Nuclear thermometers for heavy-ion collisions.
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Biomedical subjects
Publications and source records attributed to S Pratt.
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The effects of dopamine and octopamine on adenylate cyclase activity were studied on the head homogenate of adult Culex pipiens mosquitoes in vitro. Both dopamine and octopamine were shown to increase the cyclic AMP content in the homogenate. The antagonist haloperidol blocked the production of cyclic AMP induced from dopamine but had no effect on the production of cyclic AMP induced by octopamine at the concentrations tested. The opiate agonist etorphine was ineffective at reducing cyclic AMP levels induced by either dopamine or octopamine at the concentrations tested.
Morphine stimulates food consumption in the land snail Helix aspersa. This stimulation of food consumption can be blocked by naloxone, the potent opiate antagonist. In addition, this opiate-induced food consumption exhibits tolerance by the sixth day of treatment. This study further highlights opioid mechanisms in relatively simple organisms and also suggests that these mechanisms are "ancient" signal systems.
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The histogenic origin of squamous carcinoma of the stomach (SCS) is controversial. We report the case of a 55-year-old man who developed SCS following successful chemotherapy for generalized well-differentiated lymphocytic lymphoma. The patient's stomach contained both squamous carcinoma arising in squamous metaplasia and chronic atrophic gastritis with intestinal metaplasia. This case is compared to three additional cases of SCS where no such antecedent mucosal changes were evident. The SCS literature is reviewed and the histogenesis regarding the development of pure squamous tumors of the stomach is discussed.
The mechanism of the protective action of methionine and N-acetylcysteine against the toxicity of paracetamol was investigated in vivo. N-acetylcysteine inhibited the O-deethylation of ethoxyresorufin (cytochrome P-448) while methionine enhanced the N-demethylation of benzphetamine (cytochrome P-450) and increased hepatic microsomal levels of cytochrome P-450. These observations indicate that N-acetylcysteine, but not methionine, could afford protection against paracetamol hepatotoxicity, at least partly, by inhibiting cytochrome P-448 activity and thus the generation of the reactive intermediate. However, previous studies demonstrating no decrease in the urinary excretion of glutathione conjugates of paracetamol (derived from the reactive intermediate) in animals treated with N-acetylcysteine suggest that this is unlikely to be the prevailing mechanism of action. Administration of a large dose of paracetamol, as expected, depleted glutathione levels and inhibited cytosolic glutathione transferase activity. Administration of either N-acetylcysteine or methionine 1 h after paracetamol prevented both effects. On the basis of the present work and previously published observations, it is concluded that the major mechanism of action of N-acetylcysteine and methionine in vivo is by acting as precursors of intracellular glutathione.
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The coat protein (CP) open reading frame (ORF) of brome mosaic virus (BMV) has been mutated to study host-related CP functions in barley, a systemic host, and in Chenopodium hybridum L. which supports both local lesion formation and systemic spread of BMV. To test the role of the N-terminal region of CP, mutants C1 to C3, which synthesized the CP lacking first seven amino acids, and mutant D1, which had Trp 22 and Thr 23 replaced with Phe-Gly-Ser, were generated. C1 to C3 inhibited virus systemic spread in C. hybridum but not in barley while D1 only reduced virus accumulation in noninoculated leaves of C. hybridum. More internal CP regions were tested by mutation of Lys 63 to Leu (mutant SP3) and Lys 129 to Arg (mutant SP1). SP1 behaved similarly to C1 to C3 while SP3 similarly to D1. In addition, SP3 reduced concentrations of RNA3 and RNA4 in both hosts. Apparently, various CP regions differentially affect, either directly or indirectly, virus translocation in different hosts, suggesting both the CP and host factors to be important for virus spread. Larger deletions in the CP ORF (mutants BB4 and SX1) or a decrease of CP production by using a frameshift mutant C, inhibited virus systemic spread in both hosts, and delayed the appearance of smaller local lesions on C. hybridum. Thus, the CP is not required for cell-to-cell movement but is required for systemic translocation of BMV.