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Biomedical subjects

J Pierce

Publications and source records attributed to J Pierce.

At least 19 recordsLinked to original sources
PubMed1992

First-year impact of the 1989 California cigarette tax increase on cigarette consumption.

We employed a time series design to evaluate the impact of the 1989 California cigarette tax increase on cigarette consumption in California. Adult per capita consumption data from 1980 to 1990 were analyzed for California and the United States. Trend data indicated a sharp drop in California cigarette consumption coincident with the tax increase. Time-series regression analyses support this observation, and suggest that a 5% to 7% decline in consumption is attributable to the tax increase.

California↗
PubMed1992

The California Diabetes and Pregnancy Program: implementation of a multicenter experience with diabetic pregnancies.

The California Diabetes and Pregnancy Program (CDAPP) began in 1984 as a multicenter, collaborative project with support provided by the state Department of Health Services, Maternal and Child Health Branch. Between its inception and 1988, it expanded from three to eight perinatal regions, making the CDAPP model of care available to patients in 19 clinical affiliate sites. The care was provided by a multidisciplinary team composed of physicians, a diabetes educator, a registered dietician, a social worker, and appropriate consultants. The elements of this model of care included comprehensive patient education, active patient participation in care, maternal and perinatal medical assessment, and collection of standardized patient information adequate to allow a programmatic and medical evaluation of the CDAPP. Despite impressive growth of the program by December 1988, statewide implementation of CDAPP is incomplete.

Adolescent↗
PubMed1992

Humoral and cell surface interactions during gamma-irradiation leukemogenesis in vitro.

Gamma-irradiation of plateau phase cultures of the clonal murine bone marrow stromal cell line D2XRII followed by cocultivation of a clonal interleukin 3 (IL-3) (granulocyte-macrophage colony-stimulating factor (GM-CSF)-dependent hematopoietic progenitor cell line FDC-P1JL26 results in a significant increase in "cobblestone islands" of attachment and emergence of subclonal factor-independent malignant sublines. Biochemical purification of conditioned medium from irradiated D2XRII cells yielded a 75,000-dalton glycoprotein termed leukemogenic stromal factor (LSF) that was neutralized by a polyclonal antiserum to murine macrophage colony-stimulating factor (M-CSF). A monoclonal antibody to the murine M-CSF receptor (c-fms) neutralized the biological activity of this molecule in a manner comparable to its effect on recombinant human or murine M-CSF. FDC-P1JL26 parent cells were positive for Ly5, MEL-14, mGR, VLA-4, PGP-1 (CD44), and Thy1.2. After culture in LSF, Thy1.2, MEL-14, and mGR became undetectable; however, significant cell surface MAC-1 antigen and c-fms (M-CSF receptor) were expressed. Neither line was positive for Ly6, Ly22, I-CAM-1, or B220 antigen. LSF-precultured FDC-P1JL26 cells transferred as single cells to microwell culture with 5000-cGy-irradiated D2XRII cells revealed a 60-fold increase in frequency of cobblestone island formation and evolution of factor-independent subclones compared to the parent line. Both parent and LSF-precultured cells became factor independent at a 100-fold lower frequency if kept in suspension in LSF in the absence of stromal cells. Antiserum to M-CSF or monoclonal antibody to the murine M-CSF receptor (c-fms) did not inhibit or displace cobblestone island formation by either clone of FDC-P1 on irradiated stromal cells indicating a mechanism of binding not involving the M-CSF receptor. However, anti-serum to the M-CSF receptor inhibited growth of one factor-independent subclone. In separate studies, a subclone of IL-3-dependent 32Dc13 cells, expressing the transfected murine c-fms protooncogene but not the parent 32Dc13 cell line or another subclone expressing the transfected gene for the human M-CSF receptor, showed adherence and became factor independent when cocultivated with irradiated D2XRII stromal cells. Thus, irradiated stromal cells bind M-CSF receptor-positive hematopoietic progenitor cells and induce c-fms-dependent factor-independent tumorigenic subclones. The cellular interactions in this model may be relevant to gamma-irradiation leukemogenesis in vivo.

Animals↗
PubMed1991

Mouse platelet-derived growth factor receptor alpha gene is deleted in W19H and patch mutations on chromosome 5.

The mouse W19H mutation is an x-ray-induced deletion of more than 2 centimorgans on chromosome 5 encompassing the white spotting mutation W (encoded by the Kit protooncogene), patch (Ph), and recessive lethal (l) loci. The platelet-derived growth factor receptor alpha gene (PDGFRA) like Kit encodes a transmembrane receptor tyrosine kinase. By using mouse-Chinese hamster somatic cell hybrids and haplotype analysis in interspecific backcross mice, mouse Pdgfra was mapped to chromosome 5 in tight linkage with Kit. Hybridization of a PDGFRA probe to DNAs from W19H/ + heterozygous mice and patch heterozygous mice, and their wild-type littermates, demonstrated deletion of Pdgfra. Pulsed-field gel electrophoresis indicated that Kit and Pdgfra are linked on a 630-kilobase Mlu I DNA fragment. Thus the W19H deletion removes at least two receptor tyrosine kinases and the results suggest Pdgfra as a candidate for the Ph locus.

Animals↗
PubMed1991

The kinase insert domain of colony stimulating factor-1 receptor is dispensable for CSF-1 induced phosphatidylcholine hydrolysis.

Mouse NIH 3T3 fibroblasts transfected with human colony stimulating factor-1 receptor produced diacylglycerol in response to CSF1 and this correlated with elevated phosphatidylcholine hydrolyzing activity measured in an in vitro assay. Treatment of cells with the isoflavone derivative genistein attenuated PC hydrolysis in vitro suggesting a role for CSF1R tyrosine kinase activity. A CSF1R mutant lacking 67 amino acids of the kinase insert domain, which may affect the association of receptor with certain substrates, stimulated PC hydrolysis in response to CSF1. Coupling to PC hydrolysis is likely a general property of CSF1R and the kinase insert domain is dispensable for this activity.

Animals↗
PubMed1991

A mutational analysis of phosphatidylinositol-3-kinase activation by human colony-stimulating factor-1 receptor.

Colony-stimulating factor-1 (CSF1) is a cell lineage-specific hemopoietin required for the growth, differentiation, and survival of macrophages and their precursors. The human CSF1 receptor (CSF1R) is a 150-kDa transmembrane glycoprotein whose cytoplasmic tyrosine kinase domain is split by a kinase insert (KI) region of approximately 70 amino acids. We tested the ability of CSF1R KI domain deletion mutants to stimulate phosphatidylinositol-3-kinase (PtdIns-3-kinase), an enzyme whose activity is augmented by tyrosine kinase oncogenes and receptor tyrosine kinases, and to support mitogenesis in transfected cells. Receptor immunoprecipitates from CSF1-stimulated cells contained greater than 5-fold more PtdIns-3-kinase activity compared to nonstimulated cells. High performance liquid chromatography analysis of the PtdIns-3-kinase product scraped from thin layer chromatography plates indicated that PtdIns-3-P was produced. CSF1R KI domain deletion mutants retained tyrosine kinase activity in vitro. Receptor immunoprecipitates of two partially overlapping 28 and 30 amino acid KI deletion mutants of CSF1R retained some PtdIns-3-kinase activity, in contrast to immunoprecipitates of CSF1R lacking 67 amino acids of the KI domain. Each deletion mutant stimulated CSF1-dependent DNA synthesis in transfected cells at much reduced levels compared to wild-type receptor expressing cells. These data suggest a role for the CSF1R KI domain in PtdIns-3-kinase association and for CSF1-induced thymidine incorporation into DNA.

1-Phosphatidylinositol 4-Kinase↗
PubMed1989

Quantification of aminofluorene adduct formation and repair in defined DNA sequences in mammalian cells using the UVRABC nuclease.

Using the UVRABC nuclease as a reagent coupled with DNA restriction and hybridization analysis we have developed a method to quantify N-acetoxy-2-acetylaminofluorene (NAAAF)-induced DNA damage in the coding and noncoding sequences of the dihydrofolate reductase (DHFR) gene in Chinese hamster ovary (CHO) cells. High performance liquid chromatography analysis shows that the only DNA adduct formed in NAAAF-treated CHO cells is N-(deoxyguanosine-C8-yl)-2-aminofluorene (dG-C8-AF). DNA sequencing analysis demonstrates that the UVRABC nuclease incises at all potential sites in which dG-C8-AF adduct may form in linear DNA fragments. We have found that the formation and removal of dG-C8-AF adducts in the coding and 3' downstream noncoding sequences of the DHFR domain are similar in cells treated with 10 microM NAAAF (3.1 adducts/14 kilobases); DNA adduct removal attains 70% for both sequences within 24 h. This result contrasts with that obtained for the repair of cyclobutane dipyrimidines in the DHFR gene, in which the repair efficiency is much higher in the coding region than in the 3' downstream noncoding region. Our results suggest that in CHO cells the repair pathway for aminofluorene DNA adducts is not the same as that for cyclobutane dipyrimidines. This new technique has the potential to detect a variety of chemical carcinogen induced DNA adducts at the gene level in cultured cells and in DNA isolated from animal tissues.

2-Acetylaminofluorene↗
PubMed1989

Carbonyl sulfide: an alternate substrate for but not an activator of ribulose-1,5-bisphosphate carboxylase.

Carbonyl sulfide, a competitive inhibitor of ribulose-bisphosphate carboxylase with respect to CO2 (Laing, W. A., and Christeller, J. T. (1980) Arch. Biochem. Biophys. 202, 592-600), is an alternate substrate. Thiocarboxylation was monitored by mass spectrometry as the stoichiometric consumption of carbonyl sulfide. The product, 1-thio-3-phosphoglycerate, was identified by 13C NMR and UV absorption spectroscopy and measured by enzymic conversion to thiolactate, coupled to the oxidation of NADH. The expected stoichiometry of thiocarboxylation was confirmed. The maximal rates of thiocarboxylation for the spinach and Rhodospirillum rubrum enzymes were close to the maximal rates of carboxylation for these two enzymes. Both enzymes favored CO2 over carbonyl sulfide (with Mg2+ as metal ion) by a factor of about 110. Thiocarboxylation could only be demonstrated with enzymes carbamylated with CO2. Incubation of the carbamylated E.ACO2.Mg complex with excess carbonyl sulfide caused the displacement of the activator carbamate. The thiocarbamylated enzyme was catalytically incompetent and did not form a stable quaternary complex with 2'-carboxyarabinitol bisphosphate. Incubation of the thiocarbamylated enzyme with excess CO2 resulted in the displacement of the thiocarbamate, the re-formation of the carbamylated E.ACO2.Mg complex and the restoration of catalytic competence. Computergraphic simulation of the thiocarbamylated quaternary complex indicated unfavorable van der Waals interactions associated with the thiocarbamate.

Binding Sites↗
PubMed1989

Isolation of a novel receptor cDNA establishes the existence of two PDGF receptor genes.

A genomic sequence and cloned complementary DNA has been identified for a novel receptor-like gene of the PDGF receptor/CSF1 receptor subfamily (platelet-derived growth factor receptor/colony-stimulating factor type 1 receptor). The gene recognized a 6.4-kilobase transcript that was coexpressed in normal human tissues with the 5.3-kilobase PDGF receptor messenger RNA. Introduction of complementary DNA of the novel gene into COS-1 cells led to expression of proteins that were specifically detected with antiserum directed against a predicted peptide. When the new gene was transfected into COS-1 cells, a characteristic pattern of binding of the PDGF isoforms was observed, which was different from the pattern observed with the known PDGF receptor. Tyrosine phosphorylation of the receptor in response to the PDGF isoforms was also different from the known receptor. The new PDGF receptor gene was localized to chromosome 4q11-4q12. The existence of genes encoding two PDGF receptors that interact in a distinct manner with three different PDGF isoforms likely confers considerable regulatory flexibility in the functional responses to PDGF.

Amino Acid Sequence↗
PubMed1989

A cyanobacterial mutant requiring the expression of ribulose bisphosphate carboxylase from a photosynthetic anaerobe.

Ribulose bisphosphate carboxylase is essential for both photoautotrophic and photoheterotrophic growth of the cyanobacterium Synechocystis 6803. However, a mutant lacking cyanobacterial carboxylase could be obtained by replacing the natural carboxylase gene with the corresponding gene from Rhodospirillum rubrum, a photosynthetic anaerobe. This treatment produced an organism whose growth depended on the activity of the structurally and functionally dissimilar foreign carboxylase. As a further consequence of this mutagenic replacement, the mutant also lacked microscopically observable carboxysomes, the subcellular inclusion bodies in which the wild-type carboxylase naturally resides. The mutant, dependent on a carboxylase with an inferior relative specificity for CO2 versus O2 and apparently lacking carboxysomes, is extremely sensitive to the CO2/O2 ratio supplied during growth and is unable to grow at all in air. This response to the gas composition should prove useful for selection of various R. rubrum carboxylase mutants with altered specificities for CO2 and O2.

Anaerobiosis↗
PubMed1989

Patterns of Doppler recordings and its relationship to varicocele in infertile men.

Incompetence of the testicular vein appears to be the basic pathology of testicular dysfunction in varicocele. Doppler recording is a very sensitive method for detecting this reflux even when varicocele is not evident clinically. One hundred and seventy-eight men with infertility were studied. The presence of reflux in the pampiniform plexus as demonstrated by Doppler recording was compared with clinical varicocele. Reflux patterns were recorded on graph paper and various grades of reflux were observed. The three grades of reflux identified varied between a momentary reflux during vigorous Valsalva manoeuvre to significant reflux on minimal increase in intra-abdominal pressure brought about by normal respiration and deep breathing. Ninety-four per cent of the patients with clinical signs of varicocele had refluxes of grade 2 and 3 on Doppler study. Forty per cent of the patients without clinical evidence of varicocele were found to have reflux of grade 1 and 2 in the testicular veins.

Humans↗
PubMed1989

Coronary risk factor outcomes following coronary artery bypass surgery.

The coronary risk factor status of patients prior to and following coronary artery bypass surgery (CABG) has been poorly investigated. Two consecutive series of CABG patients were surveyed following CABG. One hundred and thirty patients were assessed immediately following CABG and 530 patients were assessed 12-30 months following CABG. For the long-term post-CABG group, over 80% of those who had ever smoked had ceased. Sixty-four per cent of these males and 50% of females were classified as being overweight. Twenty-five per cent of males and 34% of females reportedly had high serum cholesterol (i.e. greater than or equal to 6.5 mmol/L). Comparing these CABG data with age-adjusted National Heart Foundation Risk Factor Prevalence Survey data, there was a higher prevalence of ex-smokers, overweight, hypertension, and elevated cholesterol. It was concluded that on most coronary risk factors, except for smoking, these CABG patients had a worse profile than the general Australian community. This problem warrants further research and the development of appropriate treatment programs.

Adult↗
PubMed1988

Recognition of the DNA helix stabilizing anthramycin-N2 guanine adduct by UVRABC nuclease.

The binding of the anti-tumor antibiotic anthramycin to a defined linear DNA fragment was investigated using both exonuclease III and lambda exonuclease. We show that most of the guanine residues are reactive toward anthramycin; however, several guanine residues showed preferential reactivity for the drug. Using purified UVRA, UVRB and UVRC proteins we present evidence that these three proteins in concert are able to recognize and produce specific strand cleavage flanking anthramycin-DNA adducts. The cleavage of anthramycin adducts by UVRABC nuclease is specific and results in strand breaks at five or six bases 5' and three or four bases 3'-flanking an adduct. At some guanine residues single incisions were observed only on one side of the adduct. The 5' strand breaks observed often occurred as doublet bands on sequencing gels, indicating plasticity in the site of 5' cleavage whereas the 3' cleavage did not show this effect. When DNA fragments modified with elevated levels of anthramycin were used as substrates the activity of the UVRABC nuclease toward the anthramycin adducts decreased. Possible mechanisms for the recognition and specific cleavage of the helix-stabilizing anthramycin DNA adduct and other helix destabilizing lesions by the UVRABC nuclease are discussed.

Anthramycin↗
PubMed1988

Cooperation of V-oncogenes in human epithelial cell transformation.

The development of tissue culture systems for propagation of human epithelial cells has aided the investigation of events that lead epithelial cells to become neoplastic. In the present study, nontumorigenic human epidermal keratinocytes, immortalized by Ad12-SV40 virus or pSv3-neo, were transformed by a variety of retroviruses containing bas, H-ras, fes, fms, erbB and src oncogenes. Such transformants showed morphological alterations and induced carcinomas when transplanted into nude mice. These findings demonstrate the malignant transformation of human primary epithelial cells in culture by the combined action of Ad12-SV40 virus and retroviral oncogenes and support a multistep process for neoplastic conversion. This in vitro system may be useful in studying the interaction of a variety of retroviral oncogenes and human epithelial cells.

Adenoviridae↗