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Biomedical subjects

R Rapoport

Publications and source records attributed to R Rapoport.

27 records · Page 2Linked to original sources
PubMed1975

Metabolic disposition and cardiovascular effects of methyldopate in unanesthetized rhesus monkeys.

Methyldopate, the ethyl ester hydrochloride salt of alpha-methyldopa (alpha-MD), is used extensively in the treatment of severe hypertension. We have developed a high-pressure liquid chromatographic assay to determine the plasma-time concentrations of alpha-MD after intravenous administration of methyldopate and alpha-MD in the monkey in an effort to evaluate the bioavailability of alpha-MD and the extent of in vivo hydrolysis of the amino ester to the amino acid. The results establish that in this experimental situation methyldopate is not metabolically equivalent to alpha-MD.

Animals↗
PubMed1969

Social prognosis.

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Computers↗
PubMedDate not supplied

Fast spin-echo imaging of the temporomandibular joint.

The applicability of a fast spin-echo (FSE) technique for magnetic resonance imaging of the temporomandibular joint (TMJ) was studied, and the technique compared with a conventional spin-echo (CSE) technique. Sagittal T1-weighted CSE and dual-echo FSE images of 50 TMJs in 25 patients with symptoms of internal TMJ derangement were compared. CSE and FSE images were diagnostically comparable in 22 TMJs (44%). The FSE technique was rated better than CSE imaging for delineation of the disk in 26 joints (52%), whereas the CSE technique was rated better in only two joints (4%). The FSE technique was preferred overall in 54% of the joints. Mild to moderate joint effusion was detected in 17 joints because additional T2-weighted data were provided with the dual-echo FSE technique. The study showed that FSE imaging is an effective technique for evaluation of the TMJ. It is faster and diagnostically comparable to or better than CSE imaging, with the added advantage of providing T2-weighted data.

Adult↗
PubMedDate not supplied

Routes and regulation of NADPH production in steroidogenic mitochondria.

The first and rate-limiting step of steroidogenesis is catalyzed by the mitochondrial cholesterol side chain cleavage system that is dependent on NADPH. The pathways of NADPH generation in steroidogenic mitochondria include three major routes catalyzed by: 1. NADP-linked malic enzyme, 2. NADP-linked isocitrate dehydrogenase, and 3. nicotinamide nucleotide transhydrogenase. The main route may differ among cell types and across species. Generally operation of alternative routes, with different substrates is not excluded. The oxidation of NADPH by the mitochondrial P450 systems is not tightly coupled with substrate metabolism, as these systems can reduce O2 by a single electron to produce harmful superoxide radical. To minimize such futile NADPH oxidation, NADPH generation may be regulated by two types of mechanisms: 1. Feedback mechanisms that maintain the ratio of NADPH/NADP+ at a steady-state level by enhancing the rate of NADPH production to keep up with its rate of oxidation, e.g., allosteric regulation of enzymes involved in NADPH production. 2. Hormonal signals that enhance the level of NADPH production in coordination with steroidogenesis. One major hypothesis with experimental evidence is that stimulation of mitochondrial NAD(P)H synthesis is mediated by Ca++ as a second messenger of tropic factors. Tropic stimulation of cells increases the levels of Ca++ in the cytosol and then in the mitochondrial matrix, and the rise in Ca++ activates enzymes involved in NAD(P)H synthesis. These regulatory mechanisms most probably operate in concert adjusted to the steroidogenic activity of the cell.

Animals↗
PubMedDate not supplied

The genetics of autoantibody production in MRL/lpr lupus mice.

We have investigated the influence of background genes in the MRL strain, as compared to C57BL/6, on the induction of autoimmunity in homozygous lpr/lpr mice. We have concentrated on two autoantibodies, anti-Sm and anti-chromatin. The propensity to make anti-Sm is controlled by dominant genes from the MRL background. However, the prevalence of this response is under the control of additional recessive genes. The anti-chromatin response is found in both MRL/Mp-lpr/lpr and in C57BL/6-lpr/lpr mice, but it appears earlier and in higher titers in the former strain. This high responder effect is controlled by dominant genes. In F1 mice between these two strains, both anti-Sm and anti-chromatin antibodies preferentially use the b Igh allotype from the low responder B6/lpr parent. In addition, in the progeny of backcross of the F1 to the MRL/lpr strain, the production of both anti-Sm and anti-chromatin is linked to the b allotype. These results demonstrate the contribution of dominant genes from the MRL background on the induction of severe autoimmunity. They also suggest that the B6 background expresses an Igh allotype particularly amenable to autoantibody production, in spite of the relatively mild SLE-like syndrome in this strain.

Animals↗