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Biomedical subjects

M A Moore

Publications and source records attributed to M A Moore.

At least 469 records · Page 26Linked to original sources
PubMed1977

Proliferation of erythroid colonies in semi-solid agar.

Growth of human erythroid cells in soft-agar culture with no added erythropoietin was demonstrated. This growth was particularly marked in patients with diseases such as myelofibrosis (MF) in which patients had a previous history of polycythaemia vera (PV) characterized by excessive red cell production. A rapid assessment of the proportion of erythroid colonies was obtained by directly staining the culture with benzidine. Fixed and stained preparations of these agar-grown cells revealed elements in all stages of erythroid maturation. The morphology of these erythroid colonies was characteristic of 'erythroblastic islands' containing central, iron-containing macrophages, surrounded by erythrocytic precursors, with the more mature erythrocytes found at the periphery of the colony. These observations document that erythropoiesis may be maintained in agar cultures, and suggest that this technique may be of diagnostic value in disease states characterized by abnormalities of red cell production.

Agar↗
PubMed1977

Cell-free granulocyte colony inhibiting activity derived from human polymorphonuclear neutrophils.

Human PMN (non-adherent: density greater than 1.070 g/cm3) were used to prepare cell-free colony inhibiting activity (CIA). Intact PMN, PMN conditioned media (serum-free or serum-containing) and supernatant from immediately lysed PMN equally reduced the numbers of spontaneous bone marrow (density less than 1.070 g/cm3; depleted of PMN) colonies and clusters. Addition of CIA reproducibly reduced colony and/or cluster numbers by 35-70%. CIA was heat labile being inactivated at 37 degrees C. Daily additions of CIA reduced colony numbers even further; inhibition was dependent on [PMN] used to prepare CIA and on the potency of stimulation produced by colony stimulating cells (CSC). PMN from some patients with leukemia were inactive as inhibitors and did not condition media with CIA. All experiments were thereafter controlled by parallel assessment of supernatant of lysed PMN not demonstrating any CIA. CIA appears to be not only stored in PMN but released from viable, as well as degranulating PMN. Although not species-specific, CIA was specific in its nontoxic action on CSC; colony forming cells and cell-free colony stimulating activity were not affected. The influence of CIA on CSC could be reversed within 10 minutes, but not within 35 minutes of incubation. CIA may have possible physiological relevance.

Animals↗
PubMed1977

The characteristics and mortality of outpatient-acquired pneumonia.

One-hundred fifty-four cases of pneumonia occurring over a 6-month period were analyzed. Population characteristics, admission diagnoses, causative pathogens, frequency of associated illnesses, antibiotic usage and mortality were evaluated. Despite population characteristics known to predispose to a poor clinical outcome, the mortality was low, probably because of rapid institution of a single, appropriate antibiotic.

Adult↗
PubMed1977

Characterization of colony-stimulating activity produced by human monocytes and phytohemagglutinin-stimulated lymphocytes.

Human colony-stimulating activity (CSA) may support the proliferation of both human and murine granulocyte-macrophage progenitor cells (CFU-C) or, in the case of human urinary CSA, may only stimulate murine bone marrow CFU-C. CSA produced in the culture media of monocytes and macrophages and phytohemagglutinin-stimulated lymphocytes from human peripheral blood was characterized for both human and mouse marrow CFU-C stimulating activities. During the initial phase of a long-term cultures of monocytes, both human- and mouse-active CSA (MnCM-HM) were produced. In later phases of culture, however, only mouse-active CSA (MnCM-M) was produced. Fractionation on Sephadex G-150 revealed two functionally distinct species from MnCM-HM and lymphocytes conditioned medium, a high molecular weight factor (MW greater than 150,000) which stimulated mouse but not human colony formation, and a low molecular weight species (MW 25,000-35,000) which was active against both mouse and human target cells. However, MnCM-M revealed only one high molecular weight species (greater than 150,000), active only on mouse marrow. The possible biologic significance of such an activity is discussed.

Animals↗
PubMed1976

Lysozyme synthesis by established human and murine histiocytic lymphoma cell lines.

A human cell line established in culture from a histiocytic lymphoma patient synthesizes and secretes the monocyte-granulocyte specific enzyme lysozyme. 18 other human cell lines with characteristics of T-lymphocyte, B-lymphocyte, Burkitt's lymphoma, non-Burkitt's lymphoma, myeloma, and bone marrow epithelial cells were not associated with lysozyme. Among murine cell lines, lysozyme was produced by (a) three histiocytic lymphoma or macrophage lines, which mediate antibody-dependent phagocytosis and cytolysis; (b) myelomonocytic leukemia line which also secretes myeloid colony-stimulating factor; and (c) a spontaneous lymphoma and an Abelson leukemia virus-induced lymphoma. Lysozyme-negative lines include another Abelson lymphoma, myelomas, T lymphomas, and mastocytoma.

Cell Line↗
PubMed1976

Growth of B-lymphocytes clones in semisolid culture is mitogen dependent.

A substance which was mitogenic for murine B lymphocytes in the presence of 2-mercaptoethanol was isolated from agar. Stimulating activity of this material was stable to proteolysis or protein denaturants but was destroyed by periodate treatment. Agar-derived mitogen stimulation was distinct from that obtained with dextran sulfate or lipopolysaccharide and may define different populations of B lymphocytes.

Agar↗
PubMed1976

Prediction of relapse and remission in AML by marrow culture criteria.

Bone marrow culture studies in semi-solid agar have been performed on 250 patients presenting with acute myeloid leukemia. The detection of a spectrum of qualitative defects in the proliferation, differentiation and biophysical characteristics of leukemic colony forming cells (CFU-c) has permitted a detailed analysis of the relapse-remission status based on transition from qualitatively abnormal cell growth in vitro to a normal pattern of proliferation and differentiation. Changes in vitro generally preceded clinical or morphological evidence of the onset of relapse or remission and serve as a valuable additional parameter in monitoring clinical status. Marked cyclic changes in CFU-c incidence appeared to characterize the remission phase of AML and were frequently associated with fluctuations in marrow blast cell count which can lead to mis-diagnosis of incipient relapse. Detection of qualitative defect in marrow culture serves to distinguish patients with preleukemic disorders at high risk of termination in acute myeloid leukemia from patients with clinically similar disease who have not undergone further progression over a 2-4 year period of observation.

Bone Marrow↗
PubMed1976

Clinical utility of bone marrow culture.

Standardized culture of bone marrow in soft agar permits the detection of a population of granulocyte-macrophage progenitor cells (CFU-c). A spectrum of qualitative abnormalities serves to distinguish myeloid leukemic CFU-c from normal and remission populations. These abnormalities in maturation and proliferation are diagnostic of a myeloid leukemic state and serve to functionally reclassify acute myeloid leukemia at diagnosis into a number of categories based on in vitro growth pattern. The virtue of this classification is that it permits detection of a substantial number of patients who are refractory to conventional remission induction protocols. The clear distinction between normal and leukemic growth in vitro permits early detection of emerging remission CFU-c during induction therapy and of early onset of relapse in patients who are otherwise in complete remission. In patients with leukemia undergoing allogeneic bone marrow engraftment, marrow culture has proved of value in documenting the reconstitution of the patient and in detecting re-emergence of the original leukemic stem line prior to its detection by cytogenetic and hematological techniques. Serial studies on patients with chronic myeloid leukemia have allowed early diagnosis of blastic transformation and classification of blastic phase disease on the basis of in vitro growth pattern has revealed a similar spectrum of in vitro abnormalities as seen in AML. The cloning of normal or leukemic human myeloid progenitor cells (CFU-c) in agar or methylcellulose has permitted analysis of both quantitative and qualitative changes in this cell compartment in leukemia and other myelodysplastic states (1-7). Among these changes are abnormalities in maturation of leukemic cells in vitro (4, 5, 6), defective proliferation as measured by colony size or cluster to colony ratio (5, 6), abnormalities in biophysical characteristics of leukemic CFU-c (4, 5), regulatory defects in responsiveness to positive and negative feedback control mechanisms (8, 9) and the existence of cytogenetic abnormalities in vitro (10, 11). Detection of this spectrum of abnormalities has proved of clinical utility in diagnosis of leukemia and preleukemic states (5, 6, 12), in classification of leukemias and myeloproliferative diseases (5, 6), in predicting remission prognosis and response to therapy (5, 13), in predicting onset of remission or relapse in AML (13) and in monitoring the progression of chronic myeloid leukemia or preleukemic disease (4, 14). The present communication serves to illustrate the clinical applications of bone marrow culture in these various areas.

Blood Cells↗
PubMed1976

Aplastic anemia: presence in human bone marrow of cells that suppress myelopoiesis.

Bone marrow from a patient with aplastic anemia was shown by multiple criteria to have a block in early myeloid differentiation. This block was overcome in vitro by elimination of marrow lymphocytes. Furthermore, this differentiation block was transferred in vitro to normal marrow by coculturing with the patient's marrow. We suggest that some cases of aplastic anemia may be due to an immunologically based suppression of marrow cell differentiation rather than to a defect in stem cells or their necessary inductive environment.

Adult↗
PubMed1976

Relation between plasma renin activity, angiotensin, and aldosterone and blood pressure in mild untreated hypertension.

Plasma renin activity, arterial and venous angiotensin II (A II), plasma aldosterone, and sodium excretion were measured in a group of 101 patients with mild essential hypertension. For the total hour; arterial A II was 5.2 +/- 1.0 pg/ml; venous A II was 4.2 +/- 0.6 pg/ml; and plasma aldosterone was 5.0 +/- 0.45 ng/100 ml. All values were lower corresponding values for normal subjects on a high salt intake despite the fact that salt intake in the normal subjects exceeded that for the hypertensive group more than 3-fold. Moreover, when the range of diastolic blood pressure up to 114 mm Hg was divided into three successive class intervals of increasing severity, there was a negative correlation between diastolic blood pressure and both PRA and plasma aldosterone. Arterial A II showed an anomalous increase in the class interval 105-114 mm Hg, despite the fact that this group exhibited the lowest level of PRA. At diastolic blood pressures above 114 mm Hg, the PRA appears to rise again. The anomalous increase in arterial A II in the presence of marked suppression of PRA is consistent with the presence of a renin activator or accelerator factor in hypertensive plasma as postulated by others. It also identifies a possible mechanism whereby even small increases in PRA could exert an adverse effect on the hypertensive state.

Adolescent↗
PubMed1976

Arterial and venous angiotensin II in normal subjects. Relation to plasma renin activity and plasma aldosterone concentration, and response to posture and volume changes.

Plasma renin activity, arterial and venous angiotensin II (A II) concentrations, and plasma aldosterone concentration were measured in 16 normal subjects (mean age = 34 years) after 8 hours of recumbency, following 2 hours of ambulation, and again 30 minutes after administration of furosemide intravenously. Measurements were obtained during periods of sodium restriction and again during sodium surfeit. Both arterial and venous A II exhibited a 3-fold increase from low values of 8.8 +/- 2.5 and 8.6 +/- 2.5 pg/ml of plasma, respectively, during recumbency on high sodium intake to values of 23.9 +/- 4.1 and 26.5 +/- 6.2 pg/ml, respectively, following intravenous furosemide during sodium restriction. Corresponding values for aldosterone exhibited a 5-fold rise from 5.6 ng/100 ml to 32.0 ng/100 ml, whereas plasma renin activity (PRA) measured by an in vitro assay exhibited a 20-fold rise from 0.6 +/- 0.2 ng of angiotensin I (AI) generated per ml per hour to 13.1 ng/ml per hour. Despite the disparity in the magnitude of these increases, significant correlations were identified between all four of the measured parameters, indicating a major role of the renin-angiotensin system in regulating aldosterone output in response to volume and posture-related stimuli. Values of arterial and venous immunoreactive A II were closely correlated ( r = +0.72, P less than 0.005), but significant differences were demonstrated between low and high salt periods, suggesting that changes in metabolism of A II in the peripheral circulation may occur during sodium restriction.

Adult↗