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Biomedical subjects

R C Tripathi

Publications and source records attributed to R C Tripathi.

At least 109 records · Page 6Linked to original sources
PubMed1986

Congenital pupillary-iris-lens membrane with goniodysgenesis (a new entity).

We encountered two clinically similar but genetically unrelated cases of a disorder characterized by an unusual white pupillary-iris-lens membrane with extension to a prominent Schwalbe's line, the membranes were vascularized and their appearance changed over time. In both cases the abnormality was unilateral. Anomalous chamber angles were seen on gonioscopy. The clinical appearance is similar to a combination of iridogoniodysgenesis and pupillary membrane. However, our two cases are unique and fit into neither category. We postulate that this is a new entity consisting of an anomalous chamber angle and iris-lens membrane resulting from a localized iris (pupillary membrane), infarct with secondary neovascularization, during formation of the chamber angle.

Anterior Chamber↗
PubMed1985

Subjective past, present, and future fit: effects on anxiety depression, and other indicators of well-being.

Hypotheses were tested regarding the effects of subjective current, retrospected, and anticipated person-environment fit on affective and somatic strain and well-being. Two-hundred seven university students preparing for annual academic examinations at an Indian university completed self-administered questionnaires measuring parameters of the hypotheses. A distinction was made between cognitive (e.g., meeting demands for intelligence, good memory) and motivational (e.g., being able to muster the effort) fit. Cognitive poor fit had a greater effect on predicting high levels of strain across all time frames but did best in the past and current frames. Motivational poor fit had its greatest effect on strain when poor fit dealt with anticipated or current fit. These findings are discussed in terms of hypotheses, which suggest that the more subjectively uncontrollable a dimension of fit, the more salient it is in the past time frame, whereas the more subjectively controllable the dimension, the more salient it is in the future time frame.

Affect↗
PubMed1985

Species variations in distribution of S100 in retina. Demonstration with a monoclonal antibody and a polyclonal antiserum.

The S100 protein has been found consistently in glial cells both in the central nervous system (CNS) and peripheral nervous system (PNS). However, in the retina we find substantial species variation in the distribution of this protein. Immunohistochemically, in the human retina we do not find any S100. In the rabbit retina it is present both in Müller cells and in astrocytes and in the chicken retina it is in neurons. This demonstrates how misleading it can be to use the distribution of a protein in one species to generalize about the distribution of the same protein in other species. It is also clear that even though immunohistochemical staining for the S100 protein could be used to study pathologic conditions that involve Müller cells in guinea pigs, hamster, rat, and rabbit retina it is going to be of limited value in investigations of the same conditions in the human eye.

Animals↗
PubMed1984

Effect of epinephrine in vitro on the morphology, phagocytosis, and mitotic activity of human trabecular endothelium.

Epinephrine exerts a direct effect on cell morphology, phagocytosis and mitotic activity of human trabecular endothelium in primary culture. Its action is probably mediated through both beta and alpha adrenoceptors in a dose-time dependent manner. Younger cells and cells that were loosely attached to the substrate were found to be affected more rapidly and severely than were older cells and those in confluent regions where cell-to-cell attachment and stress fibers were well established. Continuous exposure to epinephrine at a concentration of 10(-5) M led to cessation of the normal cytokinetic cell movements, inhibition of mitotic and phagocytic activity, marked cell retraction, separation from the substrate, and, by 4-5 days, degeneration of cells. Similar, but less marked changes were seen with a concentration of 10(-6) M, the cell degeneration becoming apparent after one week of exposure. A still weaker concentration of epinephrine, 10(-7) M, did not result in cell degeneration even after 10 days of exposure and observation. On complete withdrawal of the drug, the cellular effects were reversible even after 3 days' exposure to 10(-5) M and 5-7 days' exposure to 10(-6) M epinephrine. The action of epinephrine was partially blocked by pretreatment of cultured trabecular cells with the beta-blocker, timolol. Available evidence suggests that the mechanism of action of epinephrine is mediated through both beta and alpha adrenoceptors, and that it intimately involves the cytoskeletal system of the cells. Extrapolation of our findings in vitro suggests that use of maximal doses of epinephrine over a prolonged time may contribute to tissue damage in certain conditions of glaucoma.

Adolescent↗
PubMed1984

Distribution of S-100 protein and glial fibrillary acidic protein in normal and gliotic human retina.

Monoclonal antibodies and polyclonal antisera were used to examine the distribution of S-100 protein in human retinas both immunohistochemically and immunochemically and to compare it to that of glial fibrillary acidic protein (GFAP). S-100 was not found in normal retinas nor in retinas with areas of reactive gliosis. GFAP was found in perikarya and processes of cells the nuclei of which were in the nerve fiber layer of normal retina. In areas of reactive gliosis there was intense staining with antiserum against GFAP extending from the internal limiting membrane to the external limiting membrane. Some of the glial cells in human retina and fibrillary astrocytes in the brain are identical in their expression of GFAP. However, absence of S-100 from both quiescent and reactive retinoglia distinguishes them from astrocytes in brain and spinal cord.

Adolescent↗
PubMed1984

Glaucoma in Sturge-Weber syndrome.

Trabeculectomy specimens from three eyes with Sturge-Weber syndrome were examined histopathologically. Changes in the trabecular meshwork-Schlemm's canal system were similar to findings in old age and in primary open-angle glaucoma. Two mechanisms for glaucoma are theorized. In cases with buphthalmos and congenital glaucoma, the chamber angle is often anomalous, as in other types of congenital glaucoma. In later onset juvenile cases, the chamber angle more often appears normal. A premature aging of the trabecular meshwork Schlemm's canal complex, as shown by us histopathologically, is a primary cause of juvenile glaucoma. It is suggested that both mechanisms relate to the abnormal hemodynamics of episclera and chamber angle, due to persistence of Streeter's primordial vascular plexus.

Angiomatosis↗
PubMed1984

Cellular and subcellular events in retinopathy of oxygen toxicity with a preliminary report on the preventive role of vitamin E and gamma-aminobutyric acid: a study in vitro.

Using freshly excised, pure, immature retinal vascular explants from neonatal rabbits as well as vascular cells harvested from such explants in a tissue culture environment, we established the direct cytocidal effect of hyperoxia on the vascular cells. One hundred percent oxygen at one atmosphere induced a marked cellular retraction after 4 to 6 hours of exposure and caused progressive increase in the number and size of lysosomal bodies and autophagic vacuoles. Between 12 to 18 hours, the Golgi apparatus enlarged and focal cytoplasmic degeneration ensued; the various changes in the endoplasmic reticulum, mitochondria, and nucleus became apparent between 18 to 24 hours. After 36 to 48 hours continuous exposure to hyperoxia, the cellular degradation with nuclear pyknosis led to granular and membranous debris. In contrast, the macrophages in the same culture were more resistant to the effect of hyperoxia. Our findings suggest multiple loci for oxygen toxicity in immature retinal vessels and cultured vascular cells. We believe that the cellular retraction is mediated through the prostanoid cascade. The initial event in cytotoxicity of hyperoxia is probably membrane injury, especially of the lysosomal system. The generation of the hydroxyl free radical invokes specific injury to the lysosomes; severe cellular damage occurs due to increased autophagocytosis, probably compounded upon by the inhibition of membrane pumps in the cell and the resulting intracellular acidosis. Injury to cell organelles such as mitochondria, endoplasmic reticulum, and nucleus which occurs at later stages and contributes to the final cell degeneration, may be partly related to the hyperoxic insult. The addition of vitamin E or gamma-aminobutryic acid to the culture medium partially retarded the hyperoxic injury to the vascular cells. In short term experiments, no significant damage occurred with exposure to 30% oxygen. The fact that immature, and not the mature, retinal vascular cells are rapidly and adversely affected by hyperoxia probably entails that the former are deficient in free radical scavenging enzymes but a protective mechanism against oxygen toxicity is acquired with the developmental maturity of these cells.

Animals↗
PubMed1983

Mucolipidosis I.

A case of mucolipidosis I had clinical and histopathologic features that were a combination of changes found in both mucopolysaccharidoses and sphingolipidoses. Corneal clouding, spokelike cataracts, tortuous conjunctival and retinal vessels, and strabismus were clinical findings. Histopathologically, there were inclusion vacuoles similar to those seen in mucopolysaccharidoses; lamellar bodies typical of sphingolipidoses were rare. These vacuoles were seen in conjunctival and corneal epithelium and fibrocytes, conjunctival and retinal vessel endothelium, and all retinal cell layers.

Conjunctiva↗
PubMed1983

Lens morphology, aging, and cataract.

The human lens is a uniquely transparent, biconvex, avascular structure responsible for focussing the image onto the retina. It is enclosed by a thick capsular basement membrane. The accommodative process in the lens is dependent upon the inherent elasticity of the lens capsule and the contractile property of the lens cells or fibers. In contrast to the ocular dimensions, the lens shows marked changes in size and weight with aging. Impairment in lens transparency and significant morphologic changes in the nucleus, cortex, and capsule occur with aging process. The optical zones of discontinuities of the lens result from light scatter through the various parts of the lens and are of great clinical significance in the assessment of cataract. The lens preserves its entire population of cells from fetal life until death and provides an excellent model for defining aging parameters of other ectodermally derived structures.

Adult↗
PubMed1982

Corneal keloid in Lowe's syndrome.

Bilateral corneal keloids in a boy wih Lowe's syndrome were examined by conventional light and electron microscopy. There were no signs of perforating corneal trauma or iridocorneal incarceration in either eye. The corneal keloids consisted of haphazardly arranged bundles of collagen fibers, fibroblasts, and fenestrated blood vessels. The anterior region of the keloids showed signs of active progression and epithelial epidermalization. The etiology of keloids in Lowe's syndrome remains obscure. Considerations include excessive local delivery of amino acids and unknown noxious substances through the leak corneal vessels, seepage of similar substances across the defective blood-aqueous barrier and the decompensated endothelium, repeated external trauma with associated inflammation, phenytoin (Dilantin) therapy, and congenital predisposition. No data are available on the management of the progressive course of corneal keloids. Possible empirical regimens include local excision, pressure therapy, topical corticosteroids, and cromolyn sodium.

Child↗
PubMed1982

Human retinal vessels in tissue culture. A preliminary report of the effect of acute glucose poisoning on cultured vascular cells.

To delineate the factors involved in the pathogenesis of human retinal vasculopathies, as in vitro model of human retinal vascular cells was developed by using cadaver eyes enucleated four to eight hours after death and stored at +4 C for three to seven days. A pure, viable capillary explant was obtained by microdissection and gentle agitation; the more rapidly occurring postmortem changes in the surrounding nervous tissue of the retina facilitated separation of the vascular explants. Factor VIII indirect immunofluorescent staining revealed that 85% to 90% of the cells harvested from capillaries of 3- to 5-day-old cadaver eyes and all cells cultured from 1-week-old postmortem eyes reacted positively, indicating their endothelial nature. High-glucose medium caused degenerative changes in the cells of the initial explant as well as in the cells of confluent cultures within 24 to 72 hours. The cytotoxic effect of glucose was manifested by accumulation of PAS-positive granules, cytoplasmic vacuolation, and eventual cell degeneration.

Cells, Cultured↗
PubMed1982

In vivo specular microscopy of edematous human corneal epithelium with light and scanning electron microscopic correlation.

A wide-field contact specular microscope was used to examine and to photograph the corneal epithelium in 35 eyes with chronic corneal edema. Seven of the patients subsequently underwent corneal transplantation allowing for correlation of the in vivo findings with the light and electron microscopic appearance. The early findings on specular microscopy included loss of the clear superficial epithelial cell outlines with easy dislodgement of these cells and a fine pattern of edema outlining basal cells. Individual cellular edema and fluid-filled cysts occurring at various epithelial layers and subepithelially appeared with worsening swelling. Subepithelial connective tissue and anamalous basement membrane were present at later stages.

Cornea↗
PubMed1982

The differential diagnosis of Descemet's tears (Haab's striae) and posterior polymorpous dystrophy bands. A clinicopathologic study.

Band-like structures, clinically similar to Haab's striae, occur in posterior polymorphous dystrophy (PPMD) and are often confused with them. The difference in clinical appearance based on difference in histopathology allows a clear differentiation. The edge of Haab's striae are thickened, curled, and secondarily proliferate Descemet's membrane, while the area between the edge is thin and smooth. Posterior polymorphous dystrophy bands are the exact opposite. The band is a thickening of Descemet's membrane between the edges with thinner, more normal Descemet's membrane outside of them. PPMD bands may be associated with typical vesicles or appear as the only sign of dystrophy, even in the eyes of patients with a known family history.

Adolescent↗
PubMed1982

Lowe's syndrome.

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Child↗
PubMed1982

Mucolipidosis I.

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Cataract↗