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Protein-mediated adhesion of Lactobacillus fermentum strain 737 to mouse stomach squamous epithelium.

The mechanism of adhesion of Lactobacillus fermentum strain 737 to mouse stomach squamous epithelium was investigated. Adhesion inhibition tests involving chelators, monosaccharides, periodate and concanavalin A and the use of bacteria grown in the presence of tunicamycin failed to clarify the adhesive mechanism. Washed bacterial cells had reduced adhesive capacity, except in the presence of spent broth culture supernatant fraction or cell washings. Spent culture supernatant fractions of erythrosine-supplemented broth did not enhance adhesion of washed cells. The adhesion-promoting factor(s) in the spent broth culture supernatant fractions and cell washings bound to both bacterial and epithelial cell surfaces, but did not promote adhesion of two other Lactobacillus strains which were not of mouse origin, thereby indicating host specificity for the adhesion-promoting activity. Chemical characteristics of the adhesion-promoting factor were determined by pretreatment of the dialysis retentate of spent broth culture supernatant fractions with proteolytic enzymes, concanavalin A-Sepharose or periodate before the adhesion assay. The adhesin was non-dialysable, pronase-sensitive, heat sensitive at 100 degrees C, had no affinity for concanavalin A-Sepharose and contained no carbohydrate groups active in the adhesion process. The protein profiles of dialysis retentates of spent broth culture supernatant fractions after bacterial growth in the absence and presence of erythrosine were determined by 2-dimensional SDS-PAGE. Gel filtration by HPLC was used for purification of an adhesion-promoting fraction. The host-specific adhesion of L. fermentum strain 737 was mediated by a protein, with an Mr of 12-13000, that was not detectable in cells grown in the presence of erythrosine. A model for the mode of binding of the adhesin to host epithelia and bacterial surfaces is proposed.

Adhesins, Bacterial↗

Effect of salivary secretory IgA on the adhesion of Candida albicans to polystyrene.

Attachment of Candida albicans to plastic materials of dental prostheses or to salivary macromolecules adsorbed on their surface is believed to be a critical event in the development of denture stomatitis. In an earlier study, it was shown that adhesion of C. albicans to polystyrene, a model system to study the adhesion of C. albicans to plastic materials, can be partially inhibited with an mAb directed against cell wall polysaccharides of C. albicans. In the present study, the role of whole saliva in the adhesion of C. albicans to polystyrene has been investigated, and three mAbs directed against epitopes of cell wall mannoproteins have been used to mimic the inhibitory effect observed with salivary secretory IgA (sIgA) on the adhesion of C. albicans to polystyrene. In the absence of whole saliva, adherence of C. albicans 3153 increased with germination. However, the presence of whole saliva enhanced the adhesion to polystyrene of C. albicans 3153 yeast cells but decreased the adhesion of germinated cells. The enhancement of adhesion of yeast cells to polystyrene mediated by saliva was confirmed with an agerminative mutant of C. albicans 3153. The inhibition of the adhesion of C. albicans 3153 germ tubes to polystyrene was due to the salivary sIgA since sIgA-depleted saliva enhanced the adhesion of C. albicans 3153 to polystyrene. The inhibitory effect mediated by sIgA was not related to the inhibition of germination but to the blockage of adhesins expressed on the cell wall surface of the germ tubes. The three mAbs studied reduced the adhesion of C. albicans 3153 to polystyrene at levels equivalent to those for purified sIgA. The highest reduction in the adhesion was obtained with the IgA mAb N3B. The best results were obtained when the three mAbs were combined. The results suggest that whole saliva plays a different role in the adhesion of C. albicans to polystyrene depending on the morphological phase of C. albicans. These results may give new insights into the conflicting role of saliva in the adhesion of C. albicans to plastic materials of dental prostheses.

Antibodies, Monoclonal↗

Effect of omentectomy on adhesion formation in horses.

OBJECTIVE: To determine if omentectomy would decrease the frequency of postoperative intraabdominal adhesions. STUDY DESIGN: Retrospective study. ANIMALS OR SAMPLE POPULATION: 44 horses that had either two ventral median celiotomies or a ventral median celiotomy and a necropsy more than 4 days later; 19 of these horses had their omentum removed at the initial surgery. METHODS: Data retrieved from the records included location and type of intraabdominal adhesions; location of the surgical lesion; relationship of adhesions to the surgical lesion; surgical procedures; duration of initial surgery; time interval between procedures; age, gender, and breed of the horse; and clinical outcome. Fisher's exact test was used to evaluate the association between categorical explanatory and outcome variables. The effect of potential risk factors on the incidence rate of adhesion formation was estimated using a proportional hazards regression model. RESULTS: Of 25 horses in the nonomentectomy group, 15 (60%) had postoperative adhesions that resulted in the need for a second surgical intervention, whereas of 19 horses that had omentectomy initially, only 4 (21%) had postoperative adhesions that required a second procedure. Rate of adhesion formation was higher in horses that did not have omentectomy initially (incidence ratio rate [IRR], 0.46; 90% confidence interval [CI], 0.18 to 1.19). At initial surgery, 24 horses had a small intestinal lesion, and 20 horses had a large intestinal lesion. Fifteen horses (63%) with small intestinal lesions subsequently developed adhesions compared with four horses (20%) with an initial large intestinal lesion (P = .006). At the second procedure, small intestine lesions were identified in 32 horses and large intestine lesions in 12 horses (1 horse had both small and large intestine lesions), and 1 horse had a gastric lesion. Adhesions were identified as the cause of colic signs in 19 (61%) horses with small intestinal lesions and in none of the horses with large intestine lesions. The frequency of adhesion development leading to colic associated with only the small intestine at the second surgery or necropsy was significantly greater (P = .001) than the frequency only in the large intestine. CONCLUSIONS: Omentectomy reduced the rate of postoperative adhesion formation. Adhesions are more likely to occur after small intestinal surgery and if they do occur likely involve the small intestine. CLINICAL RELEVANCE: Omentectomy is a safe procedure and should be considered prophylactically for reduction of adhesion formation after abdominal surgery in horses.

Animals↗

Bonding characteristics of self-etching adhesives to intact versus prepared enamel.

PURPOSE: This study tested the null hypothesis that the preparation of the enamel surface would not affect the enamel microtensile bond strengths of self-etching adhesive materials. MATERIALS AND METHODS: Ten bovine incisors were trimmed with a diamond saw to obtain a squared enamel surface with an area of 8 x 8 mm. The specimens were randomly assigned to five adhesives: (1) ABF (Kuraray), an experimental two-bottle self-etching adhesive; (2) Clearfil SE Bond (Kuraray), a two-bottle self-etching adhesive; (3) One-Up Bond F (Tokuyama), an all-in-one adhesive; (4) Prompt L-Pop (3M ESPE), an all-in-one adhesive; and (5) Single Bond (3M ESPE), a two-bottle total-etch adhesive used as positive control. For each specimen, one half was roughened with a diamond bur for 5 seconds under water spray, whereas the other half was left unprepared. The adhesives were applied as per manufacturers' directions. A universal hybrid composite resin (Filtek Z250, 3M ESPE) was inserted in three layers of 1.5 mm each and light-cured. Specimens were sectioned in X and Y directions to obtain bonded sticks with a cross-sectional area of 0.8 +/- 0.2 mm2. Sticks were tested in tension in an Instron at a cross-speed of 1 mm per minute. Statistical analysis was carried out with two-way analysis of variance and Duncan's test at p < .05. Ten extra specimens were processed for observation under a field-emission scanning electron microscope. RESULTS: Single Bond, the total-etch adhesive, resulted in statistically higher microtensile bond strength than any of the other adhesives regardless of the enamel preparation (unprepared = 31.5 MPa; prepared = 34.9 MPa, not statistically different at p < .05). All the self-etching adhesives resulted in higher microtensile bond strength when enamel was roughened than when enamel was left unprepared. However, for ABF and for Clearfil SE Bond this difference was not statistically significant at p > .05. When applied to ground enamel, mean bond strengths of Prompt L-Pop were not statistically different from those of Clearfil SE Bond and ABF. One-Up Bond F did not bond to unprepared enamel. Commercial self-etching adhesives performed better on prepared enamel than on unprepared enamel. The field-emission scanning electron microscope revealed a deep interprismatic etching pattern for the total-etch adhesive, whereas the self-etching systems resulted in an etching pattern ranging from absent to moderate.

Acid Etching, Dental↗

Endothelial cell adhesion in real time. Measurements in vitro by tandem scanning confocal image analysis.

Real time measurements of cell-substratum adhesion in endothelial cells were obtained by tandem scanning confocal microscopy of sites of focal contact (focal adhesions) at the abluminal cell surface. Focal contact sites were sharply defined (low radiance levels) in the living cell such that the images could be enhanced, digitized, and isolated from other cellular detail. Sites of focal contact are the principal determinant of cell-substratum adhesion. Measurements of (a) the focal contact area and (b) the closeness of contact (inverse radiance) were used to nominally define the adhesion of a single cell or field of cells, and to record spontaneous and induced changes of cell adhesion in real time. The topography of focal contacts was estimated by calculating separation distances from radiance values using a calibration technique based on interference ring optics. While slightly closer contact was noted between the cell membrane and substratum at or near the center of each focal contact, separation distances throughout the adhesion regions were always < 50 nm. Subtraction of consecutive images revealed continuous spontaneous remodeling of individual focal adhesions in unperturbed cells during periods of < 1 min. Despite extensive remodeling of focal contact sites, however, cell adhesion calculated for an entire cell over extended periods varied by < 10%. When cytoskeletal stability was impaired by exposure to cytochalasin or when cells were exposed to proteolytic enzyme, endothelial adhesion declined rapidly. Such changes were recorded at the level of single cells, groups of cells, and at single focal adhesions. In both unperturbed and manipulated cells, the dynamics of remodeling and cell adhesion characteristics varied greatly between individual sites within the same cell; disappearance of existing sites and appearance of new ones often occurred within minutes while adjacent sites underwent minimal remodelling. Tandem scanning confocal microscopy image analysis of living cells in real time provides repetitive spatial, temporal, and quantitative information about cell adhesion. Such an approach should allow more precise quantitative analyses to be made of the interactions between extracellular matrix, adhesion proteins, integrins, and the cytoskeleton in the living cell.

Actins↗

Expression pattern and regulation of genes differ between fibroblasts of adhesion and normal human peritoneum.

BACKGROUND: Injury to the peritoneum during surgery is followed by a healing process that frequently results in the attachment of adjacent organs by a fibrous mass, referred commonly as adhesions. Because injuries to the peritoneum during surgery are inevitable, it is imperative that we understand the mechanisms of adhesion formation to prevent its occurrence. This requires thorough understanding of the molecular sequence that results in the attachment of injured peritoneum and the development of fibrous tissue. Recent data show that fibroblasts from the injured peritoneum may play a critical role in the formation of adhesion tissues. Therefore, identifying changes in gene expression pattern in the peritoneal fibroblasts during the process may provide clues to the mechanisms by which adhesion develop. METHODS: In this study, we compared expression patterns of larger number of genes in the fibroblasts isolated from adhesion and normal human peritoneum using gene filters. Contributions of TGF-beta1 and hypoxia in the altered expression of specific genes were also examined using a semiquantitative RT-PCR technique. RESULTS: Results show that several genes are differentially expressed between fibroblasts of normal and adhesion peritoneum and that the peritoneal fibroblast may acquire a different phenotype during adhesion formation. Genes that are differentially expressed between normal and adhesion fibroblasts encode molecules involved in cell adhesion, proliferation, differentiation, migration and factors regulating cytokines, transcription, translation and protein/vesicle trafficking. CONCLUSIONS: Our data substantiate that adhesion formation is a multigenic phenomenon and not all changes in gene expression pattern between normal and adhesion fibroblasts are the function of TGF-beta1 and hypoxia that are known to influence adhesion formation. Analysis of the gene expression data in the perspective of known functions of genes connote to additional targets that may be manipulated to inhibit adhesion development.

Cell Hypoxia↗

Dual functions of transglutaminase in novel cell adhesion.

Transglutaminases (TGases) are enzymes which catalyze cross-link formation between glutamine residues and lysine residues in substrate proteins. In the present study, we report for the first time that a representative enzyme, blood coagulation factor XIIIa (FXIIIa), is capable of mediating adhesion of various cells. When coated on plastic surfaces FXIIIa promoted adhesion and spreading of various cells of both normal and tumor origin, in a concentration-dependent manner. The adhesion was not inhibited by antibodies against possible contaminants in the enzyme preparation such as fibronectin and vitronectin, but was completely inhibited by a polyclonal antibody against the enzyme. Therefore, if there were any contaminating cell adhesive substrates in the enzyme preparation, they cannot account for the observed cell adhesion to the enzyme; FXIIIa itself mediates the cell adhesion. Furthermore, phosphorylation of tyrosine residues in 120 kDa and 70 kDa proteins was clearly shown in human fibroblasts adhering to the enzyme. Formation of actin stress fibers was also unambiguously observed in the adhering cells. These biochemical reactions, which are also observed when cells adhere to a typical cell adhesion protein, fibronectin, are believed to be of importance in the process of cell adhesion. This adhesion activity of FXIIIa was dependent on its TGase activity, because both a modification of the active center cysteine with iodoacetamide and the addition of ammonium ion abolished the cell adhesion activity along with the enzyme activity. The cell adhesion to fibronectin, however, was not affected by these treatments. The effects of various anti-integrin antibodies suggested that both alpha v beta 3 and beta 1 family integrins participated in the cell adhesion to FXIIIa. Taken together, these data demonstrate for the first time that there is a unique TGase activity-mediated cell adhesion. This novel function of the enzyme may be of physiological importance.

Alkylating Agents↗

Adhesion of human red blood cells and surface charge of the membrane.

To elucidate the mechanism by which red blood cells (RBC) participate in thrombus formation, we investigated the mechanism of adhesion between human RBC. Our study showed that the morphology of RBC was changed by various cationic reagents, inducing adhesion between RBC. When RBC suspended in PBS buffer containing sodium phosphate (PBS(Na)) or potassium phosphate (PBS(K)) were treated with cationic reagents, stronger adhesion occurred between RBC treated with the latter. When concentrations of the reagents were low, adhesion was released and the RBC resumed its original morphology after washing. However, when the concentrations of reagents were high, the morphology did not normalize, although the adhesion was released. When fresh RBC were treated with cationized ferritin (CF), CF bound to the periphery of RBC membranes and induced adhesion. However, when RBC were induced to adhere strongly by a cationic reagent, no binding of CF to the membrane was not observed. When RBC were treated with CF, bindings between substances outside the membranes and bindings between the membranes and substances outside the membranes were observed. When RBC treated with neuraminidase to remove 85-90% of sialic acid were treated with the cationic reagents, both adhesion between RBC and morphological change were reduced. When RBC were pretreated with polyclonal antibody against human RBC membrane band 3 protein, treatment with the cationic reagents did not induce adhesion and morphological change of RBC. Further, when RBC induced to adhere by the cationic reagents were treated with the polyclonal antibody against band 3, in the case of weak adhesion, the adhesion was released and the RBC resumed its original morphology. However, in the case of strong adhesion, the morphology did not return to normal although the adhesion was released. These results suggest that the adhesion between RBC induced by cationic reagents was due to changes in the charge on the membrane surface, involving polysaccharide chains and membrane surface proteins.

Anion Exchange Protein 1, Erythrocyte↗

A three-year clinical evaluation of two-bottle versus one-bottle dentin adhesives.

BACKGROUND: The authors conducted an in vivo investigation to compare the clinical performance of two commercial one-bottle adhesives and a two-bottle adhesive for restoration of noncarious cervical lesions (NCCLs). METHOD: The patient pool consisted of 57 patients and 171 teeth (three teeth per patient), with one NCCL per tooth. Each patient received three resin-based composite restorations, each with a different adhesive: one tooth with a two-bottle, water-based adhesive as the control; another tooth with a one-bottle, ethanol-based adhesive; and a third tooth with a one-bottle, solvent-free adhesive. The authors assessed restorations in terms of retention, marginal integrity, margin discoloration and air sensitivity at baseline, six months, one year, two years and three years after initial placement. RESULTS: The retention rates at 36 months were 88 percent for the first adhesive, 81 percent for the second adhesive and 90 percent for the third adhesive. No statistically significant differences in retention rates could be shown, with 86 percent of restorations retained overall. Measures of marginal integrity, marginal discoloration and sensitivity also had no statistically significant differences between the three adhesives (P > .05). CONCLUSIONS: All three adhesives performed with acceptable outcomes after a 36-month period, with small differences between the one- and two-bottle systems and between the various solvents. Retention rate was moderately high and air sensitivity was markedly reduced; however, superficial marginal discoloration and marginal degradation was notable. Certain lesion, tooth and patient characteristics may predispose restorations to retention failure. CLINICAL IMPLICATIONS: The type of solvent may not be a major factor in retention of Class V restorations in NCCLs. Both single-bottle adhesives and conventional two-bottle adhesives performed acceptably.

Adhesives↗

[Evaluation of postoperative adhesions in rats submitted to peritoneostomy with polypropylene mesh associated to nitrofurazone].

BACKGROUND: Peritoneal injuries, common in per and postoperative, lead to the formation of adhesions. The use of polypropylene mesh increases the postoperative adhesions incidence. Based on the fact of nitrofurazone accelerates the healing process, a possible action on peritoneal adhesions was cogitated. AIM: To evaluate postoperative adhesions in rats submitted to peritoneostomy with polypropylene mesh fixation associated to nitrofurazone. METHODS: Thirty-three Wistar rats were separated into three groups of eleven animals each one. In group I was performed the laparotomy with exposition of the abdominal cavity followed by the laparotomy suture; in group II was performed the resection of a abdominal wall fragment followed by polypropylene mesh fixation on the gap and in group III was performed the same done in group II, but the mesh was previously impregnated with nitrofurazone. After 45 days the animals were sacrificed and necropsied. RESULTS: Seven animals of group I had no adhesions (degree 0), two had degree 1 adhesions and two had degree 2. In group II, one animal was classificated as degree 3 and ten as degree 4. In group III, one had degree 0, eight had degree 3 and one had degree 4 (one animal died before 45 days). All adhesions found involved the abdominal wall; ten animals had adhesions involving only omentum (group I = 4; group II = 1 and group III = 5); eleven animals had adhesions involving omentum, small bowel and other abdominal organs (group II = 10; group III = 1); three animals had adhesions involving only small bowel, all belonged to group III. Fourteen animals had adhesions involving small bowel, of these ten belonged to group II (nine with more than one fixation point) and four belonged to group III (three with just one fixation point). CONCLUSION: The association of nitrofurazone with polypropylene mesh did not reduce significantly the postoperative adhesions incidence in rats, but reduced the intensity and severity of these adhesions.

Animals↗

Peritoneal molecular environment, adhesion formation and clinical implication.

Whether induced by infection, inflammation, ischemia, and/or surgical injury, peritoneal adhesions are the leading cause of pelvic pain, bowel obstruction and infertility. It is clear that while postsurgical peritoneal wounds heal without adhesions in some patients, others develop severe scarring from seemingly equal procedures; in addition, in the same patient, adhesions can develop at one surgical site and not in another. The mechanisms underlying the predisposition to form adhesions as well as their site specificity are completely unknown. However, a large number of intraperitoneal surgical procedures are performed each day in the USA, and thus many patients are at risk of developing postoperative adhesions. Therefore, understanding of adhesion formation at the molecular level is essential and in the absence of such information, attempts to prevent patients from developing adhesions will remain an empirical process. The unprecedented advancement in molecular biology during the past decade has led to the identification of many biologically active molecules with the potential of regulating inflammatory and immune responses, angiogenesis and tissue remodeling, events that are central to normal peritoneal wound healing and adhesion formation. Although, the insight into their importance in the development of tissue fibrosis has substantially increased, their major roles in peritoneal biological functions and adhesion formation remain at best speculative. This article reviews the clinical implications of adhesions and attempts to highlight some of the key molecules i.e. growth factors, cytokines, chemokines, proteases and extracellular matrix, that are recognized to regulate inflammation, fibrinolysis, angiogenesis, and tissue remodeling, events that are central to peritoneal wound repair and adhesion formation. Finally, the article discusses the potential application and site specific delivery of several active compounds that are developed to alter the local inflammatory and immune response i.e., cytokine/chemokine network, targeted gene delivery and development of a new generation of biomaterials to prevent adhesion formation. Such understanding of peritoneal biology not only assist us to better manage patients with adhesion, but also those with endometriosis and malignant diseases that affect the peritoneal cavity.

Biocompatible Materials↗

Preventive effects of chitosan on peritoneal adhesion in rats.

AIM: To study the effects of chitosan gel and blending chiston/gelatin film on preventing peritoneal adhesion in rats. METHODS: SD rats were randomly divided into 2 groups, group A treated with chitosan gel and group B with blending chiston/gelatin film. In group A, rats were randomly subdivided into 3 subgroups as groups A1, A2 and A3, and different methods were used to induce peritoneal adhesions at the dead end of vermiform process in each group as follows: Group A1 with trauma, A2 with talc powder and A3 with ligation of blood vessel. In each subgroup, rats were redivided into control group and experimental group whose treated vermiform processes were respectively coated with chitosan gel and normal saline immediately after the adhesion-induced treatments. In group B, all the rats received traumatic adhesion-induced treatments and then were randomly divided into 4 groups (groups B1, B2, B3, B4). Group B1 served as control group and were coated with normal saline in the vermiform processes immediately after the treatments, and groups B2, B3 and B4 with 100% chitosan film, chitosan film containing 10% gelatin and chiston film containing 50% gelatin, respectively. At 2 and 4 wk after the above treatments, half of the rats in each terminal group were belly opened, and the peritoneal adhesive situation was graded and histopathological changes were examined. RESULTS: (1) In group A, regarding peritoneal adhesion situation: At both 2 and 4 wk after the treatments, for groups A1 and A3, the adhesive grades of experimental groups were significantly lower than those of the control group (2 wk: H = 4.305, P < 0.05 for A1, H = 6.743, P < 0.01 for A3; 4 wk: H = 4.459, P < 0.05 for A1, H = 4.493, P < 0.05 for A3). However, of group A2, there was no significant difference between the experimental and control groups (2 wk: H = 0.147, P > 0.05; 4 wk: H = 1.240, P > 0.05). Regarding pathological changes: In groups A1 and A3, the main pathological change was fibroplasia. In group A2, the main changes were massive foreign-body giant cell reaction and granuloma formation with fibroplasia of different degrees. (2) In group B, regarding degradation of film: With increase of the blended gelatin concentration, degrading speed of the film accelerated significantly. Regarding peritoneal adhesion situation: At both 2 and 4 wk after the treatments, the adhesive grades of B1 were the lowest among the four subgroups of B (2 wk: H = 29.679, P < 0.05; 4 wk: H = 18.791, P < 0.05). At 2 wk after the treatments, the grades of group B2 were significantly lower than that of groups B3 and B4 (H = 4.025, P < 0.05 for B2 vs B3; H = 4.361, P < 0.05 for B2 vs B4). At 4 wk, there were no significant differences of the grades between groups B2, B3 and B4. Regarding pathological changes: Inflammatory cell infiltration and fibroplastic proliferation were observed in the local treated serous membranes, which was the mildest in group B1. Slight foreign-body giant cell reactions were also found in groups B2, B3, and B4. CONCLUSION: (1) Chitosan gel has preventive effect on traumatic or ischemic peritoneal adhesion, but no obvious effect on foreign body-induced peritoneal adhesion. (2) Chitosan film may exacerbate the peritoneal adhesion. Blending with gelatin to chitosan film can accelerate the degradation of the film, but can simultaneously facilitate the formation of peritoneal adhesion.

Animals↗

Dressing spray enhances the adhesive strength of surgical dressing tapes.

BACKGROUND: The use of surgical adhesive tapes after minor surgical and dermatologic operations is widespread. Their use reduces the wound tension and separation and they ultimately improve the postoperative scar. The most commonly used wound adhesives to enhance the adhesiveness of the surgical tapes, are tincture of benzoin and mastisol. AIM: The purpose of the present study is to demonstrate the role of adhesive power of dressing spray with the adhesive tape application on the skin, which is widely used in clinics after the skin closure. METHODS: Fifteen volunteers who were chosen among the medical personnel of the hospital comprised the study group. The skin of the flexor aspect of the 1/3 middle forearm of the subjects was used as the procedure region. The data is collected in the first, second and eighth days of the study. At the first stage of the study, an adhesive wound closure tape was applied to the skin without any compound of adhesives (group A). In the second and third stages, a thin coat of transparent film dressing spray (group B) and an adhesive compound of tincture of benzoin (group C) were applied to the skin before the adhesive tape placement, respectively. Different values of weights ranging between 50-900 gm were hanged by hooking into the center of the adhesive tape. The weights that caused complete separations of the tape from the skin after exactly 20 seconds were recorded in all groups. The data was analyzed by using Friedman test in order to calculate statistical significance between groups A, B and C. RESULTS: The difference in adhesive power between control and groups B and C was found to be highly significant ( p CONCLUSION: The results indicated that dressing spray tested has an additional adhesive power besides its well known features and that it can be used as an efficient alternative material among other adhesive compounds.

Humans↗

Synthetic peptides inhibit adhesion of human tumor cells to extracellular matrix proteins.

Human tumor cell progression and metastasis are partially dependent on the ability of a tumor cell to adhere to the proteins of the extracellular matrix (ECM) and survive at the distant location. Six novel D-amino acid-containing peptides were analyzed for their ability to adhere to human prostate tumor cells, support tumor cell adhesion, and inhibit tumor cell adhesion to ECM proteins or human dermal fibroblasts. Of these, two peptides called RZ-3 (kmviywkag) and HYD-1 (kikmviswkg) bound to tumor cell surfaces and compared favorably with the previously reported AG-73 (RKRLQVQLSIRT) L-amino acid peptide, as determined by fluorescence-activated cell sorting analysis. A scrambled peptide derivative of HYD-1, called HYDS-1 (wiksmkivkg), was not active. The RZ-3, HYD-1, and AG-73 peptides supported maximal cancer cell adhesion at 5 microg, 10 microg, and 50 microg/well, respectively. The ECM proteins fibronectin, laminin 1, and collagen IV supported maximal cell adhesion at 1 microg, >10 microg, and 50 microg/well, respectively. Prostate tumor cell adhesion to immobilized RZ-3 and HYD-1 peptides was inhibited by alpha2-6- and beta1-integrin-blocking antibodies. Conversely, tumor cell adhesion to a beta1-integrin-specific antibody was blocked by both RZ-3 and HYD-1. Epithelial cell adhesion to dermal fibroblasts was inhibited by HYD-1 and unaffected by the scrambled peptide, HYDS-1. Cell adhesion to immobilized peptides was unaffected by EDTA. The soluble RZ-3 and HYD-1 peptides inhibited tumor cell adhesion to each of the immobilized four ECM proteins (1.0 microg/well) in a time- and concentration-dependent manner. The IC(50) of the RZ-3 peptide for blocking adhesion to fibronectin, laminin 1, laminin 5, and collagen IV was 2.4 microg, 1.8 microg, 4.6 microg, and 2.8 microg/well, respectively. The IC(50) of the HYD-1 peptide for blocking adhesion to fibronectin, laminin 1, laminin 5, and collagen IV was 6.9 microg, 5.7 microg, >10 microg, and 6.2 microg/well, respectively. Taken together, these results indicate that RZ-3 and HYD-1 are biologically active D-amino acid-containing peptides that can themselves support tumor cell adhesion and can inhibit tumor cell adhesion to immobilized ECM proteins or dermal fibroblasts.

Carcinoma, Squamous Cell↗

[Adhesion of hepatocellular carcinoma cells to collagen IV coated surfaces].

OBJECTIVES: To quantitatively describe the adhesion of hepatocellular carcinoma (HCC) cells and hepatocytes to collagen IV/laminin coated surfaces and to investigate the relevance of cell adhesion forces to the coating concentration of collagen IV and, when laminin was co-coated along with collagen IV, the incorporation concentration of laminin. METHODS: A stepwise coating protocol was adopted to prepare the collagen IV/laminin coated surfaces, in which poly-D-lysine and collagen IV/laminin were successively coated onto glass surfaces and finally, bovine serum albumin was used to block the non-specific adhesion. Cell adhesion forces were measured by means of micropipette aspiration technique. RESULTS: Cell adhesion forces showed good dependence on the coating concentration of collagen IV. However, the amplitude for the increase of adhesion forces of HCC cells (202 x 10(-10) N, 26%) was far more less than that for hepatocytes(1,566 x 10(-10) N, 742%) when coating concentration increased from 1 microgram/ml to 5 micrograms/ml. No further increase in the adhesion forces of HCC cells was observed when the coating concentration of collagen IV increased beyond 2 micrograms/ml. The incorporation of laminin along with 2 micrograms/ml collagen IV did not readily result in an increase in the adhesion forces of the two kinds of cells to the surfaces. Among the concentration of laminin tested, only in certain concentration(0.625 microgram/ml or 1.25 micrograms/ml) did the incorporation of laminin along with 2 micrograms/ml collagen IV lead the adhesion forces of hepatocytes and HCC cells to the coated surfaces to reach their corresponding maximum values, otherwise this incorporation led the adhesion forces to decrease. CONCLUSION: The present method is efficient in investigating cell-matrix adhesion. The cell adhesion behavior to collagen IV for HCC differs obviously from those for normal hepatocytes. Laminin might be an important factor for the regulation of cell adhesion forces to matrix components.

Carcinoma, Hepatocellular↗

Dental adhesives of the future.

The current trend in the development of dentin adhesives attempts to simplify bonding steps and make them more user-friendly. However, optimizing speed and efficiency should be accomplished without major tradeoffs in the quality or durability of resin bonds. Although dentin adhesives have improved tremendously over the past decade, postoperative sensitivity, incomplete marginal seal, premature bond degradation, biocompatibility, and compromised bonding to abnormal substrates are still considered potential problems associated with their use. Advances in different scientific disciplines will enrich the pool from which ideas may be drawn in designing future dentin adhesives. It is probably on the molecular level that we will see the greatest expansion of horizons. With the advances in biomimetics, future dentin adhesive monomers may contain domains derived from protein-based, underwater bioadhesives secreted by aquatic animals such as mussels and barnacles, making them less dependent on the surface energy of the bonding substrates as well as less susceptible to hydrolytic degradation. As adhesive joints produced by contemporary adhesives are brittle in nature, future adhesive design may incorporate biomimetic intermediate-strength domains that can undergo stepwise reversible unfolding in response to varying functional stress levels before ultimate catastrophic failure of the adhesive joint occurs. These domains may also re-establish folded configurations on stress relaxation, making the adhesive both strong and tough. Using the concept of controlled release, future adhesives may contain fluorescent biosensors that can detect pH changes around leaking restorations. They may even have the capacity to heal autonomously, in response to microcracks formed by functional stresses within the adhesive joint. The ability to self-diagnose and self-repair will increase the life expectancy of adhesive restorations. Future dentin adhesives may also assume a more instrumental role in therapeutics apart from caries prevention. These features may include the controlled release of noncollagenous proteins to promote remineralization of collagen matrices in sound and caries affected dentin, and growth factors to induce controlled formation of reparative dentin.

Adhesives↗

Mechanisms of lymphocyte adhesion to endothelial cells: studies using a LFA-1-deficient cell line.

In order to investigate the role of lymphocyte function-associated antigen 1 (LFA-1) in lymphocyte adhesion to endothelial cells (EC), we have studied the adhesion of a LFA-1-deficient lymphoblastoid cell line, ICH-KM, which has < 10% of the cell surface LFA-1 expressed on a normal lymphoblastoid cell line, ICH-BJ. The adhesion of ICH-KM cells to unstimulated EC was 49.9 +/- 8.6% (mean +/- SD) that of ICH-BJ cells. Moreover, phorbol ester-stimulated ICH-KM cells showed a considerably weaker increase in adhesion to unstimulated EC compared with ICH-BJ cells (mean +/- SD increase in percentage adhesion, 3.8 +/- 2.3 compared with 18.5 +/- 8.0; P<0.025). In contrast, there was no significant difference between the enhanced adhesion of ICH-KM cells and ICH-BJ cells to interleukin-1 (IL-1)-stimulated EC. Thus ICH-KM cells showed a 22.7 +/- 11.0 (mean +/- SD) increase in percentage adhesion to IL-1-stimulated EC compared with the 24.8 +/- 8.5 increase in percentage adhesion of ICH-BJ cells. Anti-LFA-1 monoclonal antibodies had no effect on the enhanced adhesion of ICH-KM and ICH-BJ cells to IL-1-stimulated EC but abolished the differences in adhesion between the two cell lines. The study therefore indicates that although a major part of unstimulated and phorbol ester-stimulated lymphocyte-EC adhesion is dependent upon LFA-1, the enhanced adhesion due to stimulation of EC with IL-1 is not dependent upon this molecule. The data therefore supports the existence of cytokine-inducible LFA-1-independent adhesion molecules for lymphocytes on EC.

Antibodies, Monoclonal↗

[Intestinal blood flow alterations in postoperative intraabdominal adhesion formation and the role of Endothelin-1 blockade].

BACKGROUND: The current study was planned to investigate intestinal blood flow alterations and the role of ET-1 receptor blockade in the formation of postoperative intraperitoneal adhesion formation. METHODS: Twenty-eight adult Wistar Albino rats weighing between 250 g and 300 g were divided into four groups. Control group (group 1; n=7) did not undergo any operation. Sham group (group 2; n=7) had only laparotomy. In the adhesion group (group 3; n=7), peritoneal patch (1x1 cm) excision from the right abdominal wall and cecal abrasion were done as "adhesion model operation". One week following this, treatment group (group 4; n=7) received a non-selective ET-1 receptor blocking agent bosentan (30 mg/kg, IP) intra-abdominally, once a day for four days. Intestinal blood flow through the superior mesenteric artery was measured, on postoperative seventh day. Adhesion severity and extension as well as myeloperoxidase activity in the adhesion were calculated. RESULTS: Mean intestinal blood flow significantly increased in adhesion group (81.9+/-5.6 ml/100 g) when compared to group 1 (65.5+/-1.2 ml/100 g). Bosentan caused a significant decrease (44.3+/-6.9 ml/100 g) in intestinal blood flow when compared to group 1 and group 2. Sham group (62.2+/-1 ml/100 g) had similar blood flow level with the control group (65.5+/-1.2 ml/100 g). Adhesion scores were similar in adhesion and Bosentan groups. Sham group had almost no adhesions. Myeloperoxidase activity in adhesion tissue was significantly higher in bosentan group. CONCLUSION: Non-selective ET-1 receptor blockade has no effect on prevention of the formation of intra-abdominal adhesion, but causes a decrease in intestinal blood flow. Adhesion formation increases intestinal blood flow. Adhesion formation is accompanied by increased polymorphonuclear infiltration despite bosentan treatment.

Abdomen↗