Search PubMed⌕ Search

Biomedical subjects

D A Foster

Publications and source records attributed to D A Foster.

71 records · Page 4Linked to original sources
PubMed1991

Cholera toxin induces expression of the immediate-early response gene JE via a cyclic AMP-independent signaling pathway.

Cholera toxin (CT) activates expression of two immediate-early response genes (JE and TIS10) in quiescent BALB/c 3T3 cells. Increases in cyclic AMP (cAMP) levels in response to CT are likely responsible for the induction of TIS10 gene expression, since treatment with 8-Br-cAMP and increasing the intracellular levels of cAMP by treatment with forskolin induce TIS10 gene expression. In contrast, neither forskolin nor 8-Br-cAMP induces JE gene expression. 3-Isobutyl-1-methylxanthine, which stabilizes intracellular cAMP, potentiates CT-induced TIS10 gene expression but has no effect on CT-induced JE gene expression. Thus, induction of JE by CT is independent of the cAMP produced in response to CT. Induction of JE by CT does not require protein kinase C (PKC), since depleting cells of PKC activity has no effect on the induction of JE by CT. CT-induced expression of JE can be distinguished from CT-induced TIS10 gene expression by using protein kinase inhibitors and inhibitors of arachidonic acid metabolism, further suggesting distinct signaling pathways for CT-induced JE and TIS10 gene expression. Thus, induction of JE gene expression by CT results from the activation of an intracellular signaling pathway that is independent of cAMP production. This pathway is independent of PKC activity and uniquely sensitive to inhibitors of protein kinases and arachidonic acid metabolism.

1-Methyl-3-isobutylxanthine↗
PubMed1991

v-Src increases diacylglycerol levels via a type D phospholipase-mediated hydrolysis of phosphatidylcholine.

Activating the protein-tyrosine kinase of v-Src in BALB/c 3T3 cells results in rapid increases in the intracellular second messenger, diacylglycerol (DAG). v-Src-induced increases in radiolabeled DAG were most readily detected when phospholipids were prelabeled with myristic acid, which is incorporated predominantly into phosphatidylcholine. Consistent with this observation, v-Src increased the level of intracellular choline. No increase in DAG was observed when cells were prelabeled with arachidonic acid, which is incorporated predominantly into phosphatidylinositol. Inhibiting phosphatidic acid (PA) phosphatase, which hydrolyzes PA to DAG, blocked v-Src-induced DAG production and enhanced PA production, implicating a type D phospholipase. Consistent with the involvement of a type D phospholipase, v-Src increased transphosphatidylation activity, which is characteristic of type D phospholipases. Thus, v-Src-induced increases in DAG most likely result from the activation of a type D phospholipase/PA phosphatase-mediated signaling pathway.

Animals↗
PubMed1991

v-Src activates both protein kinase C-dependent and independent signaling pathways in murine fibroblasts.

Activating the protein-tyrosine kinase activity of v-Src rapidly induced expression of the two 'primary response' genes, TIS10 and Egr-1, in Balb/c 3T3 cells. Depleting cells of protein kinase C (PKC) by prolonged exposure to 12-O-tetradecanoylphorbol 13-acetate (TPA), blocked v-Src-induced TIS10 expression, but had no effect on v-Src-induced Egr-1 gene expression. In addition, the induction of TIS10 and Egr-1 by v-Src could be distinguished using protein kinase inhibitors. Thus, v-Src induced gene expression in murine fibroblasts via two distinguishable signaling pathways: one dependent upon PKC and another that is independent of PKC. Consistent with the use of PKC-mediated signaling pathway by v-Src in murine fibroblasts, we found that activating the kinase activity of v-Src led to increased phosphorylation of a major PKC substrate. Thus, data presented here suggest that v-Src-induced transformation involves the activation of multiple signalling pathways, one of which requires PKC.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

Antibody response to inactivated influenza vaccines of various antigenic concentrations.

Four inactivated influenza vaccines (containing the recommended antigens for the 1985-1986 influenza season) of various antigenic concentration levels were randomly administered to 140 study participants. The effect of the increasing antigen concentration resulted in significantly higher influenza hemagglutination inhibition (HI) antibody levels 3 weeks after vaccination for the A/H1N1 antigen but not for the A/H3N2 or B antigens. Also, at 3 weeks after vaccination, there were significantly lower antibody titer levels associated with increasing age for the A/H1N1 and B antigens (adjusting for the prevaccination antibody titer and antigen content).

Adult↗
PubMed1990

Use of the confidence interval function.

Graphics displaying all confidence intervals around a point estimate have been referred to as P-value functions and consonance intervals. We recommend use of the term confidence interval function (CI function) rather than P-value function. The CI function is useful because it simultaneously depicts point estimation, variability, and the relation of these two factors to the null value. The usefulness of the CI function in demonstrating the concepts of effect modification and confounding, in meta-analysis, and in the comparison of various confidence interval procedures is evaluated. Software packages that produce CI functions are described.

Confidence Intervals↗
PubMed1989

Evidence that v-src and v-fps gene products use a protein kinase C-mediated pathway to induce expression of a transformation-related gene.

Induction of the transformation-related gene 9E3 by the v-src and v-fps gene products (v-Src and v-Fps) is blocked in chicken embryo fibroblasts depleted of protein kinase C (PKC). PKC agonists induce 9E3 gene expression. Protein kinase inhibitors block v-Src- and v-Fps-induced 9E3 gene expression with the same dose-response curves seen for PKC agonist-induced 9E3 gene expression. These data suggest that v-Src and v-Fps use a PKC-mediated signal-transduction pathway to induce expression of the transformation-related 9E3 gene. Consistent with this hypothesis, we find that both v-Src and v-Fps rapidly induce phosphorylation of a 67-kDa PKC substrate.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1986

Isolation of chicken cellular DNA sequences with homology to the region of viral oncogenes that encodes the tyrosine kinase domain.

A library of chicken genomic DNA was screened for sequences that could hybridize to a cloned DNA fragment containing the transforming gene (v-fps) of Fujinami sarcoma virus. In addition to c-fps, two unique chicken cellular DNA sequences were isolated that hybridized weakly to v-fps. These sequences hybridized with many other viral oncogenes encoding tyrosine kinases. Sequence analysis of the region where homology was detected revealed a region that is highly conserved among the tyrosine kinases both at the nucleotide and amino acid levels. Although we were unable to detect expression of either chicken cellular DNA sequence in a variety of avian tissues, the data suggest the existence of additional members of the tyrosine kinase gene family. Screening genomic libraries for sequences that hybridize weakly to functional regions of other genes may prove useful for the isolation and characterization of additional members of other gene families.

Animals↗
PubMed1985

Activation of the transformation potential of the cellular fps gene.

Chicken cellular-fps (c-fps) sequences were substituted for viral-fps (v-fps) sequences in two retroviral genome structures, one that expressed a c-fps gene product that was indistinguishable from the normal c-fps gene product expressed in chicken bone marrow cells, and another that expressed a gag-fps fusion protein. When c-fps gene sequences (without linked gag gene sequences) were expressed at high levels in a viral vector, no transformation of fibroblasts was detected. It was previously demonstrated that the corresponding v-fps sequences could transform fibroblasts. When the same c-fps sequences were expressed in a form linked to gag gene sequences, transformation of fibroblasts and induction of tumors were observed. The data suggest that the c-fps gene product lacks transformation potential by itself even when overexpressed and that the transformation potential of the c-fps gene can be activated by either mutation (or mutations) in the fps coding region or by fusion with viral gag gene sequences.

Animals↗
PubMed1983

A fps gene without gag gene sequences transforms cells in culture and induces tumors in chickens.

From molecularly cloned DNAs of Fujinami sarcoma virus (FSV) and the Schmidt-Ruppin-A strain of Rous sarcoma virus (SRA), viral DNA was constructed in which fps-specific sequences encoded in FSV replaced the src gene of SRA. A 3' fragment of FSV DNA, from an ATG methionine coding sequence 148 base pairs downstream from the gag-fps junction through the long terminal repeat, was joined to cloned SRA DNA at the translation start site for the src gene. The resultant DNA clone contained the splice acceptor site for src mRNA processing in SRA, but contained no src coding sequences from SRA nor any gag sequences from FSV. All genes for the replication of SRA were retained. Transfection of this cloned viral DNA genome into chicken embryo fibroblasts induced morphological transformation of the cells in culture. However, the morphology of the transformed cells was distinct from that observed in cells infected with wild-type FSV. The transformed cells produced a nondefective transforming virus called F36 which contained a hybrid FSV-SRA long terminal repeat. F36-infected cells produced a protein with the expected molecular weight of 91,000, which had an associated protein kinase activity and was immunoprecipitated by antibodies raised against fps gene determinants but not by antibodies raised against gag or src proteins. Injection of F36 virus into 8-day-old chicks produced tumors at the site of inoculation, detectable within 7 days. These results demonstrated that the gag portion of the gag-fps fusion protein of FSV is not required for transformation or tumorigenesis.

Animals↗
PubMed1982

Resistance of adenoviral DNA replication to aphidicolin is dependent on the 72-kilodalton DNA-binding protein.

Aphidicolin is a highly specific inhibitor of DNA polymerase alpha and has been most useful for assessing the role of this enzyme in various replication processes (J. A. Huberman, Cell 23:647-648, 1981). Both nuclear DNA replication and simian virus 40 DNA replication are highly sensitive to this drug (Krokan et al., Biochemistry 18:4431-4443, 1979), whereas mitochondrial DNA synthesis is completely insensitive (Zimmerman et al., J. Biol. Chem. 255:11847-11852, 1980). Adenovirus DNA replication is sensitive to aphidicolin, but only at much higher concentrations. These patterns of sensitivity are seen both in vivo and in vitro (Krokan et al., Biochemistry 18:4431-4443, 1979). A temperature-sensitive mutant of adenovirus type 5 known as H5ts125 is able to complete but not initiate new rounds of replication at nonpermissive temperatures (P. C. van der Vliet and J. S. Sussenbach, Virology 67:415-426, 1975). When cells infected with H5ts125 were shifted from permissive (33 degrees C) to nonpermissive (41 degrees C) conditions, the residual DNA synthesis (elongation) showed a striking increase in sensitivity to aphidicolin. The temperature-sensitive mutation of H5ts125 is in the gene for the 72-kilodalton single-stranded DNA-binding protein. This demonstrated that the increased resistance to aphidicolin shown by adenovirus DNA replication was dependent on that protein. It also supports an elongation role for both DNA polymerase alpha and the 72-kilodalton single-stranded DNA-binding protein in adenovirus DNA replication. Further support for an elongation role of DNA polymerase alpha came from experiments with permissive temperature conditions and inhibiting levels of aphidicolin in which it was shown that newly initiated strands failed to elongate to completion.

Adenoviruses, Human↗
PubMedDate not supplied

Epidemiology of Reye's syndrome, United States, 1991-1994: comparison of CDC surveillance and hospital admission data.

This investigation describes the epidemiology of Reye's syndrome (RS) during 1991-1994 and compares two different sources of information in the United States. Estimates of the incidence of RS from the Centers for Disease Control and Prevention (CDC) are compared with hospital inpatient data from approximately one third of the hospitals from HCIA, Inc. During 1991-1994, 48 RS cases were reported to the CDC and 93 RS hospitalizations based on HCIA data. When the HCIA data are extrapolated to the US population, there were an estimated 284 hospitalizations. Cases reported from both data sources were similar in distribution by onset, age, and sex. CDC data probably underestimate the incidence of RS due to incomplete reporting and HCIA data may overestimate it because not all cases were known to meet the CDC case definition. The true annual incidence of RS during the study years was probably between 0.2 and 1.1 cases per million population <18 years of age.

Adolescent↗