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Biomedical subjects

W R Green

Publications and source records attributed to W R Green.

At least 19 recordsLinked to original sources
PubMed1992

Generation of anti-AKR/gross murine leukemia virus cytotoxic T lymphocytes (CTL). An analysis of precursor CTL frequencies in the AKR.H-2b and C57BL/6 mouse strains.

C57BL/6 mice, after immunization and secondary in vitro restimulation with AKR/Gross murine leukemia virus (MuLV)-induced tumors, generate AKR/Gross MuLV-specific CTL. After similar immunization protocols, AKR-H-2b mice fail to generate CTL specific for AKR/Gross MuLV. The basis for nonresponsiveness in AKR.H-2b mice is unknown, however, unlike C57BL/6 mice, AKR.H-2b mice carry endogenous proviruses and express N-ecotropic viral Ag. Thus, clonal deletion of pCTL populations due to the expression of AKR/Gross MuLV-like Ag is a likely mechanism for the nonresponsiveness. To determine if nonresponsiveness is due to clonal deletion, limiting dilution cultures were performed to assess the presence of pCTL specific for AKR/Gross MuLV. Our study demonstrates that the frequencies of pCTL specific for AKR/Gross MuLV are similar in both the responder C57BL/6 and nonresponder AKR.H-2b strains. The observation that normal levels of AKR/Gross MuLV-specific pCTL exist in AKR.H-2b mice, suggests that clonal deletion of pCTL is not responsible for the inability of AKR.H-2b mice to generate anti-AKR/Gross virus-specific CTL.

Animals↗
PubMed1992

CD4-CD8+ T lymphocytes mediate AKR/gross murine leukemia virus nonresponsiveness in moderately aged AKR.H-2b:Fv-1b mice.

Previously we reported that as AKR.H-2b:Fv-1b mice become older than 9 wk of age they begin to specifically lose the ability to generate anti-AKR/Gross murine leukemia virus (MuLV) CTL responses after immunization and in vitro restimulation with cells expressing AKR/Gross MuLV-encoded Ag. Interestingly, the frequency of virus-specific precursor cytotoxic T lymphocytes (CTL) observed in moderately-aged AKR.H-2b:Fv-1b mice was not substantially decreased from that found in their young responder counterparts. To further investigate the mechanism(s) responsible for the inability of moderately-aged AKR.H-2b:Fv-1b mice to mount AKR/Gross MuLV-specific CTL responses, adoptive transfer experiments were performed in the present study. Transferring splenocytes from moderately-aged AKR.H-2b:Fv-1b donors into young AKR.H-2b:Fv-1b recipients resulted in inhibition of AKR/Gross MuLV-specific CTL responsiveness. Anti-Thy-1.1 plus complement depletion of T cells from the donor cell population before adoptive transfer resulted in a near complete restoration of AKR/Gross MuLV responsiveness of young recipient AKR.H-2b:Fv-1b mice suggesting that the inhibition observed in moderately aged mice was mediated by T lymphocytes. Additional experiments using depletion of T subsets before cell transfer demonstrated that inhibition of AKR/Gross MuLV-specific CTL responsiveness was mediated by a CD4-CD8+ T lymphocyte.

AKR murine leukemia virus↗
PubMed1992

Ocular histopathologic characteristics of cobalamin C type vitamin B12 defect with methylmalonic aciduria and homocystinuria.

The eyes of a 22-month-old girl with the cobalamin C complementation type of combined methylmalonic aciduria and homocystinuria were studied with light and electron microscopy. We observed vacuolization of the iris pigment epithelium, loss of photoreceptors in the central 3.3 mm of the macula, partial loss of the nerve fiber and ganglion cell layers between the fovea and optic disk, and partial optic atrophy. The sclera in the posterior pole was thickened with deposition of mucopolysaccharide. Electron microscopy showed inclusions containing fine granular material in conjunctival fibrocytes; corneal epithelium, keratocytes, and endothelial cells; iris pigment epithelium; ganglion cells; retinal pigment epithelium; and choroid and scleral fibrocytes. Enlarged mitochondria and clear vacuoles distended the corneal endothelial cells. We found evidence of possible lysosomal dysfunction and mucopolysaccharide storage, as well as a clinicopathologic correlation of the macular degeneration in this disease.

Eye↗
PubMed1992

Clinicopathologic correlation of occult choroidal neovascularization in age-related macular degeneration.

We report the clinicopathologic features of an eye with occult choroidal neovascularization associated with age-related macular degeneration. Ophthalmoscopic findings at presentation included subretinal fluid and lipid. We noted angiographic staining of irregularly elevated areas of retinal pigment epithelium. In the late phase of the angiogram, fluorescein leakage at the level of the outer retina was observed that did not correspond to well-demarcated areas of hyperfluorescence in earlier phases. The patient was randomized to treatment in a pilot trial comparing the effects of grid laser treatment with the effects of no treatment for occult choroidal neovascularization. Three weeks after treatment, some of the subretinal fluid had cleared and vision improved. The patient died 6 weeks after laser treatment. Histopathologic study disclosed a subretinal pigment epithelial fibrovascular membrane. Neovascularization originated from the choroid.

Aged↗
PubMed1992

Toxicity of intravitreous ceftazidime in primate retina.

Squirrel monkeys were anesthetized and given intravitreous injections of 0.1 mL of balanced salt solution containing 0 mg (two eyes), 1 mg (three eyes), 2.25 mg (three eyes), or 10 mg (three eyes) of ceftazidime, a third-generation cephalosporin that provides excellent coverage for gram-negative infections. Ophthalmoscopic examinations were performed 48 hours after the injections and results were completely normal in all eyes except for those that were injected with 10 mg of ceftazidime, all three of which showed the appearance of cystic change in the macula. The monkeys were killed and the eyes were removed and examined by light and electron microscopy. All eyes were normal by light microscopy except for those injected with 10 mg of ceftazidime, which showed disruption of photoreceptors (primarily outer segments) in the foveas with cystic changes in all three and macular holes in two of three. Electron microscopy showed mild swelling of mitochondria and perinuclear halos around photoreceptor nuclei in both control eyes and in eyes injected with 1 and 2.25 mg. An eye injected with 10 mg showed severe damage to central photoreceptor outer segments consisting of disruption of plasma membranes and accumulation of intracytoplasmic granular material. Inner segments showed mild changes and there was loss of apical microvilli of the retinal pigmented epithelium. The inner retina was normal. These data suggest that high doses of intravitreous ceftazidime show toxicity primarily to photoreceptor cells, but a dose of 2.25 mg is safe as studied in this model and can be used instead of intravitreous aminoglycosides that have a narrow therapeutic window.

Animals↗
PubMed1992

Retinal hemorrhages in newborn piglets following cardiopulmonary resuscitation.

OBJECTIVE: To determine whether conventional cardiopulmonary resuscitation causes retinal hemorrhages in piglets. DESIGN: Nonrandomized observations. SETTING: Animal physiology laboratory. PARTICIPANTS: Six 3.5- to 4.5-kg piglets. INTERVENTIONS: Fifty minutes of conventional, closed chest cardiopulmonary resuscitation. MEASUREMENTS/MAIN RESULTS: Intrathoracic venous pressure (right atrium) and intracranial venous pressure (sagittal sinus) were directly measured. At 5 minutes of cardiopulmonary resuscitation, the mean (+/- SEM) sagittal sinus pressure was 41 +/- 8 mm Hg and the mean right atrial pressure was 58 +/- 9 mm Hg. The pressures were sustained throughout the 50 minutes of cardiopulmonary resuscitation. At autopsy, there was no gross or microscopic evidence of retinal hemorrhages. CONCLUSION: These results support the conclusion that cardiopulmonary resuscitation does not cause retinal hemorrhages.

Animals↗
PubMed1992

Inadvertent corneal button inversion during penetrating keratoplasty.

Inadvertent inversion of a corneal button during corneal transplantation for pseudophakic bullous keratopathy occurred with subsequent intense intraocular inflammation but a relatively compact graft. The diagnosis was made by a superficial corneal biopsy of Descemet's membrane, and a repeat corneal transplantation resulted in a clear graft and no evidence of epithelial downgrowth. Histology revealed the persistence of the donor epithelium on the inverted donor button but no residual endothelium on the externalized surface. Although laboratory attempts to duplicate an inversion of a corneal graft revealed that this occurs only with considerable difficulty, this operative complication may explain some of the unexpected primary graft failures reported in the literature.

Aged↗
PubMed1992

Histopathology of commotio retinae.

The pathogenesis of commotio retinae in animal models has included extracellular edema, intracellular edema, and photoreceptor outer segment disruption. Histopathologic findings obtained within 24 hours of blunt trauma in a human eye with clinically-observed commotio retinae revealed photoreceptor outer segment disruption and damage to the retinal pigment epithelium. The major site of injury in commotio retinae seems to be at the level of the photoreceptor outer segment-retinal pigment epithelium junction.

Adult↗
PubMed1992

A histopathologic study of the pigmented fundus lesions in familial adenomatous polyposis.

A postmortem examination of the eyes of a 61-year-old woman with familial adenomatous polyposis was performed using light microscopy and transmission and scanning electron microscopy. Numerous lesions of the retinal pigment epithelium (RPE) were identified, which had one of three basic configurations: a monolayer of hypertrophic cells, a mound of RPE cells interposed between the RPE basement membrane and the inner collagenous layer of Bruch's membrane, or a multilayered mound of hyperplastic cells. The presence of abnormal pigment granules in cells within the lesions and cells from areas of grossly normal RPE indicates a generalized defect in melanogenesis. Although the pigmented fundus lesions of familial adenomatous polyposis are often referred to clinically as congenital hypertrophy of the RPE, the prominent component of cellular hyperplasia more appropriately designates them as hamartomas of the RPE. Their development is likely the result of the same loss of regulatory control of cell growth and replication that gives rise to the multiple colorectal polyps and soft tissue tumors that characterize this condition.

Adenocarcinoma↗
PubMed1992

Pathologic findings in pathologic myopia.

A retrospective study was conducted of 308 eyes with pathologic myopia obtained from 202 patients (23 surgical eyes; 285 post mortem eyes) over a 67-year period. Histopathologic findings and percentage of eyes affected, in decreasing order of frequency, were myopic configuration of the optic nerve head, 37.7%; posterior staphyloma, 35.4%; degenerative changes of the vitreous, 35.1%; cobblestone degeneration, 14.3%; myopic degeneration of the retina, 11.4%; retinal detachment, 11.4%; retinal pits, holes, or tears, 8.1%; subretinal neovascularization, 5.2%; lattice degeneration, 4.9%; Fuchs spot, 3.2%; and lacquer cracks, 0.6%. The reasons for enucleation in the surgically obtained eyes included, in decreasing order of frequency: degeneration after retinal detachment; secondary glaucoma; endophthalmitis; postsurgical epithelial ingrowth; expulsive hemorrhage; degeneration after cataract extraction; and presumed intraocular tumor. Clinicopathologic correlations are discussed.

Adolescent↗
PubMed1992

Clinicopathologic study of idiopathic macular pucker in children and young adults.

Clinically significant idiopathic macular pucker was observed in 11 patients aged 30 years or younger. In these patients, the tissue was well defined and fibrous in appearance, in contrast to the thin, cellophane appearance that is typical of macular pucker in elderly patients. Vitrectomy and epiretinal membrane peeling were performed in each case. Visual acuity improved after surgery in seven cases and worsened in one case, and follow-up data was not obtained in three cases. Recurrent membranes were noted in four cases, two of which detached spontaneously. Ultrastructural studies were performed on the removed specimens in each case. Myofibroblasts, myoblastic differentiation of retinal pigment epithelial cells and fibrous astrocytes, and new collagen formation were more common than in idiopathic macular pucker in older patients. The clinical and ultrastructural features of juvenile macular pucker reflect more rapidly changing, contractile tissue compared with the usually more quiescent features in series involving older patients.

Adolescent↗
PubMed1992

Foveal hypoplasia in complete oculocutaneous albinism. A histopathologic study.

Histopathologic and ultrastructural findings in an eye from a patient with complete oculocutaneous albinism are reported. Examination revealed posterior embryotoxon, high myopia, no foveal differentiation, and absence of melanin pigment in all ocular structures. A few nonmembrane-bound electron-dense granules of lipofuscin were present in the iris and retinal pigment epithelial cells.

Aged↗
PubMed1992

Clinicopathologic study of bilateral macular holes treated with pars plana vitrectomy and gas tamponade.

The clinicopathologic findings of light and electron microscopic examination of a 78-year-old woman who underwent successful bilateral pars plana vitrectomy for bilateral stage III macular holes are reported. Examination disclosed anatomical repair of the full-thickness macular holes by glial cell proliferation in the left eye. The hole apparently collapsed with no glial cell proliferation in the right eye. The photoreceptors adjacent to the healed macular holes appeared normal. Defects in the internal limiting membrane in the foveal area were noted in both eyes.

Aged↗
PubMed1992

Cytolytic T lymphocytes specific for tumors and infected cells from mice with a retrovirus-induced immunodeficiency syndrome.

LP-BM5 retrovirus complex-infected C57BL/6 mice develop immunodeficiency, somewhat analogous to AIDS, termed murine AIDS (MAIDS). After secondary stimulation with syngeneic B-cell lymphomas from LP-BM5-infected mice, C57BL/6 mice produced vigorous CD8+ cytotoxic T lymphocytes specific for MAIDS-associated tumors. An anti-LP-BM5 specificity was suggested because spleen and lymph node cells from LP-BM5-infected mice served as target cells in competition assays, and cells from LP-BM5, but not ecotropic, virus-infected mice functioned as secondary in vitro stimulators to generate cytotoxic T lymphocytes to MAIDS tumors.

Animals↗
PubMed1992

Peripapillary subretinal neovascularization. A review.

Peripapillary choroidal neovascularization is an important feature in the pathogenesis and treatment of a number of disorders affecting the optic nervehead and adjacent chorioretinal areas. Although less well understood than its macular counterpart, peripapillary subretinal neovascularization possesses characteristic clinical and histopathologic features that directly affect its prognosis and management. This review provides a summary of the diseases in which peripapillary subretinal neovascularization occurs and an overview of studies on the natural history, clinicopathologic findings, and therapy. In addition, a pathogenetic model of peripapillary subretinal neovascularization is discussed based on these findings.

Choroid Neoplasms↗
PubMed1992

Multicentric gastrointestinal and extraintestinal leiomyosarcomatosis: a case report.

This article presents a case of synchronous polypoid primary adenocarcinoma of the transverse colon without lymph node or distance metastasis. During the postmortem examination, polypoid smooth muscle tumors in the patient's gastrointestinal tract and extensive extraintestinal smooth muscle tumors in the patient's liver, lungs, and visceral organs, including the diaphragm, parathyroid gland, bone marrow of the vertebrae, and subcutaneous tissue of the left wrist, were reviewed to determine their origin. Histomorphologically, all of the tumors were classified as leiomyosarcomas.

Adenocarcinoma↗