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J F Davis

Publications and source records attributed to J F Davis.

At least 19 recordsLinked to original sources
PubMed1993

Mouse ethanol-inducible cytochrome P-450 (P450IIE1). Characterization of cDNA clones and testosterone induction in kidney tissue.

A mouse cDNA clone for the ethanol-inducible cytochrome P-450 (P450IIE1) was obtained by screening a liver cDNA library with an oligonucleotide representing a consensus sequence found in the orthologous rat, human, and rabbit sequences. The protein sequence deduced from the cDNA sequence had an identity of 93% to rat, 81% to rabbit, and 76% to human orthologous sequences. The highest levels of P450IIE1 mRNA were found in liver of both sexes, and male kidney. Developmentally, C57BL/6 female liver P450IIE1 mRNA was detectable 1 day postpartum and reached steady-state levels in animals approximately 16-20 days of age. Kidney and adrenal gland P450IIE1 mRNA was found to be induced 25-50-fold and 4-fold by testosterone treatment, respectively, and the level in both tissues reached maximum levels between 12 h and 2 days after treatment. Nuclear run-on experiments demonstrated that testosterone treatment for 24-48 h resulted in a slight transcriptional activation of the P450IIE1 gene in the kidney. However, the increase in transcription rate was far below the increase in mRNA level, suggesting that much of the induction occurs by posttranscriptional mechanisms. This process requires the androgen receptor since mutant Tfm mice lacking receptor are not inducible.

Amino Acid Sequence↗
PubMed1993

Victory at last....

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American Dental Association↗
PubMed1992

Cholylglycine measured in serum by RIA and interleukin-1 beta determined by ELISA in differentiating viral hepatitis from chemical liver injury.

Serum bile acids have been shown to serve as useful indicators of liver disease. We have confirmed these findings and added an analysis of interleukin-1 beta (IL-1 beta) profiles to further differentiate viral hepatitis from toxic liver damage associated with exposure to vinyl chloride (VC) or trinitrotoluene (TNT). The frequency of elevated cholylglycine (CG) was 100%, 75%, and 37.5% in viral hepatitis, VC- and TNT-linked liver injury patients, respectively. The mean levels, expressed in micrograms/dL, were 578, 507, 142, and 65 in hepatitis B, hepatitis non-A non-B, VC and TNT liver injury patients, respectively. Thus, the CG test could detect viral hepatitis and, VC liver injury, and (less frequently) liver injury associated with exposure to TNT. The mean level of IL-1 beta in patients with hepatitis type B was 424 pg/mL and hepatitis non A non B was 384 pg/mL compared with a mean of 33-40 pg/mL in those with VC or TNT-linked liver disease. The IL-1 beta detection test proved further to be an important distinguishing parameter as it was 100% positive in patients with viral hepatitis but only 12.5% to 25% positive in patients with VC/TNT-induced liver damage.

Adult↗
PubMed1986

Corneal epithelial cells produce thromboxane in response to interleukin 1 (IL-1).

Synthesis of thromboxane, a product of arachidonic acid formed via the cyclooxygenase pathway, was studied in rabbit corneal epithelial cells (SIRC cell line) under resting conditions and under the influence of interleukin 1 (IL-1). IL-1 potentiated the production of thromboxane 3-10-fold in a dose-dependent manner. This finding assumes added significance in view of the previous observations that the same cells are capable of producing IL-1. Thus, the corneal epithelial cells may be viewed in this context as an autocrine cell producing two biologically active substances which can serve as mediators of inflammation, one of which can augment the production of the other.

Animals↗
PubMed1984

Isolation of immunogenic neuraminidases of human influenza viruses by a combination of genetic and biochemical procedures.

Neuraminidases were purified from reassortant viruses (H6N1 and H6N2) containing the two antigenic subtypes (N1 and N2) found in human influenza viruses. Surface glycoproteins were solubilized with octylglucoside, and the neuraminidase was isolated by chromatography on DEAE-Sephadex. Neuraminidase isolated by this technique coeluted with viral lipids and spontaneously formed liposomes on dialysis. The purified neuraminidase was immunogenic in rabbits, producing a significant antibody response at dose levels as low as 1 microgram.

Animals↗
PubMed1980

Incorporation of influenza virus M-protein into liposomes.

M-protein from influenza virus vaccine was purified by sodium dodecyl sulfate-gel chromatography and incorporated into liposomes by solubilization with octylglucoside and subsequent dialysis. Liposomes containing M-protein formed a distinct population with a density of 1.22 g/ml on sucrose-gradient centrifugation, regardless of the net charge on the liposomes. Treatment of the liposomes by freeze-fracture followed by electron microscopic examination showed multilamellar structures in those liposomes without M-protein; liposomes containing M-protein were mulberry-like structures which appeared unilamellar. These studies show incorporation of M-protein into the lipid bilayer.

Chemical Phenomena↗
PubMedDate not supplied

Incidence of anemia and polycythemia in clinically ill Georgia broilers.

The incidence of anemia and polycythemia was established in clinically ill Georgia broilers that were tested for packed cell volume (PCV) during 1988 and 1989. More than 66% (324/488 = 66.4%) of PCV-tested broiler chicks were anemic, and less than 2% (8/488 = 1.6%) of PCV-tested chicks were polycythemic. The incidence of anemia was significantly (P less than 0.001) higher than expected (2.5%) at age 7 days (56.9%), 14 days (83.9%), 21 days (74.7%), 28 days (58.7%), and 35 days (57.9%). The incidence of polycythemia was significantly (P less than 0.001) higher than expected (2.5%) in 35-day-old broilers (21.1%) but was not significantly different from the expected rate in broilers at age 7 days (0%), 14 days (1.8%), 21 days (0.3%), and 28 days (4.3%). The established rates for anemia were much higher than we would have hypothesized. This led us to believe that either 1) an etiology for anemia is present in epizootic proportions in Georgia broilers, or 2) the standard method for establishing reference intervals for anemia in animals does not apply to broiler chicks.

Anemia↗
PubMedDate not supplied

Increasing incidence of anemia among clinically ill Georgia broilers: 1988-89 vs. 1990.

The incidence of anemia in clinically ill Georgia broilers climbed from 66.4% (324/488) during 1988-89 to 80.9% (531/656) during 1990. The incidence of polycythemia fell from 1.6% (8/488) during 1988-89 to 1.5% (10/656) during 1990. Specifically, compared with 1988-89, the 1990 incidence of anemia increased significantly in chicks at age 7 days (P = 0.0002) and 28 days (P = 0.05). We have no certain explanation for this shifting incidence of anemia in clinically ill Georgia broilers. Anemic chicks have plasma that contains virus particles with morphologic characteristics consistent with a virus (chicken anemia agent [CAA]) known to cause anemia in chickens. If CAA is the predominant etiology for anemia in clinically ill Georgia broilers, then our observation could be easily explained. The increasing rate of anemia could indicate a decline in broiler health over time.

Anemia↗