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Biomedical subjects

A K Asbury

Publications and source records attributed to A K Asbury.

10 recordsLinked to original sources
PubMed1979

Endoneurial lipid composition of normal human sural nerve.

The endoneurial lipid composition was determined in 7 human sural nerves from subjects without known neurological disease. The nerves were morphologically normal, with myelinated fiber density of 7,710 +/- 1,210/mm2 (mean +/- SD). Endoneurium contained 30.7 +/- 1.5 mg total lipid per 100 mg of dry weight. Cholesterol was the predominant lipid (9.1 +/- 1.0 mg). Cholesterol ester was present only in very small quantities (0.2 +/- 0.1 mg). Cerebroside concentration was 4.5 +/- 0.3 mg, and sulfatide was 1.5 +/- 0.3 mg. The most abundant phospholipid was sphingomyelin (4.3 +/- 0.3 mg), followed by phosphatidylethanolamine (4.1 +/- 0.2 mg), phosphatidylcholine (3.8 +/- 0.2 mg), and phosphatidylinositol-phosphatidylserine (1.7 +/- 0.2 mg). Eighty-one percent of cerebroside nonhydroxy fatty acids were long chain (C20 to C26), and 67% were saturated. Technological advances now permit microchemical lipid analysis of human sural nerve biopsies in cases of neuropathy. When compared with our normative data, such studies may further the understanding of peripheral nerve disorders.

Adolescent↗
PubMed1979

Nerve lipid abnormalities in human diabetic neuropathy: a correlative study.

To study endoneurial lipid composition in human diabetic neuropathy, we biopsied sural nerves from 3 middleaged men with adult-onset diabetes mellitus. Magnitude of electrophysiological abnormalities and myelinated fiber loss paralleled the clinical severity of neuropathy in all cases. Cholesterol ester concentration was elevated to about 800% of normal in diabetic nerves. Reduction in total endoneurial lipid concentration correlated best with decrease in myelin volume as calculated from measured fiber diameters. Cholesterol, cerebroside, and most phospholipids were reduced in keeping with the severity of fiber loss in each nerve. The phosphatidylinositol-phosphatidylserine fraction was most reduced in the least affected nerves. Cerebroside nonhydroxy fatty acids in diabetic nerves were of shorter chain length and more saturated than normal. It is not yet clear whether the abnormalities of phosphatidylinositol-phosphatidylserine and cerebroside fatty acids are of pathogenetic importance or whether these changes may be the nonspecific consequence of axonal degeneration.

Adult↗
PubMed1978

Antiserum-mediated demyelination in vivo: a sequential study using intraneural injection of experimental allergic neuritis serum.

Primary segmental demyelination accompanied by mononuclear phagocytes was induced by injection of antiserum into rat peripheral nerve, and the morphologic sequence of events was studied. Antisera were obtained from rabbits with experimental allergic neuritis (EAN) produced by the inoculation of emulsified bovine peripheral nerves in complete Freund's adjuvant. Sera were injected directly into rat sciatic nerve to circumvent the blood-nerve barrier. Recipient rats developed sensorimotor paralysis on the side injected with experimental allergic neuritis sera. Intense focal demyelinative lesions resulted from injection of experimental allergic neuritis sera. Control sera obtained from rabbits inoculated with bovine serum albumin in complete Freund's adjuvant did not produce paralysis or demyelination. The earliest change was damage to Schwann cells, seen 20 minutes after antiserum injection. Within a few hours lamellar splitting and vacuolation of myelin began to paranodal regions and Schmidt-Lanterman clefts and there were infiltrating polymorphonuclear cells. By 8 hours without the detectable presence of monocytes or macrophages, myelin vesiculation became advanced and widespread. By 15 hours, endoneurial edema had reached its maximum. Macrophages were found in association with myelinated nerve fibers. From that time through the next 5 days, demyelination progressed to complete denudation of axons by macrophage phagocytosis of myelin. Activated cytoplasm of Schwann cells reinvested demyelinated axons, often in concert with persisting phagocytic macrophages. Peripheral nerve demyelination thus transferred evolved rapidly, and myelin destruction occurred prior to the appearance of monocytes or macrophages. Demyelinating activity was lost after absorption by purified peripheral nerve myelin but not by liver or kidney and was heat-labile and complement dependent (T. Saida, K. Saida, D. H. Silberberg, and M. J. Brown: Nature 272: 639, 1978).

Animals↗
PubMed1976

Microdissection of peripheral nerve: collagen and lipid distribution with morphological correlation.

Peripheral nerve is a complex tissue composed of endoneurial fascicles surrounded by perineurium and epineurium. We separated endoneurium from peri- and epineurium in human sural nerves by "endoneurial plucking", a method of microdissection. Endoneurial contents (axons, myelin sheaths, Schwann cells, vessels, and interstitial collagen) were cleanly separated in high yield from enveloping connective tissue, by both microscopic and biochemical criteria. Most of the nerve sulfatide and unesterified sterol was found in the endoneurial fraction while most of the collagen was in the peri-epineurial fraction. This microdissection method should prove useful in biochemical investigations of peripheral nerve.

Adult↗
PubMed1975

Glue-sniffing neuropathy.

Although industrial exposure to n-hexane is known to cause neuropathy, it is less well recognized that inhalation of n-hexane present in the vapors of some commercial contact cements is also neurotoxic to peripheral nerves. A young man with a long history of addictive glue-sniffing developed severe distal symmetrical polyneuropathy several months after switching to a cement containing n-hexane and gradually improved several months after switching to another cement containing no n-hexane. Fascicular biopsy of radial cutaneous nerve showed striking segmental distention of axons by neurofilamentous masses with secondary thinning of myelin sheath, paranodal myelin retraction, and widening velocities were correspondingly slow. We conclude that n-hexane used as a solvent in some contact cements may be neurotoxic when inhaled to excess and, further, that the neuropathy has characteristic electrophysiological and pathological features.

Acetates↗
PubMed1975

Physiological studies of the dying-back phenomenon. Muscle stretch afferents in acrylamide neuropathy.

(1) The responses of 1,001 medial gastrocnemius afferents with conduction velocities of 24-126 m/sec have been studied in cats with experimental acrylamide neuropathy. (2) Many units which conducted at velocities indicating that they innervated muscle stretch receptors failed to discharge during muscle stretch or contraction. In animals with mild neuropathy 10 per cent of 366 units were non-responsive. In animals with moderate or severe neuropathy the proportion of non-responsive units was 68 per cent of 315 fibres and 89 per cent of 320 fibres respectively. Group I fibres were involved to a greater extent than Group II fibres. (3) The distributions of identified functioning units with respect to conduction velocity were normal, indicating that acrylamide did not produce conduction slowing before failure of function. (4) Electrophysiological and histological findings indicate that acrylamide initially produces failure of impluse conduction and subsequent fibre breakdown in the terminal axon while normal impulse conduction is preserved more proximally.

Acrylamides↗