PubMed Health⌕ Search

Biomedical subjects

R Butler

Publications and source records attributed to R Butler.

At least 181 records · Page 10Linked to original sources
PubMed1975

Arthritis in the prehistoric Southeastern United States: biological and cultural variables.

Recent research shows that a bacterial life form, Erysipelothrix insidiosa, can produce rheumatoid arthritis in deer, swine, and dogs, and that a number of animals, including man, birds, and fish, may be infected by the organism. Examination of the archaeological record suggests that both cultural and biological variables may be interrelated in the maintenance of some forms of arthritis over long periods of time in geographically disparate populations. Re-examination of Cherokee folk beliefs concerning arthritis suggests that they had some recognition of this connection, and it also suggests that they had some recognition of this connection, and it also suggests that the term "magical" may relate more to the world view of the observer than to any actual inability of preliterate peoples to draw causal relations on the basis of their own intimate knowledge of their environments.

Alabama↗
PubMed1974

Enhanced phagocytic capacity. The biologic basis for the elevated histochemical nitroblue tetrazolium reaction.

The biologic basis for the elevated histochemical reduction of nitroblue tetrazolium dye (NBT) in neutrophils from patients with acute bacterial infection or polycythemia vera was studied. A precipitin reaction followed mixing NBT with heparin. NBT was reduced after phagocytosis of this complex (H-NBT) by polymorphonuclear leukocytes (PMNs). Ingestion required divalent cations and was facilitated by the presence of complement. H-NBT incubated with normal but not with C2-deficient human serum converted native C3 to its inactive form. Phagocytic indices were determined in patients and controls by measuring O(2) utilization and hexose monophosphate shunt activity and by visually counting cell-associated latex particles. Significant elevations above controls were observed in phagocytes isolated from all patients with elevated histochemical NBT scores when H-NBT complex, latex, or zymosan was employed as the phagocytic particle. Increased indices were observed in the presence of fresh AB serum, heat-inactivated AB serum, or without serum. Serum from patients with elevated NBT scores did not alter phagocytosis in control phagocytes. With NADH and NADPH as substrates, total NBT diaphorase activity of sonicated leukocytes was normal in all patients. These results suggest that increased phagocytic capacity of PMNs is the primary cause of increased histochemical NBT reduction. The PMNs of patients with acute bacterial infection or polycythemia vera may have alterations in their cell membranes which lead to an enhanced rate of phagocytosis.

Animals↗
PubMedDate not supplied

Impact of dialysis modality and acidosis on nutritional status.

Experimental evidence suggests that acidosis may have a deleterious effect on protein metabolism. We evaluated 124 chronic dialysis patients (59 +/- 17 years) and defined acidosis as an anion gap >18 meq/L. A direct correlation (p < 0.0001 was found between anion gap and serum albumin (R = 0.402), BUN (R = 0.488), and serum creatinine (R = 0.473) concentrations. Acidotic patients (43%), when compared with nonacidotic patients, had greater serum albumin concentrations (3.95 +/- 0.50 vs. 3.60 +/- 0.48 g/dl, p = 0.0001, respectively), higher normalized protein catabolic rates (1.12 +/- 0.27 vs. 0.96 +/- 0.26 g/kg/d, respectively; p = 0.0004), and higher BUN (70 +/- 19 vs. 55 +/- 17 mg/dl, p = 0.0001) and serum creatinine (11.1 +/- 3.4 vs. 8.3 +/- 3.2, p = 0.0001 mg/dl) concentrations. However, no differences in midarm muscle circumference, fat free mass, or body cell mass were noted between groups when assessed by dialysis modality or acidosis status. In conclusion, mild chronic metabolic acidosis, likely caused by increased dietary protein intake, does not independently and adversely impact nutritional status in chronic dialysis patients.

Acid-Base Equilibrium↗
PubMedDate not supplied

Ag(c): recognition by a monoclonal antibody.

A monoclonal antibody directed against human apolipoprotein B, which was previously shown in family studies to detect allelic variations (J Biol Chem 1984; 259:6423-6430), has now been identified with the Ag(c) factor. This identification allows the location of the Ag system on the structural gene for apolipoprotein B and on the short arm of human chromosome 2. The epitope corresponding to Ag(c) is located within the amino acid sequence common to apolipoproteins B-100 and B-48. Since a single molecule of apolipoprotein B-100 is present on human LDL, individual LDL possesses either the epitope corresponding to Ag(c) or that corresponding to Ag(g). These studies on allelic variation among human apolipoprotein B species parallel similar studies in animals in which a relationship to atherosclerosis was found.

Alleles↗
PubMedDate not supplied

Two DNA restriction fragment length polymorphisms associated with Ag(t/z) and Ag(g/c) antigenic sites of human apolipoprotein B.

Several high frequency restriction fragment length polymorphisms (RFLPs) associated with the human gene for apolipoprotein B have been previously reported by Priestly et al. The EcoRI RFLP here was shown to be very strongly associated with the Ag(t/z) immunochemical polymorphism of human low density lipoproteins, allowing correct Ag(t/z) phenotyping of 17 (out of 17 tested) unrelated individuals. The Xbal RFLP was associated with the Ag(g/c) immunochemical polymorphism, permitting correct phenotyping of 14 (out of 17 tested) unrelated individuals. Its close association with an RFLP permitted localization of the Ag(t/z) polymorphism to the C-terminal end of the apolipoprotein B peptide, and allowed detailed discussion of its probable molecular basis.

Apolipoproteins B↗