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Alteration of the cell/substratum adhesive structures of rat fibroblasts (3Y1 cells) upon transformation by Rous sarcoma virus (RSV) was investigated by immunofluorescence microscopy. In serum-containing culture medium, 3Y1 cells developed focal adhesions as their main adhesive structures, while BY1 cells expressed peculiar close contacts along the cell periphery with the vitronectin receptor integrin, in addition to podosomes. These peripheral close contacts are referred to as the peripheral adhesions. The peripheral adhesions were observed as a darker region than podosomes by interference reflection microscopy. They were more easily destroyed by incubating the cells with RGD-containing peptide than were the focal adhesions. In contrast to focal adhesions and podosomes, actin bundles were not detected within the peripheral adhesions, where pp60v-src and tyrosine-phosphorylated proteins accumulated. Expression of the integrin was determined by the substratum composition when BY1 cells were cultured in serum-free culture medium. Under such conditions, BY1 cells expressed the peripheral adhesions within 3 hours on adhesion molecule-coated glass. On the other hand, in serum-containing medium, they first developed focal adhesions transiently at their early stage of adhesion, and then the peripheral adhesions were predominantly expressed within 12 hours. Podosomes were formed in a time course similar to that of the peripheral adhesions. These findings suggest that the peripheral adhesion is a class of stable adhesive structure distinct from the focal adhesion or podosome of BY1 cells. Similar close contact-type peripheral adhesions with the integrin were also observed in a variety of cultured cells such as normal fibroblasts at their logarithmic growth phase, phorbol ester-treated fibroblasts, and several malignant tumor cells, with poorly organized focal adhesions and stress fibers. These findings further suggest that the peripheral adhesions may be widely involved in the adhesion of cells that inadequately develop stress fibers and focal adhesions.
BACKGROUND: Tissue adhesives have been used for many years to close simple lacerations as an alternative to standard wound closure (sutures, staples, adhesive strips). They offer many potential advantages over standard wound closure, including ease of use, decrease in pain and time to apply, as well as not requiring a follow-up visit for removal. Many studies have compared tissue adhesives and standard wound closure to determine the cosmetic outcome as well as these other secondary outcomes in their respective study populations. However, due to the wide variation in study parameters, there are no generalisable, definitive answers about the effectiveness of tissue adhesives. No study has been adequately powered to assess differences in complications, which are rare. OBJECTIVES: To summarize the best available evidence for the effect of tissue adhesives in the management of traumatic lacerations in children and adults. SEARCH STRATEGY: We searched the Cochrane Controlled Trials Register (CD ROM 2001 Issue 4), the Cochrane Wounds Group Specialized Trials Register (Nov 2001), MEDLINE (1966 to Oct 1, 2001), and EMBASE (1988 to Sept 1, 2001) for relevant randomised controlled trials (RCTs). We also searched the citations of selected studies, and we contacted relevant authors and manufacturers of tissue adhesives to inquire about other published and unpublished trials. SELECTION CRITERIA: We included RCTs comparing tissue adhesives versus standard wound closure or tissue adhesive versus tissue adhesive for acute, linear, low tension, traumatic lacerations in an emergency or primary care setting. Trials evaluating tissue adhesives for surgical incisions or other types of wounds were not considered. DATA COLLECTION AND ANALYSIS: Data from eligible studies were extracted by one reviewer and checked for accuracy by a second reviewer. Two reviewers independently assessed masked copies for quality. Outcomes of cosmesis (subgroups of age, wound location and need for deep sutures), pain, procedure time, ease of use and complications were analysed separately for two comparisons: 1) tissue adhesive versus standard wound care; and 2) tissue adhesive versus tissue adhesive. MAIN RESULTS: Eight studies compared a tissue adhesive with standard wound care. No significant difference was found for cosmesis at any of the time points examined, using either Cosmetic Visual Analogue Scale (CVAS) or Wound Evaluation Score (WES). Data were only available for subgroup analysis for age; no significant differences were found. Pain scores (Parent VAS WMD -15.7 mm; 95% CI -21.9, -9.5) and procedure time (WMD -5.6 minutes; 95% CI -8.2, -3.1) significantly favoured tissue adhesives. No studies reported on ease of use. Small but statistically significant risk differences were found for dehiscence (favouring standard wound care NNH 25 95% CI 14, 100) and erythema (favouring tissue adhesive NNH 8 95% CI 4, 100). Other complications were not significantly different between treatment groups. Only one study was identified that compared two tissue adhesives (butylcyanoacrylate (Histoacryl TM) versus octylcyanoacrylate (Dermabond TM)) for pediatric facial lacerations. No significant difference was found for cosmesis using CVAS at 1-3 months, or using WES at 5-14 days and 1-3 months. Similarly, no significant difference was found in pain, procedure time or complications. Results for ease of use were incomplete as reported. REVIEWER'S CONCLUSIONS: Tissue adhesives are an acceptable alternative to standard wound closure for repairing simple traumatic lacerations. There is no significant difference in cosmetic outcome between tissue adhesives and standard wound closure, or between different tissue adhesives. They offer the benefit of decreased procedure time and less pain, compared to standard wound closure. A small but statistically significant increased rate of dehiscence with tissue adhesives must be considered when choosing the closure method (NNH 25).
Many arthropods and vertebrates possess tarsal adhesive pads densely covered with setae. The striking morphological convergence of ;hairy' pads in lizards, spiders and several insect orders demonstrates the advantage of this design for substrate adhesion. Early functional explanations of hairy adhesive organs focused on the performance on rough substrates, where flexible setae can make more intimate contact. Recent theoretical and experimental work shows that the hairy design can also help to achieve self-cleaning properties, controllable detachment and increased adhesion. Several arguments have been proposed to explain why adhesive forces are maximised. First, the ;Force scaling' hypothesis states that when adhesive forces scale linearly with the dimensions of the contact, adhesion is increased by dividing the contact zone into many microscopic subunits. Second, the ;Fracture mechanics' argument implies that adhesion is maximised when the size of adhesive contacts is smaller than the critical crack length. Third, the ;Work of adhesion' model suggests that adhesion increases due to the bending and stretching of setae and associated energy losses during detachment. Several morphological traits of hairy adhesive pads can be explained by the need to maximise the work of adhesion, while avoiding the sticking of setae to each other (self-matting). Firstly, if setae are oblique and convex toward the foot tip as typical of most hairy pads, arrays should achieve greater adhesion. Secondly, a branched seta morphology not only confers the advantage that setae can adapt to roughness at different length scales but also prevents self-matting and increases the work of adhesion. It is predicted from the ;Work of adhesion' model that adhesion of pads with unbranched setae cannot be increased by subdividing the contact zone into ever finer subcontacts, because this would increasingly cause self-matting. However, contact splitting can increase adhesion if setae are branched. The greater density of setae in large animals has been interpreted by ;Force scaling'. However, the existing data can be explained by the effect of seta branching and by a fundamental difference between ;wet' and ;dry' adhesive systems. As insects employ adhesive fluids, they can cope with small-scale surface roughness even with relatively blunt seta tips, whereas the dry systems of lizards and spiders require extremely fine endings.
A retrospective study using the American Fertility Society's Adhesion Scoring Method and the MCASM (More Comprehensive Adhesion Scoring Method) and a prospective, randomized, controlled, multicenter trial (Canadian Task Force Classification I) were conducted. Of 2124 cases operated by laparoscopy, 465 patients had adhesions. Fifty-one female patients underwent open or laparoscopic myomectomy procedures with vs. without application of SprayGel adhesion barrier prevention, followed by second-look laparoscopy to evaluate postoperative adhesions. Details of the 465 cases of adhesiolysis are given. In subgroup 1 (n = 34) there were no preexisting adhesions. All 34 patients were assessed at a second-look laparoscopy for adhesion occurrence after 6-8 weeks; 29.4% were found to have no adhesions and 70.6% of patients had significant or mild adhesions. In subgroup 2, 21 patients who had undergone previous surgery for adhesiolysis were operated upon again, and 24% revealed an increased adhesion score, 57% the same adhesion score, and 19% a reduced adhesion score at second-look laparoscopy. Out of 51 patients enrolled, 45 were randomized to either treatment (n = 24) or control (n = 21). Three to sixteen weeks following surgery, 18 of 24 treatment patients (75%) and 13 of 21 controls (61.9%) had second-look laparoscopies (SLL). SLL showed 5 of 18 treatment patients (27.8%) were adhesion free vs. 1 in 13 of controls (7.7%). Patients randomized to SprayGel treatment were 3.6 times more likely to be adhesion free than patients randomized to control. Compared to the initial surgery, the severity score showed a 22% reduction in the treated group vs. a 39% increase in the control group, and a 12% reduction of adhesion area in the treated group vs. a 37% increase in the control group at SLL. New data confirmed previous knowledge: To avoid adhesions you must avoid surgery. If surgery has to be performed, laparoscopic surgery causes fewer adhesions than laparotomy. SprayGel was shown to be effective in reducing postoperative adhesions after laparoscopic and open myomectomy. Application of this adhesion barrier prevention system is fast, easy, and safe. Further studies are needed to confirm the promising results of this interim analysis.
BACKGROUND: Adhesion to lymph nodes, rather than growth stimulation, accounted for preferential colonization of lymph nodes by a metastatic B16 melanoma. We investigated these adhesive interactions. METHODS: Four classes of molecules were tested for inhibition of melanoma adhesion to cryostat sections of lymph node. RESULTS: Calcium chelators ethylenediaminetetraacetic acid and ethyleneglycol-bis-(beta-aminoethylether)-N,N,N',N'-tetra ace tic acid completely inhibited adhesion (50% adhesion, half-maximal inhibition, at 1 to 3 mmol/L). Cytochalasin B, which impairs contractile microfilaments, inhibited adhesion (60% adhesion at .001 mmol/L, 28% at .01 mmol/L). Colchicine, which disaggregates microtubules, had a similar effect (20% at .01 mmol/L, lowest dose tested). Trypsin slightly increased adhesion (125% adhesion at 10 micrograms/ml). Neuraminidase, which removed sialic acid residues, inhibited it (50% adhesion at 5 micrograms/ml). Gly-arg-gly-asp-ser, a peptide with a cell binding sequence of fibronectin, did not consistently inhibit adhesion (69% adhesion at 0.1 mg/ml, 83% adhesion at 1 mg/ml) or substantially differ from gly-arg-gly-glu-ser-pro (59% adhesion at 0.1 mg/ml, 90% adhesion at 1 mg/ml). In contrast, a peptide with a cell binding region of laminin (tyr-ile-gly-ser-arg) inhibited adhesion (50% adhesion at .05 mg/ml). CONCLUSIONS: Tumor cell-lymph node adhesion is a calcium-dependent process, requiring a functional cytoskeleton, that is mediated by both sialic acid moieties and trypsin-resistant, laminin-related, adhesion molecules.
BACKGROUND AND METHODS: Intercellular reactions and cell-matrix interactions are mediated by a number of specific adhesion molecules. For the intravascular reactivity of leukocytes and thrombocytes the endothelial expression of adhesion ligand molecules is of main importance. This condition may be of special relevance for the organ-specific manifestation of immune reactions in heart and lung transplants. The question was investigated as to whether organ-specific differences exist on arterial, venous, and capillary endothelial lining cells in heart and lung transplants and whether this condition is modified during transplant rejection. Transplant biopsy specimens of 24 heart transplant recipients (n = 303) and lung transplant recipients who underwent retransplantation for rejection (n = 4), as well as normal heart (n = 7) and lung tissue (n = 4), were studied. Cell-cell adhesion molecules (intercellular adhesion molecule-1 (CD54) and -2; LFA-3; CD31; vascular cellular adhesion molecule-1; neural cellular adhesion molecule; E-/P-selectin; CD44) and cell-matrix adhesion molecules (very late antigen-1 through -6; CD51) were studied on cryostat sections by means of standard immunohistology. RESULTS: (1) Arterial, venous, and capilary endothelia in lung and heart tissue show a distinct pattern of cell-cell and cell-matrix adhesion molecules: capillary and venous endothelia are in contrast to arterioles negative for vascular cellular adhesion molecule-1 and P-selectin. Arterial endothelia of the lung, in contrast to veins and capillaries, express no receptors for laminin (very late antigen-2 and very late antigen-6). (2) With transplant rejection, an induction of a number of adhesion molecules was noted on all endothelial lining cells in heart and lung transplants (intercellular adhesion molecule-1[CD54], intercellular adhesion molecule-2, lymphocyte function antigen-3, very late antigen-2, and very late antigen-6). Capillaries of the lung, in contrast to heart capillaries, displayed no inducibility of vascular cellular adhesion molecule-1 and E-selectin. In heart transplants, differences between capillaries and arteriovenous endothelia were found for virus-like agent-2 and -3. CONCLUSIONS: These results show a distinct expression of a both cell-cell and cell-matrix adhesion molecules on arterial, venous, and capillary endothelia of heart and lung transplants. This expression may influence the local regulation of leukocyte and thrombocyte adhesion during transplant rejection. Especially lung capillaries show a lack of inducibility for vascular cellular adhesion molecule-1 and E- and P-selectin required for the induction phase of leukocyte adhesion. This lack was not found in heart transplants. This observation may explain differences in intravascular adhesion and infiltration between vessel compartments in hearts and lungs and could be of relevance for therapeutic interventions to modify leukocyte and thrombocyte adhesion, as during transplant rejection and reperfusion damage.