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C Scott-Moncrieff

Publications and source records attributed to C Scott-Moncrieff.

9 recordsLinked to original sources
PubMed1998

Effects of human intravenous immunoglobulin on canine monocytes and lymphocytes.

OBJECTIVE: To evaluate interactions of human intravenous immunoglobulin (IVIG) with canine lymphocytes and monocytes. SAMPLE POPULATION: Heparinized blood samples from 4 clinically normal Beagles. PROCEDURE: Binding ability of IVIG to canine lymphocytes and monocytes was measured by flow cytometry and an indirect immunofluorescent assay. Dual-staining fluorescent assays were done to determine lymphocyte subsets that bind IVIG. Competitive assays were done, using intact canine IgG and Fc fragments, and inhibition of binding was compared with that of F(ab)2 fragments. Ability of IVIG to inhibit phagocytosis of antibody-coated canine RBC also was determined, using a canine mononuclear cell phagocytic assay. RESULTS: IVIG concentrations (10, 1, 0.1, and 0.01 mg/ml) bound to (mean+/-SD) 99.6+/-0.4, 92.4+/-6.1, 20.4+/-24.6 and 2.0+/-5.1 % of canine lymphocytes, respectively, Dual staining analyses with IVIG and canine lymphocyte markers indicated that IVIG bound to CD4, CD8, and B lymphocytes. The aforementioned 4 IVIG concentrations bound to 98.0+/-2.1, 85.5+/-13.5, 64.7+/-32.8, and 26.5+/-17.1 % of monocytes, respectively. Inhibition of IVIG (0.01 mg/ml) binding to monocytes was significant (P< 0.05) in the presence of 1 and 10 mg of canine IgG/ml and 1 mg of canine Fc fragments/ml. In the presence of F(ab')2 fragments of canine IgG, inhibition was not significant, suggesting that binding is Fc mediated. Co-culturing of monocytes, opsonized RBC, and the 4 concentrations of IVIG and no IVIG resulted in 11.8+/-5.1, 27.7+/-12.3, 31.8+15.1, 53.8+/-6.7, and 45 + 12% of the monocytes containing RBC, respectively. Phagocytosis inhibition was significant (P < 0.05) at an IVIG concentration of 10 mg/ml. CONCLUSIONS: IVIG binds to canine lymphocytes and monocytes; binding to the latter is Fc mediated. IVIG also inhibits Fc-mediated phagocytosis of antibody-coated RBC. CLINICAL RELEVANCE: Owing to its ability to inhibit Fc-mediated phagocytosis of antibody-coated RBC, IVIG may be an effective short-term treatment for dogs with immune-mediated hemolytic anemia.

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PubMed1996

Validation of an immunoassay for canine thyroid-stimulating hormone and changes in serum concentration following induction of hypothyroidism in dogs.

OBJECTIVE: To validate a new immunoradiometric assay for canine thyroid-stimulating hormone (cTSH) and to document changes in serum cTSH concentration during induction of hypothyroidism in dogs. ANIMALS: Six healthy adult male Beagles. PROCEDURE: Sensitivity, specificity, precision, and accuracy of the cTSH assay were evaluated in vitro. Hypothyroidism was induced in dogs by i.v. administration of sodium iodide I 131 solution. Subsequently, L-thyroxine was administered orally to normalize serum thyroxine concentrations. RESULTS: The cTSH assay appeared to be specific and was sufficiently sensitive to detect cTSH in the serum of these dogs prior to induction of hypothyroidism. There was a 35-fold increase in mean serum cTSH concentration following induction of hypothyroidism, and 35 days after initiation of thyroid replacement therapy, mean serum cTSH concentration was not significantly greater than mean baseline value. CLINICAL IMPLICATIONS: Assay of serum cTSH is likely to prove helpful in the differential diagnosis of primary, secondary, and tertiary hypothyroidism in dogs, and in monitoring response to thyroid hormone replacement treatment.

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PubMed1991

Gentamicin pharmacokinetics in diabetic dogs.

Reduction of the prolonged terminal elimination phase of gentamicin may be caused by diabetes mellitus, irrespective of the model of diabetes. To test this hypothesis, five normal dogs, three dogs with alloxan-induced diabetes mellitus, and four dogs with naturally occurring diabetes mellitus (all of which were given exogenous insulin to control hyperglycemia) were given 4.4 mg/kg gentamicin intravenously. Serum pharmacokinetics were analyzed using non-compartmental pharmacokinetics assuming a sum of exponential terms. Gentamicin pharmacokinetics during the first 8 h were the same in normal and diabetic dogs. Over 7 days, MRT in normal dogs (5830 +/- 2970 min, mean +/- SD) was longer (P less than 0.01) than in diabetic dogs (136 +/- 164 min). In diabetic dogs, Cls was greater (3.01 +/- 0.86 ml/min/kg) than in normal dogs (1.45 +/- 0.11 ml/min/kg; P less than 0.01), whereas Vd(ss) was smaller in diabetic dogs (0.405 +/- 0.508 l/kg) than in normal dogs (8.56 +/- 4.48 l/kg; P less than 0.01). Serum gentamicin concentrations were less than 0.020 microgram/ml by 2 days in all of the diabetic dogs, but were 0.048 +/- 0.018 microgram/ml at 7 days in normal dogs. Thus, diabetes mellitus, either induced by alloxan administration or naturally occurring, abolished the terminal elimination phase of gentamicin disposition in a non-rodent species.

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