Exchange reaction, clustering, and surface segregation at the Al/InSb(110) interface.
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Biomedical subjects
Publications and source records attributed to Y Shapira.
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Head injury was induced in the left hemisphere of rats. The rats were killed at various time intervals after trauma (immediately, 15 min, 1 and 18 h, and 4 and 10 days), and the rates of synthesis and release of prostaglandin PGE2, 6-keto-PGF1 alpha, and thromboxane TXB2 from cortical slices of both hemispheres were studied. The rate of synthesis of PGE2 after 18 h was six and four times higher than control in the contused and contralateral hemispheres, respectively. By 10 days post-trauma, both hemispheres had normal rate of PGE2 release. TXB2 and 6-keto-PGF1 alpha synthetases were affected already 15 min after the injury, and a similarly elevated rate of synthesis was found in both hemispheres. The maximal effect was detected after 1 or 18 h with return to normal after 4 or 10 days for TXB2 and 6-keto-PGF1 alpha, respectively. Tissue specific gravity was determined for both hemispheres using linear gradient columns. The results of these determinations indicate that development of edema occurs in the contused hemisphere as early as 15 min post trauma; it reaches its maximal level at 18 h and returns to normal at 10 days. Arterial pressure was monitored, and a transient increase was found at 10 min post trauma. We suggest that the production of edema after brain injury may be related to the increased rate of PGE2 and PGI2 synthesis, which occurs at similar time intervals after injury.
Three siblings presented with fatal cardiomyopathy confirmed by electron microscopy, and normal serum but low muscle carnitine concentrations. A fourth had similar signs but remained asymptomatic. He was treated with carnitine orally which increased the concentration in muscle, though it remained below normal. Electron microscopic features were unchanged.
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A pop-off valve system for use with intermittent mandatory ventilation that employs high flow and a reservoir bag is described. It ensures constancy of the mechanical tidal volume regardless of the flow rate of fresh gases into the reservoir bag of the spontaneous breathing circuit.
A female child and her father with cerebellar ataxia and retinitis pigmentosa are described. The father's clinical onset was in middle age, the course of his disease mild and his pneumoencephalogram showed cerebellar atrophy. On the other hand, his daughter's clinical onset was in late infancy, her course was rapidly progressive with manifestations of brainstem dysfunction. She had abnormal brainstem auditory evoked potentials and the computerized tomography scan showed atrophy of the posterior fossa. Recently a paternal aunt developed cerebellar ataxia at the age of fifty. The unusual early age of onset of dominantly inherited cerebellar ataxia and the extreme variation in expression of clinical manifestation are discussed.
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Two siblings, a 14.5-year-old boy and his 11.5-year-old sister, with congenital nemaline myopathy presented with severe respiratory failure and, in the case of the older patient, with cor pulmonale and systemic hypertension. The children were treated initially by continuous mechanical ventilation, but after a few weeks they only required ventilation at night. At the start of treatment, both were found to have a decreased ventilatory response to CO2 which apparently improved during 4 to 5 years of follow-up treatment. It has not been possible to wean them from nocturnal mechanical ventilation, but during the daytime they attend school and function almost normally. It is postulated that respiratory failure in nemaline myopathy may not be related to the severity of the muscle weakness but may result from a disturbance of the feedback required for normal control of breathing.
Strenuous work or sports activities in a hot environment can cause significant fluid and salt losses due to excessive sweating. Fluid replacement is commonly accepted to be beneficial, but controversy surrounds the necessity of adding salt to the dietary intake in hot climates. Five healthy young men participated in a self-controlled experiment designed to investigate the effects of salt loading on acclimatized people exercising under controlled laboratory conditions. The additional salt ingestion was found to cause an increase in body weight, rectal temperature, heart rate, urinary sodium and potassium concentrations and in the total amounts of sodium and chloride excreted in urine during the exercise. Furthermore, it decreased plasma aldosterone level and sweat chloride excretion, but did not affect fluid intake, urine output, sweat rate, skin temperature, excretion of sodium and potassium in sweat or urinary potassium content and chloride concentration. Neither did the additional salt intake affect plasma electrolyte levels, renin activity or acid base balance. It is concluded that acclimatized people living in a hot dry climate need no supplementary salt to their daily dietary intake while engaging in physical exercise or sports activities up to two hours a day. Salt loading has no beneficial effects in these conditions and may even be hazardous.
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