Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ADHESIONS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 811 records · Page 45Linked to original sources
PubMed1989

[Bonding strength of metal frameworks and adhesive agents in the resin-bonded bridge technic. 3. Comparative research on various retention mechanisms and adhesive systems].

In fixed denture prosthetics, macro- and micromechanical as well as chemical adhesive mechanisms may be used between metal and bonding agent. The in vitro research presented here determines the adhesive strength of six different bonding agents and five different retention mechanisms on twelve precious and nonprecious metal alloys using shearing stress. The evaluation of the results should help to assess the suitability of the various combinations of materials and anchoring methods for the fixation of adhesive bridges. On the basis of the adhesive strengths and the examination of the various clinical advantages and disadvantages of the different methods that were analyzed, the electrolytic etching of nonprecious metal alloys appears to be particularly suitable for fixed denture prostheses. An efficient combination between alloy and bonding agent is of particular importance in this area. Macromechanical mesh and negative retentions can only be used to a limited clinical extent due to their high space requirements. Very good results were produced by the preconditioning of inner anchor surfaces with silanes. Sandblasting, however, provided unsatisfactory shear-stress results over a broad front independently of the type of alloy.

Dental Alloys↗
PubMed1992

Elevated expression of beta 1 and beta 2 integrins, intercellular adhesion molecule 1, and endothelial leukocyte adhesion molecule 1 in the skin of patients with systemic sclerosis of recent onset.

OBJECTIVE: To investigate the possible role of integrins and cell adhesion molecules in the pathogenesis of the mononuclear cell infiltration and fibrosis of skin that occurs in systemic sclerosis (SSc). METHODS: The presence and topographic distribution of beta 1, beta 2, and beta 4 integrins, as well as of endothelial leukocyte adhesion molecule 1 (ELAM-1) and intercellular adhesion molecule 1 (ICAM-1), was examined immunohistochemically in affected skin from 8 patients with rapidly progressive SSc of recent onset. The expression of the beta 1 integrin gene was also investigated by in situ hybridization with a human sequence-specific complementary DNA. RESULTS: The presence of beta 1 integrin epitopes and the corresponding messenger RNA within inflammatory cells surrounding small vessels was demonstrated in SSc skin but not in normal skin. Lymphocytes positive for beta 2 integrin were also found only in SSc skin, and they appeared in close proximity to small blood vessels and collagen bundles. Immunostaining for beta 4 integrin epitopes revealed no differences between normal and SSc skin. ELAM-1 and ICAM-1 monoclonal antibodies, which identify epitopes indicative of endothelial cell activation, stained endothelial cells in SSc skin but not normal skin. CONCLUSION: These observations suggest that the complex interactions of beta 1 and beta 2 integrins, as well as ELAM-1 and ICAM-1, may be intimately involved in the pathogenesis of SSc, perhaps by mediating the homing and targeting of pathogenetic lymphocytes to the affected tissues.

Antibodies, Monoclonal↗
PubMed1996

Effects of pulse methylprednisolone on cell adhesion molecules in the synovial membrane in rheumatoid arthritis. Reduced E-selectin and intercellular adhesion molecule 1 expression.

OBJECTIVE: To investigate the effects of a 1,000-mg intravenous pulse of methylprednisolone succinate (MP) on cell adhesion molecule expression on the synovial vascular endothelium in patients with rheumatoid arthritis (RA). METHODS: Sequential arthroscopic biopsy samples were taken before and 24 hours after MP administration (10 patients) and at the time of RA flare (2 patients) and after retreatment with MP (1 patient). Immunoperoxidase staining for E-selectin (CD62E), P-selectin (CD62P), intercellular adhesion molecule 1 (ICAM-1; CD54) and platelet-endothelial cell adhesion molecule (PECAM; CD31) was performed, and the staining was quantified by color video image analysis. RESULTS: MP caused a rapid (within 24 hours) and substantial decrease in the expression of E-selectin on the synovial vascular endothelium, with a smaller reduction in ICAM-1 expression on synovial vascular endothelium and the synovial lining. There were no similar effects on synovial membrane P-selectin or PECAM expression. CONCLUSION: A potential mechanism by which MP impairs neutrophil trafficking into inflamed RA joints might be by reducing E-selectin, and possibly, ICAM-1, expression in the synovial membrane.

Aged↗
PubMed2001

Vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 serum level in patients with chest pain and normal coronary arteries (syndrome X).

BACKGROUND: Plasma levels of soluble vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) mediators of leukocyte adhesion to vascular endothelium may implicate in the pathogenesis of the syndrome of chest pain with normal coronary arteries. HYPOTHESIS: We attempted to determine whether markers of endothelial activation are raised in patients with chest pain and normal coronary arteries. METHODS: We measured plasma VCAM-1, ICAM-1 (ng/ ml) in 36 patients (34 men, 2 women, aged 62 +/- 9 years) with stable angina, coronary artery disease (CAD), and a positive response to exercise test; in 21 patients (6 men, 15 women, aged 56 +/- 9 years) with chest pain and normal coronary arteriograms (syndrome X); and in 11 healthy control subjects (8 men, 3 women, aged 49 +/- 14 years). RESULTS: Plasma ICAM-1 levels were significantly higher both in patients with CAD (mean +/- standard error of the mean) (328 +/- 26, p < 0.05), and in syndrome X (362 +/- 22, p < 0.01) than in controls (225 +/- 29). VCAM-1 levels were also higher in syndrome X (656 +/- 42 ng/ml) and in patients with CAD (626 +/- 42 ng/ml) than in controls (551 +/- 60, p = 0.09). CONCLUSIONS: ICAM-1 and VCAM-1 levels are increased both in patients with CAD and with syndrome X compared with control individuals. These findings may suggest the presence of chronic inflammation with involvement of the endothelium in patients with anginal chest pain and normal coronary angiograms.

Adult↗
PubMed1988

Functional evidence that intercellular adhesion molecule-1 (ICAM-1) is a ligand for LFA-1-dependent adhesion in T cell-mediated cytotoxicity.

Although intercellular adhesion molecule-1 (ICAM-1) has been implicated as a ligand in some LFA-1-dependent adhesion, its importance to T cell function has not been established. The present studies investigate the importance of ICAM-1 for human cytotoxic T lymphocytes (CTL), both in their formation of antigen-independent conjugates (AIC) and in their lysis of targets. Analysis of monoclonal antibody (mAb) inhibition of AIC formation indicate that ICAM-1 mAb 1 blocks (a) AIC formation with some but not all targets; (b) the LFA-1 pathway but not the CD2/LFA-3 pathway of adhesion; (c) by binding to the target cell, not the T cell. In studies of cell-mediated lysis (CML) ICAM-1 mAb inhibited lysis of some targets, such as U-937, that use ICAM-1 predominantly in AIC formation; CML on some other targets is not inhibited by ICAM-1 mAb. These data indicate that ICAM-1 is a ligand for AIC formation, antigen-specific CTL recognition and cytolysis of particular target cells. The data also indicate that ICAM-1 is not used in LFA-1-dependent CTL interactions with all kinds of target cells, suggesting the existence of alternative ligands for LFA-1.

Antibodies, Monoclonal↗
PubMed1995

Different forms of human vascular adhesion protein-1 (VAP-1) in blood vessels in vivo and in cultured endothelial cells: implications for lymphocyte-endothelial cell adhesion models.

Vascular endothelium plays a pivotal role in controlling leukocyte extravasation from the blood into the tissues. Vascular adhesion protein-1 (VAP-1) is a novel endothelial cell molecule which mediates lymphocyte binding to the vascular lining (Salmi, M., and Jalkanen, S., Science 1992. 257:1407). In this study, we analyzed endothelial cell type-specific differences of VAP-1. In vivo, VAP-1 is a 90/170-kDa molecule which is mainly expressed on the lumenal surface and in cytoplasmic granules of peripheral lymph node-type postcapillary venules (high endothelial venules, HEV). In tonsil HEV, VAP-1 is modified with abundant sialic acids. VAP-1 is also detectable in the cytoplasm of human umbilical vein endothelial cells (HUVEC) and in an endothelial cell hybrid EaHy-926, although both cell types lack detectable surface VAP-1. Cultured endothelial cells do not express MECA-79-defined peripheral lymph node addressins either. VAP-1 was not translocated onto the endothelial cell surface after stimulation with multiple cytokines, mitogens or secretagogues which induced expression of other known endothelial adhesion molecules. Biochemical analyses revealed that VAP-1 is a approximately 180-kDa protein in these endothelial cell types. Digestions with neuraminidase, O-glycanase and N-glycanase, as well as treatment of cells with tunicamycin and benzyl-N-acetylgalactosaminide, did not alter the molecular mass of VAP-1 in EaHy-926. Pulse-chase experiments showed that VAP-1 is directly synthesized as a 180-kDa molecule without any detectable precursors. Thus, in cultured endothelial cells, VAP-1 is a 180-kDa protein which is devoid of post-translational modifications, and in particular, lacks the sialic acids crucial for the function of VAP-1 in tonsil vessels. Notably, the endothelial cell types commonly used as a model in studying lymphocyte-endothelial cell interactions lack surface expression of VAP-1 and peripheral node addressins, and hence are inherently of limited use in analyses of the initial adhesion of lymphocytes.

Acetylgalactosamine↗
PubMed1995

Adhesion molecule expression and adhesion properties of murine intestinal intraepithelial lymphocyte hybridomas.

We used mouse intraepithelial lymphocyte hybridomas (IELH) to study the role of adhesion molecules, especially beta 7 integrins, in the adherence of IELH to intestinal epithelial cells. Unstimulated 9.1 gamma delta IELH cells expressed high levels of CD11a, CD11a/CD18, CD44, and CD45; medium levels of CD45RB and integrin alpha 4; low levels of alpha M290, beta 7, and 33D1; and very low levels of ICAM-1 and VCAM-1. PHA and TGF-beta stimulated IELH cells--but not control BW5147 cells (alpha 4/beta 7 integrin negative fusion partner)--to bind to IEC-18 and CMT-93 intestinal epithelial cells, but not to renal mesangial cells. The binding was partially blocked by mAbs to integrin alpha 4 and/or alpha M290. The two mAbs in combination did not completely block the binding, suggesting that epitopes not recognized by these two mAbs are also involved in binding. The adhesion of 9.1 gamma delta cells to IEC-18 cells was also partially inhibited by mAbs to VCAM-1, LFA-1, and CD44, but not by mAbs CD45 and a control rat IgG. Thus, IELH may be a useful model system with which to study the role of adhesion molecules in the interaction between IEL and intestinal epithelial cells.

Animals↗
PubMed1995

Modulation of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 on human coronary smooth muscle cells by cytokines.

Adhesion molecules have been demonstrated immunohistochemically on smooth muscle cells in atherosclerotic plaques. In endothelial cells cytokines are potent modulators of adhesion molecule expression. We therefore investigated the effects of cytokines on adhesion molecule expression on cultured human coronary and pulmonary smooth muscle cells by cell ELISA and confocal microscopy. Human coronary and pulmonary smooth muscle cells expressed ICAM-1 and VCAM-1 but not E-selectin. ICAM-1 expression was upregulated by TNF alpha, Il-1 beta and IFN-gamma. VCAM-1 expression was increased by TNF alpha and weakly by Il-1 beta, IFN-gamma had no effect on VCAM-1 expression. Cytokine effects on ICAM-1 and VCAM-1 were based on de novo synthesis. These results demonstrate that cytokines regulate ICAM-1 and VCAM-1 expression on human coronary and pulmonary smooth muscle cells. These effects may play an important role in the immune mechanisms in atherosclerosis.

Cells, Cultured↗
PubMed1998

Adhesive activity of gicerin, a cell-adhesion molecule, in kidneys and nephroblastomas of chickens.

Gicerin, a cell-adhesion molecule belonging to the immunoglobulin superfamily, has both homophilic and heterophilic binding activities to neurite outgrowth factor, an extracellular matrix molecule in the laminin family. Gicerin is thought to play a role in the normal development of chicken kidney, because it is expressed abundantly in the embryonic organ and only slightly in the mature organ. In this study, we have examined the adhesive activity of gicerin in the kidney to characterize its function in organogenesis. We have also examined the function of gicerin in chicken nephroblastomas ("embryonic nephromas"), which show various structures resembling those in embryonic kidneys. Immunohistochemically, the expression patterns of gicerin and neurite outgrowth factor in nephroblastomas are similar to those of embryonic kidneys. Cell-aggregation assays have shown that primary culture cells from both embryonic kidneys and nephroblastomas have strong aggregation activities, and that each aggregation is partially inhibited by gicerin antibody. In contrast, cells from adult kidney exhibit weak aggregation activity that is not inhibited by the antibody. In addition, ligand blot analysis has revealed that gicerins in embryonic kidney and nephroblastoma bind to purified neurite outgrowth factor, whereas extracts from adult kidney show no positive reaction. These findings suggest that the homophilic and heterophilic adhesive activities of gicerin are involved in the formation of both normal kidney and nephroblastoma.

Animals↗
PubMed1989

Cell adhesion activity of non-specific cross-reacting antigen (NCA) and carcinoembryonic antigen (CEA) expressed on CHO cell surface: homophilic and heterophilic adhesion.

Cell adhesion activity of carcinoembryonic antigen (CEA) and non-specific cross-reacting antigen (NCA) has been analysed by using CHO cells which had been transfected with cDNAs and are ectopically expressing each antigen on their surface. CEA expressing CHO tended to aggregate easily within 30 min after being suspended by trypsinization. Cell adhesion assay between 51Cr labelled cells and monolayered cells showed both homophilic and heterophilic interaction, the extent of which was CEA-CEA much greater than CEA-NCA greater than NCA-NCA. These reactions were completely inhibited by Fab' fragment of anti-CEA antibody. The results strongly suggested that CEA and NCA function as Ca++ independent cell adhesion molecules by homophilic and heterophilic interactions.

Animals↗
PubMed1987

Localization of the L2 monoclonal antibody binding site on chicken neural cell adhesion molecule (NCAM) and evidence for its role in NCAM-mediated cell adhesion.

Recent studies have described the localization of functional and structural domains on the neural cell adhesion molecule NCAM. In the present study we have extended these observations to examine the location of the carbohydrate epitope recognized by the L2 monoclonal antibody. This carbohydrate moiety is localized to the 65,000-dalton amino-terminal fragment of NCAM (previously designated Fr1), but is not present in the amino-terminal 25,000-dalton region of NCAM that contains the heparin-binding domain. We have also examined the role of this domain in NCAM-mediated cell adhesion, and have shown that incubation of an NCAM substratum with L2 monoclonal antibody inhibits cell attachment to this substratum. These data therefore suggest that the carbohydrate moiety recognized by L2 monoclonal antibody may be involved in the modulation of NCAM-mediated cell adhesion.

Animals↗
PubMed2005

Mediating specific cell adhesion to low-adhesive diblock copolymers by instant modification with cyclic RGD peptides.

One promising strategy to control the interactions between biomaterial surfaces and attaching cells involves the covalent grafting of adhesion peptides to polymers on which protein adsorption, which mediates unspecific cell adhesion, is essentially suppressed. This study demonstrates a surface modification concept for the covalent anchoring of RGD peptides to reactive diblock copolymers based on monoamine poly(ethylene glycol)-block-poly(D,L-lactic acid) (H(2)N-PEG-PLA). Films of both the amine-reactive (ST-NH-PEG(2)PLA(20)) and the thiol-reactive derivative (MP-NH-PEG(2)PLA(40)) were modified with cyclic alphavbeta3/alphavbeta5 integrin subtype specific RGD peptides simply by incubation of the films with buffered solutions of the peptides. Human osteoblasts known to express these integrins were used to determine cell-polymer interactions. The adhesion experiments revealed significantly increased cell numbers and cell spreading on the RGD-modified surfaces mediated by RGD-integrin-interactions.

Adhesiveness↗
PubMed2005

Serum P-selectin, soluble vascular cell adhesion molecule-I (s-VCAM-I) and soluble intercellular adhesion molecule-I (s-ICAM-I) levels in bladder carcinoma patients with different stages.

Adhesion molecules are thought to have a role in the host defense against carcinogenesis. In this study, we measured serum platelet-(P-) selectin, soluble vascular cell adhesion molecule-I (s-VCAM-I), and soluble intercellular adhesion molecule-I (s-ICAM-I) levels in 51 sequential bladder cancer patients at our urology clinic and 8 controls. Serum levels of P-selectin, s-VCAM-I and s-ICAM-I were significantly higher in all patients than controls. Serum P-selectin and s-ICAM-I levels did not differ based on tumor (T) stage and tumor grade, whereas serum levels of s-VCAM-I were significantly higher in patients with muscle invasive tumors than those with superficial tumors. Further, s-VCAM-I levels correlated with T stage. In conclusion, significantly increased P-selectin, s-VCAM-I, and s-ICAM-I levels were observed in patients with bladder cancer, and s-VCAM-I levels correlated with T stage. Thus, we suggest that the analysis of serum s-VCAM-I levels may provide a prognostic test for T stage and bladder cancer progression during and/or following therapy.

Adult↗
PubMed1999

Levels of soluble vascular cell adhesion molecule-1 and soluble intercellular adhesion molecule-1 are increased in women with ovarian hyperstimulation syndrome.

OBJECTIVE: To determine whether plasma and peritoneal fluid levels of soluble vascular cell adhesion molecule-1 (sVCAM-1) and soluble intercellular adhesion molecule-1 (sICAM-1) are altered in women with ovarian hyperstimulation syndrome (OHSS). DESIGN: Prospective, case-control study. SETTING: Lis Maternity Hospital and the Sara Racine IVF Unit, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. PATIENT(S): The study group comprised 16 women with severe OHSS. The control groups comprised 10 women treated with controlled ovarian hyperstimulation and 8 women with normal findings at diagnostic laparoscopy. INTERVENTION(S): Plasma samples were obtained from the study group and the first control group. Peritoneal fluid samples were obtained during paracentesis from the study group and during diagnostic laparoscopy from the second control group. MAIN OUTCOME MEASURE(S): Samples were assayed by specific ELISA for sVCAM-1 and sICAM-1. RESULT(S): The mean peritoneal fluid levels of sVCAM-1 and sICAM-1 and the mean plasma levels of sVCAM-1 were significantly higher in the women with OHSS than in the control groups. However, the mean plasma levels of sICAM-1 were comparable. A positive correlation was demonstrated between the levels of sVCAM-1 and plasma E2 at the time of hCG administration and between the levels of sICAM-1 and number of ova retrieved. CONCLUSION(S): Our findings suggest that soluble cell adhesion molecules may have a role in the pathogenesis and progression of OHSS.

Adult↗
PubMed1997

New indices of ischemic heart disease and aging: studies on the serum levels of soluble intercellular adhesion molecule-1 (ICAM-1) and soluble vascular cell adhesion molecule-1 (VCAM-1) in patients with hypercholesterolemia and ischemic heart disease.

It is known that the expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) on the surface of vascular endothelial cells is closely related to the formation of early atherosclerotic lesions. In this study, serum soluble ICAM-1(sICAM-1) and soluble VCAM-1(sVCAM-1) were determined by sandwich ELISA both in normal healthy individuals (n = 114) and in patients with hypercholesterolemia (HC, n = 112) or ischemic heart disease (IHD, n = 38) to clarify the significance of the soluble forms of the adhesion molecules in the development of atherosclerotic diseases. IHD patients, not HC patients, showed significant elevation of sICAM-1, but not of sVCAM-1, compared with controls in age and sex-matched subjects. In addition, multiple linear regression analysis showed that sICAM-1 was correlated only to the presence of IHD but not to age and lipids. Multiple logistic regression analysis revealed that sICAM-1 was the most powerful independent predictor of the presence of IHD. On the other hand, sVCAM-1, not sICAM-1, was positively correlated to age. Multiple linear regression analysis showed that age was the most powerful independent predictor of the level of sVCAM-1. These data suggest that sICAM-1 and sVCAM-1 are useful as indices of clinical manifestations of atherosclerosis and aging, respectively.

Adult↗
PubMed1999

Deposition of eosinophil-granule major basic protein and expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 in the mucosa of the small intestine in infants with cow's milk-sensitive enteropathy.

BACKGROUND: Cow's milk-sensitive enteropathy (CMSE) is an important cause of chronic diarrhea and failure to thrive in infancy. The immunopathology of the mucosal lesion associated with CMSE has not yet been described. OBJECTIVES: This study investigated the eosinophil activation and the role of adhesion molecules in the pathogenesis of intestinal mucosal damage associated with CMSE. METHODS: Twenty-one patients with chronic diarrhea and abnormal mucosa on duodenal biopsy specimens were included. The patients had negative responses to skin prick tests and RASTs with milk. Fourteen patients were diagnosed with CMSE by milk challenge test and were designated as the CMSE group. Seven patients with no milk intolerance were defined as the non-CMSE group. Four infants with frequent vomiting and no mucosal abnormalities were also studied as the control group. Immunohistochemical stains for eosinophil major basic protein (MBP), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 on endoscopic duodenal biopsy specimens were performed. RESULTS: The degree of eosinophil degranulation, as evidenced by localization of extracellular MBP, was significantly greater in the CMSE group compared with the non-CMSE and control groups (P <.05). Expression of VCAM-1 on mononuclear cells was higher in the CMSE group compared with the non-CMSE and control groups (P <.05). The severity of villous atrophy was positively correlated with the deposition of MBP (r = 0.79, P <.001). CONCLUSION: These results strongly suggest eosinophils and VCAM-1 are implicated in the pathogenesis of mucosal damage associated with CMSE.

Biopsy↗
PubMed2001

Regulation of bovine intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) on cultured aortic endothelial cells.

Endothelial cell adhesion molecules (AM) intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) are important mediators of cell migration from blood into tissue. The kinetics of ICAM-1 mRNA and VCAM-1 protein expression in bovine aortic endothelial cells (BAEC) were determined using quantitative reverse transcriptase polymerase chain reaction (Q-RT-PCR) and flow cytometric analysis, respectively. Stimulation of BAEC with recombinant bovine tumor necrosis factor alpha (rbTNF-alpha) resulted in protein expression of VCAM-1 on less than 5% of all cultured BAECs at 1h post-stimulation, followed by a significant increase at 3h that was maintained until 48h when the proportion of VCAM-1 positive (+) cells decreased significantly, but not to baseline proportions. The expression kinetics for VCAM-1 were similar on cells stimulated with lipopolysaccharide (LPS) except at 24h, when there was a significantly higher proportion of BAEC expressing VCAM-1 than at any other time. The expression of ICAM-1 mRNA differed significantly between stimuli. Expression of ICAM-1 mRNA peaked at 12-18h and then diminished but remained at amounts above baseline up to 72h after stimulation. Stimulation with LPS induced a significant increase in ICAM-1 mRNA expression between 1 and 12h after which the amounts rapidly decreased to baseline. In summary, different stimuli produced similar expression kinetics of VCAM-1 surface protein but different kinetics of ICAM-1 mRNA expression.

Animals↗
PubMed1999

Circulating intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin in patients with type 2 diabetes mellitus.

Serum levels of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin in patients with type 2 diabetes mellitus (n = 64) and control subjects (n = 40) were studied. Serum ICAM-1 concentrations in diabetic patients were significantly higher than those of control subjects (378.2 +/- 70.0 versus 220.4 +/- 31.8 ng/ml, P < 0.01). By multiple regression analysis, hemoglobin A1c was independently associated with serum ICAM-1 concentration in patients with diabetes. The serum VCAM-1 concentration of diabetic patients with macroangiopathy was higher than those of patients without macroangiopathy and of control subjects (806.9 + 276.5 versus 639.0 +/- 146.0 (P < 0.01), and 652.1 +/- 146.9 ng/ml (P < 0.01), respectively). There was no difference in serum E-selectin concentration between diabetic patients with or without macroangiopathy and normal control subjects. These results suggest that adhesion molecules may contribute to the development of atherosclerosis in the diabetic state.

Adult↗