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R D Estensen

Publications and source records attributed to R D Estensen.

50 records · Page 3Linked to original sources
PubMed1974

Cytochemical electron microscopic studies of the action of phorbol myristate acetate on platelets.

Phorbol myristate acetate (PMA), the active principle of croton oil, is a potent platelet aggregating agent. A previous electron microscopic study indicated that PMA caused selective labilization of platelet granules. The present investigation has employed cytochemical procedures to clarify problems concerning the action of PMA on platelets. Results of this study confirm the suggestion that vacuoles in PMA-treated platelets derive primarily from granules, and demonstrate that the swollen vacuoles are continuous with channels of the open canalicular system (OCS) and surrounding plasma. Despite loss of the barrier separating vacuolated granules from the OCS, the contents of the organelles were not extruded from the PMA aggregated platelets. Stabilization of platelet surface membranes did not inhibit the action of PMA on platelet granules, and examination of replicas of freeze-fractured PMA platelets failed to reveal any specific injury produced by the agent. The findings have elucidated some of the effects of PMA on platelet structure, but have not solved the basic mechanism of drug action.

Alcohols↗
PubMed1972

Cytochalasin B. VI. Competitive inhibition of nucleoside transport by cultured Novikoff rat hepatoma cells.

Cytochalasin B competitively inhibits the transport of uridine and thymidine by Novikoff rat hepatoma cells growing in suspension culture with apparent K(i)'s of 2 and 6 microM, respectively, but has no effect on the intracellular phosphorylation of the nucleosides. Choline transport is not affected by cytochalasin B. Results from pulse-chase experiments indicate that cytochalasin B has no direct effect on the synthesis of RNA, DNA, or uridine diphosphate-sugars. The inhibition of uridine and thymidine incorporation into nucleic acids by cytochalasin B is solely the consequence of the inhibition of nucleoside transport.

Animals↗
PubMed1972

Degranulation of discoid platelets.

Platelet degranulation is a characteristic feature of platelet response to aggregating agents, but the mechanism and route by which secretory organelles are transferred to plasma are still uncertain. In the present study, human platelets were incubated with cytochalasin B, an agent which stabilizes discoid shape, and trypsin, which is known to cause release reaction and degranulation. Platelets treated in this manner retained their disc form, but were nearly devoid of granules and dense bodies. Electron-dense tracers indicated that degranulation was accomplished by fusion of secretory organelles with channels of the open canalicular system. The degranulated discoid platelet appears to survive exposure to cytochalasin B and trypsin and may prove to be a useful model for in vivo and in vitro experimental studies.

Biological Products↗
PubMed1970

Introduction of a heterologous nucleus into enucleated cytoplasms of cultured mouse L-cells.

Mouse L-cells exposed to cytochalasin B undergo random nuclear protrusion and, occasionally, total enucleation. The anucleate cell remains viable for several days. Chick erythrocytes were fused to L-cells with inactivated Sendai virus. The resulting hybrids, containing one or more erythrocyte nuclei in addition to the L-cell nucleus, were treated with cytochalasin B. Through the process of random enucleation, the L-cell nucleus was extruded from some hybrid cells while the erythrocyte nucleus was retained in the hybrid. In other experiments, chick erythrocytes were fused directly to enucleated L-cells. The result in both instances is the introduction of an erythrocyte nucleus into L-cell cytoplasm. The erythrocyte nucleus swells and the hybrid cell is capable of incorporating radioactive uridine.

Animals↗
PubMed1966

Puromycin-induced necrosis of crypt cells of the small intestine of mouse.

Chemical and radioautographic analysis of the small intestine of mice injected intraperitoneally with puromycin revealed an immediate decrease of precursor incorporation into DNA and protein and a delayed decrease of precursor incorporation into RNA. In addition to this decrease of precursor incorporation, damage to the crypt cells, but not to the cells of the villus of the small intestine, was observed. Further examination of other dividing cells (spleen) and nondividing cells (liver and heart) of these mice showed again that only cells of actively dividing tissues were damaged. The metabolic inhibitors actinomycin D, cytosine arabinoside, actidione, and puromycin aminonucleoside were used in an attempt to clarify the mechanism of cell damage by puromycin. The results showed that there was no clear correlation between cell necrosis and the pattern of inhibition of synthesis of DNA, RNA, or protein.

Animals↗