PubMed Health⌕ Search

Biomedical subjects

R J Pickering

Publications and source records attributed to R J Pickering.

At least 19 recordsLinked to original sources
PubMed1989

Setting educational priorities for learning the concepts of population health.

Following the World Health Organization's policy of 'Health for All by the Year 2000', doctors are increasingly being seen as health care providers to populations of patients, in addition to their more traditional role as doctors to individuals in a one-to-one encounter. In order for doctors to take on this expanded role, they must learn the knowledge and skills appropriate to population health. In this paper, we propose a method of educational priority-setting which allows educational planners to identify those diseases and adverse health conditions most appropriate for studying the concepts of population health. Using the Measurement Iterative Loop of Tugwell and colleagues as a framework, a table of Priority Illness Conditions was developed and compared with a previous priority list developed from a survey of clinical teachers at the McMaster University Medical School. Discussion of the implications for this approach in setting educational priorities at undergraduate, postgraduate and continuing medical education levels is presented, along with a review of possible shortcomings and caveats in using this approach.

Community Medicine↗
PubMed1985

Effect of prostaglandins on complement production by tissue macrophages.

Tissue macrophages produce several proteins of the complement system. The mechanisms that regulate this process are poorly understood. The established ability of certain prostaglandins to influence macrophage secretory activity suggests that these lipid mediators may also modulate complement production (CP). Using the guinea pig peritoneal macrophages, we determined the effects of selected prostaglandins on in vitro CP and found that PGE2 inhibited production of complement proteins but not lysozyme; the response of elicited and resident peritoneal cells to PGE2 was identical; and PGE1, PGF2 alpha, and PGI2 had no detectable effect. PGE2 may contribute to regulation of CP in vivo.

Animals↗
PubMed1984

Arachidonic acid-mediated and serum-opsonized-zymosan-mediated inhibition of complement production by macrophages. Lack of requirement for endogenous arachidonic acid metabolites.

The ability of exogenous prostaglandins to inhibit complement production (CP) by monocytes and macrophages (M phi) suggests that endogenous arachidonic acid metabolites produced by these cells may also regulate their rate of CP. We assessed the regulatory influence of endogenous metabolites on CP by M phi utilizing exogenous arachidonic acid and serum-opsonized zymosan as stimulators of production of cyclooxygenase and lipoxygenase metabolites. The results of this study show that (i) the inhibition of CP caused by both agents is is independent of arachidonic acid metabolites, suggesting that endogenously produced metabolites do not influence CP, and (ii) arachidonic acid and serum-opsonized zymosan inhibit production by independent mechanisms.

Animals↗
PubMed1983

Enhancement of granulocyte oxidative metabolism in sera from patients with C2 deficiency and systemic lupus erythematosus.

Serum or plasma from 3 patients with C2 deficiency (C2D) and systemic lupus erythematosus (SLE) significantly enhanced chemiluminescence and superoxide anion production by polymorphonuclear leukocytes (PMN) after stimulation with phorbol myristate acetate or latex beads. PMN from patients and normal individuals were supranormally activated when resuspended in plasma from these patients. No such effect was seen with plasma from a patient with C2D but with no evidence of SLE, from patients with SLE but not C2D, from patients with C1q or C8 deficiency, from C4-deficient guinea pigs, or NZB-NZW mice. Because oxygen-derived free radicals may cause joint or tissue damage, C2D patients who have or develop this activity in their plasma may be more prone to SLE or other collagen-vascular diseases.

Adolescent↗
PubMed1979

Abnormalities of the complement system in Reye syndrome.

Sixteen patients with Reye syndrome had diminished concentration of serum complement proteins and/or hemolytic activity in the earliest blood sample. All 12 studied with hemolytic methods had significantly reduced C1 activity; total hemolytic complement activity was reduced in only three. Low Cl activity was accompanied by equivalent reduction of Cls in 11 of 12 patients; Clq was less than normal in only two of 12. Decreased levels of at least one other classical pathway complement hemolytic activity or protein concentration were found in 13 patients, whereas factor B or the alternate complement pathway was normal or elevated in the ten patients studied. The consistent reduction of Cls protein concentration in Reye syndrome suggests that early metabolic abnormalities regularly affect the production or catabolism of this protein. Although normal serum Clq concentration in the majority of these patients does not support an immune pathogenesis, decreased Clq, C4, and C2 in three patients does suggest that immune mechanisms may be responsible for the serum complement abnormalities in this latter group of patients.

Adolescent↗
PubMed1979

Regional deficiency of secretory IgA in a patient with combined immunodeficiency of the ADA deficient type.

The IgA system in a patient with SCID and ADA deficiency showed heterogeneity. Serum IgA and stool secretory IgA (SIgA) levels were normal, but with altered kappa/lambda and A1/A2 subclass ratios; IgA in saliva and urine was deficient. Amounts of secretory component were normal. Jejunal and rectal biopsies showed prominent lymphonodular hyperplasia, but no cells containing IgA. A normal serum IgA level therefore does not always predict an intact secretory IgA system.

Adenosine Deaminase↗
PubMed1978

Heterogeneity of the clinical syndrome in patients with systemic lupus erythematosus and genetic deficiency of the second complement component.

Two patients with systemic lupus erythematosus associated with homozygous deficiency of the second complement component (SLE-C2D) illustrate the different clinical disease patterns found in patients with this illness. Despite the differences in extent and severity of clinical manifestations and serological findings, the renal disease was similar and kidney function was well preserved in both patients. Renal microscopic changes were focal and segmental, deposits of immuno-globulins and complement components were present by immunofluorescent staining, and dense deposits were seen by electron microscopy. Tubulo-reticular inclusion bodies were found in glomerular endothelial cells and lymphocytes of both patients, but not in the lymphocytes of a clinically healthy C2D sibling. The findings in these two patients stress the importance of careful evaluation to determine the presence of systemic disease in patients with SLE-C2D and suggest that an intact classic complement pathway is important in the development of severe lupus, nephritis, but is not needed in the pathogenesis of lupus skin lesions.

Adult↗
PubMed1976

Disseminated intravascular coagulation induced by Liquoid in the rat. II. Effect of heparin on hematologic and complement abnormalities and renal lesions studied by light, fluorescence, and electron microscopy.

A single intravenous injection (12.5 mg.) of Liquoid (polyanethol sulfonate) was given to anticoagulated (heparinized) rats. Fibrinogen concentrations, platelet counts, total serum complement (CH50),C3 protein, and terminal components (C3 to C9) were measured. Histopathology was assessed by light, fluorescence, and electron microscopy. Heparin given before Liquoid remarkably diminished the seferity of the histologic lesions, with good correlation among light, fluorescence, and electron microscopy. Levels of clotting factors, CH50, C3 and C3 to C9, however, were not statistically different in the heparinized rats injected with Liquoid from those of animals receiving Liquoid alone. Actually C3 protein concentration was lower in the anticoagulated (Liquoid-heparin) rats. It is postulated that under the present experimental conditions, heparin did not antagonize the procoagulant and precipitating or complement-activating Liquoid effects. The attenuated histopathology observed was perhaps the result of either local or systemic, as yet undefined, heparin effects other than anticoagulation.

Animals↗
PubMed1976

C4 synthesis in C4-deficient guinea pig radiation chimeras: restoration of the classic complement pathway.

Bone marrow transplants from normal Albany strain guinea pigs established a functional classical pathway of complement (C) in C4-deficient (C4D) guinea pigs. Seventeen days after transplant the Albany leads to C4D chimeras had detectable C4 and total hemolytic C activities. Maximum C4 levels (2 to 8% of normal were reachered by day 73 and restored total C to 40% of normal. Classical pathway function persisted for about 150 days and, thereafter, declined to undetectable levels by day 385. In contrast, Albany guinea pigs transplanted with C4D marrow maintained normal C4 levels throughout the experiment, suggesting that the C4-producing cells are radioresistant and long-lived. Unlike unmanipulated C4D animals, Albany leads to C4D chimeras were unable to produce antibodies to guinea pig C4 when immunized with normal guinea pig serum. These experiments suggest that bone marrow cell progeny produce C4 in vivo.

Animals↗
PubMed1975

Endothelial injury induced by bacterial endotoxin: effect of complement depletion.

The role of complement activation in the pathogenesis of endothelial injury caused by bacterial endotoxin was investigated in the rat. DNA synthesis in aortic endothelium was compared 48 hours after an intravenous injection of endotoxin (50 - 500 mug) in normal rats and in rats depleted of haemolytic complement by purified cobra venom factor. At the time of endotoxin administration the rats treated with cobra venom factor had less than 3% of the normal haemolytic complement level, their fibrinogen level was increased and clot retraction was impaired. Endotoxin stimulated endothelial DNA synthesis to the same degree in normal and in complement-depleted rats. Cobra venom factor alone did not stimulate endothelial DNA synthesis. The complement-depleted rats given 500 mug endotoxin were less thrombocytopenic than normal rats at the time of sacrifice, but the difference was not statistically significant. We conclude that the injurious effect endotoxin has on endothelium is not mediated by activation of late components of complement.

Animals↗
PubMed1975

Combined immunodeficiency disease associated with adenosine deaminase deficiency. Report on a workshop held in Albany, New York, October 1, 1973.

Fifty-five children with CID and known ADA status were studies at a workshop held in Albany, New York. Erythrocyte ADA determinations were performed in 22 of the 55 patients, 13 of whom were ADA negative. The ADA defect appears to be transmitted as an autosomal recessive trait. Some patients with CID and ADA deficiency have characteristic radiologic abnormalities of the skeleton, which are not found in other illnesses. The thymus glands of all patients with CID and ADA deficiency who could be examined have evidence of thymic involution manifested by presence of Hassall's corpuscles and differentiated germinal epithelium; this is in contrast to "classic" thymus findings in CID with normal ADA. Adenosine deaminase probably plays an important, although as yet undefined, role in lymphocyte development and/or function. The deficiency of ADA in CID is the first enzyme defect observed in a deficiency disease of specific immunity.

Adenosine↗