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)

Late-onset cerebellar degeneration can be induced transplacentally in mice by a single low-dose (1 mg/kg) injection of the direct-acting DNA alkylating agent N-methyl-N-nitrosourea (MNU) on day 16 of pregnancy. The offspring develop a mild ataxia that manifests by 12-16 weeks of age postnatally when the animals are challenged with a motor coordination task. Morphological evidence of degeneration includes pyknosis of Purkinje cells and abnormal foliation patterns. Additionally, these animals demonstrate a progressive retinopathy characterized by thinning of the nuclear and plexiform layers of the retina. Efforts to retard the cerebellar degeneration were undertaken in the present study. MNU-exposed and control animals were fed a standard mouse chow diet supplemented with 0.75% butylated hydroxytoluene (BHT), an antioxidant. This supplementation commenced 24 h following exposure to the teratogen and continued throughout the life of the offspring. A second group of MNU-exposed and control mice were fed a non-BHT-supplemented, standard Purina mouse chow diet. Quantitative histological evaluation of cerebellar coronal sections indicated that by 4 weeks of age BHT-fed, MNU-exposed mice had significantly fewer pyknotic Purkinje cells than non-BHT-fed, MNU-exposed animals. This was true for the vermal, paravermal, and lateral areas of the cerebellum. The findings suggest the usefulness of teratogenic models of degenerative diseases for the testing of potential intervention strategies.
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PMID:The antioxidant butylated hydroxytoluene can retard cerebellar degeneration induced transplacentally by a single low dosage of N-methyl-N-nitrosourea. 256 66

A rheological study was performed on blood samples from 10 insulin-treated diabetics with retinopathy. As part of their treatment, they all received 4 tablets of Daflon 500 mg per day for 30 days. Three complementary rheological criteria were used to characterize blood samples: 1) viscometry, using a Couette viscometer, which produces data on viscosity, shear-thinning, viscoelasticity and tixotropy of blood, 2) aggregametry, using an apparatus based on light reflectometry, using a filtrometer based on the deformations red cells undergo as they pass through narrow pores which produces information on red cell deformability. The main results were: a better red blood cell disaggregability, a decrease in red blood cell aggregation and no change in red blood cell deformability.
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PMID:Activity of Daflon 500 mg on the hemorheological disorders in diabetes. 263 48

The ocular and systemic findings in 112 Mayo Clinic patients with relapsing polychondritis were reviewed. The incidence of males and females was equal, with median age at diagnosis of 51 years and the median follow-up of 6 years. Most patients had several organ systems involved at the time of the diagnosis. Twenty-one patients had ocular symptoms at the onset, and 57 developed ocular symptoms during their course. Major ocular complications included proptosis, lid edema, episcleritis/scleritis, corneal infiltrates/thinning, iridocyclitis, retinopathy, and optic neuritis. The major system involvement included otorhinolaryngeal, respiratory, arthritic, renal, cardiovascular, dermatologic, and neurologic diseases. Generally, laboratory studies were not helpful in making the diagnosis but were valuable in monitoring the disease. Based on the experience in these cases, the indications for the various therapeutic modalities are offered.
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PMID:Ocular and systemic findings in relapsing polychondritis. 352 58

A female infant with brain and muscle abnormalities characteristic of Warburg syndrome had an atypical retinal dysplasia which appeared clinically as a 'leopard spot' retinopathy. The retinal histology is described in detail and is remarkable for periodic thinning of the inner nuclear layers and for isolated rosettes in the periphery. We believe 'leopard spot' retinopathy is yet another ocular manifestation of the Warburg syndrome.
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PMID:'Leopard spot' retinopathy in Warburg syndrome. 378 83

The clinical and pathological features of an early-onset autosomal dominant photoreceptor degeneration in the Abyssinian cat are described. Ophthalmoscopic evidence of retinal disease at 8-12 weeks of age was always preceded by marked dilatation of the pupils, impairment of the pupillary light reflex, and nystagmus. The electroretinogram was unrecordable in all but one of the affected individuals examined. Abnormal photoreceptor development was observed by both light and electron microscopy in retinas of a 22-day-old kitten; in this individual, no outer segment material was detected, and inner segments showed impaired development which was more severe towards the posterior pole. In a 40-day-old kitten, the inner segments were relatively well-formed, whereas the outer segments, though present, showed marked disorganization and degenerative change. The retinas of older individuals showed more advanced photoreceptor degeneration, with thinning of the neural retina. This early-onset retinopathy, which may be classified as a rod-cone dysplasia, is distinct from the hereditary retinal dystrophy (progressive retinal atrophy) previously described in this breed. The gene symbol Rdy has been adopted.
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PMID:An early-onset retinal dystrophy with dominant inheritance in the Abyssinian cat. Clinical and pathological findings. 380 43

Two patients (a 28-year-old woman and a 23-year-old man) with acute pancreatitis developed severe visual loss. The acute stage of retinopathy consisted of retinal edema, cotton-wool patches, and retinal hemorrhages, predominantly in the posterior pole of both eyes. During the five-year follow-up period, visual acuity improved and sequential fluorescein angiography of both patients demonstrated reperfusion of previously occluded retinal vessels. After resolution of the cotton-wool patches, the previously edematous areas were replaced by foci of retinal thinning which created irregularities in the internal limiting membrane light reflex. Visual fields demonstrated scotomas corresponding to the areas of the previous cotton-wool patches.
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PMID:Retinopathy associated with acute pancreatitis. 402 66

Six hundred and twenty-five patients with diabetes mellitus were studied by standardised clinical methods, resting and exercise electrocardiography (ECG) and digitised echocardiography to determine the prevalence of coronary and non-coronary heart disease. Clinical evidence of coronary artery disease (angina and infarction) was present in 110 (18 per cent) normotensive patients. Hypertension (blood pressure greater than 165/95 mmHg) was present in 172 (27 per cent) of whom 32 had cardiac symptoms. Heart failure or left ventricular dilatation was seen in 18 of whom 11 had either hypertension or coronary artery disease and six asymptomatic patients had unexplained ventricular hypertrophy. Echocardiograms in 245 of 290 asymptomatic patients with normal ECG showed that relaxation was prolonged (p less than 0.001) and mitral valve opening delayed (p less than 0.001) from normal especially in those with severe microangiopathy (proliferative retinopathy and/or heavy proteinuria). The peak rates of cavity dimension increase and posterior wall thinning were reduced from normal (both p less than 0.001) and patients with severe microangiopathy had the most marked changes. Redivision of these 245 diabetics by abnormalities of left ventricular function showed that 147 had normal function in whom only one of 23 (random 15 per cent sample) had a positive exercise ECG. Prolonged relaxation or delayed mitral valve opening alone (a nonspecific abnormality) was present in 41 and only three of 28 had a positive exercise ECG. Thirty-one had delayed mitral valve opening with inco-ordinate relaxation (abnormalities very suggestive of coronary artery disease) of whom 20 of 29 had a positive exercise ECG. Twenty-six had delayed mitral valve opening with slow cavity dimension increase or wall thinning (without hypertrophy) of whom 21 of 25 had a negative exercise ECG. This is a relatively specific abnormality similar to that found in left ventricular hypertrophy. Coronary artery disease is common in symptomatic and asymptomatic forms in diabetes mellitus. Non-coronary left ventricular diseases, such as dilation and hypertrophy, are probably no more common in diabetics than non-diabetics. A small number of diabetics with severe microangiopathy had abnormal relaxation and reduced peak rate of dimension increase or wall thinning which may represent left ventricular disease due to microangiopathy.
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PMID:A prospective study of heart disease in diabetes mellitus. 670 23

Male rats of the WBN/Kob strain, which are known to spontaneously develop diabetes with aging, were examined for histopathological changes in the retina. Five rats (10 eyes) each of WBN/Kob and Wistar/ST as a control were used, and the thickness of the retinal layers, both the central region and the peripheral region of the retina, were measured on weeks 1, 2, 3, 5, 9, 13, 17, 23, 27, 36, 45, 54, 67 and 80 after birth. The rod and cone cell layer in WBN/Kob rats was under-grown, and its thickness decreased 71.7% in the central zone and 59.3% in the peripheral zone of the retina compared with that of the control. In the central and peripheral retina, the rod and cone cell layer, outer nuclear layer and outer plexiform layer, as well as the inner plexiform layer in the central retina, gradually decreased in thickness from 5-45 weeks of age. In the central and peripheral parts of the retina, the number of nuclei decreased in accordance with the thinning of the nuclear layer. The thinned layers showed only cell loss. The rod and cone cell layer of the peripheral retina was thinner than that of the central retina. We obtained the following findings in the retina of male WBN/Kob rats. First, the rod and cone cell layer is undergrown compared with that of the control. Second, the first change occurred in the rod and cone cell layer. Third, the thinning of the rod and cone cell layer appeared at 5 weeks of age, and thinning with aging was slow. And finally, the thinning of the peripheral retina was more severe than that of the central retina. From the above findings, it seems that retinal changes in WBN/Kob rats are similar to the retinal degeneration of rds mice (retinal degeneration slow mice) and that WBN/Kob rats provide a useful animal model for human retinopathy.
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PMID:[Age-related changes in the retina of WBN/Kob rats--a pathological study]. 749 29

An epidemic of subacute bilateral visual failure has affected large numbers of teenagers and young adult Africans in coastal Tanzania since 1988. Previous work had indicated that many patients had sensory symptoms, but the nature of the neurological involvement was uncertain. The primary objective of this study was to characterize the accompanying neurological disorder. Furthermore, the nature of the visual loss was uncertain from previous reports as both retinopathy and optic neuropathy had been suggested. Full ophthalmic and neurological examinations were carried out at the Muhimbili University Hospital in Dar es Salaam. Nerve conduction studies, pattern electro-retinograms and cortical visually evoked responses and colour contrast sensitivity tests were carried out. Thirty eight young Africans and 12 controls were included in the study. The characteristic fundus picture was symmetrical temporal optic atrophy, and thinning of the caeco-central nerve fibre layer. Fluorescein angiography was normal. The electrophysiological and colour contrast sensitivity tests confirmed optic neuropathy in the majority of cases but primary retinal involvement was indicated in some. Neurological examination and nerve conduction measurements showed evidence of a peripheral neuropathy in 47% of the patients. The peripheral neuropathy is likely to have involved large fibres (from the nerve conduction studies) but the symptoms suggest small fibre loss also. 42% had developed hearing loss. Urinary thiocyanate levels were uniformly low. Serum was negative for antibodies to HTLV-1. DNA analysis from three cases was negative for three known mutations associated with Leber's hereditary optic atrophy (11778, 3460 and 14484). This entity, occurring predominantly in a young age group, does not correspond closely to other tropical neurological syndromes previously described from East Africa although it is clinically very similar to Strachan's syndrome (originally described in the Caribbean and more recently in prisoners of war) and also to an epidemic of optic and peripheral neuropathy that has recently occurred in Cuba. The aetiology has not yet been determined. A micronutrient deficiency is likely but has not been established.
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PMID:An epidemic of optic neuropathy in Tanzania: characterization of the visual disorder and associated peripheral neuropathy. 939 33

Cystoid macular edema (CME) is a classical complication of ocular inflammation. This syndrome was already described by Irvine in 1953 but the pathogenesis of this condition remains unclear. Cystoid macular edema can result either from a rupture of the inner or from the outer blood ocular barrier. Clinical CME that is responsible for a low visual acuity must be differentiated from angiographic CME that can be present even without any decrease in visual acuity. Fluid progressively accumulates into the outer plexiform layer of the retina and pools into cystic spaces. Fluid accumulation can now be better seen with optical coherence tomography (OCT). In chronic CME fluid accumulation is associated with thinning of the retina and fibrosis. At this stage irreversible lesions are present and CME does not respond to medical therapies. Inflammatory CME must be differentiated from CME resulting from irreversible vascular damage such as in diabetic CME or due to vein occlusions. Experimental research on cystoid macular edema has been hampered by the lack of animal model: most of laboratory animals have no macula, monkeys appear to be highly resistant to macular edema. Five major causes have been suspected to be at the origin of CME: (1) photic retinopathy, (2) trauma of ocular tissue, (3) secondary irritation of the ciliary body, (4) vitreous traction and (5) pharmaceutically induced CME. Clinical experience has shown that pseudophakic CME usually responds well to local therapy of steroids and non-steroidal antiinflammatory drugs (NSAIDs) and/or in association with systemic acetazolamide. Acetazolamide is increasing fluid resorption through the retinal pigment epithelium. Postoperative CME rarely needs additional posterior subtenon's injections to resolve. But in CME occurring secondary to uveitis additional posterior sub-Tenon's steroid injections or systemic steroids may be necessary to decrease the constant release of inflammatory mediators.
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PMID:The pathogenesis and clinical presentation of macular edema in inflammatory diseases. 1089 43


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