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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A collagen network, composed largely of type I and III fibrillar collagens, is found in the extracellular space of the myocardium. This network has multiple functions which includes a preservation of tissue architecture and chamber geometry. Given its tensile strength, collagen is a major determinant of tissue stiffness. Its disproportionate accumulation, in the form of either a reactive or a reparative fibrosis, further increases stiffness. A degradation of collagen tethers, on the other hand, is an anatomic requisite for a distortion in tissue architecture and a reduction in stiffness that can lead to chamber dilatation, wall thinning, and even rupture of the myocardium. Collagen turnover in the myocardium is dynamic. When synthesis exceeds degradation, an adverse accumulation of collagen appears to distort tissue structure. This is true for either the hypertrophied and/or nonhypertrophied ventricle. Factors that contribute to the appearance of myocardial fibrosis are largely different from those that promote cardiac myocyte growth. Included amongst these fibrogenic factors are effector hormones of the reinin-angiotensin-aldosterone system (RAAS). Studies conducted both in intact animals (relative to dietary sodium intake) and in cultured adult cardiac fibroblasts have pointed toward the association between collagen accumulation and chronic elevations in circulating angiotensin II and aldosterone. A tissue hormonal system involving angiotensin II, endothelins and bradykinin, may likewise regulate fibrogenesis. In this regard, angiotensin converting enzyme is found in connective tissue of the normal heart, including the matrix of heart valves and the adventitia of the intramural coronary arteries, and fibrous tissue that forms following infarction or with chronic RAAS activation. The importance of ACE in the regulation of local angiotensin II and bradykinin levels and their contribution to collagen turnover is a fruitful area of research with important clinical implications. The myocardium also contains a proteolytic system, including collagenase. The characteristics and regulation of matrix metalloproteinases and their tissue inhibitors in various cardiovascular disease states requires further investigation.
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PMID:Collagen network of the myocardium: function, structural remodeling and regulatory mechanisms. 802 11

In order to analyse the incorporation pattern of synthetic prosthesis made of Teflon and Dacron in the arterial system, 21 prostheses removed surgically and seven prostheses obtained from autopsies were examined; the duration of the implantation periods ranged from 30 min up to 10 years. Essentially the early phase of prosthetic incorporation (phase I) includes exudative inflammatory reactions as part of acute inflammatory processes. The degree of order within the tissue architecture and the mutual influence of matrix and cells in the reaction appeared to be slight. The cellular infiltrate found on the outer prosthetic surface is of local origin whereas the inner prosthetic lining contains cells of haematogenous origin. The organisation phase (phase II), which is comparable to the reparative-proliferative phase of an inflammatory reaction, showed activation of the reticulo-endothelial system together with the start of phagocytosis and a thinning of the prosthetic structures. Collagen type I and type III and fibronectin served both as a guidance and a growth tract for the cells during the cellular permeation of the prosthesis. Fibronectin and collagen type III have a special "catalytic" function. Collagen type I causes the firm anchoring of the vascular prosthesis in the periprosthetic tissue. The loss of stability of the prosthesis due to phagocytosis of fibres is balanced by the newly formed connective tissue within the wall of the vessel. The fibroblasts involved in the organisation must be derived from the flowing blood and from local mesenchymal cells. A chronic inflammatory reaction persisted during the late phase. In some cases increased proliferation of the inner mesenchymal lining of the prosthesis was observed together with regressive changes. The lack of a continuous surrounding stromal architecture on the luminal side of the vessel can be regarded as the main reason for this proliferation. Transformation of haematogenous cells into angioblasts or endothelial cells was not seen. Small endothelialised areas were only seen in the vicinity of anastomoses and following transprosthetic permeation by capillaries.
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PMID:The pathology of vascular grafts. 816 12

Light microscopy and electron microscopic examination were carried out on the corneal buttons of two patients who required penetrating keratoplasty for treatment of corneal complication following the intraocular injection of silicone oil to repair recurrent retinal detachments in aphakic eyes. Light microscopic examination demonstrated increased cellularity and irregularity of collagen fibers of stromal layer, defect of endothelial cell layer and endothelial degeneration. Electron microscopy examination demonstrated marked decrease in endothelial cell population density, accompanied by flattening and thinning of the remaining cells and attenuation of cell borders. There were silicone droplets in the endothelial cell layer and collagenous layer posterior to endothelial layer. These findings are well correlated to clinical manifestation and are thought to be rather due to barrier effect of silicone oil than direct toxicity.
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PMID:Silicone oil keratopathy. 818 37

We selected a subclone of HeLa-S3 cells to depict the relationship between cellular adherence to the extracellular matrix and pathological features of tumors derived from these cells. The selected subclone (PA cells) adheres poorly to type-IV collagen as compared to the wild type cells (EA cells) which attach easily to type-IV collagen. In vitro, it was confirmed that PA cells adhered poorly to type-IV collagen even after a long term of culture and showed weaker chemotactic activity toward this BM component. Injected into nude mice, PA cells formed smaller tumors than EA cells. Histologically, both derived tumors showed construction of basement membrane-like scaffolds that stained positively for type-IV collagen and laminin. EA cell tumors demonstrated frequent absence of and thinning and gaps in their basement membrane, which shows the invasive activity of the tumors. PA cell tumors showed a more regular basement membrane with predominant desmoplasia.
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PMID:[Correlation between adherence ability and construction of basement membrane-like scaffold of HeLa-S3 cells in nude mouse tumor]. 825 2

A patient with hollow visceral myopathy is reported in whom light microscopical studies of the small and large intestine showed typical features of degeneration, thinning, and fibrous replacement of smooth muscle of the gastrointestinal tract. Electron microscopy showed a striking increase in collagen with minimal fibroblast proliferation. Smooth muscle fibres had a range of ultrastructural abnormalities including myofilament disarray, electron lucency of the cytoplasm, and proliferation of the endoplasmic reticulum. Some fibres seemed to have typical ultrastructural characteristics of myofibroblasts, and others to be transition forms between typical smooth muscle cells and typical myofibroblasts. It seems likely that the fibrosis typical of this disorder has its origin in the transformation of smooth muscle fibres from a purely contractile to a myofibroblast collagen synthetic phenotype.
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PMID:Myofibroblasts in hollow visceral myopathy: the origin of gastrointestinal fibrosis? 834 91

Keratoconus, a bilateral corneal disease, is characterized by modifications in corneal shape and thinning of the stroma. It affects young people. From a biochemical point of view, a decrease in collagen content, probably due to the high collagenase activity, has been reported. In these experiments, we have studied the membrane receptors for interleukin 1 alpha, and the corresponding dissociation constant (KD). We also investigated synthesis of prostaglandin E2 (PGE2) and collagen, as well as kinetics of cyclooxygenase. Data from normal human corneas and from keratoconus were compared. Fibroblasts from keratoconus proved to bear four fold more IL1 binding sites than those from normal cornea, with similar KD. Both types of cells synthesize prostaglandin E2, even if IL1 is not added to the medium, but the keratoconus cells produce ten times more than the normal cornea cells. When the cells are stimulated with IL1, synthesis of PGE2 strongly increases and the amounts produced by keratoconus cells are always higher than those of the normal cornea cells. Kinetics of the cyclooxygenase show that Vmax. is 10 times higher in keratoconus than in normal cornea cells; Km's are the same. The amounts of collagen synthesized by keratoconus cells are slightly lower than those of normal cornea cells. Addition of IL1 to the cultures enhances synthesis of collagenase by the cells and decreases collagen found in the culture media. The drop of collagen is more important in keratoconus than in normal cornea cell cultures.
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PMID:Modification of prostaglandin E2 and collagen synthesis in keratoconus fibroblasts, associated with an increase of interleukin 1 alpha receptor number. 840 71

Osteogenesis imperfecta (OI) is a heritable disorder of connective tissue associated with fractures, osteopenia, and short stature. OI results from mutations affecting the pro alpha 1 or pro alpha 2 gene of type I collagen. We describe a strain of mice with a nonlethal recessively inherited mutation (oim) that results in phenotypic and biochemical features that simulate moderate to severe human OI. The phenotype of homozygous oim mice includes skeletal fractures, limb deformities, generalized osteopenia, and small body size. Their femurs are smaller and demonstrate marked cortical thinning and fewer medullary trabeculae than those of wild-type mice. Breeding studies show the mutation is inherited in most crosses as a single recessive gene on chromosome 6, near the murine Cola-2 gene. Biochemical analysis of skin and bone, as well as isolated dermal fibroblast cultures, demonstrate that alpha 1(I) homotrimeric collagen accumulates in these tissues and is secreted by fibroblasts. Short labeling studies in fibroblasts demonstrate an absence of pro alpha 2(I) collagen chains. Nucleotide sequencing of the cDNA encoding the COOH-propeptide reveals a G deletion at pro alpha 2(I) nucleotide 3983; this results in an alteration of the sequence of the last 48 amino acids. The oim mouse will facilitate the study of type I collagen-related skeletal disease.
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PMID:Defective pro alpha 2(I) collagen synthesis in a recessive mutation in mice: a model of human osteogenesis imperfecta. 844 83

Human type IV collagen discs were found to support proliferation and adhesion of rabbit corneal epithelial cells in tissue culture. To assess the biocompatibility of this synthetic collagen for epikeratoplasty, seven eyes of seven rhesus monkeys underwent epikeratoplasty with lenticules made of human type IV collagen. Eye rubbing by the animals expulsed two of the lenticules and caused failure of two to epithelialize completely. The remaining three lenticules epithelialized, remained clear, and caused no adverse effects on the eye. Two of these lenticules developed focal areas of subepithelial thinning 3 months postoperatively and the third lenticule has remained stable for 30 months. The presence of epithelial attachment components at the epithelial-lenticule interface was demonstrated by immunolocalization. Histopathologic and ultrastructural examination revealed focal areas of epithelial invasion and degradation of the lenticule. Neutral proteases were detected in the thinning region of one specimen. Human type IV collagen supports epithelialization in vivo and may have potential as a biomaterial for epikeratoplasty, but the stability of the material must be improved.
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PMID:Synthetic epikeratoplasty in rhesus monkeys with human type IV collagen. 845 30

A 14-year-old female with microscopic hematuria was admitted for a renal biopsy. She had a family history of renal disease without deafness. The findings of light microscopy and conventional immunofluorescence were normal. Electron microscopy showed a diffuse thinning of the glomerular basement membrane (GBM) with its mild splitting. Irregular thickening of GBM and glomerular small dense particles was not observed. Thin basement membrane syndrome was suspected from these findings. However, it was difficult to differentiate from Alport syndrome. Immunofluorescence analysis using the monoclonal antibody to the 28-kilodalton monomers of the noncollagenous domain of type IV collagen verified the diagnosis of heterozygous Alport syndrome.
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PMID:Alport syndrome diagnosed by immunofluorescence using a new monoclonal antibody. 849 40

Administration of hGH during the acute phase of experimental myocardial infarctions in pigs showed several aspects which clearly distinguished the treated group from the control one. In the first case the necrotic segment appeared considerably smaller than in the control group but also exhibit a qualitative different necrotic pattern in the histologic aspect, i.e. the infarcted area is shown itself reduced to isolated cells; scarce clusters of them interspersed where found within larger areas of preserved tissue. Affected cells have been defined as "injured fibres" according to their particular aspect which notably differs to the classic expected picture of a 25th day infarction and exhibits itself as an "arrested necrosis". A remarkable preservation of capillary vessels has also been found in the treated cases by a contrasting disappearance of the capillary bed in the control group. Ventricular contractility was also explored with ECHO B which showed significant differences between both groups: wall thinning of the ventricular wall in the affected area did not appear in treated cases and normal contractility in the same area reappeared a few hours after the infarction. Contractility was never restored in the control group. hGH main action is directed towards the preservation of the myocardial collagen matrix, helping to maintain the structural integrity of ventricular wall. There are, however, other possible effects on immunological aspects of the macrophages partially noticed, and to be disclosed in the future.
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PMID:[The reduction of the extension and severity of experimental myocardial infarct in pigs with growth hormone. The preservation of the microcirculation]. 850 20


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