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Biomedical subjects

A J Bellingham

Publications and source records attributed to A J Bellingham.

At least 73 records · Page 4Linked to original sources
PubMed1980

The effect of methylprednisolone sodium succinate on erythrocyte and haemoglobin function.

1. As it has been suggested that the beneficial effect of methylprednisolone in shock is due to its effect on erythraocyte oxygen affinity, we studied its effect on incubated erythrocytes and on haemoglobin solution. 2. Incubation of fresh whole blood anticoagulated with acid/citrate/dextrose with methylprednisolone (7 mmol/l) produced a significant decrease in oxygen affinity, which was not seen with lower concentrations of methylprednisolone. When either acid/citrate/dextrose blood stored for 10 days or fresh heparinized blood was used, no significant increase in the partial pressure of oxygen at 50% haemoglobin saturation (P50) was demonstrated even with methylprednisolone at 7 mmol/l. At the highest concentration achieved in plasma with standard therapeutic doses (56 mumol/l) there was no increase in P50 under all the conditions studied. 3. Methylprednisolone reduced the oxygen affinity of haemoglobin in solution. The reduction in oxygen affinity was less than that produced by 2,3-diphosphoglycerate and more than that of either sodium succinate or sodium chloride. 4. From the results of this study we conclude that the effect observed in whole cells is probably due to a direct effect of methylprednisolone on haemoglobin. To produce a significant decrease of oxygen affinity of while blood in vitro requires a plasma concentration of methylprednisolone above that obtained in plasma in vivo, with the currently used therapeutic doses.

Cells, Cultured↗
PubMed1979

Immunotherapy using BCG during remission induction and as the sole form of maintenance in acute myeloid leukaemia.

Thirty-two adults with acute myeloid leukaemia (AML) were randomized to receive, from the time of diagnosis, either chemotherapy alone (C group) or chemotherapy plus Bacille Calmette-Guérin vaccine (BCG) (C+I group). After remission induction and consolidation, chemotherapy was stopped in both groups but BCG was continued in the C+I group. The overall survival of the C+I group was significantly increased (P less than 0.05). There was no significant increase in the duration of first remission in the C+I group (0.05 less than P less than 0.1) nor in the time from first relapse to death (0.05 less than P less than 0.1). There was no significant difference in the incidence of first or second remissions, and the time taken to enter remission did not differ significantly between the two groups. Comparison with the results of other trials suggests that the use of maintenance chemotherapy in addition to immunotherapy produces longer remissions. Five patients in the C group developed leukaemic central-nervous-system (CSN) involvement, in comparison with none in the C+I group. CNS relapse did not produce a significant decrease in remission length (P greater than 0.1) but reduction in survival after CNS relapse was highly significant (P = 0.001). These results suggest that administration of BCG from an early stage in the treatment of AML may protect the CNS against leukaemic infiltration and therefore serve as a simple, innocuous form of CNS prophylaxis.

Adolescent↗
PubMed1979

Thrombocytopathy in preleukaemia: association with a defect of thromboxane A2 activity.

Platelet aggregation and the platelet prostaglandin pathway have been investigated in two patients with preleukaemic states who had a haemorrhagic tendency but a normal platelet count. In both patients platelet aggregation induced by collagen adenosine diphosphate (ADP) and arachidonic acid (AA) were abnormal. Malonyldiadehyde (MDA) production from exogenous AA was normal in both patients thus excluding cyclo-oxygenase deficiency. The platelet aggregating and rabbit aorta contracting activities of thromboxane A2 (TxA2) were very low in both patients. Production of thromboxane B2 (TxB2) assessed by thin layer chromatographic separation of the metabolites of [1(-14)C]AA and by radioimmunoassay, was normal. These abnormalities of platelet function appear to be due to the production of TxA2 with a low biological activity.

Adenine Nucleotides↗
PubMed1977

Defective platelet lipid peroxidation in myeloproliferative disorders: a possible defect of prostaglandin synthesis.

Platelet lipid peroxidation induced by the sulphydryl blocking reagent n-ethylmaleimide [NEM] was measured by production of malonyldialdehyde [MDA]. Lipid peroxidation was decreased in five of 10 patients with proven myeloproliferative disease. The low levels of lipid peroxidation correlated well with in vitro and in vivo tests of platelet function and the bleeding and bruising problems. The reduction in lipid peroxidation with NEM may be due to one or more of the following: [i] an aged platelet population; [ii] an abnormal cell line; [iii] a reduction of the cyclo-oxygenase enzyme activity in the platelet prostaglandin synthetic pathway; [iv] a reduction of the substrate for platelet prostaglandin synthesis, Arachidonic acid; and [v] an abnormality of phospholipase A activation.

Blood Platelet Disorders↗
PubMed1977

The significance of the Philadelphia chromosome in acute lymphoblastic leukaemia: a report of two cases.

Two cases of Philadelphia chromosome (Ph1) positive acute lymphoblastic leukaemia are reported, both of which lost the Philadelphia chromosome during remission. In one patient remission of the acute lymphoblastic leukaemia continued but classical Ph1 positive chronic granulocytic leukaemia developed. In the other patient relapse of the acute lymphoblastic leukaemia occurred associated with the return of the Ph1 chromosome. The evidence suggests that the chromosome aberration occurred in a pluripotential stem cell, which in one case proliferated along both a lymphoid cell line and a myeloid cell line. Both cases responded well to conventional therapy for acute lymphoblastic leukaemia.

Adult↗
PubMed1977

A rare presentation of splenic rupture.

Traumatic rupture of the spleen is a well known problem, complicating many types of abdominal injury. In contrast, a spontaneous rupture is a rare occurrence, mainly associated with a large spleen resulting from infections, the most common in this country being infectious mononucleosis. It is also a rare complication of leukaemias and lymphomas and the case presented here demonstrates a peculiar diagnostic problem.

Adult↗
PubMed1975

Transfer factor in Hodgkin's disease.

In a controlled studiy, six patients with stage-IV Hodgkin's disease were given transfer factor (T.F.) prepared from patients with Hodgkin's disease in long remission. There was an apparent increase in cell-mediated immune responses as evidenced by a significant increase in the recipients' lymphocyte responses to phytohaemagglutinin stimulation. Three out of six patients converted to positive delayed-hypersensitivity tests. These three all had the nodular sclerosing type of Hodgkin's disease. These results warrant the further investigation of the use of Hodgkin's disease-specific T.F. as a therapeutic agent in this condition.

Hodgkin Disease↗
PubMed1974

The sickling process in relation to clinical manifestations.

Knowledge of the detailed molecular mechanisms of the sickling process has led to an understanding of factors precipitating crises and hence allowed a reasoned approach to therapy. At present amelioration of the symptoms of sickle cell disease rests primarily on the avoidance and prompt treatment of the basic precipitating factors of the sickling process--fever, hypoxia, acidosis, and dehydration. Over the years many drugs have been claimed to have anti-sickling properties but have not stood the test of time. The current partial success of cyanate stems directly from this molecular knowledge. As further details of the site of intermolecular binding involved in the sickling process become available the possibility of developing more specific anti-sickling drugs becomes clearer.

Acidosis↗
PubMed1973

Hemoglobin olympia ( 20 valine leads to methionine): an electrophoretically silent variant associated with high oxygen affinity and erythrocytosis.

In a family with erythrocytosis, electrophoretic and chromatographic studies failed to demonstrate a hemoglobin variant. However, the oxygen dissociation curves of affected individuals were shifted to the left of normal and this shift persisted when oxygen equilibria were studied in 2.3-diphosphoglycerate-stripped hemolysates. A mutant hemoglobin was evidently present in the red blood cells of the affected persons and was responsible for the increased oxygen affinity and erythrocytosis. Specific staining of tryptic peptide maps of beta-chains from the propositus showed that peptide betaT(3) was positive for a sulfur-containing amino acid. Amino acid analysis yielded a composition identical to that of normal betaT(3), except that there were 2.6 residues of valine and 0.4 residues of methionine (normal composition: Val = 3.0, Met = 0). This suggested that the beta-chains of affected individuals consisted of a mixture of two kinds of chains, 40% of which had a methionyl residue in betaT(3). Structural studies of isolated cyanogen bromide fragments demonstrated unequivocally that, in the abnormal beta-chains, valine in position 20 is replaced by methionine. The new hemoglobin mutant is designated hemoglobin Olympia (beta20 (B2) valine --> methionine).

Adult↗