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Biomedical subjects

D R Anderson

Publications and source records attributed to D R Anderson.

At least 253 records · Page 14Linked to original sources
PubMed1982

Heterogeneity of asparagine-linked oligosaccharides of five glycosylation sites on immunoglobulin M heavy chain from mineral oil plasmacytoma 104E.

Mouse myeloma immunoglobulin IgM heavy chains were cleaved with cyanogen bromide into nine peptide fragments, four of which contain asparagine-linked sites of glycosylation. Three of these glycopeptides contain a single site located at asparagines 171, 403, and 563 in the sequence of the intact heavy chain. Another glycopeptide contains two sites of glycosylation at asparagines 332 and 364. All sites contain multiple oligosaccharide structures with a trend towards increased processing from the COOH to the NH2 terminus. Structures present at asparagine 563, located only exclusively high mannose oligosaccharides. Asparagine 403, located penultimate to the COOH terminus, has a major component that is of a complex nature but is incompletely processed. Other sites contain predominantly complex structures consisting of biantennary or triantennary branches. The unusual structure found at asparagine 403 contains fucose even though only one branch has been processed to a terminal galactose. These studies suggest that each site has a unique set of heterogeneous oligosaccharides derived from a complex processing system which utilizes a combination of "position completeness" and polypeptide structure to determine final carbohydrate structure.

Amino Acid Sequence↗
PubMed1982

Outer retina ischemic infarction--a newly recognized complication of cataract extraction and closed vitrectomy. Part 2. An animal model.

Intraocular pressure was artificially elevated above systolic blood pressure in 40 owl monkey eyes. Diffuse retinal whitening of the posterior pole and subsequent retinal pigment epithelial disruption were produced in nine of ten eyes with high pressure for 90 minutes or longer, but also in a few eyes with high pressure for a shorter duration. Fluorescein angiography and histologic examination demonstrated damage of the photoreceptors and retinal pigment epithelium with sparing of the inner retinal layers. This animal model duplicates the acute visual loss due to outer retinal infarction that sometimes occurs after closed vitrectomy or after continuous external ocular compression in preparation for surgery.

Animals↗
PubMed1982

Programmed visual field testing.

The use of programmed static spot-checking is remarkably accurate in detecting the presence of visual field defects, even the earliest abnormality, provided the correct stimulus (or stimuli) is chosen to check an appropriate number of spots, and the location of each missed response is retested. Automatic quantitation of visual field defects (so it can later be determined if the defects are worsening) can be accomplished automatically with some of the more expensive new instruments. The less elaborate instruments require repetitive testing or manual interaction, achieving accurate results, but typically with a cumbersome record of the results that is difficult to interpret. An efficient plan for the usual office at present is to use an automated spot-checking instrument for screening and diagnosis, but to depend upon the tangent screen or Goldmann perimeter for quantitation unless the most expensive automated instruments can be afforded.

Automation↗
PubMed1981

Rapid axonal transport in primate optic nerve. Distribution of pressure-induced interruption.

Six primate eyes were studied after four hours of elevated intraocular pressure. Tissue specimens from the region of the lamina cribrosa were examined in cross section by transmission electron microscopy. Interruption in fast orthograde and retrograde axonal transport was identified in individual axons by noting accumulation of membraneous microorganelles, such as mitochondria and microvesicles within axon cylinders. Although organelle accumulation varied from bundle to bundle, involvement of individual axons was diffuse across the extent of a specific axon bundle. This observation contradicts the apparent association of axonal transport block with crosswise-oriented trabecular beams at the level of the lamina cribrosa as seen in tissue specimens examined in longitudinal section. It also fails to support the notion that blocked axonal transport with elevated pressure is produced by kinking of axons at the lamina.

Animals↗
PubMed1981

Documentation of change in problem behaviors among anxious and hostile-aggressive children enrolled in a therapeutic preschool program.

A relatively simple, straightforward procedure is utilized to identify and document changes in problem behaviors among children enrolled in a therapeutic preschool program. Results of two outcome measures indicated a significant overall reduction in problem behaviors for the total group. When subgroups of anxious and hostile/aggressive children were considered, however, there was a significantly greater probability that anxious children would benefit more from the program than hostile/aggressive children. The need to consider subgroups of patients when documented treatment effectiveness is emphasized, and the advantage of building documentation techniques into the record-keeping system is discussed.

Aggression↗
PubMed1981

Morphology of axonal transport abnormalities in primate eyes.

The ultrastructure of the retina and optic nerve head was studied in primate eyes after central retinal artery occlusion. Within 2 hours of the vascular occlusion the inner retinal layers undergo watery (isosmotic) swelling. This watery swelling of axons and astroglia extends into the nerve head as far back as the anterior boundary of the scleral lamina cribrosa. The swelling is increased 4 hours after the occlusion, and by 24 hours disintegration has occurred. At the optic nerve head mitochondria and vesicles of smooth endoplasmic reticulum begin to accumulate within 2 hours. The accumulation increases at 4 hours and persists to 24 hours. The watery swelling seems characteristic of ischaemic axons. Membranous organelles accumulate at the boundary of an ischaemic zone when material carried by axonal transport is brought via the healthy axon segment to the boundary, but they cannot proceed further into the ischaemic zone. Such accumulation is typical of locations where rapid orthograde axonal transport or retrograde axonal transport is blocked. In contrast, when slow axonal flow is impaired, the swelling is characterised by an excess of cytoplasmic gel without a marked accumulation of organelles. Rapid orthograde transport and retrograde transport seem to be closely related to one another, while slow axoplasmic flow seems fundamentally different. From morphological findings we suspect that, in experimental glaucoma, intraocular pressure first affects the intracellular physiological process of rapid orthograde and retrograde axonal transport. Watery swelling may not occur unless the ischaemic injury to cell metabolism is more advanced. In contrast, in experimental papilloedema, the swelling results predominantly from impaired slow axoplasmic flow.

Animals↗
PubMed1981

The development of the trabecular meshwork and its abnormality in primary infantile glaucoma.

Tissue from ten eyes with infantile glaucoma and from 40 normal eyes of fetuses and infants without glaucoma were examined by light and electron microscopy. In normal development, the corneoscleral coat grows faster than the uveal tract during the last trimester, leading to a posterior migration of the ciliary body attachment from Schwalbe's line (5th month) to the scleral spur (9th month), and then to a location behind the scleral spur (postnatally). In infantile glaucoma, the insertion of the anterior ciliary body and iris overlaps the trabecular meshwork, similar to the late fetal position. The trabecular sheets are perforated, and there is no membrane over the surface of the trabecular meshwork. The trabecular beams are thicker than in normal infant eyes. There is both histologic and clinical evidence of traction on the iris root exerted by the thickened trabecular beams. These findings suggest that in congenital glaucoma the thickened beams had prevented the normal posterior migration of the ciliary body and iris root. This traction may compact the thickened trabecular beams, obstructing aqueous humor outflow. Release of the traction by an incision (goniotomy or trabeculotomy) of the thickened meshwork may relieve the obstruction. Of uncertain pathological significance is that there are no vacuoles in the endothelium of Schlemm's canal and there is a broad layer of collagen and amorphous material in the juxtacanalicular connective tissue. The ciliary processes are elongated inward, as if they were pulled by zonular traction (perhaps created by an enlarging diameter of the limbus with a fixed lens diameter).

Child↗
PubMed1980

The mode of progressive disc cupping in ocular hypertension and glaucoma.

Serial disc photographs of 259 patients with elevated intraocular pressures were studied retrospectively up to 15 years. Twenty-nine eyes showed progressive enlargement of the optic cup. Early vertical extension of the cup occurred in vertical extension of the cup occurred in five eyes and horizontal extension in one. In 23 eyes, a generalized expansion of the cup (retaining its round appearance) was the first change observed, typically preceding visual field loss by several years. Thus, serial disc photographs are necessary for the earliest detection of optic nerve damage in ocular hypertension. Of 18 eyes with normal visual fields at the time progression of cupping was first noted, typical glaucomatous field loss developed in 50% during a follow-up of one to six years (average, two years). Therefore, treatment is indicated for eyes exhibiting progressive disc cupping, even in the absence of visual field defects.

Adult↗
PubMed1980

Nonglaucomatous excavation of the optic disc.

In order to test the hypothesis that glaucomatous and nonglaucomatous optic disc cupping can be distinguished ophthalmoscopically, three ophthalmologists experienced in assessing optic dics were asked to view fundus stereophotographs as "unknowns". Of 29 eyes with nonglaucomatous optic atrophy, 13 (44%) were misdiagnosed as showing glaucoma by at least one observer. Of four optic disc features specifically analyzed, neuroretinal rim pallor proved to be 94% specific for nonglaucomatous atrophy, while focal or diffuse obliteration of the neuroretinal rim was 87% specific for glaucoma. These two signs are the most useful in making the distinction. Thinning of the rim was more common in glaucoma than in nonglaucomatous atrophy, but was only 47% specific for glaucoma. Laminar dots were present in both types of excavation.

Diagnosis, Differential↗
PubMed1980

Failure of unilateral carotid artery ligation to affect pressure-induced interruption of rapid axonal transport in primate optic nerves.

Previous experiments showed that optic nerve axonal transport can be blocked at the level of the lamina cribrosa by elevated intraocular pressure. In an effort to discover if this blockage might be secondary to pressure-induced ischemia, we studied the effect of unilateral common carotid artery ligation upont the pressure-induced interruption of axonal transport. In 13 owl monkeys (Aotus trivirgatus), the right common carotid artery was ligated within the anterior cervical triangle. Three days later, ophtalmodynomometry was performed on all experimental eyes. In nine of the 13 animals, this estimate of ophthalmic artery pressure was 10 to 20 mm Hg less in the right compared to the left eye. Optic nerve axonal transport was studied in right and left eyes during 5 hours of increased intraocular pressure (ocular pressure 35 mm Hg less than mean femoral artery blood pressure). No significant difference in the extent to which the transport mechanisms were interrupted could be demonstrated when comparing right and left eyes of the experimental animals. These observations fail to support a vascular mechanism for this pressure-induced interruption of axonal transport.

Animals↗
PubMed1980

Fast axonal transport in early experimental disc edema.

Previous work has documented impairment of slow axonal transport in papilledema, but the abnormalities in rapid transport were less certain. Therefore fast axonal transport was studied in 19 primate eyes subjected to ocular hypotony for 6 to 72 hr following surgical fistulization of the anterior chamber. Mild, irregular alterations in fast axonal transport were detected only after nerve head swelling was apparent. These changes in fast transport mechanisms in cases of nerve head edema occur after, and may be secondary to, impaired slow axoplasmic flow and the resultant axonal swelling. Furthermore, since prolonged complete interruption of axonal transport is theoretically inconsistent with the continued normal neuron function characteristic of papilledema and, moreover, since previous data shows a "slowdown" rather than complete blockade of axonal transport in papilledema, it is likely that in eyes with papilledema there does not exist a complete flock of axonal transport. Therefore we hypothesize that the swelling results when slow axoplasmic flow is locally slowed down but not totally stopped, with the axon distention producing secondary mild, irregular changes in fast axonal transport.

Animals↗
PubMed1980

Breakdown of the normal optic nerve head blood-brain barrier following acute elevation of intraocular pressure in experimental animals.

Five hours of elevated intraocular pressure produced evidence of an altered blood-brain barrier at the optic nerve head in 27 of 29 monkey eyes. The change in vascular permeability was documented by fluorescein angiography (18 of 21 eyes), by Evans blue fluorescence microscopy (21 of 23 eyes), or by both methods. Leakage occurred from major blood vessels as well as from microvasculature of the nerve head. In 22 eyes, rapid axonal transport was studied after intravitreal injection of tritiated leucine. In 18 of these 22 eyes, autoradiography demonstrated a local interruption of axonal transport. In 15 eyes examined by all three methods, leakage from microvasculature (as opposed to leakage from the major vessels) was loosely associated with severe and widespread blockade of axonal transport at the lamina cribrosa. Although cause-and-effect relationships are not proved, ischemia may be responsible both for the focal endothelial damage with breakdown of the normal blood-brain barrier and for the local abnormalities of axonal transport.

Animals↗