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@# Objective: To investigate the value of intercellular adhesion molecule 1 (ICAM-1) for the diagnosis and prognosis of pancreatic cancer. Methods: Eighty patients with pancreatic cancer (pancreatic cancer group), forty patients with benign pancreatic disease (benign disease group) who were admitted to Department of Hepatobiliary and Pancreatic Surgery in Cancer Hospital of Hubei Province fromApril 2015 to December 2017 were included in the study; and thirty healthy subjects during the same period were included as control. Serum ICAM-1 and carbohydrate antigen 19-9 (CA19-9) levels were determined in all the three groups. The receiver operating characteristic curve (ROC) was used to analyze the diagnostic characteristics of ICAM-1 for pancreatic cancer. The COX regression model was used to analyze whether serum ICAM-1 was independently associated with the prognosis of patients with pancreatic cancer. Results: The levels of ICAM-1 and CA19-9 in pancreatic cancer group were significantly higher than those in benign disease group and control group (P<0.01). The level of CA19-9 in benign disease group was significantly higher than that in control group (P<0.01). ROC curve analysis showed that the area under the curve (AUC) of serum ICAM-1, CA19-9 and the combinations of both was 0.732 (95% CI: 0.658-0.807, P=0.000), 0.691 (95% CI: 0.620-0.762, P=0.000), and 0.747 (95% CI: 0.674-0.821, P=0.000), respectively. There was a significant positive correlation between ICAM-1 and CA19-9 (r=0.472, P=0.000). The survival time of patients with serum ICAM-1< 2 308 U/ml was significantly longer than that of patients with ICAM-1≥2 308 U/ml (χ2=28.357,P=0.000); COX regression analysis showed that ICAM-1≥2 308 U/ml was an independent influence factor for prognosis, with an OR of 3.08 (2.14-7.23). Conclusion: Serum ICAM-1 contributes to the early diagnosis and prognosis evaluation of pancreatic cancer.
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Background : Detecting the active state of systemic lupus erythematosus (SLE) is important but challenging. This study aimed to determine the diagnostic accuracy of serum endothelial cell adhesion molecules (ICAM-1 and VCAM-1) and anti-C1q antibody in discriminating between active and non-active SLE. Methods: Using SELENA-SLE disease activity index (SLEDAI), 95 SLE patients (45 active and 50 non-active) were assessed. A score above five was considered indicative of active SLE. The blood samples were tested for serum ICAM-1, VCAM-1 and anti-C1q antibody using enzyme-linked immunosorbent assay (ELISA). Results: The levels of serum VCAM-1 and anti-C1q antibody were significantly higher in active SLE patients. Both VCAM-1 and anti-C1q were able to discriminate between active and non-active SLE ( p -value < 0.001 and 0.005, respectively). From the receiver operating characteristic curves (ROCs) constructed, the optimal cut-off values for VCAM-1 and anti-C1q antibody in discriminating between active and non-active SLE were 30.5 ng/mL (69.0% sensitivity, 60.0% specificity, PPV 58.5%, NPV 66.7%) and 7.86 U/mL (75.6% sensitivity, 80% specificity, PPV 77.3%, NPV 78.4%), respectively. However, serum ICAM-1 level was unable to discriminate between the two groups ( p -value = 0.193). Conclusion: Anti-C1q antibody demonstrated the best diagnostic accuracy in discriminating between active and non-active SLE patients
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Objective To elucidate the spreading dynamics of β2 integrin expressed human neutrophils (PMNs) on ICAM-1-immobilized substrate. Methods The fraction of PMN spreading on the substrate pre coated by 10, 20, or 100 μg/mL intercellular adhesive molecule-1 (ICAM-1) was quantified when that on 2% human serum albumin (HSA) immobilized or that on blank substrate was served as control. The site density of β2 integrin expressing on PMNs was determined using flow cytometry and the regulation of β2 integrin subunits was defined using the fraction of PMN spreading on 100 μg/mL ICAM-1 substrate by blocking CD11a or CD11b subunit of β2 integrin. Results PMN spreading was presented on ICAM-1-immobilized substrate but absent on 2% HSA-immobilized substrate, supporting the specificity of β2 integrin induced spreading. Time course of neutrophil spreading on ICAM-1 substrate was density dependent of both ICAM-1 and β2 integrin molecules. The fraction of PMN spreading was reduced significantly when the expression of CD11b subunit was blocked. Conclusions PMN spreading was mediated specifically by β2 integrin-ICAM-1 interactions and determined by the expression of β2 integrin and ICAM-1, in which CD11b subunit played a dominate role.
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@#Objective To study the effects of hyperbaric oxygen （HBO） therapy in patients with acute intracerebral hemorrhage on serum adhesion molecules. Methods 66 cases with acute intracerebral hemorrhage were divided into routine treatment group (n=33) and HBO treatment group (n=33). 30 health persons were selected as normal trontrol. The level of adhesion molecules, including intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin, were measured before and after treatment. Results The levels of adhesion molecules in routine and HBO treatment groups were higher than those in normal control group when hospitalized (P<0.01). All the adhesion molecules levels in two treatment group were decreased after the treatment, and more significantly in HBO group (P<0.05). Conclusion HBO therapy may ameliorate the adhesion molecule abnormalities after intracerebral hemorrhage.
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Objective To investigate the effect of administration intravenously of rosiglitazone (ROSI) on severe acute pancreatitis (SAP) in rats and its mechanisms. Method Fifty-four male Wistar rats were randomly divided into sham operation group (SO group), severe acute panereatitis model group (SAP group) and rosiglita-zone pretreatment group (ROSI group),18 rats in each group.SAP model was induced by retrograde inufsion of 5% sodium taurecholate into the biliopancreatic duct. The rats in SO group and SAP group were injected with 10% DMSO (0.2 ml/100 g) by femoral vein 30 minutes piror to the operation. In ROSI group,rosiglitazone partes ae-quales(6 mg/kg) was injected instead of 10% DMSO. Rats were killed at 3, 6 and 12 h after operation. Serum amylase level and myelopemxidase activity were detected. Pancreatic tissue samples were stained with hematoxylin and eosin for histopathological evaluation. Reverse transcription-polymerase chain reaction was used for detecting the levels ofTNF-α mRNA and ICAM-1 mRNA in pancreatic tissue. Results Amylase level, myeloperexidase ac-tivity, pathologic score and the expression of TNF-α and ICAM-1 mRNA were increased significantly in SAP group at each time point than those in SO group (P<0.05). Compared with SAP group, pretreatment with rosiglitazone reduced serum amylase level and pathologic score at time point of 6 h and 12 h (P<0.05), decreased myeloper-oxidase activity at 12 h (P<0.05), downregulatied the expression of TNF-α mRNA at all time pointy, (P<0.05),ICAM-1 mRNA at 6 h and 12h(P<0.05). Conclusions Rosightazone has the effect on pancreatitis in SAP through downregulating the expression of TNF-α mRNA and ICAM-1 mRNA.
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Objective: To explore the correlation between endothelia cells activation and cytokines (ET-1, NO) levels in patients with pulmonary hypertension (PH), and to discuss their roles in the development of PH. Methods: Twenty patients with simple ventricular septal defect (VSD) were chosen as controls, and 30 patients with PH were studied. Plasma levels of ET-1 and NO were measured by radioimmunoassay or colorimetric method. Before cardiopulmonary bypass was established, the specimens from right lung were fixed with formaldehyde solution, embedded with paraffin and stained by SP immunohistochemistry. Intercellular adhesion molecule-1 (ICAM-1) expression was measured through the determination of the light density with computer imaging technology. Results: Compared with that of the patients with simple VSD, the light density of ICAM-1 and plasma level of ET-1 increased in patients with PH; but plasma level of NO decreased (P<0.05). Positive correlation was observed between ICAM-1 and ET-1/NO (P<0.05). Conclusion: Endothelia cells activation and imbalance of ET-1/NO might play an important role in the development of PH.
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Objective To explore the correlation between endothelia cells activation and cytokines (ET-1, NO) levels in patients with pulmonary hypertension (PH), and to discuss their roles in the development of PH. Methods Twenty patients with simple ventricular septal defect (VSD) were chosen as controls, and 30 patients with PH were studied. Plasma levels of ET-1 and NO were measured by radioimmunoassay or colorimetric method. Before cardiopulmonary bypass was established, the specimens from right lung were fixed with formaldehyde solution, embedded with paraffin and stained by SP immunohistochemistry. Intercellular adhesion molecule-1 (ICAM-1) expression was measured through the determination of the light density with computer imaging technology. Results Compared with that of the patients with simple VSD, the light density of ICAM-1 and plasma level of ET-1 increased in patients with PH; but plasma level of NO decreased (P<0.05). Positive correlation was observed between ICAM-1 and ET-1/NO (P<0.05). Conclusion Endothelia cells activation and imbalance of ET-1/NO might play an important role in the development of PH.
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It has been well-documented that ICAM-1 implicates in pathophysiology of ischemic-reperfusion injury of the kidney.Renal injury after ischemia appears to be a consequence of tissue hypoxia not only from interrupted blood supply but also from the process of reperfusion which leads to an active inflammatory process.Infiltrating leukocytes are potential source of reactive oxygen species.Proteolytic enzymes and cytokines,which during reperfusion may play a detrimental role.It has been suggested that ICAM-1 plays a key role during leukocyte adhesion and recruitment to inflamed tissue.The goal of the review is to explore the effect and significance of ICAM-1 as well as its mechanism in renal ischemia-reperfunsion.
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Objective To examine the distribution of HA in monocytes and expression of CD44 and ICAM-1 on the monocytes and effects of HA and HA receptors on adhesion and migration of the monocytes. Methods Canine peripheral blood monocytes were isolated by non-continuous density centrifugation with percoll solution.HA on the cell surface,intracellular HA,CD44 and ICAM-l of the monocytes were labeled with immunofluorescence.Effects of HA on the cell surface,substrate HA and free HA on adhesion and migration of the monocytes were examined by digesting HA on the cell surface with HAase,coating the bottom of the dishes and the membrane of the cell culture inserts with HA and adding HA into the medium.Regulating effects of HA receptors on adhesion and migration of the monocytes were investigated after blockade of the receptors. Results There was HA on the surface and in the cytoplasm of the monocytes.CD44 and ICAM-1 were expressed on the monocytes.The adhered and migrated monocytes decreased after HA on the cell surface was digested with HAase.The numbers of the adhered and migrated monocytes were greater when the cells were incubated on HA-coated dishes and membranes of the cell culture inserts.The adhered and migrated monocytes decreased after HA was added into the medium.When CD44 was blocked with antibody,the adhered and migrated monocytes decreased.There were not significant changes in the numbers of the adhered and migrated monocytes after ICAM-1 was blocked with antibody.Conclusion There is HA on the surface and in the cytoplasm of monocytes.HA on the cell surface is essential for adhesion and migration of the monocytes.HA substrate promotes adhesion and migration of the monocytes,while free HA reduces adhesion and migration of the cells.CD44 mediates HA-induced adhesion and migration of the monocytes.
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BACKGROUND: The endothelial expresson and upregulation of ICAM-1 and epidermal keratinocyte expression of ICAM-1 are well documented in psoriasis. ICAM-1 mediates the adhesion and trafficking of circulating activated skin-seeking CD45RO+ memory CD4+ T lymphocytes from the vessel into the dermis and epidermis of psoriatic skin by binding to its ligand LFA-1(lymphocyte function-associated antigen-1) expressed on lymphocyte membranes. OBJECTIVE: The purpose of this study was to investigate the expression of ICAM-1 in vascular endothelium and keratinocyte of psoriatic skin and the difference of ICAM-1 expression between early and fully developed psoriatic lesions. METHODS: We have studied the expression of ICAM-1 in twelve psoriatic patients who had not been treated for psoriatic lesions for 1 month and three normal human skin samples by immunohistochemical staining using monoclonal antibody against ICAM-1. RESULTS: Immunohistochemical staining revealed anti-ICAM-1 antibody positively stained only in the subpapillary endothelial cells of normal skin. But in all psoriatic lesions studied, anti- ICAM-1 antibody was stained positively in the endothelium of papillary and subpapillary plexus, and in fully developed psoriatic lesions, anti-ICAM-1 antibody was stained focally in epidermal keratinocytes. CONCLUSION: The results suggest that ICAM-1 expression on papillary microvessels and keratinocytes may play an important role in the transendothelial and transepidermal migration of lymphocytes from the vessel into the dermis and epidermis of psoriatic skin.
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Humans , Dermis , Endothelial Cells , Endothelium , Endothelium, Vascular , Epidermis , Intercellular Adhesion Molecule-1 , Keratinocytes , Lymphocytes , Membranes , Memory , Microvessels , Psoriasis , Skin , T-Lymphocytes , Up-RegulationABSTRACT
PURPOSE: The early and efficient diagnosis of neonatal sepsis still remains a difficult task. Reliable laboratory test is not available yet and treatment is mainly based on the physical appearance of infants. And high number of negative blood cultures in cases of clinically diagnosed sepsis further emphasize the need for a more reliable index for early diagnosis. Intercellular adhesion molecule 1 (ICAM-1) has been known important in various immunological processes early in inflammation, and recently circulating ICAM-1 (cICAM-1) has been detected in serum and supernatant of cytokine-activated endothelial cell cultures. The purpose of our study was to evaluate cICAM-1 as a marker in neonatal sepsis. METHODS: Using enzyme linked immunosorbent assay (ELISA), we measured serial cICAM-1 over the first week of admission in 48 neonates who were admitted at NICU due to clinically suspected sepsis. RESULTS: We found the levels of cICAM-1 on admission in 9 culture proven and 20 clinically dignosed septic neonates (1723.3+/-669.7ng/ml and 994.9+/-358.5ng/ml, respectively) were significantly higher (P<0.001) than those in neonates showing systemic inflammatory signs without evidence of sepsis and healthy controls (380.6+/-235.8ng/ml and 238.8+/-96.6ng/ml, respectively). The cICAM-1 levels on admission in septic neonates with high severity score were higher than those with low severity score (P<0.01). Fatal cases exhibited higher cICAM-1 on admision than did survivals (1710.8+/-634.5ng/ml versus 963.4+/-411.4ng/ml, P<0.0001) and there seemed to be a positive correlation between cICAM-1 levels and mortality. The elevation of cICAM-1 on admission in septic neonates appeared earlier than the rise of c-reactive protein (CRP) above 10mg/L. CONCLUSIONS: The measurement of cICAM-1 on admisson might be useful for the early detection of neonatal sepsis and high cICAM-1 level suggests poor prognosis.
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Humans , Infant , Infant, Newborn , C-Reactive Protein , Diagnosis , Early Diagnosis , Endothelial Cells , Enzyme-Linked Immunosorbent Assay , Inflammation , Intercellular Adhesion Molecule-1 , Mortality , Prognosis , SepsisABSTRACT
PURPOSE: The early and efficient diagnosis of neonatal sepsis still remains a difficult task. Reliable laboratory test is not available yet and treatment is mainly based on the physical appearance of infants. And high number of negative blood cultures in cases of clinically diagnosed sepsis further emphasize the need for a more reliable index for early diagnosis. Intercellular adhesion molecule 1 (ICAM-1) has been known important in various immunological processes early in inflammation, and recently circulating ICAM-1 (cICAM-1) has been detected in serum and supernatant of cytokine-activated endothelial cell cultures. The purpose of our study was to evaluate cICAM-1 as a marker in neonatal sepsis. METHODS: Using enzyme linked immunosorbent assay (ELISA), we measured serial cICAM-1 over the first week of admission in 48 neonates who were admitted at NICU due to clinically suspected sepsis. RESULTS: We found the levels of cICAM-1 on admission in 9 culture proven and 20 clinically dignosed septic neonates (1723.3+/-669.7ng/ml and 994.9+/-358.5ng/ml, respectively) were significantly higher (P<0.001) than those in neonates showing systemic inflammatory signs without evidence of sepsis and healthy controls (380.6+/-235.8ng/ml and 238.8+/-96.6ng/ml, respectively). The cICAM-1 levels on admission in septic neonates with high severity score were higher than those with low severity score (P<0.01). Fatal cases exhibited higher cICAM-1 on admision than did survivals (1710.8+/-634.5ng/ml versus 963.4+/-411.4ng/ml, P<0.0001) and there seemed to be a positive correlation between cICAM-1 levels and mortality. The elevation of cICAM-1 on admission in septic neonates appeared earlier than the rise of c-reactive protein (CRP) above 10mg/L. CONCLUSIONS: The measurement of cICAM-1 on admisson might be useful for the early detection of neonatal sepsis and high cICAM-1 level suggests poor prognosis.
Subject(s)
Humans , Infant , Infant, Newborn , C-Reactive Protein , Diagnosis , Early Diagnosis , Endothelial Cells , Enzyme-Linked Immunosorbent Assay , Inflammation , Intercellular Adhesion Molecule-1 , Mortality , Prognosis , SepsisABSTRACT
Objective:To investigate the effect of allitride injection preconditioning and ischemic preconditioning on renal ischemia/ reperfusion(I/R)injury in rats.Methods:Rat's I/R injury model was established.A total of 75 rats were randomized into five groups(n=15,in each);control group(CON),I/R control group(IR),ischemic preconditioninggroup(IPC),allitride preconditioninggroup(APC),allitride preconditioning and ischemic preconditioning group(AIPC).Kidney tissue and blood specimen were collected from all groups 24 hours after operation.The changes of the renal pathological morphology were observed by hematoxylin-eosine(HE)staining.The levels of serum creatinine(Cr)and urea nitrogen(BUN) were determined.The levels of malonaldehyde(MDA)were determined by thibabituric acid(TBA).The levels of superoxide dismutase(SOD)were determined by xanthine oxidase.Intercellular adhesion molecule-1(ICAM-1)expression in kidney was tested by immunohistoehemistry.Results:IPC or APC group had less necrosis in HE staining than IR group.BUN,Cr,MDA contents in IPC or APC group are less than that in IR group(P
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Objective To investigate the protective effect of felodipine on reactive oxygen species (ROS) generation,mRNA level of inflammatory factors such as intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1),in human umbilical vein endothelial cells (HUVECs) injured by oxidized low-density lipoprotein (ox-LDL) so as to explore felodipine's anti-atherosclerosis mechanism independent of its anti-hypertensive effect. Methods Isolated HUVECs were treated with ox-LDL at different concentrations (6,12.5 and 25 mg/L) for 24 hours so that the optimal concentration and time of ox-LDL treatment were selected. Then the cells were incubated with ox-LDL and treated with felodipine at different concentrations (0.1,1 and 10 ?mol/L). Intracellular ROS level was determined by flow cytometry (FCM). Expressions of inflammatory factors ICAM-1 and VCAM-1 were measured by real time-polymerase chain reaction (real time-PCR). Results ROS generation was increased in HUVECs after treatment with different concentrations (6,12.5 and 25 mg/L) of ox-LDL for 24 hours and there was a significant difference at 25 mg/L ox-LDL (P
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Objective To investigate how vascular endothelial growth factor(VEGF) up-regulates intercellular adhesion molecule-1 via protein kinase C(PKC)/ nitric oxide(NO) pathway in the retina of diabetic rats.Methods All the rats were divided into 4 groups: normal,diabetes,diabetes+PKCI and control groups.Diabetes was induced by an intraperitoneal injection of STZ.PKC inhibitor GF109203X was injected intravitreally after 5 months of streptozotocin induced diabetes.NO was determined by nitrate reductase method.VEGF and intercellular adhesion molecule-1(ICAM-1) were measured by Western blot.Results VEGF and NO expressions increased obviously in the retina of diabetic rats compared with those in the normal group(P