[ Objective] The aim of this study was to provide a theoretical basis for the prevention and treatment of highly pathogenic porcine reproductive and respiratory syndrome （HP-PRRS）. [Method] Antigen location and hist...[ Objective] The aim of this study was to provide a theoretical basis for the prevention and treatment of highly pathogenic porcine reproductive and respiratory syndrome （HP-PRRS）. [Method] Antigen location and histopathological observation in natural cases infected by highly pathogenic porcine reproductive and respiratory syndrome virus （HP-PRRSV） were analyzed by immunohistochemistry and H. E. staining. [Result] The virus antigen mainly existed in epithelial calls, and also a few in mecrophages, lymphocytes and brain nerve cells. [ Conclusion] The cell and tissue tropism of HP-PRRSV strain in natural cases is different from that of previous strains.展开更多
Objective: To observe the risk factors of thrombosis in patients with obstructive sleep apnea hypopnea syndrome (OSAHS).Methods: From February 2001 to April 2003, 24 patients with moderate and severe OSAHS (OSAHS grou...Objective: To observe the risk factors of thrombosis in patients with obstructive sleep apnea hypopnea syndrome (OSAHS).Methods: From February 2001 to April 2003, 24 patients with moderate and severe OSAHS (OSAHS group) and 19 healthy adults (control group) were recruited. Their blood samples were drawn at 6∶00 and 16∶00 respectively for testing hemocrit, platelet aggregation (PAG), whole blood viscosity (WBV), prothrombin time (PT), activated partial thromboplastin time (APTT), plasma fibrinogen (Fng) and endothelin (ET).Results: There was a significantly higher hemocrit, WBV, Fng and ET as well as a significant shortening of PT and APTT at 6∶00 than that at 16∶00 in OSAHS group. However, there was no significant difference in all testing items between 6∶00 and 16∶00 in control group. The hemocrit, WBV, PAG, plasma Fng and ET were significantly higher, and PT and APTT were obviously shorter at 6∶00 in OSAHS group than those at 6∶00 in control group. A higher hemocrit, PAG, plasma Fng and ET, a longer PT and APTT were observed at 16∶00 in OSAHS group, compared with those at 16∶00 in control group.Conclusion: In OSAHS patients there were striking risk factors of thrombosis, which is more remarkable in the early morning than in the afternoon.展开更多
AIM： To investigate the major steps of thrombogenesis and to identify the differences in these steps between idiopathic patient group and control group. METHODS： Fibrinogenesis was studied by measuring the activated...AIM： To investigate the major steps of thrombogenesis and to identify the differences in these steps between idiopathic patient group and control group. METHODS： Fibrinogenesis was studied by measuring the activated factor Ⅶ, total and free levels of tissue factor pathway inhibitor （TFPI）. The fibrinolysis step was investigated by determining the global fibrinolytic capacity. The endothelial function was assessed by measuring the levels of soluble adhesion molecules, namely soluble intercellular adhesion molecule 1 （sICAM-1）, soluble vascular cell adhesion molecule 1 （sVCAM-1） and soluble E-selectin molecule. The exclusion criteria from ＂idiopat- hic＂ patient group were abdominal surgery, pregnancy, use of oral contraceptives, anti-phospholipid syndrome, Behet＇s disease, cancer, myeloproliferative diseases. The congenital factors like mutations of factor-Ⅴ Leiden and prothrombin, deficiencies of proteins C and S, antithrombin, hyperhomocysteinemia and hyperfibrinogenemia were ruled out. The total number of patients was reduced from 96 to 9 （7 with portal vein thrombosis, 2 Budd Chiari syndrome） by exclusion criteria. RESULTS： The levels of adhesion molecules sICAM-1, sVCAM-1, free TFPI levels and global fibrinolytic capacity were significantly different （P〈 0.05） in the patient group indicating an endothelial dysfunction and a lower fibrinolytic activity. CONCLUSION： These results show that this patient group should be tested by means of endothelial dysfunction and managed differently.展开更多
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
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
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
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
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
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
文摘[ Objective] The aim of this study was to provide a theoretical basis for the prevention and treatment of highly pathogenic porcine reproductive and respiratory syndrome （HP-PRRS）. [Method] Antigen location and histopathological observation in natural cases infected by highly pathogenic porcine reproductive and respiratory syndrome virus （HP-PRRSV） were analyzed by immunohistochemistry and H. E. staining. [Result] The virus antigen mainly existed in epithelial calls, and also a few in mecrophages, lymphocytes and brain nerve cells. [ Conclusion] The cell and tissue tropism of HP-PRRSV strain in natural cases is different from that of previous strains.
文摘Objective: To observe the risk factors of thrombosis in patients with obstructive sleep apnea hypopnea syndrome (OSAHS).Methods: From February 2001 to April 2003, 24 patients with moderate and severe OSAHS (OSAHS group) and 19 healthy adults (control group) were recruited. Their blood samples were drawn at 6∶00 and 16∶00 respectively for testing hemocrit, platelet aggregation (PAG), whole blood viscosity (WBV), prothrombin time (PT), activated partial thromboplastin time (APTT), plasma fibrinogen (Fng) and endothelin (ET).Results: There was a significantly higher hemocrit, WBV, Fng and ET as well as a significant shortening of PT and APTT at 6∶00 than that at 16∶00 in OSAHS group. However, there was no significant difference in all testing items between 6∶00 and 16∶00 in control group. The hemocrit, WBV, PAG, plasma Fng and ET were significantly higher, and PT and APTT were obviously shorter at 6∶00 in OSAHS group than those at 6∶00 in control group. A higher hemocrit, PAG, plasma Fng and ET, a longer PT and APTT were observed at 16∶00 in OSAHS group, compared with those at 16∶00 in control group.Conclusion: In OSAHS patients there were striking risk factors of thrombosis, which is more remarkable in the early morning than in the afternoon.
基金Supported by Hacettepe University Office of Scientific Research Center
文摘AIM： To investigate the major steps of thrombogenesis and to identify the differences in these steps between idiopathic patient group and control group. METHODS： Fibrinogenesis was studied by measuring the activated factor Ⅶ, total and free levels of tissue factor pathway inhibitor （TFPI）. The fibrinolysis step was investigated by determining the global fibrinolytic capacity. The endothelial function was assessed by measuring the levels of soluble adhesion molecules, namely soluble intercellular adhesion molecule 1 （sICAM-1）, soluble vascular cell adhesion molecule 1 （sVCAM-1） and soluble E-selectin molecule. The exclusion criteria from ＂idiopat- hic＂ patient group were abdominal surgery, pregnancy, use of oral contraceptives, anti-phospholipid syndrome, Behet＇s disease, cancer, myeloproliferative diseases. The congenital factors like mutations of factor-Ⅴ Leiden and prothrombin, deficiencies of proteins C and S, antithrombin, hyperhomocysteinemia and hyperfibrinogenemia were ruled out. The total number of patients was reduced from 96 to 9 （7 with portal vein thrombosis, 2 Budd Chiari syndrome） by exclusion criteria. RESULTS： The levels of adhesion molecules sICAM-1, sVCAM-1, free TFPI levels and global fibrinolytic capacity were significantly different （P〈 0.05） in the patient group indicating an endothelial dysfunction and a lower fibrinolytic activity. CONCLUSION： These results show that this patient group should be tested by means of endothelial dysfunction and managed differently.
文摘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.
基金Project (No. 021110240) supported by grants from the Foundation of the Department of Science and Technology of Zhejiang Province,China
文摘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.
文摘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.
基金Supported by National Institute of Health,NIH DK 43785
文摘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.
文摘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.
文摘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.
