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Biomedical subjects

M L Weiss

Publications and source records attributed to M L Weiss.

At least 73 records · Page 4Linked to original sources
PubMed1984

Sodium appetite during captopril blockade of endogenous angiotensin II formation.

Angiotensin II and aldosterone increase in response to sodium deficiency to promote sodium and water conservation. In addition, they may act synergistically to arouse a sodium appetite. If so, then blockade of endogenous angiotensin should decrease the appetite. In experiments reported here, captopril (SQ 14,225) was given peripherally to rats to block conversion of angiotensin I to angiotensin II. It both enhanced and suppressed sodium depletion-induced sodium appetite. The appetite was suppressed when captopril was given in high doses, which block conversion centrally as well as peripherally. The same doses of captopril had no effect on urinary sodium excretion or on sodium appetite aroused by mineralocorticoid treatment. Low doses, which block conversion only in the periphery, enhanced salt intake elicited by depletion, and the enhancement was abolished by captopril given directly into the brain. Therefore the enhancement was probably due to a captopril-induced increase of peripheral angiotensin I, which gained access to the brain and was converted there to angiotensin II.

Administration, Oral↗
PubMed1983

Plasmodium berghei: a mouse model for the "sudden death" and "malarial lung" syndromes.

A mouse model for the "sudden death" and "malarial lung" syndromes is described. Mice of the C3H/z strain succumb suddenly approximately 7 days after an infection with Plasmodium berghei becomes patent, at a time when parasitemia is still moderate (6 to 8%). Death could be shown to be due to anaphylactoid shock, probably induced by soluble immune complexes. Increased vascular permeability caused transudation and leakage of serum proteins into the interstitium and the alveoli. The lungs were found to be edematous, with a fine granular precipitate in the alveoli and adherent to the vascular walls. The precipitates reacted with antiglobulins G and M, and could be shown to also contain malaria antigens and C3/4. A dramatic drop in hematocrit was recorded several hours before death, indicating the sudden release of malaria antigens. The myocardium of animals that had died very suddenly showed a patchy loss of phosphorylase activity. This loss of activity was much more extensive, and sometimes almost total, when there had been an agonal period of several (1 to 3) hours before death. In these cases the irreversibility of the myocardial damage was also indicated by the loss of activity of the dehydrogenases, as well as by typical inflammatory reactions of granulocytic and histiocytic infiltrations. The hearts thus presented a typical picture of the acute and peracute shock syndromes. In acute shock cardiac insufficiency develops so suddenly that death ensues before irreversible damage has occurred, and cardiac insufficiency can only be demonstrated by the most sensitive of enzyme histochemical means. In the present case shock was induced by the anaphylactoid activity of immune complexes with the lung as target organ. The described syndrome appears analogous to human "malarial lung."

Animals↗
PubMed1982

Phylogenetic origins and adaptive evolution of avian and mammalian haemoglobin genes.

Recent years have seen rapid growth in amino acid sequence data on globins and nucleotide sequence data on haemoglobin genes and pseudogenes, and cladistic analysis of these data continues to reveal new facets of globin evolution. Our present findings demonstrate: (1) avian and mammalian embryonic alpha genes (pi and xi, respectively) had a monophyletic origin involving an alpha locus duplication about 400 Myr ago soon after the duplication which separated alpha and beta genes; (2) much later in phylogeny, independent beta-gene duplications produced the embryonic rho locus of birds and embryonic epsilon and fetal gamma loci of mammals. This parallels the earlier finding that myoglobins evolved more than once from generalized globin ancestors. Here we support the view that such globin evolution resulted from natural selection acting on mutations in duplicated genes. Thus, our evidence contradicts the neutralist view in which almost all amino acid substitutions in descent to extant globins evaded positive selection.

Amino Acid Sequence↗
PubMed1978

Splenic transposition with ligation of the vascular pedicle in rodents. Immunological consequences.

By splenic subcutaneous transposition and ligation of the vascular pedicle, the direct relation spleen-liver was interrupted in rodents infected with malaria. It was demonstrated that in this situation detoxification of the liver and recovery from malaria was evidently hampered by the lack of a direct splenic cell supply, due to retardation of the homing and differentiation in the spleen of precursors of immunologically competent cells. In the presence of blood-borne antigens and/or hepatotoxins, this simple 'shunt' operation appears to constitute a serious immunological handicap. However, it may be a useful model for the study of cellular and microenvironmental interrelationships of the immune response versus blood-borne antigens.

Animals↗