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Biomedical subjects

M Lowe

Publications and source records attributed to M Lowe.

At least 73 records · Page 4Linked to original sources
PubMed1988

Cloning and characterization of Bacillus subtilis homologs of Escherichia coli cell division genes ftsZ and ftsA.

The Bacillus subtilis homolog of the Escherichia coli ftsZ gene was isolated by screening a B. subtilis genomic library with anti-E. coli FtsZ antiserum. DNA sequence analysis of a 4-kilobase region revealed three open reading frames. One of these coded for a protein that was about 50% homologous to the E. coli FtsZ protein. The open reading frame just upstream of ftsZ coded for a protein that was 34% homologous to the E. coli FtsA protein. The open reading frames flanking these two B. subtilis genes showed no relationship to those found in E. coli. Expression of the B. subtilis ftsZ and ftsA genes in E. coli was lethal, since neither of these genes could be cloned on plasmid vectors unless promoter sequences were first removed. Cloning the B. subtilis ftsZ gene under the control of the lac promoter resulted in an IPTGs phenotype that could be suppressed by overproduction of E. coli FtsZ. These genes mapped at 135 degrees on the B. subtilis genetic map near previously identified cell division mutations.

Amino Acid Sequence↗
PubMed1986

Investigation of alternative mechanisms of collagen-induced platelet activation by using monoclonal antibodies to glycoprotein IIb-IIIa and fibrinogen.

Anti-HuPl-ml (reactive with IIIa) and anti-C2G7 (reactive with the carboxyl terminal of the alpha chain of fibrinogen) were used to investigate platelet aggregation, fibrinogen binding and thromboxane synthesis induced by low dose collagen (LDC) or high dose collagen (HDC) in normal or aspirin treated platelets. Anti-HuPl-ml and anti-C2G7 inhibited LDC induced platelet aggregation almost completely whilst abolishing fibrinogen binding; thromboxane production although reduced, still occurred. Thus LDC activation was dependent on fibrinogen binding to Gp IIIa. Aggregation of platelets induced by HDC was inhibited with anti-C2G7 or anti-HuPl-ml by 15-35% in association with a modest reduction in thromboxane (TxB2) production (with anti-HuPl-ml) and total inhibition of fibrinogen binding. When anti-HuPl-ml was added to aspirin treated platelets, aggregation with HDC although substantially reduced was not totally abolished. Collagen appears to activate platelets in a dose related manner in which there are at least three possible mechanisms via: (i) GpIIb-IIIa and associated fibrinogen binding; (ii) prostaglandin pathway; (iii) an alternate pathway responsible for approximately 20%-30% of platelet aggregation.

Antibodies, Monoclonal↗
PubMed1986

Overproduction of FtsZ suppresses sensitivity of lon mutants to division inhibition.

Escherichia coli lon mutants are sensitive to UV light and other DNA-damaging agents. This sensitivity is due to the loss of the lon-encoded ATP-dependent proteolytic activity which results in increased stability of the cell division inhibitor SulA. Introduction of the multicopy plasmid pZAQ containing the ftsZ gene, which is known to increase the level of FtsZ, suppressed the sensitivity of lon mutants to the DNA-damaging agents UV and nitrofurantoin. Alterations of pZAQ which reduced the expression of ftsZ reduced the ability of this plasmid to suppress the UV sensitivity. Examination of the kinetics of cell division revealed that pZAQ did not suppress the transient filamentation seen after exposure to UV, but did suppress the long-term inhibition that is normally observed. lon strains carrying pZAQ could stably maintain a multicopy plasmid carrying sulA (pBS2), which cannot otherwise be introduced into lon mutants. In addition, the increased temperature sensitivity of lexA(Ts) strains containing pBS2 was suppressed by pZAQ. These results suggest that SulA inhibits cell division by inhibiting FtsZ and that this interaction is stoichiometric.

Alleles↗
PubMed1983

Factor structure and norms for the Revised Behavior Problem Checklist in New Zealand children.

The Revised Behavior Problem Checklist (RBPC) is a recent expansion of the widely used Behavior Problem Checklist. This study attempted to replicate the factor structure of the RBPC, originally developed for U.S.A. children, and to establish norms for its use with New Zealand children. Two groups of children, aged five to 13 years, were rated on the scale by their parents. One was a clinic sample and comprised 266 patients attending two psychiatric clinics. The second was a random community sample of 267 children, from four census tracts in Auckland, selected to cover a range of socioeconomic strata representative of New Zealand. Factor analysis of the clinic data resulted in a factor structure similar to that found in American children. Only two of the six factors (Socialised Aggression and Psychotic Behaviour) differed to any degree. Using ratings from the community sample, norms were developed for screening and diagnostic purposes.

Adolescent↗
PubMed1982

Immunological approaches to the study of membrane receptors. A monoclonal antibody that inhibits the binding of asialoglycoproteins to the rat liver receptor.

The major polypeptide (43,000 daltons) of the rat liver receptor for asialoglycoproteins was isolated by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis. Antibodies raised in a goat against this SDS-treated polypeptide exhibited marked cross-reactivity toward the SDS-denatured forms of the two other prominent polypeptides (54,000 and 64,000 daltons) of the receptor preparation. Monoclonal antibodies directed against the receptor were prepared using the spleen cells of mice immunized with the soluble, active receptor purified by affinity chromatography. The most extensively characterized of the monoclonal antibodies, designated D3-5D3, recognized the solubilized receptor and bound to the exterior surface of isolated rat hepatocytes. The binding of D3-5D3 to hepatocytes prevented subsequent binding of the ligand, 125I-asialo-orosomucoid. Conversely, occupation of the receptor with ligand inhibited binding of 125I-IgG prepared from D3-5D3 ascites fluid. The secondary structure of the receptor appears to be critical for recognition by D3-5D3, since denaturation of the receptor with 1% SDS, 5% beta-mercaptoethanol at 100 degrees C abolished antibody binding. Under less denaturing conditions (0.1% SDS, 25 degrees C), antigenic reactivity was retained by the receptor. Preparative electrophoresis using the latter conditions permitted the demonstration that D3-5D3 recognized a unique determinant that is present in each of the three polypeptides.

Animals↗
PubMed1981

beta-Adrenergic receptors stimulated peroxidase secretion from rat lacrimal gland.

Incubation of rat extraorbital lacrimal gland slices with the beta-agonist isoproterenol caused peroxidase secretion but no K+ release. The peroxidase secretion was inhibited by propranolol. Addition of dibutyryl cyclic AMP or adenosine 3'5'-cyclic phosphorothioate to lacrimal slices produced peroxidase secretion at a higher rate than that obtained with optimal concentration of isoproterenol. Methyl isobutylxanthine is also a strong stimulator of peroxidase secretion. Peroxidase activity was determined by a modified sensitive guaiacol method. Membrane fraction of lacrimal cells was shown to contain an isoproterenol-stimulated adenylate cyclase activity. It is therefore suggested that there is a beta-adrenergic receptor in the rat lacrimal gland and that its stimulation causes activation of an adenylate cyclase which leads to peroxidase secretion.

1-Methyl-3-isobutylxanthine↗