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PubMed1998

Adhesion of adhesive resin to dental precious metal alloys. Part II. The relationship between surface structure of Au-In alloys and adhesive ability with 4-META resin.

Adhesion of 4-META to Au-In alloy was improved by adding In equivalent to .15% of Au content. On the basis of the results of Au-In alloys analyzed by XPS, the present study investigated the reason why adhesion of the Au-In alloy was improved. The O 1s spectrum could be separated into three oxygen chemical states, In2O3, chemisorbed H2O, and physisorbed H2O. The amount of chemisorbed H2O decreased remarkably with increasing amount of In. It is considered that the poor adhesive ability of the pure gold and alloys containing only small amounts of In was due to the chemisorbed H2O molecules and insufficient indium oxide on the alloy surface. It was established that excellent adhesion requires an oxide with chemical affinity for 4-META to cover at least 50% of the alloy surface.

Acrylic Resins↗
PubMed1995

Mast cells induce T-cell adhesion to human fibroblasts by regulating intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression.

The capacity of mast cell products to mediate T-cell adhesion to fibroblasts was explored using heterotypic coculture systems or by exposing fibroblasts to mast-cell-conditioned media (MCCM), prepared by degranulating mast cells with calcium ionophore. Experimental results indicated that fibroblasts exposed to MCCM for 24 h bound fivefold more T cells than control fibroblasts. Binding was inhibited with intercellular adhesion molecule-1 (ICAM-1) or vascular cell adhesion molecule-1 (VCAM-1) neutralizing antibodies. Enzyme-linked immunosorbent assay and fluorescence-activated cell sorter analysis revealed that fibroblasts exposed to MCCM markedly increased ICAM-1 and VCAM-1 surface expression by 4 h, with levels maximal at 16 h and returning toward baseline by 48 h. A dose-dependent response of ICAM-1 and VCAM-1 expression was noted using serial dilutions of MCCM or by altering the ratio of degranulated mast cells cocultured with fibroblasts. Similar results were obtained using human fibroblasts derived from the dermis, synovium, and lung, although lung fibroblasts were generally less responsive. Northern analysis confirmed that MCCM regulated ICAM-1 and VCAM-1 expression at the mRNA level. In summary, mast cell products stimulated fibroblast surface expression, steady-state mRNA levels, and functional expression of ICAM-1 and VCAM-1. Experimental data suggest that mast-cell-derived tumor necrosis factor-alpha may be in large part responsible for these observations, although further studies using human mast cells will be required. Using a skin-equivalent organotypic coculture model with fibroblasts admixed with mast cells, we observed increased ICAM-1 expression in both keratinocytes and fibroblasts after activation of the mast cells.

Adult↗
PubMed1993

Immunolocalization of the cellular adhesion molecules, intercellular adhesion molecule-1 (ICAM-1) and platelet endothelial cell adhesion molecule (PECAM), in human endometrium throughout the menstrual cycle.

In the present study the presence and distribution of cellular adhesion molecules involved in leukocyte binding were investigated in human endometrium. Endometrial biopsies (n = 45) were collected from women at all stages of normal menstrual cycles. Consecutive cryostat sections of endometrium were immunostained with monoclonal antibodies to intercellular adhesion molecule-1 (ICAM-1) and platelet endothelial cell adhesion molecule (PECAM) and haematoxylin and eosin. Primary antibody binding was visualized using a streptavidin-biotin system. Strong staining for PECAM was observed in endothelial cells of all vessel types and in focal areas of stroma including single cells, small clusters and larger aggregates of cells. At menstruation, however, almost the entire stroma stained for PECAM which was temporally related to a massive influx of leukocytes. ICAM-1 staining, which was consistently less intense than PECAM staining, was detected in vascular endothelial cells during the cycle, reaching a peak at menstruation. Unlike PECAM, ICAM-1 staining did not occur consistently across all vessel types. Stromal staining for ICAM-1 was rare except at menstruation, when almost the entire stroma showed positive staining for ICAM-1. No glandular or luminal epithelial staining was detected for either PECAM or ICAM-1. This study demonstrates that PECAM and ICAM-1 are expressed on endothelial cells of veins, arterioles and capillaries, and stromal cells within human endometrium.

Adult↗
PubMed2002

Influence of single low-density lipoprotein apheresis on the adhesion molecules soluble vascular cellular adhesion molecule-1, soluble intercellular adhesion molecule-1, and P-selectin.

The aim of our study was to investigate the influence of single low-density lipoprotein apheresis (heparin extracorporeal low-density lipoprotein precipitation [HELP]procedure) on plasma concentrations of soluble adhesion molecules (sAMs) such as soluble vascular cellular adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), and P-selectin in patients with familial heterozygous hypercholesterolemia and documented coronary artery disease enrolled in a chronic weekly HELP apheresis. Before HELP apheresis, the mean plasma concentration of sVCAM-1 was 515 +/- 119 ng/ml, 204 +/- 58 ng/ml for sICAM-1, and 112 +/- 45 ng/ml for P-selectin. After single HELP apheresis, plasma concentrations of sAM declined significantly by 32 +/- 7%, 18 +/- 15%, and 33 +/- 25% for sVCAM- 1,sICAM-1 and P-selectin, respectively. After a 1 week interval, sAM concentrations rose to approximately the initial values. The concentrations of all sAMs studied were significantly lower in the plasma leaving than entering the filter. Due to filtration, the decline in plasma level of sVCAM-1, sICAM-1, and P-selectin was 62 +/- 19%, 51 +/- 39%, and 67 +/- 22%, respectively. In addition to lipid reduction, single HELP apheresis significantly lowers plasma concentrations of sVCAM-1, sICAM-1, and P-selectin.

Adolescent↗
PubMed2000

The role of amniotic fluid interleukin-6, and cell adhesion molecules, intercellular adhesion molecule-1 and leukocyte adhesion molecule-1, in intra-amniotic infection.

PROBLEM: To determine amniotic fluid concentrations and correlations of interleukin-6 (IL-6), intercellular adhesion molecule-1 (ICAM-1), and leukocyte adhesion molecule-1 (LAM-1) in patients with and without intra-amniotic infection. METHOD OF STUDY: Fourteen specimens with intra-amniotic infection and 45 without intra-amniotic infection were studied. Intra-amniotic infection was defined as the presence of a positive amniotic fluid culture. Amniotic fluid IL-6, ICAM-1, and LAM-1 levels were determined by an enzyme-linked immunoassay, and normalized by amniotic fluid creatinine levels. RESULTS: Amniotic fluid concentrations of IL-6 and LAM-1 were significantly higher in patients with than without intra-amniotic infection. However, amniotic fluid ICAM-1 concentrations were not significantly different between two groups. Amniotic fluid IL-6, LAM-1, and ICAM-1 were positively correlated. CONCLUSIONS: Our data indicate that amniotic fluid IL-6 is significantly associated with an increased adhesion molecule expression in intra-amniotic infection. However, LAM-1 plays a more important role than ICAM-1 in intra-amniotic infection.

Amniotic Fluid↗
PubMed1991

Adhesion of K99 fimbriated Escherichia coli to pig intestinal epithelium: correlation of adhesive and non-adhesive phenotypes with the sialoglycolipid content.

Evidence for the existence of two phenotypes of piglets born to experimental herds was obtained based on the susceptibility of intestinal brush borders to adhesion of K99-positive Escherichia coli. The enterocytes of the K99-receptive piglets displayed a characteristic sialoglycolipid pattern, with a higher content of the monosialoglycolipids II3NeuGc-LacCer (GM3Gc), IV3NeuGc-nLcOse4Cer (SPGGc) and IV3NeuAc-nLcOse4Cer (SPG) and the oligosialogangliosides IV3NeuAc,II3NeuAc-GgOse4Cer (GD1a), II3(NeuAc)2-GgOse3Cer (GD2), II3(NeuAc)2-GgOse4Cer (GD1b) and IV3NeuAc,II3(NeuAc)2-GgOse4Cer (GT1b) when compared to the gangliosides of non-receptive piglets. The gangliosides from enterocytes of the non-receptive piglets were mainly the monosialogangliosides II3NeuAc-GgOse3Cer (GM2) and II3NeuAc-LacCer (GM3), only traces of the other sialoglycolipids being detected. Adhesion of 14C-labelled K99-positive E. coli cells to the piglet small intestinal sialoglycolipids, as tested by the thin-layer chromatogram overlay assay, revealed that the receptive enterocyte membrane was richer in glycolipids containing K99 receptor structures than the non-receptive enterocyte. Adhesion of K99-positive E. coli correlated with the degree of sialylation of the brush border glycolipids.

Animals↗
PubMed2004

Calcium rises locally trigger focal adhesion disassembly and enhance residency of focal adhesion kinase at focal adhesions.

Focal adhesion kinase (FAK) activity and Ca(2+) signaling led to a turnover of focal adhesions (FAs) required for cell spreading and migration. We used yellow Cameleon-2 (Ycam), a fluorescent protein-based Ca(2+) sensor fused to FAK or to a FAK-related non-kinase domain, to measure simultaneously local Ca(2+) variations at FA sites and FA dynamics. Discrete subcellular Ca(2+) oscillators initiate both propagating and abortive Ca(2+) waves in migrating U87 astrocytoma cells. Ca(2+)-dependent FA disassembly occurs when the Ca(2+) wave reaches individual FAs, indicating that local but not global Ca(2+) increases trigger FA disassembly. An unexpectedly rapid flux of FAK between cytosolic and FA compartments was revealed by fluorescence recovery after photobleaching studies. The FAK-Ycam recovery half-time (17 s) at FAs was slowed (to 29 s) by Ca(2+) elevation. FAK-related non-kinase domain-Ycam had a faster, Ca(2+)-insensitive recovery half-time (11 s), which is consistent with the effect of Ca(2+) on FAK-Ycam dynamics not being due to a general modification of the dynamics of FA components. Because FAK association at FAs was prolonged by Ca(2+) and FAK autophosphorylation was correlated to intracellular Ca(2+) levels, we propose that local Ca(2+) elevations increase the residency of FAK at FAs, possibly by means of tyrosine phosphorylation of FAK, thereby leading to increased activation of its effectors involved in FA disassembly.

Blotting, Western↗
PubMed1995

Adhesion molecules on intermediate TCR cells. I. Unique expression of adhesion molecules, CD44+ L-selectin-, on intermediate TCR cells in the liver and the modulation of their adhesion by hyaluronic acid.

In addition to thymus-derived T cells, it was demonstrated recently that extrathymically differentiated T cells exist in the liver and other immune organs of mice. Since such extrathymic T cells have T-cell receptors (TCR) of intermediate intensity (i.e. intermediate TCR cells) and constitutively express IL-2 receptor beta-chain (IL-2R beta) similar to natural killer (NK) cells, they are easily distinguished from thymus-derived T cells with a TCR-bright+ IL-2R beta- phenotype (i.e. bright TCR cells). In the present study, the expression of adhesion molecules CD44 and L-selectin was compared between these T-cell subsets. Intermediate TCR cells in the liver and other organs were found to be CD44+ L-selectin- and, inversely, bright TCR cells were CD44- L-selectin+. CD3- IL-2R beta+ NK cells were also estimated to be CD44+ L-selectin-. Hyaluronic acid, which is known to adhere to a CD44 ligand, bound to intermediate TCR cells, but not to bright TCR cells. Among many extracellular matrices, hyaluronic acid induced a prominent decrease in the numbers and proportions of intermediate TCR cells and NK cells in the liver from 6 to 24 hr after in vivo administration. The half-life span of injected hyaluronic acid was approximately 7 hr in the plasma. These results suggest that the CD44 molecule, which is uniquely expressed on intermediate TCR cells and NK cells, is eventually associated with their adhesion to the sinusoidal walls in the liver.

Animals↗
PubMed1996

A fundamental subdivision of circulating lymphocytes defined by adhesion to mucosal addressin cell adhesion molecule-1. Comparison with vascular cell adhesion molecule-1 and correlation with beta 7 integrins and memory differentiation.

The leukocyte integrin alpha 4 beta 7 is a receptor for the vascular mucosal addressin cell adhesion molecule-1 (MAdCAM-1). Most circulating B and T lymphocytes in man are alpha 4+, and on these cells the regulated display of the beta 7 integrin chain determines the expression of alpha 4 beta 7 and, in large part, binding to MAdCAM-1. Among CD4+ T cells, beta 7 high memory cells (including the L-selectin+ subset) bind MAdCAM-1 better than beta 7int naive cells; whereas beta 7- memory cells,including skin homing lymphocytes, interact poorly if at all. Circulating alpha E beta 7+ T cells are alpha 4 beta 7high and also bind MAdCAM-1 well. B cells are also subdivided by beta 7 expression, and beta 7+ B cells bind MAdCAM-1 better than the beta 7low/- subset. The related vascular ligand vascular cell adhesion molecule-1 (VCAM-1), expressed on endothelium primarily in nonmucosal sites of inflammation, interacts with blood lymphocytes (including beta 7high T cells) almost exclusively via alpha 4 beta 1 and binds beta 7low/-(beta 1high) better than beta 7+ B cells and memory cells better than naive CD4+ cells. beta 7-(beta 1high) memory T cells are somewhat enriched over beta 7high memory cells at low (but not at high) VCAM-1 densities. Interestingly, CD56+ NK cells, which express both alpha 4 beta 7 and alpha 4 beta 1, bind well to VCAM-1 but poorly to MAdCAM-1. The findings indicate that the display and function of alpha 4 beta 7 determine integrin-dependent blood lymphocyte interactions with MAdCAM-1, thus delineating discrete mucosal vs nonmucosal lymphocyte populations in vivo; that alpha 4 beta 1 dominates blood lymphocyte interactions with VCAM-1; and that quantitative and qualitative regulation of MAdCAM-1 vs VCAM-1 can critically control the recruitment of specialized lymphocyte subsets during inflammation.

Adult↗
PubMed1980

Analysis of the cell adhesion mechanism using somatic cell hybrids. I. Aggregation of hybrid cells between adhesive V79 and non-adhesive Ehrlich's ascites tumour cells.

V79 Chinese hamster cells dissociated with 1 nm EDTA retain 2 kinds of cell adhesion mechanisms, one dependent on Ca2+ and the other independent of Ca2+. Ehrlich's ascites tumour (EAT) cells are provided with neither Ca2+-dependent nor CA2+-independent mechanisms. Studies on the aggregation of cells of 25 different hybrid clones obtained by fusing these 2 lined cells revealed the following points with regard to adhesive properties of hybrid cells. (1) The activity of the Ca2+-independent mechanism was lower in most hybrid clones than in parental V79 cells. (2) There were a few hybrid clones whose Ca2+-dependent mechanism activity was lower than in V79 cells. In these clones, the Ca2+-independent mechanism was also less active than the parental cells. (3) A hybrid clone with reduced Ca2+-dependent mechanism activity only was not found. (4) All the hybrid clones have at least one set of chromosomes derived from V79. (5) The number of chromosomes derived from EAT cells tended to be less in hybrid clones with lower aggregative ability. These results can be explained by assuming that the activity of the Ca2+-independent and Ca2+-dependent mechanisms of V79 cells may be differently inhibited by genes contained in EAT cells.

Animals↗
PubMed1999

Adhesion molecules (E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)) in sera from patients with Staphylococcus aureus bacteraemia with or without endocarditis.

The aim of this prospective study was to evaluate if patients with endocarditis display a more extensive endothelial activation than those with bacteraemia but without endocarditis. Sixty-five patients with blood culture-verified Staphylococcus aureus bacteraemia were included and serum samples collected on admission were analysed by enzyme immunoassays. Elevated serum concentrations of adhesion molecules were found in most of the patients with S. aureus bacteraemia. Patients with endocarditis (n = 15) showed significantly higher serum E-selectin (median 156 ng/ml) and VCAM-1 (median 1745 ng/ml) concentrations compared with those with S. aureus bacteraemia but without endocarditis (80 ng/ml and 1172 ng/ml, respectively; P = 0.01 and P = 0.003). No significant difference was found between the groups concerning ICAM-1 (median 451 ng/ml versus 522 ng/ml). In addition, serum tumour necrosis factor-alpha (TNF-alpha) concentrations were significantly correlated (P < 0.002) to serum levels of E-selectin, ICAM-1 and VCAM-1.

Adolescent↗
PubMedDate not supplied

Cerebrospinal fluid and plasma concentration of soluble intercellular adhesion molecule 1, vascular cell adhesion molecule 1 and endothelial leukocyte adhesion molecule in patients with acute ischemic brain disease.

BACKGROUND: Leukocyte migration into the ischemic area is a complex process, controlled by adhesion molecules (AM) in leukocytes and endothelium, by migratory capacity of leukocytes and the presence of hemotaxic agents in the tissue. In this research it was supposed that in the blood and cerebrospinal fluid (CSF) of patients in the acute phase of ischemic brain disease (IBD) there were relevant changes in the concentration of soluble AM (sICAM-1, sVCAM-1 and sE-selectin), that could have been the indicators of the intensity of damaging processes in central nervous system (CNS). METHODS: The study included 45 IBD patients, 15 with transient ischemic attack (TIA), 15 with reversible ischemic attack (RIA), and 15 with brain infarction (BI), of both sexes, mean age 66 +/- 7. Control group consisted of 15 patients with radicular lesions of discal origin, subjected to diagnostic radiculography, without the signs of interruption in the passage of CSF. Changes of selected biochemical parameters were determined in all patients in frame 72 hours since the occurrence of an ischemic episode. Concentrations of soluble AM were determined in plasma and CSF by ELISA. Total number of leukocytes (TNL) in peripheral blood was determined by hematological analyzer. RESULTS: The results showed that during the first 72 hrs of IBD significant increases occurred in TNL and that the increase was progressive compared to the severeness of the disease. Significant increase of soluble AM concentration was shown in plasma of IBD patients. The increase was highest in BI, somewhat lower in RIA and the lowest in TIA patients compared to the control. In CSF concentrations of sICAM-1, sVCAM-1 and sE-selectin demonstrated similar increasing trend as in plasma. CONCLUSION: TNL, as well as the soluble AM concentrations in plasma and CSF, were increased during the acute IBD phase and progressive in relation to the severeness of the disease, so that they might have been the indicators of CNS inflammatory reaction intensity. Furthermore, the results indicated their role in IBD pathogenesis and offered the possibility of researching the application of antagonists and/or activity modulators of some of them in IBD therapy.

Acute Disease↗
PubMed2000

Liquid and fluid agents for preventing adhesions after surgery for subfertility.

BACKGROUND: Pelvic surgery is associated with high rates of both de novo adhesion formation and adhesion reformation. Although the role of pelvic and/or tubal surgery in the management of infertility is more limited since the development of in-vitro fertilisation such surgery remains indicated for a number of selected patients. Other forms of pelvic surgery will remain prevalent in women of reproductive age (e.g. endometriosis surgery, ovarian cystectomy, myomectomy). Since subsequent fertility is reduced with increasing severity of periadnexal adhesions, pelvic adhesions will remain a clinical problem in infertility patients. Adjuvant therapy has been promoted for many years to prevent adhesion formation. Numerous substances have been used experimentally in animal models, many have been advocated for use during human surgery, and some are widely used in clinical practice. Steroids and antihistamines are given in the belief that they will promote fibrinolysis during healing without preventing healing. OBJECTIVES: To investigate whether pharmacological and liquid agents used as adjuvants during pelvic surgery in infertility patients lead to a reduction in the incidence or severity of postoperative adhesion (re-)formation, and/or an improvement in subsequent pregnancy rates. SEARCH STRATEGY: The specialised database of the Menstrual Disorders and Subfertility Group. SELECTION CRITERIA: Randomised controlled trials investigating the use of pharmacological and liquid agents to prevent adhesion formation after pelvic surgery for infertility. DATA COLLECTION AND ANALYSIS: Data were extracted independently by the first 2 authors. Differences of opinion were registered and resolved by consensus with the senior author (RJL). Two by two tables were generated for each trial for the dichotomous outcome of pregnancy and the effects on pregnancy rate of each study is expressed as an odds ratio with 95% confidence intervals. MAIN RESULTS: None of the pharmacological or liquid agents investigated in a randomised controlled fashion was shown to improve postoperative pregnancy rates. There was some evidence that steroids reduced the incidence and severity of postoperative adhesion formation. Dextran appeared to neither reduce the incidence or severity of adhesions. REVIEWER'S CONCLUSIONS: The routine use of pharmacological agents to prevent post-operative adhesions after infertility surgery cannot be recommended on the basis of the available evidence derived from RCTs. In connection with adhesion prevention, the evidence with regard to steroids is far from perfect but tentatively suggests that they may be beneficial. Further randomised studies should be conducted to investigate this further.

Anticoagulants↗
PubMed2002

Three functionally distinct adhesions in filopodia: shaft adhesions control lamellar extension.

In this study, adhesions on individual filopodial shafts were shown to control veil (lamellar) advance and to be modulated by guidance cues. Adhesions were detected in individual filopodia of sensory growth cones using optical recordings, adhesion markers, and electron microscopy. Veils readily advanced along filopodia lacking shaft adhesions but rarely advanced along filopodia displaying shaft adhesions. Experiments altering adhesion showed that this relationship is not caused by veils removing adhesions as they advanced. Reducing adhesion with antibodies decreased the proportion of filopodia with shaft adhesions and coordinately increased veil advance. Moreover, the inhibitory relationship was maintained: veils still failed to advance on individual filopodia that retained shaft adhesions. These results support the idea that shaft adhesions inhibit veil advance. Of particular interest, guidance cues can act by altering shaft adhesions. When a cellular cue was contacted by a filopodial tip, veil extension and shaft adhesions altered in concert. Contact with a Schwann cell induced veil advance and inhibited shaft adhesions. In contrast, contact with a posterior sclerotome cell prohibited veil advance and promoted shaft adhesions. These results show that veil advance is controlled by shaft adhesions and that guidance signal cascades can alter veil advance by altering these adhesions. Shaft adhesions thus differ functionally from two other adhesions identified on individual filopodia. Tip adhesions suffice to signal. Basal adhesions do not influence veil advance but are critical to filopodial initiation and dynamics. Individual growth cone filopodia thus develop three functionally distinct adhesions that are vital for both motility and navigation.

Animals↗
PubMed2005

Matrix cell adhesion activation by non-adhesion proteins.

Cell adhesion to the extracellular matrix is important in many biological processes. Various ligands and cell surface receptors have been defined. In vitro cell adhesion to matrix proteins and to other 'adhesion' proteins is generally measured on plastic culture substrates. We have found that the presence of low levels of adhesion proteins, e.g. fibronectin, together with high concentrations of non-adhesion proteins, e.g. osteonectin, can promote cell attachment on plastic culture dishes. This promotion of adhesion occurs even when the concentrations of fibronectin, collagen and other adhesive proteins are too low to support cell attachment alone. Other non-adhesive proteins that have similar activity in 'triggering' the attachment of cells to low levels of adhesion molecules include bovine serum albumin (BSA) and cytochrome C. The non-adhesive protein must be added to the plate first, or together with the low amount of the adhesion protein, to 'activate' cell attachment. Adding the adhesion protein fibronectin to the plate first, followed by osteonectin, resulted in no 'activation' of attachment. The non-adhesive protein did not bind to the adhesive protein nor did it alter the level of adhesive protein binding to the substrate. The non-adhesive protein did, however, expose integrin-binding sites of the adhesive protein fibronectin. These data confirm and extend previous data by others demonstrating the role of non-adhesive proteins in regulating the conformation and cell adhesive activity of matrix adhesion proteins on plastic surfaces. Such findings might explain contradictions in the literature about the activity of 'adhesive proteins'.

Animals↗
PubMed1994

Improvement of interobserver reproducibility of adhesion scoring systems. Adhesion Scoring Group.

OBJECTIVE: To compare the interobserver reproducibility of two adhesion scoring methods, a more comprehensive adhesion scoring method and the American Fertility Society (AFS) adhesion scoring method. DESIGN: Eleven endoscopic surgeons independently evaluated and scored 13 surgical video recordings using both systems. MATERIAL AND METHODS: The standardized AFS adhesion scoring method and the more comprehensive adhesion scoring method were utilized to assess abdominal adhesions. The more comprehensive adhesion scoring method scored 23 individual locations in the abdominal cavity for severity (0, none; 1, filmy, avascular; 2, vascular and/or dense; 3, cohesive) and extent of total area or length (0, none; 1, < or = 25%; 2, 26% to 50%; 3, > 50%). Because the best method of representing a composite adhesion score is unclear, the more comprehensive adhesion scoring method employed two independent methods of determining total score based on the severity and extent at each location, either adding severity plus extent or multiplying severity times extent before summing all 23 locations. RESULTS: For each scoring method, a correlation coefficient was calculated for each of the 55 pairs of surgeons. Significant correlations were identified for all methods (AFS adhesion scoring method: 35 of 55, 64%; more comprehensive adhesion scoring method: severity plus extent, 49 of 55, 89%; and more comprehensive adhesion scoring method: severity times extent, 53 of 55, 96%). When the more comprehensive adhesion scoring method is limited to 13 areas in the lower pelvis corresponding to the locations represented in the AFS adhesion scoring method, the proportion of significant correlation coefficients become 54 of 55 and 50 of 55 for severity plus extent and severity times extent, respectively. CONCLUSION: Although the AFS adhesion scoring method generated significant agreement between pairs of surgeons, less than a third correlated at the 0.7 level. Use of the more comprehensive adhesion scoring method specifically demonstrating locations, severity, and extent of adhesions produced a marked increase in reproducibility between surgeon pairs in scoring pelvic adhesions.

Humans↗
PubMed1992

Role of LFA-1 and VLA-4 in the adhesion of cloned normal and LFA-1 (CD11/CD18)-deficient T cells to cultured endothelial cells. Indication for a new adhesion pathway.

Patients with the leukocyte adhesion deficiency (LAD) syndrome have a genetic defect in the common beta 2-chain (CD18) of the leukocyte integrins. This defect can result in the absence of cell surface expression of all three members of the leukocyte integrins. We investigated the capacity of T cell clones obtained from the blood of an LAD patient and of normal T cell clones to adhere to human umbilical vein endothelial cells (EC). Adhesion of the number of LAD T cells to unstimulated EC was approximately half of that of leukocyte function-associated antigen (LFA)-1+ T cells. Stimulation of EC with human rTNF-alpha resulted in an average 2- and 2.5-fold increase in adhesion of LFA-1+ and LFA-1- cells, respectively. This effect was maximal after 24 h and lasted for 48 to 72 h. The involvement of surface structures known to participate in cell adhesion (integrins, CD44) was tested by blocking studies with mAb directed against these structures. Adhesion of LFA-1+ T cells to unstimulated EC was inhibited (average inhibition of 58%) with mAb to CD11a or CD18. Considerably less inhibition of adhesion occurred with mAb to CD11a or CD18 (average inhibition, 20%) when LFA-1+ T cells were incubated with rTNF-alpha-stimulated EC. The adhesion of LFA-1- T cells to EC stimulated with rTNF-alpha, but not to unstimulated EC, was inhibited (average inhibition, 56%) by incubation with a mAb directed to very late antigen (VLA)-4 (CDw49d). In contrast to LAD T cell clones and the LFA-1+ T cell line Jurkat, mAb to VLA-4 did not inhibit adhesion of normal LFA-1+ T cell clones to EC, whether or not the EC had been stimulated with rTNF-alpha. We conclude that the adhesion molecule pair LFA-1/intercellular adhesion molecule (ICAM)-1 plays a major role in the adhesion of LFA-1+ T cell clones derived from normal individuals to unstimulated EC. Adhesion of LFA-1-T cells to TNF-alpha-stimulated EC is mediated by VLA-4/vascular cell adhesion molecule (VCAM)-1 interactions. Since we were unable to reduce significantly the adhesion of cultured normal LFA-1+ T cells to 24 h with TNF-alpha-stimulated endothelium with antibodies that block LFA-1/ICAM-1 or VLA-4/VCAM-1 interactions, and lectin adhesion molecule-1 and endothelial leukocyte adhesion molecule-1 appeared not to be implicated, other as yet undefined cell surface structures are likely to participate in T cell/EC interactions.

Cell Adhesion↗
PubMed1995

Gonadotropin-releasing hormone agonist therapy reduces postoperative adhesion formation and reformation after adhesiolysis in rat models for adhesion formation and endometriosis.

OBJECTIVES: To evaluate the effectiveness of GnRH agonist (GnRH-a) therapy on adhesion formation and reformation in established rat models for surgically induced adhesion formation and endometriosis. DESIGN: Before surgery, female Sprague-Dawley rats were injected with GnRH-a or control diluent. Six days later, rats were assigned to one of four surgical groups: [1] endometriosis, [2] endometriosis sham, [3] adhesion model, or [4] adhesion sham. Three weeks after surgery, a second-look laparotomy was performed, adhesions were scored (0 = no adhesions to 3 = severe adhesions) and mechanically disrupted, and rats received a second GnRH-a or diluent injection either analogous to their initial injection or in a crossover design. Three weeks after the second injection, rats were killed and adhesion reformation was scored. Data were evaluated using nonparameteric tests including Mann-Whitney, Kruskal-Wallis, and Friedman's tests comparing GnRH-a treatments with diluent controls. RESULTS: Preoperative GnRH-a therapy reduced adhesion scores in rats with surgically induced endometriosis (mean +/- SEM; GnRH-a 1.1 +/- 0.2 versus diluent 2.2 +/- 0.2) and adhesions (GnRH-a 0.3 +/- 0.1 versus diluent 0.6 +/- 0.1). Pretreatment GnRH-a therapy did not affect adhesion scores in the endometriosis sham procedure. Combined preoperative and postoperative GnRHa therapy (GnRH-a-GnRH-a) but not postoperative GnRH-a therapy alone (diluent-GnRH-a) reduced adhesion reformation after adhesiolysis in the endometriosis model (GnRH-a-GnRH-a 1.1 +/- 0.3, diluent-GnRH-a 1.6 +/- 0.7), the endometriosis sham (GnRH-a-GnRH-a 0.7 +/- 0.2, diluent-GnRHa 1.8 +/- 0.1), and the adhesion model (GnRH-a-GnRH-a 0.3 +/- 0.2, diluent-GnRHa 1.0 +/- 0.5). No adhesions were observed in the adhesion sham group. CONCLUSIONS: Gonadotropin-releasing hormone agonist therapy was successful in reducing adhesion formation and reformation. These studies suggest that GnRH-a therapy for adhesion prevention in women should be explored.

Animals↗