27 research outputs found
P 155 Decreased central corneal sensitivity in the 50% galactose-FED rat model of diabetic ocular complications
Detector Description and Performance for the First Coincidence Observations between LIGO and GEO
For 17 days in August and September 2002, the LIGO and GEO interferometer
gravitational wave detectors were operated in coincidence to produce their
first data for scientific analysis. Although the detectors were still far from
their design sensitivity levels, the data can be used to place better upper
limits on the flux of gravitational waves incident on the earth than previous
direct measurements. This paper describes the instruments and the data in some
detail, as a companion to analysis papers based on the first data.Comment: 41 pages, 9 figures 17 Sept 03: author list amended, minor editorial
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Ablação ocular no camarão Macrobrachium rosenbergii (De Man) (Crustacea, Decapoda, Palaemonidae): efeitos sobre a reprodução, pigmentação epidérmica e atividade alimentar
Retinal Capillary Dilation: Early Diabetic-Like Retinopathy in the Galactose-Fed Rat Model
Diabetic-like loss of corneal sensitivity in the 50% galactose fed rat is ameliorated with topical administration of an aldose reductase inhibitor
Dose-Dependent Reduction of Retinal Vessel Changes Associated with Diabetic Retinopathy in Galactose-Fed Dogs by the Aldose Reductase Inhibitor M79175
Retinal Vascular Changes Induced by the Oxidative Stress of α-Tocopherol Deficiency Contrasted with Diabetic Microangiopathy
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Decreased DNA repair in familial Alzheimer's disease
Alterations in the capacity of a cell to repair DNA lesions play an important role in a number of human diseases. We and others have demonstrated defective DNA repair of alkylation damage in cells from patients with Alzheimer's disease. It has been hypothesized that this defect is related to the cause of Alzheimer's disease and results in the accumulation of lesions in the central nervous system neurons. One prediction of this hypothesis is that in dominantly inherited Alzheimer's disease, the repair defect will be present in half of the offspring of affected patients long before they develop symptoms of the disease. In order to test the hypothesis that decreased DNA repair is responsible for familial Alzheimer's disease and their at-risk offspring we have studied DNA repair in these individuals after exposure of lymphoblasts to alkylating agents. Our results indicate that cell lines from affected patients repair significantly less damage in 3 h than cell lines from healthy controls. A small number of at-risk individuals were also studied and some of these had lower levels of repair, although more cell lines from individuals in this group must be studied. These findings provide further support for defective DNA repair playing a role in the pathogenesis of Alzheimer's disease