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Biomedical subjects

R C Tripathi

Publications and source records attributed to R C Tripathi.

At least 145 records · Page 8Linked to original sources
PubMed1979

Experimental retinal branch vein occlusion in rhesus monkeys. III. Histopathological and electron microscopical studies.

Experimental retinal vein occlusion in monkeys was followed by an immediate increase in capillary permeability which was accompanied by retinal oedema. This functional capillary change was followed at about 6 hours after occlusion by structural damage to the capillary wall. Thrombus formation occurred in the damaged vessels, and areas of stasis were thus produced with associated retinal haemorrhages. Finally, there was complete loss of the capillary endothelium and pericytes, and the acellular capillaries were invaded by proliferating glial cell processes, so producing permanent capillary closure.

Animals↗
PubMed1977

Corneal mucus plaques.

Corneal mucus plaques adhered to the anterior corneal surface in 17 of 67 advanced cases of keratoconjunctivitis sicca. The plaques were translucent to opaque and varied in size and shape, from multiple isolated islands to bizarre patterns involving more than half the corneal surface. Ultrastructurally, they consisted of mucus mixed with desquamated degenerating epithelial cells and proteinaceous and lipoidal material. The condition may be symptomatic but can be controlled and prevented in most cases by topical ocular application of 10% acetylcysteine.

Acetylcysteine↗
PubMed1976

Vitreous opacities in primary amyloid disease. A clinical, histochemical, and ultrastructural report.

Three patients who initially presented to the ophthalmologist with a history of gradual deterioration of visual acuity showed, on biomicroscopic examination, a linear meshwork of opacities in the vitreous attached to the posterior surface of the lens in the form of pseudopodia lentis. Amyloidosis of the vitreous associated with systemic amyloid disease was diagnosed because of the characteristic nature of the opacities. This was confirmed initially in two of the cases by light and electron microscopical examination of a biopsy of the clinically normal conjunctiva, subsequently by systemic investigations, and finally, by direct histochemical and elecron microscopical examination of the vitreous which became available after vitrectomy in all three cases. It was not possible to examine other members of the families. The relevant literature on vitreous amyloidosis is reviewed in relation to our own findings and the importance of a diagnostic conjunctival biopsy is emphasized. This paper is the first British report on primary vitreous amyloidosis. The pathogenesis of vitreous amyloid opacities is discussed in the light of current concepts of amyloidosis. Since the vitreous opacities due to amyloid deposits appear to be one of the manifestations of systemic amyloid disease, surgical removal of the opacities by vitrectomy may not produce longlasting results. Moveover, in contemplating surgical treatment the ophthalmologist should bear in mind the poor prognosis of systemic amyloidosis.

Adult↗
PubMed1976

Pigmented lens striae.

The clinical features of pigmented lens striae were studied biomicroscopically in seven patients. The lenses of three of these, obtained by cataract surgery, were examined by electron microscopy to determine the structure of the striae. We concluded that the striae are not formed by remnants of tunica vasculosa lentis, as earlier workers believed, but consist of fine fibrils of zonular bundles entrapping pigment granules of uveal origin.

Aged↗
PubMed1976

Anatomy of passive arthus reaction in the cornea. A preliminary communication.

Corneal changes in passive Arthus reaction are essentially the same as that reported to occur in active Arthus reaction and consist of accumulation of polymorphonuclear leucocytes around the deposits of immune complexes, release of lysosomes and fragmentation and dissolution of collagen fibrils. In addition, degenerative changes were found in the corneal endothelium and Descemet's membrane.

Animals↗
PubMed1976

Experimental retinal branch vein occlusion in the monkey. Histopathological and ultrastructural studies.

Light and electron microscopical studies of monkey retinae after experimental branch vein occlusion by argon laser reveal that the immediate reaction in the corresponding region is one of capillary engorgement and dilatation followed by oedema (intra- and extracellular), and plasma leakage as shown by intravenous injection of horseradish peroxidase. Vascular stasis is characterized by packing of erythrocytes in the capillary lumen, early thrombus formation, and focal haemorrhages. Progressive degenerative changes in the endothelium and pericytes are seen in specimens taken a few hours to a few days after occlusion; within 3 to 4 weeks many vessels in the occluded region are reduced to basement membrane "ghosts" and the lumen and the cellular lodges of some vessels are subsequently invaded by proliferating glia, thus producing permanent capillary closure.

Animals↗
PubMed1975

Secondary anterior crocodile shagreen of Vogt.

The clincopathological features and pathogenesis of secondary mosaic degeneration of the cornea (anterior crocodile shagreen of Vogt) are described. The structural basis for the normal anterior corneal mosaic pattern seems to lie in the particular arrangement of many prominent collagen lamellae of the anterior stroma that thake an oblique course to gain insertion into Bowman's layer. Since, at normal intraocular pressure, Bowman's layer is under tension, when viewed from the anterior surface the cornea appears smooth. By releasing the tension, however, a reproducible polygonal ridge pattern becomes manifest. It is suggested that a prolonged phthisical state of the eye is one condition wherein the mosaic pattern may become permanent and that, as a secondary event, this is followed by irregular calcification of Bowman's layer which particularly involves the ridges projecting into the epithelium. Biomicroscopically these ridges corresponded to the branching reticular arrangement of the mosaic opacities.

Aged↗
PubMed1975

Calcium deposition as a cause of spoilation of hydrophilic soft contact lenses.

A series of 75 spoilt soft lenses with opacities (mostly manifesting as discrete spots or as large areas of cloudiness, chalk-white in appearance) were subjected to histochemical, electron microscopical, electron probe x-ray microanalytical, x-ray diffraction, atomic absorption spectro-photometric, and biochemical analyses. The results showed that in many cases calcium was implicated in the deposit formation and that a broad correlation existed between the amount of calcium present and the degree of opacification. The possible mode of calcium deposition and resulting implications in lens intolerance are discussed. It is advocated that a search should be made for a modified or new soft lens material which does not permit calcium deposition, and that the medical practitioner should strive towards improved assessment of the systemic and ocular conditions which may help in identifying patients at risk of early lens failure.

Calcium↗