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B J Clarke

Publications and source records attributed to B J Clarke.

45 records · Page 3Linked to original sources
PubMed1980

Monocytes do not inhibit peripheral blood erythroid burst forming unit colony formation.

To determine a possible role of peripheral blood monocytes in erythroid differentiation, various fractions of peripheral blood mononuclear cells were prepared from normal volunteers. The fractions contained 3-95% monocytes. These freshly prepared monocytes did not inhibit erythroid burst forming unit expression in plasma clot erythroid colony culture. Null cell preparations contaminated by up to 84% monocytes expressed erythroid burst forming unit colony formation when either T lymphocytes or T-cell conditioned medium was added. These results indicate that certain peripheral blood null cells engage the program of erythroid differentiation in the presence of T cells and erythropoietin. Monocytes do not inhibit this engagement.

Adult↗
PubMed1979

The effects of rubidium on mammary tumour growth in C57 blk/6J mice.

A high pH therapy for cancer arrived at theoretically was tested in mice by feeding them rubidium carbonate. Tumours were transplanted in the abdomen of mice and allowed to grow for 8 days. The mice were then divided into two groups. The control group was continued on conventional mouse chow. The test group, in addition to the mouse chow, was force-fed 1.11 mg of rubidium carbonate dissolved in distilled water. At the end of 13 more days the tumours in the controls had grown to a large size so all the mice were sacrificed. The tumours were then removed and weighed. The tumours in the test animals weighed essentially one eleventh of those in the controls. In addition the test animals were showing no adverse effects from the cancers. The probability that this marked difference in tumour size could have come about by chance is exceedingly small.

Animals↗
PubMed1978

Normal erythropoietic helper T cells in congenital hypoplastic (Diamond-Blackfan) anemia.

To examine the erythropoietic function of T and null cells in congenital hypoplastic (Diamond-Blackfan) anemia, we fractionated the peripheral blood of three normal subjects and three affected patients into subclasses of null, T and B cells. Mixtures of these cells were co-cultured in plasma clots in the presence of erythropoietin. Erythroid colonies grew in cultures of normal null cells if either normal or patient T cells were co-cultured with them. Null cells of patients with hypoplastic anemia did not produce erythroid colonies under any culture conditions. We conclude that in this disorder, T cells function normally as helper cells in erythropoiesis and do not suppress colony formation, whereas the erythroid progenitor cells in the peripheral blood null-cell fractions are deficient in either number of function.

Adolescent↗
PubMed1978

Erythroid precursors in congenital hypoplastic (Diamond-Blackfan) anemia.

To explore the etiology of congenital hypoplastic anemia (CHA) or the Diamond-Blackfan anemia, erythropoietin responsive committed erythroid precursors were enumerated by the plasma clot method. These included blood and marrow erythroid burst-forming units (BFU-E) and marrow erythroid colony-forming units (CFU-E). The peripheral blood nucleated cells of 11 patients and the marrow cells of seven of these patients were examined. Studies were repeated in several patients during relapse and after induction of remission. BFU-E were undetectable in the marrow and blood of all but one relapsed patient, and the numbers of marrow CFU-E were depressed in all relapsed patients. Blood BFU-E remained low in all of the patients in remission. No evidence was obtained for suppression of normal CFU-E or BFU-E by CHA lymphocytes. Erythropoietin dose-response curves performed in two patients revealed a 10-fold increase in erythropoietin requirement for marrow CFU-E colony growth. This marked unresponsiveness to erythropoietin was strikingly improved by steroid therapy in one patient. We suggest that CHA is the result of a qualitative and/or quantitative deficiency of BFU-E. If BFU-E are produced, they must be relatively unresponsive to erythropoietin. The abnormal BFU-E give rise to erythropoietin unresponsive CFU-E and, thence, to proerythroblasts that are, in turn, trapped in that early stage of development because of their poor erythropoietic response. Hence, red cell production is deficient. Steroids appear to improve the erythropoietin response of CHA erythroid precursors.

Adolescent↗
PubMed1977

Characterization of an erythroid precursor cell of high proliferative capacity in normal human peripheral blood.

We have found that the peripheral blood of normal humans contains a significant number of committed erythroid stem cells of high proliferative capacity. These erythroid stem cells closely resemble the murine erythroid burst-forming unit (BFU-E) with respect to proliferative capacity, colony morphology, and erythropoietin requirement. BFU-E were isolated from the peripheral blood of normal individuals by Ficoll-Hypaque density gradient centrifugation and cultured in vitro using the plasma culture technique. Macroscopic erythroid colonies of between 100 and 1000 cells were observed after 10-14 days of culture in the presence of either sheep or human erythropoietin at 0.5-4 units/ml. Individual colonies contained between 3 and 20 subcolonies and reached a maximum mean size of approximately 500 cells. Colony number was linearly related to the cell input, suggesting that a single cellular entity was precursor to each colony. The frequency of cells capable of giving rise to an erythroid colony was at least 100 per ml of blood in a number of individuals tested. The ability to assay significant numbers of erythroid precursor cells of high proliferative capacity from normal peripheral blood should facilitate the study of both normal erythropoiesis and of disease states affecting erythropoiesis in which marrow samples are not available on a routine basis.

Blood Cells↗
PubMed1976

Friend spleen focus-forming virus production in vitro by a nonerythroid cell line.

We developed a cell line (IS) that continuously produced both Friend spleen focus-forming virus (SFFV) and XC plaque-forming virus in vitro. The line was derived from the enlarged spleen of an inbred SIM mouse previously infected with a polycythemic strain of Friend leukemia virus in vivo. Friend SFFV titers of 10(4) spleen focus-forming units/ml of culture medium were maintained for more than 200 cell generations. The virus from IS cells induced the splenomegaly and high hematocrit typical of Friend virus-induced erythroid disease in SIM mice. Cells of the IS line were adherent and phagocytic and had a low saturation density. They produced no tumors after being injected sc into normal syngeneic hosts and no spleen colonies after being injected iv into supralethally irradiated hosts. IS cells did not have the character of erythroid cells: They did not contain detectable heme as measured by benzidine-peroxide reagent, did not contain globin mRNA in detectable amounts, and did not produce erythroid colonies in plasma culture in the absence or presence of erythropoietin. According to these criteria, growth in the presence of dimethyl sulfoxide did not stimulate erythroid differentiation of IS cells. We concluded that Friend SFFV can infect nonerythroid spleen cells but that replication of the virus was not obligatorily coupled to expression of genes associated with the erythroid phenotype.

Animals↗
PubMed1975

Erythroid colony induction without erythropoietin by Friend leukemia virus in vitro.

Erythroid colonies could be produced without the addition of erythropeietin in plasma cultures seeded with bone marrow cells from normal C3Hf/Bi mice by exposure of the cells in vitro to medium from a cell line (IS) that continuously produces Friend leukemia virus in culture. The activity in the culture medium was viral rather than erythropoietin-like, since it was sedimentable by high-speed centrifugation and heat labile. Erythroid colonies did not develop when the bone marrow cells exposed to virus-containing medium were from mice genetically resistant to Friend virus. IS culture medium contained both Friend spleen focus-forming and XC-plaque-forming activities. No erythroid colonies were induced when genetically sensitive cells were exposed to a preparation from which the spleen focus-forming activity had been removed, but which contained XC plaque-forming activity in high concentration. Thus the spleen focus-forming component of Friend virus appeared to be responsible for inducing erythroid colony formation without erythropoietin in vitro. Some erythroid colonies were also found in control cultures to which neither virus nor erythropoietin had been added. Reduction in the concentration of fetal calf serum in the culture medium substantially decreased the number of these colonies but had only a minor effect on the number of virus-induced colonies. The number of erythroid colonies produced after 2 days of culture without erythropoietin or fetal calf serum was approximately proportional to the titer of Friend spleen focus-forming virus to whcih the bone marrow cells had been exposed. This system should prove useful for investigation in vitro of Friend virus--host cell interactions which lead to erythropoietin-independent erythropoiesis.

Animals↗