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Biomedical subjects

V G Wong

Publications and source records attributed to V G Wong.

At least 19 recordsLinked to original sources
PubMed1991

Effect of rH tumor necrosis factor on experimental intraocular tumors.

Local and systemic tumor necrosis factor (TNF) have been shown to have marked tumorcidal effect on VX2 intraocular tumors. Complete ablation or remission of the experimental ocular tumor was not achieved in doses employed. TNF is a potent immune modulator of acute and chronic inflammation. Local toxic effect of TNF to the eye was severe and occurred only in the presence of tumor. Intravitreal TNF will cause severe necrosis of the normal eye. This toxic effect was not seen when intravitreal TNF was injected into a tumor-bearing eye. Chronic perfusion and low doses of TNF in combination with other antitumor agents may be tried in future studies to avoid local and systemic toxicity.

Animals↗
PubMed1983

Retinal atrophy induced by intravitreous colchicine.

Colchicine is known to inhibit axoplasmic transport in ganglion cells. Previous studies have shown considerable, but largely reversible, retinal changes after low dosages of intravitreal colchicine in experimental animals. In the present study, the effects of 1.0 to 100 micrograms of intravitreal colchicine in monkeys were studied by ophthalmoscopy, light microscopy, and electron microscopy. Optic atrophy was ophthalmoscopically evident within 4 weeks after a single dose of 10 micrograms or more. Morphologic changes included progressive swelling of retinal neurons, accumulation of a fibrillogranular material, displacement of organelles, and loss of microtubules. Plasmalemmal rupture was observed in ganglion cells and in photoreceptors after as little as 1 microgram of colchicine. Relative sparing of the cone cells was noted. The retina of monkeys appears to be more sensitive to intravitreal colchicine than that of certain lower animals.

Animals↗
PubMed1981

Aetiology of sympathetic ophthalmitis.

The aetiology of sympathetic ophthalmitis is still unknown. Recent investigations on patients and experimental studies on allergic uveitis in guinea-pigs suggest that sympathetic ophthalmitis may be due to delayed hypersensitivity to one of the retinal antigens associated with photoreceptor membranes (called the retinal 's' antigen). It is postulated that a penetrating injury causes a reversal of normal tolerance by introducing an adjuvant effect from bacterial or viral contamination along with the release of the intraocular antigen. The antigen then gains access to the regional lymphatics by way of the penetrating wound. A specific cell-mediated immune response is then initiated followed by the onset of sympathetic ophthalmitis.

Animals↗
PubMed1979

A heat-stable protein inhibitor of cyclic 3',5'-nucleotide phosphodiesterase.

A heat-stable, non-dialyzable inhibitory factor of cyclic nucleotide phosphodieterase was detected in and partially purified from bovine retina. The factor appears to be a protein, since the inhibitory activity was abolished by trypsin digestion but not by DNAase or RNAase treatment. The protein inhibitor from bovine retina effectively inhibits the Ca2+-independent phosphodiesterase from several sources, including bovine retina, bovine rod outer segment, and a human lymphoblastic leukemia cell line, indicating lack of tissue and species specificity.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1979

Experimental intraocular malignancy: the effect of intracameral perfusion.

Transplantable Brown-Pearce carcinoma was adapted successfully in the rabbit anterior chamber. Regression of tumor growth was attained on tri-weekly perfusion of the AC with 10 micromolar of methotrexate. Tumor cyclic nucleotide phosphodiesterase (PDE) and protein activator were found to be markedly depressed during the course of chemotherapy and the PDE cAMP/cGMP ratio was similarly altered. Corroborative light and electron-microscopic studies showed specific alterations of intracellular organelles in relation to MTX and tumor cell death. These findings suggest that metabolic pathways of cyclic nucleotides are important biochemical modulators of neoplastic cells. The method of intraocular perfusion precludes systemic toxic effects and avoids compromising the animals' immunocompetence.

Animals↗
PubMed1977

Congenital cerebral and ocular malformations induced in rhesus monkeys by Venezuelan equine encephalitis virus.

Rhesus monkey fetuses were inoculated with Venezuelan Equine Encephalitis (VEE) vaccine virus by the direct intracerebral route at approximately 100 days gestation to determine possible teratogenicity of the virus. Congenital micrencephaly, hydrocephalus and cataracts were found in all animals and porencephaly in 67 percent of the cases. The virus replicated in the brain and other organs of the fetus. VEE vaccine virus is teratogenic for non-human primates and must be considered a potential teratogen of man.

Animals↗
PubMed1977

Cyclic nucleotide phosphodiesterase and protein activator in human cancer cell lines and Brown-Pearce carcinoma.

3':5'-Cyclic-AMP phosphodiesterase (EC 3.1.4.17) and the activating factor of cyclic nucleotide phosphodiesterase were detected in cultured human cell lines from patients with lymphoblastic leukemia and retinoblastoma and in the Brown-Pearce (rabbit) carcinoma. The homogenate of lymphoblasts contained levels of the activating factor in excess of that required to produce maximal activation of the endogenous phosphodiesterase. The activating factor found in these malignant cells appears to be similar to the calcium-binding protein activator of bovine brain phosphodiesterase on the basis of the molecular weight obtained from gel filtration, electrophoretic patterns, calcium requirement for the activity, and the effect of calcium on the proteolysis. In addition, the tumor-derived activator was able to restore the activity of activator-deficient phosphodiesterase from the bovine brain.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1977

Rhodopsin and blindness.

Systemic immunization with purified homologous rhodopsin from retinal outer segments induced blindness in primates (Macaca mulatta). Inflammation and characteristic retinal changes were the earliest clinical signs of the disease. Perivasculitis, subretinal exudations and bullous detachments of the retina were progressive and unrelenting pathological processes leading to rapid and irreversible visual deterioration. Electroretinographic responses (ERG) at this stage of the disorder became abolished. Antibodies and delayed hypersensitivity to rhodopsin were demonstrated only in the experimental diseased animals. Homologous visual purple appears to be organ and immunopathologically specific. Histological confirmation of these findings showed a pathological spectrum of destructive alterations confirmed specifically to the outer segments of the entire retina. The pathologic reaction was supported by a distinct and pronounced granulomatous inflammatory response.

Animals↗
PubMed1976

The propensity of different strains of guinea pigs to develop experimental autoimmune uveitis.

We compared the propensity of several strains of guinea pigs to develop autoimmune experimental uveitis and autoimmunity following immunization with retinal-uveal antigens in complete Freund's adjuvant. The Hartley and NIH strains developed the disease more frequently and more severely than the strain 13 animals. The strain 2 guinea pigs did not develop the disease at all. In addition, the strain 2 did not make as much delayed hypersensitivity or as much antibody as the Hartley and NIH strain animals. NIH guinea pigs lacking the fourth component of complement made as much disease as those with that enzyme.

Animals↗
PubMed1975

Homologous retinal outer segment immunization in primates. A clinical and histopathological study.

Immune intraocular inflammation was induced in primates with homologous retinal outer segments. Perivascular retinitis, uveitis, and edema of the optic nerve head were the prominent acute clinical features. Acute and chronic inflammation was seen in the central and peripheral retinal vessels and granulomatous infiltration was present in the choroid of the uvea. Selective degeneration of the outer segments of the photoreceptor cells of the retina with sparing of the inner segments and of the adjacent pigment epithelium was confirmed by light and electron microscopy. This study strongly suggests that photoreceptor outer segments are highly and specifically immunogenic. The inciting antigen has yet to be identified. Implication of rhodopsin will have to await further studies since it exists as the essential protein in the outer segment.

Animals↗
PubMed1975

Prevention of experimental allergic uveitis. Treatment and methotrexate.

These experiments were undertaken to determine if methotrexate therapy, initiated after immunization, could prevent the development of experimental allergic uveitis. Strain 13 guinea pigs were immunized with Strain 13 guinea pig retina-uvea extract that had been emulsified in Freund complete adjuvant. Some were treated with methotrexate twice a week until the 21st day. Each week, all of their eyes were examined with a slit-lamp. At the end of the study, some were skin tested, and the sera of selected animals were tested by immunodiffusion for antibody. The eyes of certain groups were examined histologically. Results show methotrexate prevented the development of this type of uveitis, even when therapy was initiated seven days after immunization. The disease did not appear after therapy was stopped. Methotrexate also inhibited the development of skin sensitivity and antibody to retina-uvea antigen.

Animals↗
PubMed1975

Koch's stulates and experimental ocular histoplasmosis.

The present study shows clearly that focal choroiditis is produced in rabbits by infecting the animals with a mycelial form of H. capsulatum. Identification of this organism as the pathogenic agent was made by histopathological and mycological observations. This fungus was recovered from infected ocular lesions in those eyes enucleated within four weeks following the appearance of uveitus-a time period consistent with the clinical and pathological appearance of multiple granulomas in the choroid. The absence of organisms in the contralateral eyes of these same animals at eight weeks suggests perhaps that recovery was associated with the emergence of immunity by two months following the appearance of uveitus. This is supported in part by our previous study, which supplied evidence that animals were protected from further uveitis on subsequent reinfections (after they had recovered from their initial infection) by a mycelial or yeast form of the fungus. Similar protection was also seen in animals that had prior exposures to heat-killed organisms. Moreover, onset of the ocular changes occurred usually two weeks after infection. This evidence strongly suggests that the experimental choroiditis may be immunologically induced. H. capsulatum recovered from infected eyes (Groups I and II) produced identical ocular lesions clinically and histopathologically when injected into normal animals (Groups IA and IIA). Fulfillment of Koch's postulates in experimental ocular histoplasmosis was achieved within only one month following the appearance of uveitis. This may be of fundamental importance in that efforts to demonstrate a causal relationship between the ocular picture and benign systemic histoplasmosis have been unsuccessful in man. Because of the striking similarity between the experimental choroiditis in rabbits and the changes observed in presumed ocular histoplasmosis in man, studies in primates are necessary. Since the ocular anatomy is similar in monkeys and in man, there remains the necessity to reproduce the hemorrhagic disciform lesion of the macula, which represents the gravest aspect of presumed ocular histoplasmosis.

Animals↗