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Biomedical subjects

S Shibolet

Publications and source records attributed to S Shibolet.

At least 37 records · Page 2Linked to original sources
PubMed1981

1,25-dihydroxyvitamin D3 and the regulation of macrophage function.

Vitamin D3 deficient (D-) mice show a depressed inflammatory response and both inflammatory peritoneal macrophages and bone marrow polymorphonuclear leukocytes of D- mice exhibit a decreased spontaneous migration under agarose. The impaired phagocytic response of peritoneal macrophages from D- mice can be corrected by incubation with 1,25-dihydroxyvitamin D3 and is not affected by interaction with other vitamin D3 metabolites. Transfer of mice from the D- to the D+ state results in correction of both the inflammatory and the phagocytic response. Intactness of phagocyte function is thus directly dependent on vitamin D3 metabolism.

Animals↗
PubMed1981

Recurrent septic arthritis due to Pseudomonas sp.

Two episodes of Pseudomonas septic arthritis occurred in an 84-year-old diabetic man separated by a 6 year interval. Pseudomonas is an unusual cause of septic arthritis requiring vigorous antibiotic therapy. The recurrence of the infection may be related to the inadequate response to treatment in the first episode, however, the long interval remains unexplained.

Aged↗
PubMed1980

Dynamic changes in acid base balance during heatstroke in dogs.

The dynamic changes in acid base balance and respiratory metabolism during the development of heatstroke in dogs were studied. Three groups of five unanesthetized dogs each were exposed to different climatic conditions while at rest: A) 24 degrees C, 50% relative humidity (RH); B) 35 degrees C, 35% RH, and C) 45 degrees C , 25% RH. These conditions were maintained for 4 h or until the dogs collapsed. The heatstroke dogs were cooled in tap water bathes and were observed for another 4 h. Dogs of groups A and B did not show any notable changes in rectal temperature (Tre) and acid base balance. All dogs in group C developed heatstroke. Their peak mean Tre (44.1 degrees C) was reached after a mean of 111 min of exposure, with respiratory alkalosis followed by increasingly severe metabolic acidosis above Tre of 42 degrees C. At peak Tre mean arterial pH was 7.26. Acidosis increased (pHa = 7.17) following cooling, as panting subsided. At Tre above 42 degrees C blood lactate increased and bicarbonate decreased significantly, attaining mean values of 58 mg% and 8 mEq/l, respectively. Bicarbonate changes correlated linearly with lactate changes. During recovery lactate decreased and blood pH increased approximating normal by the end of the experiment. The results illustrate the body's ability to spontaneously correct arterial pH without therapeutic means.

Acid-Base Equilibrium↗
PubMed1979

Recurrent miliary tuberculosis secondary to infected ventriculoatrial shunt.

The placing of a ventriculoatrial anastomosis because of elevated CSF pressure secondary to tuberculous meningitis resulted in repeated dissemination of Mycobacterium tuberculosis from the anastomosis. The consequent clinical picture showed recurrent appearance and clearing of miliary tuberculosis of the lung in spite of antituberculosis chemotherapy. While this possibility was considered early, the diagnosis was not established until the shunt was replaced shortly before the patient's death.

Antitubercular Agents↗
PubMed1978

Low levels of serum calcium, phosphorus and plasma 25-hydroxy vitamin D in cirrhosis of the liver.

In a retrospective analysis of 78 patients with liver cirrhosis, we found low serum levels of calcium and phosphorus. The low calcium levels showed a better correlation with high activity of aspartate aminotransferase than with low levels of albumin. In addition, there was a relationship between low calcium and low phosphorus levels. Therefore, factors other than, and in addition to, hypoalbuminemia seem to be responsible for the low calcium and phosphorus levels in cirrhosis patients. Although low levels of serum 25-hydroxyvitamin D were found in 23 of our patients, there was no indication that hypovitaminosis D was causative factor in the hypocalcemia and hypophosphatemia.

Aspartate Aminotransferases↗
PubMed1978

Familial hyperpotassemia and hypertension accompanied by normal plasma aldosterone levels: possible hereditary cell membrane defect.

Hypertension and hyperpotassemia that were accompanied by normal plasma aldosterone and low renin levels and were responsive to chlorothiazide administration were found in a 29-year-old patient and two decades later in his 21-year-old son. Their renal function is normal, including response to sodium sulfate, mannitol, and aldosterone infusions. Adrenal insufficiency was excluded. The renin-aldosterone system was proved intact by physiological and pharmacologic stress and angiotensin-II infusion. Also normal were values for blood counts, blood volumes, and erythrocyte and exchangeable body potassium. The postulation of a defective cell membrane impeding potassium influx is supported by the failure of glucose and insulin infusions to substantially reduce hyperpotassemia. In the context of a hereditary disorder (the pedigree, compatible with autosomal dominant inheritance, includes five affected in two generations), hypertension is a second phenotypic character of a single defective pleiotropic gene although its pathogenesis remains unclear.

Adult↗
PubMed1977

Prediction of heat tolerance from heart rate and rectal temperature in a temperate environment.

To determine if heat tolerance could be predicted from responses to exercise in temperature conditions, 51 young men performed 15 min of bench stepping at an average work load of 80 W at 23 degrees C. On the following day they attempted to perform 3 h of bench stepping at 40 W in heat (39.3 degrees C dry bulb, 30.3 degrees C wet bulb). Of these subjects, 4 were heat intolerant, judged by previous heat stroke episodes during field marches, 12 were heat acclimated, and 35 were unacclimated. The heat-intolerant subjects showed the highest heart rates (HR) and rectal temperatures (Tre) at 23 degrees C and in heat, and the acclimated subjects showed the lowest corresponding values. HR and Tre in each environment were combined into a single score, from 10, indicating the poorest responses, to 100, indicating the best responses. These scores at 23 degrees C when correlated with the corresponding scores in heat resulted in a linear correlation coefficient of r = 0.94 with a standard error of estimate of 8.6%. Scores of the heat-intolerant subjects were below 35, and those of the acclimated subjects were between 70 and 100. Thus heat tolerance can accurately be predicted for HR and Tre responses to exercise at room temperature.

Acclimatization↗
PubMed1976

Heat stroke: a review.

Heat stroke is a complex clinical picture caused by extreme elevation of body temperature and is especially prevalent in hot climates. The danger of heat stroke has apparently always accompanied unacclimatized man on his way through arid zones, and was often the cause of man's fatal adventures in the desert. Large numbers of unacclimatized urban dwellers have suffered when the urban areas have been involved in heat waves. Heat stroke has also been a major problem in hot industrial environments. This paper is a review of pertinent literature on this subject.

Acclimatization↗
PubMed1975

Controlled trial of propranolol in intermittent claudication.

Seven patients (5 with arteriosclerosis obliterans and 2 with Buerger's disease) completed a two-phase double-blind crossover trial of propranolol in intermittent claudication. Performance was measured on a moving treadmill. In the initial phase, the patients were hospitalized in order to determine an "effective" dose of propranolol. Improvement was noted in all: after 1,600 mg in 5 and after 240 mg and 600 mg in the others. The controlled phase was carried out on an outpatient basis over 8 weeks, the patients receiving propranolol and placebo in a random manner, each for two 2-week periods. Comparison of matched periods of drug and placebo revealed no advantage for propranolol. Patients' performances deteriorated with time. None of the patients evidenced deterioration of occlusive peripheral arterial disease that could be attributed to propranolol, in spite of the high doses used.

Adult↗
PubMed1972

Altered membrane sodium transport in Bartter's syndrome.

To explore the possibility that Bartter's syndrome is the manifestation of an inherited abnormality of sodium transport, we have measured various parameters of sodium transport in erythrocytes from patients with Bartter's syndrome, their siblings, and their parents. Sodium transport in six of the eight patients with Bartter's syndrome differed significantly from that in the other two patients. On the basis of this difference, the patients were divided into two groups (type I and type II). In the six type I patients, fractional sodium outflux (0.38+/-0.05/hr [SD]) was significantly less than normal (0.50+/-0.07) and erythrocyte sodium concentration (9.48+/-0.84 mmoles/liter cells per hr) was significantly greater than normal (5.24+/-0.66). In the two type II patients, none of the measured parameters of sodium transport differed significantly from normal. Erythrocyte sodium transport in the relatives of three type I patients was altered in a way similar to that in the type I patients and was significantly different from that in the relatives of a type II patient. These findings indicate the presence of inherited alterations of erythrocyte sodium transport in certain patients with Bartter's syndrome.

Adolescent↗