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Biomedical subjects

M J Cline

Publications and source records attributed to M J Cline.

At least 73 records · Page 4Linked to original sources
PubMed1982

Humoral stimulation of hemopoietic progenitors from human fetal liver.

Hemopoietic cells from human fetal livers of 9-21 weeks gestation were cultured in semisolid media in vitro and in diffusion chambers implanted in mice. Myeloid colony formation in agar (CFU-C) was detected only in the presence of colony-stimulating factor. Formation of erythroid bursts in vitro was enhanced by addition of erythropoietin or erythroid-potentiating activity derived from a human T cell line (Mo). Fetal liver cells implanted in diffusion chambers gave rise to myeloid (CFU-DG) and occasionally to erythroid colonies. Administration of colony-stimulating factor derived from the T cell line to the host mice did not effect CFU-DG numbers. In contrast, a partially purified preparation containing erythroid-potentiating activity, caused a significant increase in the formation of CFU-DG. Similar stimulation was achieved by pretreatment of the diffusion chamber hosts with cyclophosphamide. None of these manipulations effected erythroid colony formation in diffusion chambers in mice.

Animals↗
PubMed1982

Human T-lymphocyte products stimulate human hemopoietic progenitor cell proliferation in diffusion chambers in vivo.

Human myeloid colony formation in diffusion chambers in mice (CFU-DG) was enhanced following administration of a human T-cell-line-derived conditioned medium (Mo). The Mo cell line also elaborates activities stimulating human myeloid colony formation in vitro in agar (CSF) and potentiating erythroid colony formation in vitro in methylcellulose (EPA). Depletion of CSF from Mo conditioned medium by heat inactivation or gel exclusion chromatography did not affect CFU-DG formation. EPA and CFU-DG stimulating activities are heat stable and have approximately the same molecular weight. Culture of human bone marrow cells in diffusion chambers in mice for 4 days under the influence of Mo conditioned medium resulted in significant increment of BFU-E and CFU-DG as judged by subculture of diffusion chamber contents. No effect on CFU-C could be detected.

Animals↗
PubMed1982

Cryopreservation of the human multipotent stem cell.

Light density human bone marrow cells were cryopreserved, then thawed and tested for their ability to form myeloid (CFUGM), erythroid (BFUE) and mixed myeloid-erythroid colonies in vitro. Proliferation of mixed hematopoietic colonies was supported by conditioned media from a human T-lymphocyte cell line and erythropoietin. All mixed colonies contained neutrophil and erythroid precursors and approximately 25% had mononuclear phagocytes. Following cryopreservation the bone marrow retained its capacity to form mixed colonies without apparent loss. The recovery of CFUGM and BFUE was 76% and 72% respectively.

Bone Marrow↗
PubMed1981

Insertion of new genes into bone marrow cells of mice.

Drug resistance genes such as those coding for a methotrexate-resistant dihydrofolate reductase (DHFR) or the thymidine kinase from herpes simplex virus can be used to confer a proliferative advantage on bone marrow cells of mice. As a result of this proliferative advantage, transformed cells become the predominant population in the bone marrow. Efficient gene expression was obtained for both the thymidine kinase and DHFR genes inserted into mouse bone marrow. Such gene insertion techniques may ultimately lead to the cure of life-threatening globinopathies such as sickle cell disease or the beta thalassemias. They may also be useful in reducing the hematopoietic toxicity of anticancer drugs.

Animals↗
PubMed1981

High-dose combined-modality therapy and autologous bone marrow transplantation in resistant cancer.

Fourteen patients with resistant cancers received high-dose chemotherapy and total body irradiation followed by rescue with autologous cryopreserved bone marrow cells. In seven patients, disease has remained in remission for periods up to two years. These data indicate that effectiveness of high-dose combined-modality therapy and bone marrow autotransplantation in patients with resistant cancer. The high incidence of non-marrow toxicity may be reduced by the use of this modality before patients have received extensive therapy.

Adolescent↗
PubMed1981

Chronic myelocytic leukaemia: a pluripotent haemopoietic cell is involved in the malignant clone.

Haemopoietic cells with pluripotent capabilities, were grown in soft-gel cultures from the peripheral blood of a glucose-6-phosphate dehydrogenase (G6PD) electrophoretic A,B heterozygous female with chronic myelocytic and granulocytic progeny. Only type B isoenzyme of G6PD was found in mixed colonies, in mature neutrophils, erythrocytes, and committed granulocyte and isoenzymes of G6PD. This study provides direct evidence that a pluripotent haemopoietic stem cell is involved in the malignant clone in CML.

Adult↗
PubMed1981

Proliferation in liquid culture of myeloid progenitor cells from the blood of normals and patients with aplastic anaemia.

We studied myeloid progenitor cells (CFUc) from peripheral blood mononuclear leukocytes (MNL) of normals and patients with severe aplastic anaemia (AA). Baseline CFUc averaged 4.4 +/- 1.5 (range 0--17)/10(6) MNL in fifteen normals and 0 +/- 1/10(6) MNL in six patients with severe AA (P less than 0.05). To assess CFUc proliferative capacity, 10(7) MNL were put into liquid culture in Marbrook chambers with colony-stimulating activity and sub-cultured in agar at intervals up to 10 days. CFUc from normal MNL increased from 44 +/- 15/chamber at Day 0 to 156 +/- 33/chamber at peak value (P less than 0.02). In contrast, CFUc from AA MNL remained undetectable throughout the period of liquid culture (AA peak v. normal peak; P less than 0.001). These results indicate a marked decrease in circulating CFUc in patients with severe AA, and a profound abnormality in CFUc proliferation in vitro. This abnormality could be due to defective replication of CFUc, a lack of feed-in from more primitive precursors, or both.

Adult↗
PubMed1981

Intensive chemotherapy for acute myelogenous leukemia.

A complete remission rate of 82% was obtained in a group of 68 patients with acute myelogenous leukemia treated with a high-dose induction chemotherapy (TAD) consisting of 7-day courses of 6-thioguanine, cytarabine, and daunorubicin. The patients who achieved remission received intensive consolidation chemotherapy and were randomized to receive maintenance chemotherapy with or without immunotherapy. Median remission duration was 13 months and median survival, 21 months. Neither central nervous system prophylaxis nor the addition of immunotherapy to the maintenance regimen prolonged remissions or improved survival. Age, sex, and subclassification of acute myelogenous leukemia had no effect on the remission rate or survival. These data indicate that a large proportion of patients with acute myelogenous leukemia can achieve remission with intensive induction chemotherapy. Attempts to prolong remission have been less successful.

Adolescent↗
PubMed1981

Growth hormone stimulation of normal and leukemic human T-lymphocyte proliferation in vitro.

In order to investigate the effect of human growth hormone on T lymphocytes, we utilized a clonogenic assay for mitogen-responsive human peripheral blood T lymphocytes. Lymphocytes were purified by density gradient centrifugation and incubated in the presence of phytohemagglutinin using a two-layer agar technique for CFU- T-lymphocyte culture. Nanogram concentrations of human growth hormone, ovine prolactin, human chorionic somatomammotropin, or growth hormone fragment were added to cell cultures. Growth hormone potentiated normal T-cell colony formation in a species-specific manner. Cells from a homogeneous T-lymphoblast line derived from a patient with a T-cell variant of hairy cell leukemia also showed augmentation of colony growth in the presence of human growth hormone. These studies provide evidence for a direct effect of growth hormone on normal and some neoplastic human T cells.

Animals↗
PubMed1981

Plasma thromboplastin antecedent (Factor XI) deficiency in a black family.

A black man with a prolonged partial thromboplastin time has a severe deficiency of plasma thromboplastin antecedent (PTA) (factor XI) measured both in clotting assays and immunoassays, suggesting a diagnosis of homozygous PTA deficiency. His offspring seemed to be heterozygous carriers of PTA deficiency. Additionally, the proband and two of his children had decreased Hageman factor (factor XII) levels consistent with those of heterozygous carriers of Hageman trait. To our knowledge, this is the first case known of PTA deficiency in a black person. Its pattern of inheritance was independent of that of factor VII deficiency.

Black People↗
PubMed1981

Effect of cryopreservation on recovery of cells forming colonies in diffusion chambers in mice (CFUD).

The effect of cryopreservation on human and murine hematopoietic precursor cell survival was assessed. A large proportion of CFUC and CFUS was recovered following freezing and thawing. At the same time there was a substantial decrease in the number of cells which form myeloid (CFUDG) and megakaryocytic (CFUDM) colonies in diffusion chambers in mice. We suggest that the CFUDG and CFUDM number should be determined in the autologous bone marrow transplantation setting.

Animals↗
PubMed1981

The progeny of a single progenitor cell can develop characteristics of either a tissue or an alveolar macrophage.

Alveolar and peritoneal macrophages differ in their energy metabolism. Alveolar macrophages are mainly aerobic whereas peritoneal macrophages are mainly anaerobic in their energy generation. We investigated the question of whether these differences in metabolism are preprogrammed in subsets of macrophage precursors in the bone marrow, or develop in proliferating cells as a consequence of exposure to different tissue environments. The progeny of single mouse macrophage progenitor cells were grown in vitro for 4 days; the resultant colonies were divided into two roughly equal populations, which were cultured in either a high or low oxygen environment corresponding to that of the alveoli or tissues. Following 4 days incubation at 5% or 20% O2, the activities of the two glycolytic enzymes lactate dehydrogenase (LDH) and pyruvate kinase (PK) were two- to threefold higher in the half of the colonies grown in the low O2 environment, whereas the activity of the oxidative phosphorylative enzyme glutamate dehydrogenase (GDH) was two- to threefold higher in the half colony grown in the aerobic environment. Re-exposure of the cells from the low O2 environment to high O2 conditions for an additional 4 days caused a rise in the GDH activity and a decrease in the LDH and PK. The recovery of the GDH activity after the re-exposure was time dependent. Our results support the theory that macrophages arising from a single progenitor cell can develop different metabolic features depending on the O2 environment in which they mature. A single precursor cell can give rise to mature cells with metabolic characteristic of either alveolar or tissue macrophages.

Animals↗
PubMed1981

An in vitro model of hematopoietic injury in chronic hypoplastic anemia.

Mice treated with high-dose busulfan develop a 'latent' form of bone marrow failure characterized by near-normal peripheral blood counts and marrow cellularity, but marked reductions in marrow pluripotent stem cells (CFUs) and myeloid progenitor cells (CFUc). Spleen cell suspensions from control and 'latent' mice were placed in liquid culture in the presence of colony-stimulating activity. Cells were harvested at intervals up to 14 days and sub-cultured in agar to assay for CFUc. Baseline splenic CFUc did not differ significantly between control and 'latent' mice. Splenic CFUc from control mice increased 50-fold and reached a peak at day 10 in liquid culture. In contrast, splenic CFUc from 'latent' mice increased only 7-fold and reached a peak at day 3. Our results indicate that although splenic CFUc are present in normal numbers in 'latent' mice, their proliferative capacity is markedly reduced, either as the result of defective CFUc self-renewal or defective feed-in from CFUs or both.

Anemia↗