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Biomedical subjects

J B Pickett

Publications and source records attributed to J B Pickett.

9 recordsLinked to original sources
PubMed1992

Insulin increases amino acid transport into rat soleus motor axons.

Hyperosmotic neurosecretion was used to measure basal and insulin-stimulated amino acid and myoinosital transport into rat motor nerve terminals. L-Alanine and alpha(methylamino)-isobutyric acid (a nonmetabolizable system A-specific analog) transport was rapid into motor nerve terminals innervating a fast-twitch muscle, the extensor digitorum longus, and slow into motor nerve terminals innervating the soleus, a slow-twitch muscle. A physiological concentration of insulin, 10 microU/mL, increased L-alanine and alpha(methylamino)-isobutyric acid transport into motor nerve terminals in the soleus. Large doses of insulin, 100 or 1000 microU/mL, had no effect on L-alanine or alpha(methylamino)-isobutyric acid transport into nerve terminals in the extensor digitorum longus. There was negligible basal or insulin-stimulated transport of D-alanine or myoinositol into nerve terminals of the soleus or extensor digitorum longus. These studies show that insulin regulates sterospecific amino acid transport into soleus motor axons, but has no effect on the rapid amino acid transport into extensor digitorum longus motor axons. Differences in basal and insulin-stimulated transport suggest that motor axons differ in their metabolism, and might be selectively vulnerable to disease processes.

Amino Acids↗
PubMed1988

AAEE case report #16: Botulism.

Botulinal toxin causes a marked reduction in the number of quanta released by autonomic and motor nerve terminals. As a result it causes blurred vision, inability to move the eyes, weakness of other cranial nerve-innervated muscles, dyspnea progressing to apnea, and generalized weakness. Electrodiagnostic findings in severe botulism can be relatively nonspecific, with low amplitude and short duration motor unit action potentials and small M wave amplitudes. A modest increment in M wave amplitude with rapid repetitive nerve stimulation may help to localize the disorder to the neuromuscular junction. Identification of the toxin in the patient's serum is diagnostic. The treatment of botulism is mainly supportive.

Adolescent↗
PubMed1988

Insulin improves rat soleus axon function by increasing glucose transport.

The effect of varying glucose and insulin concentration on neuromuscular transmission was investigated in rat soleus and extensor digitorum longus (EDL) nerve-muscle preparations using conventional microelectrode techniques. Soleus and EDL axons were similar in that both failed after approximately 70 min of glucose deprivation and often did not recover from glucose deprivation. Soleus and EDL axons differed in the following ways: 1) soleus axons required greater than 7.64 mM of glucose to give sustained function vs. greater than 2.78 mM of glucose for the EDL; 2) 30 microU/ml of insulin improved soleus axon function over a range of glucose concentrations from 4.17 to 9.72 mM vs. no effect of 1,000 microU/ml on EDL axons; 3) resting glucose transport was slow into soleus axons and rapid into EDL axons; and 4) 10 microU/ml of insulin increased glucose transport into soleus axons vs. no effect of 1,000 microU/ml of insulin on glucose transport into EDL axons. These results suggest that insulin improves soleus axon function by increasing glucose transport, whereas insulin has no effect on EDL axons.

Animals↗
PubMed1985

Localizing peroneal nerve lesions.

The main result of a peroneal nerve lesion, foot drop, is so obvious that few patients can ignore its presence. However, the detailed knowledge of peroneal nerve anatomy needed to localize the lesion may tax even a seasoned clinician. Examination of the strength of five muscles--the tibialis anterior, peroneus longus and brevis, posterior tibial, gluteus medius and quadriceps--provides information necessary to localize the site of the neuropathy. This tentative localization can be confirmed by electromyography. Treatment is directed to the cause of the lesion and stabilization of the ankle if necessary.

Electromyography↗
PubMed1979

Inhibition of the evoked release of acetylcholine by the porphyrin precursor delta-aminolevulinic acid.

The effect of delta-aminolevulinic acid (ALA) on neuromuscular transmission were studied. High concentrations (0.6 to 18 mM) of ALA caused significant reductions in the amplitudes of curarized end-plate potentials (epps). Changing the ratio of calcium to magnesium in the bathing solution allowed the quantal content of the epps to be directly measured. Under these conditions, ALA reduced the quantal content of epps without affecting the depolarization produced by a single quantum of acetylcholine. It was concluded that ALA, in high concentrations, inhibits the release of acetylcholine evoked by a nerve impulse but is unlikely to be the cause of the neurological defects of acute porphyria.

Acetylcholine↗
PubMed1978

Late components of motor unit potentials in a patient with myoglobinuria.

A 45-year-old woman had severe weakness, myoglobinuria, and elevated muscle enzyme levels in the serum after a flulike illness. Electromyography some four weeks later showed motor unit potentials with late components; these remained present on subsequent electromyographic examinations performed at approximately monthly intervals for the following year. The persistence of motor unit potentials with late components is taken to imply that the late components were caused either by sprouts that failed to undergo myelination or, more likely, by ectopically innervated muscle fibers.

Electromyography↗
PubMed1975

Neuromuscular complications of acromegaly.

Seventeen consecutive acromegalic patients were evaluated for evidence of neuromuscular dysfunction and followed for 1 year after hypophysectomy. Before treatment, four patients had both a myopathy and the carpal tunnel syndrome, five had myopathy alone, four had carpal tunnel syndrome alone, and four had neither. The myopathy was caracterized by mild, strictly promixal weakness and flabbiness of muscles; electromyography revealed typical myopathic abnormalities, but serum enzymes and muscle biopsy usually were normal. The presence of myopathy or the carpal tunnel syndrrome could not be correlated with the magnitude of growth hormone elevation or any secondary endocrine derangement, but myopathy was associated with a longer duration of acromegaly. Carpal tunnel symptoms usually improved in the first 6 weeks after hypophysectomy, while myopathy improved more slowly and sometimes was detectable 1 year later.

Acromegaly↗