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At least 469 records · Page 26Linked to original sources
PubMed2003

No volume effect on retrograde colonic spread of rectally-administered ropivacaine gel.

BACKGROUND: Rectal administration of enemas, foams and suppositories is the most efficient way to deliver locally acting drugs to the distal colon. Ropivacaine, a long-acting local anaesthetic, was chosen as a candidate for a new rectal treatment of ulcerative colitis. AIM: To determine the colonic spread of a rectal ropivacaine formulation. METHODS: In this randomized, incomplete cross-over study, 12 male volunteers were given 200 mg ropivacaine HCl rectally in 20, 40, 60 and 80 mL hydroxypropyl methylcellulose gel. The viscosity of the gel was 1.1 Pa s. The spread of the radiolabelled (99mTc-labelled diethylenetriaminepenta-acetic acid) formulations was assessed by gamma-scintigraphy. Plasma was collected and analysed for ropivacaine base. RESULTS: The retrograde spread was limited to the descending colon and the difference between the studied volumes was not statistically significant. Only the 80-mL volume tended to have a larger distribution, although the 20-mL volume showed the same maximal distribution in two subjects. No distinct relationship between volume, retrograde colonic spread and plasma concentrations could be found. Ropivacaine was well tolerated. CONCLUSIONS: Rectal ropivacaine gel in all volumes between 20 and 80 mL can spread up to the descending colon. There was no relationship between either retrograde colonic spread or the administered volume and the ropivacaine plasma concentrations.

Administration, Rectal↗
PubMed2002

Determination of the water droplet size distribution of fat spreads using confocal scanning laser microscopy.

Knowledge of the water droplet size distribution of fat spreads is necessary for the development and production of high quality microbiological safe products. Fat spreads are water-in-oil emulsions. The water droplet size distribution can be determined by confocal scanning laser microscopy (CSLM) after staining the fat with Nile Red. The profiles of the non-fluorescent water droplets in the 2D images are identified and measured using image analysis. The 'true' water droplet size distribution is calculated from the distribution of the measured profile diameters using a Wicksell transformation of log-normal distributions. The influence of the fluorescent staining and CSLM parameters on the information were studied. The CSLM method was tested on fat spreads with a fat content ranging from 40% to 80%. The results were compared with those obtained by nuclear magnetic resonance spectroscopy (NMR). The distribution parameters [volume weighed geometric mean diameter (D3,3) and the standard deviation (sigma) of the logarithm of the droplet diameter] calculated for 80% fat spreads are in good agreement with those obtained by NMR (within +/- 7% relative). Small differences were found for 65% fat spreads and large differences were identified for 40% fat spreads. The precision for the determination of the D3,3 value by CSLM is worse than that of NMR, even when three images were used to calculate this parameter [3-11% and 1-6% relative standard deviation (RSD), respectively]. The precision for the determination of exp(sigma) by CSLM is comparable or better than that of NMR (1-5% and 3-6% RSD, respectively). CSLM proved to be a reliable method for the determination of the water droplet size distribution of margarines (80% fat). The advantage of CSLM compared to NMR is that visual information is given about the water droplet size distribution in the sample.

Journal Article↗
PubMed2000

The relationship between accessory foramina and tumour spread on the medial mandibular surface.

The medial cortical surface of the mandible can be involved by tumour infiltration from the floor of the mouth. A detailed study of spread via accessory foramina through the edentulous alveolar crest has been previously undertaken, but no similar study has been carried out for the medial surface. In order to gain further appreciation of the mode of tumour spread, a study of the number and distribution of accessory foramina on the medial mandibular surface was performed on 89 mandibles. The number of foramina varied greatly from specimen to specimen. In the ascending ramus above the inferior dental foramen, 3 mandibles showed no foramina; the condylar section possessed the greatest proportion followed by the sigmoid and the coronoid. On the rest of the medial surface below the inferior dental foramen, all specimens showed at least 1 accessory foramen; the greatest concentration was in the middle third along the path of the inferior dental canal, followed by the upper third and the lower third section. Accessory foramina were repeatedly present at certain dedicated sites. The medial facing wall of the inferior dental foramen was found to be the commonest dedicated site (98.3%) followed by foramina on either side of the genial tubercles (71.9%), the digastric fossa (71.9%) and the median foramen above the genial tubercles (64%). The findings of this study are in keeping with the current observation that the lower border is least commonly involved in tumour spread. In view of the presence of accessory foramina along the inferior dental canal and especially on the medial facing wall of the inferior dental foramen, it is imperative to preclude tumour spread in this region prior to undertaking the conservative rim resection procedure. Medial to the symphysis the alveolar mucosa dips down almost to the level of the dedicated foramina in the vicinity of the genial tubercles. As a general rule the attached muscle forms a barrier to tumour spread except in the later stages, however, in irradiated mandibles resistance to spread has been previously reported to be diminished. Under these circumstances, it is possible that the numerous accessory foramina reported in this study could facilitate a direct pathway into the cancellous bone.

Adult↗
PubMedDate not supplied

Spread of injectate during C6 stellate ganglion block and fascial arrangement in the prevertebral region: an experimental study using donated cadavers.

BACKGROUND AND OBJECTIVES: The precise fascial space through which the injectate spreads during stellate ganglion block (SGB) remains unclear. Recent studies using magnetic resonance imaging or computed tomography have suggested that the injectate is deposited around and/or within the longus colli muscle during SGB. However, a fascial space, close to the longus colli, is the most likely route of spread. We identified the prevertebral interlaminal space (PVILS), situated between the anterior and posterior laminae of the prevertebral layer of the fascia, as an important route for the spread of the injectate and as a potential pathway to the ganglion. The danger of downward spread of deep infections through this space has previously been recognized. METHODS AND RESULTS: Using the 6th cervical vertebra paratracheal approach technique, we performed experimental SGB with 10 mL latex on donated cadavers. Spreading of latex into the PVILS was observed in 45 of 52 (86.5%) cadavers that had been fixed with formaldehyde after death, and 5 of 8 (62.5%) fresh cadavers. In these experiments, the latex usually reached the ganglion via the PVILS (39 of 45 and 5 of 5, respectively). Moreover, after direct injection into the PVILS, latex reached the ganglion in 13 of a further 19 (68.4%) postmortem-fixed donated cadavers. CONCLUSION: These results suggest that the PVILS plays a critical role in the spread of injectate as well as being a potential pathway to the stellate ganglion during SGB.

Autonomic Nerve Block↗
PubMed2005

Spread dynamics of invasive species.

Species invasions are a principal component of global change, causing large losses in biodiversity as well as economic damage. Invasion theory attempts to understand and predict invasion success and patterns of spread. However, there is no consensus regarding which species or community attributes enhance invader success or explain spread dynamics. Experimental and theoretical studies suggest that regulation of spread dynamics is possible; however, the conditions for its existence have not yet been empirically demonstrated. If invasion spread is a regulated process, the structure that accounts for this regulation will be a main determinant of invasion dynamics. Here we explore the existence of regulation underlying changes in the rate of new site colonization. We employ concepts and analytical tools from the study of abundance dynamics and show that spread dynamics are, in fact, regulated processes and that the regulation structure is notably consistent among invasions occurring in widely different contexts. We base our conclusions on the analysis of the spread dynamics of 30 species invasions, including birds, amphibians, fish, invertebrates, plants, and a virus, all of which exhibited similar regulation structures. In contrast to current beliefs that species invasions are idiosyncratic phenomena, here we provide evidence that general patterns do indeed exist.

Journal Article↗
PubMed2006

Predicting the global spread of H5N1 avian influenza.

The spread of highly pathogenic H5N1 avian influenza into Asia, Europe, and Africa has resulted in enormous impacts on the poultry industry and presents an important threat to human health. The pathways by which the virus has and will spread between countries have been debated extensively, but have yet to be analyzed comprehensively and quantitatively. We integrated data on phylogenetic relationships of virus isolates, migratory bird movements, and trade in poultry and wild birds to determine the pathway for 52 individual introduction events into countries and predict future spread. We show that 9 of 21 of H5N1 introductions to countries in Asia were most likely through poultry, and 3 of 21 were most likely through migrating birds. In contrast, spread to most (20/23) countries in Europe was most likely through migratory birds. Spread in Africa was likely partly by poultry (2/8 introductions) and partly by migrating birds (3/8). Our analyses predict that H5N1 is more likely to be introduced into the Western Hemisphere through infected poultry and into the mainland United States by subsequent movement of migrating birds from neighboring countries, rather than from eastern Siberia. These results highlight the potential synergism between trade and wild animal movement in the emergence and pandemic spread of pathogens and demonstrate the value of predictive models for disease control.

Animals↗
PubMed2001

Tissue spreading on implantable substrates is a competitive outcome of cell-cell vs. cell-substratum adhesivity.

While the interactions of cells with polymeric substrata are widely studied, the influence of cell-cell cohesiveness on tissue spreading has not been rigorously investigated. Here we demonstrate that the rate of tissue spreading over a two-dimensional substratum reflects a competition or "tug-of-war" between cell-cell and cell-substratum adhesions. We have generated both a "library" of structurally related copolymeric substrata varying in their adhesivity to cells and a library of genetically engineered cell populations varying only in cohesiveness. Cell-substratum adhesivity was varied through the poly(ethylene glycol) content of a series of copolymeric substrata, whereas cell-cell cohesiveness was varied through the expression of the homophilic cohesion molecules N- and R-cadherin by otherwise noncohesive L929 cells. In the key experiment, multicellular aggregates containing about 600 cells were allowed to spread onto copolymeric surfaces. We compared the spreading behavior of aggregates having different levels of cell-cell cohesiveness in a series of copolymeric substrata having different levels of cell-substratum adhesivity. In these experiments, cell-cell cohesiveness was measured by tissue surface tensiometry, and cell-substratum adhesivity was assessed by a distractive method. Tissue spreading was assayed by confocal microscopy as the rate of cell emigration from similar-sized, fluorescence-labeled, multicellular aggregates deposited on each of the substrata. We demonstrate that either decreasing substratum adhesivity or increasing cell-cell cohesiveness dramatically slowed the spreading rate of cell aggregates.

Animals↗
PubMed1989

Effect of cell spreading on cytoplasmic pH in normal and transformed fibroblasts.

Growth of normal fibroblasts requires an adhesive substratum on which to spread, whereas transformed cells can grow in suspension. Since an alkaline cytoplasm has been shown to be required for growth, we measured cytoplasmic pH in individual cells as a function of spreading. The degree of spreading was controlled by coating tissue culture plastic with varying amounts of the nonadhesive polymer polyHEMA. Completely round BALB/c 3T3 cells were 0.15 pH unit more acidic than spread cells. In short-term experiments, cells were treated with the peptide Gly-Arg-Gly-Asp-Ser-Pro to induce rounding or by plating on fibronectin to induce spreading. When cells were induced to change shape, pH changed rapidly and reversibly. All of the anchorage-dependent cell lines tested behaved similarly, but 3T3 cells transformed by the plasma membrane oncogene src or ras were able to maintain a relatively alkaline pH even when completely round. Cells transformed by the nuclear oncogene myc behaved like normal cells. Our results suggest that the requirement for spreading may in part be mediated by cytoplasmic pH. Anchorage-independent growth due to oncogenes that localize to the plasma membrane is associated with loss of this control mechanism.

Animals↗
PubMed1996

Embryonic mesoderm cells spread in response to platelet-derived growth factor and signaling by phosphatidylinositol 3-kinase.

Abnormal mesoderm movement, leading to defects in axial organization, is observed in mouse and Xenopus laevis embryos deprived of platelet-derived growth factor (PDGF) AA signaling. However, neither the cellular response to PDGF nor the signaling pathways involved are understood. Herein we describe an in vitro assay to examine the direct effect of PDGF AA on aggregates of Xenopus embryonic mesoderm cells. We find that PDGF AA stimulates aggregates to spread on fibronectin. This behavior is similar to that of migrating mesoderm cells in vivo that spread and form lamellipodia and filipodia on contact with fibronectin-rich extracellular matrix. We go on to show two lines of evidence that implicate phosphatidylinositol 3-kinase (PI3K) as an important component of PDGF-induced mesoderm cell spreading. (i) The fungal metabolite wortmannin, which inhibits signaling by PI3K, blocks mesoderm spreading in response to PDGF AA. (ii) Activation of a series of receptors with specific tyrosine-to-phenylalanine mutations revealed PDGF-induced spreading of mesoderm cells depends on PI3K but not on other signaling molecules that interact with PDGF receptors including phospholipase C gamma, Ras GTPase-activating protein, and phosphotyrosine phosphatase SHPTP2. These results indicate that a PDGF signal, medicated by PI3K, can facilitate embryonic mesoderm cell spreading on fibronectin. We propose that PDGF, produced by the ectoderm, influences the adhesive properties of the adjacent mesoderm cells during gastrulation.

Androstadienes↗
PubMed2001

Patterns of spread in biological invasions dominated by long-distance jump dispersal: Insights from Argentine ants.

Invading organisms may spread through local movements (giving rise to a diffusion-like process) and by long-distance jumps, which are often human-mediated. The local spread of invading organisms has been fit with varying success to models that couple local population growth with diffusive spread, but to date no quantitative estimates exist for the relative importance of local dispersal relative to human-mediated long-distance jumps. Using a combination of literature review, museum records, and personal surveys, we reconstruct the invasion history of the Argentine ant (Linepithema humile), a widespread invasive species, at three spatial scales. Although the inherent dispersal abilities of Argentine ants are limited, in the last century, human-mediated dispersal has resulted in the establishment of this species on six continents and on many oceanic islands. Human-mediated jump dispersal has also been the primary mode of spread at a continental scale within the United States. The spread of the Argentine ant involves two discrete modes. Maximum distances spread by colonies undergoing budding reproduction averaged 150 m/year, whereas annual jump-dispersal distances averaged three orders of magnitude higher. Invasions that involve multiple dispersal processes, such as those documented here, are undoubtedly common. Detailed data on invasion dynamics are necessary to improve the predictive power of future modeling efforts.

Animals↗
PubMed1995

Cell spreading in Colo 201 by staurosporin is alpha 3 beta 1 integrin-mediated with tyrosine phosphorylation of Src and tensin.

Staurosporin, a broad-spectrum kinase inhibitor, induced cell spreading in a human colon cancer cell line, Colo 201. On collagen and laminin, cell spreading was induced in more than 90% of the cells and was dependent on very late activation antigen-3, as shown by an antibody inhibition assay. Cell spreading required divalent cations and showed the order of preference Mn2+ > Mg2+ > Ca2+. On fibronectin, only about 30% of the cells were observed to spread, and spreading occurred via a non-integrin, RGD-independent pathway. Staurosporin-induced spreading was inhibited by treatment with tyrosine kinase inhibitors herbimycin A and methyl 2,5-dihydroxycinnamate. Despite the presence of staurosporin, seven proteins (220, 175, 150, 98, 62, 58, and 45 kDa) showed increased levels of tyrosine phosphorylation in association with cell adhesion. Two of these (58 and 220 kDa) were identified by immunoprecipitation as Src product and tensin, respectively. Flow cytometric analysis showed that the Colo 201 cells expressed the alpha 2, alpha 3, alpha 6, and beta 1 chains of integrin, but expression of these chains was not influenced by staurosporin. Immunofluorescence microscopy revealed that the alpha 3 chain, diffusely expressed on the cell surface in the absence of staurosporin, was concentrated at focal adhesion plaques after staurosporin treatment. Neither alpha 2 nor alpha 6 was focalized by the treatment.

Alkaloids↗
PubMed1997

Fibroblasts spread on immobilized fibrin monomer by mobilizing a beta1-class integrin, together with a vitronectin receptor alphavbeta3 on their surface.

Human and murine fibroblasts were found to spread far more avidly on fibrin monomer monolayers than on immobilized fibrinogen, indicating that removal of fibrinopeptides by thrombin is a prerequisite for the fibrin-mediated augmentation of cell spreading. In fact, cell spreading was not efficiently augmented on monolayers of a thrombin-treated dysfibrinogen lacking the release of fibrinopeptide A due to an Aalpha Arg-16 --> Cys substitution. Since a synthetic Arg-Gly-Asp (RGD)-containing peptide inhibited the fibrin-mediated cell spreading, subsequent dissociation of the carboxyl-terminal globular domain of the Aalpha-chains appears to render the RGD segments accessible to the cell-surface integrins. In support of this, fibrin-augmented cell spreading was inhibited by an antibody recognizing a 12-kDa peptide segment with gamma Met-89 at its amino terminus, which is located in close association with the RGD segment at Aalpha 95-97 in the helical coiled-coil interdomainal connector. The fibrin-mediated augmentation of cell spreading was inhibited not only by an antibody against human vitronectin receptor (LM 609) but also by an antibody against the beta1 subunit of integrin (mAb13), suggesting that the beta1-class integrin together with a vitronectin receptor, alphavbeta3, is mobilized onto the surface of fibroblasts upon contact with the fibrin monomer monolayer.

Animals↗
PubMed1998

Lipid products of phosphoinositide 3-kinase and phosphatidylinositol 4',5'-bisphosphate are both required for ADP-dependent platelet spreading.

We have shown previously that ADP released upon platelet adhesion mediated by alphaIIb beta3 integrin triggers accumulation of phosphatidylinositol 3',4'-bisphosphate (PtdIns-3,4-P2) (Gironcel, D. , Racaud-Sultan, C., Payrastre, B., Haricot, M., Borchert, G., Kieffer, N., Breton, M., and Chap, H. (1996) FEBS Lett. 389, 253-256). ADP has also been involved in platelet spreading. Therefore, in order to study a possible role of phosphoinositide 3-kinase in platelet morphological changes following adhesion, human platelets were pretreated with specific phosphoinositide 3-kinase inhibitors LY294002 and wortmannin. Under conditions where PtdIns-3, 4-P2 synthesis was totally inhibited (25 microM LY294002 or 100 nM wortmannin), platelets adhered to the fibrinogen matrix, extended pseudopodia, but did not spread. Moreover, addition of ADP to the medium did not reverse the inhibitory effects of phosphoinositide 3-kinase inhibitors on platelet spreading. Although synthetic dipalmitoyl PtdIns-3,4-P2 and dipalmitoyl phosphatidylinositol 3',4', 5'-trisphosphate restored only partially platelet spreading, phosphatidylinositol 4',5'-bisphosphate (PtdIns-4,5-P2) was able to trigger full spreading of wortmannin-treated adherent platelets. Following 32P labeling of intact platelets, the recovery of [32P]PtdIns-4,5-P2 in anti-talin immunoprecipitates from adherent platelets was found to be decreased upon treatment by wortmannin. These results suggest that the lipid products of phosphoinositide 3-kinase are required but not sufficient for ADP-induced spreading of adherent platelets and that PtdIns-4,5-P2 could be a downstream messenger of this signaling pathway.

Adenosine Diphosphate↗
PubMed1999

Integrin-mediated muscle cell spreading. The role of protein kinase c in outside-in and inside-out signaling and evidence of integrin cross-talk.

Muscle cell survival depends upon the presence of various integrins with affinities for different extracellular matrix proteins. The absence of either alpha(5) or alpha(7) integrins leads to degenerative disorders of skeletal muscle, muscular dystrophies. To understand the cell survival signals that are mediated by integrin engagement with matrix proteins, we studied the early signaling events initiated by the attachment of muscle cells to fibronectin, an interaction that is mediated primarily by alpha(5) integrins. Cells that express alpha(5) integrin rapidly spread on fibronectin, and this process is associated with the phosphorylation of focal adhesion kinase (FAK). Cells deficient in alpha(5) integrin failed to spread or promote FAK phosphorylation when plated on fibronectin. For alpha(5)-expressing cells, both spreading and FAK phosphorylation could be blocked by inhibitors of protein kinase C (PKC), indicating that PKC is necessary for this "outside-in signaling" mediated by alpha(5) integrin. Surprisingly, activators of PKC could promote spreading and FAK phosphorylation in alpha(5)-deficient muscle cells plated on fibronectin. This PKC-induced cell spreading appeared to be due to activation of alpha(4) integrins ("inside-out signaling") since it could be blocked by peptides that specifically inhibit alpha(4) integrin binding to fibronectin. A model of integrin signaling in muscle cells is presented in which there is a positive feedback loop involving PKC in both outside-in and inside-out signaling, and the activation of this cycle is essential for cell spreading and downstream signaling to promote cell survival. In addition, the data indicate a cross-talk that occurs between integrins in which the outside-in signaling via one integrin can promote the activation of another integrin via inside-out signaling.

Animals↗
PubMed2000

Alpha(1)-proteinase inhibitor, alpha(1)-antichymotrypsin, or alpha(2)-macroglobulin is required for vascular smooth muscle cell spreading in three-dimensional fibrin gel.

It is assumed that vitronectin and other adhesion molecules induce cell spreading. We found that vascular smooth muscle cells require unidentified plasma components besides adhesion molecules to spread in fibrin gel, a likely provisional matrix at wound sites. By purification, the plasma components were found to be alpha(1)-proteinase inhibitor, alpha(1)-antichymotrypsin, and alpha(2)-macroglobulin. The chemically inactivated alpha(1)-proteinase inhibitor and alpha(2)-macroglobulin lose the spreading activity, indicating that these proteins function as proteinase inhibitors but not as adhesion molecules. Not only anti-integrin (alpha(v)beta(3) and alpha(5)beta(1)) antibodies but also anti-fibronectin antibodies inhibit the cell spreading. The spreading occurs without the addition of fibronectin and integrins, suggesting that cells produce these molecules. In the absence of the proteinase inhibitors, Western blot analysis shows that the fibronectin is degraded in fibrin gel, while it is intact in the presence of the inhibitors. Thus, the proteinase inhibitors prevent adhesion molecules such as fibronectin from being degraded by a cell-derived proteinase(s) and thus play a role in cell spreading.

Animals↗
PubMed2005

Interleukin-8 secretion by fibroblasts induced by low density lipoproteins is p38 MAPK-dependent and leads to cell spreading and wound closure.

We have previously reported (Dobreva, I., Waeber, G., Mooser, V., James, R. W., and Widmann, C. (2003) J. Lipid Res. 44, 2382-2390) that low density lipoproteins (LDLs) induce activation of the p38 MAPK pathway, resulting in fibroblast spreading and lamellipodia formation. Here, we show that LDL-stimulated fibroblast spreading and wound sealing are due to secretion of a soluble factor. Using an antibody-based human protein array, interleukin-8 (IL-8) was identified as the main cytokine whose concentration was increased in supernatants from LDL-stimulated cells. Incubation of supernatants from LDL-treated cells with an anti-IL-8 blocking antibody completely abolished their ability to induce cell spreading and mediate wound closure. In addition, fibroblasts treated with recombinant IL-8 spread to the same extent as cells incubated with LDL or supernatants from LDL-treated cells. The ability of LDL and IL-8 to induce fibroblast spreading was mediated by the IL-8 receptor type II (CXCR-2). Furthermore, LDL-induced IL-8 production and subsequent wound closure required the activation of the p38 MAPK pathway, because both processes were abrogated by a specific p38 inhibitor. Therefore, the capacity of LDLs to induce fibroblast spreading and accelerate wound closure relies on their ability to stimulate IL-8 secretion in a p38 MAPK-dependent manner. Regulation of fibroblast shape and migration by lipoproteins may be relevant to atherosclerosis that is characterized by increased LDL cholesterol levels, IL-8 production, and extensive remodeling of the vessel wall.

Atherosclerosis↗
PubMed1998

Recombinant TIMP-1 and -2 enhance the proliferation of rabbit corneal epithelial cells in vitro and the spreading of rabbit corneal epithelium in situ.

PURPOSE: The repair of the corneal epithelium is modulated by matrix metalloproteinases. The present study examined the effects of recombinant (r-) tissue inhibitors of metalloproteinases-1 and -2 (TIMP-1 and -2) on the proliferation of cultured epithelial cells from rabbit cornea, and on the spreading of a sheet of squamous epithelium of rabbit cornea placed in an organ culture system. METHODS: DNA synthesis of the cells, with or without r-TIMPs, was determined by an immunoassay for BrdU incorporation. Cell proliferation was assayed by measuring MTT mitochondrial activity. Epithelial spreading was evaluated by culturing small corneal blocks for 24 h in the presence or absence of each agent. Cryosections were prepared and the epithelial growth on the cut stromal surface was measured. RESULTS: Each agent, r-TIMP-1 (at 50 and 100 ng/ml) and r-TIMP-2 (at 50 ng/ml) significantly enhanced the DNA synthesis and MTT activity of the corneal epithelial cells in vitro. Relative to the untreated control cells, DNA synthesis was increased 2.4-fold by r-TIMP-1 and 2.3-fold by r-TIMP-2. r-TIMP-1 (at 100 and 200 ng/ml) and r-TIMP-2 (at 10 and 50 ng/ml) each significantly enhanced the spreading of the corneal epithelium. Relative to the untreated control tissue, spreading of the epithelial sheet was increased 1.7-fold by r-TIMP-1 and 1.4-fold by r-TIMP-2. Higher concentrations of r-TIMP-1 and r-TIMP-2 did not further enhance either the DNA synthesis of the cultured cells or the spreading of the epithelium. CONCLUSIONS: Exogenous TIMPs enhanced the spreading of the corneal epithelium and proliferation of cultured corneal epithelial cells. Findings suggest that endogenous TIMPs may influence the healing of corneal epithelium in vivo.

Animals↗
PubMed1998

Spreading of platelets: a morphological marker for platelet reactivity in peripheral arterial occlusive disease.

Platelet-surface contact is the first step in thrombus formation. Platelet spreading makes this initial contact irreversible. On the other hand plasma lipids and fibrinogen have been described to activate platelets or promote adhesion. We therefore investigated whether platelet spreading under stagnation-point flow conditions correlated with plasma concentrations of cardiovascular risk factors such as fibrinogen and high density lipoprotein (HDL)-cholesterol. Platelet rich plasma (PRP) from patients with peripheral arterial occlusive disease and healthy controls was examined by means of the Stagnation-Point Flow Adhesio- Aggregometer (SPAA). The SPAA comprises a microscopic setup with a flow chamber that permits direct observation and quantitation of platelet deposition onto standardized surfaces. After the flow experiments the deposited platelets were analyzed morphometrically for the degree of spreading expressed as inverse circularity (1/C). 1/C was correlated over 2 X 2 tables of fibrinogen combined with plasma levels of HDL-cholesterol, each of which was divided into a low and high value group. The patient and control group differed significantly with regard to 1/C, i.e. patient platelets demonstrated more adhesive platelets with a more extensive degree of spreading. 1/C was inversely correlated with HDL-cholesterol and showed significant differences between the patient and the control group. Increased 1/C values were found when associated with high fibrinogen levels and simultaneously with low HDL-cholesterol concentrations. Platelet spreading shows a correlation with increased levels of independent plasmatic risk factors for thrombosis in PAOD patients. Obtained during stagnation-point flow, spreading seems to be a morphological marker for platelet hyperreactivity.

Journal Article↗