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S Brody

Publications and source records attributed to S Brody.

152 records · Page 9Linked to original sources
PubMed1965

Mechanism studies of suppressor-gene action.

Brody, Stuart (Stanford University, Stanford, Calif.), and Charles Yanofsky. Mechanism studies of suppressor-gene action. J. Bacteriol. 90:687-695. 1965.-Mutations which change the primary structure of the A protein of the tryptophan synthetase of Escherichia coli can be reversed by allele-specific suppressor mutations. Normally, the suppressors of a particular A mutant lead to the appearance of small amounts of a wild-type-like A protein (su-A protein), in addition to the cross-reacting material antigenically similar to the normal A protein (CRM-A protein). In some cases, the particular ratio of su-A protein to CRM-A protein, indicative of a given suppressor gene, was increased when that suppressor gene was transduced into a different strain, such as a K-12 Hfr stock of E. coli. In these cases, there was a general correlation between an increased ratio and a marked instability of the suppressor gene. However, stable suppressed stocks were isolated in the Hfr strain, which also produced a high proportion of su-A protein. The ratios of su-A protein to CRM-A protein remained relatively constant under conditions of tryptophan repression in three different suppressor stocks, suggesting that the formation of each of the su-A proteins does not involve the interaction of a CRM-A protein with any other cellular constituent. It would appear, then, that the changes in the primary structure of the A protein which lead to the formation of the su-A proteins are determined before or during, but not after, the synthesis of the polypeptide chain. The specificity of amino acid activation was investigated in strains bearing one of the suppressor genes. These studies failed to reveal any significant alteration in the amino acyl ribonucleic acid (RNA) synthetases or the transfer RNA molecules for arginine, glycine, histidine, and tyrosine.

Escherichia coli↗
PubMedDate not supplied

Psychoneurocardiology: psychosomatic and somatopsychic approaches to hypertension research.

We introduce the field of psychoneurocardiology, and cite examples of research into psychosomatic and somatopsychic bases for hypertensive development. Beta-adrenergic hyperreactivity (a possible precursor of hypertension), as indexed by electrocardiographic T-wave amplitude suppression, was greater during active than passive coping tasks. The rise in tonic mean arterial blood pressure in normotensives over a 19-month period was a joint function of self-reported daily stress and baroreceptor-dependent pain dampening (as determined by the PRES method of noninvasive controlled carotid baroreceptor manipulation). The latter finding provides support for the learned model of hypertension. In this model, phasic blood pressure increases stimulate the baroreceptors, which in turn dampen pain and stress. The long-term effect of this relief is initially to increase the frequency of such phasic increases, and eventually to produce a tonic elevation in blood pressure.

Humans↗
PubMedDate not supplied

Sensorineural hearing loss due to cochlear otospongiosis: theoretical considerations of etiology.

Several theories have been advanced to explain the sensorineural hearing loss that occurs in patients with otospongiosis: toxic substances produced by the otospongiotic focus; vascular shunts betwen the inner ear vessels and the otospongiotic focus; and atrophy of the organ of Corti and stria vascularis due to unknown causes. Presented here is yet another theory: impingement upon the cochlear walls by the otospongiotic focus, causing a narrowing of the lumen of the cochlea and distortion of the basilar membrane.

Arteriovenous Fistula↗
PubMedDate not supplied

Patients misrepresenting their risk factors for AIDS.

To determine the truthfulness of patients' and research subjects' self-reports of their sexual and drug use histories in studies of human immunodeficiency virus (HIV) transmission and acquired immunodeficiency syndrome (AIDS) risk factors, studies of or pertinent to lying about AIDS risk factors were extracted from MEDLINE and PSYCLIT. The present paper describes normal and pathological motives for misrepresenting risk factors, and reviews the literature on such underreporting. There is much evidence for lying about anal intercourse and intravenous drug use risk factors, implying that the estimates of risk for vaginal transmission of HIV (particularly in Pattern-I industrialized countries) have been inflated. Research on HIV/AIDS behavioural risk factors must include sophisticated methods for the assessment of self-report validity, such as the use of behavioural markers, improved lie scales and interview methods, and physical methods.

Acquired Immunodeficiency Syndrome↗