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韩-薛-柯氏综合征1例
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作者 马玉新 白海平 +3 位作者 李增生 余俐 张锦宏 孙纪民 《西北国防医学杂志》 CAS 1998年第1期19-19,共1页
韩-薛-柯氏综合征1例马玉新1白海平1李增生1余俐1张锦宏1孙纪民2关键词综合征网状内皮细胞系疾病诊治中国图书资料分类法分类号R442.8患者,男,7岁。发现左颞部一蚕豆大包块4月余。2月前增大至2cm×2cm,... 韩-薛-柯氏综合征1例马玉新1白海平1李增生1余俐1张锦宏1孙纪民2关键词综合征网状内皮细胞系疾病诊治中国图书资料分类法分类号R442.8患者,男,7岁。发现左颞部一蚕豆大包块4月余。2月前增大至2cm×2cm,无疼痛。头颅CT检查示左颞骨结节待查,... 展开更多
关键词 综合征 网状内皮细胞疾病 诊治
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Anges MG/Goodman的涂膜支架
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作者 金伟秋 《国外药讯》 2003年第9期10-11,共2页
关键词 AngesMG Goodman 涂膜支架 NF—kappa B 内皮细胞疾病 控制
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Human hepatic sinusoidal endothelial cells can be distinguished by expression of phenotypic markers related to their specialised functions in vivo 被引量:13
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作者 PF Lalor SM Curbishley +1 位作者 S Shetty DH Adams 《World Journal of Gastroenterology》 SCIE CAS CSCD 2006年第34期5429-5439,共11页
The hepatic sinusoids are lined by a unique population of hepatic sinusoidal endothelial cells (HSEC), which is one of the first hepatic cell populations to come into contact with blood components. However, HSEC are n... The hepatic sinusoids are lined by a unique population of hepatic sinusoidal endothelial cells (HSEC), which is one of the first hepatic cell populations to come into contact with blood components. However, HSEC are not simply barrier cells that restrict the access of blood- borne compounds to the parenchyma. They are func- tionally specialised endothelial cells that have complex roles, including not only receptor-mediated clearance of endotoxin, bacteria and other compounds, but also the regulation of inflammation, leukocyte recruitment and host immune responses to pathogens. Thus understand- ing the differentiation and function of HSEC is critical for the elucidation of liver biology and pathophysiology. This article reviews methods for isolating and studying human hepatic endothelial cell populations using in vitro models. We also discuss the expression and functions of phe- notypic markers, such as the presence of fenestrations and expression of VAP-1, Stabilin-1, L-SIGN, which can be used to identify sinusoidal endothelium and to permit discrimination from vascular and lymphatic endothelial cells. 展开更多
关键词 HUMAN Liver ENDOTHELIUM SINUSOID PHENOTYPE
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Immortalization of human umbilical vein endothelial cells with telomerase reverse transcriptase and simian virus 40 large T antigen 被引量:7
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作者 边昶 赵葵 +2 位作者 童国新 朱永良 陈鹏 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE EI CAS CSCD 2005年第7期631-636,共6页
Objective: To establish normally conditionally-immortalized human umbilical vein endothelial cells (HUVECs) by ectopic expression of the human telomerase catalytic enzyme (hTERT) and simian virus 40 large T (SV40 LT) ... Objective: To establish normally conditionally-immortalized human umbilical vein endothelial cells (HUVECs) by ectopic expression of the human telomerase catalytic enzyme (hTERT) and simian virus 40 large T (SV40 LT) antigen. Methods:Primary HUVECs were transfected with recombinant retrovirus containing hTERT or SV40 LT respectively. Subsequently drug resistant cell clones were screened and expanded for further studies. Endothelial cell biomarkers were confirmed by examination.Results: The morphological phenotype of the transfected cells was similar to the non-transfected cells. Von Willebrand factor,hTERT and SV40 LT could be detected in transfected HUVECs. Moreover, higher telomerase activity in transfected cells was maintained for over 50 population doublings compared with only low level of endogenous telomerase transiently at early population doublings in primary HUVECs. When exposed to TNF-α (tumor necrosis factor-α), the expression of E-selectin in transfected cells was significantly up-regulated, but no alteration of endothelial lipase was found. Conclusion: Ectopic coexpression of hTERT and SV40 LT can effectively immortalize HUVECs without tumorigenicity in vitro. Immortalized HUVECs may be an ideal target of further molecular function studies. 展开更多
关键词 Endothelial cell Telomerase activity IMMORTALIZATION
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Thalidomide effect in endothelial cell of acute radiation proctitis 被引量:10
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作者 Ki-Tae Kim Hiun-Suk Chae +6 位作者 Jin-Soo Kim Hyung-Keun Kim Young-Seok Cho Whang Choi Kyu-Yong Choi Sang-Young Rho Suk-Jin Kang 《World Journal of Gastroenterology》 SCIE CAS CSCD 2008年第30期4779-4783,共5页
AIM: To determine whether thalidomide prevents microvascular injury in acute radiation proctitis in white rats. METHODS: Fourteen female Wistar rats were used: six in the radiation group, six in the thalidomide group,... AIM: To determine whether thalidomide prevents microvascular injury in acute radiation proctitis in white rats. METHODS: Fourteen female Wistar rats were used: six in the radiation group, six in the thalidomide group, and two in normal controls. The radiation and thalidomide groups were irradiated at the pelvic area using a single 30 Gy exposure. The thalidomide (150 mg/kg) was injected into the peritoneum for 7 d from the day of irradiation. All animals were sacrificed and the rectums were removed on day 8 after irradiation. The microvessels of resected specimens were immunohistochemically stained with thrombomodulin (TM), von Willebrand Factor (vWF), and vascular endothelial growth factor (VEGF). RESULTS: The microscopic scores did not differ significantly between the radiation and thalidomide groups, but both were higher than in the control group. Expression of TM was significantly lower inthe endothelial cells (EC) of the radiation group than in the control and thalidomide groups (P < 0.001). The number of capillaries expressing vWF in the EC was higher in the radiation group (15.3 ± 6.8) than in the control group (3.7 ± 1.7), and the number of capillaries expressing vWF was attenuated by thalidomide (10.8 ± 3.5, P < 0.001). The intensity of VEGF expression in capillaries was greater in the radiation group than in the control group and was also attenuated by thalidomide (P = 0.003). CONCLUSION: The mechanisms of acute radiation- induced proctitis in the rats are related to endothelial cell injury of microvessel, which may be attenuated with thalidomide. 展开更多
关键词 Radiation proctitis Von Willebrand factor THROMBOMODULIN Vascular endothelial growth factor THALIDOMIDE
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Role of the endothelium in inflammatory bowel diseases 被引量:11
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作者 Walter E Cromer J Michael Mathis +2 位作者 Daniel N Granger Ganta V Chaitanya J Steven Alexander 《World Journal of Gastroenterology》 SCIE CAS CSCD 2011年第5期578-593,共16页
Inflammatory bowel diseases(IBD) are a complex group of diseases involving alterations in mucosal immunity and gastrointestinal physiology during both initiation and progressive phases of the disease.At the core of th... Inflammatory bowel diseases(IBD) are a complex group of diseases involving alterations in mucosal immunity and gastrointestinal physiology during both initiation and progressive phases of the disease.At the core of these alterations are endothelial cells,whose continual adjustments in structure and function coordinate vascular supply,immune cell emigration,and regulation of the tissue environment.Expansion of the endothelium in IBD(angiogenesis),mediated by inflammatory growth factors,cytokines and chemokines,is a hallmark of active gut disease and is closely related to disease severity.The endothelium in newly formed or inflamed vessels differs from that in normal vessels in the production of and response to inflammatory cytokines,growth factors,and adhesion molecules,altering coagulant capacity,barrier function and blood cell recruitment in injury.This review examines the roles of the endothelium in the initiation and propagation of IBD pathology and distinctive features of the intestinal endothelium contributing to these conditions. 展开更多
关键词 MICROVASCULATURE ENDOTHELIUM Inflamma-tion Nitric oxide Adhesion molecules Crohn's disease Ulcerative colitis CYTOKINES CHEMOKINES Growth factors
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Involvement of interleukin-15 and interleukin-21, two γ-chain-related cytokines, in celiac disease 被引量:3
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作者 Daniela De Nitto Ivan Monteleone +2 位作者 Eleonora Franzè Francesco Pallone Giovanni Monteleone 《World Journal of Gastroenterology》 SCIE CAS CSCD 2009年第37期4609-4614,共6页
Celiac disease (CD), an enteropathy caused by dietary gluten in genetically susceptible individuals, is histologically characterized by villous atrophy, crypt cell hyperplasia, and increased number of intra-epithelial... Celiac disease (CD), an enteropathy caused by dietary gluten in genetically susceptible individuals, is histologically characterized by villous atrophy, crypt cell hyperplasia, and increased number of intra-epithelial lymphocytes. The nature of CD pathogenesis remains unclear, but recent evidence indicates that both innate and adaptive immune responses are necessary for the phenotypic expression and pathologic changes characteristic of CD. Extensive studies of molecules produced by immune cells in the gut of CD patients have led to identification of two cytokines, namely interleukin (IL)-15 and IL-21, which are thought to play a major role in orchestrating the mucosal inflammatory response in CD. Here we review the current knowledge of the expression and function of IL-15 and IL-21 in CD. 展开更多
关键词 INTERLEUKIN-21 INTERLEUKIN-15 Celiac disease
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VASCULAR ENDOTHELIAL INJURIES AND CHANGES OF BLOOD COAGULATION AND FIBRINOLYSIS INDEXES IN PATIENTS WITH ACUTE RESPIRATORY DISTRESS SYNDROME 被引量:4
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作者 Xiao-linHe ZhiLiu Shu-yueXia 《Chinese Medical Sciences Journal》 CAS CSCD 2004年第4期252-256,共5页
Objective To study endothelial damage by observing changes of circulating endothelial cells (CECs) in blood, coagula-tion and fibrinolysis index in patients with acute respiratory distress syndrome. Methods CECs were ... Objective To study endothelial damage by observing changes of circulating endothelial cells (CECs) in blood, coagula-tion and fibrinolysis index in patients with acute respiratory distress syndrome. Methods CECs were separated by isopycnic centrifugation method in 14 patients with acute lung injury (ALI), 7 patients with acute respiratory distress syndrome (ARDS), 10 intensive care unit (ICU) controls, and 15 healthy controls. Plasma prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (FG), fibrin degradation products (FDP), and D-dimer were examined simultaneously. Acute physiology and chronic health evaluation (APACHE)Ⅱand lung injury score (LIS) were recorded to evaluate severity of illness and lung injury. Results (1) The number of CECs in ALI (10.4 ±2.3) and ARDS groups (16.1 ±2.7) was higher than that in the healthy (1.9 ±0.5) (P< 0.01). In both ALI and ARDS, the number of CECs correlated with APACHEⅡ(r=0.55, P< 0.05 and r=0.62, P< 0.05, respectively)and LIS (r=0.60, P< 0.05 and r=0.53, P< 0.05, respectively). CEC number was negatively correlated with PaO 2 in ALI and ARDS (r=-0.49, P< 0.05 and r=-0.64, P< 0.05, respectively). (2) The level of FDP and D-dimer were higher in ALI and ARDS patients than that in ICU and healthy control groups (P< 0.05). The level of FG in ARDS group was significantly higher than in the ICU and healthy control groups (P< 0.05). But in ALI group, the level of FG was significantly higher than only healthy control group (P< 0.05). Conclusions Endothelial cell damage occurs in ARDS patients, which may play a major role in the pathophysiology of ARDS. Changes of endothelial cell activation and damage markers, such as CECs, plasma coagulation and fibrinolysis index, to some extent reflect severity of illness and lung injury in ARDS. 展开更多
关键词 acute respiratory distress syndrome endothelial cell FIBRINOGEN FIBRIN D-DIMER
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Common immunologic mechanisms in inflammatory bowel disease and spondylarthropathies 被引量:7
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作者 Massimo C Fantini Francesco Pallone Giovanni Monteleone 《World Journal of Gastroenterology》 SCIE CAS CSCD 2009年第20期2472-2478,共7页
Spondyloarthropathies (SPA) are commonly observed extra-intestinal manifestations of both Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of inflammatory bowel diseases ([BD). However, t... Spondyloarthropathies (SPA) are commonly observed extra-intestinal manifestations of both Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of inflammatory bowel diseases ([BD). However, the immunological link between these two clinical entities is still poorly understood. Several lines of evidence indicate that SpA may originate from the relocation to the joints of the immune process primarily induced in the gut. The transfer of the intestinal inflammatory process into the joints implicates that immune cells activated in the gut-draining lymph nodes can localize, at a certain point of the intestinal disease, either into the gut or into the joints. This is indicated by the overlapping expression of adhesion molecules observed on the surface of intestinal and synovial endothelial cells during inflammation. Moreover bacterial antigens and HLA-B27 expression may be implicated in the reactivation of T cells at the articular level. Finally, accumulating evidence indicates that a T helper 17 cell-mediated immune response may contribute to IBD and IBD-related SpA with a crucial role played by tumor necrosis factor-α in CD and to a lesser extent in UC. 展开更多
关键词 Cell adhesion molecules ANTIGENS TH17 Helper T-cells Tumor necrosis factor-α
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Microscopic colitis 被引量:5
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作者 Gianluca Ianiro Giovanni Cammarota +4 位作者 Luca Valerio Brigida Eleonora Annicchiarico Alessandro Milani Massimo Siciliano Antonio Gasbarrini 《World Journal of Gastroenterology》 SCIE CAS CSCD 2012年第43期6206-6215,共10页
Microscopic colitis may be defined as a clinical syndrome, of unknown etiology, consisting of chronic watery diarrhea, with no alterations in the large bowel at the endoscopic and radiologic evaluation. Therefore, a d... Microscopic colitis may be defined as a clinical syndrome, of unknown etiology, consisting of chronic watery diarrhea, with no alterations in the large bowel at the endoscopic and radiologic evaluation. Therefore, a definitive diagnosis is only possible by histological analysis. The epidemiological impact of this disease has become increasingly clear in the last years, with most data coming from Western countries. Microscopic colitis includes two histological subtypes [collagenous colitis (CC) and lymphocytic colitis (LC)] with no differences in clinical presentation and management. Collagenous colitis is characterized by a thickening of the subepithelial collagen layer that is absent in LC. The main feature of LC is an increase of the density of intra-epithelial lymphocytes in the surface epithelium. A number of pathogenetic theories have been proposed over the years, involving the role of luminal agents, autoimmunity, eosinophils, genetics (human leukocyte antigen), biliary acids, infections, alterations of pericryptal fibroblasts, and drug intake; drugs like ticlopidine, carbamazepine or ranitidine are especially associated with the development of LC, while CC is more frequently linked to cimetidine, non-steroidal antiinflammatory drugs and lansoprazole. Microscopic colitis typically presents as chronic or intermittent watery diarrhea, that may be accompanied by symptoms such as abdominal pain, weight loss and incontinence. Recent evidence has added new pharmacological options for the treatment of microscopic colitis:the role of steroidal therapy, especially oral budesonide, has gained relevance, as well as immunosuppressive agents such as azathioprine and 6-mercaptopurine. The use of anti-tumor necrosis factoragents, infliximab and adalimumab, constitutes a new, interesting tool for the treatment of microscopic colitis, but larger, adequately designed studies are needed to confirm existing data. 展开更多
关键词 Microscopic colitis Lymphocytic colitis Collagenous colitis Watery diarrhea Immunosuppressive agents Anti-tumor necrosis factoragentsThe requested resource could not be loaded. libcurl returned the error:
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