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Biomedical subjects

C D Davis

Publications and source records attributed to C D Davis.

At least 73 records · Page 4Linked to original sources
PubMed1990

Intake, serum concentrations, and urinary excretion of manganese by adult males.

Nutritional status of manganese in 10 adult males was monitored through a 47-d period by measuring manganese in serum and urine and by chemically analyzing duplicate portions of all foods and beverages consumed on 3 d, with computer analysis of dietary records for 10 additional days. Subjects consumed 0.52-5.33 mg Mn/d; 50% of the time they consumed less than the 1980 Estimated Safe and Adequate Daily Dietary Intake for manganese. Subjects on average (+/- SEM) excreted 7.0 +/- 0.5 nmol Mn/g creatinine; their average serum manganese concentration was 19.3 +/- 1 nmol/L. These potential indices of manganese exposure were not correlated with the subjects' dietary intakes of manganese or other minerals. However, serum manganese concentrations tended to be elevated (p less than 0.064) in five subjects who consumed 15 mg chelated Mn/d for 7 d.

Adult↗
PubMed1990

Manganese, iron and lipid interactions in rats.

The interactive effects of manganese, iron and lipid on mineral status, manganese-dependent superoxide dismutase (MnSOD) activity and lipoprotein composition were investigated by feeding weanling rats two levels of manganese (0.4 or 56 micrograms Mn/g diet), two levels of iron (29 or 109 micrograms Fe/g diet) and either 12% high-linoleic acid safflower oil or 12% high-oleic acid safflower oil for 8 wk. Rats fed the manganese-deficient diets had decreased heart MnSOD activity; depressed tibia and kidney manganese concentrations; lowered plasma and high density lipoprotein (HDL) cholesterol, HDL protein and HDL apo E concentrations; and elevated HDL protein/cholesterol ratios. Ingestion of supplemental iron slightly decreased heart MnSOD activity and tibia and kidney manganese concentrations but had no effect on hematocrits or on plasma and HDL cholesterol levels. Rats fed the linoleic acid-rich rather than the oleic acid-rich oil had increased heart MnSOD activity but had unchanged plasma and HDL cholesterol levels. The decrease in plasma and HDL cholesterol levels with manganese deficiency appeared not to be a result of increased lipid peroxidation but may have resulted from decreased cholesterol synthesis and/or secretion.

Analysis of Variance↗
PubMed1990

Selective binding of Trypanosoma cruzi to host cell membrane polypeptides.

An adaptation of the immunoblotting technique was used to investigate binding interactions between Trypanosoma cruzi and mammalian host cells at the molecular level. A specific binding interaction was observed between T. cruzi and two host cell membrane polypeptides with molecular masses of approximately 32 and 34 kilodaltons. This molecular interaction was observed with antigen extracts of T. cruzi and with live, infective trypomastigote stages of the parasite, suggesting that the observed phenomenon may have relevance to the initial attachment of the parasite to the host cell membrane before invasion.

Animals↗
PubMed1990

Detection of antigens with affinity for host cell membrane polypeptides in culture supernatants of Trypanosoma cruzi.

Parasite antigens which bind to host cell molecules of approximately 32 and 34 kilodaltons (kDa) were identified in supernatant fluids obtained from axenic cultures of Trypanosoma cruzi. These parasite components were first detected in culture supernatants obtained after 2 weeks in culture. Immunoblot analysis of culture supernatants exhibiting binding activity revealed the presence of several parasite antigens ranging in molecular mass from approximately 26 to 290 kDa. Gel filtration (Sephacryl S-300) analysis of culture supernatants revealed four major peaks, but only the highest-molecular-mass peak (containing several parasite antigens ranging from 27 to 250 kDa) possessed binding activity for the host cell molecules.

Animals↗
PubMed1990

Corporate negligence doctrine expanded in recent Nevada ruling.

In summary, Texas courts generally do not hold hospitals liable for negligent acts of non-employee physicians under the theory of corporate liability. Hospitals should take care to maintain fair and efficient procedures for granting and reviewing physician staff privileges. Hospitals clearly have a duty to maintain competent staff members and should withhold staff privileges if a physician is incompetent. Unfortunately, some plaintiffs' attorneys attempt to equate incompetence with a particular, and often singular, act. No Texas court has upheld this claim, and none should. A bad result, a negligent act or a medical accident does not, by itself, constitute incompetence.

Clinical Competence↗