Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Healing process of operative cardiac wounds was studied histopathologically in 14 patients who died 28 hours to 5 years after the operation of cardiac valve replacement. Repair of wounds in aorta and free wall of atrium was characterized by production of neointima and proliferation of collagen fiber at adventitia of aorta or epicardium of heart. Adhesion with granulation tissue at left ventricular venting wounds was observed in the case of 18th post-operative day. Reticulofibrosis of surrounding intracardiac muscle played an important role in development of granulation tissue. Cicatrix with collagen fiber was appeared from one month after the operation. In spite of attenuation of ventricular scar, aneurysmal bulging could not be observed. The basic healing pattern of wound in atrial septum was production and thickening of neointima. Granulation tissue rarely developed at the septum. Adhesion between sutured edges of atrial septal endocardium could not be observed and the dead space there remained over a period of 7 months after the operation. These findings indicated the continuous presence of unexpected weakness of the sutured septum until sufficient thickening of neointima had developed.
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PMID:[Healing of operative cardiac wounds]. 400 Jan 3

By implantation of BSp73 ascites cells in a subcutaneous site and subsequent subcutaneous passage of either the local tumor node or metastatic lung tissue, variants were obtained which differed with respect to morphology and to metastatic capacity. The highly metastasizing variant ASML showed spherical morphology in culture, while the nonmetastatic variant AS showed adhesion and spreading. Upon cloning it was observed that colonies with fully expressed morphotypes were readily obtained from solid tissue of both variants. Parental ascites as well as the tumor line derived from the primary solid tumor gave rise to stable expression of either morphotype only after prolonged culturing. Mixing of established clones did not result in an interclonal adaptation of growth rates in vivo. Further characterization of variants AS and ASML revealed marked differences in the outer cell surface. Adhesion of AS cells onto plastic was found to be mediated by fibronectin, laminin and 4 out of 5 collagen types. ASML cells showed adhesion only with collagen type III at higher concentrations. Cytogenetic analysis revealed that the adaptation of BSp73 cells to ascitic growth ultimately led to an increase in chromosome numbers, and this was conserved in ASML cells (modal number 63, range 49-74). AS cells on the other hand showed a modal number of 47 (range 45-49). The chromosome count distribution was rather narrow in ascites cells in vivo, but it was very broad in clones derived thereof, indicating that diversity was obtained in culture rather than in vivo. The data are compatible with the assumption that the nonmetastatic variant was not preexisting in BSp73 ascites but represents a stable phenotype which infrequently arises in a particular microenvironment by chromosome loss from a hyperdiploid parental population.
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PMID:Clonal analysis of diversity in the BSp73 rat tumor. 406 7

The interaction of several common strains of bacteria with rabbit or human platelets in vitro has been examined sequentially with scanning and transmission electron microscopy. Bacteria were added to platelets in their native plasma or to washed platelets in a balanced salt solution at ratios of about 1:1 or at low bacteria to platelet ratios (down to 1:100). The platelet-bacterial interaction (PBI) was studied with recording nephelometry. Matched samples were fixed for microscopy at various points in the aggregation response. The results support these conclusions: a) Bacteria stimulate platelet aggregation by direct contact and adhesion with the platelet surface. b) Adhesion between the two cell types requires divalent cations, occurs through fusion of normal cell-surface coats and appears identical in the presence or absence of extracellular plasma protein. c) The morphologic transformation of platelets during PBI is identical to that produced by collagen. d) During PBI the bacteria are incorporated into the forming platelet aggregates and reside predominantly intercellularly. e) Phagocytosis of bacteria by a single platelet is very rare. f) Bacteria which have resided within platelet aggregates for one hour are unaltered morphologically. g) PBI occurs even at very low bacterial numbers and produces platelet-bacterial aggregates in small numbers without stimulating generalized platelet aggregation. Methods for concentration of thrombocytopenic plasma and washing human platelets are presented.
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PMID:Platelet interaction with bacteria. 3. Ultrastructure. 463 8

The adhesion of SV40-3T3 cells to collagen has been used as a model to investigate factors which may influence the arrest and attachment of metastatic cells in the blood circulation. Adhesion of the transformed cells to collagen films was stimulated by pretreatment of the substrate with human plasma, a source of the cell attachment factor fibronectin, and equally effectively by platelets previously sedimented on to the collagen substrate. Platelet-facilitated adhesion of the transformed cells was related to the number of platelets deposited but there was no requirement for plasma components or for the release of platelet constituents.
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PMID:Platelet-facilitated adhesion of SV40-3T3 cells to collagen. 609 29

Glycosaminoglycans (GAGs) and glycoprotein-derived glycopeptide from mouse BALB/c3T3 and simian virus 40-transformed 3T3 whole cells or their adhesion sites, which are left bound to the serum-coated tissue culture substratum after detachment of cells mediated by [ethylenebis-(oxyethylenenitrilo]tetraacetic acid (EGTA), were analyzed for specific binding to Sepharose columns derivatized with cold-insoluble globulin (CIg). CIg is the serum-contained form of fibronectin and is required for the adhesion of these fibroblasts to the substratum. Of the various GAGs present in these fractions of either cell type, only the highly N-sulfated sequences of heparan sulfate and a small subset of dermatan sulfate bind to CIg-Sepharose. There was no detectable binding of glycopeptide, undersulfated heparan sulfate, the various chondroitin species, or hyaluronate. Adhesion sites from newly attaching cells were greatly enriched in CIg-binding heparan sulfate when compared to long-term-growth adhesion sites or EGTA-detached cells. Various properties of binding were determined. The reference standard standard GAGs heparin (or heparan sulfate) and dermatan sulfate were able to displace bound radiolabeled adhesion site GAG from the column, whereas the other GAGs had no effect. CIg has been shown to be the only adhesion-promoting activity in the serum layer of this culture system. Because these fibroblast adhesion sites do not contain collagen, which could potentially mediate adhesion to the substratum-bound CIg, these data support other evidence that multivalent heparan sulfate proteoglycans mediate substratum adhesion of these cells by coordinate binding to fibronectin on the cell surface and CIg on the substratum.
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PMID:Glycosaminoglycans that bind cold-insoluble globulin in cell-substratum adhesion sites of murine fibroblasts. 625 52

Platelet interactions with cultured bovine endothelial cells were studied following freeze-thaw damage or detergent treatment. Platelets from whole blood, platelet-rich plasma, or gel-filtered plasma did not interact directly with freeze-thaw-damaged endothelial cells. Freezing and thawing did result in the exposure of an extracellular matrix located beneath the cells, which proved very thrombogenic. Platelets from all sources attached to both microfilament and amorphous components of the extracellular matrix, although only platelets from whole blood demonstrated aggregation and extensive pseudopodia formation. Treatment of cells with Triton-X detergent resulted in exposure of an intracellular cytoskeleton. Most platelets attached to the cytoskeleton were located near the cell border and had one or more pseudopodia either in contact with extracellular or intracellular material. Adhesion of platelets to the extracellular matrix may represent platelet-collagen or platelet-fibronectin interactions since both are produced by an incorporated into the extracellular matrix. Platelet interaction with endothelial cytoskeletons may represent contact of pseudopodia with the now exposed matrix located beneath the cells. The possibility that platelets also adhered to intracellular components could not be eliminated. These findings are in agreement with data from a freeze-thaw injury model of perfused aorta. In addition, they tend to indicate that physical insult is not sufficient to induce platelet interaction with the endothelial surface, but that chemical modification enhances platelet deposition.
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PMID:Platelet-endothelial cell interactions in vitro following freeze-thaw injury or detergent treatment. 638 63

Adhesion of platelets from the platelet-rich plasma (PRP) of patients with von Willebrand's disease (vWD) and healthy donors has been studied in a simple model system - wells of multiwell tissue culture plates coated with fibrillar calf skin collagen (CSC). This model is characterized by: (i) the presence of only one constituent of the vessel wall connective tissue matrix (collagen), (ii) the absence of surface-bound aggregates and thrombi, (iii) absence of overlapping of neighbouring spread platelets. A morphometric quantitation of adhesion by scanning electron microscopy (SEM) has been carried out. It allows to subdivide this process into three stages: 1) initial attachment of unspread platelets to the substrate, 2) platelet spreading on the substrate, and 3) attachment of unspread platelets to the upper surface of spread platelets. It was established that the PRP of vWD patients, compared to that of healthy donors, is characterized by a decreased total adhesion of platelets to a CSC-coated surface, which is manifested in the impairment of both the initial attachment and subsequent spreading of platelets. Addition of platelet-free plasma from healthy donors to the vWD PRP completely restores platelet spreading on collagen but little affects the initial attachment. These experiments performed on isolated collagen preparations provide further evidence for the initial attachment and spreading of platelets on collagenous constituents of the subendothelium being factor VIII/von Willebrand factor (FVIII/vWF)-dependent. In contrast to the adhesion on the collagen substrate, the adhesion of platelets from vWD PRP to a foreign surface, polystyrene plastic of uncoated wells, is the same as that of the normal PRP and, thus, FVIII/vWF-independent.
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PMID:Step-by-step analysis of adhesion of human platelets to a collagen-coated surface defect in initial attachment and spreading of platelets in von Willebrand's disease. 661 Feb 24

Cell-substratum adhesion of rat hepatocytes was inhibited by antisera raised against purified plasma membranes of rat liver (anti-liver-antiserum) and Morris hepatoma 7777 (anti-hepatoma-antiserum). It is assumed that substances which block the adhesion-inhibiting activity of the antisera are involved in cell-substratum adhesion. Adhesion-involved molecules of rat liver monitored as 'blocking activity' were compared with those of Morris hepatoma 7777 and 9121. They were found to be integral membrane glycoproteins, which could be solubilized only by detergents. Fractionation of plasma membrane extracts by size exclusion HPLC revealed two blocking activity peaks representing molecules involved in the adhesion to plastic (P-AIM) and collagen (C-AIM). In rat liver both adhesion-involved molecules were found; yet P-AIM seemed to be the major type of adhesion-involved molecule. In the relatively well differentiated Morris hepatoma 9121 also both types were detected. In membrane extracts of the high malignant and poorly differentiated Morris hepatoma 7777, however, no P-AIM but only C-AIM were found. Estimation by size exclusion HPLC revealed molecular weights of 120 kD for C-AIM and approx. 105 kD for P-AIM. On SDS gel electrophoresis proteins in the region of 95 kD were found in C-AIM containing fractions, whereas proteins of 105 kD are likely candidates for P-AIM.
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PMID:Integral membrane antigens involved in cell-substratum adhesion of hepatocytes and hepatoma cells. 670 41

A simple turbidimetric method is described that permits quantitation of both the number and the rate at which human fixed washed platelets adhere to fibrillar collagen in suspension. Fixed washed platelets were mixed with buffer or test sample in an aggregometer cuvette. Collagen was added, and the change in light transmission was recorded at 37 degrees C. Percent adhesion was obtained from the maximum change in light transmission within 5 minutes, and the adhesion rate was calculated from the initial slope of the adhesion curve. In this system, the percent adhesion was optimal at ionic strengths of 0.1 to 0.15 in a pH range of 7.0 to 8.0. Percent adhesion could be increased either by lowering the platelet number or by increasing the collagen concentration. No adherence of fixed washed platelets to heat-denatured collagen or Cytodex 3 beads was observed. Adhesion rate increased with greater stirring speed, but decreased with increasing concentrations of bovine serum albumin or normal human plasma, but the percent adhesion remained relatively constant. The rate of adhesion in 20% normal human plasma was greater than that in 1% to 4% bovine serum albumin buffer. This suggests that normal plasma contains some factor(s) that can overcome the inhibitory effect of protein on the rate of adhesion of fixed washed platelets to fibrillar collagen.
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PMID:A quantitative method for studying platelet adhesion to collagen. 671 55

The effect of 2 strains of Haemophilus somnus on bovine endothelial cells in cultured arterial segments was investigated and compared with the effects of Escherichia coli and Salmonella typhimurium. In cultures inoculated with either strain of H somnus, there was widespread contraction and desquamation of endothelial cells, exposing large areas of subendothelial collagen. Many bacteria were adherent to endothelial cells and some were in phagosomes within cells. Endothelial changes were milder in arterial cultures inoculated with E coli or S typhimurium than in those inoculated with either strain of H somnus. Adhesion of H somnus to vascular endothelial cells followed by exposure of subendothelial collagen may initiate the thrombosis, vasculitis, and ischemic necrosis characteristic of infectious thromboembolic meningoencephalitis in cattle. Arterial cultures might be useful in assaying the virulences of different strains of H somnus, and could be used to investigate the mechanism of their action on endothelial cells.
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PMID:Effect of Haemophilus somnus on bovine endothelial cell in organ culture. 702 Apr 97


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