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Adhesion measured on the attachment pads of Tettigonia viridissima (Orthoptera, insecta).

The tarsi of the cricket Tettigonia viridissima bear flexible attachment pads that are able to deform, replicating the profile of a surface to which they are apposed. This attachment system is supplemented by a secretion produced by epidermal cells and transported onto the surface of the pad through the pore canals of the pad cuticle. This study shows that the secretion alone is necessary, but not sufficient, for adhesion. To account for the full adhesive force, the deformation of the pad and the resulting changes in contact area were considered. In two series of experiments, the adhesive properties of the secretion and the adhesion of the whole pad were measured using a force tester, the sensitivity of which ranged from micronewtons to centinewtons. The adhesive forces of the secretion measured between a smooth sapphire ball with a diameter of 1.47 mm and a flat silicon surface ranged from 0.1 to 0.6 mN. In a control experiment on the silicon surface without secretion, no adhesive force was measured. There was no dependence of the adhesive force on the applied compressive force. When an intact pad was pulled off a flat silicon surface, the adhesive force increased with increasing applied compressive force, but it did not increase further once the applied force exceeded a certain value. The saturated adhesive force, ranging from 0.7 to 1.2 mN, was obtained at applied forces of 0.7-1.5 mN. The hemispherical surface of the pad had a larger contact area and demonstrated greater adhesion under a larger applied force. Adhesion became saturated when a pad was deformed such that contact area was maximal. The tenacity (the adhesive force per unit area) was 1.7-2.2 mN mm(-)(2).

Adhesiveness↗

Cadherin-mediated cell-cell adhesion and tissue segregation in relation to malignancy.

We review evidence concerning the basis for tissue segregation during embryonic development. This compartmentalization is shown to be an immiscibility phenomenon caused by changes in the strengths of adhesions between mobile cells which accompany their differentiation and generate interfacial tensions at cell population boundaries. The mobile cells exchange neighbors in response to these adhesion-generated forces which impel the system toward the configuration of maximal binding. Cadherins dominate these intercellular adhesions, but integrin-fibronectin-based adhesions also contribute to them as well as to cell-matrix adhesions. At the interface between two segregating cell populations are three kinds of cell-cell interfaces: a-a, b-b and a-b. Tissue immiscibility (segregation) results when the cross-adhesion is weaker than the mean value of the two kinds of self-adhesions, does not require (although it permits) qualitative changes in cell adhesion molecules and is easily generated even by moderate changes in the quantities of adhesion molecules on the cell surfaces. All type I and II cadherins tested cross-adhere, in most cases with strengths close to those of their self-adhesions. Is malignant invasion a process of cell segregation in reverse, in which the cross-adhesion between cancer cells and host tissue components is strong relative to their self-adhesions? We review evidence for cadherin involvement in breast, prostate and brain cancers. Despite evidence that N-cadherin enhances the invasiveness of certain cancer cells, we have found that increasing the expression not only of functional E-cadherin but also of P- or N-cadherin restrains the spreading of other malignant cell lines over (and through) a reconstituted extracellular matrix.

Animals↗

Adhesion of human glioma cell lines to fibronectin, laminin, vitronectin and collagen I is modulated by gangliosides in vitro.

Adhesion of eight cell lines, derived from human gliomas of different histological types, to fibronectin, collagen I, vitronectin, and laminin was investigated in vitro. The glioma cell lines were found to attach to these substrates to different extents. Interestingly, all cell lines strongly attached to laminin. In addition, glioma cell adhesion was found to be dose dependent. Moreover, adhesion of three cell lines to fibronectin and collagen I was partially inhibited and to vitronectin completely prevented by GRGDTP peptide, indicating the involvement of integrin receptors in glioma cell adhesion. We have demonstrated, recently, that gangliosides play an important role in promoting glioma cell invasion of the reconstituted basement membrane, Matrigel, in vitro. In order to study the mechanism of action of gangliosides in this process, the role of six gangliosides (GM1, GM3, GD3, GD1a, GD1b, and GT1b) in cell adhesion to the four proteins was investigated in three cell lines. Although all gangliosides, with the exception of GM3, were found to enhance cell adhesion to these proteins to different extents, GD3 proved to be the most effective adhesion-promoting ganglioside in all three cell lines. GM3 was found to inhibit cell adhesion to the four proteins in one cell line but enhanced cell adhesion in two other cell lines. The three cell lines were found to express both GD3 and gangliosides recognised by the A2B5 antibody. Furthermore, adhesion of the three cell lines to fibronectin, vitronectin, laminin, and collagen I was inhibited by incubation with A2B5, demonstrating the involvement of intrinsic cell membrane gangliosides in adhesion of glioma cells to these proteins. Taken together with the observation that gangliosides modulate integrin receptor function, these data suggest that gangliosides may play a central role in the control of the adhesive and invasive properties of human glioma cells.

Amino Acid Sequence↗

Requirement for RhoA kinase activation in leukocyte de-adhesion.

Leukocyte migration from bloodstream to tissue requires rapid coordinated regulation of integrin-dependent adhesion and de-adhesion. Whether de-adhesion is an active process mediated by a distinct signaling pathway(s) or a passive decay of initial adhesion remains undetermined. We found that blockade of RhoA with C3 exoenzyme or inhibition of RhoA kinase by the specific inhibitor Y-27632 enhanced phorbol ester-stimulated alpha(4)beta(1)-dependent adhesion of Jurkat cells at 30 min. Similarly, Y-27632 treatment increased stimulated beta(2) integrin-dependent neutrophil adhesion at 30 min but not at 5 min. Because reduced de-adhesion could mimic augmentation of adhesion at later time points, we developed an assay to measure de-adhesion specifically. Treatment of phorbol ester-or bacterial chemoattractant peptide-but not Mn(2+)-stimulated neutrophils adherent to serum-coated plastic or endothelial cells with Y-27632 or C3 exoenzyme markedly reduced the rate of de-adhesion, while markedly increasing their spreading. RhoA kinase inhibitor effects on de-adhesion and spreading were reversed by treatment with the cytoskeletal-disrupting agent cytochalasin D. Treatment with Y-27632 influenced neither integrin activation epitope nor integrin clustering. We conclude that activation of RhoA kinase promotes leukocyte de-adhesion by inhibiting cytoskeletal-dependent spreading, and that these effects of RhoA kinase constitute a new mechanism for regulation of integrin receptor avidity.

ADP Ribose Transferases↗

Thrombin induces mast cell adhesion to fibronectin: evidence for involvement of protease-activated receptor-1.

Thrombin activates mast cells to release inflammatory mediators through a mechanism involving protease-activated receptor-1 (PAR-1). We hypothesized that PAR-1 activation would induce mast cell adhesion to fibronectin (FN). Fluorescent adhesion assay was performed in 96-well plates coated with FN (20 microg/ml). Murine bone marrow cultured mast cells (BMCMC) were used after 3-5 wk of culture (>98% mast cells by flow cytometry for c-Kit expression). Thrombin induced beta-hexosaminidase, IL-6, and matrix metalloproteinase-9 release from BMCMC. Thrombin and the PAR-1-activating peptide AparafluoroFRCyclohexylACitY-NH(2) (cit) induced BMCMC adhesion to FN in a dose-dependent fashion, while the PAR-1-inactive peptide FSLLRY-NH(2) had no effect. Thrombin and cit induced also BMCMC adhesion to laminin. Thrombin-mediated adhesion to FN was inhibited by anti-alpha(5) integrin Ab (51.1 +/- 6.7%; n = 5). The combination of anti-alpha(5) and anti-alpha(4) Abs induced higher inhibition (65.7 +/- 7.1%; n = 5). Unlike what is known for FcepsilonRI-mediated adhesion, PAR-1-mediated adhesion to FN did not increase mediator release. We then explored the signaling pathways involved in PAR-1-mediated mast cell adhesion. Thrombin and cit induced p44/42 and p38 phosphorylation. Pertussis toxin inhibited PAR-1-mediated BMCMC adhesion by 57.3 +/- 7.3% (n = 4), indicating that G(i) proteins are involved. Wortmannin and calphostin almost completely inhibited PAR-1-mediated mast cell adhesion, indicating that PI-3 kinase and protein kinase C are involved. Adhesion was partially inhibited by the mitogen-activated protein kinase kinase 1/2 inhibitor U0126 (24.5 +/- 3.3%; n = 3) and the p38 inhibitor SB203580 (25.1 +/- 10.4%; n = 3). The two inhibitors had additive effects. Therefore, thrombin mediates mast cell adhesion through the activation of G(i) proteins, phosphoinositol 3-kinase, protein kinase C, and mitogen-activated protein kinase pathways.

Animals↗

The CC chemokine MCP-1 stimulates surface expression of CX3CR1 and enhances the adhesion of monocytes to fractalkine/CX3CL1 via p38 MAPK.

The membrane-anchored form of CX3CL1 has been proposed as a novel adhesion protein for leukocytes. This functional property of CX3CL1 is mediated through CX3CR1, a chemokine receptor expressed predominantly on circulating white blood cells. Thus far, it is still uncertain at what stage of the trafficking process CX3CR1 becomes importantly involved and how the CX3CR1-dependent adhesion of leukocytes is regulated during inflammation. The objective of this study was to examine the functional effects of chemokine stimulation on CX3CR1-mediated adhesion of human monocytes. Consistent with previous reports, our data indicate that the activity of CX3CR1 on resting monocytes is sufficient to mediate cell adhesion to CX3CL1. However, the basal, nonstimulated adhesion activity is low, and we hypothesized that like the integrins, CX3CR1 may require a preceding activation step to trigger firm leukocyte adhesion. Compatible with this hypothesis, stimulation of monocytes with MCP-1 significantly increased their adhesion to immobilized CX3CL1, under both static and physiological flow conditions. The increase of the adhesion activity was mediated through CCR2-dependent signaling and obligatory activation of the p38 MAPK pathway. Stimulation with MCP-1 also induced a rapid increase of CX3CR1 protein on the cell surface. Inhibition of the p38 MAPK pathway prevented this increase of CX3CR1 surface expression and blunted the effect of MCP-1 on cell adhesion, indicating a causal link between receptor surface density and adhesion activity. Together, our data suggest that a chemokine signal is required for firm CX3CR1-dependent adhesion and demonstrate that CCR2 is an important regulator of CX3CL1-dependent leukocyte adhesion.

Animals↗

Platelet adhesion to collagen type I, collagen type IV, von Willebrand factor, fibronectin, laminin and fibrinogen: rapid kinetics under shear.

Extracellular matrix proteins in the blood vessel wall fulfill an essential role in haemostasis by promoting platelet adhesion at the site of vessel injury. We have combined a continuous-flow system with affinity chromatography to study platelet adhesion under conditions mimicking arterial flow and have examined the adhesion kinetics of unstimulated platelets to collagens type I and IV, von Willebrand factor (vWf), fibronectin, laminin and to fibrinogen. In the absence of red cells, in ACD-prepared plasma adhesion to collagens type I and IV or vWf was rapid, efficient (>50% in <1 s ) and independent of shear rates from 650 to 3400 s(-1) with kinetics following an inverse exponential decay curve. We introduced a simple mathematical model in which this type of kinetics arises, and which may be more generally applicable to various adhesion processes under flow conditions. The model is characterized by the rate of platelet deposition on the adhesive surface being proportional to the number of platelets in the flow. Adhesion to fibronectin was independent of shear rate, but revealed a lag phase of approximately 1.5 s before significant adhesion began. Laminin and fibrinogen supported efficient adhesion at low shear rates (650-1000 s(-1)), but a lag phase of approximately 1.5 s was seen at high shear rates (1700-3400 s(-1)). Control proteins (albumin and gelatin) supported minimal adhesion. Nonspecific adhesion to poly-L-lysine differed from that to other substrate proteins in that the kinetics were linear. In conclusion, human platelets adhered specifically, rapidly (within seconds) and efficiently to several proteins under flow conditions and the kinetics of adhesion depended on the protein serving as substrate as well as on shear rate.

Blood Platelets↗

The judgement of adhesion formation following laparoscopic and conventional cholecystectomy in an animal model.

INTRODUCTION: The development of postoperative adhesions remains an almost inevitable consequence of visceral and gynaecologic surgery, appearing in 50-95% of all patients. Although decreased adhesion formation is one of the accepted advantages of laparoscopic surgery, only a small number of prospective studies have been done to support this claim. AIMS OF THE STUDY: To evaluate the extent of postoperative adhesion formation after laparoscopic and open cholecystectomy. MATERIAL AND METHOD: 60 experimental laparoscopic cholecystectomies (LC) were performed by qualified surgeons in dogs with the aim to acquire the laparoscopic technique. To assess the relation between the complications during the operation (bleeding, injury to the liver substance or gallbladder perforation) and the formation of adhesions, the surviving animals were divided into 4 groups according to the complications occurred. The assessment of the results was made by second--look laparoscopy 4 weeks following LC using the adhesion index. As a control group open cholecystectomy was then performed in 5 dogs without intraoperative complications. RESULTS: No adhesion formation was observed in the groups where no intraoperative complications occurred. In all the cases where bleeding or injury to the liver bed occurred adhesion formation occurred. No adhesion formation was observed in case of gallbladder perforation. In all the animals of the control group adhesion formation was observed. CONCLUSION: It seems that LC has a reduced rate of adhesion formation when compared with the open technique. Complications such as bleeding or injury to the liver substance during LC can enhance adhesion formation. No adhesion formation can be mentioned in relation with gallbladder perforation when the laparoscopic technique is applied.

Adjuvants, Immunologic↗

New range of light-activated surgical adhesives for tissue repair.

A new range of light-activated surgical adhesives has been developed for laser-assisted tissue repair. The surgical adhesive is composed of a polymer scaffold doped with the traditional protein solder mix of serum albumin and a chromophoric dye. Problems associated with inflexibility in conforming to various tissue geometries, instability in a hydrated environment due to non-uniform tissue adhesive denaturation, and solubility in physiological fluids prior to denaturation are overcome using the adhesives. The new adhesives offer a viable alternative to conventional fasteners, including sutures, staples and clips, currently used for tissue repair. In addition, it could be possible to use patches prepared from the adhesive in the field as a simple and effective method to stop bleeding and repair tissue quickly in an emergency situation. First, studies were conducted to improve the flexibility of traditional protein solders to enable them to be tailored to a wide range of clinically relevant geometry's including tubes, crescents and tape. Second, the creation of a chromophore concentration gradient across the thickness of the adhesive was investigated as a means to allow control of the heat source gradient through the adhesive. Increased deposition of the laser energy near the vital solder/tissue interface was thus achieved. Finally, predenaturation of the adhesive was investigated as a means for enhancing its stability in a hydrated environment thus improving the handling characteristics of the adhesive for clinical application. The application of the new surgical adhesives to augment laser tissue repairs is shown to enhance edge co-optation, improve repair strength and to reduce thermal tissue injury. The moldable, absorption controllable and flexible nature of the new adhesives greatly improves the clinical applicability of laser-solder tissue repair.

Animals↗

Inhibition by heparin and derivatized dextrans of Staphylococcus aureus adhesion to fibronectin-coated biomaterials.

Recent data on cardiovascular device-centered infections suggest that some plasma and extracellular matrix proteins contribute to bacterial adhesion and colonization on biomaterials. We previously developed an in vitro assay to study the Staphylococcus aureus adhesion-promoting effect of surface-adsorbed fibronectin on flat PMMA coverslips coated with a monolayer amount of fibronectin. We screened the potential anti-adhesive properties of a group of substituted dextrans, previously shown to exhibit potent anticoagulant and anticomplementary activities. In comparison to unsubstituted dextran which showed no significant (< 20%) adhesion inhibition at 1 mg/ml, dextrans increasingly substituted with carboxylic and benzylamide groups (CMBD) exhibited increasing anti-adhesive activities. Three CMBD derivatives showing an increasing proportion (5-14%) of benzylamide groups showed inhibition of bacterial adhesion increasing from 33 to 51% at 1 mg/ml. Another category of substituted dextrans having a variable proportion (2-26%) of sulfonated benzylamide groups (CMBDS) produced active inhibition of S. aureus adhesion. In comparison to these heparin-like dextran derivatives, native heparin produced inhibition values of S. aureus adhesion which were intermediate between those of CMBD and CMBDS compounds. Furthermore, the anti-adhesive activity was still expressed when substituted dextrans were preincubated with fibronectin-coated PMMA but washed away at the time when radiolabeled bacteria were added to the adhesion assay. This indicates that the anti-adhesive effects of CMBDS could be exerted at the level of the S. aureus binding site of fibronectin. In conclusion, S. aureus adhesion on fibronectin-coated biomaterials can be efficiently blocked in vitro by soluble compounds such as dextran derivatives.

Adsorption↗

Minimal adhesions to ePTFE mesh after laparoscopic ventral incisional hernia repair: reoperative findings in 65 cases.

OBJECTIVES: Laparoscopic ventral incisional hernia repair involves intraabdominal placement of a synthetic mesh, and the possibility of formation of severe visceral adhesions to the prosthesis is a principal concern. Little clinical information based on reoperative findings is available about adhesions to biomaterials placed intraabdominally. We conducted a multiinstitutional study of adhesions to implanted expanded polytetrafluoroethylene (ePTFE) mesh at reoperation in patients who had previously undergone laparoscopic incisional hernia repair done with the same mesh implantation technique. METHODS: Nine surgeons retrospectively assessed the severity of adhesions to ePTFE mesh at reoperation in 65 patients. For each case, adhesions were assigned a score of 0 to 3, with 0 indicating no adhesions and 3 severe adhesions. RESULTS: The mean time from mesh implantation to reoperation was 420 days (range, 2 to 1739 days). No adhesions were observed in 15 cases. Forty-four cases received an adhesion score of 1, and 6 cases a score of 2; no scores of 3 were assigned. Thus, 59 patients (91%) had either no or filmy, avascular adhesions. No enterotomies occurred during adhesiolysis. CONCLUSIONS: In this large series of reoperations after laparoscopic incisional hernia repair, no or minimal formation of adhesions to implanted ePTFE mesh was observed in 91% of cases, and no severe cohesive adhesions were found. Comparative analyses of newer materials based on clinical reoperative findings are warranted to assess the safety of intraabdominally placed meshes.

Adult↗

Adhesion in gynecology complication, cost, and prevention: a review.

The objective of this chapter is to evaluate the magnitude of the problems of adhesions in Gynecology, complications, cost for the health care, and methods to prevent adhesion formation. It contains a review of relevant literature on intra-abdominal adhesion, adhesion-reducing substances, and their related cost. Adhesions can cause infertility, abdominal pain, or bowel obstruction. The impact of adhesions to the health-care system is huge. The total cost of adhesion-related problems in the United States is more than dollar 1 billion dollars annually. Modification in surgical technique, such as the use of laparoscopy, can minimize adhesion formation. Another approach is by using adhesion-reducing substances. Many substances and materials have been used to decrease the adhesion formation; however, there remains no unequivocally effective adhesion-reducing substance. Also, its use is costly. To our knowledge, no study has been published to date that addresses the use of adhesion-reducing substances as relates to the risk of bowel obstruction or long-term costs to the health-care system.

Abdomen↗

IL-1-induced adhesion of polymorphonuclear leukocytes to cultured human endothelial cells. Role of platelet-activating factor.

In early studies we found that IL-1 stimulated endothelial cells (EC) to produce platelet-activating factor (PAF, 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine). Inasmuch as this phospholipid has a wide range of biologic activities, including polymorphonuclear leukocytes (PMN) aggregation and chemotaxis, we investigated whether EC-associated PAF could contribute to IL-1-induced PMN adhesion to EC. When four selective PAF antagonists were added to IL-1-stimulated EC during the PMN adhesion assay, adhesion was reduced in a concentration-related way. Similarly, pre-treatment of PMN with PAF before the adhesion assay to induce desensitization to this phospholipid reduced PMN adhesion to IL-1-treated EC. However, comparing the time course and the concentration response curve of IL-1-induced EC adhesivity and PAF synthesis, we found that increased EC adhesivity to PMN required a shorter incubation time and lower concentration of IL-1 to become apparent than PAF production. When acetyl-coenzyme A was added to EC cultures at a concentration that raised PAF synthesis by 60%, no significant increase in PMN adhesion was observed. In addition, after 9 to 10 doublings, the EC ability to synthesize PAF decreased by 85 to 90%, whereas IL-1-induced EC adhesivity to PMN was only slightly diminished. When IL-1-alpha and -beta were tested on EC, we observed that both were equally active in promoting PMN adhesion to EC but only the alpha-form was able to stimulate PAF production. When PMN were seeded on IL-1-treated EC, increased amounts of PAF were detected even when EC were fixed; in addition, the inhibitory effect of a PAF antagonist was evident also in these conditions. Overall these results indicate that IL-1-induced PAF production by EC does not significantly contribute to PMN adhesion to them. We hypothesize that the observed inhibitory effect of PAF antagonists and PAF desensitization of PMN might be directed at PAF produced by PMN themselves during adhesion to IL-1-treated EC.

Cell Adhesion↗

Adhesion of sickle cells to vascular endothelium is critically dependent on changes in density and shape of the cells.

Experiments were performed to explore whether adhesion differences among different density sickle (SS) cells are mainly caused by deformability characteristics attendant to density variations, which could affect their surface contacts with the endothelium, or caused by any changes in their membrane surface (eg, receptors). Also, what is the contribution of morphologic attributes of SS cells in adhesive and obstructive events? To resolve these issues, controlled modifications of cell density were performed using Nystatin and sucrose. This allowed elevation of the mean corpuscular hemoglobin concentration (MCHC) of light-density SS2 discocytes to that of SS4 native dense cells, as well as its normalization in both native and artificially dehydrated cells. Hemodynamic and adhesive characteristics of these individual SS cell populations and their defined mixtures were investigated in the ex vivo mesocecum vasculature. Dehydrated (high MCHC) SS2 discocytes, alone or with SS2 control cells, caused a higher peripheral resistance but no persistent microvascular blockage. Nevertheless, dehydrated SS2 discocytes resulted in a significantly decreased adhesion in venules (adhesion sites). Rehydration of these high MCHC discocytes completely restored their adhesivity, similar to that of SS2 control cells. In contrast, irreversibly sickled cell (ISC)-rich SS4 dense cell class (dense discocytes and 66% to 72% ISCs) was less adherent than dehydrated SS2 discocytes, but caused a persistent blockage of small diameter postcapillary venules when infused with SS2 control or dehydrated discocytes. In the areas of adhesion, SS4 dense discocytes outnumbered ISCs by 4 to 1, demonstrating that ISCs, because of their shape characteristics, are minimally adherent but play a distinct role in postcapillary obstruction. When MCHC (density) of SS4 cells was decreased by rehydration, it resulted in an almost complete reversal of their hemodynamic and adhesive behavior, confirming a profound influence of cell density. These findings demonstrate for the first time that, under shear flow, adhesion of different density SS cells to the endothelium is dependent on the inverse of cell density rather than any changes in their adhesion potential. Finally, the trapping of ISC-rich native dense cells, but not of dehydrated discocytes, in the areas of adhesion shows a distinct contribution of ISC in adhesion-initiated vasoocclusion.

Adult↗

Adhesion formation after laparoscopic anterior resection in a porcine model: a pilot study.

Although decreased adhesion formation is one of the accepted advantages of laparoscopic colorectal surgery, no prospective studies have been done to support this claim. Therefore, we prospectively assessed adhesion formation following laparoscopic anterior resection of the rectum in a porcine model. Five domestic female pigs underwent the procedure with a double-stapled intracorporeal anastomosis. After completion of the laparoscopic procedure, 50 cm of ileum was retrieved through the right lower port site. Controlled serosal abrasion of the antimesenteric surface was performed using a fresh knife. The abraded loop was returned into the peritoneal cavity and the fascia closed at all port sites. All animals underwent a midline laparotomy 3 weeks later to assess adhesions using a 0-3 score according to the density vascularity, and extent of adhesions. All animals survived the study period. The mean level of the anastomosis was 8 cm (range, 7-10) above the anal verge; all anastomoses were intact and completely healed. None of the animals had adhesions to the port sites. The anastomotic site was completely free of adhesions in four animals, and only one animal (20%) had grade 1 adhesions between the urine horns and the anastomosis. Conversely, all animals had adhesions of the abraded loop involving 60 cm (range, 40-75) of bowel and 7 cm (range, 4-9) of the abdominal wall (remote to the port sites); no other adhesions were noted. In this pilot study, serosal abrasion of the small bowel resulted in severe adhesion formation in the porcine model. However, laparoscopic anterior resection of the rectum in the same animals was associated with only minimal insignificant adhesions. Furthermore, unlike in laparotomy incisions, adhesions to port sites did not occur.

Abdomen↗

Reduction of intraperitoneal adhesion formation by use of non-abrasive gauze.

BACKGROUND: Adhesion formation is potentially harmful. Surgical swabs may contribute to adhesions by trauma to the peritoneum. The purpose of this study was to evaluate whether standard surgical gauze (Medipres) has an adhesion-promoting effect, and to determine whether a soft textile (Fastsorb), used in the electronics industry, might be less traumatic and therefore lead to less adhesion formation. METHODS: A reproducible rat model allowing semiquantitative scoring of adhesion formation was used. Three different adhesion models representing increasing degrees of peritoneal trauma (minimal, moderate and severe) were employed. The model inflicting minimal peritoneal trauma was combined with standardized rubbing of the peritoneum with surgical gauze or non-surgical textile. RESULTS: Minimal peritoneal trauma resulted in a significantly lower mean adhesion percentage (21 per cent) than moderate (44 per cent) or severe (60 per cent) peritoneal trauma (P < or = 0.005). Rubbing of the peritoneum with surgical gauze after minimal peritoneal trauma induced significantly more adhesion formation (58 versus 23 per cent, P < 0.0001). After minimal peritoneal trauma, rubbing with surgical gauze produced significantly more adhesions than rubbing with non-surgical textile (63 versus 19 per cent, P < 0.0001). Moreover, rubbing the peritoneum with non-surgical textile after minimal peritoneal trauma did not induce any additional adhesion formation (35 versus 24 per cent, P = 0.23). CONCLUSION: The extent of adhesion formation correlates significantly with the degree of peritoneal damage. Standard surgical gauze is traumatizing to the peritoneum and promotes adhesion formation whereas a less abrasive non-surgical textile does not.

Animals↗

Periovarian peritoneal adhesions in women with endometriosis. Structural patterns.

OBJECTIVE: To draw attention to the structural features of adhesions associated with pelvic endometriosis since they are less well studied than endometriosis proper. STUDY DESIGN: Sixty-two samples of periovarian adhesions were laparoscopically obtained from 24 infertile women 26-38 years of age and were prepared for detailed histologic analyses. RESULTS: Macroscopically, the adhesions were either velamentous or cordlike and grossly were free of endometriosis. Most adhesions were attached to the connective tissue of the ovarian tunica albuginea; in two cases they were attached to the corpus luteum. Upon microscopic analysis, velamentous adhesions consisted of fibrous sheets of collagen connective tissue, with the surface lined with single-layered coelomic epithelium. The cord-like adhesions consisted of "hyalinized" fibrous tissue and were either avascular or vascularized. Irregular cystic or tubular structures that could be regarded as endometriosis were found in four patients. Hyaline cartilage within the tissue of the adhesion was an unexpected finding in one patient. CONCLUSION: Microscopic analysis permitted grouping of the adhesions in the following way: (1) Connective tissue adhesions (23 patients) with the following subcategories: (A) fibrous, either avascular or encompassing degenerating blood vessels (6 patients); (B) vascularized, containing granulomatous tissue (12 patients); (C) vascularized with stromoglandular endometrioid cysts or tubules (4 patients); (D) rare types, such as that encompassing hyaline cartilage (1 patient). (2) Fibrin adhesions (1 patient). From the clinical point of view, the presence of endometrial tissue within adhesions raises the question of whether there is a need for removal, rather than just lysis, of adhesions to avoid persistent pain.

Adult↗

Roles of secretion and the cytoskeleton in cell adhesion and polarity establishment in Pelvetia compressa zygotes.

During the establishment of polarity, fucoid algal zygotes adhere to the substratum and select a growth axis according to environmental cues. Since little is known about the early events leading to axis selection, we investigated the chronology of cell adhesion, adhesive deposition, and axis selection induced by light (photopolarization). The requirements for secretion and the cytoskeleton in these processes and in the process of changing the orientation of an axis in response to new environmental cues (axis realignment) were also tested. Adhesive deposition occurred in two distinct stages: it was deposited uniformally on young zygotes (uniform primary adhesive) and later was deposited asymmetrically (polar secondary adhesive). Uniform primary adhesive deposition, cell adhesion, and photopolarization occurred simultaneously, and shortly thereafter, polar secondary adhesive deposition occurred at the future growth site. Uniform primary adhesive deposition and cell adhesion required secretion, but were independent of filamentous-actin (F-actin) and microtubule function. Photopolarization of young zygotes and polar secondary adhesive deposition required secretion but not microtubules. F-actin served to localize secondary adhesive deposition at the rhizoid pole; its function in polarization was more complex. F-actin was required for axis selection; however, its role in realignment of an axis depended on the light regime. The differing requirements for F-actin during development indicates that the axis is not static, but changes with time. These findings indicate that previous and future work on "axis formation" must be interpreted in the context of the developmental stage of the zygote.

Actins↗