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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study of immunofluorescence of unfractionated Type IV collagen, non-collagenous (NC-1) domain of Type IV collagen, basement membrane (GBM) component detected by Goodpasture's syndrome patient's serum and laminin (LN) in the glomeruli from 10 patients with IgA nephropathy was described. Type IV collagen, non-collagenous (NC-1) domain of Type IV collagen, GBM component or LN was observed linearly in the glomerular capillary walls in all patients with IgA nephropathy examined. The deposition of IgA, IgM or C3 was marked in the glomerular capillary walls in patients in the moderate or advanced stage of IgA nephropathy. However, the staining of Type IV collagen, GBM component or LN in such walls was not altered by the depositions of IgA, IgM and C3. In particular, a wrinkled pattern of NC-1 domain of Type IV or GBM component was detected in the glomerular capillary walls of totally sclerotic glomeruli in some patients with IgA nephropathy. It appears that the deposits of IgA and/or C3 did not influence the major components of glomerular capillary walls in patients with IgA nephropathy. It is concluded that the initiating factors of the collapse and/or sclerosis of glomerular capillary walls might be due to various factors other than the deposition of glomerular IgA-dominant immune-complexes in patients with IgA nephropathy.
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PMID:Immunofluorescent studies on IgA nephropathy: type IV collagen and glomerular basement membrane component detected by Goodpasture's syndrome serum and laminin. 307 23

The surgical repair of subglottic stenosis (SGS) is often unsuccessful because of recurrence of the scar contracture. Over the past few years, two lathyrogenic agents (compounds that inhibit collagen cross-linking) have been shown effective in prevention of stenosis in animal models that have deep caustic esophageal burns. Since the principles of induced lathyrism have not been applied to the treatment of laryngotracheal stenosis, a pilot study using a canine model was conducted to test the efficacy of penicillamine and N-acetyl-L-cysteine in reduction of the rate of reformation of SGS. In all six animals used, a complete, 10 to 15 mm thick, mature SGS was induced experimentally, then opened with a CO2 laser. The dogs that were treated with lathyrogenic agents exhibited a lower rate of re-stenosis (one maintained patency throughout the 5 weeks of treatment) when compared to the two control dogs. Histologic sections of the subglottis in each dog revealed severe cricoid collapse, necrosis, and scarring, and thus demonstrated similarities to SGS in human beings. The two lathyrogenic agents used in this study are already approved for human use and may represent a valuable form of adjunctive therapy in the surgical management of SGS.
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PMID:Lathyrogenic agents as therapy for subglottic stenosis--a pilot study. 312 Jan 20

The clinical feature of rheumatoid arthritis (RA) is characterized by systemic-immunological, local-inflammatory phenomena. But it is the joint destruction which gives RA its dramatic course. Through the years we evaluated joint tissues of app. 14,500 patients with defined RA and besides the conventional inflammatory processes we could prove a mechanism which is responsible for the joint destruction and which is typical for RA. Following an exudative episode, compact, homogeneous cell masses can occur in the synovial membrane which consist of macronuclear, immature, synoviogenous cells. These masses can encroach on the adjacent structures of articular cartilage and subchondral bone which consequently enzymatically will be degraded and destroyed. Since these rapidly growing cell masses are avascular in their aggressive stage, they soon will collapse. The surviving cells "modulate" to fibroblast which start collagen synthesis and thus form the well-known pannus. In the area of the compact, homogeneous cell masses of synovial origin, there are no lymphocytes and plasma cells nor PMN or macrophages. Macrophages only occur after the breakdown of the cell masses and the beginning of pannus formation, this also is the case with lymphocytes and plasma cells. Thus, the immature synoviogenous cell masses are in contrast to the initial synovitis not of inflammatory character. Their cytological and aggressive behavior rather shows oncological analogies. This also corresponds to our proof of the expression of myc and ras to a high degree in the aggressive cell masses in RA.
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PMID:Synovial processes in rheumatoid arthritis. 325 51

The herbicide paraquat induces irreversible progressive pulmonary fibrosis in human beings and animals. The mechanisms of the fibrosis are still unresolved. There is histological and ultrastructural evidence that an early destructive phase followed by a proliferative phase occurs in the lungs post paraquat-exposure. In this study, lungs obtained from a dog 7 days following intravenous administration of paraquat (12 mg paraquat dichloride per kg bodyweight) are compared with lungs obtained from a normal dog. Examination included gross post mortem inspection, histology, transmission electron microscopy (TEM) and scanning electron microscopy (SEM). Comparison of the TEM of the paraquat affected canine lung with the normal showed: alveolar collapse; detachment of alveolar epithelial cells from the basement membrane; alteration of the type II alveolar cell morphology; infiltration of granulocytes and erythrocytes into both the interstitium and alveolar air spaces; and fibroblasts associated with collagen fibrils. The SEM of the paraquat-exposed canine lung, reported here for the first time, demonstrated irregular, alveolar walls with type I alveolar epithelial cell detachment, and erythrocyte and alveolar macrophage infiltration. These findings suggest that the detachment of alveolar epithelial cells and the alveolar macrophage play a significant role in paraquat-induced pulmonary fibrosis.
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PMID:Ultrastructure of canine lung during the proliferative phase of paraquat toxicity. 334 60

A case of hip osteoarthrosis associated with ochronosis in a 65-year-old woman is reported. Characteristic features of both conditions were observed macroscopically and on light and electron microscopic examination. In the cartilage the pigment deposits were located on and between thick collagen fibrils. In the synovial membrane there were embedded packets of cartilage shards of which the collagen fibrils and pigment were phagocytosed, as well as calcified bone debris whose disaggregation might have explained the presence of some apatite deposits free of any underlying collagen structure. As also previously observed, the present case of ochronotic hip osteoarthrosis is remarkable for the minor osteophyte formation and for the inclusion of pigmented cartilage shards in the osteomedullar remodeled territory. It also demonstrates a collapse of the femoral head cortex presumably related to the rapid clinical and radiologic evolution. By the well-known origin of its chondropathy and by the pigment labeling of the cartilage, ochronotic arthropathy provides an almost experimental model for analyzing a broader problem, i.e., that of the various components of an osteoarthrotic remodeling.
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PMID:Rapidly progressive osteoarthrosis of ochronotic origin. A pathologic study. 338 49

In this paper we describe two simple experimental models of diffuse interstitial renal fibrosis in the rat. One develops 25 days after unilateral renal vein ligation, and the other 15 days after unilateral ureteral double ligation and section. In both models fibrosis is examined morphologically and biochemically, the latter with emphasis on collagen turnover. In addition to a description of the histology, also presented are quantitative biochemical data on four features of tissue collagen turnover, namely total content, concentration, biosynthesis, and degradation. Although the microscopic picture of both models can be adequately described as interstitial diffuse renal fibrosis, their mechanisms are different: unilateral renal vein ligation is an example of collapse fibrosis, whereas unilateral ureteral double ligation and section is a model of absolute fibrosis. In both models however, decreased collagen degradation is the significant metabolic abnormality.
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PMID:Experimental diffuse interstitial renal fibrosis. A biochemical approach. 340 76

Proliferative vitreoretinopathy (PVR) is the leading cause of failure of retinal detachment surgery. In this disorder, contractile cellular membranes form within the vitreous cavity. Retinal pigment epithelial (RPE) cells are an early and important component of these membranes. Contraction is mediated by cellular events and this contraction results in the formation of traction retinal detachments. Using the techniques of time-lapse cinemicrography, the authors studied the interaction of single RPE cells with individual strands of collagen. RPE cells pull the collagen fibers toward them using alternating extension and retraction of their lamellipodia. (The mechanism can be likened to sailors pulling in sheets of a sal in a hand-over-hand manner.) The collagen is not engulfed by the cell, but instead is piled up in a small bundle adjacent to the cell. Using this mechanism, each cell can reel in several times its length of collagen in 1 hour. In this manner, a small number of RPE cells may be able to collapse the vitreous gel and exert tractional forces.
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PMID:Proliferative vitreoretinopathy. The mechanism of development of vitreoretinal traction. 358 12

By using intranasal tissues for lining, employing cartilage battens to brace against contraction or collapse, designing axial skin flaps from exact three-dimensional patterns, using the topographic subunits of the nose as templates, and refining the result by subcutaneous sculpturing, a new nasal part that is nearly normal in appearance can be created in a few stages. It should be remembered that the restored part is not a nose, but merely a collage of forehead skin, cheek skin, mucosa, vestibular lining, nasal septum, and ear cartilage fragments all stuck together with collagen, as with glue. It is taken for a nose only because its contour, color, and texture are exact. The principles of aesthetic reconstruction are valid, and the results are consistent.
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PMID:Aesthetic restoration of the nose. 389 49

Seven cases in which interstitial fibrosis developed in patients who had acute interstitial pneumonia were studied ultrastructurally to elucidate the pathogenesis of the interstitial thickening seen by light microscopy. Interstitial fibrosis is generally thought to result from fibroblast proliferation and collagen deposition, and this mechanism was confirmed. However, two additional mechanisms that also contributed to the interstitial thickening were identified. One, which was not described previously, involves folding of portions of alveolar septa or collapse of entire alveoli and permanent apposition of their walls. This process occurred in areas that had been denuded of alveolar lining epithelium. Granular pneumocytes attempting to re-epithelialize the denuded basal lamina proliferated over the surface of apposed septa, thereby combining the folded or collapsed alveoli and forming a single thickened septum. The second mechanism involves incorporation of intra-alveolar exudates into alveolar septa. It occurred when granular pneumocytes re-epithelialized along the luminal surface of intra-alveolar debris overlying denuded alveolar epithelial basal laminae. The relative importance of each of these mechanisms in the pathogenesis of interstitial fibrosis and their role in the more common chronic interstitial pneumonias are unknown. However, their recognition may inspire new approaches for the prevention and treatment of interstitial fibrosis.
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PMID:Pathogenesis of "fibrosis" in interstitial pneumonia: an electron microscopic study. 404 50

To allow a more valid comparison between our previous ultrastructural data and the immunolocalization of type IX and other minor collagen species in cryosectioned cartilage, we examined both normal and testicular hyaluronidase-digested canine tibial cartilage by electron microscopy. Removal of matrix proteoglycans caused the pericellular capsule to collapse against the cell surface, suggesting that its normal anatomical position is mediated by pericellular matrix hydration. Detailed examination of the pericellular capsule and pericellular channel revealed fine, faintly banded fibrils and an amorphous component somewhat similar in structure to basement membrane collagens. Matrix vesicles and the electron-dense material of the interterritorial matrix were only partially digested by hyaluronidase. We propose that the pericellular capsule is composed of a "felt-like" network of minor collagen species which act synergistically to maintain both the composition of the pericellular matrix and the integrity of the chondrocyte/pericellular matrix complex during compressive loading.
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PMID:Morphology of the pericellular capsule in articular cartilage revealed by hyaluronidase digestion. 405 39


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