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Biomedical subjects

L W Powell

Publications and source records attributed to L W Powell.

At least 181 records · Page 10Linked to original sources
PubMed1982

Demonstration of previously undetected hepatitis B viral determinants in an Australian Aboriginal population by monoclonal anti-hbs antibody radioimmunoassays.

High-affinity IgM and IgG monoclonal antibodies (anti-HBs) against hepatitis B surface antigen (HBsAg) determinants were used to study a confined Australian Aboriginal population, 51% of which showed evidence of exposure to hepatitis B virus (HBV). A conventional radioimmunoassay which uses polyvalent anti-HBs antisera indicated that 4.4% of the subjects were positive for HBsAg; a monoclonal IgM anti-HBs radioimmunoassay detected all these HBsAg-positive samples and showed enhanced binding activity in a further 5.4% of subjects. Detailed analysis of this binding activity in serum by different IgG and IgM monoclonal anti-HBs antibodies demonstrated additional HBsAg-associated determinants as well as remarkable homogeneity of the determinants in this population. It was concluded that there are HBV or HBV-like agents in this community not previously detected by conventional assays.

Adult↗
PubMed1982

Idiopathic hemochromatosis: demonstration of homozygous-heterozygous mating by HLA typing of families.

In five families with idiopathic (hereditary) hemochromatosis, clinical and biochemical expression of the disease occurred in offspring of probands, suggesting an autosomal dominant mode of inheritance. However, HLA typing of subjects indicated that a homozygous-heterozygous mating almost certainly had occurred in four of the five families, resulting in homozygous offspring. Thus, in these families inheritance of the hemochromatosis trait was best explained in terms of an autosomal recessive or intermediate mode of inheritance. This study demonstrates the value of HLA typing in identifying homozygous-heterozygous matings in hemochromatosis families.

Adolescent↗
PubMed1982

Iron overload.

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Adult↗
PubMed1982

Ferritin synthesis in peripheral blood monocytes in idiopathic hemochromatosis.

RE ferritin synthesis in IHC was studied in M0s isolated from peripheral blood. Twelve phlebotomized hemochromatosis patients with normal body iron stores and 12 healthy control subjects were studied. M0s in culture were exposed to iron as either ferric ammonium citrate or iron dextran, and ferritin synthesis was determined by measurement of 3H-leucine incorporation after isolation of ferritin by a quantitative immunoadsorbent technique. Iron at concentrations of 150 and 300 microM induced de novo ferritin synthesis, increasing both 3H-leucine incorporation into ferritin and cellular ferritin content. However, no differences were observed between hemochromatosis and control M0s with respect to basal or iron-stimulated ferritin synthesis. The study has demonstrated that M0 ferritin synthesis in IHC does not differ from M0 ferritin synthesis in normal subjects and therefore suggests that the reported abnormalities in RE iron storage in IHC are not related to an inability of RE cells to synthesize ferritin.

Cells, Cultured↗
PubMed1981

Idiopathic haemochromatosis in the Australian population: HLA linkage and recessivity.

Studies of 78 unrelated patients and 19 families with idiopathic haemochromatosis are reported. The unrelated patients showed a highly significant association between the disease and HLA-A3. There was a less strong association with HLA-B7 and HLA-DRw2 attributed to the linkage disequilibrium between HLA-A3, B7, and DRw2. Lod scores and haplotype analysis of the families indicated a recessive mode of inheritance for an idiopathic haemochromatosis susceptibility factor in close linkage with the HLA region. These results, for Australian caucasoid patients, are not in total agreement with those reported in studies of other populations.

Australia↗
PubMed1981

Regulation of plasma ferritin by the isolated perfused rat liver.

The isolated perfused rat liver has been used to investigate the regulation of plasma ferritin in normal, iron-deficient and iron-overloaded states. Both 125I-labelled and non-labelled rat liver ferritins were rapidly cleared from the perfusion circuit with a half-life of approximately 30 min. Perfusion of livers from normal, iron-loaded or iron-deficient rats with blood obtained from normal, iron-loaded or iron-deficient rats showed that the liver takes up plasma ferritin, and releases ferritin into the perfusate to achieve a perfusate ferritin level appropriate to the iron stores of the animal from which the liver was taken. It is concluded that the liver is capable of both uptake and release of ferritin and that within the liver there resides a mechanism which maintains circulating ferritin concentrations at a level appropriate to body iron stores.

Animals↗
PubMed1981

Serum prednisolone levels in Crohn's disease and coeliac disease following oral prednisolone administration.

Serum prednisolone levels have been measured following the oral administration of 20 mg prednisolone in 10 normal subjects, in 9 patients with Crohn's disease and in 6 with coeliac disease. Serum prednisolone levels showed more variation in patients with Crohn's disease when compared to normal subjects. In those patients with Crohn's disease who failed to respond to corticosteroid therapy, adequate serum levels of prednisolone were achieved. Patients with coeliac disease had levels similar to normal. Serum protein binding of prednisolone was not significantly different between the groups. We conclude that, even in the presence of mucosal damage, patients with coeliac disease and Crohn's disease achieve therapeutic serum prednisolone levels.

Administration, Oral↗
PubMed1980

Alterations of drug metabolism in rats exposed to cigarette smoke.

In male rats exposed to cigarette smoke, antipyrine clearance was enhanced to the same extent as has been observed in human cigarette smokers. The activity of aryl hydrocarbon hydroxylase, a representative microsomal mixed function oxidase, was increased significantly in lung and kidney of smoke-exposed rats compared with controls. The activity of this enzyme in the liver, however, was not altered by cigarette smoke. Although aryl hydrocarbon hydroxylase activity in extrahepatic tissues was significantly enhanced after cigarette smoke exposures, the total drug metabolizing capacity of these tissues remained trivial compared with that of the liver. Hence, extrahepatic drug metabolism is unlikely to account for enhanced antipyrine elimination in cigarette smokers. The present study has established an animal model for studying the changes produced by cigarette smoke which result in enhanced drug metabolism in man.

Animals↗
PubMed1980

Antigen-dependent physical interaction between human monocytes and T lymphocytes.

The physical interaction between human monocytes and autologous T lymphocytes was studied in cultures of cells from tuberculin-sensitive individuals to which purified protein derivative of tuberculin had been added. Such cultures displayed formation of cell aggregates, each typically consisting of one or two monocytes to which several lymphocytes adhered by means of uropods. The capacity of monocyte-T-lymphocyte mixtures to produce this type of aggregate in response to tuberculin correlated with the tuberculin sensitivity of the cell donor as measured by skin test.

Adolescent↗
PubMed1980

Effect of long-term corticosteroid therapy on monocyte chemotaxis in man.

The influence of prednisolone on monocyte chemotactic activity in vitro at prednisolone concentrations comparable with those achieved in man following oral dosage has been investigated. Chemotactic activity of monocytes from each of sixteen normal subjects was suppressed by concentrations of prednisolone as low as 25 ng/ml (suppression of chemotaxis, 20%). Maximal suppression occurred at 100 ng/ml (suppression of chemotaxis, 48%) and no significant increase in suppression was produced by increasing the concentration to 200 ng/ml (suppression of chemotaxis, 53%). In contrast, monocytes isolated from ten patients receiving corticosteroid therapy showed no significant suppression of chemotactic activity when exposed to these concentrations of prednisolone, even though they exhibited a normal ability to respond to a chemotactic stimulus. The lack of suppression of monocyte chemotaxis in patients receiving corticosteroid therapy is unexplained, but may represent a change in the circulating monocyte or lymphocyte populations.

Administration, Oral↗
PubMed1980

Cell-mediated immunity to liver antigen in toxic liver injury. II. Role in pathogenesis of liver damage.

The possible pathogenetic role of lymphocytes sensitized to liver antigens was investigated in CBA mice in which sublethal hepatic necrosis had been induced by carbon tetrachloride (CCl4). Sensitized lymphocytes from CCl4-treated mice were administered to syngeneic recipients. The recipients developed sensitivity to liver antigens but showed no evidence of liver damage. The cell mediating the immune response both in the donor and the recipient was a T cell. This was demonstrated further by studies involving mice rendered T cell deficient. These mice did not develop sensitized lymphocytes when they were treated with CCl4 but the extent of liver damage was similar in both T cell-depleted and intact animals. These findings suggest that T cell sensitization to liver antigens occurs as a result of toxic liver damage and does not play a role in the pathogenesis of the hepatic necrosis.

Animals↗
PubMed1980

Cell-mediated immunity to liver antigen in toxic liver injury. I. Occurrence and specificity.

To investigate the possible role of cell-mediated immunity in the pathogenesis of liver disease lymphocyte function was studied in CBA mice in which predictable sublethal liver necrosis had been included by the administration of the hepatotoxin carbon tetrachloride (CCl4). Non-specific lymphocyte function, as assessed by the response to the mitogen phytohaemagglutinin (PHA) was normal in over 90 percent of the animals. Forty-three per cent of the treated mice demonstrated specific lymphocyte sensitivity to liver antigen preparations. Such specific sensitivity was transient and apparent in only one case for more than 2 weeks after the CCl4 treatment. The lymphocyte sensitization was not reproduced by the addition of CCl4 to the lymphocyte cultures. There was no correlation between the severity of the liver disease and the detection of sensitized lymphocytes. Although these data may not be extrapolated directly to human liver disease, they demonstrate that cell-mediated immune reactivity to liver-derived antigens can occur as a result of non-immunological toxic liver injury.

Animals↗
PubMed1979

The nature of piecemeal necrosis in chronic active hepatitis.

On the basis of histological studies, it is proposed that the type of liver-cell death in piecemeal necrosis is apoptosis. The characteristic inconspicuousness of apoptosis explains why the mode of hepatocyte elimination in piecemeal necrosis has hitherto remained obscure. Cell-mediated immune attack induces apoptosis, not classical necrosis, and the occurrence of apoptosis in piecemeal necrosis links the observed morphological changes in chronic active hepatitis with the other evidence for an autoimmune pathogenesis. It is significant that apoptosis does not evoke inflammation or fibroplasia. In attempting to elucidate the cause of the fibrosis that accompanies progression to cirrhosis in chronic hepatitis, it may thus be more relevant to study the effect on fibroblasts of substances liberated during lymphocyte-hepatocyte interactions than the death of the hepatocytes.

Autoimmune Diseases↗