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At least 415 records · Page 23Linked to original sources
PubMed1995

Adhesion or anti-adhesion in cancer: what matters more?

The regulation of adhesion processes between normal epithelial cells is an essential condition for the maintenance of appropriate tissular architecture and differentiation. Quantitative and qualitative alterations in these homotypic adhesions occur during the transformation of normal into malignant epithelium. How these complex alterations in various homotypic adhesions modify the ability of tumor cells to detach from the original neoplastic site, to grow and move as single or clumped cells, and to invade the stroma are current issues in tumor biology. This review contrasts tumor cell adhesion mediated by E-cadherin which is consistently decreased in carcinomas, with adhesion mediated by CD44 and CEA which are increased in the tumors. A model proposing to resolve the apparent paradox of simultaneous adhesion and anti-adhesion mediated by the same protein is proposed.

Cadherins↗
PubMed1989

[Postoperative, intra-abdominal adhesions--a new standardized and objective animal model and testing of substances for the prevention of adhesions].

80 male Sprague Dawley rats were divided in 8 groups of equal size. After median laparotomy defined abrasions of the serosa of abdominal wall, cecum and ileum were performed (400p, abrasive paper 280 grains/cm2, 8 cm2). The control group (I) received no medication. In the treatment groups 5 ml of the following agents were instilled before closure of the abdominal wall: normal saline (II), 16,250 IE Neomycin with 1250 IE Bacitracin (III), 30% dextrose (MW 70,000) (IV), 50,000 IE Streptokinase with 12,500 IE Streptodornase (V), or TCDO in concentrations of 10% (VI), 50% (VII), and 100% (VIII). All animals were relaparotomized on the 7th postoperative day, the adhesions were dissected and their extent was calculated by computer aid. Furthermore specimens were obtained for microscopic studies. Compared to the controls no reduction of adhesions could be achieved by dextrose. Significantly more adhesions were observed after treatment with Neomycin/Bacitracin. A reduction of about 23% was registered with normal saline and TCDO 10%. The greatest reduction of adhesions was seen after application of Streptokinase/Streptodornase as well as TCDO in concentrations of 50% and 100% (63%). The results were significant after evaluation with the t-test. Histologically there was a correlation between the extent of adhesions and the fibrin film. The new animal model has proven to result in reproducible data if used to evaluate substances for prevention of adhesions. Clinical studies with the best of these agents could serve as an approach to solve the problem of adhesion ileus.

Abdomen↗
PubMed2000

Initial homotypic cell pair adhesion in regenerating Hydra facilitates subsequent adhesion of homotypic cells.

In Hydra vulgaris at the level of dissociated single cells endodermal cells adhere to each other more readily than to ectodermal cells at the initial adhesion. The time required for adhesion to occur between two adjacent cells is shorter for both endodermal and ectodermal homotypic cell adhesions once the initial adhesion of the first pair of cells has been established. It is confirmed that contact of an aggregated pair with additional homotypic cells facilitates the occurrence of homotypic adhesions; heterotypic adhesions are discouraged. This suggests that adhesion of homotypic cells contributes to an increased readiness for subsequent homotypic cells to adhere.

Animals↗
PubMed1985

Adhesion mutants of Dictyostelium discoideum lacking the saccharide determinant recognized by two adhesion-blocking monoclonal antibodies.

A mutant of Dictyostelium discoideum, strain HL260, was isolated based on its failure to bind d-41, a monoclonal antibody that blocks developmentally regulated cell-cell adhesion. The mutant fails to normally acquire cell-cell adhesion as assayed with cells shaken in 10 mM EDTA, but aggregates and and constructs fruiting bodies. Other mutant strains, HL216 and HL220, previously shown to have impaired cell-cell adhesion, also lack the determinant that binds d-41. The three strains all carry mutations in a gene designated mod B, which directs a post-translational modification of several developmentally regulated D. discoideum glycoproteins. Diploids formed between independent mod B mutant haploid strains also lack this determinant and show marked impairment of cell-cell adhesion in EDTA, indicating that mutations in mod B, rather than other mutations not shared by the haploid strains, are related to the adhesion defect. The results are consistent with other evidence that an oligosaccharide carried on several developmentally regulated glycoproteins plays an essential role in EDTA-resistant cell-cell adhesion in D. discoideum. However, this type of adhesion is not essential for morphogenesis in that the only defect detected thus far in mod B mutant strains is that they construct relatively smaller fruiting bodies that contain fewer spores.

Animals↗
PubMed1996

Hydrogen peroxide and superoxide modulate leukocyte adhesion molecule expression and leukocyte endothelial adhesion.

While endothelial oxidant generation and subsequent leukocyte chemotaxis and activation are important mechanisms of tissue damage in ischemic organs, it is not known if oxidant generation may be involved in triggering the subsequent leukocyte-mediated injury which occurs. Questions remain whether particular oxidants and oxygen-free radicals are capable of modulating the expression of leukocyte adhesion molecules and effecting leukocyte endothelial adhesion. Studies were performed to determine the effect of different biologically occurring oxidant molecules and oxygen free radicals including: .O2-, .OH, and H2O2 on the expression of integrin and selectin adhesion molecules on the surface of human PMNs and to determine the effect of these alterations on PMN adhesion to the endothelium. Adhesion molecule expression on the surface of human PMNs was measured by immunofluorescence flow cytometry. Electron paramagnetic resonance spectroscopy was applied to characterize the presence of exogenous free radical generation as well as that from activated PMNs. It was observed that these oxidants can cause up-regulation of CD11b and CD18 expression with shedding of L-selectin. The kinetics and dose-response of these effects were analyzed and their functional significance determined by measuring PMN adhesion to cultured human aortic endothelial monolayers. These studies demonstrate that oxygen free radicals and non-radical oxidants can directly trigger PMN activation and adhesion to vascular endothelium.

Antigens, CD↗
PubMed2001

Lymphocyte migration to inflamed lacrimal glands is mediated by vascular cell adhesion molecule-1/alpha(4)beta(1) integrin, peripheral node addressin/l-selectin, and lymphocyte function-associated antigen-1 adhesion pathways.

Sjogren's syndrome is an autoimmune disease characterized by inflammation and destruction of lacrimal and salivary glands. The development of the inflammation requires the migration of lymphocytes from the blood into these tissues. This migration involves multistep cascades with binding of lacrimal gland endothelial adhesion molecules to their ligands on circulating lymphocytes. We used nonobese diabetic mice, which develop autoimmune-mediated lacrimal gland inflammation, as an experimental model to define the adhesion molecules that control lymphocyte migration into inflamed lacrimal glands. We found that vascular endothelia in inflamed areas of lacrimal gland expressed vascular cell adhesion molecule (VCAM)-1 and the peripheral node addressin (PNAd), but not mucosal addressin cell adhesion molecule-1. Most lymphocytes in the inflamed glands expressed alpha(4) integrin, L-selectin, and lymphocyte function-associated antigen (LFA)-1. In vivo studies revealed that antibodies against VCAM-1, alpha(4) integrin, PNAd, L-selectin, or LFA-1 almost completely blocked lymphocyte migration from blood into inflamed lacrimal glands. There was no inhibition of migration by antibodies against mucosal addressin cell adhesion molecule-1 or alpha(4)beta(7) integrin. These results indicate that endothelial/lymphocyte adhesion cascades involving VCAM-1/alpha(4)beta(1) integrin, PNAd/L-selectin, and LFA-1 control the migration of lymphocytes into inflamed lacrimal gland. These adhesion molecules offer potential therapeutic targets to block the development of lacrimal gland inflammation and destruction.

Aging↗
PubMed2000

A role for the cell adhesion molecule CD44 and sulfation in leukocyte-endothelial cell adhesion during an inflammatory response?

CD44 is a widely expressed cell adhesion molecule that has been implicated in a variety of biological processes including lymphopoiesis, angiogenesis, wound healing, leukocyte extravasation at inflammatory sites, and tumor metastasis. The adhesive function of CD44, like other molecules involved in inducible adhesion, is tightly regulated. Post-translational modifications, isoform expression, aggregation state, and protein associations all can affect the ligand binding properties of CD44, and these can vary depending on the cell type and the activation state of the cell. The most extensively characterized ligand for CD44 is hyaluronan, a component of the extracellular matrix. Interactions between CD44 and hyaluronan can mediate both cell-cell and cell-extracellular matrix adhesion. In the immune system, both the selectin molecules and CD44 have been implicated in the initial binding of leukocytes to endothelial cells at an inflammatory site. Sulfation is required for selectin-mediated leukocyte-endothelial cell interactions, and, recently, inducible sulfation also was shown to regulate CD44-mediated leukocyte adhesion to endothelial cells. Sulfation, therefore, may be important in the regulation of cell adhesion at inflammatory sites. In this commentary we have reviewed the molecular aspects of CD44 and the mechanisms that regulate its binding to hyaluronan. In addition, we have summarized the role of CD44 and hyaluronan in mediating leukocyte-endothelial cell interactions and have discussed how this interaction may be regulated. Finally, we examined the potential role of sulfation as an inducible means to regulate CD44-mediated leukocyte adhesion and as a more general mechanism to regulate leukocyte-endothelial cell interactions.

Animals↗
PubMed1998

Reduction of de novo postsurgical adhesions by intraoperative precoating with Sepracoat (HAL-C) solution: a prospective, randomized, blinded, placebo-controlled multicenter study. The Sepracoat Adhesion Study Group.

OBJECTIVE: To assess the efficacy and safety of Sepracoat (HAL-C; Genzyme Corporation, Cambridge, MA) solution in reducing the incidence, severity, and extent of de novo adhesion formation at sites without direct surgical trauma or adhesiolysis at the time of gynecologic laparotomy. DESIGN: Prospective, randomized, blinded, placebo-controlled multicenter study. Patients underwent gynecologic procedures via laparotomy; approximately 40 days later, surgeons assessed their adhesions during second-look laparoscopy. SETTING: Twenty-three North American institutions. PATIENT(S): Two hundred seventy-seven women for safety evaluations; 245 women for efficacy studies. INTERVENTION(S): Intraoperative serosal coating with Sepracoat (treatment) or phosphate-buffered saline (placebo) after opening of the abdominal cavity, after irrigation or every 30 minutes during surgery, and at the completion of surgery. MAIN OUTCOME MEASURE(S): Incidence, severity, and extent of de novo adhesions to 23 intraabdominal sites. RESULT(S): The Sepracoat group had a significantly lower incidence of de novo adhesions than the placebo group as assessed by the proportion of sites involved (0.23 +/- 0.02 versus 0.30 +/- 0.02, respectively) and the percentage of patients without de novo adhesions (13.1% versus 4.6%, respectively), as well as significantly reduced adhesion extent and severity. Sepracoat was well tolerated, with a safety profile nearly identical to that of the placebo. CONCLUSION(S): Sepracoat was significantly more effective than placebo and was safe in reducing the incidence, extent, and severity of de novo adhesions to multiple sites indirectly traumatized by gynecologic surgery via laparotomy.

Administration, Topical↗
PubMed2004

Mechanism of adhesion and detachment at the anterior end of Merizocotyle icopae (Monogenea: Monocotylidae) including ultrastructure of the anterior adhesive matrix.

The anterior adhesive mechanism was studied for Merizocotyle icopae (Monogenea: Monocotylidae). Adult anterior apertures can open and close. In addition, duct endings terminating within the apertures are everted or retracted depending on the stage of attachment. Adhesive in adults is synthesized from all 3 secretory types (rod-shaped, small and large spheroidal bodies) found within anterior apertures. All exit together and undergo mixing to produce the adhesive matrix, a process that depletes duct contents. A greater number of ducts carrying rod-shaped bodies is depleted than ducts containing spheroidal bodies which changes the ratio of secretory types present on detachment. Detachment involves elongation of duct endings and secretion of additional matrix as the worm pulls away from the substrate. The change in secretory type ratio putatively modifies the properties of the secreted matrix enabling detachment. Only after detachment do ducts refill. During attachment, individual secretory bodies undergo morphological changes. The larval and adult adhesive matrix differs. Anterior adhesive in oncomiracidia does not show fibres with banding whereas banded fibres comprise a large part of adult adhesive. The data suggest that this is the result of adult spheroidal secretions modifying the way in which the adult adhesive matrix forms.

Adhesiveness↗
PubMed2000

Adhesion to fibronectin via beta1 integrins regulates p27kip1 levels and contributes to cell adhesion mediated drug resistance (CAM-DR).

The tumor cell environment may influence drug response through interactions with the extracellular matrix (ECM). We recently reported that adhesion of myeloma cells to fibronectin (FN) via beta1 integrins is associated with a cell adhesion mediated drug resistance (CAM-DR). Activation of beta1 integrins is known to influence both apoptosis and cell growth. We hypothesized that the FN mediated cytoprotection may be in part due to perturbations in cell cycle progression. In this report we demonstrate that adhesion of myeloma cells to FN results in a G1 arrest associated with increased p27kip1 protein levels and inhibition of cyclin A and E associated kinase activity. Disruption of cells from FN adhesion resulted in a rapid recruitment of cells into S phase, a decrease in p27kip1 levels, and reversion to a drug sensitive phenotype. Treatment of cells with p27Kip1 antisense oligonucleotides did not affect FN adhesion; however, p27Kip1 protein levels were reduced and cells became sensitive to cytotoxic drugs. These studies demonstrate that beta1 mediated adhesion of myeloma cells to FN regulates p27kip1 levels and that p27kip1 levels are causally related to CAM-DR. Disruption of beta1 integrin mediated FN adhesion may represent a potential target for the potentiation of drug induced apoptosis.

CDC2-CDC28 Kinases↗
PubMed1991

Relationship between neuronal migration and cell-substratum adhesion: laminin and merosin promote olfactory neuronal migration but are anti-adhesive.

Regulation by the extracellular matrix (ECM) of migration, motility, and adhesion of olfactory neurons and their precursors was studied in vitro. Neuronal cells of the embryonic olfactory epithelium (OE), which undergo extensive migration in the central nervous system during normal development, were shown to be highly migratory in culture as well. Migration of OE neuronal cells was strongly dependent on substratum-bound ECM molecules, being specifically stimulated and guided by laminin (or the laminin-related molecule merosin) in preference to fibronectin, type I collagen, or type IV collagen. Motility of OE neuronal cells, examined by time-lapse video microscopy, was high on laminin-containing substrata, but negligible on fibronectin substrata. Quantitative assays of adhesion of OE neuronal cells to substrata treated with different ECM molecules demonstrated no correlation, either positive or negative, between the migratory preferences of cells and the strength of cell-substratum adhesion. Moreover, measurements of cell adhesion to substrata containing combinations of ECM proteins revealed that laminin and merosin are anti-adhesive for OE neuronal cells, i.e., cause these cells to adhere poorly to substrata that would otherwise be strongly adhesive. The evidence suggests that the anti-adhesive effect of laminin is not the result of interactions between laminin and other ECM molecules, but rather an effect of laminin on cells, which alters the way in which cells adhere. Consistent with this view, laminin was found to interfere strongly with the formation of focal contacts by OE neuronal cells.

Animals↗
PubMed1976

Intercellular adhesive selectivity. III. Species selectivity of embryonic liver intercellular adhesion.

A species difference in the intercellular adhesive selectivity of mixtures of embryonic liver cells is reported. This is first quantitative assessment of species differences in the intercellular adhesive properties of embryonic cells. A collecting aggregate assay, a new double-label assay procedure, and histological and autoradiographic procedures were used to elucidate the intercellular adhesive selectivity of developing mammalian and avian liver cells. Evidence is presented that the reported adhesive differences are not due to the different cell types composing the respective embryonic mammalian and avian livers. Finally, such heterolgous-homotypic selectivity of adhesion is not a property of all tissues, since it is shown that developing brain cells (mesencephalon) do not exhibit the avove intercellular adhesive selectivity (mammalian vs. avian). These findings provide further support for the hypothesis that generic identity as well as cell type may play an important part in determining the intercellular adhesive behavior of heterologous-homotypic mixtures of embryonic cells. A possible evolutionary divergence of morphogenetic mechanisms is discussed.

Animals↗
PubMed1998

Serine and threonine phosphorylation of the paxillin LIM domains regulates paxillin focal adhesion localization and cell adhesion to fibronectin.

We have previously shown that the LIM domains of paxillin operate as the focal adhesion (FA)-targeting motif of this protein. In the current study, we have identified the capacity of paxillin LIM2 and LIM3 to serve as binding sites for, and substrates of serine/threonine kinases. The activities of the LIM2- and LIM3-associated kinases were stimulated after adhesion of CHO.K1 cells to fibronectin; consequently, a role for LIM domain phosphorylation in regulating the subcellular localization of paxillin after adhesion to fibronectin was investigated. An avian paxillin-CHO.K1 model system was used to explore the role of paxillin phosphorylation in paxillin localization to FAs. We found that mutations of paxillin that mimicked LIM domain phosphorylation accelerated fibronectin-induced localization of paxillin to focal contacts. Further, blocking phosphorylation of the LIM domains reduced cell adhesion to fibronectin, whereas constitutive LIM domain phosphorylation significantly increased the capacity of cells to adhere to fibronectin. The potentiation of FA targeting and cell adhesion to fibronectin was specific to LIM domain phosphorylation as mutation of the amino-terminal tyrosine and serine residues of paxillin that are phosphorylated in response to fibronectin adhesion had no effect on the rate of FA localization or cell adhesion. This represents the first demonstration of the regulation of protein localization through LIM domain phosphorylation and suggests a novel mechanism of regulating LIM domain function. Additionally, these results provide the first evidence that paxillin contributes to "inside-out" integrin-mediated signal transduction.

Amino Acid Sequence↗
PubMed1990

Mouse thymic epithelial cell lines interact with and select a CD3lowCD4+CD8+ thymocyte subset through an LFA-1-dependent adhesion--de-adhesion mechanism.

Differentiation of bone-marrow-derived precursor cells into mature mouse T lymphocytes occurs in the thymus and involves sequential interactions with MHC-positive hemopoietic and epithelial stromal cells. To study the in vitro molecular mechanisms at play during the lympho-epithelial cell adhesion, we derived thymic stromal cell lines which were shown to possess cytokeratin filaments and tight junctions. These mouse thymic epithelial (MTE) cell lines did not express the classical hemopoietic stromal cell surface markers (i.e. LFA-1, Mac-1, and CD45) but expressed ICAM-1, NCAM, J11d, CD44, and MHC molecules. A quantitative cell adhesion assay was used to evaluate the interaction of various lymphoid cell subsets with MTE cells. Two cell interaction patterns could be defined: first, a rapid adhesion of a fraction of CD4+CD8+ and of a few CD4-CD8- immature thymocytes to MTE cells was observed at 4 degrees C. The CD8 molecule was shown to be partially involved in this initial contact. The strength of adhesion between MTE cells and distinct thymocyte subsets was evaluated and found to be maximal with neonatal thymocytes. Second, a temperature-dependent adhesion step characterized by a rapid and active stabilization of the interaction of MTE cells with 20% of CD4+CD8+CD3low thymocytes was seen, followed by a more progressive de-adhesion step. This active process of engagement was highly LFA-1-dependent, involved the CD4 and CD8 molecules, and required protein kinase C activation and cytoskeletal integrity. The results are consistent with the involvement of LFA-1 in a transient and regulated cell adhesion under the control of the TCR-CD3 complex that progressively appears on maturing cells. This phenomenon might contribute to the selection of a subset of immature thymocytes by epithelial cells occurring during the process of maturation of these cells.

Animals↗
PubMed2001

Adhesion of corneal epithelial cells to cell adhesion peptide modified pHEMA surfaces.

Epithelialization of a corneal implant is a desirable property. In this study we compared surface modification of poly (2-hydroxyethyl methacrylate) (pHEMA) with the cell adhesion peptides RGDS and YIGSR. Various parameters in the tresyl chloride activation and modification reactions were considered in order to maximize surface coverage with the peptide including tresyl chloride reaction solvent. tresyl chloride reaction time, tresyl chloride concentration, peptide concentration, and peptide reaction pH. Surface chemistry and corneal epithelial cell adhesion to the modified surfaces were examined. X-ray photoelectron spectroscopy data suggested that while peptide modification had occurred, surface coverage with the peptide was incomplete. Acetone was found to result in a higher fraction of nitrogen and surface bound carboxyl groups compared to dioxane and ether. Furthermore, corneal epithelial cell adhesion to the surfaces for which acetone was used for the activation reaction was significantly greater. Statistical analysis of the various samples suggests that lower peptide concentrations and higher tresyl chloride reaction times result in better cell adhesion. Furthermore, modification with YIGSR resulted in higher surface concentrations and better cell adhesion than modification with RGDS. Little or no cell adhesion was noted on the unmodified pHEMA controls. Protein adsorption results suggest that the differences in cell adhesion cannot be attributed to differences in serum protein adsorption from the culture medium. We conclude that YIGSR modified surfaces have significant potential for further development in corneal applications.

Adsorption↗
PubMed1991

Chemotactic factors regulate lectin adhesion molecule 1 (LECAM-1)-dependent neutrophil adhesion to cytokine-stimulated endothelial cells in vitro.

Monoclonal antibodies recognizing CD18, CD11a, CD11b, and neutrophil lectin adhesion molecule 1 (LECAM-1), i.e., the human homologue of the murine MEL-14 antigen, were used to assess the relative contribution of these glycoproteins to neutrophil-endothelial adhesion. Under static conditions, the adhesion of neutrophils to IL-1-stimulated human umbilical vein endothelial cell (HUVEC) monolayers was inhibited by antibodies to CD18, CD11a, and the neutrophil LECAM-1, and the effect of combining anti-LECAM-1 and anti-CD11a was almost additive. Under flow at a wall shear stress 1.85 dyn/cm2, a condition where CD18-dependent adhesion is minimal, anti-LECAM-1 inhibited adhesion by greater than 50%. Chemotactic stimulation of neutrophils induced a rapid loss of LECAM-1 from the neutrophil surface, and the level of neutrophil surface LECAM-1 was closely correlated with adhesion under flow. Neutrophils contacting the activated endothelial cells for 30 min lost much of their surface LECAM-1, a phenomenon induced by a soluble factor or factors released into the medium by the stimulated monolayers, and a high percentage migrated through the HUVEC monolayer. This migration was almost completely inhibited by anti-CD18, but was unaffected by antibodies to neutrophil LECAM-1. These results support the concept that LECAM-1 is a neutrophil adhesion molecule that participates in the adherence of unstimulated neutrophils to cytokine-stimulated endothelial cells under conditions of flow, and is then lost from the neutrophil surface coincident with the engagement of CD18-dependent mechanisms leading to transendothelial migration.

Adult↗
PubMed1994

Recipient mononuclear cell recognition and adhesion to graft endothelium after human cardiac transplantation. Lymphocyte recognition leads to monocyte adhesion.

Transendothelial migration of mononuclear cells is crucial in the development of allograft rejection and transplant coronary disease. Adhesion of circulating cells to endothelium is the initial step in transendothelial migration. Human aortic endothelial cell cultures were established from aortic tissue harvested at the time of organ donation for cardiac transplantation which allowed specific recipient mononuclear cell-graft endothelial interactions to be studied. Confluent untreated endothelial cells were incubated with recipient mononuclear cells for 15 min to assess adhesion. Adhesion of recipient mononuclear cells to endothelium derived from their graft was threefold higher than adhesion to nonspecific endothelium (93 +/- 20 vs. 30 +/- 11 cells/high power field, P < 0.005). Graft-specific adhesion was inhibited by preincubation of the endothelium with antibodies to class I HLA (34 +/- 16 cells/high power field, P < 0.005). Immunofluorescence performed after adhesion showed that 73 +/- 6% of both specific and nonspecific adherent cells were monocytes. The use of purified lymphocyte and monocyte preparations showed that graft-specific lymphocytes induce unrelated monocytes to become adherent. These results suggest that lymphocytes are primed in vivo to recognize endothelium derived from their graft which leads to a rapid increase in lymphocyte and monocyte adhesion. Such allo-recognition may involve endothelial class I HLA molecules.

CD3 Complex↗
PubMedDate not supplied

Use of fibrin adhesive to reduce post-surgical adhesion reformation in rabbits.

Following surgery on fallopian tubes, the development of adhesions is a natural consequence of wound healing and may result in infertility. Using a rabbit model, we evaluated the anti-adhesive properties of a sponge-like equine collagen sheet (TachoComb), which is coated on one side with human fibrinogen and bovine thrombin. TachoComb is applied by affixing the sheet over the area of perforation or bleeding and acts as a haemostatic agent, capable of sealing perforations to prevent leakage. In our rabbit model, adhesions were induced by mechanical and chemical irritants during laparotomy. After a 1-month recovery period, adhesions were lysed using microsurgical techniques and TachoComb, or physiological saline applied. Evaluation of adhesion reformation was determined after a minimum of 10 days. TachoComb significantly reduced the area of adhesion reformation compared with rabbits treated using physiological saline only. Our study demonstrated that TachoComb is effective not only as a haemostatic agent, but is also capable of reducing adhesion reformation.

Animals↗