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Biomedical subjects

J Guy

Publications and source records attributed to J Guy.

At least 19 recordsLinked to original sources
PubMed1992

Surfactant-producing rabbit pulmonary alveolar type II cells synthesize and secrete an antiinflammatory protein, uteroglobin.

Neonatal respiratory distress syndrome (RDS) caused by surfactant deficiency is a common disorder in premature infants. Exogenous surfactant therapy improves survival in infants with RDS. However, the phospholipid component of the surfactant has been suggested to be inactivated by a phospholipid hydrolyzing enzyme, phospholipase A2 (PLA2). Although alveolar type II cells produce the surfactant, it is not known whether these cells have any mechanism to protect surfactant from PLA2 hydrolysis. Since alveolar Clara cells express uteroglobin (UG), a PLA2 inhibitory and antiinflammatory protein, and since it has been suggested that alveolar type II cells are derived from Clara cells, we sought to elucidate whether type II cells are also capable of expressing UG gene. By using radioimmunoassay, immunoprecipitation and Western blotting techniques we demonstrate for the first time that type II cells, isolated from mature rabbit lungs, synthesize and secrete UG. The transcription of the UG gene was detected by in situ hybridization using rabbit UG cDNA probe. These results imply that UG, synthesized by type II cells, may protect both endogenous and exogenous surfactant from PLA2 hydrolysis. Moreover, the antiinflammatory properties of UG may prevent the development of chronic inflammatory lung disease, a frequent complication of RDS.

Animals↗
PubMed1992

Enhancement and demyelination of the intraorbital optic nerve. Fat suppression magnetic resonance imaging.

Conventional spin-echo magnetic resonance imaging (MRI) of intraorbital optic neuritis is hampered by the adjacent high signal and chemical shift artifact of orbital fat. Frequency-selective saturation pulse MRI reduces these problems and was used to determine its utility in evaluation of intraorbital optic neuritis. Eight consecutive patients with optic neuritis underwent MRI within 1 week of the onset of visual loss. Conventional MRI with T1, proton density, and T2 weighting and frequency-selective saturation pulse MRI with T1, proton density, and T2 weighting were performed. After administration of intravenous gadopentetate dimeglumine, T1-weighted conventional and frequency-selective saturation pulse MRI were performed. Frequency-selective saturation pulse MRI showed gadopentetate dimeglumine enhancement in the intraorbital optic nerve in 7 patients and the intracranial optic nerve in 3 patients. Conventional MRI failed to show optic nerve gadopentetate dimeglumine enhancement in patients with intraorbital lesions, but did show intracranial lesions. Frequency-selective saturation pulse MRI showed bilateral optic nerve enhancement in 3 patients with unilateral visual signs and symptoms. Proton density and T2-weighted conventional MRI of the brain showed no convincing signal aberrations in the optic nerves. In the MRI evaluation of intraorbital optic neuritis: (1) frequency-selective saturation pulse fat suppression MRI is superior to T1-weighted conventional MRI in the detection of gadopentetate dimeglumine enhancement; (2) frequency-selective saturation pulse proton density and T2-weighted MRI is superior to proton density and T2-weighted conventional MRI; (3) frequency-selective saturation pulse MRI showed gadopentetate dimeglumine enhancement as well as proton density/T2-weighted signal aberration in exactly the same portion of the intraorbital optic nerve.

Adult↗
PubMed1992

Intraorbital optic nerve and experimental optic neuritis. Correlation of fat suppression magnetic resonance imaging and electron microscopy.

To provide magnetic resonance imaging (MRI)-ultrastructural correlations of demyelinating lesions of the intraorbital optic nerve, the authors performed gadolinium-enhanced/T2-weighted fat-suppressed MRI and transmission electron microscopy of the optic nerves of animals with experimental allergic encephalomyelitis. Gadolinium enhancement of the optic nerve adjacent to the globe was seen on fat-suppressed T1-weighted MRI as early as 3 days after antigenic sensitization, increased in severity involving longer segments of nerve at 10 to 14 days, and persisted at 30 days. Gadolinium enhancement preceded T2-weighted signal aberrations. Ultrastructural evaluation of the intraorbital nerve revealed: (1) expansion of the extracellular space and inflammatory infiltrate that correlated with the intensity of gadolinium enhancement; (2) the degree of demyelination correlated with T2-weighted signal aberrations; (3) as deduced from gadolinium enhancement and T2 signal aberrations, breakdown of the blood-brain barrier preceded widespread demyelination; (4) lesions appeared to start at the optic nerve insertion into the globe and then progress toward the orbital apex.

Adipose Tissue↗
PubMed1992

Human antiglioma monoclonal antibodies from patients with astrocytic tumors.

The current management of malignant gliomas is unsatisfactory compared to that of other solid tumors; the expected median survival period is less than 1 year with the patient undergoing conventional surgery, radiotherapy, and chemotherapy treatment. Immunological reagents could be a useful adjunct. Human monoclonal antibodies derived from patients with astrocytic tumors might recognize subtle antigenic specificities that would differ from those recognized by xenogeneic (murine) systems. Five hybridomas, designated as BT27/1A2, BT27/2A3, BT32/A6, BT34/A5, and BT54/B8, were produced from the fusion of peripheral blood lymphocytes of four patients with astrocytic tumors to the human myeloma-like cell line TM-H2-SP2. This cell line has a 46, XX karyotype and is negative for hypoxanthine guanine phosphoribosyltransferase. All five human monoclonal antibodies produced 2.4 to 44 micrograms/ml of immunoglobulin M, had a similar but not identical pattern of reactivity against a panel of human tumor cell lines, and failed to react with normal human astrocytes. Labeling of four neuroectodermal tumor explant cultures by BT27/2A3 was demonstrated by flow cytometry. Karyotyping of three of the five hybridomas demonstrated that two were pseudodiploid (2-3n) and one hypodiploid (less than 2n). The monoclonality of the hybridomas was evaluated by Southern blot analysis of JH gene rearrangements, revealing two types of rearrangements for each hybridoma, both consistent with monoclonality. Preliminary antigen characterization indicated that at least four of the five human monoclonal antibodies were directed to cell-surface glycolipids.

Adolescent↗
PubMed1991

Inhibition of ribonucleotide reductase by gallium in murine leukemic L1210 cells.

Our previous studies of the mechanism of cell growth inhibition by gallium have suggested that the block in cellular iron uptake induced by transferrin-gallium results in an inhibition of the iron-dependent M2 subunit of ribonucleotide reductase. However, it is not known whether the inhibitory effect of gallium on ribonucleotide reductase is solely the result of limiting iron availability for enzyme activity or whether a direct effect of intracellular gallium on the enzyme is also involved. In the present study, utilizing a cell-free assay, we show that gallium nitrate directly inhibits CDP and ADP reductase activity. Inhibition of DNA synthesis by gallium nitrate thus appears to be due to a combination of a block in iron availability to ribonucleotide reductase and a direct inhibition of the enzyme by gallium.

Animals↗
PubMed1991

Central retinal and posterior ciliary artery occlusion after particle embolization of the external carotid artery system.

A 15-year-old boy underwent neuroradiologic embolization of the left internal maxillary artery with polyvinyl alcohol to stop traumatic epistaxis after failure of surgical clipping and nasal packing. Selective catheterization of the external carotid artery before embolization showed a faint choroidal blush. Although the procedure provided hemostasis, embolization to the central retinal artery and ciliary arteries resulted in loss of vision. The route of the emboli to the eye was via the anastomotic network of the lacrimal artery supplied by the external carotid artery system. Neuroradiologic embolization of the external carotid artery is an effective mode of therapy for dural-cavernous fistulas when fed by the external carotid artery system. Because the blood flow to the brain and eye is predominantly supplied by the internal carotid artery, embolization of the external carotid artery is considered relatively safe. The authors document the importance of recognition of the choroidal blush during selective external carotid artery angiography as a sign of collateral blood flow to the eye. Physicians and patients need to be aware of the risk of blindness as a complication of external carotid artery embolization when this sign is present.

Adolescent↗
PubMed1991

Radiation-induced optic neuropathy: a magnetic resonance imaging study.

Optic neuropathy induced by radiation is an infrequent cause of delayed visual loss that may at times be difficult to differentiate from compression of the visual pathways by recurrent neoplasm. The authors describe six patients with this disorder who experienced loss of vision 6 to 36 months after neurological surgery and radiation therapy. Of the six patients in the series, two had a pituitary adenoma and one each had a metastatic melanoma, multiple myeloma, craniopharyngioma, and lymphoepithelioma. Visual acuity in the affected eyes ranged from 20/25 to no light perception. Magnetic resonance (MR) imaging showed sellar and parasellar recurrence of both pituitary adenomas, but the intrinsic lesions of the optic nerves and optic chiasm induced by radiation were enhanced after gadolinium-diethylenetriaminepenta-acetic acid (DTPA) administration and were clearly distinguishable from the suprasellar compression of tumor. Repeated MR imaging showed spontaneous resolution of gadolinium-DTPA enhancement of the optic nerve in a patient who was initially suspected of harboring recurrence of a metastatic malignant melanoma as the cause of visual loss. The authors found the presumptive diagnosis of radiation-induced optic neuropathy facilitated by MR imaging with gadolinium-DTPA. This neuro-imaging procedure may help avert exploratory surgery in some patients with recurrent neoplasm in whom the etiology of visual loss is uncertain.

Aged↗
PubMed1991

Maintenance of myelinated fibre g ratio in acute experimental allergic encephalomyelitis.

The spectra of myelin sheath thickness and g ratio (axon diameter/fibre diameter) of guinea pig optic nerves for 8 animals with acute experimental allergic encephalomyelitis (EAE) were compared with those for 6 normal animals. The mean myelin sheath thickness of 0.12 microns for the animals with EAE was significantly lower than the value of 0.16 microns for the normal animals. Since fibre diameter comprises axon diameter plus the thickness of its surrounding myelin sheath, a reduction in mean fibre diameter from 1.52 microns in normals to 1.20 microns in EAE was expected, but it was surprising to find that a mean g ratio of 0.85 obtained for normal nerves was not substantially different from a value of 0.86 for demyelinated optic nerves. A decrease in the mean axon diameter of 1.24 microns for normal animals to 0.94 microns for those with EAE tended to offset the decrease in mean myelin sheath thickness and contributed to the relative stability of the g ratio with acute demyelination. Our results showing reduction in axonal calibre and myelin sheath thickness may offer an explanation for apparent discrepancies between electrophysiological delays in conduction characteristics of experimental and, if not the result of a maturational effect on myelination, human primary demyelinating disorders associated with the scant histopathological demyelination of initial attacks of EAE and the visually asymptomatic patients with multiple sclerosis.

Animals↗
PubMed1990

Hydrogen peroxide localization in experimental optic neuritis.

The association of reactive oxygen species to altered permeability of the blood-brain barrier in acute experimental encephalomyelitis was investigated by ultrastructural cytochemical localization of hydrogen peroxide (H2O2) to sites in the optic nerve previously identified by extravasation of intravascular horseradish peroxidase. Using a modified cerium method, we found electron-dense cerium-derived H2O2 reaction product was localized to the perivascular space at the lamina retinalis, lamina choroidalis, and lamina scleralis. In the optic nerve head, electron-dense reaction product was observed in the presence of intravascular leukocytes, although adjacent perivascular and interstitial inflammatory cells at this site were scant. In the myelinated retrobulbar optic nerve, cerium-derived H2O2 reaction product was seen in the intravascular space of blood vessels and surrounding perivascular and interstitial foci of inflammatory cells. Reaction product was also observed in the extracellular space adjacent to the plasmalemma of axons and glial cells in the optic nerve head and retrobulbar nerve. The perivascular and intravascular distribution of cerium-derived reaction product suggests that H2O2 may play a role in the pathogenesis of altered vascular permeability in experimental optic neuritis and supports our previous observations of suppression of blood-brain barrier permeability by detoxification of H2O2 with the exogenous administration of antioxidant enzymes.

Animals↗
PubMed1990

Gadolinium-DTPA-enhanced magnetic resonance imaging in experimental optic neuritis.

Magnetic resonance imaging (MRI) with gadolinium-diethylenetriaminepentaacetic acid (Gd-DTPA) was used to investigate disruption of the blood-optic nerve barrier associated with acute autoimmune demyelination. Leakage of Gd-DTPA was seen in the optic nerves and optic chiasm of adult guinea pigs sensitized for acute experimental allergic encephalomyelitis, but not in normal unsensitized animals. This finding occurred as early as 5 to 8 days after antigenic sensitization with the myelin emulsion and before the onset of paralysis or ataxia. Pathologic examination at this early stage of experimental allergic encephalomyelitis showed an absence of demyelination in the optic nerves and optic chiasm, although scant perivascular foci of inflammatory cells were seen. Leakage of Gd-DTPA in the optic nerve before demyelination of this white matter tract illustrates that increased permeability of the blood-optic nerve barrier is an early, if not the initial, event in autoimmune demyelination, and the optic nerve is a common site of central nervous system involvement during the initial phase of acute experimental allergic encephalomyelitis. Findings in this animal model appear comparable with the results of MRI with Gd-DTPA in patients with optic neuritis, and they suggest that disruption of the blood-optic nerve barrier is a common denominator for both disorders of primary demyelination.

Animals↗
PubMed1990

Pathogenesis of corneal oedema associated with herpetic eye disease.

Corneal oedema and stromal disease, induced in rabbits by intrastromal injection of herpes simplex virus, type 1, strain RE (HSV-1, RE), reached a peak of 12-15 days after infection. Corneal oedema as measured by ultrasonic pachymetry, and stromal disease as measured by a subjective scoring system, were closely related for 30 days after infection. Morphometric analysis of wide field specular micrographs showed that no immediate endothelial cell damage occurred in either control or HSV-1 infected corneas. Alizarin red S staining of corneas taken during the period of most severe oedema indicated no significant endothelial cell loss; however, visual inspection indicated numerous staining abnormalities. Scanning and transmission electron microscopy provided evidence of an intact endothelial layer possessing integrated infiltrating cells. Virus antigen could not be detected on endothelial cells by immunoperoxidase staining at any time during development of corneal oedema. The results indicate that corneal oedema associated with HSV-1 induced disease can occur in the absence of detectable virus replication and cytolysis of corneal endothelial cells.

Animals↗
PubMed1990

Treatment of visual loss in pseudotumor cerebri associated with uremia.

Ten patients with pseudotumor cerebri associated with renal insufficiency had papilledema and elevated intracranial pressure, but neurologic examinations and CT were normal. The 40% frequency of severe visual loss, 20/100 or worse, was higher than expected for pseudotumor cerebri. While furosemide was effective in 3 patients with renal transplants, administration of corticosteroids to 2 other patients did not halt progressive loss of vision. The visual function of 2 patients deteriorated even after lumboperitoneal shunting. Five patients underwent fenestration of the optic nerve sheath. This procedure improved the visual acuity of 3 patients and stabilized vision in the others. While the pathogenesis of pseudotumor cerebri in renal insufficiency is unknown, optic nerve sheath fenestration is the surgical treatment of choice for visual loss unresponsive to medical therapy.

Adolescent↗
PubMed1990

[University by radio and television in Great Britain. The Open University].

There are some 20 years since Great Britain was given a new and important University (established by a Royal Charter in 1969), especially intended for students wanting to achieve their education at home. The whole teaching, guided by tutors, is supported by various materials: booklets, audio- and videotapes which are completed by television and radio broadcasts for many courses and informations. After successful examinations are obtained the usual degrees and certificates delivered by the British Universities. Furthermore, this kind of education begins to be available in a few other countries (Belgium, Luxembourg, The Netherlands, Cyprus, Hong Kong).

Audiovisual Aids↗
PubMed1990

Gadolinium-DTPA-enhanced magnetic resonance imaging in optic neuropathies.

Magnetic resonance imaging (MRI), after intravenous administration of the paramagnetic agent gadolinium-diethylenetriaminepentaacetic acid (Gd-DTPA), showed enhancement of the optic nerve in 7 of 13 patients with acute optic neuritis. Four of these patients had Gd-DTPA enhancement of the intracranial optic nerve and two had involvement of the optic nerve at the orbital apex, ipsilateral to the eye with visual loss. Gadolinium-DTPA enhancement of both intracranial optic nerves was seen in one of two patients with bilateral retrobulbar neuritis. Two patients with acute radiation-induced optic neuropathy also had Gd-DTPA enhancement of the intracranial optic nerve. The authors recommend MRI with Gd-DTPA as the neuro-diagnostic procedure of choice for visualization of increased permeability of the blood-brain barrier in acute optic neuritis and radiation-induced optic neuropathy.

Adolescent↗
PubMed1989

Spectra of G ratio, myelin sheath thickness, and axon and fiber diameter in the guinea pig optic nerve.

The spectra of fiber and axon diameter, myelin sheath thickness, fiber density, and g ratio of the optic nerve were analyzed for the strain-13 guinea pig, an animal extensively utilized in the investigation of experimental disorders of demyelination. Our detailed analytical study of the normal guinea pig optic nerve provides the basis for comparison to disease states and the morphology of other species. As in the rat, mouse, and chipmunk, fiber diameters in the guinea pig were unimodal, but dissimilar to the trimodal fiber spectra of the cat and primate. The predominance of medium-sized fibers (0.80-2.00 microns), common to most species, contributed to the larger mean fiber diameter (1.45 microns) of the guinea pig optic nerve, in which small fibers (0.50 microns or less) were infrequent and fibers larger than 5.00 microns in diameter, seen in the cat and primate, were absent. While myelin sheath thickness increased with axon diameter in the guinea pig, as in other species, a g ratio of 0.81 in the guinea pig was greater than in most mammals. Since conduction velocity is dependent on axon size, as well as myelin properties, the relatively larger mean axon diameter of the guinea pig optic nerve (1.18 microns) may compensate for the decrease in its myelination.

Animals↗
PubMed1989

Contralateral trochlear nerve paresis and ipsilateral Horner's syndrome.

Two patients had paresis of the trochlear nerve contralateral to the site of lesions in the brainstem. Both patients had ipsilateral blepharoptosis and miosis suggesting oculosympathetic paresis from involvement of the descending sympathetic tract, adjacent to the fourth cranial nerve nucleus and its fascicles, in the caudal mesencephalon. Cerebral antiography documented an arteriovenous malformation of the brainstem in Case 1. Magnetic resonance imaging disclosed a lesion of high signal intensity on T2-weighted images involving the dorsal mesencephalon in Case 2. Involvement of the superior cerebellar peduncle produced ipsilateral dysmetria and ataxia. Lesions involving the fourth cranial nerve nucleus or its fascicles, before decussation in the superior medullary velum, and adjacent sympathetic fibers may produce an ipsilateral Horner's syndrome and contralateral superior oblique muscle paresis.

Adult↗