Networks Modulating the Retinal Response to Injury: Insights from Microarrays, Expression Genetics, and Bioinformatics

Abstract. We studied 45 IDDM without c-peptide response, duration 7-22 years, without proliferative retinopathy. After 2 months run-in period, they were randomly assigned to: (P) 15 received CSII: (C) 15 received muliple s.c. injections via butterfly 5-6x daily;: (M) 15 received twice daily mixed rapid and long acting insulin. All groups improved blood glucose control in the run-in period (p<0.0001). After change of treatment (P) and (M) improved further (p<0.01) but (C) was unchanged. GFR was supranormal and decreased in (P) and (M). No regression of retinopathy was shown in any group. One in (P) had transient florid pre-proliferative retinopathy which regressed spontaneously without laser treatment. We conclude that retinal response to strict control is complex. A transient deterioration may been seen.

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An electrically evoked slow potential of the frog's retina. II. Identification with PII component of electroretinogram

Journal of Neurophysiology ◽

10.1152/jn.1975.38.1.198 ◽

1975 ◽

Vol 38 (1) ◽

pp. 198-209 ◽

Cited By ~ 18

Author(s):

R. W. Knighton

Keyword(s):

Electrical Current ◽

Photoreceptor Cells ◽

Slow Potential ◽

Synaptic Terminals ◽

Electrical Stimuli ◽

Retinal Response

1. To show conclusively that the electrically evoked retinal response (EERG) is in fact an electrically evoked component of the usual ERG, it is necessary to show that the two responses have the same intraretinal pattern of current generators. A method for determining when two responses have the same origin has been developed. This method utilizes measurements from a single microelectrode penetrating the retina. 2. The method was sensitive enough to detect differences in the origins of two responses when they were present. 3. The EERG had the same intraretinal origin as the PII component of the ERG, and thus is the PII component evoked by electricity rather than by light. 4. The hypothesis that electrical stimuli act on the synaptic terminals of the photoreceptor cells predicts that electrical current will evoke components of the ERG. The fact that the EERG is an electrically evoked component of the ERG fulfills that prediction.

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Review of Current Theories for Abdominal Aortic Aneurysm Pathogenesis

Vascular ◽

10.2310/6670.2009.00046 ◽

2009 ◽

Vol 17 (5) ◽

pp. 253-263 ◽

Cited By ~ 62

Author(s):

Ian M. Nordon ◽

Robert J. Hinchliffe ◽

Peter J. Holt ◽

Ian M. Loftus ◽

Matthew M. Thompson

Keyword(s):

Abdominal Aortic Aneurysm ◽

Aortic Aneurysm ◽

Systemic Disease ◽

Aortic Aneurysms ◽

Atherosclerotic Plaques ◽

Search Terms ◽

Abdominal Aortic ◽

Expression Genetics ◽

Shared Risk ◽

Similar Risk

Atherosclerotic plaques are a feature of abdominal aortic aneurysms (AAAs). Atherosclerosis and AAA appear to share similar risk factors. These observations have led to the conclusion that AAAs are a consequence of advanced atherosclerosis. This review explores current theories regarding the pathogenesis of AAA and their implications for treatment. A systematic literature search was conducted using the search terms abdominal aortic aneurysm, atherosclerosis, pathogenesis, and systemic disease. Articles were categorized according to the association of AAAs with atherosclerosis, arteriomegaly, peripheral aneurysm, systemic expression, genetics, autoimmunity, oxidative stress, and systemic disease. Twenty-nine articles reporting changes in the systemic vasculature associated with AAA and 12 articles examining the shared risk factor hypothesis were identified. There is insufficient evidence to confirm that AAAs are the result of advanced atherosclerosis. The bulk of evidence points to AAA disease being a systemic disease of the vasculature, with a predetermined genetic susceptibility leading to a phenotype governed by environmental factors.

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