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Biomedical subjects

M Greaves

Publications and source records attributed to M Greaves.

At least 253 records · Page 14Linked to original sources

Phenotypes of 'null' lymphoid cells in human blood.

F(ab')2 antibody fragments of heteroantisera directed against p28,33 (or 'Ia-like') antigen, T-cell antigen(s) (T), myeloid antigen (M), and immunoglobulin have been used along with rosetting techniques to analyse the antigenic heterogeneity of 'null' or 'unclassified' lymphoid cells purified 'negatively' from human blood by E rosette depletion of T cells and B removal on an anti-immunoglobulin immunoabsorbent. The results confirm that considerable heterogeneity exists within the 'null' cell population; the majority of cells are p28,33+ and Fcgamma-receptor-positive, and a proportion but not all of these p28,33+, Fcgamma+ cells are also C3-receptor-positive but negative for the other heteroantigens (T and M). 2-6% were 'pre-B' by the criteria of immunofluorescent staining for cytoplasmic IgM in the absence of detectable cell surface Ig. 1-3% stained intensely with anti-IgM, anti-IgG or anti-IgA, or anti-k plus anti-lambda and were presumed to be plasma cells or their immediate precursors. No null cells stained with antibody to terminal deoxynucleotidyl transferase enzyme, a marker for early T lineage cells, and less than 1% expressed an acute ('non-T, non-B') lymphoblastic-leukaemia-associated membrane antigen which is believed to be an 'early' lymphoid lineage differentiation marker. A minor subpopulation made sheep 'E' rosettes, and another made mouse 'E' rosettes after neuraminidase pretreatment of the lymphoid cells. A small proportion of 'lymphoid', 'null cells' were reactive with an anti-myelomonocytic (M) antibody. It is suggested that 'null' lymphoid cells in blood are heterogeneous and that most are not immature T or B precursors but either a relatively mature B lymphocyte population with a very low density of membrane immunoglobulin or a distinct non-T, non-B cell type.

Animals↗

Erythropoietin.

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Animals↗

Small intestinal transit in diabetics.

Small intestinal transit was assessed in diabetic patients and healthy controls by measuring the breath hydrogen appearance time after the ingestion of lactulose. Transit in diabetics with autonomic neuropathy was significantly slower than in diabetics without neuropathy and controls. Delayed transit is probably due to vagal denervation. These slower transit times would allow bacteria to proliferate, which might explain why some diabetics have diarrhoea. The test cannot be used in patients with bacteria in the small bowel because these may metabolise lactulose and release hydrogen prematurely.

Autonomic Nervous System↗

Analysis of human leukaemic cells using cell surface binding probes and the fluorescence activated cell sorter.

Cell surface binding fluorescent ligands have been used to distinguish between different types of leukaemic cells and between leukaemic cells and their presumed normal counterparts or progenitors. Binding of these probes was evaluated using the Fluorescence Activated Cell Sorter (FACS) which provides both rapid, objective and quantitative recording of fluorescent signals from individual cells plus physical separation of cells of particular interest. Binding sites for cholera toxin (monosialoganglioside GM1) were found to be normally expressed in chronic leukaemias but greatly diminished or absent in acute leukaemias irrespective of their morphological type. Antibodies specific for the common form of acute lymphoblastic leukaemia (ALL, non-T, non-B) have been produced in rabbits. After extensive absorption and testing these were shown to define a cell surface antigen of non-T, non-B type ALLs. The antigen is absent from other leukaemias with two interesting exceptions--the majority of acute undifferentiated leukaemias express the antigen as do a proportion of chronic granulocytic leukaemias in blast crisis relapse. The anti-ALL antibodies can therefore be used to distinguish different leukaemias and, more significantly, can identify the existence of relatively rare leukaemic cells in the blood of untreated patients and the marrow of treated patients considered to be in remission.

Antibodies, Neoplasm↗

Association of ventricular extrasystoles and ventricular tachycardia with idioventricular rhythm.

Patients with acute myocardial infarction were monitored for ventricular arrhythmias in the first 48 hours. Idioventricular rhythm (rate less than 100/minute) occurred in 35 out of 224 patients (15.6%) during the first day and in 13 out of 192 patients not receiving treatment on the second day (6.8%). This arrhythmia was frequently preceded by late ventricular extrasystoles, which often showed variation of their coupling intervals to the preceding QRS. Double ventricular extrasystoles separated by larger than or equal to 600 ms were also precursors of idioventricular rhythm. Idioventricular rhythm at times could be described as an escape rhythm, but on other occasions it was undoubtedly an accelerated rhythm. Spontaneous changes in the idioventricular cycle length were frequent on single one-minute electrocardiographic recordings. The rate of the dominant rhythm in patients with episodes of idioventricular rhythm was significantly slower than the heart rate of patients without this arrhythmia. Idioventricular rhythm was more frequent in patients with inferior infarction. Idioventricular rhythm sometimes preceded ventricular tachycardia but there was only a significant association between ventricular tachycardia and idioventricular rhythms with rates of over 75/minute. Irregular idioventricular rhythm frequently accelerated to ventricular tachycardia. It is suggested that the term benign idioventricular rhythm be reserved for those rhythms below 75/minute, and that the term rapid idioventricular rhythm should be used for rhythms between 75 and 120/minute. The rate of idioventricular rhythm is related to the probability of development of life-threatening ventricular arrhythmias during the first 48 hours after myocardial infarction.

Cardiac Complexes, Premature↗

Amino acid composition of human nail, as measured by gas-liquid chromatography.

We describe a quantitative method for determination of histidine and 16 other amino acids in a nail hydrolysate. This is based on the formation of trifluoroacetyl amino acid methyl esters and gas-liquid chromatographic analysis with use of two columns of mixed stationary phases. Histidine is determined as a triple derivative Nalpha-trifluroacetyl-Nim-carbethoxy methyl histidinate. The specificity and reproducibility of the method are illustrated. As little as 1 mg of amino acid per gram of nail can be determined, and 15 hydrolysates can be completely analyzed in 10 working days. Data obtained from multiple analyses of 10 nail hydrolysates by the method described closely parallel those obtained in another laboratory, in which an amino acid analyzer was used.

Amino Acids↗

Immunological determination of muscle-type enolase in the serum as a diagnostic test for myocardial infarction.

An antiserum raised in the chicken against purified rat skeletal muscle enolase neutralized 86% of the enolase activity of human heart muscle and 8.7% +/- 4.8% (mean +/- S.D.) of the enolase activity in normal human serum. The fraction of enolase inhibited by the antiserum, designated as 'immunologically reacting muscle enolase', promptly rose after myocardial infarction in the serum of affected subjects, reaching peak values in excess of 40% in all but one of 23 subjects. Only one subject with ischaemic heart disease, but without infarction, and 2 with miscellaneous conditions, among 117 such patients tested, yielded comparable values. The test appears to be highly specific for myocardial infarction when muscle disease can be excluded and would not be difficult to introduce as a laboratory routine.

Diagnosis, Differential↗

Ligand-induced redistribution of lymphocyte membrane ganglioside GM1.

Dynamic aspects of the binding of cholera toxin to lymphocyte membranes have been studied. We have shown that the receptor for this ligand--the GM1 ganglioside--can be laterally redistributed into aggregates and caps. Exogenous purified GM1 inserted into GM1-deficient human leukaemic cells can undergo a similar pattern of ligand-induced mobilisation. These observations may have important implications for both the general behaviour of cell surface glycolipids and the mode of action of cholera toxin on adenyl cyclase.

Animals↗

Leukemia-associated antigens in man.

Rabbit antisera raised against acute lymphoblastic leukemia (ALL) cells were used to distinguish ALL from other leukemias, to identify rare leukemia cells in the bone marrow of patients in remission, and to define human leukemia-associated antigens. Antibody binding was studied with the use of immunofluorescence reagents and the analytic capacity of the Fluorescence Activated Cell Sorter-1 (FACS-1). The results indicated that most non-T-cell ALL have three leukemia-associated antigens on their surface which are absent from normal lymphoid cells: 1) an antigen shared with myelocytes, myeloblastic leukemia cells, and fetal liver (hematopoietic) cells; 2) an antigen shared with a subset of intermediate normoblasts in normal bone marrow and fetal liver; and 3) an antigen found thus far only on non-T-cell ALL and in some acute undifferentiated leukemias, which we therefore regard as a strong candidate for a leukemia-specific antigen. These antigens are absent from a subgroup of ALL patients in which the lymphoblasta express T-cell surface markers. Preliminary studies on the bone marrow samples of patients in remission indicated that rare leukemia cells were present in some samples. The implications of these findings with respect to the heterogeneity and cell origin(s) of ALL, its diagnosis, and its potential monitoring during treatment were discussed.

Absorption↗