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Biomedical subjects

J A Lewis

Publications and source records attributed to J A Lewis.

At least 145 records · Page 8Linked to original sources
PubMed1980

Antifolate-resistant Chinese hamster cells. Evidence for dihydrofolate reductase gene amplification among independently derived sublines overproducing different dihydrofolate reductases.

Purification of a cDNA probe specific for dihydrofolate reductase mRNA has allowed the relative quantification of dihydrofolate reductase gene numbers and mRNA levels between a line of Chinese hamster lung fibroblasts sensitive to the antifolate drugs methotrexate and methasquin and sublines which by virtue of their overproduction of the target enzyme dihydrofolate reductase are cross-resistant to these site-specific inhibitors. Previous results have shown that resistant sublines could overproduce one of two molecular weight forms of dihydrofolate reductase, one parental-like (Mr = 21,000) and one nonparental-like (Mr = 20,000), each encoded by a different mRNA present in elevated amounts in resistant cells (Melera, P. W., Wolgemuth, D., Biedler, J. L., and Hession, C. (1980). J. Biol. Chem. 255, 319--322). The cDNA-RNA and cDNA-DNA hybridization experiments reported here confirm the elevated levels of dihydrofolate reductase-specific mRNA in resistant cells and show that the overproduction of either molecular weight form of dihydrofolate reductase is accompanied by amplification in dihydrofolate reductase gene number.

Animals↗
PubMed1980

The effects of amino acid starvation on regulation of polypeptide chain initiation in Ehrlich ascites tumor cells.

The ratio of initiation of protein synthesis in Ehrlich ascites tumor cells in culture is reduced by over 60% in the absence of a single essential amino acid. Cell-free extracts prepared from control and amino acid-starved cells retain some of the translational characteristics of these cells and are able to form [40 S.Met-tRNAfMet] initiation complexes. Studies with inhibitors show that up to 63% of the translation directed by endogenous mRNAs in vitro depends on reinitiation of polypeptide chains. Amino acid starvation inhibits this activity, as well as protein synthesis due to in vitro polysomal run-off, by up to 75%. Analysis of [40 S.Met-tRNAfMet]initiation complexes formed in vitro on native 40 S subunits shows that amino acid starvation causes up to a 77% decrease in the concentration of these complexes relative to the corresponding fed controls. This difference is eliminated by the addition of highly purified eukaryotic initiation factor eIF-2. Factor eIF-3 also stimulates [40 S.Met-tRNAfMet] formation in the cell extracts but does not abolish the difference between fed and starved preparations. Mixing experiments have not so far revealed any inhibitor of initiation complex formation in the starved cell extracts.

Amino Acids↗
PubMed1980

The genetics of levamisole resistance in the nematode Caenorhabditis elegans.

We have characterized a small group of genes (13 loci) in the nematode Caenorhabditis elegans that, when mutated, confer resistance to the potent anthelmintic levamisole. Mutants at the 7 loci conferring the most extreme resistance generally possess almost identical visible and pharmacological phenotypes: uncoordinated motor behavior, most severe in early larval life, extreme resistance to cholinergic agonists and sensitivity to hypo-osmotic shock. Mutants with exceptional phenotypes suggest possible functions for several of the resistance loci. The most extreme mutants can readily be selected by their drug resistance (211 mutants, as many as 74 alleles of one gene). The more common resistance loci are likely to be unessential genes, while loci identified by only a few alleles may be essential genes or genes conferring resistance only when mutated in a special way. We propose that these mutants represent a favorable system for understanding how a small group of related genes function in a simple animal. The extreme drug resistance of these mutants makes them useful tools for the genetic manipulation of C. elegans. And, as the most resistant class of mutants might lack pharmacologically functional acetyl-choline receptors (LEWIS et al. 1980), these mutants may also be of some neurobiological significance.

Alleles↗
PubMed1980

Multicentre post-infarction trial of propranolol in 49 hospitals in the United Kingdom, Italy, and Yugoslavia.

A multicentre study of survivors of an anterior myocardial infarction is reported. The trial consisted of 720 patients and was a double-blind, placebo-controlled study with propranolol 40 mg three times a day. Trial entry was at two to 14 days (mean 8.5 days) and follow-up at one, three, and in most centres, six and nine months. The trial was designed to detect a 50 per cent reduction in mortality and this was not shown. The non-fatal reinfarction rate was similar in both groups. Subgroup analysis identified several prognostic risk factors for death, none of which interacted with treatment.

Clinical Trials as Topic↗
PubMed1980

Poriomania.

Explore the source record for details and available documents.

Electroencephalography↗
PubMed1979

Neuropsychological impairment with schizophrenia vs. acute and chronic cerebral lesions.

Performed detailed neuropsychological evaluations with 25 recently hospitalized schizophrenics in whom systematic neurologic workups had failed to reveal CNS disease. Efforts were made to minimize possible effects of drug-induced extrapyramidal symptoms on test performance. Although the schizophrenics showed some neuropsychological impairment relative to 25 normals, their deficits were not as severe as those of patients known to have either acute or chronic brain disorders (N = 25). The diagnostic accuracy achieved by the tests supports their use in short-term treatment facilities when the differential diagnosis includes schizophrenia and brain disorder, especially acute brain disorder. Schizophrenics' neuropsychological impairment was more correlated with degree of EEG abnormality than with degree of psychosis, which suggests a possible organic basis for the deficits that they showed on testing.

Acute Disease↗
PubMed1979

Influence of soil texture on survival and saprophytic activity of Rhizoctonia solani in soils.

Survival of Rhizoctonia solani in precolonized tablebeet seed was greater in a light-textured sandy loam (SL 1) than in a heavy-textured silty clay loam (SiCL). Reduction in survival as well as competitive saprophytic activity of the pathogen resulted when clays (kaolinite and montmorillonite) were added to SL to prepare soils of heavier texture. Survival and activity of R. solani, however, were not increased when sand was added to SiCL (suppressive to R. solani survival) to make this soil lighter in texture. In natural soils of different textures, activity of R. solani was maintained longer in two light-textured sandy loam soils than in a light-textured loamy sand or loam. During investigation of soil chemical and biological influences on R. solani survival, high K2O content in soil was significantly correlated with low saprophytic activity of the pathogen. In all instances where soil microbial activity as determined by a dehydrogenase assay was high, low saprophytic activity was found. Since high microbial activity or K2O content in soil were not associated with any particular soil type, biological or chemical factors may be more important than soil texture in influencing survival and activity of R. solani in soil.

Glucose↗
PubMed1977

Specific neuroanatomical changes in chemosensory mutants of the nematode Caenorhabditis elegans.

Eight of nineteen chemotactic mutants of the nematode Caenorhabditis elegans have morphological defects in the sensory endings of neurons at the tip of the head. The mutants were obtained as worms swimming away from attractant or found amongst male potency mutants or mutants exhibiting erratic behavior. The nineteen mutants fall into at least twelve complementation groups. Mutants E1034 and E1035, alleles of che-1, show morphological alterations in the sensory endings of amphidial neurons and inner labial type 2 neurons, both prospective chemosensory neurons. Both mutants contain non-complementing ts sterile mutations linked to the chemosensory mutation. E1066 shows abnormalities in all the sheath cells associated with the sensory neurons and in the bundling pattern of the amphidial neurons. E1126 is structurally abnormal only in the sensory endings of inner labial type 2 neurons, supporting a chemosensory role for these neurons. E1033 (che-2) and E1124 (che-3) cause defects in the ciliary structure of all but one type of ciliated sensory neuron in the head. E1062 is grossly defective in head structure and the structure of the male copulatory organ, suggesting these opposite ends of the nematode rich in sensory structures share gene functions in embryogenesis. Our study illustrates the possibilities for genetic dissection of the development of a small set of nerves in a simple organism.

Animals↗