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Biomedical subjects

M M Johnson

Publications and source records attributed to M M Johnson.

At least 91 records · Page 5Linked to original sources
PubMed1980

Correlation between fibrinogen binding to human platelets and platelet aggregability.

Fibrinogen is essential for aggregating platelets with adenosine diphosphate (ADP) and was recently shown to bind to platelets stimulated with ADP. The present work confirms the specific and saturable nature of the platelet-fibrinogen interaction. Binding of 125iodine-labeled fibrinogen to human gel-filtered platelts was maximal at 1 min, and the receptors were saturated when the fibrinogen concentration in the suspending medium approached 0.8 mg/ml. Assuming that one fibrinogen molecule interacts with a single receptor, experiments with 9 normal donors revealed the presence of 12,896 +/- 2456 receptors per platelet. Much of the bound material dissociated from platelets after incubation with apyrase or EDTA. Binding was markedly inhibited at pH 6.5, in the presence of EDTA, and with platelets from 3 thrombasthenic patients but not with those from a patient with the Bernard-Soulier syndrome. Fibrinogen binding was also virtually absent with platelets that had been incubated with EDTA for 8 min at 37 degrees C and pH 7.8. These platelets could not aggregate when mixed with ADP and adequate CaCl2 and fibrinogen, although they could still change their shape. Thus, ADP-induced binding of fibrinogen correlates with platelet aggregability.

Adenosine Diphosphate↗
PubMed1979

Cytogenetic localisation of the purine 1 and guanosine 1 loci of Drosophila melanogaster; the purine 1 locus specifies a vital function.

Three auxotrophic mutants at two loci (pur 1 and gua 1) apparently involved in purine metabolism were mapped cytologically to region 9E1-9E3 on the X-chromosome of Drosophila. Because mutants of pur 1 behaved as semi-lethals against deficiencies even on permissive medium, it appears that the pur 1 locus is vital to the fly and its auxotrophic mutants are hypomorphs.

Animals↗
PubMed1979

Platelet membrane glycoproteins in thrombasthenia, Bernard-Soulier syndrome, and storage pool disease.

Quantitative polyacrylamide gel electrophoresis has been carried out on patients with Bernard-Soulier syndrome, Glanzmann's thrombasthenia, and storage pool defect in order to clarify the abnormalities in their platelet membrane glycoproteins. Normal individuals had values (expressed as PAS staining units/mg of membrane protein) of 5.11 +/- 0.63 for glycoprotein 1 (Mr 150,000), 2.35 +/- 0.35 for glycoprotein II (Mr 120,000), 0.89 +/- 0.22 for glycoprotein III (Mr 100,000), and 1.34 +/- 0.64 for glycoprotein IV (Mr 85,000). Total PAS staining of these four major bands was 9.70 +/- 1.26 PAS units/mg of membane protein. Patients with Bernard-Soulier syndrome completely lacked glycocalicin and had about one half (1.90 PAS units/mg) of the glycoprotein I of normal controls. These was no significant reduction in glycoproteins II, III, and IV, but total PASstaining was reduced to 4.40 units/mg, reflecting the importance of the contribution of glycoprotein I to this parameter. Thrombasthenic platelets gave values for glycoprotein II of 0.66, which were about 25% of controls, and the values for glycoprotein III (0.34) were about 40% of controls. Patients with storage pool disease gave values within the normal range with the exception of one family which showed, in addition, small platelets and an associated lipid defect. In thic case of glycoprotein (2.71) was significantly elevated.

Blood Platelet Disorders↗
PubMed1978

Nerve extract induces increase and redistribution of acetylcholine receptors on cloned muscle cells.

The effect of rat spinal cord explants and cell-free nerve extract on acetylcholine receptor site density and distribution was studied using (125)I- and rhodamine-labeled alpha-bungarotoxin on L(6), a cloned rat muscle cell line. Control L(6) myotubes have a low and uniform distribution of acetylcholine receptors (20 +/- 3 sites per mum(2) in the present study). The addition of spinal cord explants caused an increase in average receptor site density of about 6 times on myotubes within 2 mm of the explant, while a smaller increase of 3 times was observed at distances greater than 5 mm. The formation of high-density patches of receptors was also stimulated. These observations suggested that a diffusible substance originating from the explant was responsible for these changes. Cell-free homogenates of the central nervous system were prepared and found to produce the same effects. The effect of the homogenate was not strongly dependent on the age of the fetus from which the tissue was isolated, and fetal liver had little or no effect. The active component(s) appears to be a protein(s) with a molecular weight of about 100,000. Because the nerve homogenates make the L(6) cells resemble primary muscle cultures, we suggest that a common factor is responsible for regulating the acetylcholine receptor in the two types of muscle culture. The normally acetylcholine receptor-poor L(6) cells may provide a more sensitive assay for these factors than do primary muscle cultures.

Acetylcholine↗
PubMed1978

Absence of the platelet receptor for drug-dependent antibodies in the Bernard-Soulier syndrome.

The platelet membrane receptor for quinidine- and quinine-dependent antibodies was studied in three patients with the Bernard-Soulier syndrome (BSS) and in normal subjects with immunologic techniques based on the release of 51Cr from labeled platelets. The receptor could not be detected on BSS platelets but was present on platelets from each of 180 normal subjects. BSS platelets reacted normally with other allo- and autoantibodies. In confirmation of previous reports, BSS platelets were found to be deficient in glycoproteins Ib and Is. However, after apparently total cleavage of these proteins from the membrane of normal platelets by controlled hydrolysis with trypsin or chymotrypsin, 80% of the drug-dependent antibody receptor activity was retained. These observations suggest the existence of an additional, hitherto unrecognized membrane defect in Bernard-Soulier platelets.

Antibodies↗
PubMed1975

Hereditary giant platelet syndrome. Absence of collagen-induced coagulant activity and deficiency of factor-XI binding to platelets.

The platelets from two related patients with the hereditary giant platelet syndrome were examined. They were larger than normal but otherwise ultrastructurally normal; they contained increased storage pools of adenine nucleotides and heparin-neutralizing activity and took up serotonin at an increased rate. They aggregated normally with ADP and collagen but failed to aggregate with bovine factor VIII and Ristocetin. Some change in shape occurred with ADP, and the reduction in adenylate energy change after addition of ADP to platelet-rich plasma was smaller than normal. Platelet coagulant activities including contact product forming activity, intrinsic factor-Xa forming activity and platelet factor 3 activity were normal or increased, but collagen-induced coagulant activity was absent whether tested in washed platelet suspensions or platelet-rich plasma. Platelet washing experiments showed decreased binding of factors V and VIII to hereditary giant platelets and no detectable factor XI in washed platelet suspensions. It is concluded that (1) the hereditary giant platelets studied lacked a binding mechanism for factors, V, VIII and XI; (2) the normal development of collagen-induced coagulant activity apparently depends upon the binding of factor XI to the platelet membrane; and (3) the defective prothrombin consumption observed in these patients may have resulted from the failure of their platelets to bind factor XI.

Adenine Nucleotides↗
PubMedDate not supplied

Suppression of in vitro haematopoiesis following human immunodeficiency virus infection.

Viral infections are frequently associated with haematological disorders. Abnormalities including leukopenia, anaemia and thrombocytopenia are commonly observed in patients with the acquired immune deficiency syndrome (AIDS) or the AIDS-related complex (ARC). The underlying cause of these haematological abnormalities is poorly understood. We report here that bone marrow progenitors isolated from AIDS or ARC patients are responsive to recombinant human granulocyte-macrophage colony stimulating factor (rGM-CSF) and recombinant erythropoietin. Antibodies present in the serum of patients infected with the human immunodeficiency virus (HIV), however, could suppress the growth of these progenitors, but not the growth of progenitors from HIV seronegative controls. A component of this immune-mediated suppression appears to be antibodies directed towards the envelope glycoprotein (gp120) of HIV.

AIDS-Related Complex↗