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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adhesion of leukocytes to endothelial cells is a critical step in the development of acute and chronic inflammatory lesions. We report here that estradiol treatment of cultured human umbilical vein endothelial cells stimulated up to a twofold increase in TNF-induced adhesion of both polymorphonuclear leukocytes and PMA-activated peripheral blood mononuclear cells. This effect was more evident (threefold increase) when endothelial cells were cultured on the basement membrane glycoprotein laminin. Progesterone, but not testosterone, had a similar stimulatory effect. Estradiol also promoted a slight increase in interferon gamma-stimulated endothelial cell adherence for peripheral blood mononuclear cells, but no effect of estradiol was observed when adhesion of leukocytes to endothelial cells was stimulated with IL-1 or IL-4. The estradiol-induced increase in leukocyte binding to human umbilical vein endothelial cells was partially blocked by antibodies to the adhesion molecules E-selectin, intercellular adhesion molecule type 1 (ICAM-1), and vascular cell adhesion molecule type 1 (VCAM-1). Indirect immunofluorescence techniques showed that estradiol produces an increase in TNF-induced cell surface expression of these molecules. Northern blot analysis demonstrated a transient increase in TNF-induced expression of mRNA for E-selectin, ICAM-1, and VCAM-1 in endothelial cells treated with estradiol. Our data demonstrate that estradiol has important regulatory functions in promoting leukocyte-endothelial cell interactions that might contribute to the observed predominance in females of some autoimmune inflammatory diseases.
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PMID:Estradiol enhances leukocyte binding to tumor necrosis factor (TNF)-stimulated endothelial cells via an increase in TNF-induced adhesion molecules E-selectin, intercellular adhesion molecule type 1, and vascular cell adhesion molecule type 1. 750 11

Standard tensile strength and peel adhesion tests were carried out to investigate interactions of pressure-sensitive adhesives (PSAs) with several backing foils used for transdermal patches. Seven branded transdermal patches (Alora, Cutanum, Estraderm MX 50, Estraderm TTS 50, Fem7 -50 micrograms, Menorest, Oesclim) were included in the investigation. Their skin adhesion measured in several clinical trials was compared with the results of the laboratory measurements according to PSTC-1 (Peel Adhesion for Single Coated Tapes 180 degrees Angle, Pressure Sensitive Tape Council, Illinois, 1996), such as Young's modulus at 3% elongation and peel adhesion to stainless steel. Data obtained for the PSA-coated backings (laminates) show increasing elasticity with increasing PSA thickness. Interactions of PSAs with backing foil became evident in significant changes in Young's modulus by low PSA thickness, as seen for the silicone adhesive. The Young's moduli of the laminates were found to be influenced not only by the elasticity of the backing foil but also by the chemical structure of the PSA. There was no correlation between the elasticity and peel adhesion of both the laminates and the branded patches. Likewise, for the branded patches the peel adhesion to stainless steel does not correlate with skin adhesion values obtained from clinical trials. The Young's modulus of the branded patches was between 4 N/mm2 (Oesclim) and 501 N/mm2 (Fem7). For the branded transdermal patches no correlation was found between Young's modulus and both the peel force on stainless steel and the skin adhesion reported in studies.
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PMID:Adhesive backing foil interactions affecting the elasticity, adhesion strength of laminates, and how to interpret these properties of branded transdermal patches. 1247 71

Osteoporosis caused by estrogen deficiency is characterized by enhanced bone resorption mediated by osteoclasts. Adhesion to bone matrix and survival of differentiated osteoclasts is necessary to resorb bone. The aim of our study was to investigate the in vitro effects of estradiol on murine osteoclasts. RAW 264.7 cells treated with 30 ng/ml RANK-L were used as a model for osteoclastogenesis. Estradiol (10(-8)M) for 5 days induced an inhibition of osteoclast differentiation and beta3 expression. Estradiol inhibited significantly the adhesion of mature osteoclasts by 30%. Furthermore estradiol-induced apoptosis shown by with nuclear condensation and Bax/Bcl2 ratio. In addition, estradiol enhanced caspase-3, -8 and -9 activities. This effect completely disappeared using specific caspase-8 inhibitor. However, increased caspase-3 activity by estradiol was observed in the presence of caspase-9 inhibitor, indicating the preferential involvement of caspase-8 pathway. Fas and FasL mRNA expression was not regulated by estradiol. However, estradiol enhanced caspase-3 activity in Fas-induced apoptosis on mature osteoclasts, suggesting that this might interact with the Fas-signaling pathway. These data suggest that estradiol decreases bone resorption by several mechanisms including adhesion and apoptosis of osteoclasts.
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PMID:Estradiol inhibits adhesion and promotes apoptosis in murine osteoclasts in vitro. 1662 21

Application of antimicrobial chemicals is a general procedure in the cleaning and disinfection of food-contacting surfaces. Adhesion to glass surfaces and chemically induced detachment of Pseudomonas fluorescens ATCC 13525(T) were studied in situ, under flow conditions, in a well-controlled parallel plate flow chamber (PPFC). Ortho-phthalaldehyde (OPA) and cetyltrimethyl ammonium bromide (CTAB) were applied separately, at several concentrations, to attached bacteria and their subsequent detachment was monitored. Following treatments the remaining adhered bacteria were characterized in terms of viability and cell size. Simultaneously, the planktonic cell surface was characterized in order to correlate PPFC results with thermodynamic approaches for adhesion evaluation, and surface free energy of chemically treated cells with adhesion strength. About 2.8x10(6) cells/cm(2) adhered to the glass surface after 30 min of bacterial flow, although thermodynamic analyses evidenced unfavourable adhesion. The independent application of OPA and CTAB promoted bacterial detachment to a small extent (16% of total cells). The remaining adhering bacteria were totally non-viable for OPA> or =0.75 mM and CTAB> or =0.25 mM, showing a lack of correlation between bacterial viability and detachment. The cellular size decreased as attachment proceeded and with chemical treatment. Both chemicals altered the cell surface properties, increasing the cell-glass adhesion strength, and promoting the emergence of polar characteristics. The overall results emphasize that OPA and CTAB were markedly ineffective in removing glass-attached P. fluorescens, demonstrating that bacteria can be non-viable but remain strongly attached to the adhesion surface.
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PMID:The effects of a biocide and a surfactant on the detachment of Pseudomonas fluorescens from glass surfaces. 1815 93