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This article is from Cell Adhesion & Migration , volume 6 . Abstract The survival, proliferation, self-renewal and differentiation of human pluripotent stem cells (hPSCs, including human embryonic stem cells and human induced pluripotent stem cells) involve a number of processes that require cell-cell and cell-matrix interactions. The cell adhesion molecules (CAMs), a group of cell surface proteins play a pivotal role in mediating such interactions. Recent studies have provided insights into the essential roles and mechanisms of CAMs in the regulation of hPSC fate decisions. Here, we review the latest research progress in this field and focus on how E-cadherin and several other important CAMs including classic cadherins, Ig-superfamily CAMs, integrins and heparin sulfate proteoglycans control survival and differentiation of hPSCs

This article is from Cell Adhesion & Migration , volume 6 . Abstract The survival, proliferation, self-renewal and differentiation of human pluripotent stem cells (hPSCs, including human embryonic stem cells and human induced pluripotent stem cells) involve a number of processes that require cell-cell and cell-matrix interactions. The cell adhesion molecules (CAMs), a group of cell surface proteins play a pivotal role in mediating such interactions. Recent studies have provided insights into the essential roles and mechanisms of CAMs in the regulation of hPSC fate decisions. Here, we review the latest research progress in this field and focus on how E-cadherin and several other important CAMs including classic cadherins, Ig-superfamily CAMs, integrins and heparin sulfate proteoglycans control survival and differentiation of hPSCs

This article is from Cell Adhesion & Migration , volume 6 . Abstract The survival, proliferation, self-renewal and differentiation of human pluripotent stem cells (hPSCs, including human embryonic stem cells and human induced pluripotent stem cells) involve a number of processes that require cell-cell and cell-matrix interactions. The cell adhesion molecules (CAMs), a group of cell surface proteins play a pivotal role in mediating such interactions. Recent studies have provided insights into the essential roles and mechanisms of CAMs in the regulation of hPSC fate decisions. Here, we review the latest research progress in this field and focus on how E-cadherin and several other important CAMs including classic cadherins, Ig-superfamily CAMs, integrins and heparin sulfate proteoglycans control survival and differentiation of hPSCs

This article is from Cell Adhesion & Migration , volume 6 . Abstract The survival, proliferation, self-renewal and differentiation of human pluripotent stem cells (hPSCs, including human embryonic stem cells and human induced pluripotent stem cells) involve a number of processes that require cell-cell and cell-matrix interactions. The cell adhesion molecules (CAMs), a group of cell surface proteins play a pivotal role in mediating such interactions. Recent studies have provided insights into the essential roles and mechanisms of CAMs in the regulation of hPSC fate decisions. Here, we review the latest research progress in this field and focus on how E-cadherin and several other important CAMs including classic cadherins, Ig-superfamily CAMs, integrins and heparin sulfate proteoglycans control survival and differentiation of hPSCs

Synaptic adhesion molecules regulate synapse development and maintenance. Neurexins and neuroligins have been implicated in psychiatric disorders, and shown that they are related to vascular system and carcinomas in recent studies. In the present study we focused neurexin 1 and neuroligin1, and investigated the relationship between those two molecules expression and clinical features of oral cancer.

This article is from PLoS ONE , volume 9 . Abstract Differential cell adhesive properties are known to regulate important developmental events like cell sorting and cell migration. Cadherins and protocadherins are known to mediate these cellular properties. Though a large number of such molecules have been predicted, their characterization in terms of interactive properties and cellular roles is far from being comprehensive. To narrow down the tissue context and collect correlative evidence for tissue specific roles of these molecules, we have carried out whole-mount in situ hybridization based RNA expression study for seven cadherins and four protocadherins. In developing chicken embryos (HH stages 18, 22, 26 and 28) cadherins and protocadherins are expressed in tissue restricted manner. This expression study elucidates precise expression domains of cell adhesion molecules in the context of developing embryos. These expression domains provide spatio-temporal context in which the function of these genes can be further explored.

This article is from PLoS ONE , volume 9 . Abstract Differential cell adhesive properties are known to regulate important developmental events like cell sorting and cell migration. Cadherins and protocadherins are known to mediate these cellular properties. Though a large number of such molecules have been predicted, their characterization in terms of interactive properties and cellular roles is far from being comprehensive. To narrow down the tissue context and collect correlative evidence for tissue specific roles of these molecules, we have carried out whole-mount in situ hybridization based RNA expression study for seven cadherins and four protocadherins. In developing chicken embryos (HH stages 18, 22, 26 and 28) cadherins and protocadherins are expressed in tissue restricted manner. This expression study elucidates precise expression domains of cell adhesion molecules in the context of developing embryos. These expression domains provide spatio-temporal context in which the function of these genes can be further explored.

Class 12: Adhesion molecules and chemokines

Class 12: Adhesion molecules and chemokines

The evaporative channels for the unimolecular dissociation of metastable AgXlY+ (X = 5-25; Y = 0-4) clusters made by fast atom bombardment of silver foil in the presence of CH3I vapor are observed in the first field free region of a double focussing mass spectrometer. We found three dominant neutral evaporative channels: Ag loss, Ag2 loss and AgI loss. Only Agl2I3+ is found to have an additional channel involving an (AgI)3 loss. Consistent with our previous studies of stable AgXlY+ clusters, we assume a structural formula of (AgX-Y)+(AgI)Y where the metallic part of the cluster conforms to Jellium model predictions. In comparing the relative evaporative loss of AgI from these metastable clusters, we observe: (a) evidence for significant AgI-AgI interaction for clusters whose metallic part has a ls2, IP2 or Is2,Ip4 Jellium configuration; (b) a near constant fractional loss of AgI as the number of AgI units in the parent cluster increases for clusters whose metallic part has a closed main Jellium shell; (c) a relative increase in the fraction loss of Agl as the number of AgI molecules in the parent cluster increases for clusters with an open shell configuration for the metallic part. These observations are discussed in terms of evaporative loss of AgI from structures in which the AgI molecules solvate the metallic part of the cluster. It is proposed that the heat of AgI evaporation is greatly determined by dipole/induced-dipole interactions between the permanent dipole of AgI and the polarizable delocalized electron density of the metallic part of the cluster.

We discuss some interesting physical features stemming from our previous analytical study of a simple model of a fluid with dipolar-like interactions of very short range in addition to the usual isotropic Baxter potential for adhesive spheres. While the isotropic part is found to rule the global structural and thermodynamical equilibrium properties of the fluid, the weaker anisotropic part gives rise to an interesting short-range local ordering of nearly spherical condensation clusters, containing short portions of chains having nose-to-tail parallel alignment which runs antiparallel to adjacent similar chains.

This article is from Reproductive Biology and Endocrinology : RB&E , volume 9 . Abstract Objective: In this study, we determined circulating levels of C-reactive protein, several cytokines, chemokines, adhesion molecules and angiogenic factors along with those of leptin in healthy non-pregnant and pregnant women and preeclamptic patients, and investigated whether serum leptin levels were related to the clinical characteristics and measured laboratory parameters of the study participants. Methods: Sixty preeclamptic patients, 60 healthy pregnant women and 59 healthy non-pregnant women were involved in this case-control study. Levels of leptin and transforming growth factor (TGF)-beta1 in maternal sera were assessed by ELISA. Serum levels of interleukin (IL)-1beta, IL-1 receptor antagonist (IL-1ra), IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p40, IL-12p70, IL-18, interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interferon-gamma-inducible protein (IP)-10, monocyte chemotactic protein (MCP)-1, intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 were determined by multiplex suspension array. Serum C-reactive protein (CRP) concentrations were measured by an autoanalyzer. Serum total soluble fms-like tyrosine kinase-1 (sFlt-1) and biologically active placental growth factor (PlGF) levels were determined by electrochemiluminescence immunoassay. For statistical analyses, non-parametric methods were applied. Results: There were significant differences in most of the measured laboratory parameters among the three study groups except for serum IL-1beta and TGF-beta1 levels. Serum leptin levels were significantly higher in preeclamptic patients and healthy pregnant women than in healthy non-pregnant women. Additionally, preeclamptic patients had significantly higher leptin levels as compared to healthy pregnant women. Serum leptin levels were independently associated with BMI in healthy non-pregnant women. In healthy pregnant women, both BMI and serum CRP concentrations showed significant positive linear association with leptin levels. There were significant positive correlations between serum leptin concentrations of healthy pregnant women and systolic blood pressure, as well as serum levels of IP-10, while their serum leptin levels correlated inversely with fetal birth weight. In preeclamptic patients, a significant positive correlation was observed between serum concentrations of leptin and IP-10. Furthermore, elevated serum leptin level and sFlt-1/PlGF ratio had an additive (joint) effect in the risk of preeclampsia, as shown by the substantially higher odds ratios of their combination than of either alone. Conclusions: Simultaneous measurement of leptin with several inflammatory molecules and angiogenic factors in this study enabled us to investigate their relationship, which can help to understand the role of circulating leptin in normal pregnancy and preeclampsia.

This article is from Reproductive Biology and Endocrinology : RB&E , volume 9 . Abstract Objective: In this study, we determined circulating levels of C-reactive protein, several cytokines, chemokines, adhesion molecules and angiogenic factors along with those of leptin in healthy non-pregnant and pregnant women and preeclamptic patients, and investigated whether serum leptin levels were related to the clinical characteristics and measured laboratory parameters of the study participants. Methods: Sixty preeclamptic patients, 60 healthy pregnant women and 59 healthy non-pregnant women were involved in this case-control study. Levels of leptin and transforming growth factor (TGF)-beta1 in maternal sera were assessed by ELISA. Serum levels of interleukin (IL)-1beta, IL-1 receptor antagonist (IL-1ra), IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p40, IL-12p70, IL-18, interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interferon-gamma-inducible protein (IP)-10, monocyte chemotactic protein (MCP)-1, intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 were determined by multiplex suspension array. Serum C-reactive protein (CRP) concentrations were measured by an autoanalyzer. Serum total soluble fms-like tyrosine kinase-1 (sFlt-1) and biologically active placental growth factor (PlGF) levels were determined by electrochemiluminescence immunoassay. For statistical analyses, non-parametric methods were applied. Results: There were significant differences in most of the measured laboratory parameters among the three study groups except for serum IL-1beta and TGF-beta1 levels. Serum leptin levels were significantly higher in preeclamptic patients and healthy pregnant women than in healthy non-pregnant women. Additionally, preeclamptic patients had significantly higher leptin levels as compared to healthy pregnant women. Serum leptin levels were independently associated with BMI in healthy non-pregnant women. In healthy pregnant women, both BMI and serum CRP concentrations showed significant positive linear association with leptin levels. There were significant positive correlations between serum leptin concentrations of healthy pregnant women and systolic blood pressure, as well as serum levels of IP-10, while their serum leptin levels correlated inversely with fetal birth weight. In preeclamptic patients, a significant positive correlation was observed between serum concentrations of leptin and IP-10. Furthermore, elevated serum leptin level and sFlt-1/PlGF ratio had an additive (joint) effect in the risk of preeclampsia, as shown by the substantially higher odds ratios of their combination than of either alone. Conclusions: Simultaneous measurement of leptin with several inflammatory molecules and angiogenic factors in this study enabled us to investigate their relationship, which can help to understand the role of circulating leptin in normal pregnancy and preeclampsia.

This article is from BMC Genomics , volume 15 . Abstract None

Synaptic adhesion molecules regulate synapse development and maintenance. Neurexins and neuroligins have been implicated in psychiatric disorders, and shown that they are related to vascular system and carcinomas in recent studies. In the present study we focused neurexin 1 and neuroligin1, and investigated the relationship between those two molecules expression and clinical features of oral cancer.

Synaptic adhesion molecules regulate synapse development and maintenance. Neurexins and neuroligins have been implicated in psychiatric disorders, and shown that they are related to vascular system and carcinomas in recent studies. In the present study we focused neurexin 1 and neuroligin1, and investigated the relationship between those two molecules expression and clinical features of oral cancer.

Synaptic adhesion molecules regulate synapse development and maintenance. Neurexins and neuroligins have been implicated in psychiatric disorders, and shown that they are related to vascular system and carcinomas in recent studies. In the present study we focused neurexin 1 and neuroligin1, and investigated the relationship between those two molecules expression and clinical features of oral cancer.

We consider an anisotropic version of Baxter's model of `sticky hard spheres', where a nonuniform adhesion is implemented by adding, to an isotropic surface attraction, an appropriate `dipolar sticky' correction (positive or negative, depending on the mutual orientation of the molecules). The resulting nonuniform adhesion varies continuously, in such a way that in each molecule one hemisphere is `stickier' than the other. We derive a complete analytic solution by extending a formalism [M.S. Wertheim, J. Chem. Phys. \textbf{55}, 4281 (1971) ] devised for dipolar hard spheres. Unlike Wertheim's solution which refers to the `mean spherical approximation', we employ a \textit{Percus-Yevick closure with orientational linearization}, which is expected to be more reliable. We obtain analytic expressions for the orientation-dependent pair correlation function $g(1,2) $. Only one equation for a parameter $K$ has to be solved numerically. We also provide very accurate expressions which reproduce $K$ as well as some parameters, $\Lambda_{1}$ and $\Lambda_{2}$, of the required Baxter factor correlation functions with a relative error smaller than 1%. We give a physical interpretation of the effects of the anisotropic adhesion on the $g(1,2) $. The model could be useful for understanding structural ordering in complex fluids within a unified picture.

We consider an anisotropic version of Baxter's model of `sticky hard spheres', where a nonuniform adhesion is implemented by adding, to an isotropic surface attraction, an appropriate `dipolar sticky' correction (positive or negative, depending on the mutual orientation of the molecules). The resulting nonuniform adhesion varies continuously, in such a way that in each molecule one hemisphere is `stickier' than the other. We derive a complete analytic solution by extending a formalism [M.S. Wertheim, J. Chem. Phys. \textbf{55}, 4281 (1971) ] devised for dipolar hard spheres. Unlike Wertheim's solution which refers to the `mean spherical approximation', we employ a \textit{Percus-Yevick closure with orientational linearization}, which is expected to be more reliable. We obtain analytic expressions for the orientation-dependent pair correlation function $g(1,2) $. Only one equation for a parameter $K$ has to be solved numerically. We also provide very accurate expressions which reproduce $K$ as well as some parameters, $\Lambda_{1}$ and $\Lambda_{2}$, of the required Baxter factor correlation functions with a relative error smaller than 1%. We give a physical interpretation of the effects of the anisotropic adhesion on the $g(1,2) $. The model could be useful for understanding structural ordering in complex fluids within a unified picture.

We consider an anisotropic version of Baxter's model of `sticky hard spheres', where a nonuniform adhesion is implemented by adding, to an isotropic surface attraction, an appropriate `dipolar sticky' correction (positive or negative, depending on the mutual orientation of the molecules). The resulting nonuniform adhesion varies continuously, in such a way that in each molecule one hemisphere is `stickier' than the other. We derive a complete analytic solution by extending a formalism [M.S. Wertheim, J. Chem. Phys. \textbf{55}, 4281 (1971) ] devised for dipolar hard spheres. Unlike Wertheim's solution which refers to the `mean spherical approximation', we employ a \textit{Percus-Yevick closure with orientational linearization}, which is expected to be more reliable. We obtain analytic expressions for the orientation-dependent pair correlation function $g(1,2) $. Only one equation for a parameter $K$ has to be solved numerically. We also provide very accurate expressions which reproduce $K$ as well as some parameters, $\Lambda_{1}$ and $\Lambda_{2}$, of the required Baxter factor correlation functions with a relative error smaller than 1%. We give a physical interpretation of the effects of the anisotropic adhesion on the $g(1,2) $. The model could be useful for understanding structural ordering in complex fluids within a unified picture.

We consider an anisotropic version of Baxter's model of `sticky hard spheres', where a nonuniform adhesion is implemented by adding, to an isotropic surface attraction, an appropriate `dipolar sticky' correction (positive or negative, depending on the mutual orientation of the molecules). The resulting nonuniform adhesion varies continuously, in such a way that in each molecule one hemisphere is `stickier' than the other. We derive a complete analytic solution by extending a formalism [M.S. Wertheim, J. Chem. Phys. \textbf{55}, 4281 (1971) ] devised for dipolar hard spheres. Unlike Wertheim's solution which refers to the `mean spherical approximation', we employ a \textit{Percus-Yevick closure with orientational linearization}, which is expected to be more reliable. We obtain analytic expressions for the orientation-dependent pair correlation function $g(1,2) $. Only one equation for a parameter $K$ has to be solved numerically. We also provide very accurate expressions which reproduce $K$ as well as some parameters, $\Lambda_{1}$ and $\Lambda_{2}$, of the required Baxter factor correlation functions with a relative error smaller than 1%. We give a physical interpretation of the effects of the anisotropic adhesion on the $g(1,2) $. The model could be useful for understanding structural ordering in complex fluids within a unified picture.

Philip Morris Records; report; study

Philip Morris Records; report; study

We have compared the metallic evaporation channels from metastable Ag(X=5,7,11)(AgI)(Y=1-4)(+) clusters in the 1st FFR of a double focussing mass spectrometer with that of the corresponding pure metallic clusters, Ag(X=5,7,11) (+). It is found that the presence of the polar AgI molecules increases the rate of silver monomer evaporation relative to that of silver dimer evaporation. Using thermodynamic expressions for the heat of evaporation of the different evaporation processes and assuming the absence of reverse activation energies, an expression for the difference between the activation energy of silver monomer and dimer evaporation is derived. It is shown that dipole/induced-dipole forces resulting from the presence of AgI polar molecules lead to an enhancement of silver monomer evaporation if the polarizability of the pure metallic cluster ions increases with the number of Jellium electrons. Our theoretical calculations of the static polarizabilities of (Ag(x))(+) using time dependent density functional theory within the local density approximation, shows a smooth increase in the polarizabilities with the number of the Jellium electrons in these clusters. Finally, we observe that the enhancement of Ag monomer evaporation per AgI added is smaller for clusters with even number of AgI molecules than with odd numbers. This was proposed to result from the contribution of configurations with dipole 'pairing' of the AgI molecules in clusters with even number of AgI molecules. Dipole pairing would decrease the average dipole/induced-dipole interaction between the AgI molecules and the metallic part of these 'mixed' clusters.

Eosinophils are nonimmune inflammatory cells which are intricately involved in helminthic infections and allergic hypersensitivity reactions (1, 2). Activated eosinophils produce a host of mediators, including cytokines which can be both detrimental as well as helpful to the host (3, 4, 5). Cytokines such as IL-lalpha, IL-1beta and TNFalpha, also produced by eosinophils, upregulate adhesion molecule expression on both endothelial and tumor cells (6, 7). Increased expression of adhesion molecules such as ICAM-1, V-CAMl and E-Selectin (ELAM-l) on tumor cells is correlated with increased invasiveness and metastasis (8, 9, 10). Multicellular tumor spheroids are three-dimensional cell culture systems which have been shown to model the growth characteristics of tumors as well as their metastatic potential(11, 12, 13). In light of this, tumor spheroids have more recently been used as a model for examining tumor-endothelial cell interactions in order to better understand the interactions of the tumor with its microvascular environment. We have utilized the tumor spheroid model system to study not only its interaction with endothelial cells, but also examine the effector role of eosinophils in tumor:endothelial cell interaction. We have shown that peripheral blood eosinophils from allergic and asthmatic individuals can inhibit the growth of both breast and prostate tumor cells (14, 15). In this study we attempted to examine the hypothesis that eosinophils infiltrate breast spheroids (14) release of their contents into the tumor microenvironment and that these eosinophil mediators, to include cytokines, can modulate spheroid adherence and invasion. In order to do this we attempted to set up an eosinophil tumor spheroid:endothelial tri-cell complex (16).

We have developed a rodent model of decompression sickness and have used it to characterize the pathophysiology of cord injury using quantitative histopathology, immunocytochemistry, flow cytometry and hemodynamic measurements. The results of this work indicate that accumulation of nitrogen gas extravascularly or intravascularly does not play a role in the cord injury. The expression of ICAM-l in the endothelium of the cord increases after decompression. However, there is no corresponding increase in surface expression of adhesion counterreceptors on leucocytes. No recruitment of leucocytes to the cord or activation of endogenous effector cells was identified. These results indicate that the cellular inflammatory reaction is not activated and does not contribute to the cord injury induced by decompression sickness. We have also used the rat model to develop a rapid quantitative assay of cord trauma that will be useful for testing pharmacologic interventions designed to decrease the severity of the injury and enhance recovery. (AN)

Critical progress has been made in the identification and characterization of cells and mediators involved in allergic inflammation. Accumulating evidence supports the importance of cell adhesion molecule expression as an initiating process in tissue inflammation. Despite progress made to date, much is still unknown about the exact mechanisms responsible for this inflammatory response. Scientists have been working to understand the selective cell recruitment operating in allergic disease with the hope of discovering therapeutic intervention strategies that will prevent the accumulation of unwanted cells in inflamed airways. Research has been directed at developing various approaches to generate specific antagonists. Some approaches under study interrupt airway inflammation in its early stages during leukocyte-endothelial interactions. Other approaches inhibit cell recruitment at the endothelial wall. Many studies have been done, both in vivo and in vitro, and the advances that have been made suggest that these therapeutic interventions may be the keys to controlling and, possibly, curing asthma and allergic reactions.

Critical progress has been made in the identification and characterization of cells and mediators involved in allergic inflammation. Accumulating evidence supports the importance of cell adhesion molecule expression as an initiating process in tissue inflammation. Despite progress made to date, much is still unknown about the exact mechanisms responsible for this inflammatory response. Scientists have been working to understand the selective cell recruitment operating in allergic disease with the hope of discovering therapeutic intervention strategies that will prevent the accumulation of unwanted cells in inflamed airways. Research has been directed at developing various approaches to generate specific antagonists. Some approaches under study interrupt airway inflammation in its early stages during leukocyte-endothelial interactions. Other approaches inhibit cell recruitment at the endothelial wall. Many studies have been done, both in vivo and in vitro, and the advances that have been made suggest that these therapeutic interventions may be the keys to controlling and, possibly, curing asthma and allergic reactions.

Critical progress has been made in the identification and characterization of cells and mediators involved in allergic inflammation. Accumulating evidence supports the importance of cell adhesion molecule expression as an initiating process in tissue inflammation. Despite progress made to date, much is still unknown about the exact mechanisms responsible for this inflammatory response. Scientists have been working to understand the selective cell recruitment operating in allergic disease with the hope of discovering therapeutic intervention strategies that will prevent the accumulation of unwanted cells in inflamed airways. Research has been directed at developing various approaches to generate specific antagonists. Some approaches under study interrupt airway inflammation in its early stages during leukocyte-endothelial interactions. Other approaches inhibit cell recruitment at the endothelial wall. Many studies have been done, both in vivo and in vitro, and the advances that have been made suggest that these therapeutic interventions may be the keys to controlling and, possibly, curing asthma and allergic reactions.

Critical progress has been made in the identification and characterization of cells and mediators involved in allergic inflammation. Accumulating evidence supports the importance of cell adhesion molecule expression as an initiating process in tissue inflammation. Despite progress made to date, much is still unknown about the exact mechanisms responsible for this inflammatory response. Scientists have been working to understand the selective cell recruitment operating in allergic disease with the hope of discovering therapeutic intervention strategies that will prevent the accumulation of unwanted cells in inflamed airways. Research has been directed at developing various approaches to generate specific antagonists. Some approaches under study interrupt airway inflammation in its early stages during leukocyte-endothelial interactions. Other approaches inhibit cell recruitment at the endothelial wall. Many studies have been done, both in vivo and in vitro, and the advances that have been made suggest that these therapeutic interventions may be the keys to controlling and, possibly, curing asthma and allergic reactions.

This article is from Annals of Saudi Medicine , volume 31 . Abstract BACKGROUND AND OBJECTIVES:: The expression of soluble adhesion molecules inter-cellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), besides activation of endothelial cells and transendothelial migration of leukocytes, play an important role in inflammation and progression of ischemic injury after acute stroke. The aim of this study was to determine serum levels of soluble ICAM-1 and VCAM-1 in patients with acute ischemic stroke and controls and correlate them according to etiological subtypes (thromboembolic or lacunar stroke), stroke severity and disability after acute stroke. PATIENTS AND METHODS:: Hospital-based prospective study of acute stroke patients hospitalized between December 2008 and September 2009 at the University Hospital Sestre Milosrdnice in Zagreb, Croatia. METHODS:: We enrolled 110 patients with acute ischemic stroke and 93 healthy individuals as controls. Serum concentrations of VCAM-1 and ICAM-1 were determined by means of quantitative sandwich enzyme immunoassay. Patients were classified according to etiological subtype, clinical severity of stroke and disability after stroke. RESULTS:: There was no significant difference between levels of soluble adhesion molecules VCAM-1 and ICAM-1 in patients and in controls. Levels of VCAM-1 were significantly higher in patients with thromboembolic stroke than in controls. There was no significant correlation between levels of soluble adhesion molecules VCAM-1 and ICAM-1 and stroke severity and disability. There was marked biological interindividual variability in all patient groups. CONCLUSION:: This study confirms the role of adhesion molecule VCAM-1 in the pathogenesis of acute thromboembolic stroke.

This article is from Annals of Saudi Medicine , volume 31 . Abstract BACKGROUND AND OBJECTIVES:: The expression of soluble adhesion molecules inter-cellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), besides activation of endothelial cells and transendothelial migration of leukocytes, play an important role in inflammation and progression of ischemic injury after acute stroke. The aim of this study was to determine serum levels of soluble ICAM-1 and VCAM-1 in patients with acute ischemic stroke and controls and correlate them according to etiological subtypes (thromboembolic or lacunar stroke), stroke severity and disability after acute stroke. PATIENTS AND METHODS:: Hospital-based prospective study of acute stroke patients hospitalized between December 2008 and September 2009 at the University Hospital Sestre Milosrdnice in Zagreb, Croatia. METHODS:: We enrolled 110 patients with acute ischemic stroke and 93 healthy individuals as controls. Serum concentrations of VCAM-1 and ICAM-1 were determined by means of quantitative sandwich enzyme immunoassay. Patients were classified according to etiological subtype, clinical severity of stroke and disability after stroke. RESULTS:: There was no significant difference between levels of soluble adhesion molecules VCAM-1 and ICAM-1 in patients and in controls. Levels of VCAM-1 were significantly higher in patients with thromboembolic stroke than in controls. There was no significant correlation between levels of soluble adhesion molecules VCAM-1 and ICAM-1 and stroke severity and disability. There was marked biological interindividual variability in all patient groups. CONCLUSION:: This study confirms the role of adhesion molecule VCAM-1 in the pathogenesis of acute thromboembolic stroke.

This article is from Annals of Saudi Medicine , volume 31 . Abstract BACKGROUND AND OBJECTIVES:: The expression of soluble adhesion molecules inter-cellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), besides activation of endothelial cells and transendothelial migration of leukocytes, play an important role in inflammation and progression of ischemic injury after acute stroke. The aim of this study was to determine serum levels of soluble ICAM-1 and VCAM-1 in patients with acute ischemic stroke and controls and correlate them according to etiological subtypes (thromboembolic or lacunar stroke), stroke severity and disability after acute stroke. PATIENTS AND METHODS:: Hospital-based prospective study of acute stroke patients hospitalized between December 2008 and September 2009 at the University Hospital Sestre Milosrdnice in Zagreb, Croatia. METHODS:: We enrolled 110 patients with acute ischemic stroke and 93 healthy individuals as controls. Serum concentrations of VCAM-1 and ICAM-1 were determined by means of quantitative sandwich enzyme immunoassay. Patients were classified according to etiological subtype, clinical severity of stroke and disability after stroke. RESULTS:: There was no significant difference between levels of soluble adhesion molecules VCAM-1 and ICAM-1 in patients and in controls. Levels of VCAM-1 were significantly higher in patients with thromboembolic stroke than in controls. There was no significant correlation between levels of soluble adhesion molecules VCAM-1 and ICAM-1 and stroke severity and disability. There was marked biological interindividual variability in all patient groups. CONCLUSION:: This study confirms the role of adhesion molecule VCAM-1 in the pathogenesis of acute thromboembolic stroke.

This article is from PLoS ONE , volume 8 . Abstract Background: Currently available methods for diagnosis and staging of prostate cancer lack the sensitivity to distinguish between patients with indolent prostate cancer and those requiring radical treatment. Alterations in key adherens (AJ) and tight junction (TJ) components have been hailed as potential biomarkers for prostate cancer progression but the majority of research has been carried out on individual molecules. Objective: To elucidate a panel of biomarkers that may help distinguish dormant prostate cancer from aggressive metastatic disease. Methods: We analysed the expression of 7 well known AJ and TJ components in cell lines derived from normal prostate epithelial tissue (PNT2), non-invasive (CAHPV-10) and invasive prostate cancer (LNCaP, DU145, PC-3) using gene expression, western blotting and immunofluorescence techniques. Results: Claudin 7, α –catenin and β-catenin protein expression were not significantly different between CAHPV-10 cells and PNT2 cells. However, in PC-3 cells, protein levels for claudin 7, α –catenin were significantly down regulated (−1.5 fold, p = 

This article is from Experimental & Molecular Medicine , volume 44 . Abstract Homophilic interaction of the L1 family of cell adhesion molecules plays a pivotal role in regulating neurite outgrowth and neural cell networking in vivo. Functional defects in L1 family members are associated with neurological disorders such as X-linked mental retardation, multiple sclerosis, low-IQ syndrome, developmental delay, and schizophrenia. Various human tumors with poor prognosis also implicate the role of L1, a representative member of the L1 family of cell adhesion molecules, and ectopic expression of L1 in fibroblastic cells induces metastasis-associated gene expression. Previous studies on L1 homologs indicated that four N-terminal immunoglobulin-like domains form a horseshoe-like structure that mediates homophilic interactions. Various models including the zipper, domain-swap, and symmetry-related models are proposed to be involved in structural mechanism of homophilic interaction of the L1 family members. Recently, cryo-electron tomography of L1 and crystal structure studies of neurofascin, an L1 family protein, have been performed. This review focuses on recent discoveries of different models and describes the possible structural mechanisms of homophilic interactions of L1 family members. Understanding structural mechanisms of homophilic interactions in various cell adhesion proteins should aid the development of therapeutic strategies for L1 family cell adhesion molecule-associated diseases.

This article is from Current Molecular Medicine , volume 14 . Abstract The low molecular weight GTP-binding protein RhoA regulates many cellular events, including cell migration, organization of the cytoskeleton, cell adhesion, progress through the cell cycle and gene expression. Physical forces influence these cellular processes in part by regulating RhoA activity through mechanotransduction of cell adhesion molecules (e.g. integrins, cadherins, Ig superfamily molecules). RhoA activity is regulated by guanine nucleotide exchange factors (GEFs) and GTPase activating proteins (GAPs) that are themselves regulated by many different signaling pathways. Significantly, the engagement of many cell adhesion molecules can affect RhoA activity in both positive and negative ways. In this brief review, we consider how RhoA activity is regulated downstream from cell adhesion molecules and mechanical force. Finally, we highlight the importance of mechanotransduction signaling to RhoA in normal cell biology as well as in certain pathological states.

The structures and energetics of organic molecules adsorbed onto clean and H-passivated Si(001)-(2$\times$1) surfaces have been calculated using density functional theory. For benzene adsorbed on the clean Si surface the tight-bridge structure was found to be stable and the butterfly structure metastable. Both carbonic acid H$_2$CO$_3$ and propane C$_3$H$_8$ dissociate on contact with the surface. Passivation of the Si surface with H-atoms has a dramatic effect on the surface properties. The passivated surface is very inert and the binding energy of all the molecules is very weak.

This article is from Neuro-Oncology , volume 16 . Abstract Background: Cellular adhesion molecules (CAMs), which are normally associated with leukocyte trafficking, have also been shown to play an essential role in tumor metastasis to non-CNS sites. However, the role played by CAMs in brain metastasis is largely unexplored. It is known that leukocyte recruitment to the brain is very atypical and that mechanisms of disease in peripheral tissues cannot be extrapolated to the brain. Here, we have established the spatiotemporal expression of 12 key CAMs in the initial phases of tumor seeding in 2 different models of brain metastasis. Methods: BALB/c or SCID mice were injected intracardially (105 cells/100 μL phosphate-buffered saline with either 4T1-GFP or MDA231BR-GFP cells, respectively (n = 4–6/group), and expression of the CAMs was determined by immunohistochemistry and immunofluorescence colocalisation. Results: Endothelial expression of E-selectin, VCAM-1, ALCAM, ICAM-1, VLA-4, and β4 integrin was markedly increased early in tumor seeding. At the same time, the natural ligands to these adhesion molecules were highly expressed on the metastatic tumor cells both in vitro and in vivo. Two of these ligands showed particularly high tumor cell expression (ALCAM and VLA-4), and consequently their functional role in tumor seeding was determined. Antibody neutralization of either ALCAM or VLA-4 significantly reduced tumor seeding within the brain (>60% decrease in tumor number/mm2 brain; P < .05–0.01). Conclusions: These findings suggest that ALCAM/ALCAM and VLA-4/VCAM-1 interactions play an important functional role in the early stages of metastasis seeding in the brain. Moreover, this work identifies a specific subset of ligand-receptor interactions that may yield new therapeutic and diagnostic targets for brain metastasis.

This article is from Neuro-Oncology , volume 16 . Abstract Background: Cellular adhesion molecules (CAMs), which are normally associated with leukocyte trafficking, have also been shown to play an essential role in tumor metastasis to non-CNS sites. However, the role played by CAMs in brain metastasis is largely unexplored. It is known that leukocyte recruitment to the brain is very atypical and that mechanisms of disease in peripheral tissues cannot be extrapolated to the brain. Here, we have established the spatiotemporal expression of 12 key CAMs in the initial phases of tumor seeding in 2 different models of brain metastasis. Methods: BALB/c or SCID mice were injected intracardially (105 cells/100 μL phosphate-buffered saline with either 4T1-GFP or MDA231BR-GFP cells, respectively (n = 4–6/group), and expression of the CAMs was determined by immunohistochemistry and immunofluorescence colocalisation. Results: Endothelial expression of E-selectin, VCAM-1, ALCAM, ICAM-1, VLA-4, and β4 integrin was markedly increased early in tumor seeding. At the same time, the natural ligands to these adhesion molecules were highly expressed on the metastatic tumor cells both in vitro and in vivo. Two of these ligands showed particularly high tumor cell expression (ALCAM and VLA-4), and consequently their functional role in tumor seeding was determined. Antibody neutralization of either ALCAM or VLA-4 significantly reduced tumor seeding within the brain (>60% decrease in tumor number/mm2 brain; P < .05–0.01). Conclusions: These findings suggest that ALCAM/ALCAM and VLA-4/VCAM-1 interactions play an important functional role in the early stages of metastasis seeding in the brain. Moreover, this work identifies a specific subset of ligand-receptor interactions that may yield new therapeutic and diagnostic targets for brain metastasis.

This article is from Korean Journal of Anesthesiology , volume 66 . Abstract Background: The aim of this study was to investigate the effects of anesthetic techniques used during general anesthesia (GA) and spinal anesthesia (SA) on endothelial adhesion molecules in the fetal circulation of healthy parturients undergoing elective cesarean section. Methods: Patients were randomly assigned to either the general anesthesia (n = 20) or spinal anesthesia (n = 20) group. Maternal and cord blood neopterin, sE-selectin, and sL-selectin levels were measured in both groups. Results: Cord blood neopterin concentrations in the SA group were not different from those in the GA group, but maternal neopterin levels in the SA group were different from those in the GA group. Maternal blood levels of sE-selectin and sL-selectin were not different between the two groups. Similarly, the cord blood levels of sE-selectin and sL-selectin were not different between the two groups. We found an increased inflammatory process in the fetal circulation depending on the anesthetic method used. Conclusions: These results indicate the effects of general and spinal anesthetic techniques on serum sL-selectin, sE-selectin, and neopterin levels in neonates and parturients undergoing elective cesarean section. sE-selectin and neopterin concentrations and leukocyte counts were higher in the fetal circulation than in the maternal circulation during both GA and SA.

This article is from Blood Cancer Journal , volume 3 . Abstract Multiple myeloma (MM) is a largely incurable plasma cell malignancy with a poorly understood and heterogeneous clinical course. To identify potential, functionally relevant somatic mutations in MM, we performed whole-exome sequencing of five primary MM, corresponding germline DNA and six MM cell lines, and developed a bioinformatics strategy that also integrated published mutational data of 38 MM patients. Our analysis confirms that identical, recurrent mutations of single genes are infrequent in MM, but highlights that mutations cluster in important cellular pathways. Specifically, we show enrichment of mutations in adhesion molecules of MM cells, emphasizing the important role for the interaction of the MM cells with their microenvironment. We describe an increased rate of mutations in receptor tyrosine kinases (RTKs) and associated signaling effectors, for example, in EGFR, ERBB3, KRAS and MAP2K2, pointing to a role of aberrant RTK signaling in the development or progression of MM. The diversity of mutations affecting different nodes of a particular signaling network appears to be an intrinsic feature of individual MM samples, and the elucidation of intra- as well as interindividual redundancy in mutations that affect survival pathways will help to better tailor targeted therapeutic strategies to the specific needs of the MM patient.

This article is from Diabetology & Metabolic Syndrome , volume 5 . Abstract Background: The phosphodiesterase inhibitor cilostazol has beneficial effects on atherosclerosis by virtue of vasodilatory and antiplatelet effects. However, less is known about the effect of cilostazol on arterial stiffness and biochemical markers related to vascular inflammation and endothelial dysfunction in type 2 diabetic patients with metabolic syndrome. Methods: In this randomized, double-blind, crossover trial, 45 diabetic patients with metabolic syndrome were randomly assigned to either the cilostazol group (50 mg for 2 weeks, 100 mg for 6 weeks) or placebo group for an 8-week treatment phase, and then crossed over. Brachial-ankle pulse wave velocity (baPWV) and serum levels of inflammatory cytokines and vascular cellular adhesion molecules were measured before and after each treatment phase. Results: Compared with the placebo group, the mean baPWV did not improve in the cilostazol group (mean difference 31.42 cm/sec, 95% CI −55.67 to 118.5). Cilostazol treatment significantly reduced soluble vascular cellular adhesion molecule-1 (sVCAM-1) level (from 1288.7 ± 285.6 to 1168.2 ± 252.3 ng/dL, P = 0.0003), and there was also significant mean difference between groups (mean difference 105.18 ng/dL, 95% CI 10.65 to 199.71). However, other biochemical markers including lipid profiles, high sensitivity C-reactive protein, adiponectin, interleukin-6, tumor necrosis factor-alpha, monocyte chemotactic protein-1, and soluble intercellular adhesion molecule-1 did not improve with cilostazol treatment. Conclusion: Cilostazol treatment significantly reduced serum sVCAM-1 level, but this short term treatment was not associated with beneficial effect on arterial stiffness and other inflammatory markers. Trial registration: (Clinical trial reg. no. NCT00573950, clinicaltrials.gov.)

This article is from Diabetology & Metabolic Syndrome , volume 5 . Abstract Background: The phosphodiesterase inhibitor cilostazol has beneficial effects on atherosclerosis by virtue of vasodilatory and antiplatelet effects. However, less is known about the effect of cilostazol on arterial stiffness and biochemical markers related to vascular inflammation and endothelial dysfunction in type 2 diabetic patients with metabolic syndrome. Methods: In this randomized, double-blind, crossover trial, 45 diabetic patients with metabolic syndrome were randomly assigned to either the cilostazol group (50 mg for 2 weeks, 100 mg for 6 weeks) or placebo group for an 8-week treatment phase, and then crossed over. Brachial-ankle pulse wave velocity (baPWV) and serum levels of inflammatory cytokines and vascular cellular adhesion molecules were measured before and after each treatment phase. Results: Compared with the placebo group, the mean baPWV did not improve in the cilostazol group (mean difference 31.42 cm/sec, 95% CI −55.67 to 118.5). Cilostazol treatment significantly reduced soluble vascular cellular adhesion molecule-1 (sVCAM-1) level (from 1288.7 ± 285.6 to 1168.2 ± 252.3 ng/dL, P = 0.0003), and there was also significant mean difference between groups (mean difference 105.18 ng/dL, 95% CI 10.65 to 199.71). However, other biochemical markers including lipid profiles, high sensitivity C-reactive protein, adiponectin, interleukin-6, tumor necrosis factor-alpha, monocyte chemotactic protein-1, and soluble intercellular adhesion molecule-1 did not improve with cilostazol treatment. Conclusion: Cilostazol treatment significantly reduced serum sVCAM-1 level, but this short term treatment was not associated with beneficial effect on arterial stiffness and other inflammatory markers. Trial registration: (Clinical trial reg. no. NCT00573950, clinicaltrials.gov.)

This article is from Bioscience of Microbiota, Food and Health , volume 31 . Abstract A surface protein of Lactobacillus reuteri, mucus adhesion-promoting protein (MapA), is considered to be an adhesion factor. MapA is expressed in L. reuteri strains and adheres to piglet gastric mucus, collagen type I, and human intestinal epithelial cells such as Caco-2. The aim of this study was to identify molecules that mediate the attachment of MapA from L. reuteri to the intestinal epithelial cell surface by investigating the adhesion of MapA to receptor-like molecules on Caco-2 cells. MapA-binding receptor-like molecules were detected in Caco-2 cell lysates by 2D-PAGE. Two proteins, annexin A13 (ANXA13) and paralemmin (PALM), were identified by MALDI TOF-MS. The results of a pull-down assay showed that MapA bound directly to ANXA13 and PALM. Fluorescence microscopy studies confirmed that MapA binding to ANXA13 and PALM was colocalized on the Caco-2 cell membrane. To evaluate whether ANXA13 and PALM are important for MapA adhesion, ANXA13 and PALM knockdown cell lines were established. The adhesion of MapA to the abovementioned cell lines was reduced compared with that to wild-type Caco-2 cells. These knockdown experiments established the importance of these receptor-like molecules in MapA adhesion.

This article is from Journal of Clinical Medicine Research , volume 6 . Abstract Background: Accumulating evidence suggests that inflammatory mechanisms play a central role in the development, progression and outcome of atherosclerosis. Recent evidence suggests that statins improve anti-inflammatory, anti-thrombotic and endothelial functions, along with their lipid-decreasing effects. We examined the effect of statins on endothelial function using biochemical markers of endothelial dysfunction and brachial artery flow-mediated dilatation (FMD). Methods: Thirty male patients presenting with acute coronary syndrome (ACS) and 26 age-matched healthy control subjects aged 40 - 60 years who were not on any medication were enrolled in the study. The patient group was started on atorvastatin (40 mg/day) without consideration of their low-density lipoprotein (LDL)-cholesterol levels. Endothelin, sICAM and E-selectin from stored serum samples were measured using commercially available enzyme-linked immunosorbant assays (ELISAs). Endothelial function was assessed using brachial artery FMD. Results: Prior to statin treatment, E-selectin, sICAM and endothelin levels, endothelial dysfunction markers, were 99.74 ± 34.67 ng/mL, 568.8 ± 149.0 ng/mL and 0.62 ± 0.33 fmol/mL, respectively in the patient group. E-selectin and sICAM levels were significantly higher in the patients than in the control subjects (P < 0.001); however, endothelin levels were not significantly different between groups. Statin treatment significantly reduced E-selectin and sICAM levels (P < 0.001); however, the decrease in endothelin levels was not statistically significant. %FMD values were significantly increased after statin treatment (P = 0.005), and levels of C-reactive protein (CRP), an inflammation marker, were significantly reduced. Conclusion: Our results indicate that statins play an important role in treatment endothelial dysfunction by reducing adhesion of inflammatory cells.

This article is from Diagnostic Pathology , volume 6 . Abstract Background: The aim of this study was to compare histomorphometric changes and the results of immunohistochemical tests for VCAM, ICAM-1, CD4 and CD8 in normal placentas from HIV-seropositive pregnant women. Methods: Samples of normal placentas were divided into 2 groups: healthy HIV-seronegative pregnant women (control group = C = 60) and HIV-seropositive women (experimental group = E = 57). Conventional histological sections were submitted to morphometric analysis and evaluated in terms of the immunohistochemical expression of ICAM-1, VCAM, CD4 and CD8. Results: The villi in group E were smaller than those in group C. The median for the CD8+ T cell count was higher in group E than in group C (p = 0.03). Immunohistochemical expression of ICAM-1 was observed in 57% of the cases in group E, compared with 21% of those in group C (p = 0.001). There was no difference in VCAM expression or CD4+ cell counts between groups and no correlation between the data for antiretroviral therapy and morphometric or immunohistochemical data. Conclusions: The morphometric data showed that placentas of HIV-seropositive pregnant women tend to have smaller villi than those of seronegative women. In addition, immunohistochemical testing for infectious agents helped to identify cases that were positive for microorganisms (6/112) that routine pathological examination had failed to detect. The anti-p24 antibody had a limited ability to detect HIV viral protein in this study (2/57). Correlation of immunohistochemical expression of CD8+ T cells and ICAM-1 with the presence of HIV in the placenta revealed that those expressions can act as biomarkers of inflammatory changes. There was no correlation between the data for antiretroviral therapy and morphometric or immunohistochemical data.

This article is from Perioperative Medicine , volume 2 . Abstract Background: Whether inflammatory responses to surgery are comparably activated during total intravenous anesthesia (TIVA) and during volatile anesthesia remains unclear. We thus compared the perioperative effects of TIVA and isoflurane anesthesia on plasma concentrations of proinflammatory and anti-inflammatory interleukins and cell adhesion molecules. Methods: Patients having laparoscopic cholecystectomies were randomly allocated to two groups: 44 were assigned to TIVA and 44 to isoflurane anesthesia. IL-1β, IL-6, IL-8, IL-10, IL-13, and the cellular adhesion molecules intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 were determined preoperatively, before incision, and at 2 and 24 hours postoperatively. Our primary outcomes were area-under-the-curve cytokine and adhesion molecule concentrations over 24 postoperative hours. Results: The only statistically significant difference in area-under-the-curve concentrations was for IL-6, which was greater in patients given isoflurane:78 (95% confidence interval (CI): 52 to 109) pg/ml versus 33 (22 to 50) pg/ml, P= 0.006. Two hours after surgery, IL-6 was significantly greater than baseline in patients assigned to isoflurane: 47 (95% CI: 4 to 216, P

This article is from Nutrition & Metabolism , volume 9 . Abstract Background: The soluble cell adhesion molecules and adipokines are elevated in patients with obesity, hypertension, type 2 diabetes mellitus, breast cancer and atherosclerosis. Objective: To investigate the relationship between anthropometric profile, dietary intake, lipid profile and fasting glycemia with serum levels of adipokines (adiponectin and PAI-1) and adhesion molecules (ICAM-1 and VCAM-1) in women without breast cancer undergoing routine mammographic screening. Design: Transversal study. Subjects: One hundred and forty-five women over 40-years old participated in this study. Results: In 39.3% of cases the BMI was above 30 kg/m2; 46.9% had hypertension, 14.5% had type 2 Diabetes Mellitus, 31.7% had dyslipidemia and 88.3% presented a waist-to-hip ratio ≥ 0.8. A linear correlation was found between serum levels of PAI-1 and triglycerides, between serum levels of PAI-1 and WHR and between serum levels of VCAM-1 and BMI. Conclusion: We found a high prevalence of obesity and metabolic syndrome. PAI-1 and VCAM-1 levels were correlated with clinical indicators of obesity and overweight.

This article is from Diabetes Care , volume 35 . Abstract OBJECTIVE: Diabetes may accelerate atheromatosis in uremic patients. Our aim was to assess the influence of type 1 diabetes on the atheromatosis-related inflammation in patients with chronic kidney disease (CKD). RESEARCH DESIGN AND METHODS: We analyzed the expression of proinflammatory cytokines and adhesion molecules in the inferior epigastric artery walls of type 1 diabetic patients with CKD (n = 22) and compared it with nondiabetic uremic patients (n = 92) at the time of kidney transplantation. We evaluated the expression of interleukin (IL)-6, monocyte chemotractant protein (MCP)-1, vascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule-1, and the activation of nuclear factor-κβ p65 (NFkB-p65). Common carotid intima-media thickness (c-IMT) was determined by conventional echography. RESULTS: IL-6, MCP-1, and VCAM-1 proteins were elevated in type 1 diabetic patients compared with nondiabetic subjects (P < 0.05). The nuclear localization of NFkB-p65 was higher in type 1 diabetic patients (P < 0.01) and correlated with the levels of MCP-1 in this group (r = 0.726, P < 0.001). Arterial fibrosis correlated with IL-6 and MCP-1 levels (r = 0.411, P < 0.001 and r = 0.378, P = 0.001). A significant correlation was observed between VCAM-1 levels and both the degree of arterial narrowing and c-IMT. CONCLUSIONS: Type 1 diabetes produces a proinflammatory state in the arteries of end-stage CKD patients, with increased levels of IL-6, MCP-1, and VCAM-1, as well as a greater degree of p65 activation, which are associated with more severe vascular lesions and higher c-IMT. Although causality is not demonstrated, these findings support the major role of inflammation in type 1 diabetic patients with CKD.

This article is from Journal of Experimental & Clinical Cancer Research : CR , volume 32 . Abstract Background: L1 cell adhesion molecule (L1CAM) and epithelial cell adhesion molecule (EPCAM) have been implicated in the development and progression of gastric cancer. The present study investigated the clinical significance of L1CAM and EPCAM in the development, progression and prognosis of gastric cancer. Methods: Expression of L1CAM and EPCAM were examined immunochemically in 601 clinicopathologically characterized gastric cancer cases. Results: L1CAM protein was detected in 23.9% of human non-tumor mucosa samples. All samples expressed L1CAM protein at low levels. High expression of L1CAM protein was detected in 163 (27.1%) tumors. Expression of L1CAM correlated with age, tumor location, size of tumors, Lauren’s classification, depth of invasion, lymph node and distant metastases, regional lymph node stage, Tumor-Node-Metastasis (TNM) stage and prognosis. EPCAM protein was detected in 45.7% of human non-tumor mucosa samples. All samples expressed EPCAM protein at low levels. High expression of EPCAM protein was detected in 247 (41.1%) tumors. Expression of EPCAM correlated with age, tumor location, size of tumors, Lauren’s classification, depth of invasion, lymph node and distant metastases, regional lymph node stage, TNM stage and prognosis. Cumulative 5-year survival rates of patients with high expression of both L1CAM and EPCAM were significantly lower than in patients with low expression of both. Conclusions: Expression of L1CAM and EPCAM in gastric cancer was significantly associated with lymph node and distant metastasis, and poor prognosis. L1CAM and EPCAM proteins could be useful markers to predict tumor progression and prognosis.