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Biomedical subjects

M O Tso

Publications and source records attributed to M O Tso.

At least 163 records · Page 9Linked to original sources
PubMed1981

Feulgen-positive deposits in retinoblastoma. Incidence, composition, and ultrastructure.

The incidence of hematoxyphilic extracellular deposits in 159 cases of retinoblastoma was found to be 18%. Six other features of these tumors also were examined. In the majority of eyes with these deposits, the tumors were composed solely of anaplastic cells. None was well differentiated with preponderantly rosette formation. The hematoxyphilic deposits were Feulgen-positive, and this staining was diminished but not abolished by pretreatment with purified deoxyribonuclease (DNase), which did abolish nuclear staining. Feulgen staining of the deposits was totally blocked by pronase--DNase pretreatment--suggesting that the deposits may represent DNA-protein complexes. Ultrastructurally, these deposits were electron dense and finely vacuolar. The deposits may originate from degenerating tumor cell nuclei, and the possibility that they may represent immune complexes warrants future study in view of occasional spontaneous regression of this tumor.

Antigen-Antibody Complex↗
PubMed1981

Talc retinopathy in primates. A model of ischemic retinopathy: I. Clinical studies.

Four rhesus monkeys received intravenous injections of talc twice weekly for 3 1/2 to ten months. Within one month, talc particles were visible in fine perifoveal retinal vessels in the posterior pole. Continued deposition of talc could then be seen after subsequent injections. Hemorrhages in the nerve fiber layer, cotton-wool patches, and whitish plaques in the choroid were visible ophthalmoscopically. Fluorescein angiography revealed precapillary arteriolar occlusions, capillary nonperfusion, an abnormal foveal avascular zone, and retinal vascular leakage. Vitreous fluorophotometric findings were abnormal in all five eyes tested, while electroretinograms were normal in two eyes with advanced talc retinopathy. Talc retinopathy in the primate is similar to ischemic retinopathies in humans, including human talc retinopathy, sickle cell retinopathy, and hypertensive retinopathy. Subsequent reports will describe the light microscopic and ultrastructural changes in these eyes using tracer studies with in these eyes using tracer studies with horseradish peroxidase.

Animals↗
PubMed1981

Pathology and pathogenesis of drusen of the optic nervehead.

This report describes the findings of a clinicopathologic correlative study of 18 cases of drusen of the optic nervehead and reports on the observations of the first ultrastructural study of this disease in the literature. From these observations, the processes of formation of drusen of the optic nervehead are proposed: abnormal axonal metabolism leads to intracellular mitochondrial calcification. Some axons rupture and mitochondria are extruded into the extracellular space. Calcium is heavily deposited in the extracellular mitochondria. Small calcified microbodies are produced and calcium continues to deposit on the surface of these nidi to form drusen. We conclude that drusen are definitely related to axonal degeneration of the optic nervehead.

Adolescent↗
PubMed1980

Clinicopathologic study of blood-retinal barrier in experimental diabetes mellitus.

Rats with experimental diabetes (induced by streptozocin [Streptozotocin]) were studied by vitreous fluorophotometry and horseradish peroxidase tracer technique. Vitreous fluorescein sodium concentration notably increased four to eight days after a single dose of streptozocin. No leakage from the retinal vasculature could be demonstrated by the horseradish peroxidase tracer study, but three types of retinal pigment epithelial (RPE) lesions were observed. The RPE lesions seemed to be partially responsible for the increase of vitreous fluorescein concentration.

Animals↗
PubMed1980

An ultrastructural study of the corpora amylacea of the optic nerve head and retina.

We studied corpora amylacea in the optic nerve heads and retinas of four human eyes with increased intraocular pressure by light and electron microscopy. Ultrastructurally they consisted of a mass of filamentous tangle discretely bordered by normal or abnormal axoplasm within an axonal swelling. We found neurotubules, mitochondria, and the accumulation of dense bodies in the axoplasm surrounding the filamentous tangle. We noted ultrastructural similarities between corpora amylacea and cytoid bodies, swollen axons with transport block, and experimentally induced neurofibrillary tangles. We concluded that corpora amylacea are intracellular organelles found in axonal swellings and are not glial in origin, as previously believed. There is a possible relationship between corpora amylacea and distrubance of axoplasmic transport.

Axons↗
PubMed1980

An ultrastructural study of melanocytomas (magnocellular nevi) of the optic disk and uvea.

We examined by light and electron microscopy five melanocytomas from four patients. Two types of cells were observed in each tumor. The predominant cell type in most of the tumors studied consisted of plump polyhedral nevus cells that contained numerous giant melanosomes. These cells showed advanced differentiation. They appeared to be metabolically inactive and to have been the cause of the heavy pigmentation and benign nature of these tumors. The second variant of melanocytoma cells were smaller spindle-shaped cells that were lightly pigmented. Other morphologic features of these cells such as high nucleus-cytoplasm ratio, prominent nucleolus, nuclear membrane infolding, numerous mitochondria, prominent rough endoplasmic reticulum, and free ribosomes, indicated a metabolically active cell, which may explain the infiltrating behavior of these tumors.

Adult↗
PubMed1980

Pathological study of cystoid macular oedema.

Many diseases may give rise to cystoid macular oedema (CMO), which suggests that this condition is not a disease but a final common pathway of many diseases. It is not exclusively associated with retinal vascular disturbance, but may be secondary to choroidal vascular changes and alterations of the retinal pigment epithelium. In some forms of CMO, generalized ocular involvement is present and results in vascular leakage of the iris and possibly other ocular structures. Experimental pathological models suggest that leakage of the retinal vasculature and/or retinal pigment epithelium alone may not give rise to CMO. Ischaemia resulting in microinfarction may be one of the important factors in the production of CMO.

Animals↗
PubMed1980

An inherited retinopathy in collies. A light and electron microscopic study.

A recessively inherited retinopathy in collies aged 8 to 189 days was studied by light and electron microscopy. The disease is produced when the outer segments of rods and cones fail to develop normally. Retinal pigment epithelial changes found in several litters appeared to form a separate disease entity. We compared the collie retinopathy with other canine models and the collie ectasia syndrome.

Animals↗
PubMed1979

Repair and late degeneration of the primate foveola after injury by argon laser.

Each foveola of nine rhesus monkey eyes was subjected to a single, mild, calibrated exposure from an argon laser (1 to 1.4 mW for 10 to 20 min). Observations from ophthalmoscopy, fundus photography, and fluorescein angiography were correlated with light and electron microscopic studies. The ophthalmoscopic changes consisted of initial whitening and subsequent but persistent depigmentation of the foveola. Fluorescein angiography showed a pattern consistent with "window defect" of the retinal pigment epithelium (RPE). In the first 6 months after injury, the pathologic changes consisted of initial vacuolar changes of the RPE, followed by persistent hypopigmentation and slow development of membranous bodies or lipoidal degeneration in these cells. Initial alteration and subsequent incomplete reformation of cone outer segments were also noted. In animals sacrificed 3 to 4 years after injury, separation of RPE from Bruch's membrane, with production of various abnormal basement membranes and intercellular cystoid changes in the overlying retina, was observed. The morphologic observations suggest that although the mildly injured epithelial cells may recover, they may develop functional incompetence at a later date, resulting in serous detachment of RPE and foveal (macular) edema.

Animals↗
PubMed1979

Sickled erythrocytes, hyphema, and secondary glaucoma: VII. The passage of sickled erythrocytes out of the anterior chamber of the human and monkey eye: light and electron microscopic studies.

Sickled erythrocytes leave the anterior chamber of human and monkey eyes by several mechanisms: intracameral and intratrabecular hemolysis and phagocytosis; entry into and phagocytosis within the iris and ciliary body; and passage into Schlemm's canal. Sickled erythrocytes used as biologic tracers allowed definite confirmation, for the first time in the human, that intracameral erythrocytes can enter Schlemm's canal in the orthograde direction. Erythrocytes appeared to traverse the inner wall of Schlemm's canal through the cytoplasm of individual endothelial cells, rather than between adjacent endothelial cells -- a mechanism similar to that employed by red and white blood cells elsewhere in the body. Although some sickled erythrocytes did pass into Schlemm's canal, considerable obstruction appeared to occur at the corneoscleral meshwork, juxtacanalicular connective tissue, and inner wall of Schlemm's canal, caused largely by the elongated, rigid nature of the sickled cells. Total blockage of Schlemm's canal was not observed.

Anemia, Sickle Cell↗
PubMed1978

Rubeosis iridis and glaucoma associated with sickle cell retinopathy: a light and electron microscopic study.

The ultrastructure of rubeosis iridis in sickle cell-hemoglobin C disease is described for the first time. Findings included open interendothelial cell junctions, intraendothelial cytoplasmic attenuations (fenestrations), and pericyte formation. The ultrastructural appearance of rubeosis iridis gives no clue to the underlying etiology and is similar to that reported in rubeosis associated with diabetes mellitus, central retinal vein occlusion, and uveitis. The electron microscopic findings explain the functional incompetence of rubeotic vessels that are manifested by transmural leakage of fluorescein.

Anemia, Sickle Cell↗
PubMed1978

Multiple periorbital fibrous histiocytomas: a light and electron microscopic study.

Recurrent, bilateral, multiple, periorbital fibrous histiocytomas occurred in a 62-year-old woman. There were no associated serum lipid abnormalities. Histologically, the tumor was composed of an admixture of lipid-laden histiocytes and fibroblasts with a variable amount of collagen production. In many areas the fibroblasts were arranged in a storiform pattern. No cytologic evidence of malignancy was observed. Ultrastructural studies of the tumor showed histiocytic cells with a variable amount of lipid in the cytoplasm and fibroblasts with mild to moderate collagen production. Differential diagnosis and histogenesis are discussed.

Cytoplasm↗
PubMed1977

Experimental photocoagulation of the human retina. I. Correlation of physical, clinical, and pathologic data.

Thirty-eight retinal burns were inflicted by a modified xenon-arc photocoagulator in the eyes of eight human volunteers. The ophthalmoscopic characteristics of these lesions were correlated with the degree of histopathologic damage. Definitive clinical criteria that helped to predict the severity of the retinal burns were established. The dose of radiant energy received was further correlated with the histopathologic changes in determining the threshold of safety standards of bright flashes of white light to the human eye. Lesions from patients with blue irises were produced by considerably higher dose rates than comparable lesions from patients with brown irises and the fovea was more susceptible to damage than the rest of the retina.

Dose-Response Relationship, Radiation↗
PubMed1977

Experimental photocoagulation of the human retina. II. Electron microscopic study.

Minimal retinal damage in xenon-arc photocoagulation lesions in man 14 hours to three days after exposure was confined to the retinal pigment epithelium (RPE) and consisted of accumulation of lysosome-related bodies in the cytoplasm. Slightly more intense damage consisted of dilation, vacuolization, and breakdown of the lamellae of the smooth-surfaced endoplasmic reticulum, preferentially around melanin-rich cell portions. Underneath more heavily vacuolated cells of the RPE, already in the periphery of ophthalmoscopically just-visible lesions, damage extended into the endothelial cells of the choriocapillaris and into the photoreceptor elements. Macrophages escaped from the choroidal circulation to appear on both sides of the Bruch membrane and within the subretinal space. More intense lesions showed features identical to those described in monkeys and are expected to show the same morphologic pattern of healing.

Choroid↗
PubMed1977

Optic disc edema in raised intracranial pressure. III. A pathologic study of experimental papilledema.

Optic nerve heads of 21 eyes from 13 rhesus monkeys that had developed papilledema secondary to chronically raised intracranial pressure from balloon implantation in the subarachnoid space were studied by light and electron microscopy. Nine eyes were also examined with the horseradish peroxidase tracer technique. The pathologic changes in the optic nerve head included severe axonal changes and mild interstitial edema. Axonal alteration ranged from axonal swelling to formation of cytoid bodies. Interstitial edema and vascular leakage of horseradish peroxidase were noted in the posterior lamina retinalis, lamina choroidalis and lamina scleralis (prelaminar and lamina cribrosa regions), as well as in the retrolaminar myelinated optic nerve. No intracellular edema of the glial elements was noted. Axonal swelling was so prominent that it appeared to be primarily responsible for the overall swelling of the optic disc observed ophthalmoscopically.

Animals↗
PubMed1977

Optic disc edema in raised intracranial pressure. IV. Axoplasmic transport in experimental papilledema.

Tritiated leucine was injected intravitreously into the eyes of rhesus monkeys that had developed papilledema secondary to implantation of intracranial balloons. Autoradiographic studies of the optic nerve head showed that six hours after intravitreous injection of the isotope the fast component of axoplasmic transport accumulated in the regions of the lamina choroidalis and lamina scleralis. The slow component arrived at the optic nerve head two to four days after injection, and the swollen axons of the entire optic nerve head were filled with radioactive isotopes. Twelve days after injection of isotope, the axons in the optic nerve head were still diffusely labeled. Disturbance of axoplasmic transport was one of the primary events resulting in swelling of axons in papilledema. The pattern of axoplasmic disturbances in papilledema secondary to raised intracranial pressure was similar to that observed in papilledema secondary to ocular hypotony or increased intraocular pressure. Ocular hypotony, raised intracranial pressure, and increased intraocular pressure appear to share a final common pathway. All these conditions apparently converge into this final common pathway of disturbance of axoplasmic transport to give rise to papilledema.

Animals↗