American College Of Chest Physicians the American Association for Respiratory Care and the American College of Critical Care Medicine 2001Chest2001,120,6:1
14Management of small cell lung cancer: ACCP evidence-based clinical practice guidelines (2nd edition) 显示文摘Simon GR Turrisi A American College of Chest Physicians 2007Chest2007,132,3:1
15Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis显示文摘American College of Chest Physiciano Society of Critical Care Medicine Consensus Conference 1992Crit Care Med1992,20,6:1
16Definitions for sepsis and organ failure and guide- lines for the use of innovative therapies in sepsis 显示文摘American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference 1992Crit Care Med1992,20,6:1
17Critical care medicine conference显示文摘American College of Chest Physician So- ciety 1992Chest1992,101,6:1
18Definitions for sepsis and multiple organ failure and guidelines for the use of innovative therapies in sepsis显示文摘American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference 1992Crit Care Med1992,20,6:1
19American Col- lege of Chest Physicians/Society of Critical Care Medicine Consen?sus Conference: definitions for sepsis and organ failure and guide?lines for the use of innovative therapies in sepsis显示文摘Memebers of the American College of Chest Physicians/Society of Crit Care Med Consensus Conference Committee 1992Crit Care Med1992,20,6:1
20Management of small cell lung cancer:ACCP evidence-based clinical practice guidelines (2nd edition)显示文摘Simon GR Turrisi A American College of Chest Phy-sicians 0,,3:1
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