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)

Optimal conditions for in vitro adherence of Escherichia coli to uroepithelial cells, previously shown to more efficient for strains causing acute symptomatic than that for strains causing "asymptomatic" urinary tract infections, were investigated. Uroepithelial cells from fresh morning urine of healthy individuals and E. coli bacteria from patients with various forms of urinary tract infeciton were used. Adhesion was found to vary, between individuals and epithelial cell types, with epithelial cell viability, bacterial cultivation medium and growth phase, number of bacteria added to the epithelial cells, and incubation time and temperature. Adhesion was also influenced by variations in pH and osmolarity. Optimal test conditions were obtained with post-log-phase bacterial cultures grown on nutrient broth when 10(8) bacteria were added to 10(5) epithelial cells and incubated for 60 min. Considerable variation was found between experiments done on different days, whereas the variation between duplicates was small. The method described may provide a useful tool in the study of the host-parasite relationship in urinary tract infections.
Infect Immun 1977 Dec
PMID:Adhesion of Escherichia coli to human uroepithelial cells in vitro. 2 93

Adhesion of Streptococcus sanguis, Fusobacterium nucleatum and an Actinomyces sp. to enamel and epon and their interspecies cohesion was studied with scanning and transmission electron microscopy. For adhesion studies enamel or epon was coated with salivary macromolecules and then cells of S. sanguis and in some experiments also with F. nucleatum or Actinomyces sp. Cells of S. sanguis were seen scattered over the surface of a thin "pellicle" that was heavily stained, and F. nucleatum and Actinomyces sp. adhered to S. sanguis or directly to the "pellicle". For studies of cohesion S. sanguis was brought to cohere with F. nucleatum or Actinomyces sp. and then processed for transmission electron microscopy. The morphology of the cell surface structures involved was studied in negatively stained preparations or in thin sections of material treated with ruthenium red or poststained with uranyl and lead salts, phosphotungstic acid or periodic acid-thiocarbohydrazide-osmium tetroxide. S. sanguis demonstrated a fuzzy coat of fimbriae that seemed to unfold in areas of contact with other cells, while cells of F. nucleatum had 6-10 polar pilus-like fimbriae, which appeared to be instrumental in cohesion, as did a dense coat of long, slender fimbriae that covered cells of Actinomyces sp.
Scand J Dent Res 1979 Dec
PMID:Surface ultrastructure of some oral bacteria. 29 64

A case of ossified chronic subdural hematoma was reported. This patient was 56-year-old man, who suffered from mild head traumas two times in 1966 and 1969, and was a drinker. He suddenly complained of speech disturbance on May 17, 1972, and general convulsion with unconsciousness beginning from the right upper limb on May 21. Slight right hemiapresis and mental disturbance appeared gradually since then, and he was admitted to our hospital on August 15. After some examinations, total removal of the ossified cystic chronic subdural hematoma was performed on August 25. The post-operative course was almost good and he was discharged on September 21. Content of this chronic subdural hematoma was almost all old yellowish muddy substance, but while some fresh bleeding points were seen at the inner surface of the both outer and inner membrane. Microscopically, the definite bony formation and the development of capillaries in accordance with the fresh bleeding points were observed in the membranes. Adhesion between the inner membrane of the hematoma and the brain surface which related to the intracerebral hematoma was presented. From these findings, this case suggested some problems about the life cycle of chronic subdural hematoma. The ossified chronic subdural hematoma was discussed from the studies of 6 literature cases and our one case.
No Shinkei Geka 1976 Dec
PMID:[Ossified chronic hematoma--one successful operated case (autlhor's transl)]. 82 42

Adhesion molecules such as intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 are expressed in the kidney and are regulated by proinflammatory cytokines. These adhesion molecules play an important role in the binding and activation process of leukocytes and are of importance in inflammatory kidney diseases. This review article describes current knowledge regarding the structure, expression, and functional role of adhesion molecules and their significance in immune-mediated renal diseases.
J Am Soc Nephrol 1992 Dec
PMID:Intercellular adhesion molecules and vascular cell adhesion molecule-1 and the kidney. 128 78

In order to analyze the onset mechanism of experimental autoimmune uveoretinitis (EAU), two experimental models were used; one was EAU induced by one injection of purified bovine interphotoreceptor retinoid-binding protein (IRBP) with complete Freund's adjuvant in Lewis rat, and the other was an IRBP-induced autoimmune uveoretinitis that occurred spontaneously in nude (nu/nu) mice at 4 weeks of age reconstituted by the grafting of rat embryonic thymus (TG nude mouse). EAU develops when the IRBP-reactive lymphocytes in the regional lymph-nodes are activated. Activation begins when the T lymphocyte recognizes the peptide for the epitope bound to a major histocompatibility complex (MHC) molecule in the antigen-presenting cell by way of the T-cell receptor (TCR). In EAU, ten peptide residues p1182-1191 of the IRBP amino acid sequence, were revealed to be sufficiently capable of lymphocyte activation for EAU, and it was also shown that amino acid positions 1182W (tryptophane), 1185G (glycine), 1186V (valine) and 1188P (proline) of IRBP play important roles as the epitopes or agretopes in developing EAU. On the other hand, two amino acids of IRBP, amino acid positions 1182W (tryptophane) and 1194P (proline) were shown to be the agretopes inducing autoimmune uveoretinitis in the TG nude mouse. A study of the variable region of the TCR with a residual p1182-1194 specific T-cell line from the TG nude mouse revealed that as many as 96% utilized the T-cell receptor V beta 6 gene and that the peptide-MHC molecule complex was recognized by restricted receptors. Adhesion molecules such as ICAM-1 and LFA-1 were also found to play an important role as cofactors in activation of lymphocytes in the antigen-recognition process of EAU. Uveoretinitis seemed to result from an immune reaction in the eye occurring when the T lymphocyte arrives there, activating the immunological process. ICAM-1 and LFA-1 were also found to be involved in the infiltration process of inflammatory cells: our immunohistological examination revealed that ICAM-1 was present in the retinal pigment epithelium and epithelium of the ciliary body composing the blood-ocular barrier. In contrast, LFA-1 was expressed in the infiltrating cells. Finally, the tolerance of IRBP was discussed and it was experimentally demonstrated that the absence of IRBP-induced uveoretinitis in human beings and certain experimental animals resulted from endogenous IRBP serving as a tolerogen; we assumed that the breakdown of this self-tolerance would induce EAU due to thymic dysfunction or IRBP antigen injection.
Nippon Ganka Gakkai Zasshi 1992 Dec
PMID:[The onset mechanism of experimental autoimmune uveoretinitis induced by interphotoreceptor retinoid-binding protein]. 128 51

Severe adhesions were induced at laparotomy by laser ablation of the surface of one uterine horn and 1 cm2 of pelvic sidewall in 20 rabbits. Three weeks later the rabbits were selected at random for laparoscopy or laparotomy. Adhesions at the horn, sidewall and incidental sites were scored and lysed with laser at similar power densities. Three weeks later animals were killed and adhesions were blindly scored. We found a significant and similar reduction in severe adhesions at uterine horns after either laser laparoscopy or laser laparotomy, better lysis of sidewall and incidental adhesions by laser laparoscopy and formation of de novo adhesions at nonoperative sites after laparotomy but not after laparoscopy. We conclude that (1) de novo adhesions are common after laparotomy; (2) severe uterine horn adhesions can be reduced equally well by both laparoscopy and laparotomy but laparoscopy is superior to laparotomy with less severe peripheral adhesions; (3) outcome of adhesiolysis depends on several variables, including adhesion density and location and approach (laparotomy or laparoscopy), even when the tool (laser) is constant.
J Reprod Med 1992 Dec
PMID:Laser laparoscopy versus laparotomy in lysis of pelvic adhesions. 128 6

Intercellular adhesion molecule-1 (ICAM-1) is a cell surface adhesion glycoprotein that mediates leukocyte adhesion through interaction with the leukocyte CD11/CD18 adhesion complex. The aim of this study was to determine whether ICAM-1 is expressed by normal or neoplastic colonic epithelial cells. Immunohistochemical studies on human colonic tissue demonstrated focal ICAM-1 expression by colonic carcinomas but not by normal colonic epithelium. ICAM-1 expression by colonic carcinomas showed a positive correlation with the presence of a peritumoral inflammatory infiltrate. Surface expression of ICAM-1 was also observed in HT-29 cultured human colon cancer cells by both immunohistochemistry and enzyme immunoassay. Interferon-gamma and interleukin-1 beta significantly increased ICAM-1 surface expression by HT-29 cells in a dose-dependent manner. Upregulation of ICAM-1 surface expression became evident some hours after cytokine stimulation and was inhibited by both actinomycin D and cycloheximide, indicating a requirement for de novo RNA and protein synthesis. HT-29 monolayers supported adhesion of human lymphocytes as determined by a quantitative 111In-labeled leukocyte adhesion assay. Adhesion was mediated in part via interaction of ICAM-1 on HT-29 cells with lymphocyte function-associated antigen-1 (CD11a/CD18) on lymphocytes, as defined by using blocking monoclonal antibodies. Expression of ICAM-1 and/or other leukocyte adhesion receptors by neoplastic epithelial cells may play a role in directing leukocyte trafficking and leukocyte-epithelial cell interactions in colonic carcinoma.
Am J Physiol 1992 Dec
PMID:Human colon cancer cells express ICAM-1 in vivo and support LFA-1-dependent lymphocyte adhesion in vitro. 136 41

Tyrosine phosphorylation of membrane-associated proteins is involved at two distinct sites of contact between cells and the extracellular matrix: adhesion plaques (cell adhesion and de-adhesion) and invadopodia (invasion into the extracellular matrix). Adhesion plaques from chicken embryonic fibroblasts or from cells transformed by Rous sarcoma virus contain low levels of tyrosine-phosphorylated proteins (YPPs) which were below the level of detection in 0.5-microns thin, frozen sections. In contrast, intense localization of YPPs was observed at invadopodia of transformed cells at sites of degradation and invasion into the fibronectin-coated gelatin substratum, but not in membrane extensions free of contact with the extracellular matrix. Local extracellular matrix degradation and formation of invadopodia were blocked by genistein, an inhibitor of tyrosine-specific kinases, but cells remained attached to the substratum and retained their free-membrane extensions. Invadopodia reduced or lost YPP labeling after treatment of the cells with genistein, but adhesion plaques retained YPP labeling. The plasma membrane contact fractions of normal and transformed cells have been isolated form cells grown on gelatin cross-linked substratum using a novel fractionation scheme, and analyzed by immunoblotting. Four major YPPs (150, 130, 81, and 77 kD) characterize invadopodial membranes in contact with the matrix, and are probably responsible for the intense YPP labeling associated with invadopodia extending into sites of matrix degradation. YPP150 may be an invadopodal-specific YPP since it is approximately 3.6-fold enriched in the invasive contact fraction relative to the cell body fraction and is not observed in normal contacts. YPP130 is enriched in transformed cell contacts but may also be present in normal contacts. The two major YPPs of normal contacts (130 and 71 kD) are much lower in abundance than the major tyrosine-phosphorylated bands associated with invadopodial membranes, and likely represent major adhesion plaque YPPs. YPP150, paxillin, and tensin appear to be enriched in the cell contact fractions containing adhesion plaques and invadopodia relative to the cell body fraction, but are also present in the soluble supernate fraction. However, vinculin, talin, and alpha-actinin that are localized at invadopodia, are equally concentrated in cell bodies and cell contacts as is the membrane-adhesion receptor beta 1 integrin. Thus, tyrosine phosphorylation of the membrane-bound proteins may contribute to the cytoskeletal and plasma membrane events leading to the formation and function of invadopodia that contact and proteolytically degrade the extracellular matrix; we have identified several candidate YPPs that may participate in the regulation of these processes.
J Cell Biol 1992 Dec
PMID:Tyrosine phosphorylation of membrane proteins mediates cellular invasion by transformed cells. 144 4

Lipoprotein lipase (LPL) bound to vascular endothelial cells hydrolyses triglycerides in plasma lipoproteins. To explore the role of LPL in atherogenesis, the effect of LPL-mediated lipolysis of very low density lipoproteins (VLDL) on monocyte adhesion to endothelial cells was examined. Adhesion of U937 monocytes to porcine aortic endothelial cells that were incubated with VLDL and purified bovine milk LPL was markedly higher than endothelial cells that were incubated with VLDL alone. The increase in monocyte adhesion obtained with VLDL was dependent on the concentration of the lipoprotein, monocyte dose and time of incubation. The increase in adhesion correlated with generation of free fatty acids from the hydrolysis of triglycerides in VLDL by LPL. Furthermore, direct addition of oleic acid to endothelial cells also increased adhesion of monocytes. We postulate that LPL-derived lipolytic products increase monocyte adhesion to vascular endothelium and thereby promote atherogenesis.
Biochem Biophys Res Commun 1992 Dec 30
PMID:Lipoprotein lipase-mediated lipolysis of very low density lipoproteins increases monocyte adhesion to aortic endothelial cells. 148 70

Adhesion of hematopoietic cells to endothelial (En) cells plays an important role in their migration into extravascular tissue. This report characterizes the adhesion properties of naive splenocytes to syngeneic and allogeneic mouse brain microvascular endothelium isolated from the BALB/c or SJL/j mouse strains. Syngeneic adhesion reaches maximum levels by 60 min at 37 degrees C, but is more pronounced in the BALB/c system (mean adhesion = 10.7% +/- 1.0) compared to adhesion seen in the SJL/j (mean adhesion = 4.3% +/- 0.6). BALB/c, but not SJL/j adhesion, seems to be mediated, at least in part, by the interaction of CD11a/CD18 (lymphocyte function-associated antigen 1 (LFA-1] with one of its ligands, because BALB/c adhesion is partially inhibited when the assay is carried out either in the presence of chelating agents or with antibodies to the CD11a/CD18 molecule. Activation of the endothelium with recombinant interferon-gamma (rIFN-gamma), recombinant interleukin-1 alpha (rIL-1 alpha), and recombinant tumor necrosis factor-alpha (rTNF-alpha), enhances adhesion in both BALB/c and SJL/j. IFN-gamma and IL-1 alpha mediated adhesion enhancement is abrogated by antibodies to the CD11a/CD18 molecules in the BALB/c but not in the SJL/j system. The adhesion of splenocytes to mouse brain En clearly has unique properties, and whether or not the differences seen in the SJL/j system in any way influences its susceptibility to the autoimmune demyelinating disease, experimental autoimmune encephalitis, remains to be determined.
J Neuroimmunol 1991 Dec
PMID:Adhesion of splenocytes to brain microvascular endothelium in the BALB/c and SJL/j mouse systems. 168 52


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