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Biomedical subjects

M O Tso

Publications and source records attributed to M O Tso.

At least 145 records · Page 8Linked to original sources
PubMed1984

Distribution of ascorbate in normal primate retina and after photic injury: a biochemical, morphological correlated study.

The levels of reduced and oxidized ascorbates were determined in the normal baboon neural retina and pigment epithelium-choroid. The ascorbate in the neural retina was mainly in the reduced form, while in the pigment epithelium, it existed primarily in the oxidized form. One eye of each of six baboons was exposed to indirect ophthalmoscope light for 30 minutes. Morphologic study showed necrotic photoreceptors, outer segment disorganization, and abnormal pigment epithelial basal infoldings and swollen microvilli. After the light exposure, the values of the reduced ascorbate decreased in both the neural retina and pigment epithelium-choroid of the posterior pole. The possible role of ascorbate as an antioxidant and ascorbate transport into the retina are discussed.

Animals↗
PubMed1984

Pathologic studies of the blood--retinal barrier in the spontaneously diabetic BB rat.

The BB rat spontaneously develops a diabetic state that closely resembles human type I diabetes. The authors studied the pathologic changes of the retina and retinal pigment epithelium of four normal and nine diabetic BB rats using (1) light and electron microscopy with the horseradish peroxidase tracer technique, and (2) trypsin digest preparations of the retinal vessels. They observed a retinal pigment epitheliopathy characterized by (1) derangement of the plasmalemma infoldings; (2) patchy organelle degeneration leading to focal necrosis; (3) increased permeability to horseradish peroxidase; and (4) repair of the pigment epithelium. Focal thickening of the retinal vascular basement membrane was seen occasionally, but the trypsin digest preparations were unremarkable. These studies suggest that diabetic retinal pigment epitheliopathy may be one of the early changes of diabetic retinopathy and may provide a pathogenetic mechanism for early disruption of the blood-retinal barrier.

Animals↗
PubMed1983

Heredofamilial retinal dystrophy in Guinea baboons. I. A histopathologic study.

We performed a histopathologic study of a heredofamilial retinal dystrophy in a colony of Guinea baboons. A bull's-eye appearance was noted in the maculas of six baboons of three generations. Histologic examination of 13 eyes from this colony showed primary degeneration of both rod and cone cells initially in the parafoveal region, which subsequently involved the photoreceptor cells of the equator and periphery of the retina. The retinal pigment epithelium and choriocapillaris showed mild changes in the early stages. This disease in baboons was compared with various human retinomaculopathies.

Animals↗
PubMed1983

Heredofamilial retinal dystrophy in Guinea baboons. II. Electron microscopic observations.

Electron microscopic study of an inherited retinal degeneration in Guinea baboons disclosed primary pathologic alterations in photoreceptor cells. These changes were first seen in the perifoveal region. Cell death occurred in two forms: hydropic degeneration and densification and/or necrosis. The hydropic type was mainly associated with cone cells, whereas densification and/or necrosis was largely seen in rod cells. Lamellar bodies and granular membrane-bound inclusions were noted in the inner segments and soma. Mitochondria were vacuolated and formed membranous whorls. Bundles of filaments were arranged in parallel array in the soma synaptic endings. Clusters of tubules were present in the synaptic terminals. Preliminary biochemical studies on these animals have yielded no clues to the pathogenesis of the retinopathy.

Animals↗
PubMed1983

Patterns of the choriocapillaris. A method to study the choroidal vasculature of the enucleated human eye.

We examined the architecture of the choriocapillaris in enucleated human eyes by flat preparation using trypsin digestion and corrosion cast technique by injecting methacrylate into the vortex vein. The choriocapillaris in the posterior fundus had a distinct lobular pattern of about 600 mu in diameter. An arteriole entered the lobule at its center, and a ring of collector capillaries surrounded the lobule. In the equatorial and more peripheral fundus, arterioles and veins were located in the plane of the choriocapillaris, and the choriocapillaris was segmental in arrangement.

Animals↗
PubMed1983

An electron microscopic study of calcification of retinoblastoma.

We examined three eyes with retinoblastoma that had clinical evidence of calcification. The light and electron microscopic study of the retinoblastoma cells from these eyes disclosed an intramitochondrial calcium deposition after plasmalemma disruption. Morphologically, calcium deposits initially occur as needle-like structures gathered within the mitochondrial membrane. With progressive necrotic liquefaction of tumor cells, microbodies develop a central calcified cone surrounded by an electron-translucent zone with coarse needle-like calcium deposition on the surface.

Calcinosis↗
PubMed1983

Conjunctival myxoma. A clinicopathologic study.

A 54-year-old white man had a slowly growing painless epibulbar mass that clinically mimicked a lymphangioma. Morphologically, the paucicellular tumor contained stellate and spindly cells, mast cells, and dilated lymphatic channels embedded in a loose collagenous matrix. The clinical differential diagnosis included lymphangioma, amelanotic nevus, lymphoma, reactive lymphoid hyperplasia, dermoid, lipoma, and botryoid rhabdomyosarcoma. Pathologically, lymphangioma, myxoid neurofibroma, and spindle cell lipoma were all considered. The authors discuss the clinical and histopathologic features of the various tumors, and confirmation of the diagnosis of conjunctival myxoma by differential alcian blue staining properties dependent on critical electrolyte concentration.

Conjunctiva↗
PubMed1983

von Hippel angiomatosis. A light, electron microscopic, and immunoperoxidase characterization.

A 25-year-old Iranian man had undergone eye wall resection of a large von Hippel angioma to alleviate an exaggerated macular response, affording study by light and electron microscopy and immunohistochemistry before the obfuscatory effects of long-standing exudative retinal detachment, gliosis, or iatrogenic ablation supervened. We used this vantage point to assess the interrelation between the component endothelial cells, pericytes, and stromal foam cells. On the basis of staining with glial fibrillary acidic protein, factor VIII, the C3 fraction of complement, fibrinogen, and lysozyme, it is unlikely that stromal foam cells derive from glial precursors, but may represent degenerating cells, perhaps arising from a common vasoformative stem cell under hypoxic stress.

Adult↗
PubMed1983

Effect of photic injury on the retinal tissues.

In order to study the tissue damages in photic injury of the retina, the macula and posterior pole of the rhesus monkey were exposed to the light of an indirect ophthalmoscope. During the acute phase of the injury, disruption of the blood-retinal barrier appeared to be an early and sensitive indicator of retinal pigment epithelial damage and cyclic-GMP-phosphodiesterase of the photoreceptor lamella was inactivated. These lesions were followed for 2 to 5 years. Focal chronic decompensation of the blood-retinal barrier and subretinal pigment epithelial neovascularization were noted in the chronic degenerative phase of this photic maculopathy. A possible protective role of ascorbic acid in mild photic injury was proposed.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1983

Double-masked trial of fenoprofen sodium: treatment of chronic aphakic cystoid macular edema.

Aphakic cystoid macular edema is a serious eye disease. Its etiology is unknown, but a widely held theory attributes it to an inflammatory response to surgical trauma. In a double-masked study, a 1% solution of fenoprofen sodium, a topically applied antiprostaglandin agent, was evaluated against placebo in determining the effectiveness of fenoprofen in the treatment of chronic aphakic cystoid macular edema. Fourteen patients, five women and nine men, participated in the study. Fenoprofen sodium was found to have no effect on the course of chronic aphakic cystoid macular edema. We believe that the lack of effect may have been due to the duration of edema at the time of treatment or to the small sample size. Larger studies in the immediate postoperative period are suggested. The importance of iris angiography as a possible predicting technique of macular leakage is emphasized.

Aged↗
PubMed1983

Reduced and oxidized ascorbates in guinea pig retina under normal and light-exposed conditions.

Both reduced and oxidized ascorbates were measured in aqueous, neural retina, and pigment epithelium-choroid complex (PE-C) of pigmented guinea pigs. Normal values for total ascorbate of 16 mg/dl in aqueous, 22 mg/dl in neural retina, and 7 mg/dl in PE-C were found. After mild photic damage caused by varying lengths of exposure of 10,000 to 20,000 lux of fluorescent lighting, reduced ascorbate concentrations generally decreased in the neural retina, while oxidized ascorbate generally increased in PE-C. In both normal and light-exposed retinas, reduced ascorbate was predominant in the neural retina, and oxidized ascorbate was predominant in the PE-C. Histochemical localization of reduced ascorbate occurred in the Müller cell fibers and at the apices of the retinal pigment epithelium.

Animals↗
PubMed1982

Talc retinopathy in primates: a model of ischemic retinopathy. II. A histopathologic study.

Experiment talc retinopathy was produced in four adult rhesus monkeys by biweekly intravenous injections of talc for 31/2 to ten months and was studied by retinal vascular flat preparations and by light microscopy. Talc particles were lodged in the walls of the precapillary arterioles and capillaries, producing focal occlusion of retinal and choroidal capillaries. The pericyte-endothelial cell ratio was 1:0.77 in the posterior pole and 1:0.53 in the retinal periphery. The horseradish peroxidase study showed leakage of tracer from the retinal vasculature into the extracellular interstitial space, but the barrier of the retinal pigment epithelium was intact. Microinfarcts produced small cystoid spaces in the outer plexiform layer, inner nuclear layer, and ganglion cell layer of the macula. Cytoid bodies and macrophages were scattered in the retina. No retinal or vitreal neovascularization was observed.

Animals↗
PubMed1982

Talc retinopathy in primates: a model of ischemic retinopathy. III. An electron microscopic study.

Electron microscopic study of experimental talc retinopathy provides an opportunity to study the basic cytologic response of retinal and choroidal vessels to small, relatively inert emboli. Occlusion of the retinal and choroidal capillaries resulted primarily from the cellular reaction to, rather than directly from, the emboli. Mitotic figures in pericytes were observed. Even though we failed to produce retinal neovascularization (as is sometimes seen in human talc retinopathy) in this experimental model, our observations suggest that proliferation of pericytes may be an initial step in the process of retinal neovascularization.

Animals↗
PubMed1982

Pathophysiology of hypertensive retinopathy.

The effects of systemic hypertension on the posterior segment of the eye are discussed under the headings of hypertensive choroidopathy, hypertensive retinopathy, and hypertensive optic disc edema. The sympathetic nervous control and autoregulatory mechanisms of the retinal and choroidal vasculatures are briefly reviewed. In hypertensive choroidopathy focal occlusion of choriocapillaris leads to necrosis of retinal pigment epithelium (Elschnig spots). Hypertensive retinopathy is described in vasoconstrictive, exudative, and sclerotic phases, followed by complications of the sclerotic phase. Hypertensive optic disc edema is influenced by the blood supply and extracellular tissue fluid pressure of the optic nervehead. In baboons with hypertensive disc edema, accumulation of axoplasmic components is observed in the optic nervehead.

Animals↗
PubMed1982

Pathology of cystoid macular edema.

In order to define the pathology of cystoid macular edema (CME), 35 human cases with histopathologic features of CME were reviewed. The macular cysts appeared in different layers of the retina in eyes after cataract extraction, retinal vein occlusion, trauma, diabetes mellitus, and accelerated hypertension. The pathologic process varied from transudation, exudation to liquefaction necrosis. The experimental models of lens extraction and talc retinopathy in rhesus monkeys were examined. Disruption of the blood-retinal barrier at the retinal vasculature and retinal pigment epithelium were noted after lens extraction. Cystoid degeneration of the macula was seen in monkeys with talc retinopathy. The possibility that disruption of the blood-retinal barrier and microinfarction play important roles in the formation of the macular cysts is proposed.

Aged↗