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Biomedical subjects

E S Miller

Publications and source records attributed to E S Miller.

At least 55 records · Page 3Linked to original sources
PubMed1984

The bacteriophage T4 regA gene: primary sequence of a translational repressor.

The regA gene product of bacteriophage T4 is an autogenously controlled translational regulatory protein that plays a role in differential inhibition (translational repression) of a subpopulation of T4-encoded "early" mRNA species. The structural gene for this polypeptide maps within a cluster of phage DNA replication genes, (genes 45-44-62-regA-43-42), all but one of which (gene 43) are under regA-mediated translational control. We have cloned the T4 regA gene, determined its nucleotide sequence, and identified the amino-terminal residues of a plasmid-encoded, hyperproduced regA protein. The results suggest that the T4 regA gene product is a 122 amino acid polypeptide that is mildly basic and hydrophilic in character; these features are consistent with known properties of regA protein derived from T4-infected cells. Computer-assisted analyses of the nucleotide sequences of the regA gene and its three upstream neighbors (genes 45, 44, and 62) suggest the existence of three translational initiation units in this four-gene cluster; one for gene 45, one for genes 44, 62 and regA, and one that serves only the regA gene. The analyses also suggest that the gene 44-62 translational unit harbors a stable RNA structure that obligates translational coupling of these two genes.

Amino Acid Sequence↗
PubMed1984

Cloning and characterization of gdhA, the structural gene for glutamate dehydrogenase of Salmonella typhimurium.

Glutamic acid is synthesized in enteric bacteria by either glutamate dehydrogenase or by the coupled activities of glutamate synthase and glutamine synthetase. A hybrid plasmid containing a fragment of the Salmonella typhimurium chromosome cloned into pBR328 restores growth of glutamate auxotrophs of S. typhimurium and Escherichia coli strains which have mutations in the genes for glutamate dehydrogenase and glutamate synthase. A 2.2-kilobase pair region was shown by complementation analysis, enzyme activity measurements, and the maxicell protein synthesizing system to carry the entire glutamate dehydrogenase structural gene, gdhA. Glutamate dehydrogenase encoded by gdhA carried on recombinant plasmids was elevated 5- to over 100-fold in S. typhimurium or E. coli cells and was regulated in both organisms. The gdhA promoter was located by recombination studies and by the in vitro fusion to, and activation of, a promoter-deficient galK gene. Additionally, S. typhimurium gdhA DNA was shown to hybridize to single restriction fragments of chromosomes from other enteric bacteria and from Saccharomyces cerevisiae.

Cloning, Molecular↗
PubMed1981

L-Methionine SR-sulfoximine-resistant glutamine synthetase from mutants of Salmonella typhimurium.

Two mutants of Salmonella typhimurium resistant to growth inhibition by the glutamine synthetase transition state analog, L-methionine SR-sulfoximine, were isolated and characterized. These mutants are glutamine bradytrophs and cannot use growth rate-limiting nitrogen sources. Although this phenotype resembles that of mutants with lesions in the regulatory gene for glutamine synthetase, glnG, these mutations do not lie in the glnG gene. Purification and characterization of the glutamine synthetase from one of the mutants and a control strain demonstrated that the mutant enzyme is defective in the reverse gamma-glutamyltransferase activity but has biosynthetic activity that is resistant to inhibition by L-methionine SR-sulfoximine. The mutant enzyme also has a 4.4-fold higher apparent Km for glutamate (0.2 mM versus 2.1 mM, respectively) and a 13.8-fold higher Km for NH3 (6.4 mM versus 0.46 mM) than the enzyme from the control. These data show that the glutamine synthetase protein has been altered by this mutation, designated as glnA982, and suggest that the L-methionine SR-sulfoximine resistance is conferred by a change in the NH3 binding domain of the enzyme.

Drug Resistance, Microbial↗
PubMed1980

Graduate training of family practice residents in Israel.

The educational goals and the actual implementation of the Israeli residency program in family medicine are examined. Except for the lack of required training in gynecology, the program syllabus is based on a sophisticated concept of comprehensive care. The teaching clinics provide residents with excellent patient material and with generally adequate medical facilities; however, important equipment is occasionally lacking, and the administration of the clinic discourages thorough teaching. The instructors are experienced practitioners and highly motivated teachers; They provide excellent role models, but are unable to give the residents adequate feedback or to stimulate deeper personal insight. The residents have heavy service responsibility, but in such areas as the interview technique, pediatrics and gynecology, they fail to acquire necessary skills. Suggestions are made regarding an educational reform of the program that would entail the use of university departments of family practice to support regional networks of teaching clinics.

Adult↗
PubMed1975

Blindness and encephalopathy caused by Helichrysum argyrosphaerum DC. (Compositae) in sheep and cattle.

An outbreak of amaurosis and paresis was observed amongst sheep, and occasionally cattle, which had been grazing on pastures consisting mainly of Helichrysum argyrosphaerum DC. A similar syndrome was produced by feeding the suspect plant to sheep, thereby providing proof if its toxicity. Although none of the sheep became blind and only one developed paralysis, typical sponly lesions were detected in the brains and optic fasciculi of all the experimental animals. The lesion had specific predilection sites, such as the white matter around the lateral ventricles, the optic tracts plus chiasm, the pyramidal tracts and the brachium pontis. Enlargement of the optic fasciculi furthermore gave rise to malacia, papilloedema and retinal changes. Some aged sheep developed cataracts approximately 2-3 months after the initial outbreaks of amaurosis had occurred. Circumstantial and histopathological evidence suggests that the cataracts may be due to chronic Helichrysum poisoning, but this could not confirmed in the present investigation.

Animals↗