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Biomedical subjects

M Rosenthal

Publications and source records attributed to M Rosenthal.

At least 289 records · Page 16Linked to original sources

[Sharp's syndrome (mixed connective tissue disease). Clinical aspects diagnosis and prognosis].

Sharp syndrome (mixed connective tissue disease) is a distinct rheumatic syndrome with symptoms of various connective tissue diseases (rheumatoid arthritis, systemic lupus erythematodes, progressive systemic sclerosis, polymyositis and others). 15 patients with mixed connective tissue disease are described. The clinical picture and diagnostic criteria are evaluated and the course of the disease, treatment and prognosis are discussed.

Adolescent↗

[The effect of treatment on circulating immune complexes in rheumatoid arthritis (author's transl)].

Immune complexes were demonstrated by leucocyte phagocytosis assay in 37 of 55 patients with rheumatoid arthritis. After treatment with gold salts, penicillamine, alpha-mercaptopropionylglycine, immunosuppressive agents or levamisole a substantial fall or elimination of demonstrable circulating immune complexes occurred. In-vitro studies revealed that gold salts in therapeutic concentrations inhibited the phagocytosis of immune complexes, while other drugs - penicillamine, levamisole and all anti-inflammatory agents including corticosteroids - lack this effect. The reduction in circulating immune complexes under basic therapy may be due to a beneficial effect of these agents on the disease process itself. This test may, therefore, be of value in assessing the efficacy of drug treatment.

Antigen-Antibody Complex↗

[The value of RNase-ANA determinations for the diagnosis of Sharp syndrome (mixed connective tissue disease) (author's transl)].

The presence of antinuclear antibodies with speckled pattern is essential for the diagnosis of the Sharp Syndrome (moxed connective tissue disease=MCTD). It is however not a specific finding seen only in this condition. Antinuclear antibodies (ANA) with speckled pattern can be observed in sera of patients with various rheumatic diseases (rheumatoid arthritis, systemic lupus erythematosus, Sjögren Syndrome) and even in healthy persons. Yet, utilizing the differentiation system of the antinuclear antibodies, it seems to be possible to establish the diagnosis of mixed connective tissue disease. The antinuclear antibodies in mixed connective tissue disease show high titres (1:2560--1:20,480), contain IgG and bind complement. The antigen is a ribonucleoprotein (RNP) which is sensitive to ribonuclease treatment. The latter observation allows a differentiation between the ANA in mixed connective tissue disease and the ANA in other conditions, especially in systemic lupus erythematosus and Sjögren Syndrome.

Antibodies, Antinuclear↗

Phenytoin, electric, ionic, and metabolic responses in cortex and spinal cord.

Post-tetanic potentiation (PTP) of monosynaptic reflex was estimated in spinal cords in the drug-free state after the administration of a convulsant dose of penicillin and after the administration of phenytoin. There was no apparent correlation between the degree of depression of PTP and the efficacy of controlling seizure activity by phenytoin. Extracellular potassium levels were measured with ion-selective microelectrodes. The post-stimulation clearing of [K+]0 was not accelerated by phenytoin, and frequently it was slowed. Post-stimulus undershooting of [K+]0 was diminished. Oxidation of NADH in cortex and of cytochrome a, a3 in spinal cord were measured by optical methods. Stimulus-evoked transient oxidation responses evoked by electrical stimulation were depressed by phenytoin. It is concluded that systemic administration of phenytoin in therapeutic doses does not stimulate Na+-K+-activated membrane ATPase in cortex and spinal cord. Unlike other depressants, phenytoin did not cause a reduction of "resting" redox levels of respiratory enzymes. The local regulation of blood flow remained unaltered after phenytoin administration. Phenytoin caused a moderate but consistent depression of the stimulus-evoked responses of potassium activity, electric potential, and oxidative enzymes, consistent with diminished outflow of potassium from cells, owing either to lesser activation of cells or to a lesser exchange of ions.

Animals↗

Marital sexual dysfunction: female dysfunctions.

The diagnosis, treatment, and referral of married women with sexual dysfunctions require information about the current physiologic deficit, previous sexual capacity, level of sexual desire, masturbatory experience, means of orgasmic attainment, preferred sexual partner, quality of marriage, husband's sexual capacities, and method of contraception. For classification purposes, the three basic physiologic deficits--excitement phase dysfunction, orgasmic phase dysfunction, and vaginismus--are subdivided into primary and secondary types. Primary dysfunctions represent longstanding developmental problems and are usually purely psychological in origin. Secondary dysfunctions occur after a period of normal sexual functioning and may be organic or psychological in origin. The actual determinants of dysfunctions are not well understood, but those factors commonly associated are discussed. The lack of knowledge about the nature of sexual desire, prevalence of dysfunctions, and significance of the inability to attain orgasm with coitus is emphasized. The physician's role in giving advice and treatment is defined.

Adult↗

Phenobarbital actions in vivo: effects on extra cellular potassium activity and oxidative metabolism in cat cerebral cortex.

Extracellular potassium activity and changes in the reduction levels of intramitochondrial pyridine nucleotide (NAD) and cytochrome-a,a3 were monitored in the cerebral cortex of cats at rest and during electrical stimulation, before and after administration of sodium phenobarbital. Stimulation of the cortical surface evoked a transient increase in the level of oxidized NAD which was proportional in magnitude to the associated transient elevation of extracellular potassium. Phenobarbital (i.v.) produced, within minutes, a persistent shift in NAD to a more reduced level indicative of decreased oxygen consumption. Electrical excitability of the cortex also decreased within minutes, although there was no concomitant change in the resting extracellular potassium activity. Cortical stimulation produced transient elevations of [K+]0 and NADH oxidation and these responses returned to base lines more slowly following the barbiturate administration. However, the proportionality between NADH oxidation and [K+]0 elevation was not altered by phenobarbital. The kinetics of the cytochrome-a, a3 response to cortical stimulation mirrored those of NADH, implying that phenobarbital was not blocking electron transport in the respiratory chain between NADH and cytochrome-a, a3 even at doses where "resting" tissue oxygen consumption was decreased. The prolongation of recovery metabolism following phenobarbital was interpreted as being the result of protracted elevation of extracellular potassium activity. The slow return to "resting" levels of extracellular potassium is probably caused by interference with passive clearance mechanisms.

Animals↗

Metabolite studies of methamphetamine effects based upon mitochondrial respiratiory state in rat brain.

Methamphetamine-induced changes in metabolite levels were studied based upon a new approach to tissue sampling. In this procedure, the noninvasive, autoindicated redox state of intramitochondrial NADH was used to determine the point at which samples were taken rather than the time after drug injection. By this combination of in situ microfluorometry and tissue assay, a complex sequence of rapid changes in cerebral intermediary metabolism and associated mitochondrial redox shifts were observed. These changes were found to occur over a wide range of time course among animals after drug administration, and this temporal variation in response to the drug may be the factor for previously reported inconsistencies in metabolite patterns after methamphetamine. This finding emphasizes the potential difficulties that temporal variability produces in certain cerebral pharmacological responses and the value of the noninvasive, autoindicated redox keyed technique (NARK analysis) for metabolite sampling.

Anesthesia↗

Increased frequency of HLA B8 in hyperostotic spondylosis.

HLA antigens were determined in 50 patients with hyperostotic spondylosis (Forestier's disease), and compared with 1244 normal controls. There was no significant difference in the distribution of HLA B27 between the two groups. However, there was an increased incidence of HLA B8 among the patients with hyperostotic spondylosis (42 per cent), as compared to the normal controls (17.5 per cent). This difference was statistically significant (p less than 0.005). Sixteen of the 50 patients with hyperostotic spondylosis had evidence of diabetes mellitus, 12 of whom also had the HLA B8 antigen. Thus patients with hyperostotic spondylosis have an increased incidence of HLA B8, associated with an increased incidence of diabetes mellitus.

Diabetes Complications↗