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The mixed mode fracture of unidirectional composites is investigated by application of the strain energy density theory. Two analytical models are used. The first assumes that the composite is an ideal homogeneous anisotropic body, and the second assumes that failure takes place in a layer of matrix material whose edges are bonded to two orthotropic plates. The expressions for the strain energy density factor, S, are derived for both models, and brittle fracture is assumed to occur when the S-factor in an element of material ahead of the crack reaches a critical value, Sc. Results are presented for E-glass fiber reinforced plastics, stainless steel fiber reinforced aluminum and graphite fiber epoxy materials and compared with available experimental data. The latter model is preferred as it accounts for the effect of nonhomogeneity that is inherent in the filament-reinforced composites.

The effect of a high concentration of the antibiotic colistin sulfate on neuromuscular transmission was examined by recording intracellularly from rat diaphragm blocked with tubocurarine chloride. The presynaptic effect of colistin was different from that of neomycin sulfate, which reduces the probability of acetylcholine release: Colistin reduced the quantum content of the initial and the last 20 end-plate potentials of a train of 40 stimuli without altering the probability of acetylcholine release. The quantum size was reduced, while the frequency of miniature end-plate potentials was unchanged.

A 61-year-old woman had proximal muscle weakness since 38 years of age. Eventually, her distal muscles became affected and she showed widespread muscle wasting, absent tendon reflexes, and electromyographic findings of a neuropathy. On biopsy, there was a lipid storage myopathy, lipid-containing vacuoles in leukocytes, and vacuoles in Schwann cells. The muscle carnitine level was abnormally low, but the serum carnitine level was normal. The findings are consistent with a generalized disorder of carnitine metabolism that may involve carnitine transport across cell membranes.

The effects of occult carcinoma on the structure and function of the nervous system have been recognized with increasing frequency during the past decade. This association is most striking in males with a myopathy which begins after the age of 50. Frequently, the myopathy is accompanied by skin changes, and takes the form of dermatomyositis. Electromyographic confirmation of the diagnosis appears more reliable than muscle biopsy or measurement of serum enzymes.This case report is the first instance of a lateonset myopathy without dermal change recognized in association with malignant melanoma. The melanoma was found in the brain, and was of unknown primary origin.

A 4-year-old boy developed oculobulbar paralysis with fixed dilated pupils in the face of a normal level of consciousness. Serological and bacteriological studies did not confirm a diagnosis of botulism, but electromyographic changes supported the diagnosis, especially since no other cause for the patient's clinical state was found. Electromyographic abnormalities included a very small grouped muscle action potential (MAP) response to a single nerve stimulus; marked tetanic and posttetanic MAP facilitation at fast rates of repetitive nerve stimulation; increased nerve excitability; and a "supernormal" mixed nerve action potential response, enhanced after a calcium infusion.

ANTIBIOTICS produce weakness by interfering with neuromuscular transmission. Apnea in experimental animals was observed first in 1941 with tyrothricin, the first antibiotic tested for clinical application.1 In 1956, the first case of prolonged apnea in man was reported after intraperitoneally infected neomycin sulfate.2 Since 1956, a syndrome characterized by respiratory weakness, flaccid paralysis, and pupillary and visual changes has been recognized in association with a number of antibiotics.3-50 As defined, this "myasthenic syndrome" occurs in patients who do not have myasthenia gravis, although some myasthenics become weaker when given certain antibiotics.51 Recent reviews of antibiotic toxicity do not emphasize this syndrome52-54 Electromyographic (EMG) studies were mentioned in only four patients. In one, neuromuscular transmission and nerve conduction velocities were normal.49 A "currarelike"30 or nondepolarizing34,50 effect occurred in the others. In one patient50 the block was not altered by edrophonium chloride.Profound

THE OCCURRENCE of "progressive muscular tautness" was termed the "stiff-man" syndrome by Moersch and Woltman in 1956.1 Once hysteria or extrapyramidal disease are eliminated from consideration, there remains a group of patients with striking axial stiffness, sometimes with superimposed muscle spasms, in whom no apparent pathology can be found. Exacting clinical, metabolic, and electromyographic (EMG) criteria for this diagnosis were set forth in 1964.2 As a result a number of clinically similar conditions were excluded.Olafson et al in 19642 suggested that this disorder might arise because of a disturbance in spinal reflex mechanisms. They advanced this hypothesis because of similarities between the stiff-man syndrome and disorders such as tetanus, in which there is good theoretical, physiological, and anatomical evidence for interference with the normal reflex inhibitors of anterior horn cell activity. Because of certain clinical observations, Allsop argued in 19633 that the spinal reflex disturbance

Myasthenia gravis is demarcated from other syndromes of weakness and easy fatigue by its predilection for certain muscle groups, repair by rest, clinical course,1 characteristic defect in neuromuscular transmission,2 and response to anticholinesterase medication. The myasthenic patient shows improvement in strength after dosage of anticholinesterase drugs that would produce distressing effects in any other person.1,3-5Observations on a recent patient suggested that tolerance to the effects of these drugs is not limited to myasthenia gravis. Thus, such tolerance cannot be taken as incontrovertible evidence supporting that diagnosis.A survey of our records disclosed 4 additional patients (Table 1). They were all women who told of weakness and easy fatigue, without objective signs to corroborate this. Although bulbar symptoms were common, bulbar signs were absent. Psychiatric diagnoses ranged from depression with hysterical features to frank psychosis. These patients offered multiple complaints in every system. Their asthenia was improved

In the management of myasthenia gravis, it is important to avoid the use of medications such as curare and quinine which make the neuromuscular block worse. Shortly after the discovery of chlorpromazine, animal studies suggested some actions which might be deleterious to myasthenic patients.1,2,7,9-11 However, no clinical report confirming such adverse effects in myasthenia has appeared.When a psychotic myasthenic patient became weaker after oral chlorpromazine, study was made of the nature of this worsening. The results of that investigation form the basis of this report. REPORT OF A CASE This patient was the subject of an extensive report 21 years ago.5 Thus, only findings pertinent to the present study are detailed here.The patient was born in 1902. He was struck on the head with a baseball bat in 1918 and was unconscious for 5 to 6 hr.; a left peripheral facial paresis was the only sequela.

The dynamic, thermoelastic response of cylindrical shells to suddenly applied and rotating thermal inputs is investigated. Fully coupled, dynamic, thermoelastic cylindrical shell equations are derived using Galerkin’s method. Identical results were obtained independently using a variational theorem. Analytical solutions to these equations are formulated for finite-length and infinite-length cylinders. Numerical results for the response of infinite-length cylindrical shells to suddenly applied and rotating longitudinal lines of heat flux are presented. It is shown that for many thermoelastic problems involving moving thermal inputs that the maximum ratio of dynamic to quasi-static deflection can be much greater than two, that dynamic effects can be important for all thicknesses within the realm of thin shell theory, and that semicoupled theory gives incorrect results in some cases for which a fully coupled theory is required.

SOME 15% of infants born to mothers with myasthenia gravis develop respiratory and feeding difficulties and often more generalized weakness, which responds to cholinergic drugs.1 Symptoms appear within 72 hours of birth and persist for several days to three months.2 This form of myasthenia does not recur later in life.3 The implication is that a factor influencing neuromuscular transmission (NMT) crosses the placenta, and that this factor, or its effect persists for many weeks without leaving a permanent defect.4There are two accounts of electromyographic (EMG) studies of such infants.5,6 Studies of NMT in normal newborns5,7 suggest that their neuromuscular junction functions with smaller reserves than the adult. Trains of repetitive stimuli are poorly sustained, and recovery after a train is delayed.We have conducted serial EMG studies in an infant with the syndrome, an unaffected infant of a myasthenic mother, and three