Plasma glutathione peroxidase after selenium supplementation in patients with reduced selenium state.
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Biomedical subjects
Publications and source records attributed to H Menzel.
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It can be shown that 0.1% aluminum hydroxide is able to compensate a 90% difference in antigen content of a human diploid cell strain rabies vaccine in man. This conclusion, however, is drawn only from the formation of neutralizing antibodies (kinetics and antibody concentration). Further experiments should be performed to compare also the protective capacity of HDCS vaccines varying in antigen content and adjuvant. A sole reduction of viral antigen is reflected by a corresponding reduction in antibody formation provided the different doses fall within the logarithmic part of the dose-response curve.
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Three exogenous pyrogens (Escherichia coli lipopolysaccharide, synthetic double-stranded ribonucleic acid. Newcastle disease virus) were compared with respect to their mechanisms of fever induction in rabbits. All inducers stimulated the production of an endogenous pyrogen demonstrated in the blood as well as prostaglandins of the E group, and of cyclic adenosine 3',5'-monophosphate in the cerebrospinal fluid. The concentrations of these compounds were elevated approximately twofold as compared to the controls. Independently of the mode of induction, the fever reaction could be prevented by pretreatment with 5 mg of cycloheximide per kg, although the three fever mediators were induced as in febrile animals. Consequently, at least one additional fever mediator that is sensitive to a 30 to 50% inhibition of protein synthesis by cycloheximide has to be postulated. The comparable reactions of the rabbits after administration of different pyrogens argues for a similar fever mechanism. In contrast to fever induction there was no stimulation of endogenous pyrogen, prostaglandins of the E group, and cyclic adenosine 3',5'-monophosphate in hyperthermia as a consequence of exposure of the animals to exogenous overheating. Furthermore, hyperthermia could not be prevented by cycloheximide.
Histological and biochemical studies were carried out in a total of 300 patients who had died in the recovery room, and in rabbits, to investigate the frequency of deposits of calcium oxalte crystals in the kidneys, the influence of infusion therapy and the pathological significance of such deposits on the kidney tissue and on renal function. - Quite independent of any infusions, however, deposits of calcium oxalate crystals were found in the presence of kidney-specific diseases, in particular uraemia and anuric conditions. Xylitol infusions of 0.4 g/kg body weight or, in individual cases, of not more than 500 g total in 7 days, had no infllence on the appearance of calcium oxalate deposits. The blockage of the tubular system by the calcium oxalate deposits leads to a temporary reversible increase in serum urea and serum creatinine. With time, and uninfluenced by infusions, the deposits disappear out of the kidney again without having caused any organic renal damage. In the presence of a temporary excess of serum oxalate, the kidneys temporarily act like a cloaca.
Two cases of malignant hyperthermia with different clinical courses are reported. The patients showed the classical signs of malignant hyperthermia consisting of tachycardia, tachypnoea, ocasional peripheral cyanosis, high body temperature as well as characteristic rise in serum enzymes. In one of the patients the symptoms were recognized early during the operation. The immediate commencement of therapy with ice-cooled. Ringer-Lactate-Solution, Procainmedication, Corticoids as well as physical body cooling favourably influenced the clinical course and the patient survived. In both cases the patients underwent succinylcholine and halothane anaesthesia, but the symptoms of the second patient appeared after the reduction of anaesthesia. In spite of vigorous therapy the hyperpyrexia resulted in heart arrest and death. Morphologically, both patients showed signs of preexistent myopathy with volumetric alterations of the muscle fibres, centralisation of the nuclei and acute muscle fibre necrosis. On the basis of the observed variable course, the various symptom complexes reported in the literature to data are reviewed. A detailed discussion of the "carrier problem" and the available treatment possibilities is also made. Realising that malignant hyperthermia is an inheritable disease, prophylactic measures such as, f.i. the issue of medical certificates to the patient and his relatives are suggested.
Pretreatment with cycloheximide prevents virus-induced fever in rabbits. Compared to the febrile control animals, CH-pretreated afebrile animals exhibit similar concentrations of endogenous pyrogen in the blood and of prostaglandins of the E-group and adenosine 3', 5'-cycle monophosphate in the cerebrospinal fluid. The fever response seems to involve one or several additional so far unknown mediators which are sensitive to cycloheximide.
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