bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lymphoblastic lymphoma: an immunophenotype study of 26 cases with comparison to T cell acute lymphoblastic leukemia
Authors: Weiss LM , Bindl JM , Picozzi VJ , Link MP , Warnke RA 
Published: October 2019

Abstract
A series of 26 lymphoblastic lymphomas (LLs) and 13 T cell acute lymphoblastic leukemias (ALLs) were investigated using a battery of monoclonal antibodies applied to tissue frozen sections. Twenty-one of the LLs were of T lineage. All but one of the T cell LLs were of immature thymic phenotype, mostly corresponding to stage II cortical thymocyte development. The T cell LLs expressed Leu-1 in 100%, Leu-4 and Leu-9 in 95%, and Leu-5 in 85% of the cases. The high percentage of Leu-4 expression in this series is probably due to detection of cytoplasmic antigen with our methods. One LL was of pre-B or B cell and two cases were of common ALL phenotype. Two cases were of undefined phenotype, expressing markers of both B and T cell differentiation. Pediatric cases showed a greater tendency toward T cell phenotype than did adult cases. The cases of T cell ALL were immunophenotypically similar to the cases of T cell LL but showed a tendency toward a more immature phenotype.
Biochemical properties of the eosinophil cationic protein and demonstration of its biosynthesis in vitro in marrow cells from patients with an eosinophilia
Authors: Olsson I , Persson AM , Winqvist I 
Published: October 2019

Abstract
The eosinophil cationic protein (ECP), which has been shown to be secreted both in vitro and in vivo, is a cytotoxic unique constituent of eosinophil granules. To increase the understanding of the mechanisms behind the role of the eosinophil as a cytotoxic effector in disease, a detailed biochemical characterization of ECP was performed. A considerable molecular heterogeneity was revealed when purified ECP was eluted isocratically from a high-resolution cation exchange resin; the separation, reproducibly achieved, of five components was probably due to hydrophobic interaction with the resin. These polypeptides, which reacted quantitatively with anti-ECP antiserum, showed molecular weights (mol wt) of 19,500 and 16,700 and showed almost identical amino acid compositions. The amino-terminal sequence for one of the polypeptides was (in the standard one-letter code) (R-P-X-Q-F-T-R-A-Q-W- F-A-I-Q-H-I-S-L-N-P-R-R-C-T-I-A-M-R-A-I-N-N-Y-). The biosynthesis of ECP was demonstrated in marrow cells from patients with eosinophilia using labeling with (14C)-leucine, followed by immunoprecipitation with anti-ECP, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and fluorography for visualization of labeled ECP. Biosynthesis was demonstrated of mol wt 22,000 ECP, which may represent precursor ECP, since with time some of it was processed into ECP with a mol wt of 18,000 to 19,000. Monensin, a proton ionophore, blocked the processing of mol wt 22,000 ECP. This study shows that ECP consists of a family of similar polypeptides. These may, however, have different biological activities.
An abnormal plasma distribution of protein S occurs in functional protein S deficiency
Authors: Comp PC , Doray D , Patton D , Esmon CT 
Published: October 2019

Abstract
Protein S is a natural anticoagulant present in the plasma that serves as a cofactor for activated protein C. Patients deficient in protein S are subject to recurrent venous thrombotic disease. Protein S deficiency differs from other plasma protein deficiencies in that deficient patients often have normal or only mildly reduced levels of protein S in their plasma as detected by conventional immunologic methods but have markedly reduced functional protein S levels. This apparent discrepancy is due to the presence of two forms of protein S in plasma. The protein S is present free and in a complex with C4b- binding protein. The free form is functionally active, whereas the bound form is not. Examination by crossed immunoelectrophoresis of 31 functionally protein S-deficient individuals from seven families reveals that 29 of the 31 have all or most of their protein S complexed to C4b-binding protein with little or no free protein and have correspondingly low levels of protein S functional activity (type I deficiency). Two related protein S-deficient individuals show a different type of distribution with little or no protein S, either bound or free (type II deficiency). The detection and classification of protein S-deficient individuals requires the application of both a functional assay and an assessment of protein S distribution between bound and free forms.
Abnormalities of chromosome 7q and Tac expression in T cell leukemias
Authors: Brito-Babapulle V , Matutes E , Parreira L , Catovsky D 
Published: October 2019

Abstract
Clonal chromosome abnormalities were demonstrated in 13 cases of T cell leukemia with a mature membrane phenotype. The cases comprised two adult T cell lymphoma leukemia (ATLL), five Sezary syndrome (SS), three T prolymphocytic leukemia (T-PLL), and three T chronic lymphocytic leukemia (T-CLL). The presence of clonal chromosome abnormalities in the three cases of T-CLL supports the view that although clinically benign, this disorder probably represents a neoplastic process. Cells from six of 11 patients were tested and found to be reactive with monoclonal antibody (McAb) anti-Tac in the absence of mitogens (two ATLL, two SS, and two T-PLL). Only the two ATLL patients were serologically positive for the human T cell leukemia virus I (HTLV-I), and their cells showed a higher anti-Tac reactivity. Chromosome 7 abnormalities were observed in seven cases (two ATLL, three SS, two T- PLL), and a strong correlation was seen between the presence of a 7q abnormality and the expression of the Tac antigen (T cell growth factor receptor). These findings are discussed in relation to the localization of T cell receptor genes on chromosome 7 and possible mechanisms for the activation of the Tac gene.
Paroxysmal nocturnal hemoglobinuria erythrocytes are of two distinct types: positive or negative for acetylcholinesterase
Authors: Dockter ME , Morrison M 
Published: October 2019

Abstract
Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired disorder. Erythrocytes isolated from PNH patients show increased sensitivity to complement and decreased acetylcholinesterase (AChE) activity. In this study, indirect immunofluorescence analysis of a monoclonal antibody specific for a surface epitope of human erythrocyte AChE is used to quantitate the content of this enzyme at the single-cell level. Flow- cytofluorimetric analysis of erythrocytes from normal donors indicates that all erythrocytes contain detectable levels of the surface epitope with a strong correlation between cell size and enzyme content. In contrast, erythrocytes from PNH patients show two distinct populations of erythrocytes; namely, those containing a normal content of AChE and a second population containing no detectable AChE. The AChE-negative population of cells is quantitatively complement-sensitive. These data support suggestions that PNH is a clonal disorder resulting in two distinct types of circulating erythrocytes. The abnormal clone produces cells that are both surface-AChE-negative and complement-sensitive. In addition, the method described provides an attractive alternative for the diagnosis and quantitative evaluation of abnormal erythrocytes in PNH patients.
Platelet-leukocyte interaction: selective binding of thrombin- stimulated platelets to human monocytes, polymorphonuclear leukocytes, and related cell lines
Authors: Jungi TW , Spycher MO , Nydegger UE , Barandun S 
Published: October 2019

Abstract
The association of platelets with leukocytes was investigated, using gel-filtered platelets stimulated with thrombin and then fixed with formaldehyde. Evidence is presented that stimulation of gel-filtered platelets with low concentrations of thrombin (0.01 to 0.1 U/mL) induces the expression of surface determinants interacting strongly with monocytes and polymorphonuclear leukocytes (PMNs) but only weakly with lymphocytes. Both monocyte-platelet binding and PMN-platelet binding occurred at 37 degrees C and more intensively at 0 degrees C; it was Ca2+-dependent and was unaffected by the addition of sodium azide. The binding also occurred with the monocytoid cell lines HL 60 and U 937 in exponential growth and was much less two days after induction of terminal differentiation by phorbol myristate acetate (PMA). No other tested cell lines (B cells, T cells, and myeloid cells) bound thrombin-stimulated platelets. Monocyte-derived macrophages kept in culture for one week also exhibited reduced binding of thrombin- stimulated platelets. IgG and fibronectin could be ruled out as ligands that mediate binding.
Characterization of natural killer cells with antileukemia activity following allogeneic bone marrow transplantation
Authors: Hercend T , Takvorian T , Nowill A , Tantravahi R , Moingeon P , Anderson KC , Murray C , Bohuon C , Ythier A , Ritz J 
Published: October 2019

Abstract
To identify cells with potential antileukemia activity following bone marrow transplantation, we have monitored immunologic reconstitution in a patient with acute lymphocytic leukemia in second remission who received intensive chemotherapy and total body irradiation followed by infusion of allogeneic histocompatible marrow. Prior to transplantation, donor bone marrow cells were depleted of T lymphocytes by in vitro treatment with anti-T12 monoclonal antibody and rabbit complement. In the first 3 weeks following bone marrow transplantation, the predominant regenerating mononuclear cell population in peripheral blood exhibited a phenotype characteristic of natural killer (NK) cells. After 4 weeks, T lymphocytes became predominant, but NK cells persisted. Cultured peripheral blood lymphocytes obtained 12 weeks posttransplant were able to display significant cytotoxicity against leukemic blasts that had been cryopreserved at the time of relapse 5 months prior to bone marrow transplantation. To further characterize those cells with antileukemia activity, we used in vitro cloning techniques to identify four monoclonal populations, termed TC12, -48, - 50, and -59, with strong antitumor activity. Cytogenetic analysis demonstrated that each clone was of donor origin. Phenotypic characterization showed that the four clones expressed NKH1A but did not express T3, T4, or T8 antigens. Three of the four clones expressed T11/E rosette antigen. Each clone exhibited strong cytotoxicity against genetically unrelated hematopoietic tumor cell lines such as K562, Molt- 4, JM, and U937. In addition, we found that these patient clones were similar to cloned NK cells previously derived from normal individuals. Taken together, these results suggest that at least some clones with antileukemia activity following bone marrow transplantation are cells with NK-like function and phenotype. Functional analysis of these cytolytic cells in larger numbers of patients will be necessary to determine the clinical significance of this finding.
Short-term culture of acute myeloid leukemia blasts: analysis of acquired susceptibility to activated natural killer cells
Authors: Moingeon P , Ythier A , Nowill A , Delmon L , Bayle C , Pico JL , Bohuon C , Hercend T 
Published: October 2019

Abstract
Following a cryopreservation step, short-term cultures of circulating leukemic blasts from a patient with acute myeloid leukemia (AML) were performed. Because cultured tumor cells became susceptible to natural killer (NK) activity, in vitro alteration of the blasts was studied. Immediately after thawing, cell suspensions consisted of a relatively homogeneous population of undifferentiated blasts. In culture, tritiated thymidine uptake by the leukemic cells was low during the first 24 hours and then increased (X20) to a peak on day 7. The cell concentration started to increase on day 4. On day 8, less than 10% of the cultured cells still appeared as undifferentiated blasts, whereas up to 60% were granular and 30% to 40% had a monocytoid morphology. Prior to being cultured, the blasts were resistant to resting and IL2- activated natural killing. When the kinetics of in vitro acquired susceptibility were studied, it was found that maximum cytotoxicity against these leukemic cells was reached within 24 hours. Thus, the blasts had become NK-sensitive prior to increase in DNA synthesis, proliferation, and differentiation based on morphological and cytochemical criteria. In contrast, there was a positive correlation between acquired susceptibility and surface expression of an activation antigen, termed TNKtar. To dissect further the mechanisms of acquired susceptibility, a series of six NK clones representing four distinct phenotypes of NK active lymphocytes were tested against the leukemic cells. Immediately after thawing, blasts were essentially resistant to all clones, whereas they were strongly killed by 5 of 6 clones when cultured for 24 hours. Cold target inhibition assays indicated that resistance of fresh blasts was likely to be due to a binding defect. These results suggested that tumor cells became susceptible because they surface-expressed NK target structure(s) in the early phase of an activation process leading to their proliferation and/or differentiation. This hypothesis was substantiated for one clone, termed JT9, because the anti-TNKtar antibody blocked cytotoxicity of JT9 cells against the cultured blasts.
Treatment of hairy cell leukemia with recombinant alpha interferon: I. Quantitative study of bone marrow changes during the first months of treatment
Authors: Flandrin G , Sigaux F , Castaigne S , Billard C , Aguet M , Boiron M , Falcoff E , Degos L 
Published: October 2019

Abstract
Seventeen patients with hairy cell leukemia (HCL) were treated with low doses of recombinant alpha interferon (IFN) for over 4 months. Marked improvement was observed in peripheral blood and bone marrow in 15 of 17 patients. Comparison of pretreatment values and hemograms obtained after 4 months of treatment showed a marked decrease in circulating hairy cells (P less than .01), a decrease in the number of lymphocytes (P less than .01), a rise in the number of platelets (P less than .05), granulocytes (P less than .05), and monocytes (P less than .01), and a rise in the hemoglobin level (P less than .01). Transient reduction in the number of granulocytes was noted during the first month. Correction of thrombocytopenia often appeared within 2 months and usually preceded improvement of anemia, monocytopenia, and neutropenia. Bone marrow biopsy specimens were taken before treatment and 2, 4, and 7 months after its initiation. The volumes occupied by hairy cells, cells of the myeloid lines, and adipocytes were studied by stereological analysis of semithin sections. Decrease in the volume occupied by hairy cells was seen after 4 months of treatment (P less than .01), and the volume continued to decrease at the seventh month (P less than .05). Hairy cells were no longer detected on bone marrow biopsies of 4 of 17 patients by the fourth month and in 3 of 8 additional patients by the seventh month. A rise in the volume occupied by normal myeloid cells was visible by the second month of treatment (P less than .01). Nevertheless, the volume occupied by granulocytes remained lower than in the normal controls (P less than .01). After an initial increase during the first 2 months of treatment (P less than .01), the overall cellularity remained unchanged at 4 months and decreased significantly (P less than .05) at 7 months. Except for biopsies at 2 months, mean cellularity was below that of control biopsies (P less than .01).
Treatment of hairy cell leukemia with recombinant alpha interferon: II. In vivo down-regulation of alpha interferon receptors on tumor cells
Authors: Billard C , Sigaux F , Castaigne S , Valensi F , Flandrin G , Degos L , Falcoff E , Aguet M 
Published: October 2019

Abstract
Interferons (IFNs) initiate their effects by interacting with specific high-affinity cell surface receptors, but little is known about the physiology of IFN receptor interaction in vivo. Treatment of patients suffering from hairy cell leukemia (HCL) with human recombinant alpha IFN results in significant tumor regression, with clinical improvement in a high percentage of cases. To investigate a possible relevance of binding parameters as response markers, IFN receptor interaction on tumor cells responsive to IFN in vivo was studied. Binding of human alpha 2 IFN to circulating hairy cells was analyzed before and during IFN therapy in ten patients selected on the basis of high numbers of peripheral hairy cells. Binding experiments were carried out on Ficoll- Paque fractionated peripheral cell samples containing a majority of hairy cells. All patients reacted to recombinant alpha IFN treatment with a striking decrease in binding capacity within 12 hours after the first injection. As demonstrated by using a monoclonal antibody able to recognize alpha 2 IFN bound to its receptor, this decreased binding capacity was not due to blocking by circulating IFN but rather to a decrease in receptor number. This receptor “down-regulation” was partially reversible after the first IFN injection. However, upon prolonged IFN therapy, all patients displayed a stable state of decreased receptor expression. Down-regulation of IFN receptors can be regarded as a response marker to IFN treatment. This response marker, however, was not correlated with the clinical response within the first months of IFN therapy.
Monoclonal antibody 12-8 recognizes a 115-kd molecule present on both unipotent and multipotent hematopoietic colony-forming cells and their precursors
Authors: Andrews RG , Singer JW , Bernstein ID 
Published: October 2019

Abstract
A monoclonal antibody, 12–8, prepared against KG-1a cells, recognizes an approximately 115-kd cell surface antigen and reacts with 3% to 4% of bone marrow cells, including most of the blast cells. The antigen is not expressed on peripheral blood cells. Marrow cells expressing 12–8 collected by fluorescence-activated cell sorting contained nearly all of the unipotent (CFU-GM, BFU-E) and multipotent (CFU-MIX) colony- forming cells. The isolated 12–8 positive marrow population also contained precursors of these colony-forming cells. In a two-stage long- term marrow culture system employing irradiated allogeneic marrow adherent cells, 12–8 positive cells produced both unipotent and multipotent colony-forming cells for ten weeks. Moreover, the output of colony forming cells substantially exceeded the input. Antibody 12–8 appears useful for analysis and possibly enrichment of hematopoietic progenitor cells that include colony-forming cell precursors.
Purified interleukin-3 and erythropoietin support the terminal differentiation of hemopoietic progenitors in serum-free culture
Authors: Suda J , Suda T , Kubota K , Ihle JN , Saito M , Miura Y 
Published: October 2019

Abstract
We studied the effect of purified interleukin-3 (IL-3) and erythropoietin on colony formation by hemopoietic progenitors in serum- free cultures of spleen cells from 5-fluorouracil (5-FU)-treated mice. In the presence of IL-3 alone, most of the multilineage (three or more lineages) colonies did not contain erythroid cells. However, in the presence of IL-3 and erythropoietin, most of the multilineage colonies contained various numbers of erythroid cells. Replating experiments suggest that IL-3 maintains the growth of the progenitor cells, which could differentiate into erythroid cells. Erythropoietin facilitated the terminal differentiation and amplification of erythroid cells, although it did not sustain the growth of multipotential stem cells. Single-cell transfer experiments demonstrate that IL-3 supported the late stages of differentiation of neutrophils, macrophages, eosinophils, and megakaryocytes in the absence of lineage-specific factors. Therefore, IL-3 supports the differentiation of multilineage hemopoietic progenitors, and the terminal differentiation of most hemopoietic lineages, with the exception of the erythroid lineage.
The chemokinetic response of human neutrophils
Authors: Howard TH 
Published: October 2019

Abstract
A computer-assisted single cell assay that allows quantification of the locomotive behavior of individual cells and a flow-through system that allows study of response of individual cells to stimulation were utilized to study the chemokinetic response of neutrophils. The range of basal mean rate of locomotion (mROL) and chemokinetic response to 10(-9) mol/L formylmethionyl leucyl phenylalanine (FMLP) was determined for neutrophils of eight normal adults. The basal mROL was 8.2 +/- 1.5 um/min and 6.2 +/- 1.0 um/min; the rate after 10(-9) mol/L fMLP was 12.1 +/- 2.1 and 9.5 +/- 1.8 um/min in 2.0 g% and 0.05 g% HSA, respectively. The mean increase in ROL for neutrophils was 50%. Assay with the flow-through system shows that the chemokinetic response-- increase in mROL of a population of neutrophils in response to 10(-9) mol/L--is due to an increase in ROL when cells are actively moving and not due to a decrease in the amount of time the cell spends inactive. Studies of individual cells within the populations show that chemokinetic response to 10(-9) mol/L fMLP is highly variable. The majority of cells (77%) respond with an increase in ROL; the minority (23%) are nonresponders that characteristically move at ROL greater than or equal to 14 um/min prior to stimulation and do not change ROL or exhibit a net decline in ROL in response to 10(-9) mol/L fMLP. The dose response of a population of neutrophils and of individual neutrophils to serial addition of 10(-10) to 10(-6) mol/L fMLP shows that the fMLP dose dependence for maximal chemokinetic response is highly variable among individual cells. Seventeen percent of cells do not respond to any fMLP concentration; 25% of neutrophils exhibit maximal response to 10(-10) mol/L fMLP, while 50% and 25% of cells showed peak chemokinetic response to 10(-9) mol/L and greater than or equal to 10(-8) mol/L fMLP, respectively. These studies document the variability in the locomotive responses of peripheral blood neutrophils. Understanding the causes of variability in the chemokinetic responsiveness of individual neutrophils may improve our understanding of how the cellular inflammatory response in man can be modulated.