cyclic guanosine 3 5 monophosphate/atrophy

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Emergence of cyclic guanosine 3':5'-monophosphate-dependent protein kinase immunoreactivity in developing rhesus monkey cerebellum: correlative immunocytochemical and electron microscopic analysis.

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The appearance of cyclic guanosine 3':5'-monophosphate-dependent protein kinase (cGK), an enzyme that may be involved in the regulation of various aspects of neuronal function and that is highly concentrated in cerebellar Purkinje cells, was studied in the developing and adult monkey cerebellum by

Elevation of cGMP with normal expression and activity of rod cGMP-PDE in photoreceptor degenerate labrador retrievers.

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Cyclic guanosine 3',5'-monophosphate (cGMP) levels were determined in retinas from a strain of Labrador Retrievers with inherited retinal dystrophy manifesting at early stages of retinal differentiation. The cGMP contents of dystrophic retinas of dogs from 1 to 4 months of age (n = 7) were

Detection of cGMP in the degenerating retina.

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Cyclic guanosine 3'-5'-monophosphate (cGMP) plays a key role in the physiological process of light detection in photoreceptor cells of the retina. However, there is also growing evidence that cGMP may be critically involved in some pathophysiological processes of the retina since degenerating

Retinal degeneration in mice lacking the gamma subunit of the rod cGMP phosphodiesterase.

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The retinal cyclic guanosine 3',5'-monophosphate (cGMP) phosphodiesterase (PDE) is a key regulator of phototransduction in the vertebrate visual system. PDE consists of a catalytic core of alpha and beta subunits associated with two inhibitory gamma subunits. A gene-targeting approach was used to

Combination of cGMP analogue and drug delivery system provides functional protection in hereditary retinal degeneration.

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Inherited retinal degeneration (RD) is a devastating and currently untreatable neurodegenerative condition that leads to loss of photoreceptor cells and blindness. The vast genetic heterogeneity of RD, the lack of "druggable" targets, and the access-limiting blood-retinal barrier (BRB) present major

C-Type Natriuretic Peptide Ameliorates Lipopolysaccharide-Induced Cardiac Dysfunction in Rats with Pulmonary Arterial Hypertension.

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Lipopolysaccharide induces rapid deterioration of cardiac function in rats with pulmonary arterial hypertension. It was desired to investigate if this cardiac dysfunction could be treated by C-type natriuretic peptide. Rat pulmonary arterial hypertension was induced by intraperitoneal injection of

Retinal remodeling.

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Retinal photoreceptor degeneration takes many forms. Mutations in rhodopsin genes or disorders of the retinal pigment epithelium, defects in the adenosine triphosphate binding cassette transporter, ABCR gene defects, receptor tyrosine kinase defects, ciliopathies and transport defects, defects in

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