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)

The primary migration of 15 and 22 cemented acetabular and femoral prosthetic components was recorded in 23 patients operated because of type I (minimal endosteal bone loss) and type II (thinning of bone, enlargement of femoral canal and acetabulum) mechanical loosening. Roentgen stereophotogrammetric analysis was used to measure the three-dimensional displacements of the center of the acetabulum and the femoral head. All but 1 of the acetabular and 1 of 15 revised femoral stem prostheses migrated within 2 years after the operation, whereas 5 of 7 revised femoral surface arthroplasties were stable. Femoral components with type II loosening migrated, on average, 1.5 mm (range, 0.6-3.0 mm) during the first postoperative year, compared with 0.7 mm (range, 0.3-1.1 mm) in patients with type I loosening (P less than .02). Increased bone loss of the acetabulum (type II), the quality of the bone-cement interface as judged from radiographs, and the presence of perforation of the femoral cortex did not significantly influence the rate of migration in this group. Compared with previously presented studies of cemented primary hip prostheses, cemented revisions seem not only to migrate more frequently but also at a higher rate. Poor primary fixation is probably one important cause of the high frequency of clinical failures in these patients.
J Arthroplasty 1990 Sep
PMID:Early loosening of revision hip arthroplasty. A roentgen stereophotogrammetric analysis. 223 Aug 18

An outbreak of congenital hydranencephaly and cerebellar hypoplasia occurred between November 1985 and May 1986 in Miyazaki, South Kyushu, Japan. Seventy-three calves had nervous signs of varying severity such as inability to stand, locomotor difficulties, defective vision and difficulty in sucking. At necropsy, 62 calves had macroscopic lesions in the central nervous system: hydranencephaly accompanied by cerebellar hypoplasia in 47; hydranencephaly alone in eight; and dilatation of the lateral ventricle in seven; none had arthrogryposis. Microscopically, all 62 cases involved various degrees of hypoplasia of neural components, such as total or partial thinning of the cerebral or cerebellar laminae. Heterotopia, such as abnormal islands of granule cells or Purkinje cells was also observed. Fourteen of these animals had other lesions such as non-purulent encephalitis, focal gliosis, neuronal degeneration, calcification or pseudocalcification, and cholesterol deposits, activation of vascular endothelial cells and haemorrhage. From the findings, these cases were considered to represent mainly hypoplasia of nerve tissue due to infection with a virus different from Akabane virus.
Res Vet Sci 1990 Sep
PMID:An outbreak of congenital hydranencephaly and cerebellar hypoplasia among calves in South Kyushu, Japan: a pathological study. 223 6

Magnetic resonance imaging (MRI) of the knee articular cartilage is possible owing to the contrast provided by different signal intensities of adjacent menisci and subchondral bone. The objective of this study was to determine the accuracy of MRI in quantitatively detecting thinning and focal defects of articular cartilage in vivo. High resolution MRI was performed followed by dissection of the knee within one hour of amputations above the knee of eight patients (62-89 years) with peripheral vascular disease. Articular cartilage was examined for erosions, surface irregularities, and appearance. Mean thicknesses of femoral and tibial articular cartilage sagittal sections from MRI were statistically indistinguishable from matched gross thicknesses. In those joints in which cartilage erosions, thinning, or irregularities were detected by MRI the same defects were apparent by gross examination. Cartilage that appeared normal by MRI had a normal gross appearance by gross examination. Thus high resolution MRI can accurately predict gross articular cartilage appearance and thickness, allowing an objective, quantitative, noninvasive assessment of eroded cartilage.
Ann Rheum Dis 1990 Sep
PMID:Articular cartilage defects of the knee: correlation between magnetic resonance imaging and gross pathology. 224 Dec 83

Clinical, roentgenographic and biologic features of etretinate bone toxicity in a 13-year-old girl with pachyonychia congenita syndrome are reported. Etretinate is a synthetic derivative of vitamin A that infrequently induces bone and joint abnormalities in children. The following manifestations can be observed: cortical hyperostosis, pain, calcification of tendons, thinning of long bones, demineralization, premature closure of epiphyses, or abnormal remodelling. Onset of these anomalies is often delayed since etretinate has a long half-life. Mechanisms are unknown. We advocate use of the minimum effective dosage and regular monitoring of patients.
Ann Pediatr (Paris) 1990 Sep
PMID:[Bone complications from chronic etretinate intoxication in children]. 225 41

Thirteen femora that were obtained at autopsy from patients in whom a cemented total hip replacement had been implanted from forty months to 17.5 years earlier were evaluated radiographically and morphologically. All of the patients had been functioning well, and only one of the prostheses showed radiographic evidence of loosening. Serial sections of the proximal portion of the femur that enclosed the femoral component of the prosthesis showed that the host bone was intimately and directly apposed to the cement, and fibrous tissue intervened only rarely. The bone-remodeling processes had created a dense shell of substantial new bone around the cement-mantle that resembled a new cortex, attached to the outer cortex by new trabecular struts. Evidence of ingrowth of bone from this dense shell of bone into the undulating surface of the cement was found in many areas. In the adjacent femoral cortex, there was substantial osteoporosis and cortical thinning. The cement-bone interface was intact and excellent throughout, despite the presence of fractures within the cement-mantle and de-bonding at the cement-prosthesis interface in some specimens. The cemented femoral components were well tolerated by the skeleton over a long period of use, and fibrous tissue had rarely formed at the femoral cement-bone interface of these well fixed and clinically successful prostheses. The cement-mantle was well supported by extensive medullary bone-remodeling and formation of a dense shell of new bone. The internal bone-remodeling helped to maintain the cemented femoral components over time and did not cause loosening of the prosthesis.
J Bone Joint Surg Am 1990 Sep
PMID:Histomorphological studies of the long-term skeletal responses to well fixed cemented femoral components. 239 93

To determine whether aneurysms form in experimental diet-induced atherosclerosis, we reviewed our experience with cynomolgus monkeys (n = 268) and rhesus monkeys (n = 175) fed an atherogenic diet for various lengths of time. Many animals in long-term experiments were fed "regression" diets and cholestyramine to lower cholesterol levels after lesions were established. No aneurysms were found in animals on normal diet. There were no aneurysms in 252 animals fed an atherogenic diet with or without regression for 12 months or less. However, aneurysms formed in 13% of cynomolgus monkeys (4 of 31) and 1% (1 of 107) rhesus monkeys on an atherogenic regimen for 16 to 24 months. Four of the five animals with aneurysms were on a regression diet and cholestyramine for 4 to 12 months. The fifth was fed the atherogenic diet for 20 months without subsequent regression. Aneurysms were prominent and involved the thoracic and abdominal aorta, innominate artery, carotid arteries, iliac and femoral arteries, and formed in areas most involved with plaque formation in both species. Histologic evidence was found of thinning of the media and atrophy with loss of normal architecture. The higher incidence of aneurysms in cynomolgus monkeys was associated with greater media destruction than was noted in the rhesus. These data support the thesis that aneurysm formation is a manifestation of atherosclerosis. In primate atherosclerosis, aneurysms form only after prolonged exposure to the atherogenic regimen, even in the presence of declining serum cholesterol levels. Matrix fibers in plaques may provide structural support to the aortic wall where there is underlying atrophy of the media. With time or declining serum cholesterol levels or both, plaques may atrophy leaving an aortic wall too thin to support increasing mural tension, leading to aneurysmal enlargement.
J Vasc Surg 1990 Sep
PMID:Aneurysm formation in experimental atherosclerosis: relationship to plaque evolution. 239 95

We report a 5-month-old Sudanese boy with a probable diagnosis of Congenital Nephrotic Syndrome. Our case had features which are neither typical of the Finnish type nor of other hereditary renal diseases. Histologically, the most striking changes were in the glomerular basement membranes which show patchy thinning, thick segments (with reduplication) and occasional low spikes. Tubules are well preserved, and no foam cells were seen. Electron microscopy showed extensive fusion of foot processes with podocyte microvilli. In parts the glomerular basement membrane shows irregular thickening and splitting, and incorporation of podocyte cytoplasm into the membrane. In other areas there is marked thinning of the basement membrane. Immunological features include a high level of IgA and IgG. To our knowledge such features have not been described before.
Ann Trop Paediatr 1987 Sep
PMID:Congenital nephrotic syndrome in Sudan: histological and immunological features. 244 74

Observations of vascularization of the retinal pigment epithelium (RPE) and formation of vitreo-retinal membranes (VRMs) in Royal College of Surgeons (RCS) rats with inherited retinal dystrophy suggest that vascular proliferation occurs in this model. To test this hypothesis, we studied the progression of vascular changes in RCS and age-matched control rats using quantitative light microscope morphometry and electron microscopy. At 2 weeks, prior to photoreceptor degeneration, the dystrophic retina is comparable with the control. By 2 months, extensive degeneration of photoreceptor cells results in significant thinning of the dystrophic retina as compared with the control. Signs of vascular degeneration are evident at the electron microscope level--"ghost" vessels consisting of acellular basal lamina surrounded by amorphous electron-dense material; degenerating endothelial cells and pericytes; and abnormal deposits of extracellular matrix (ECM) material around blood vessels. Vascular degeneration is accompanied by glial changes in the form of necrotic perivascular glial processes and abnormal ECM deposits among the altered Muller cell processes. At 2-4 months in the dystrophic retina, numbers of vessel profiles in dystrophic retinas are decreased as compared with controls. However, vascular degeneration is overshadowed by the formation of numerous capillary tufts within the RPE layer, which together with retinal thinning results in increased vessel density. Between 4-12 months, the retinal thickness diminishes further, vascularization of the RPE increases, vitreo-retinal membranes are formed, and vascular density increases. In summary, following an initial period of vascular degeneration, vascularization of the RPE is accompanied by an increase in retinal vessel density and by the formation of vitreo-retinal membranes.
Curr Eye Res 1989 Sep
PMID:Increased vascular density and vitreo-retinal membranes accompany vascularization of the pigment epithelium in the dystrophic rat retina. 247 96

To assess the possible role of restoring forces underlying left ventricular wall motion during rapid filling, the time relations between left ventricular dimensions and filling velocity were studied by digitised M-mode and Doppler echocardiography in 23 normal children and 43 patients: 11 with mild and 17 with severe mitral regurgitation, and 15 with left ventricular hypertrophy due to aortic stenosis. In normal children, peak mitral flow velocity characteristically lagged peak rate of dimension increase by 50 +/- 15 msec, and peak rate of posterior wall thinning by 35 +/- 15 msec, (P less than 0.01 for both). Towards the apex, and along the long axis of the ventricle, these phase differences between dimension and flow velocity were not apparent. The characteristic time relations between flow velocity and transverse dimension were also present in patients with left ventricular hypertrophy or mild mitral regurgitation, but when mitral regurgitation was severe they were lost and there was no significant difference in timing between peak flow velocity and peak rate of dimension change (-2 +/- 30 msec) or wall thinning (-4 +/- 25 msec). We conclude that phase differences between left ventricular wall motion and mitral inflow velocity are present in the normal ventricles of children. They cannot be explained on the basis of simple shape changes or passive filling of the relaxing ventricle, but strongly suggest the additional presence of ventricular restoring forces. They persist in patients with left ventricular hypertrophy or mild mitral regurgitation, but are lost when the regurgitation is severe, the filling pattern reverting to that predicted for passive distension of the ventricular cavity by a high left atrial pressure.
Int J Cardiol 1989 Sep
PMID:Phase differences between left ventricular wall motion and transmitral flow in man: evidence for involvement of ventricular restoring forces in normal rapid filling. 252 30

We performed computed tomography (CT) of the nose and paranasal sinuses in 21 patients with chromium induced septal perforation or thinning. Twenty patients showed various magnitudes of septal perforation. Twelve of 20 had perforation at the mid portion of the cartilaginous nasal septum. One patient had a sheet-like thinning of septal cartilage. Sixteen patients had mucosal thinning of the nasal conchas. In most cases, unilateral involvement of the inferior concha was seen. Eleven of 21 cases showed paranasal sinus mucosal thickening and one patient had a cyst or polyp in the sinus cavity. The main finding was nodular thickening of mucosa. Septal perforation by inhalation of chromic acid was located in the cartilaginous septum and there was no destruction of the bony septum and wall of the sinuses.
Yonsei Med J 1989 Sep
PMID:CT findings of the nose and paranasal sinuses in chromium intoxication. 258 68


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