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Biomedical subjects

W K Engel

Publications and source records attributed to W K Engel.

At least 253 records · Page 14Linked to original sources

A new program for investigating adult human skeletal muscle grown aneurally in tissue culture.

With our new "explant-reexplanting" technique, abundant growth of mature human muscle in long-term tissue culture was achieved,and with the "sandwich" technique several histochemical reactions were obtained on serial cross sections of the cultured fibers. An advanced degree of maturation but lack of differentiation into reciprocally staining fiber-types was demonstrated. For electron-microscopic and electronmicroscopic-histochemical study, a method was developed in which the embedded fibers of greatest potential interest were identified by light microscopy and punched out by our specially-designed hollow drill. This selection procedure is critically important when the goal is to study in cultured diseased human muscle: (1) successive stages of development and (2) certain structural changes that often occur only in some fibers and only in certain regions of those fibers. The electronmicroscopic-histochemical appearance of developing cultured muscle fibers correlated well with the fresh-frozen light microscopic histochemical cross-sections and longitudinal whole preparations of similar fibers.

Adenosine Triphosphatases↗

99mTc-diphosphonate uptake in skeletal muscle: a quantitative index of acute damage.

In rats with ischemic myopathy induced by aortic ligation and 5-hydroxytryptamine, there was good correlation of the skeletal muscle concentration of 99mTc-diphosphonate with the increase of plasma creatine phosphokinase and the decrease in muscle potassium. This radionuclide tracer method can be used to quantitate acute injury in individual muscles and provides a basis for clinical nuclear imaging in patients with a variety of disorders involving muscle fiber damage.

Acute Disease↗

Brief, small, abundant motor-unit action potentials. A further critique of electromyographic interpretation.

The concept that there is a constellation of electromyographic (EMG) findings diagnostic of myopathy is criticized. The EMG pattern generally referred to as "myopathic" is one of brief-duration, small-amplitude overly-abundant (for the amount of power being exerted) motor-unit action potentials on slight voluntary effort. For it, the author prefers the descriptive and diagnostically noncommittal acronym "BSAP". In addition to myopathy, three hypothetical neurogenic mechanisms could equally well cause a BSAP EMG pattern: (1) Acquired functional or structural loss of a fraction of the axonal twigs in many individual motor-unit trees, (2) congenital motor-unit hypoplasia (too few muscle fibers per motor unit), and (3) acquired (atrophic) or congenital (hypotrophic) smallness of many muscle fibers. The term and concept of a diagnostic "myopathic EMG" thus is considered invalid.

Action Potentials↗

Distinct subtypes of type I fibers of human skeletal muscle.

We have identified two distinct and consistent type I fiber subtypes in histochemically normal biopsies (vastus lateralis or biceps brachialis) from 12 healthy persons, both sexes, ages 15 to 42. The type I fibers were uniformly light with the regular ATPase (9.4) and uniformly dark with the acid-preincubated reverse ATPase reactions. However, the subtype IA fibers were stained darker than subtype IB fibers with the nicotinamide adenine nucleotide dehydrogenase-tetrazolium reductase, Oil red O, reduced nicotinamide adenine dinucleotide phosphate-tetrazolium reductase, nonspecific esterase, succinic-tetrazolium reductase, nicotinamide adenine dinucleotide-linked malic-tetrazolium reductase, and "nicotinamide adenine dinucleotide-linked lactic-tetrazolium reductase," and stained lighter with the phosphorylase, periodic acid-Schiff for glycogen, and menadione-mediated alpha-glycerophosphate-tetrazolium reductase reactions. The IB fibers were not as light (or as dark, depending on the stain) as any of the type II fibers. In one pathologic case, all the "hypotrophic type I muscle fibers with central nuclei" were subtype IB. In case of chronic infantile spinal atrophy the muscle showed some type-grouping and marked type I fiber predominance--the great majority of type I fibers were subtype IB, among which were islands (subtype-groups) of IA fibers. Subtyping of type I fibers may be informative in evaluating the pathologic process of certain human neuromuscular diseases.

Adolescent↗

Neuromuscular disease in secondary hyperparathyroidism.

Neuromuscular function was evaluated in six patients with osteomalacia or secondary hyperparathyroidism, or both, as demonstrated by bone biopsy showing osteomalacia or increased immunoreactive parathyroid hormone, or both. Each patient had weakness, atrophy, and fatigability of proximal muscles, especially of the lower extremities. Most also showed involuntary fine movements of the tongue, hyperactive tendon reflexes with abnormal spread, and decreased vibration sensation, abnormalities similar to those observed in primary hyperparathyroidism. Every patient studies had evidence of neuropathic muscle disease, either on electromyography or muscle biopsy studies histochemically or both. Muscle biopsies showed no definite myopathic features. Treatment of the osteomalacia improved muscle strength. Patients with osteomalacia therefore have a treatable neuromuscular disease that is neuropathic in nature and resembles closely that found in primary hyperparathyroidism.

Adolescent↗

In vitro analysis of the general properties and junctional receptor characteristics of skeletal muscle membranes. Isolation, purification, and partial characterization of sarcolemmal fragments.

Muscle membranes were partially purified from rat leg muscles. Externally oriented membrane functions were used to monitor and characterize the resulting membrane fractions. Na(+)K(+)-stimulated Mg(++)-adenosinetriphosphatase, acetylcholinesterase, and cholinergic receptor activities are present and enriched in the density-gradient subfractions of crude sarcolemma when compared with the first pellet. The physical separation of the cholinesterase and receptor activities on the gradient subfractions is demonstrated. Receptor activity, determined by specific (125)I-labeled alpha-bungarotoxin binding, appears in fractions with densities similar to other plasma membranes (D(4) (20) 1.1015-1.1520). Acetylcholinesterase, on the other hand, is preferentially distributed in lighter density fractions (D(4) (20) 1.0507-1.0780) and parallels the gradient distribution of the ATPase. In sodium dodecyl sulfate-polyacrylamide gel electrophoresis, a high-molecular-weight glycoprotein sediments with the higher density fractions only. The data suggest a molecular dissection of the layers of the sarcolemma. The receptor is tentatively felt to be an integral component of the junctional plasma membrane. Acetylcholinesterase is felt to be superficially located on the ectolamina of the junctional sarcolemma, and may be woven within the matrix of the intersynaptic basement membrane.

Acetylcholinesterase↗