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Biomedical subjects

H I Miller

Publications and source records attributed to H I Miller.

At least 145 records · Page 8Linked to original sources
PubMed1982

Control of phage lambda development by stability and synthesis of cII protein: role of the viral cIII and host hflA, himA and himD genes.

The cII protein of bacteriophage lambda has a decisive role in the regulatory switch between the lysogenic and lytic pathways of viral development. Recent work has indicated that cII may be the primary control function providing for the initial partition between the two pathways, with other host and viral regulatory genes acting to determine the levels of cII in an infected cell. We have studied the synthesis and stability of cII protein with two experimental systems, phage infection and a cII-producing plasmid. We have found that the stability of cII is controlled by the host hflA and viral cIII genes; hflA protein facilitates degradation of cII, whereas cIII protects cII. The synthesis of cII appears to be under the positive control of the host himA and himD genes. We conclude that posttranscriptional regulation of cII by host and viral genes is critical for the choice of a developmental pathway.

Bacteriophage lambda↗
PubMed1982

Mechanisms of immune haemolysis: cell-dependent destruction of autologous red blood cells in penicillin-induced haemolytic anaemia.

The mechanisms of red blood cell destruction in 2 patients with penicillin-induced immune haemolytic anaemia were investigated. Anti-penicillin antibodies of the IgG subclass were found in the patients' sera and in the eluates of their direct antiglobulin positive red blood cells. Using a rapid 51Cr in vitro assay it was shown that fresh peripheral blood mononuclear phagocytes and granulocytes but not lymphocytes from both patients lysed and phagocytosed autologous red blood cells previously treated in vivo or in vitro by penicillin and autologous anti-penicillin antibody. Antibody-dependent cell-mediated cytotoxicity (ADCC) as well as antibody-dependent phagocytosis (ADPh) were proportional to serum concentration and to the number of attacking cells. Anti-penicillin antibody from 1 patient activated the complement system in vitro but failed to induce lysis of penicillin-treated red blood cells in the presence of complement. These results suggest that ADCC as well as ADPh participate in the destruction of red blood cells in penicillin-induced haemolysis in vivo.

Adult↗
PubMed1981

Direct role of the himA gene product in phage lambda integration.

The integration of phage lambda into the Escherichia coli chromosome is accomplished by a site-specific recombination between two unique DNA sequences (attB on the bacterial genome and attP on the phage; reviewed in refs 2, 3) and requires proteins encoded by both the bacterium and the phage. Genetic and biochemical studies have shown that bacterial strains mutant in the himA gene, located at 38 min on the E. coli map, are defective in the activity of the host-encoded component. They are, moreover, defective for the growth of bacteriophage Mu, for precise excision of transposable antibiotic resistance determinants and for the synthesis of the lambda int gene product. We now show that the himA gene product (phimA) is not solely a regulator of genes involved in integration but is one of two host polypeptides required for integrative recombination.

Bacteriophage lambda↗
PubMed1981

Multilevel regulation of bacteriophage lambda lysogeny by the E. coli himA gene.

Previous experiments have shown that the himA gene of E. coli specifies a protein that is required for bacteriophage lambda integration. lambda Forms clear plaques on himA mutants indicating a possible additional defect in the establishment of repression. We have tested the effects of a himA mutation on the establishment and maintenance of lambda repressor (cl) synthesis and on the synthesis of Int protein. The rate of synthesis of cl and Int after infection by lambda is severely reduced in a strain carrying a himA gene deletion. Synthesis of Int or repressor can occur in the himA- strain if the phage carry constitutive promoters for either the int gene or the cl gene. Maintenance of repression is unaffected by himA mutations as judged by repressor-stimulated transcription of PM fused to the lacZ gene. These results indicate that the himA gene participates in the regulation of the promoter sites specific of the establishment of lysogeny: PE for cl synthesis and PI, for Int production. Since the himA gene product is required also for lambda site-specific recombination, it appears that the himA gene regulates lambda lysogeny at several levels. I discuss the significance of this multilevel regulation to lambda development.

Bacterial Proteins↗
PubMed1981

SOS induction and autoregulation of the himA gene for site-specific recombination in Escherichia coli.

The himA gene of EScherichia coli controls the lysogenization of bacteriophage lambda at the level of catalysis of site-specific recombination and expression of the lambda int and cI genes required for lysogenic development. We have analyzed the regulation of himA by two methods: (i) beta-galactosidase synthesis from a lacZ gene inserted into the himA gene and (ii) detection of radioactive HimA protein after fractionation by two-dimensional gel electrophoresis. We find that himA- mutations produce enhanced expression of the himA gene, indicating that HimA protein controls its own synthesis. The himA gene is also induced by treatment of cells with UV or mitomycin C, suggesting control by the inducible DNA repair (SOS) system regulated by the LexA and RecA proteins. Regulation of himA follows the pattern expected for a typical SOS gene: constitutive high expression in mutants that have inactive LexA or the altered RecA conferred by the recA441 (tif1) mutation and low noninducible expression in a mutant that has a deleted recA gene. We conclude that the himA gene is a component of the inducible SoS response, repressed by LexA and induced by the capacity of activated RecA to cleave LexA. We suggest that HimA may be subject to SOS induction because it functions as an "acquisitionase" for new genetic material and thus is of special utility under conditions of impaired capacity for growth of the bacterial population.

Coliphages↗
PubMed1981

Serial electrophysiological studies in a young patient with recurrent ventricular fibrillation.

A 28-year-old male with recurrent episodes of ventricular fibrillation, which were initiated by very early ventricular premature depolarizations with a normal QT interval, was subjected to three consecutive electrophysiological studies. During the first study, which was carried out to test the efficacy of amiodarone treatment, no ventricular arrhythmias could be induced. While on amiodarone therapy, the patient experienced another syncopal episode and therefore a second electrophysiological study was done. In that study, ventricular fibrillation was induced by ventricular stimulation. During the third study, which was carried out in order to evaluate the effect of the addition of quinidine to the on-going amiodarone therapy, no more than three repetitive ventricular responses could be induced. The patient has been asymptomatic since the third study (fifteen months) with combined therapy of amiodarone and quinidine. The significance of the ability to induce ventricular fibrillation during an electrophysiological study is discussed as well as the value of such studies in determining the long-term efficacy of antiarrhythmic drug therapy.

Adult↗
PubMed1981

Free fatty acid turnover and oxidation after burn shock in guinea pigs.

We have previously shown a rapid decrease in plasma free fatty acid (FFA) concentration and turnover rate immediately after extensive full-skin-thickness burn in a guinea pig model. In the present study the relationship between plasma FFA turnover rate and oxidation after burn was investigated, since the amount of plasma FFA oxidized is determined by the turnover rate and the percent of turnover that is oxidized. Using the constant infusion of 14C-palmitate, we examined the plasma FFA concentration and turnover rate, plasma FFA contribution to carbon dioxide production, percent of plasma FFA turnover that is rapidly oxidized to carbon dioxide, oxygen consumption, carbon dioxide production, and respiratory quotient. We found that in some cases, but not all, plasma FFA concentration and turnover rate were decreased 1-6 hours postburn. Both in the presence or absence of decreased FFA turnover rate, the percent of FFA turnover that was immediately oxidized to carbon dioxide was unchanged. After burn shock, the rate of oxidation of FFA appears to be controlled by the rate of FFA delivery to the tissues.

Adipose Tissue↗
PubMed1981

Increased tissue lipoprotein lipase activity in guinea pigs following burn trauma.

Accelerated clearance of circulating triglycerides has been observed in thermally injured patients, which suggests that lipoprotein lipase (LPL) activity may be increased. The present study was initiated to ascertain if heart, skeletal muscle, or adipose tissue LPL activities are affected by burn trauma in guinea pigs. Anesthetized guinea pigs were immersed into room temperature water (nonburned) or boiling water (burned) to the iliac crest for three seconds and sacrificed seven or 24 hours later. Myocardial and adipose tissue LPL activities were 60% and 125% greater, respectively, in burned guinea pigs 24 hours after injury than in nonburned animals. LPL activity in skeletal muscle from the burned region, red vastus, was significantly increased seven hours after injury, but the change after 24 hours was not significant. Muscle LPL activities examined in the nonburned region, diaphragm and red triceps, were increased 24 hours after thermal injury. Increased tissue LPL activities after thermal injury may enhance the clearance of circulating triglycerides.

Adipose Tissue↗