Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the histologic and ultrastructural findings on two sisters with familial visceral myopathy who presented with acquired megacolon that necessitated subtotal colectomy. Both patients were mentally retarded and had repeated episodes of constipation and fecal impaction. Each presented near the age of 30 with massive dilatation of the colon and without clinical evidence of small intestinal involvement. Histologic abnormalities primarily involved smooth muscle and included marked nuclear enlargement and irregularity, interstitial fibrosis, and cytoplasmic vacuolation. These changes were most severe in the muscularis propria, but similar abnormalities were found in the muscularis mucosae and blood vessels. In the most advanced stages, collagen had completely replaced the muscularis propria, with extreme thinning of the intestinal wall. Abnormalities were noted in all segments of the colon and the appendix, but there was little correlation between severity of involvement and the segment examined. This study not only confirms the variable nature of morphologic changes in familial visceral myopathy, but also provides evidence of more extensive involvement of intestinal smooth muscle than has been previously reported.
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PMID:Familial visceral myopathy. Evidence of diffuse involvement of intestinal smooth muscle. 367 82

In order to elucidate mechanisms of contrast enhancement on computed tomography observed in non-glial tumors, tumors vessels were studied with conventional ultrathin section and freeze-fracture replica techniques. The materials were obtained from surgically removed specimens in 19 cases of tumors (6 of meningioma, 6 of hemangioblastoma, 5 of pituitary adenoma, and 2 of acoustic neurinoma). The following results were obtained. The common findings of these non-glial tumor vessels in ultrathin preparations were surface infoldings, increased pinocytotic vesticles and many fenestrations of endothelial cells, irregularity of basal laminae, and enlarged perivascular spaces. In freeze-fracture replicas of vascular endothelium, pinocytotic vesicles and fenestrations were 22 and 26 per micron2 on the average respectively. Tight junctions between endothelial cells were composed of one or two strands which appeared to be a discontinuous array of particles. As for the each non-glial tumor, menigiomas showed endothelial thickness and finger-like projections, variable lengths of tight junctions and marked enlargement of perivascular space which contained many collagen fibrils. Thinning of endothelium and many fenestrations were observed in hemangioblastomas, pituitary adenomas, and acoustic neurinomas. Fenestrations were most frequently observed in pituitary adenomas. The results indicate that extravasation of contrast material through fenestrations has an important role in marked contrast enhancement of non-glial tumors, in addition to the osmotic opening of tight junctions by contrast material. The irregular basal lamina and large perivascular space may also contribute to an increased extravasation of contrast material.
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PMID:[Ultrastructure of capillary permeability in human brain tumors. 3: Mechanisms of contrast enhancement in non-glial tumors]. 370 29

Temporal changes in infarct collagen and left ventricular topography during healing after myocardial infarction were studied in 132 dogs with coronary artery ligation: 8 sham dogs and 13 with no infarction (controls) and 111 with infarction (3 at 1 day, 54 at 2 days, 25 at 7 days, 3 at 2 weeks, 9 at 4 weeks and 17 at 6 weeks). Myocardial hydroxyproline (a marker of collagen) was measured by spectrophotometry and pathologic infarct size, arteriographic occluded bed size and topography by computerized planimetry of weighed left ventricular rings. Over 6 weeks, hydroxyproline was unchanged in normal regions (average 4.20 mg/g dry weight) but increased progressively between 7 days and 6 weeks (9.94 versus 55.55 mg/g, p less than 0.001) in infarct zones. Progressive infarct contraction occurred over 6 weeks, with infarct size at 6 weeks being 40% less than at 2 days (9.7 versus 16.3% of the left ventricle, p less than 0.001), although total infarct hydroxyproline was directly related to infarct size at each time period (r = 0.73 to 0.81, p less than or equal to 0.05). Significant (p less than or equal to 0.05) left ventricular topographic changes in infarct hearts compared with control hearts included: 1) increase in cavity area (5.0 versus 3.9 cm2), endocardial circumference (8.8 versus 7.4 cm) and expansion index (infarct/normal endocardial segment length, 1.21 versus 1.02) by 7 days; and 2) decrease in thinning ratio (infarct/normal wall thickness, 0.71 versus 0.98) by 6 weeks. Also, compared with 2 day infarcts, by 6 weeks infarct area was decreased (1.8 versus 3.4 cm2) and the noninfarcted segment length increased (6.9 versus 5.4 cm). Changes in hydroxyproline and topography were similar for anterior (n = 54) and posterior (n = 57) infarcts. Thus, healing in canine infarcts is associated with cavity dilation and infarct expansion within 7 days followed by infarct contraction and thinning by 6 weeks, whereas collagen increases between 7 days and 6 weeks. Collagen deposition in expanded and thinned infarct segments explains the permanent regional shape distortion associated with ventricular aneurysms.
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PMID:Healing after myocardial infarction in the dog: changes in infarct hydroxyproline and topography. 394 Dec 23

The healing phase of acute myocardial infarction (AMI) is initiated by proteolysis of necrotic myocardium, followed by infiltration of fibroblasts and deposition of collagen. To assess whether ibuprofen, a potent antiinflammatory agent, preserves existing collagen and enhances deposition of new collagen during infarct healing, biochemical and morphologic studies were made of experimentally induced myocardial infarcts in untreated rats and in rats treated with ibuprofen. All treated rats received 12.5 mg/kg of ibuprofen at 1, 6 and 18 hours after AMI. Group 1 rats underwent measurement of myocardial hydroxyproline (HP) content at 24 hours after AMI. Group 2 rats received ibuprofen, 12.5 mg/kg, twice a day for 2 additional days, with measurement of myocardial HP at 3 days (group 2a) or 21 days (group 2b) after AMI. Group 3 rats received ibuprofen, 12.5 mg/kg, twice a day for 6 additional days with measurement of HP content, or infarct size and degree of thinning at 21 days after AMI. Compared with untreated rats, ibuprofen-treated rats had significantly greater amounts of HP in the infarct at 24 hours (group 1, 8.9 +/- 2.2 nmol/mg dry weight vs untreated, 7.1 +/- 2.8 nmol/mg dry weight, p less than 0.04) and at 21 days (group 2b, 112 +/- 37 nmol/mg dry weight vs untreated, 91 +/- 39 nmol/mg dry weight, p less than 0.05, and group 3, 125 +/- 51 nmol/mg dry weight vs untreated, 91 +/- 39 nmol/mg dry weight, p less than 0.003). Substantial scar thinning was noted in all rats; no difference in scar thinning was noted between treated and untreated rats at 21 days after AMI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of ibuprofen on the healing phase of experimental myocardial infarction in the rat. 400 5

A moderately severe thermal injury of the central cornea of 48 Dutch-belted rabbit eyes was produced with a carbon (CO2) laser. The lesions were photographed with a slit lamp (SL) camera immediately following the injury and at 1, 2, 4, 7, 14, 21, 30 and 60 days after the exposure. Lesion size, opaqueness, and depth were graded clinically by SL biomicroscopy at the same intervals. No significant differences were found (p less than or equal to 0.05) between groups of eyes treated with flurbiprofen (0.03%), prednisolone acetate (1%), and vehicle control four-times-a-day for three weeks following injury. Additionally, eyes were studied histopathologically at 3 and 60 days following injury by light and transmission electron microscopy, and clinically at 30 and 60 days by endothelial specular microscopy. Important clinical and histopathological findings included coagulative necrosis of the corneal epithelium, epithelial sloughing, fusion of stromal collagen, stromal edema and inflammatory cell infiltration, stromal scar formation, corneal thinning, endothelial hyperplasia and metaplasia, fibrinous anterior chamber reaction with hypopyon, and retrocorneal fibrous membrane formation.
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PMID:Laser induced thermal injury of rabbit cornea and treatment with anti-inflammatory agents. 400 71

The literature contains conflicting reports about the potential value of the processed human umbilical vein graft as an arterial substitute. With a view to a better understanding of the ultimate fate of this device, a series of long-term implantation was undertaken with a nonhuman primate model. Dardik Biografts were implanted as an infrarenal aortic substitute in 13 monkeys. Nine were put to death following complications after post-operative periods ranging from 3 months to 3 years, while four animals remain alive. No calcification or lipid infiltration was found, presumably because the animals were healthy. The patency rate was poor because of complications associated with thrombotic deposits and thinning of the graft wall after implantation, which led to stenosis and fibrous hyperplasia along the anastomoses. The external polyester mesh was found to encourage external tissue proliferation, which could not prevent the graft from dilating since it contained neither elastin nor smooth muscle cells. Because the places where the graft had been damaged before or during processing were the sites of thrombotic accumulation and initial collagen degeneration, it is essential to use only defect-free material. As a consequence the long-term durability of this graft continues to be questioned.
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PMID:The fate of human umbilical vein grafts as an infrarenal aortic substitute in monkeys. 403 10

Kidneys from 7 mutant Southdown sheep with congenital hyperbilirubinemia, aged from 1 to 5 years were examined. Renal biopsies were taken from another mutant at 3 months and 12 months of age. At 3 months, lesions consisted of thin radial bands of myxomatous tissue in the medullary rays and atrophy of the adjacent collecting tubules. By 1 year collagen had replaced myxomatous tissue. Grossly, the kidneys were normal until 2 years when they became red and gray mottled and stained with bilirubin. The capsules stripped readily to reveal fine granular surfaces in sheep over 2 years of age. On the cut surface of the cortex were 0.5 mm wide radial gray streaks of fibrous tissue. Progressive fibrosis in sheep 2 to 5 years old resulted in a thinning of the cortex. With increasing fibrosis, the number of cystic tubules increased progressively. Protein casts and hyaline droplet degeneration were numerous in sheep over 2 years of age. Plasma cells and lymphocytes were frequently seen in the fibrous bands, and bile pigment was visible in the macrophages in the fibrous tissue and in the epithelium of the proximal tubule cells. Polyuria, low specific gravity urine and reduced effective renal plasma flow and glomerular filtration rates resulted from the replacement of specialized proximal tubule cells by low cuboidal cells, fibrous tissue separating the capillaries from the loops of Henle, destruction of glomeruli and segregation of glomeruli in fibrous bands. The kidney lesions may be determined by the same gene responsible for the hepatic excretion defect for bilirubin.
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PMID:Renal radial fibrosis in mutant Southdown sheep with congenital hyperbilirubinemia. 503 62

We evaluated the pathogenesis of skin thickening in three patients with acromegaly. Growth hormone levels were normal in one patient and were elevated in two patients. Skin biopsy specimens were obtained from the forearm. Hematoxylineosin staining showed slight epidermal thinning and, in two of the patients, a small increase in the number of fibroblasts. Selective stains for collagen, elastic, and reticular fibers disclosed normal connective tissue. The most striking abnormality was increased glycosaminoglycan deposition on the slides stained with colloidal iron. Glycosaminoglycan infiltration occurred mostly in the papillary and upper reticular dermis and was not directly related to the simultaneous growth hormone levels. Tissue digestion with specific enzymes identified hyaluronic acid, chondroitin-4- and 6-sulfate, and dermatan sulfate as the most prominent glycosaminoglycans in the dermis. The skin ultrastructure appeared to be preserved on electron microscopy. We conclude that cutaneous mucinoses is the main cause for the thickening of the skin in acromegaly.
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PMID:Histochemical characterization of the cutaneous involvement of acromegaly. 621 6

We have examined the collagens synthesized by cultures of normal human corneal stromal cells. Radioactively labeled products, accumulated in the culture medium during a 24-h labeling period, were treated with pepsin and analyzed by SDS-polyacrylamide gel electrophoresis. The cell layer collagen was characterized by 2.6 M and 4.4 M salt fractionation at neutral pH. CM-cellulose column chromatography, SDS-gel electrophoresis, and cyanogen bromide peptide mapping. Type I alpha 1 and alpha 2 chains were the predominant components in both the cell layer and the medium fractions of normal human stromal cultures; type III collagen was found mostly in the culture medium; and type V collagen was associated with the cell layer. Immunofluorescent techniques used to visualize collagen deposition in the cell layer confirmed the presence of these collagen types. Keratoconus is a disease characterized by thinning and scarring of the central cornea. Stromal cells grown from keratoconus corneas produced similar types of collagen (types I, III, and V) as normal human controls. Cells from keratoconus patients, however, contained more type V collagen in the cell layer than did normal cells. The difference was seen only in the 4.4 M salt precipitates. Since type V collagen is one component of cell surfaces, the primary defect in cultures from keratoconus corneas could involve cell membrane and cell surface components.
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PMID:Identification of collagens synthesized by cultures of normal human corneal and keratoconus stromal cells. 633 47

Highly purified antibodies to two ubiquitous components of basement membrane, type IV collagen and laminin, were applied to both fresh-frozen and formalin-fixed tissue sections of a variety of invasive carcinomas, carcinomas in situ, and their "look-alike" benign counterparts. These included lesions of the breast (infiltrating ductal carcinoma, comedocarcinoma, and sclerosing adenosis); lesions of the skin (squamous cell carcinoma, Bowen's disease, and pseudoepitheliomatous hyperplasia); lesions of the pancreas (adenocarcinoma and pancreatitis); lesions of the prostate (adenocarcinoma and benign prostatic hyperplasia); and other epithelial lesions of the invasive, in situ, and benign category. By both immunofluorescence and immunoperoxidase techniques, benign and in situ lesions showed intact basement membranes with linear staining of type IV collagen and laminin. The majority of invasive carcinomas, in contrast, lacked immunoreactivity for both of these basement membrane components. In cases of in situ carcinoma with microinvasion, there was thinning, fragmentation, and disruption of the basement membrane in the foci of microinvasion but not elsewhere. Utilizing antibodies to type IV collagen and laminin aids in both understanding the pathophysiology of the invasive process and the recognition of its presence in tissue sections.
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PMID:Loss of basement membrane components by invasive tumors but not by their benign counterparts. 634 6


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