Changes in serum cellular adhesion molecule and matrix metalloproteinase-9 levels in patients with cerebral infarction following hyperbaric oxygen therapy A case and intergroup control study

BACKGROUND： Animal studies have confirmed that hyperbaric oxygen （HBO） therapy can reduce matrix metalloproteinase activity and blood brain barrier permeability, thereby exhibiting neuroprotective effects. However, at present, consensus does not exist in terms of its clinical efficacy. OBJECTIVE： To validate the significance of changes in serum cellular adhesion molecule and MMP-9 levels in patients with cerebral infarction following HBO therapy. DESIGN, TIME AND SETTING： This randomized, controlled, neurobiochemical study was performed at the Department of Neurology, Affiliated Hospital of Qingdao University Medical College between December 2002 and March 2006. PARTICIPANTS： A total of 112 patients with acute cerebral infarction of internal carotid artery, comprising 64 males and 48 females, averaging （67 ±11） years, were recruited and randomized to a HBO group （n = 50） and a routine treatment group （n = 62）. An additional 30 gender- and age-matched normal subjects, consisting of 17 males and 13 females, averaging （63 ± 9） years, were enrolled as control subjects. METHODS： The routine treatment group received routine drug treatment and rehabilitation exercise. HBO treatment was additionally performed in the HBO group, once a day, for a total of 10 days. MAIN OUTCOME MEASURES： Serum levels of soluble intercellular adhesion molecule, soluble vascular cell adhesion molecule, soluble E-selectin, and matrix metalloproteinase-9 were detected by enzyme linked immunosorbent assay. RESULTS： Upon admission, serum levels of soluble intercellular adhesion molecule, soluble vascular cell adhesion molecule, soluble E-selectin, and matrix metalloproteinase-9 were significantly increased in patients with cerebral infarction, compared with control subjects （P 〈 0.01）. Following HBO and routine treatments, serum levels of the above-mentioned indices were significantly reduced in the HBO and routine treatment groups （P 〈 0.01）. Moreover, greater efficacy was observed in the HBO group, compared with the routine treatment group （P 〈 0.05 or P 〈 0.01）. CONCLUSION： Intergroup comparison and case-control results indicated that HBO noticeably reduced serum levels of soluble intercellular adhesion molecule, soluble vascular cell adhesion molecule, soluble E-selectin, and matrix metalloproteinase-9.

A clinical evaluation of serum concentrations of intercellular adhesion molecule-1 in patients with gastric cancer

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Expression of epithelial cellular adhesion molecule in gastric cancer:A meta-analysis

AIM： To obtain an accurate evaluation of the association between high expression of epithelial cellular adhesion molecule （EpCAM） and gastric cancer （GC） risk.METHODS： Studies that had examined the association between high expression of EpCAM and GC risk were identified by searching electronic databases PubMed, EMBASE, Cochrane library and Chinese Biomedical Literature database. Risk ratios （RRs） together with their 95%CIs were used to assess the association between high expression of EpCAM and GC risk. We selected eligible studies based on inclusion criteria. RevMan 5.3 software was used to calculate the pooled values.RESULTS： A total of 14 studies were included in this meta-analysis. EpCAM-positive cases were signifcantly associated with tumor size （RR： 1.68, 95%CI： 1.47-1.91, P 〈 0.00001 fxed-effect）, depth of invasion （RR： 1.37, 95%CI： 1.11-1.68, P = 0.003 random-effect）, TNM stage （RR： 2.02, 95%CI： 1.35-3.02, P = 0.0007 random-effect）, tumor location （RR： 0.80, 95%CI： 0.71-0.91, P = 0.0007 fxed-effect）, histologic differentiation （RR： 1.23, 95%CI： 1.13-1.33, P 〈 0.00001 fxed-effect） and lymph node metastasis （RR： 1.89, 95%CI： 1.28-2.80, P = 0.001 random-effect）. However, we did not observe any significant association between the presence of EpCAM with age, gender, distant metastasis, Borrmann type or Lauren classification. Additionally, EpCAM expression was not associated with the overall survival rate. The pooled HR of the overall effect was 1.39（95%CI： 0.30-6.48, P = 0.67 random-effect）.CONCLUSION： Our meta-analysis indicates that EpCAM contributes to GC risk, which acts as a prognostic factor and a marker of poor outcome.

Increased Expression of Intercellular Adhesion Molecule-1,Vascular Cellular Adhesion Molecule-1 and Leukocyte Common Antigen in Diabetic Rat Retina

Purpose: To understand the expression and distribution of intercellular adhesion molecule- 1(ICAM- 1),vascular cellular adhesion molecule- 1 (VCAM- 1)and CD45 (Leukocyte Common Antigen) in the control nondiabetic and various courses of diabetic rats retina. To explore the role of adhesion molecules (Ams) and the adhesion of leukocytes to vascular endothelial cells via Ams in diabetic retinopathy(DR).Methods: Sixty healthy adult male Wistar rats were randomly divided into diabetic groups(induced by Streptozotocin, STZ) and normal control groups. Rats in these two groups were further randomly divided into 3, 7, 14, 30, 90 and 180 days-group,including 5 rats respectively. The immunohistochemical studies of ICAM-1, VCAM-1 and CD45 were carried out in the retinal digest preparations or retinal paraffin sections, and the results were analyzed qualitatively, semi-quantitatively.Results: No positive reaction of VCAM-1 was found, and weak reactions of ICAM-1,CD45 were found in nondiabetic rats retina. The difference of 6 control groups had no statistical significance(P > 0.05). The increased ICAM-1 and CD45 staining pattern were detectable 3 days after diabetes induction, and a few VCAM-1 positive cells were observed in the retinal blood capillaries. The difference of diabetes and control is significant( P < 0.05).Following the course, the expressions of ICAM-1, VCAM-1 and CD45 were increasingly enhanced, reaching a peak at the 14th day.Conclusion: Increased expression of ICAM-1, VCAM-1 and leukocytes adhering and stacking in retinal capillaries are the very early events in DR. Coherence of expression and distribution of the three further accounts for it is the key point for the onset of DR that Ams mediates leukocytes adhesion and endothelial cell injury.

Adhesion molecule and proinflammatory cytokine gene expression in hepatic sinusoidal endothelial cells following cecal ligation and puncture

INTRODUCTIONMultiple organ dysfunction syndrome (MODS) isthought to be a frequent consequence of sepsis[1-3].Despite substantial advances in our knowledge and understanding of the basic pathophysiologic mechanisms[4-7], in critically ill patients infections and sepsis are still associated with a high mortality[8,9].

Ubiquitin Reduces Expression of Intercellular Adhesion Molecules and Tumor Necrosis Factor-α in Lung Tissue of Experimental Acute Lung Injury

Background Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are two important cytokines in inflammatory response, which may induce rolling and adhesion of both leukocytes and lymphocytes, while modulating vascular permeability at the same time. These adhesion molecules usually serve as surrogate markers of activation and injury of vascular endothelial cells. Tumor necrosis factor-α (TNF-α) is a key factor to induce the expression and production of the above cell adhesion molecules. However, it remains to be elucidated whether exogenous ubiquitin exerts any effect on the cytokines in sepsis-induced ALI. Methods Sixty mice were devided randomly into five groups with twelve mice in each group, i.e. CLP group, SHAM group, UB1 group (10 mg/kg), UB2 group (5 mg/kg) and UB3 group(1 mg/kg). Mice of SHAM group underwent sham operation, and other four groups underwent CLP. Six hours after surgery, mice of three UB groups received ubiquitin by caudal vein injection while CLP and SHAM group received vehicle. Seven hours after surgery, blood and lungs of all mice were collected. ICAM-1, VCAM-1 and TNF-α level of 9% lung homogenate and serum TNF-α level were measured by ELISA. Results Pulmonary ICAM-1, VCAM-1 and TNF-α level of three UB groups were lower than CLP and SHAM group, and there were several comparisons with a statistically significant difference. Serum TNF-α level of three UB groups were slightly lower than CLP group, but far higher than SHAM group. Pulmonary ICAM-1 level, VCAM-1 level and serum TNF-α level of UB3 group were lower than UB1 and UB2 group, and there was a significant difference in VCAM-1 between UB3 and UB1 group. Pulmonary TNF-α level of UB3 group was slightly higher than UB1 and UB2 group.

Dynamic interplay between adhesion surfaces in carcinomas:Cell-cell and cell-matrix crosstalk

Cell-cell and cell-matrix signaling and communication between adhesion sites involve mechanisms which are required for cellular functions during normal development and homeostasis; however these cellular functions and mechanisms are often deregulated in cancer. Aberrant signaling at cell-cell and cell-matrix adhesion sites often involves downstream mediators including Rho GTPases and tyrosine kinases. This review discusses these molecules as putative mediators of cellular crosstalk between cell-cell and cell-matrix adhesion sites, in addition to their attractiveness as therapeutic targets in cancer. Interestingly, inter-junctional crosstalk mechanisms are frequently typified by the way in which bacterial and viral pathogens opportunistically infect or intoxicate mammalian cells. This review therefore also discusses the concept of learning from pathogen-host interaction studies to better understand coordinated communication between cell-cell and cell-matrix adhesion sites, in addition to highlighting the potential therapeutic usefulness of exploiting pathogens or their products to tap into inter-junctional crosstalk. Taken together, we feel that increased knowledge around mechanisms of cell-cell and cell-matrix adhesion site crosstalk and consequently a greater understanding of their therapeutic targeting offers a unique opportunity to contribute to the emerging molecular revolution in cancer biology.

Effects of Ginkgo biloba extract adjuvant therapy on inflammatory reaction, adhesion molecules and antioxidant function in patients with cerebral infarction complicated with hyperhomocysteinemia

Objective: To investigate the effects of Ginkgo biloba extract adjuvant therapy on inflammatory reaction, adhesion molecules and antioxidant function in patients with cerebral infarction complicated with hyperhomocysteinemia. Methods: A total of 114 patients with cerebral infarction complicated with hyperhomocysteinemia who were conformed to the research selection criteria were selected as the research objects, according to the random data table method they were evenly divided into the control group (n=57) and the observation group (n=57), patients in the two groups were given conventional supportive treatment, on this basis, the control group patients were given folic acid tablets and vitamin B12 treatment, the observation group was treated with Ginkgo biloba extract dripping pills on the basis of the treatment of the control group. The levels of inflammatory factors, adhesion molecules and antioxidant and antioxidant function were compared between the two groups before and after treatment (after treatment 30 d). Results: There was no significant difference in the levels of hs-CRP, WBC, ICAM-1, VCAM-1, SOD and MDA between the two groups before and after treatment;After treatment, the levels of hs-CRP, WBC, ICAM-1, VCAM-1 and MDA in the observation group were significantly lower than those in control group, all significantly lower than the levels in the same group before treatment, the difference was statistically significant. After treatment, the level of SOD in the observation group was (100.37±9.45) U/mL, which was significantly higher than that of the control group (85.04±9.49) U/mL, which was significantly higher than that before the treatment, the difference was statistically significant. Conclusion: Ginkgo biloba extract adjuvant treatment of cerebral infarction significantly with high homocysteine hyperlipidemia efficacy can effectively reduce the inflammatory response to stress, reduce the release of adhesion molecules, improve the antioxidant function of oxidation, which has an important clinical value.

The role of adhesion molecules in gastri c ulcer healing

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Effect of Batroxobin on Expression of Neural Cell Adhesion Molecule in Temporal Infarction Rats and Spatial Learning and Memory Disorder

The effect of Batroxobin expression of neural cell adhesion molecule (NCAM) in left temporal ischemic rats with spatial memory disorder was investigated by means of Morri's water maze and immunohistochemical methods. The results showed that the mean reaction time and distance of temporal ischemic rats for searching a goal were significantly longer than those of sham-operated rats and at the same time NCAM expression of left temporal ischemic region was significantly increased. However, the mean reaction time and distance of Batroxobin-treated rats were shorter and they used normal strategies more often and earlier than those of ischemic rats. The number of NCAM immune reactive cells of Batroxobin-treated rats was more than that of ischemic group. In conclusion, Batroxobin can improve spatial memory disorder of temporal ischemic rats and the regulation of the expression of NCAM is probably related to the neuroprotective mechanism.

Expression of fibronectin and cell adhesion molecule CD15 in hepatocellular carcinoma

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High level of intercellular adhesion molecule-1 affects prognosis of patients with hepatocellular carcinoma

AIM: To determine the cut-off value of intercellular adhesion molecule-1(ICAM-1) and assess the correlation of ICAM-1 with clinicopathological features and the prognosis of hepatocellular carcinoma(HCC)patients who underwent surgical resection.METHODS: We prospectively collected clinicopathological data from 236 HCC patients who had undergone successful hepatectomy. Receiver operating characteristic curve analysis was performed to determine the optimal cut-off value of ICAM-1. Enzymelinked immunosorbent assay was used to measure the concentration of ICAM-1 in 236 serum samples isolated from HCC patients and the stratified analysis was used to compare the serum level of ICAM-1 in different HCC subgroups. Immunohistochemistry was performed to test the expression level of the ICAM-1 protein in76 cases of HCC tissues and their adjacent normal liver tissues(ANLT). The survival probability of HCC patients was estimated using Kaplan-Meier plots and differences between the groups were obtained using the log-rank test. Furthermore, independent indicatorsof the prognosis were acquired using a stepwise Cox proportional hazard model to analyze a series of predictors that were associated with disease-free survival(DFS) and overall survival(OS) in HCC patients.RESULTS: Our findings suggested that ICAM-1promotes HCC metastasis and high serum ICAM-1 is significantly associated with alpha-fetoprotein(AFP)(P = 0.022), clinical tumor-node-metastasis stage(P< 0.001), portal vein tumor thrombus(P = 0.005),distant metastasis(P = 0.016) and recurrence(P= 0.034). We further detected the ICAM-1 protein in HCC specimens and found that 56 of 76(73.7%)HCC tissues had ICAM-1 positive staining while only23 of 76(30.3%) ANLT were positively stained(P <0.0001). Survival analysis indicated that HCC patients with increased ICAM-1 concentrations had significantly shorter DFS and OS after resection. A multivariate analysis showed that ICAM-1 > 684 ng/mL was an independent factor for DFS(HR = 1.643; 95%CI:1.125-2.401; P = 0.010) and OS(HR = 1.692; 95%CI:1.152-2.486; P = 0.007).CONCLUSION: ICAM-1 may be a promising serological biomarker for HCC diagnosis and an independent predictor of DFS and OS after surgical resection and may provide a useful reference for the prediction of intra- and extrahepatic metastasis.

Clinical significance of serum intercellular adhesion molecule-i detection in patients with hepatocellular carcinoma

INTRODUCTION Since the late 1980s,studies on the expression ofintercellular adhesion molecule-1(ICAM-1)inpatients with malignancies have demonstrated thatICAM-1 may strongly express in two forms in suchdiseases:membranous one on the surface of tumorcells(membrane-bound ICAM-1)and soluble one incirculation(soluble ICAM-1,sICAM-1).

Intercellular adhesion molecule-1 expression in the hippocampal CA1 region of hyperlipidemic rats with chronic cerebral ischemia

Chronic cerebral ischemia is a pathological process in many cerebrovascular diseases and it is induced by long-term hypedipidemia, hypertension and diabetes mellitus. After being fed a high-fat diet for 4 weeks, rats were subjected to permanent occlusion of bilateral common carotid arteries to establish rat models of chronic cerebral ischemia with hypedipiclemia. Intercellular adhesion molecule-1 expression in rat hippocampal CA1 region was determined to better understand the mechanism underlying the effects of hypedipidemia on chronic cerebral ischemia. Water maze test results showed that the cognitive function of rats with hyperlipidemia or chronic cerebral ischemia, particulady in rats with hypedipidemia combined with chronic cerebral ischemia, gradually decreased between 1 and 4 months after occlusion of the bilateral common carotid arteries. This correlated with pathological changes in the hippocampal CA1 region as detected by hematoxylin-eosin staining. Immunohistochemical staining showed that intercellular adhesion molecule-1 expression in the hippocampal CA1 region was noticeably increased in rats with hyperlipidemia or chronic cerebral ischemia, in particular in rats with hyperlipidemia combined with chronic cerebral ischemia. These findings suggest that hyperlipidemia aggravates chronic cerebral ischemia-induced neurological damage and cognitive impairment in the rat hippocampal CA1 region which may be mediated, at least in part, by up-regulated expression of intercellular adhesion molecule-l.

Relationship between serum adhesion molecules, trace elements and delayed union of tibial and fibula fractures

Objective:To investigate the relationship between serum adhesion molecules, trace elements and delayed union of tibial and fibula fractures.Methods:A total of 46 patients with delayed union of tibial and fibula fractures in our hospital from May 2014 to June 2016 were selected as the observation group, 46 patients with normal healing of tibial and fibula fractures were selected as the control group, then the serum adhesion molecules and trace elements levels of two groups at forth, eighth and sixteenth week after the surgery were compared.Results:The serum dhesion molecules levels of observation group at forth, eighth and sixteenth week after the surgery were all higher than those of control group, the serum trace elements levels were all lower than those of control group, and the serum adhesion molecules levels of two groups at eighth week after the surgery were all higher than those at other time, the trace elements levels were all lower than those at other time (allP<0.05).Conclusions:The serum adhesion molecules and trace elements of patients with delayed union of tibial and fibula fractures show obviously abnormal state, so those indexes of those patients should be paid to more monitoring and improvement.

Changes of soluble intercellular adhesion molecule-1 in the serum from patients with acute cerebral infarction

objective: To observe the changes of soluble intercellular adhesion molecule-1(sICAM-1) in the serum of patients with acute cerebral infarctlon (ACI) and their clinical significance. Methods: The concen-tration of sICAM-1 in the serum of 91 patients with ACI was determined with ELISA and then the results were compared wlth those of 43 patients with cerebral hemorrhage and 30 healthy individuals. Results: In the 24th hour after infarction. the concentration of sICAMu-1 in the serum was significantly higher in patients with ACI than in patients with cerebral hemorrhage and normal controls (P< 0. 01). In the patients with ACI, the concentration exhibited an decreasing tendency in the period from the 24th hour to the 14th day andwas correlated with the focal size of cerebral infarction. During the first 14 days after infarction, the concen-tration was significantly higher in the patients with the complication of infection than in those without. Con-clusion: sICAM-1 is closely correlated with clinical manifestation of ACI.

Intrapulmonary expression of intercellular adhesion molecule-I inacute pancreatitis and its significance in rats

intrapulmonary expression of intercellular adhesion molecule- I (ICAM-l ) in acute hemorrhagicnecrotic pancreatitis (AHNP) and its significance were studied with imrnunohistochemistry and computer image analysis system and the therapeutic efficacy of the monoclonal antibody of tumor necrosis factora (TNFaMnAb ) was evaluated in rats. It was found during AHNP, there was an early increase of intrapulmonary expression of ICAM--l and the expression reached the peak in the 12th hour after the onset of AHNP and became stabilized in the 24th hour. ICAM-l expression correlated positively to the accumulation of polymorphonuclear neutrophils (PMNs). ICAM-l expression and PMN accumulation would be significantly attenuated if the rats were pretreated with TNFa MnAb. It is concluded that PMN infiltration in the pulmonary tissues results from intrapulmonary expression of ICAM-l and TNFa MnAb inhibits ICAM-l expression andPMN accumulation in the lungs. Consequently, administration of TNFa MnAb during AHNP can protect thelungs from being damaged.

Nerve bundle formation during the promotion of peripheral nerve regeneration:collagenⅥ-neural cell adhesion molecule 1 interaction

The formation of nerve bundles,which is partially regulated by neural cell adhesion molecule 1(NCAM1),is important for neural network organization during peripheral nerve regeneration.However,little is known about how the extracellular matrix(ECM)microenvironment affects this process.Here,we seeded dorsal root ganglion tissue blocks on different ECM substrates of peripheral nerve ECM-derived matrixgel,Matrigel,laminin 521,collagen I,and collagen IV,and observed well-aligned axon bundles growing in the peripheral nerve ECM-derived environment.We confirmed that NCAM1 is necessary but not sufficient to trigger this phenomenon.A protein interaction assay identified collagen VI as an extracellular partner of NCAM1 in the regulation of axonal fasciculation.Collagen VI interacted with NCAM1 by directly binding to the FNIII domain,thereby increasing the stability of NCAM1 at the axolemma.Our in vivo experiments on a rat sciatic nerve defect model also demonstrated orderly nerve bundle regeneration with improved projection accuracy and functional recovery after treatment with 10 mg/m L Matrigel and 20μg/m L collagen VI.These findings suggest that the collagen VI-NCAM1 pathway plays a regulatory role in nerve bundle formation.This study was approved by the Animal Ethics Committee of Guangzhou Medical University(approval No.GY2019048)on April 30,2019.

Correlation of body mass index with Th1/Th2 balance, adhesion molecules and insulin signal transduction in infertile patients

Objective: To study the correlation of body mass index with Th1/Th2 balance, adhesion molecules and insulin signal transduction in infertile patients. Methods: A total of 132 patients who received diagnostic curettage due to infertility in Tangshan Maternal and Child Health Hospital between June 2015 and March 2016 were selected as the research subjects and divided into the normal group with BMI<25 kg/m2, the overweight group with BMI 25-30 kg/m2 and the obesity group with BMI > 30 kg/m2 according to BMI, and the levels of Th1/Th2 cytokines in serum as well as the expression of Th1/Th2 transcription factors, adhesion molecules and insulin signal pathway molecules in endometrial tissue were detected. Results:IFN-γ and TNF-α levels in serum of obesity group and overweight group were significantly higher than those of control group while IL-4, IL-5 and IL-13 levels in serum as well as CD44V6, N-cadherin, FAK, ICAM-1, GLUT-4, IRS-1, PI3K and AKT mRNA expression in endometrial tissue were significantly lower than those of control group;IFN-γ and TNF-α levels in serum of obesity group were significantly higher than those of overweight group while IL-4, IL-5 and IL-13 levels in serum as well as CD44V6, N-cadherin, FAK, ICAM-1, GLUT-4, IRS-1, PI3K and AKT mRNA expression in endometrial tissue were significantly lower than those of overweight group. Conclusion: Weight gain can aggravate the Th1/Th2 disorder, reduce the adhesion molecule expression and hinder the insulin signal transduction in infertile patients.

Intercellular adhesion molecule-5 protects PAJU cells during in vitro ischemia following cerebral infarction

BACKGROUND： Intercellular adhesion molecule-5 （ICAM-5） relieves the damage of beta-amyloid protein to PAJU cells, However, little is known about how ICAM-5 works as a neurotrophic factor, or whether ICAM-5 lessens neuronal damage under ischemic conditions following cerebral infarction. OBJECTIVE： To investigate the effects of ICAM-5 on PAJU cells growth in serum-free medium under ischemic conditions following cerebral infarction. DESIGN, TIME AND SETTING： The cytological in vitro study was performed at the Central Laboratory, Second Xiangya Hospital, Central South University, China, in June 2009. MATERIALS： Human ICAM-5 gene transfected into PAJU-TLN cells was supplied by the Life Science College, Helsinki University, Finland. Empty vector transfected PAJU-NEO cells were established by the Gene Center, Second Xiangya Hospital, Central South University, China. METHODS： PAJU-TLN cells transfected with human ICAM-5 or empty vector were incubated in serum-free medium. MAIN OUTCOME MEASURES： Phase contrast microscopy was used to observe changes in PAJU cell morphology. 3-（4, 5-dimethylthiazolzyl）-2, 5-diphenyltetrazolium bromide was used to determine cell viability. Hoechst 33258 was used to stain cell nuclei. Flow cytometry was utilized to measure the apoptosis rate of both PAJU-TLN and PAJU-NEO cells. RESULTS： Both PAJU-TLN and PAJU-NEO cells were injured by cultivating in serum-free medium, but the survival rate of PAJU-TLN cells was significantly higher. CONCLUSION： ICAM-5 protects PAJU-TLN cells from serum deprivation-induced apoptosis, induces the outgrowth of PAJU cells, and diminishes their morphologic impairment.