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Biomedical subjects

W M Strauss

Publications and source records attributed to W M Strauss.

21 records · Page 2Linked to original sources

AKR murine thymic leukemias are from a distinct thymic cell lineage and do not express the beta chain of the T-cell antigen receptor.

Characterization of tumors that arise spontaneously in the AKR mouse indicates that they are derived from cells of a distinct T-cell lineage. Cells in this subclass bear surface antigens, designated Tpre, Tthy, Tind, and Tsu, which are encoded by genes in the Tsu linkage group on murine chromosome 12. We have examined the rearrangement and expression of genes encoding the T-cell alpha, beta, and gamma chains in these tumors. Although these cells contain alpha-chain mRNA, they do not produce a normal-sized beta-chain mRNA. Most of them also lack gamma-chain mRNA. Each thymic leukemia was derived from a cell arrested at a different stage of development as defined by their expression of terminal deoxynucleotidyl transferase and Thy-1 mRNA. The data presented here are consistent with a model in which thymocytes expressing Tpre, Tthy, Tind, or Tsu undergo somatic development parallel to the development of other T cells. However, these thymocytes do not appear to differentiate into cells bearing alpha-beta heterodimers of the T-cell antigen receptor.

Animals↗

Morphology and morphogenesis of cerebral ring hemorrhages in anemic monkeys.

Cerebral ring hemorrhages were observed in four species of monkeys with various forms of anemia. The lesions resembled those described in humans with a variety of diseases, including pernicious anemia. The pale centers of most lesions were surrounded by rings of erythrocytes. Also observed were petechiae, pale foci without hemorrhage, and glial nodules. Ultrastructural study revealed that the pale cores were foci of degenerating neurites associated with infiltration of fibrin into the finest interstitial spaces. Leakage of firbinogen and erythrocytes apparently occurred from capillary sized vessels. A few of these were thrombosed, some were normal and some had only small fibrin thrombi in apparent apposition to damaged endothelial tight junctions. These findings suggest that a primary effect of anemia and other insults associated with ring hemorrhages is damage to tight junctions. Consequent fibrinous exudation clogs the interstitium and results in neuritic degeneration.

Anemia↗