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Biomedical subjects

I H Wallow

Publications and source records attributed to I H Wallow.

At least 55 records · Page 3Linked to original sources
PubMed1984

Actin filaments in contracting preretinal membranes.

In 14 patients, preretinal membranes, causing retinal traction and severe visual impairment, were removed by vitrectomy and evaluated by light and electron microscopy using myosin subfragment-1 to stain actin filaments. Eight membranes were of vascular origin, six of nonvascular origin. All but one contained bundles of oriented actin filaments within a number of their nonvascular stroma cells, suggesting that the contractile protein action may have been involved in their clinically observed contraction.

Actins↗
PubMed1983

Posterior and anterior permeability defects? Morphologic observations on streptozotocin-treated rats.

Structural abnormalities of the blood-ocular barrier were examined in streptozotocin (STZ)-treated hyperglycemic rats, after 9 days, 6 months, and 10 months' duration of "diabetes," and in normoglycemic control animals using the horseradish peroxidase tracer technique combined with light and electron microscopy. The most frequent abnormalities consisted of small areas of diffuse dense staining by the tracer of (1) the retinal pigment epithelium and (2) the nonpigmented ciliary epithelium. Pigment epithelium abnormalities occurred occasionally in both groups of animals with approximately equal frequency and extent. Ciliary body abnormalities occurred also in both groups, but were frequent; statistically, the probability of these changes was not significantly different between the two groups. At the ora serrata, tracer escape was present through the retinal pigment epithelium into subretinal space and retina. Retinal vascular leakage occurred rarely and may be related to tracer toxicity rather than hyperglycemia. Thus, using the HRP method, we cannot confirm the claim that sustained STZ-induced hyperglycemia causes breakdown of the blood-retinal barrier in the rat.

Animals↗
PubMed1981

Actin filaments in diabetic fibrovascular preretinal membrane.

A vitrectomy specimen from a diabetic patient was studied by light and electron microscopy using myosin subfragment 1 to decorate and identify actin filaments. The patient had proliferative diabetic retinopathy, a shrinking fibrovascular preretinal membrane associated with retraction of the thickened posterior hyaloid, and a localized traction retinal detachment. The fibrovascular tissue comprised normal mature collagen, few cells, and occasional blood vessels. The cells contained numerous thick bundles of the contractile protein, actin. We suggest that actin may have been involved in the contraction phenomena observed clinically and that membrane contraction might be blocked by pharmacologic treatment.

Actins↗
PubMed1981

Long-term changes in photocoagulation burns.

101 argon laser and xenon arc photocoagulation burns were studied clinically and histopathologically in 8 diabetics patients treated for PDR. The age of the lesions ranged between 4 and 70 months. Our observations confirmed long-term patterns of retinal pair observed previously only in animals. Moderately severe burns, when placed in the thick paracentral retina, at times resulted in differentiated retinal repair not associated with new retinal adhesions. Severe burns created full thickness retinal defects, but spared the inner limiting membrane and allowed formation of apparently firm new retinal adhesions. These burns are considered as most suitable for the scatter treatment of PDR. Very severe burns exhausted the retinal capacity for glial repair so that the RPE became the only resource of retinal reparative tissue. In such scars the RPE bordered the vitreoretinal juncture yet did not invade the vitreous. However, glial preretinal membranes were frequently seen over very severe burns exerting tangential retinal traction.

Argon↗
PubMed1980

Endothelial fenestrae in proliferative diabetic retinopathy.

The ultrastructure of old neovascular preretinal membranes was examined in both eyes of a patient with proliferative diabetic retinopathy treated in one eye with photocoagulation. Membranes in both eyes consisted of a matrix rich in mature collagen surrounding viable new vessels and "ghost vessels." Viable vessels of different calibers frequently showed endothelial fenestrae bridged by diaphragms. Occasionally tight junctions between endothelial cells appeared altered. Fenestrae and incompetent junctions may account for the characteristic "leakiness" of newly formed vessels.

Diabetic Retinopathy↗
PubMed1980

Actin filaments in retinal pericytes and endothelial cells.

The contractile protein actin was identified within retinal capillary pericytes and endothelial cells. In capillary cross-sections, circumferential pericyte processes showed numerous parallel bundles of actin filaments forming a cap over the adjacent endothelial cells. The latter contained few actin filaments but a considerable number of intermediate filaments. Pericytes and endothelial cells communicated via gaps in the adluminal basal lamina. These special anatomic relationships are interpreted as evidence for a contractile role of retinal capillary pericytes and against a contractile role of retinal capillary endothelial cells

Actins↗
PubMed1979

Clinicopathologic correlation of xenon arc and argon laser photocoagulation. Procedure in human diabetic eyes.

Xenon arc and argon laser lesions applied as scatter treatment to two diabetic patients were studied clinically and histopathologically. Seventy-one burns were grouped as very severe, severe, and moderately severe, according to pigmentation and diameter of the retinal scar. All lesions except half of the moderately severe ones showed full-thickness retinal involvement. In very severe xenon burns, whether xenon or argon, only proliferated retinal pigment epithelium provided a thin retinal scar, corresponding to an ophthalmoscopic appearance of "bare sclera". In the center of severe and moderately severe lesions, both glial cells and pigment epithelium bridged the retinal defect, forming a thick pigmented scar that contained pigment-laden macrophages. Rephotocoagulation over such thick scars may be less hazardous than is generally assumed. Nonvascular preretinal membranes were frequently present over very severe xenon lesions but rarely over very severe argon burns.

Adult↗
PubMed1979

Impairment of isoproterenol, H2 histamine, and prostaglandin E1 response of human granulocytes after incubation in vitro with live influenza vaccines.

The release of the lysosomal enzyme beta-glucuronidase from granulocytes follows incubation in vitro with complement-activated zymosan particles. Release of beta-glucuronidase is inhibited by isoproterenol, histamine, and prostaglandin E1. This in vitro model was used to study the effect of incubating a live, bivalent (A + B) influenza vaccine on the granulocyte response to the agonists described. After incubation in vitro with the live, bivalent influenza vaccine, there was a significantly impaired granulocyte reponse to all 3 agonists. The change in the response of polymorphonuclear leukocytes to isoproterenol was similar to an impairment in beta-adrenergic response found during respiratory infections in vivo. The viral-induced changes in the granulocyte response to isoproterenol may reflect similar alteration in other tissues, such as variable control of the airways and provide one explanation for the occurrence of airway dysfunction during respiratory infections.

Adult↗
PubMed1978

Septic choroiditis with serous detachment of the retina in dogs.

The present study describes a model of multifocal septic choroiditis with serous retinal detachment after intracarotid injection of Staphylococcus aureus or Streptococcus faecalis. The fundus lesions occurred mainly in the tapetal area and, on ophthalmoscopic examination, were more extensive after S. aureus than after S. faecalis injection. On histopathologic examination there were microabscesses in the inner choroid and subretinal space, disrupting the outer retina but sparing the inner retina.

Animals↗
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

Permeability and patency of retinal blood vessels in experimental diabetes.

Increased permeability of retinal blood vessels in human diabetic retinopathy is well known clinically. Its morphologic equivalent is unknown. In dogs with 5 years of poorly controlled alloxan diabetes and nonproliferative diabetic retinopathy comparable to that of man, permeability and patency of retinal blood vessels were tested with the protein tracer horseradish peroxidase and evaluated by electron microscopy. A breakdown of the blood-retinal barrier was found associated with extensive tracer leakage around retinal blood vessels. Tracer had seemingly permeated endothial junctions, and was not transported through the endothelial cytoplasm. Blood vessels which had lost their endothelial cells and were partially occluded by glial cells retained some patency to tracer. These findings suggest the following. (1) Endothelial tight junctions are not a static cell specialization but one that can open due to chronic metabolic or osmotic factors prevailing in diabetes. Opened tight junctions may account for plasma leakage seen clinically in human diabetic retinopathy. (2) In the absence of endothelial cells perfusion does not necessarily end abruptly. The tracer method and electron microscopy may show details of vascular obstruction that are not readily demonstrated clinically.

Animals↗
PubMed1975

[Retinal reactions to intense light. I. Threshold lesions. Experimental, morphological and clinical studies of pathological and therapeutic effects of laser and white light].

The effects of intense light produced by an argon laser, a helium-neon laser and a xenon are photocoagulator in the retinas of gray chinchilla rabbits, cynomolgus monkeys, and rhesus monkeys were studied clinically and histopathologically including electron microscopy. An improved experimental set-up was used allowing a very good consistency of the inflicted lesions. Threshold lesions were produced in chinchilla rabbits and cynomolgus monkeys by an argon laser and a helium-neon laser. The lesions were evaluated ophthalmoscopically and histograms were drawn indicating ophthalmoscopic ED50 values. For the two lasers examined these values were 12 and 17 mW, respectively, for exposure durations in the range of the blink reflex (125-150 msec). Histopathologically, ophthalmoscopic threshold lesions of both laser types showed evidence of thermal damage of the outer retinal half. This damage was principally identical in both species involving the retinal pigment epithelium and the full extension of the photoreceptor cells up to their synapses within the outer plexiform layer. The ophthalmoscopic threshold value was associated, therefore, with an irreversible loss of visual function within the retinal area concerned. No evidence for primary sites of significant energy absorption within the neural retina was found. The width of ophthalmoscopic threshold lesions was determined by measuring within the histologic sections with a microscope and a calibrated graticule the extension of damage at the level of the retinal pigment epithelium and at the level of the outer nuclear layer. In the cynomolgus monkey for ophthalmoscopic argon laser threshold lesions the extension at the level of the RPE was 70-80 mum in diameter and at the level of the outer nuclear layer it was 40-50 mum in diameter. Laser lesions that had a diameter of 60 mum at the level of the RPE and of 30 mum at the level of the outer nuclear layer were ophthalmoscopically subvisible. It is concluded that probably also in man such laser lesions, as well as various other pathologic changes of this size or smaller, cannot be evaluated by clinical ophthalmoscopy. The ophthalmoscopic threshold was correlated with a histopathologic threshold as defined by minimal histopathologic damage. Very likely, such damage lies within the range of functional recovery, and the histopathologic threshold demarcates at the same time the decisive functional threshold. The conversion ratio between histopathologic-functional and ophthalmoscopic threshold for argon lesions in cynomolgus monkeys was somewhat greater than 3, e.i. the ophthalmoscopic threshold was more than 3 times higher than the histopathologic-functional threshold. Using this data together with additional biologic and optical considerations, a safety threshold for man for cw-lasers within the visible spectrum was estimated to be 1-2 mW.

Animals↗