bluuebunny/crossref_metadata_2025_split huggingface dataset:
A murine model system for the study of the human leukemia-associated inhibitory activity
Authors: Marcelletti J , Furmanski P 
Published: October 2019

Abstract
Mice inoculated with the RFV strain of Friend virus develop an erythroleukemia that spontaneously regresses. Bone marrow cells from leukemic mice produce a factor that inhibits colony formation in agar by normal CFU-Cs. CFU-Cs from leukemic animals are resistant to the factor. Bone marrow cells from some mice whose leukemia has regressed continue to produce the factor, and CFU-Cs from some regressed mice retain resistance to the factor. These observations dupllicate findings reported for patients with acute leukemias and those with leukemia in remission. The RFV system thus serves as an accurate experimental model for the study of hematopoietic cell interactions and the proliferative advantage of neoplastic cells in human leukemias.
Philadelphia chromosome positive childhood acute lymphoblastic leukemia
Authors: Priest JR , Robison LL , McKenna RW , Lindquist LL , Warkentin PI , LeBien TW , Woods WG , Kersey JH , Coccia PF , Nesbit ME Jr 
Published: October 2019

Abstract
In a 3-yr period, the Philadelphia chromosome (Ph1) was found in 4 of 43 children with acute lymphoblastic leukemia (ALL) in whom chromosomes were studied at diagnosis. The clinical, morphological, cytochemical, and immunologic findings in the Ph1-positive (PH1+) CASES WERE CONsistent with typical childhood ALL, indicating that identification of cases requires chromosome studies. A review of all reported cases of Ph1 + childhood ALL shows that Ph1 + patients are older and have higher initial platelet and white blood cell counts (WBC) than most children with ALL. However, a life table comparison between the reported cases of Ph1 + ALL in children and randomly selected age-, sex-, and WBC- matched controls with ALL shows the duration of first marrow remission to be significantly shorter (p less than 0.02) for the Ph1 + cases Ph1 + ALL is a distinct subtype of childhood ALL that is not rare and can be identified only by cytogenetic studies. The prognosis is poor. Cytogenetic studies should be done prospectively in a large group of children with ALL to define further the subgroup of patients and to confirm the findings of this retrospective analysis.
Chlorpromazine inhibition of granulocyte superoxide production
Authors: Cohen HJ , Chovaniec ME , Ellis SE 
Published: October 2019

Abstract
Superoxide production by granulocytes is a result of the activation of an NAD(P)H-dependent oxidase present in the plasma membrane. Chlorpromazine (5–50 muM) prolongs the time necessary to activation of the superoxide generating system and inhibits the extent of activation. When chlorpromazine is added after activation, there is an inhibition of further superoxide production. These effects are seen with digitonin, phorbol myristate acetate, and opsonized zymosan stimulated guinea pig and human granulocytes. Other phenothiazines (1–20 muM) and tetracaine (0.1–1.0 muM) produce similar effects. Lidocaine (1–10 mM) inhibits superoxide production but has no effect on the rate of activation. The effect of chlorpromazine on the rate of activation is reversible, but its effect on extent of activation is unaffected by extensive washing. Incubation of granulocytes with chlorpromazine results in decreased activation of the plasma membrane superoxide generating NADPH oxidase. Chlorpromazine also competes with NADPH for the membrane oxidase. These data and previously published results provide the basis of a model for the activation of the superoxide generating system.
In vitro interactions of PGE and cAMP with murine and human erythroid precursors
Authors: Rossi GB , Migliaccio AR , Migliaccio G , Lettieri F , Di Rosa M , Peschle C , Mastroberardino G 
Published: October 2019

Abstract
Addition of prostaglandins of the E series (PGE1, PGE2) in methylcellulose cultures of murine marrow results in a dose-dependent inhibition of the cloning efficiency of both BFU-E and CFU-C. However, CFU-E growth is unaffected. The inhibitory action of PGE is progressively overcome by increasing amounts of colony-stimulating factor (CSF), and with some limitations, also of erythropoietin (Ep). Addition of PGF2 alpha' associated or not with indomethacin, does not exert any significant effect on these hemopoietic precursors. In an attempt to unvail the mechanism(s) underlying these phenomena, dibutyryl-cyclic AMP (db-cAMP), theophylline (an inhibitor of phosphodiesterase), or theophylline + PGE were plated at various concentrations. Both db-cAMP and theophylline induce an inhibitory influence on both BFU-E and CFU-C growth, which mimicks that by PGEs; additionally, theophylline potentiates the inhibitory action of PGE1. In all these studies, the CFU-E number was not significantly modified. PGE action on BFU-E proliferation is clearly species-dependent, since PGE1 addition to human marrow methylcellulose cultures induces a significant enhancement of the number of both BFU-E and CFU-E derived colonies. This action was abolished upon removal of adherent cells, thus suggesting that PGE1 evokes a release of factor(s) enhancing human erythroid colony growth by adherent cells.
Hemoglobin Ohio (beta 142 Ala replaced by): a new abnormal hemoglobin with high oxygen affinity and erythrocytosis
Authors: Moo-Penn WF , Schneider RG , Shih T , Jones RT , Govindarajan S , Govindarajan PG , Patchen LC 
Published: October 2019

Abstract
Hemoglobin Ohio [beta 142 (H20) Ala replaced by Asp] was found in three members of a white family, all of whom showed erythrocytosis. The variant hemoglobin has a high oxygen affinity, a reduced Bohr effect, and diminished cooperativity. The functional abnormalities of Hb Ohio are explained by the proximity of the substituent beta 142 residue, both to beta 143 His, which is involved in the DPG binding site of hemoglobin, and to the critical C terminal region of the beta chain, which participates in the stabilization of the deoxy (T) conformation.
An undifferentiated variant derived from the human acute myelogenous leukemia cell line (KG-1)
Authors: Koeffler HP , Billing R , Lusis AJ , Sparkes R , Golde DW 
Published: October 2019

Abstract
A variant subline (KG-1a) of the human acute myelogenous leukemia (AML) cell line (KG-1) has been isolated. The cells retain the same constitutive markers as the parent line, including HLA antigens, isoenzymes, and karyotype. The cells from the subline are morphologically and histochemically undifferentiated blast cells, while the parent cells and several of its clones are at the myeloblast and promyelocyte stages of development. The variant cells do not respond to colony-stimulating factor (CSF), and they do not express the human la antigen, nor a recently characterized AML antigen. The parent KG-1 cells are stimulated to proliferate in the presence of CSF and the cells express the la and AML antigen. Variant AML cell lines, such as KG-1a, will be useful in vitro models for investigating cellular response to CSF and for studying antigen expression in leukemic cells.
Restoration of nonclonal hematopoiesis in chronic myelogenous leukemia (CML) following a chemotherapy-induced loss of the Ph1 chromosome
Authors: Singer JW , Arlin ZA , Najfeld V , Adamson JW , Kempin SJ , Clarkson BD , Fialkow PJ 
Published: October 2019

Abstract
After intensive chemotherapy, marrow cells of some patients with Philadelphia chromosome (Ph1) positive chronic myelogenous leukemia (CML) become partially or completely Ph1-negative. However, without a second marker for the neoplastic clone, it could not be determined if these Ph1-negative cells arose from normal progenitors or were still members of an abnormal clone. In the present study, a patient with Ph1- positive CML, also heterozygous for glucose-6-phosphate dehydrogenase (G6PD), was studied before and after intensive chemotherapy. Prior to treatment only G6PD type B was detected in the patient's red cells, platelets, and granulocytes, and all unstimulated marrow metaphases had Ph1. After four cycles of chemotherapy, 76% of marrow cells were Ph1- negative, and approximately 80% of the granulocytes were nonclonal by G6PD analysis. Thus, the frequency of nonclonal cells by G6PD analysis correlated closely with that of the Ph1-negative cells. The data indicate that intensive chemotherapy can restore nonclonal and presumably non-neoplastic hematopoiesis in CML.
T lymphocytes expressing human Ia-like antigens in infectious mononucleosis (IM)
Authors: Tatsumi E , Kimura K , Takiuchi Y , Fukuhara S , Shirakawa S , Uchino H , Morikawa S , Minowada J 
Published: October 2019

Abstract
In six patients with Epstein-Barr virus (EBV) induced infectious mononucleosis (IM) and in two patients with IM-like syndrome, peripheral blood lymphocytes in the acute and convalescent phase were tested for human la-like antigens as well as other cell surface markers. The major population of T lymphocytes in the acute phase showed la-like antigens, as detected by indirect immunofluorescence with heteroantisera, and the number of la-like antigen-positive T lymphocytes decreased with convalescence. The crossabsorption study indicated that the amount of la-like antigen on the surface of IM T cells was less than that of Raji cells.
Cellular phenotypes of normal and leukemic hemopoietic cells determined by analysis with selected antibody combinations
Authors: Janossy G , Bollum FJ , Bradstock KF , Ashley J 
Published: October 2019

Abstract
Individual leukemic cells and the corresponding rare normal cell types in nonleukemic bone marrow were analyzed with various combinations of antisera (labeled with different fluorochromes: TRITC and FITC). Double staining for membrane Ia-like molecules (TRITC) and nuclear terminal transferase (FITC) was a very useful combination that distinguished common non-T, non-B ALL (Ia+,TdT+) and thymic ALL (Ia-,TdT+) from the rare cases of B ALL (Ia+,TdT-) and from AML (frequently Ia+, TdT-; in some cases Ia-, TdT-). Additional antisera (such as anti-ALL, anti- HuTLA, anti-immunoglobulin reagents, etc.) confirmed the diagnosis and further characterized the leukemic blasts. Ia+,TdT+ cells could be observed in low numbers in normal and nonleukemic regenerating marrow and were probably normal precursor cells; this reagent combinations was, therefore, not useful for monitoring residual non-T, non-B ALL blasts in treated patients. Other marker combinations detecting pre-B ALL blasts (double staining for cytoplasmic IgM and nuclear TdT) and Thy-ALL blasts (HuTLA+,TdT+) were, however, virtually leukemia specific in the bone marrow and could be used to effectively monitor residual leukemic cells throughout the disease. These combined single-cell assays are not only economical and informative but are also important for assessing the heterogeneity of leukemia and for standardizing new mouse or rat monoclonal antibodies for diagnosis.
Effect of interferon on colony formation in culture by blast cell progenitors in acute myeloblastic leukemia
Authors: Taetle R , Buick RN , McCulloch EA 
Published: October 2019

Abstract
The effect of purified human fibroblast interferon on primary and secondary colony formation by blast progenitors from the peripheral blood of patients with acute myelogenous leukemia was examined. Interferon inhibited blast progenitors and normal granulocyte/macrophage progenitors (CFU-C) in a dose-dependent manner. The magnitude of this effect on blast progenitors and CFU was similar. Interferon also inhibited secondary plating of blast progenitors (self- renewal). This effect was in marked contrast to the effect of adriamycin, which reduced primary plating efficiency of blast progenitors but did not affect self-renewal. Inhibition of blast progenitor proliferation by interferon was markedly reduced when interferon was added after 24 hr of culture and was absent when added after 72 hr. Inhibition of self-renewal was observed even when interferon was added at 72 hr. We conclude that interferon inhibits both primary proliferation and self-renewal of blast progenitors and that this effect is not due to reduction in the number of primary colonies. These experiments provide an example of how cell culture techniques may be used to test antitumor agents for effects on important cellular events other than general cytotoxicity.
Sequential surface marker and cytokinetic studies on individual cells from children with acute lymphoid leukemia
Authors: Wagner HP , Hirt A 
Published: October 2019

Abstract
Sequential immunological and cytokinetic studies were done on individual lymphoid cells in the peripheral blood of 10 children with previously untreated acute lymphoid leukemia (8 non-T--non-B, 1 T, and 1 B-ALL) and on lymphoid bone marrow cells (4 non-T--non-B ALL). The results obtained suggest that some, but not all, of the children considered to have non-T--non-B ALL had proliferating leukemic cells with surface immunoglobulin (Sig) in the peripheral blood. The absolute number of these SIg+ proliferating leukemic cells, however, was always smaller than the absolute number of SIg- proliferating leukemic cells. A similar observation was made in the child with B-ALL. On the other hand, in the blood of the child with T-ALL, no SIg+ proliferating leukemic cells were detected. The results indicate that sequential analyses of different parameters on single cells might permit a more precise investigation of relations between cell proliferation and cell differentiation or of interactions between normal and neoplastic lymphoid cells.
Peripheral blood lymphocyte receptors for B-lymphoblastoid cell lines (B-LCL)
Authors: Zighelboim J , Lichtenstein A 
Published: October 2019

Abstract
Because interactions between B cells and T lymphoyctes are of fundamental importance in the generation of the immune response to most antigens, we attempted to identify the cells capable of binding B- lymphoblastoid cell lines (B-LCL), their tissue distribution, and their presence in other species. Cells bearing a surface receptor for B-LCL were found in human peripheral blood, tonsil, and bone marrow, as well as mouse and rat spleen. Binding cells were phenotypically heterogeneous. The majority are T cells as defined by their ability to bind sheep red blood cells (E-rosettes). However, a subpopulation of non-T-lymphocytes were capable of binding B-LCL. This was demonstrated by depleting T cells with an E-rosette centrifugation technique and then performing a double rosette assay. The wide distribution of T lymphocytes with receptors for B-lymphoblastoid cells within peripheral lymphoid organs and their presence in several species suggest that these surface molecules may represent one of the means by which T cells and B cells interact in the induction of the immune response to T- dependent antigens.
Late-appearing Philadelphia chromosome in two patients with chronic myelogenous leukemia
Authors: Lisker R , Casas L , Mutchinick O , Perez-Chavez F , Labardini J 
Published: October 2019

Abstract
We describe two patients with typical myelogenous leukemia, who at the beginning of the disease lacked the Philadelphia chromosome in bone marrow cells, and 90 and 42 days later, respectively, its presence was shown in all cells analyzed from that tissue. These findings are compatible with the possibility that at least occasionally Ph1 occurs secondarily in already leukemic cells. The rapid change form Ph1- to Ph1+ CML in one of the patients (42 days), suggests the possibility that in addition to Ph1+ cells enjoying marked selective advantage, this change is induced simultaneously in multiple bone marrow cells.
Regulation of platelet arachidonic acid oxygenation by cyclic AMP
Authors: Schafer AI , Levine S , Handin RI 
Published: October 2019

Abstract
Intracellular cyclic adenosine monophosate (AMP) levels regulate the generation of thromboxane by platelets by inhibiting the hydrolysis of arachidonic acid from membrane phospholipids. However, there is conflicting evidence regarding the role of cyclic AMP in the control of the subsequent oxygenation of arachidonic acid by cyclooxygenase. We studoed the regulation of cyclooxygenase activity by agents that elevate platelet cyclic AMP (dibutyryl cyclic AMP and prostaglandins), measuring arachidonate-induced aggregation, O2 consumption, and malonaldehyde formation. In platelet-rich cyclic AMP. This inhibitory effect of cyclic AMP was absent in gel-filtered platelets suspended in buffer containing 0.5% albumin, and was progressively restored as plasma was added in increasing concentrations. Increasing the albumin concentration in platelet buffer suspensions likewise increased the ability of cyclic AMP to block the arachidonate-induced O2 burst and MDA production. We conclude that (1) the presence of plasma proteins is important in investigating platelet plasma milieu or at least in the presence of physiologic albumin concentrations.
Differentiation-linked expression of cell surface markers on HL-60 leukemic cells
Authors: Boss MA , Delia D , Robinson JB , Greaves MF 
Published: October 2019

Abstract
The cell surface antigenic phenotype of HL-60, a human acute promyelocytic leukemia cell line, has been analyzed before and after maturation induction with dimethylsulfoxide (DMSO) using a panel of markers including a “library” of monoclonal antibodies and “conventional” antisera in conjunction with the fluorescene-activated cell sorter. HL-60 cells express granulocyte and “leukocyte” differentiation antigens but not antigens of the lymphoid, platelet, and erythroid lineages. DMSO-induced morphological maturation was found to be associated with a decrease in the proportion of cells in mitotic cycle, induction of C3d receptors, increased expression of granulocytic and leukocyte antigens, and diminished expression of HLA-A,B,C and beta 2-microglobulin determinants. HL-60 cells have no detectable expression of HLA-DR-associated determinants as assayed by rabbit anti-p28,33 monoclonal anti-HLA-DR (monomorphic determinant), and HLA-DRw typing alloantisera. The relationship of these changes in cell surface properties to normal granulocytic differentiation is discussed.
A technique for the flow cytometric analysis of lymphocytes bearing histamine receptors
Authors: Osband ME , Cohen EB , McCaffrey RP , Shapiro HM 
Published: October 2019

Abstract
Histamine receptors have been demonstrated on lymphocyte membranes by a variety of techniques. We now report a method that allows for the flow cytometric analysis of histamine receptors on human peripheral T cells. Histamine is conjugated to fluoresceinated human albumin by the coupling agent ECDI. This conjugated histamine compound (FHA-his) binds to approximately 45% of T cells. Fluoresceinated human albumin alone (FHA), not conjugated to histamine, does not bind to T cells. In addition, unconjugated histamine can inhibit completely the binding seen with FHA-his. We conclude that this technique demonstrates specific FHA-his binding to histamine receptors on T cells and can be used to determine the number of cells bearing such receptors. In addition, the reagent could be used with a cell sorter to isolate distinct histamine-receptor-bearing (HR+) cells for further immunologic study.
Alpha-gene deletions in black newborn infants with Hb Bart's
Authors: Ohene-Frempong K , Rappaport E , Atwater J , Schwartz E , Surrey S 
Published: October 2019

Abstract
The presence of increased Hb Bart's (gamma 4) in cord blood is believed to be an indication of alpha-thalassemia. We have used restriction endonuclease nalyses of DNA to compare the number of alpha-genes with the percentage of Hb Bart's in 6 older children who had Hb Bart's at birth and 17 newborns. Four children with > 2% Hb Bart's had Eco R1 alpha-gene patterns and hematologic data consistent with the presence of two alpha-genes, one per chromosome. Of the remaining 19 children, all of whom had < 2% Hb Bart's, 8 had 3, while 11 had 4 alpha-genes. Three infants with Hb Bart's between 1% or less Hb Bart's. infants with 3 alpha-genes may therefore have elevated or normal levels of Hb Bart's at birth. DNA analysis is the definitive method for the determination of heterozygous alpha-thalassemia syndromes in newborns.
Effect of plasma from cyclophosphamide-treated mice on CFU-S in an in vivo culture system
Authors: Fried W , Barone-Varelas J , Helfgott M , Berman M 
Published: October 2019

Abstract
Various studies suggest that humoral substances, capable of stimulating CFU-S proliferation, are released into the plasma in response to depletion of the CFU-S population by cytotoxic substances such as cyclophosphamide. To test this hypothesis, we placed 0.25 ml of a murine marrow cell suspension with an equal volume of plasma from either normal mice or from mice previously injected with 5 mg of cyclophosphamide into cellulose dialysis tubing. These tubes were then incubated in the peritoneal cavity of mice for 1–7 days. The CFU-S content of the tubes was then assayed. The CFu-S content of suspensions in normal mouse plasma declined to one-fourth of the initial value after 7 days, whereas those in plasma from mice that received cyclophosphamide 7 days previously were essentially unchanged in number. These data suggest that 7 days after injection of cyclophosphamide, the plasma contains a factor that either prevents death of CFU-S or stimulates them to proliferate. An alternative explanation is that normal plasma contains an inhibitor of CFU-S growth that is lacking in plasma of cyclophosphamide-treated mice.
Effect of oxygenated sterol compounds on human bone marrow granulocytic progenitor cells
Authors: Hoffman PC , Richman CM , Hsu RC , Chung J , Scanu AM , Yachnin S 
Published: October 2019

Abstract
Oxygenated sterol compounds are potent inhibitors of sterol and DNA synthesis in mammalian cells. We studied the effects of oxygenated sterols on human marrow granulocytic progenitor cells in vitro (CFU-C). 25-Hydroxycholesterol was found to be a potent inhibitor of sterol synthesis in marrow mononuclear cells, with 50% inhibition occurring at approximately 10(-7) M. This compound, as well as 6-ketocholestanol, 7- ketocholesterol, and 20 alpha-hydroxycholesterol, also demonstrated marked inhibition of CFU-C proliferation. The latter effect, which was not a result of direct cytoxicity of the compounds, was reversible by cholesterol, but not by mevalonic acid. We conclude that inhibition of sterol synthesis by oxygenated sterol compounds may be insufficient to explain their suppression of CFU-C proliferation.
Chronic hemolytic anemia due to a monoclonal IgG cold agglutinin with anti-Pr specificity
Authors: Dellagi K , Brouet JC , Schenmetzler C , Praloran V 
Published: October 2019

Abstract
Immunologic studies performed in a case of autoimmune chronic hemolytic anemia with low titer cold agglutinins (1/16) demonstrated that the cold agglutinins corresponded to monoclonal IgG with anti-Pr specificity. This antibody had a large thermal amplitude, being active at 37 degrees C. These unusual characteristics may define a distinct subset of chronic cold agglutinin disease.