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Dive into the research topics where Guillermo de Venecia is active.

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Featured researches published by Guillermo de Venecia.


Ophthalmology | 1978

Photocoagulation Treatment of Proliferative Diabetic Retinopathy: The Second Report of Diabetic Retinopathy Study Findings

Arnall Patz; Stuart L. Fine; Daniel Finkelstein; Thaddeus E. Prout; Lloyd Paul Aiello; Robert Bradley; Jose C. Briones; Frank L. Myers; George H. Bresnick; Guillermo de Venecia; Thomas S. Stevens; Ingolf H. L. Wallow; Suresh R. Chandra; Edward W.D. Norton; George W. Blankenship; John E. Harris; William H. Knobloch; Frederick C. Goetz; Robert C. Ramsay; J. Wallace McMeel; Donald Martin; Morton F. Goldberg; Felipe U. Huamonte; Gholam A. Peyman; Bradley R. Straatsma; Stanley M. Kopelow; W.A.J. van Heuven; Aaron Kassoff; Stephen S. Feman; Robert C. Watzke

Data from the Diabetic Retinopathy Study (DRS) show that photocoagulad inhibited the progression of retinopathy. These beneficial effects were noted to some degree in all those stages of diabetic retinopathy which were included in the Study. Some deleterious effects of treatment were also found, including losses of visual acuity and constriction of peripheral visual field. The risk of these harmful effects was considered acceptable in eyes with retinopathy in the moderate or severe retinopathy in the moderate or severe proliferative stage when the risk of severe visual loss without treatment was great. In early proliferative or severe nonproliferative retinopathy, when the risk of severe visual loss without treatment was less, the risks of harmful treatment effects assumed greater importance. In these earlier stages, DRS findings have not led to a clear choice between prompt treatment and deferral of treatment unless and until progression to a more severe stage occurs.


American Journal of Ophthalmology | 2003

Central serous chorioretinopathy associated with administration of sympathomimetic agents

John C. Michael; John Pak; Jose S. Pulido; Guillermo de Venecia

PURPOSE To report central serous chorioretinopathy associated with excessive use of compounds with sympathomimetic activity. DESIGN Observational case series. METHODS Four patients presented with clinical and fluorescein angiographic evidence of central serous chorioretinopathy. All patients expressed a concomitant psychogenic stress and high-dose ingestion of pseudoephedrine, oxymetazoline, or 3,4-methylenedioxymethamphetamine, all of which possess sympathomimetic properties. RESULTS In all cases, resolution of central serous chorioretinopathy coincided with cessation of the medication. CONCLUSIONS Patients afflicted with central serous chorioretinopathy should be notified about its possible association with sympathomimetic medications.


American Journal of Ophthalmology | 1976

Ocular and Cerebral Involvement in Familial Lymphohistiocytosis

Richard E. Appen; Steven W. Weber; Guillermo de Venecia; Gabriele M. Zu Rhein

A 5-month-old infant girl died of familial lymphohistiocytosis. The central nervous system showed widespread perivascular infiltration of the cerebral pia and arachnoid, the cerebral white matter and deep gray matter, the cerebellum, and brain stem by lymphocytes, benign appearing histiocytes, and macrophages with erythro-and lymphophagocytosis. The eyes had mild infiltration of the anterior uveal tract, moderate involvement of the inner retina, and marked infiltration of the optic nerves by identical cells.


American Journal of Ophthalmology | 1978

Meningeal carcinomatosis with blindness.

Richard E. Appen; Guillermo de Venecia; Joseph H. Selliken; Laurence T. Giles

A 53-year-old man had bilateral blindness secondary to meningeal carcinomatosis from pulmonary adenocarcinoma. Histopathologic examination of the visual system showed extensive infiltration of the arachnoid of the proximal optic nerves and chiasm, with minimal invasion of the optic nerves themselves. The visual pathways within the cerebral cortex were not affected.


American Journal of Ophthalmology | 1980

Optic Disk Vasculitis

Richard E. Appen; Guillermo de Venecia; James R. Ferwerda

A 44-year-old woman developed progressive loss of vision associated initially with a swollen optic disk, and later with optic atrophy and a diffuse retinal vasculopathy, which caused extensive retinal hemorrhagagic. Histopathologic examination showed hemorrhagagic infarction of the retina, as well as infarction of the anterior optic nerve. In the optic nerve, the central retinal vessels showed extensive phlebitis and occlusion of many small arterioles.


Retina-the Journal of Retinal and Vitreous Diseases | 1990

Immunocytochemical study of an eye with proliferative vitreoretinopathy and retinal tacks.

T. Michael Nork; Ingolf H. L. Wallow; Stephen J. Sramek; Thomas S. Stevens; Guillermo de Venecia

After an eye-wall resection for a choroidal melanoma, a 32-year-old woman had subsequent retinal detachment with proliferative vitreoretinopathy (PVR), and an unsuccessful attempt at repair with retinal tacks. Gross and light-microscopic examination of the globe revealed a total retinal detachment with extensive preretinal and subretinal membranes. The membranes surrounded the tack heads and extended in taut bands to form a tractional detachment of the pars plana. The membranes contained glial and nonglial cells. The glial cells immunolabeled for glial fibrillary acidic protein (GFAP), carbonic anhydrase-C (CA-C), vimentin, and glutamine synthetase (GS), thus suggesting that they were Müllers cells. While the tacks did not seem to cause PVR, in this case they may have provided an anchoring point from which membranes were able to exert traction on the retina and pars plana.


American Journal of Ophthalmology | 1995

Retinal trypsin digest study of cystoid macular edema associated with peripheral choroidal melanoma

John C. Michael; Guillermo de Venecia

PURPOSE Although the association of cystoid macular edema with peripheral choroidal melanoma has been studied previously, the pathogenesis of cystoid macular edema as evaluated by light and electron microscopy remains controversial. We evaluated the cause of cystoid macular edema at the retinal capillary level. METHODS We clinicopathologically correlated petaloidlike changes noted on fluorescein angiography with the corresponding morphologic changes, as documented by retinal trypsin digest preparation. RESULTS The angiographic foci of fluorescein leakage were found to correspond to sites of endothelial cell proliferation that resembled intraretinal microvascular abnormalities in the retinal trypsin digest preparation. CONCLUSIONS The source of cystoid macular edema at the level of the retinal capillary network are intraretinal microvascular abnormalities resembling endothelial cell proliferation. We examine the relationship between endothelial cell proliferation and vascular leakage.


Ophthalmology | 1984

Neuronal Ceroid Lipofuscinosis: A Retinal Trypsin Digest Study

Guillermo de Venecia; Michael B. Shapiro

Neuronal ceroid lipofuscinosis, also known as the Batten-Vogt syndrome, is clinically manifested by seizures, loss of intellect, and deterioration of vision. The retinal histopathologic and ultrastructural changes have been well-described. This report adds the findings of trypsin digest preparation of the retinae in three such patients with varying duration of this disease. Acellular retinal capillaries, or ghost vessels, were observed, and the degree of this change correlated with the duration of clinical symptoms. These changes, as well as the histopathologic abnormalities, are discussed.


Archives of Ophthalmology | 1971

Cytomegalic Inclusion Retinitis in an Adult: A Clinical, Histopathologic, and Ultrastructural Study

Guillermo de Venecia; Gabriele M. Zu Rhein; Mary V. Pratt; William Kisken


Archives of Ophthalmology | 1975

Retinal Ischemia in Diabetic Retinopathy

George H. Bresnick; Guillermo de Venecia; Frank L. Myers; James A. Harris; Matthew D. Davis

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George H. Bresnick

University of Wisconsin-Madison

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Frank L. Myers

University of Wisconsin-Madison

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Ingolf H. L. Wallow

University of Wisconsin-Madison

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James C. Allen

University of Wisconsin-Madison

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John C. Michael

University of Wisconsin-Madison

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Matthew D. Davis

University of Wisconsin-Madison

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Richard E. Appen

University of Wisconsin-Madison

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Thomas S. Stevens

University of Wisconsin-Madison

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