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Biomedical subjects

E White

Publications and source records attributed to E White.

At least 289 records · Page 16Linked to original sources
PubMed1988

Association of food frequency questionnaire estimates of vitamin A intake with serum vitamin A levels.

To assess the validity of nutrient intake estimates from a food frequency questionnaire, the authors compared estimates of intake of preformed retinol (dietary plus supplements), beta-carotene, other active carotenoids, and total vitamin A computed from questionnaire responses with serum retinoid and carotenoid concentrations. Data were obtained from 302 male and female current or former smokers, participants in a lung cancer chemoprevention trial at the Fred Hutchinson Cancer Research Center in Seattle, Washington, during 1985-1986. Both serum beta-carotene and serum alpha-carotene were associated, although weakly, with food frequency estimates of total vitamin A intake, dietary vitamin A, beta-carotene, other carotenoids, and total carotenoids (0.18 less than or equal to r less than or equal to 0.26). Serum retinol was associated with supplementary vitamin A intake (r = 0.16). Nondietary factors were also associated with serum nutrient concentrations--in particular, cigarette smoking, alcohol intake, and body mass index. Cigarette smoking emerged as an important modifying factor of the relation between serum beta-carotene and dietary beta-carotene (r = 0.14 for current smokers, r = 0.30 for former smokers).

Aged↗
PubMed1988

Differential distribution of the adenovirus E1A proteins and colocalization of E1A with the 70-kilodalton cellular heat shock protein in infected cells.

Five distinct localization patterns were observed for the adenovirus E1A proteins in the nuclei of infected HeLa cells: diffuse, reticular, nucleolar, punctate, and peripheral. The variable distribution of E1A was correlated with the time postinfection and the cell cycle stage of the host cell at the time of infection. All staining patterns, with the exception of peripheral E1A localization, were associated with the early phase of infection since only the diffuse, reticular, nucleolar, and punctate staining patterns were observed in the presence of hydroxyurea. Because the E1A proteins (12S and 13S) stimulate the expression of the cellular heat shock 70-kilodalton protein (hsp70), we examined the intracellular distribution of hsp70 in the adenovirus-infected cells. Whereas hsp70 was predominantly cytoplasmic in the cells before infection, after adenovirus infection most of the protein was now found within the nucleus. Specifically, hsp70 was found within the nucleoli as well as exhibiting reticular, diffuse, and punctate nuclear staining patterns, analogous to those observed for the E1A proteins. Double-label indirect immunofluorescence of E1A and hsp70 in infected cells demonstrated a colocalization of these proteins in the nucleus. Translocation of hsp70 to the nucleus was dependent upon both adenovirus infection and expression of the E1A proteins. The localization of hsp70 was unaltered by infection with an E1A 9S cDNA virus which does not synthesize a functional E1A gene product. Moreover, the discrete nuclear localization patterns of E1A and the colocalization of E1A with hsp70 were not observed in adenovirus-transformed 293 cells which constitutively express E1A and E1B. E1A displayed exclusively diffuse nuclear staining in 293 cells; however, localization of E1A into the discrete nuclear patterns occurred after adenovirus infection of 293 cells. Immunoprecipitation of labeled infected-cell extracts with a monoclonal antibody directed against the E1A proteins resulted in precipitation of small amounts of hsp70 along with E1A. These data indicate that the adenovirus E1A proteins colocalize with, and possibly form a physical complex with, cellular hsp70 in infected cells. The relevance of this association, with respect to the function of these proteins during infection and the association of other oncoproteins with hsp70, is discussed.

Adenoviridae↗
PubMed1988

Role of the adenovirus E1B 19,000-dalton tumor antigen in regulating early gene expression.

Mutations in the adenovirus gene encoding the E1B 19-kilodalton protein (the 19K protein) result in pleiotropic phenotypes that affect the host cell and virus growth. Examination of viral gene expression in HeLa cells infected with E1B 19K mutant viruses revealed synthesis and accumulation of E1A proteins to higher steady-state levels than those proteins synthesized during infection with the wild-type virus. As a consequence of elevated E1A levels, another early gene product, the 72K DNA-binding protein, accumulated earlier in mutant-infected cells. In a 12S E1A cDNA virus background, E1B 19K gene mutations had a more profound effect. Larger amounts of the 12S E1A product were present in E1B mutant-infected cells. A deletion mutation that eliminated expression of the 19K protein was also responsible for a 200-fold increased plaque-forming efficiency of the 12S cDNA virus in HeLa cells and an increased rate of virus production. Therefore, the E1B 19K tumor antigen may function to down-regulate virus replication by repressing E1A-dependent gene transcription. Eliminating expression of the E1A 13S and 12S gene products by substitution of an E1A 9S cDNA gene, however, uncovered a stimulatory effect of the E1B 19K protein on early gene expression and virus replication. An E1A 9S virus with a wild-type gene encoding the E1B 19K protein displayed increased early gene transcription, synthesized more 72K DNA-binding protein, and replicated more efficiently than an E1A 9S virus containing a mutation that eliminated expression of the 19K protein. Therefore, the E1B 19K protein has both positive and negative effects on early gene expression and virus replication. In the presence of functional E1A gene products, the 19K protein repressed E1A-dependent gene expression, but in the absence of E1A, the 19K protein stimulated viral gene expression and DNA synthesis. This raises the possibility that the E1B 19K protein functions to repress transcription by modifying the activity of the E1A proteins. Independent of E1A, however, the E1B 19K protein can increase viral gene expression and DNA synthesis, which then leads to increased virus replication.

Adenoviridae↗
PubMed1988

The stability of uric acid in ammonium hydroxide.

We examined the stability of uric acid in dilute aqueous ammonium hydroxide solution by mass spectrometry. Uric acid decomposes in ammonium hydroxide even as dilute as 15 mmol/L when the mole ratio of ammonium hydroxide to uric acid is 50:1. There are at least four products of the decomposition, two of which have been identified as allantoin and urea. The slope of the decomposition curve indicates that uric acid is destroyed at an initial rate of 2-3% per hour. In ammonium hydroxide at a concentration of 1 mmol/L and a mole ratio of ammonium hydroxide to uric acid of less than or equal to 3.4, uric acid is not detectably decomposed. Evidently, any method for determination of uric acid that involves treating the analyte with ammonium hydroxide before analysis may destroy it. Therefore, a published method described as being "definitive" for uric acid (J Clin Chem Clin Biochem 1985; 23:129-35) could produce incorrect results because it involves storing the uric acid in 15 mmol/L ammonium hydroxide at a mole ratio of ammonium hydroxide to uric acid of greater than 120:1.

Ammonium Hydroxide↗
PubMed1987

Oncogenes in radioresistant, noncancerous skin fibroblasts from a cancer-prone family.

Li-Fraumeni syndrome is manifested in a variety of neoplasms that are transmitted in a dominantly inherited pattern. The noncancerous skin fibroblasts of family members exhibit a unique characteristic of being resistant to the killing effect of ionizing radiation. A three- to eightfold elevation in expression of c-myc and an apparent activation of c-raf-1 gene have been observed in these noncancerous skin fibroblasts. These results may provide insight into the heritable defect underlying the familial predisposition to a variety of cancers.

Animals↗
PubMed1987

Decreasing incidence of invasive cervical cancer in young women.

Although the overall incidence of invasive cervical cancer is decreasing, there is concern that the disease might be increasing in younger women. Analysis of data from the Cancer Surveillance System, a population-based cancer registry in western Washington, shows a decreasing incidence of cervical cancer in women of all ages.

Adult↗
PubMed1987

Biochemical and genetic approaches to microtubule function in Dictyostelium discoideum.

Methods have been developed for analyzing tubulin and microtubules from the cellular slime mold D. discoideum. alpha- and beta-tubulin have been identified on high-resolution 2D gels, and microtubules have been isolated in cytoskeleton preparations from amoebae (White et al., 1983). These studies have revealed properties unique to Dictyostelium tubulin. Amoebal microtubules can be visualized by indirect immunofluorescence, which has aided in the identification of inhibitors which specifically depolymerize microtubules and block amoebae in mitosis. The mitotic inhibitors CIPC, NOC, and TBZ have been used to select resistant mutants which are currently the subjects of biochemical, morphological, and genetic analysis (Katz et al., 1982; White, 1983). One mitotic inhibitor-resistant mutant, CIPC 6, was found to be temperature-sensitive for growth at 27 degrees C as well as CIPC-resistant. At the restrictive temperature amoebae from this mutant are deficient in the passage through mitosis. After incubation for 12 hours at the restrictive temperature, 20% of the CIPC 6 amoebae displayed condensed chromosomes, compared to 2% at the permissive temperature, as determined by Giemsa staining. Examination of the microtubules of this mutant by indirect immunofluorescence showed abnormal spindle microtubule formation at the restrictive temperature, which is the likely cause of the mitotic arrest (White, 1983). Cytoplasmic microtubules were also disrupted in nonmitotic amoebae of CIPC 6 at 27 degrees C. This temperature-sensitive loss of microtubule function suggested the possibility that tubulin from CIPC 6 might be altered. When tubulin from CIPC 6 was examined on 2D gels, no reproducible electrophoretic change was observed from that of the wild type. Through further characterization of mitotic inhibitor-resistant mutants like CIPC 6, more mitotic or microtubule mutants will be identified. Among these mutants, some should contain electrophoretically altered tubulin, microtubule-associated proteins, or components of the amoebal cytoskeleton. Possessing Dictyostelium mutants with known biochemical alterations in cytoskeletal proteins should reveal significant information regarding the function of these proteins in eukaryotic growth and development.

Cytoskeletal Proteins↗
PubMed1987

Expression of adenovirus E1B mutant phenotypes is dependent on the host cell and on synthesis of E1A proteins.

Adenovirus mutants containing genetic alterations in the gene encoding the E1B 19,000-molecular-weight (19K) tumor antigen induce the degradation of host cell chromosomal DNA (deg phenotype) and enhanced cytopathic effect (cyt phenotype) after infection of HeLa and KB cells. The deg and cyt phenotypes are a consequence of viral early gene expression in the absence of the E1B 19K protein. The role of the E1A proteins in induction of the cyt and deg phenotypes was investigated by constructing E1A-E1B double mutant viruses. Viruses were constructed to express the individual E1A 13S, 12S, or 9S cDNA genes in the presence of a mutation in the gene encoding the E1B 19K tumor antigen. Expression of either the 13S or 12S E1A proteins in the absence of functional E1B 19K protein produced the deg and cyt phenotypes. In contrast, a virus which expressed exclusively the 9S E1A gene product in the absence of the E1B 19K gene product did not induce the deg and cyt phenotypes, even at high multiplicities of infection. Therefore, both the 13S and 12S E1A gene products could directly or indirectly cause the deg and cyt phenotypes during infection of HeLa cells with an E1B 19K gene mutant virus. Furthermore, the deg phenotype was found to be host cell type specific, occurring in HeLa and KB cells but not in growth-arrested human WI38 cells. These results indicate that expression of the E1A trans-activating and transforming proteins is necessary for the induction of the cyt and deg phenotypes and that host cell factors also play a role.

Adenovirus Early Proteins↗