bluuebunny/crossref_metadata_2025_split huggingface dataset:
Assessment of Complement Binding by Anti‐D and Anti‐M Antibodies Employing Labelled Antiglobulin Antibodies
Authors: Freedman J. , Massey A. , Chaplin H. , Monroe M. C. 
Published: March 2008

Summary The presence of small amounts of C3d on freshly obtained normal red blood cells (RBC) was demonstrated by a radio‐labelled antiglobulin technique; this increased 1·5‐fold after incubation in fresh normal serum. No significant further increase in bound C3d was demonstrated for cDE/cDE, CDe/CDe, ‐D‐/‐D‐ RBC maximally sensitized with any of three potent anti‐D antibodies. When anti‐c, anti‐D and anti‐E antibodies were used in combination to sensitize cDE/cDE RBC, bound C3d increased by approximately 22%; however, a similar increase occurred with cde/cde RBC and was therefore considered non‐Rh specific. Umbilical cord RBC from four infants severely affected by anti‐D haemolytic disease of the newborn did not exhibit more bound C3d than cord RBC from normal controls.One serum containing IgM anti‐M bound a small amount of complement in vitro; two IgG anti‐M sera did not.
Human Factor IX in Animals: Kinetics from Isolated, Radiolabelled Protein and Platelet Destruction following Crude Concentrate Infusions
Authors: Thompson Arthur R. , Forrey Arden W. , Gentry Patricia A. , Smith Kenneth J. , Harker Laurence A. 
Published: March 2008

Summary Crude, concentrated and isolated, labelled human factor IX was prepared and infused into animals. Initially, two dogs with severe haemophilia B received both preparations and factor IX clotting activity and label survived well. Kinetic parameters fit a two‐compartment open model.For 12 infusions of concentrates into normal baboons, clotting and antigen data again fit the model. Similar kinetics, with less variability, were found for nine infusions of [125I]factor IX. Radioactivity of the first post‐infusion samples was >90% precipitated in the double antibody system with an average of 84% of counts adsorbable to barium citrate. Compared to plasma, barium adsorbable counts gave a shorter t1/2β‐elimination phase suggesting a small recirculating 125iodide pool. When [125I]factor IX was rechromatographed over heparin‐agarose, variable amounts of altered, labelled protein were present; this species was more rapidly cleared from plasma post‐infusion.Twelve infusions of crude concentrates into baboons were given to animals whose platelets had been labelled with 51Cr. Platelet counts as well as survival were then followed. For seven of these animals, mean counts decreased and the labelled platelets were destroyed, to an average of 21%, during the first 4 h post‐infusion. Subsequent platelet survival was normal. Three infusions of gel‐filtered, crude concentrates and two infusions of ‘activated’commercial concentrates did not significantly alter platelet survival.
Serum Ferritin in Ascorbic Acid Deficiency
Authors: Roeser H. P. , Halliday J. W. , Sizemore D. J. , Nikles A. , Willgoss D. 
Published: March 2008

Summary Serum ferritin levels were monitored in guinea‐pigs rendered scorbutic by dietary deprivation of ascorbic acid (AA). Hepatic and splenic concentrations of AA fell rapidly during the first 8 d of deprivation, and then declined more slowly to reach approximately 10% of control values after 14 d. Normal levels of serum ferritin (geometric mean, 324 μg/1) were observed for 20 d but a significant fall occurred between days 20 and 23 of deficiency (143 γg/1; P<0·05).Intramuscular administration of iron dextran to scorbutic animals (75 mg Fe per kg body weight) resulted in a non‐significant elevation of serum ferritin levels (geometric mean, 470 μg/1; P>0·1). In control animals, the same dose of iron dextran caused a 10‐fold rise in serum ferritin levels (3400 μg/1). A single subcutaneous dose of AA (75 mg/kg weight) given to scorbutic animals caused a significant rise in serum ferritin levels to 599 μg/1 (P<0·001) but had no effect in control animals. The same dose of AA given to iron loaded, scorbutic animals elevated serum ferritin levels from 554 μg/1 to 1297 μg/1 (P<0·025).Thus, AA deficiency in guinea‐pigs caused serum ferritin levels to fall and blocked the rise in serum ferritin levels observed in response to acute iron loading in control animals. Adequate tissue concentrations of AA appeared to be necessary for the maintenance of a quantitative correlation between tissue iron stores and serum ferritin levels. The mechanisms by which AA influences serum ferritin levels are at present unknown.
The Association of Eosinophilia with Lymphoblastic Leukaemia or Lymphoma: a Study of Seven Patients
Authors: Catovsky D. , Bernasconi C. , Verdonck P. J. , Postma A. , Hows J. , van der Does‐van den Berg A. , Rees J. K. H. , Castelli G. , Morra E. , Galton D. A. G. 
Published: March 2008

Summary Seven patients with hypereosinophilia in association with a lymphoblastic malignancy are described. The eosinophilia preceded or was present at diagnosis in all patients. Eosinophil counts fell during complete remission but rose significantly before or during relapses in five patients. Hypogranular and sometimes Pelgereosinophils were seen in five cases. Surface and enzyme markers defined the malignancy in six cases as common‐ALL (three), T‐ALL (two) and T‐lymphoblastic lymphoma (one). Although a diagnosis of eosinophilic leukaemia or acute myeloid leukaemia with cosinophil differentiation was considered in three patients, cytochemical and ultrastructural studies failed to show any evidence of myeloid differentiation in the blast cells. The bone marrow karyotype was normal in the four patients studied.All seven patients had one or more relapses and six died 6–62 months from diagnosis. Severe complications of the hypereosinophilic syndrome developed in one patient.As T‐lymphocytes have been shown to be involved in the induction of eosinophilia in rodents, it is suggested that the hypereosinophilia in these patients was induced by eosinopoietic stimuli produced by lymphoblasts.
Behaviour of Myeloid Precursors in Homozygous β Thalassaemia
Authors: Gabutti V. , Miniero R. , Piga A. , Incarbone E. , Sacchetti L. , Balegno G. 
Published: March 2008

Summary Maintaining a high haemoglobin level, through a high transfusion regime, is the best method for treating thalassaemia. Not much is known about the effect of this treatment on medullary or extramedullary haemopoiesis, particularly on the extent of erythropoietic inhibition and on the behaviour of myelopoiesis.In order to analyse some aspects of the problem, we studied the myeloid stem cells (CFU‐c) in the bone marrow and in the peripheral blood of children with homozygous thalassaemia, using the agar culture technique. The number of circulating CFU‐c observed in 68 patients was higher than in normal subjects. This number was significantly increased after splenectomy.A positive correlation was demonstrated between the number of circulating CFU‐c and the time elapsed since the last transfusion. Patients with a high Hb level displayed a marked reduction in the number of CFU‐c in their peripheral blood.In 10 patients, before the beginning of transfusions, bone marrow CFU‐c were lower than in normal subjects; their number increased after therapy. Most circulating CFU‐c were proliferating as shown by the thymidine suicide technique.
The Erythrocyte Membrane Disturbances in Protein‐Energy Malnutrition: Nature and Mechanisms
Authors: Fondu Pierre , Mozes Nava , Neve Pierre , Sohet‐Robazza Lucienne , Mandelbaum Israël 
Published: March 2008

Summary. In protein‐energy malnutrition (PEM), as observed in Kivu, the RBC have an increased ratio of surface area to volume which is demonstrated by the presence of target cells on light microscopy and cup cells with scanning electron microscopy. The osmotic fragility is decreased. These abnormalities can be attributed to the accumulation of cholesterol and phosphatidylcholine (PC) in the RBC membrane. The molar ratio of cholesterol to phospholipids is moderately increased.Several findings suggest that the cholesterol and PC build‐up results from disturbed exchanges in these lipids between the RBC and the plasma lipoproteins. Firstly, the osmotic fragility of a patient's RBC gradually becomes normal when the cells are transfused into a healthy recipient. Secondly, the cholesterol flux between the RBC and the plasma LDL seems to be low. Thirdly, the increase in RBC PC cannot be explained by a diminished fatty acids transport between the deep RBC PC pool and the RBC phosphatidylethanolamine (PE) pool. Finally complex disturbances of the plasma lipoproteins are obvious.It is improbable that the cholesterol and PC build‐up accounts for the premature RBC destruction which has been described in Kivu PEM. However, the observation of an increased fatty acid turnover in RBC PC and PE, as well as other data previously obtained in Kivu PEM, lead to the conclusion that membrane peroxidation may be a major cause of the shortened erythrocyte life‐span in this syndrome.
The Morphological Classification of Acute Lymphoblastic Leukaemia: Concordance among Observers and Clinical Correlations
Authors: Bennett J. M. , Catovsky D. , Daniel M. T. , Flandrin G. , Galton D. A. G. , Gralnick H. R. , Sultan C. 
Published: March 2008

Summary. The degree of concordance in the morphological classification of ALL was assessed by the FAB group after two successive reviews of 200 and 100 slides respectively. As a result, a simple scoring system for types L1 and L2 is proposed based on the following four features: (1) nuclear cytoplasmic ratio, (2) presence, prominence and frequency of nucleoli, (3) regularity of nuclear membrane outline, and (4) cell size. By this method, the overall concordance by seven observers (agreement of 7:0 or 6:1 only) increased from 63% to 84%.A significant difference in the incidence of the ALL morphological types in children (15 years) and adults (>15 years) was found: 74% of L1 cases were children while 66% of L2 cases were adults (P<0.001). No significant differences were observed in the incidence of L3 in children and adults or between L1 and L2 according to the membrane phenotype of the blast cells. All L3 cases had B‐cell characteristics.A better prognosis for L1 and a higher relapse rate for L2 has been found in several recent reports; the present study may facilitate the morphological analysis of ongoing clinical trials in ALL by improving the reproducibility of the FAB classification.
Inhibitor of in Vitro Neutrophil Migration in Sera of Children with Homozygous Sickle Cell Gene during Pain Crisis
Authors: Akenzua Gregory I. , Amiengheme Okpiaifo R. 
Published: March 2008

Summary. There is conflicting evidence for a causal relationship between infection and haematological crisis of sickle cell disease. To find out whether changes in leucotaxis occur during pain crisis, in‐vitro neutrophil migration was determined in 38 children with Hb SS during steady state and during pain crisis. Migration of neutrophils of sickle cell patients was 29 12 μm in steady state and 27.5 10.5 μm during pain crisis. These rates were comparable to migration of neutrophils of control children with normal haemoglobin of 34 9.6 μm. However, with addition of autologous serum to the cell suspension, neutrophil migration of patients in pain crisis was significantly retarded (16 13 μm) as compared to those in steady state (26 10.2 μm) and control children (28.7 10 μm). Sera of children in pain crisis also inhibited migration of neutrophils of healthy adults with normal Hb. Pooled normal plasma reversed inhibitory action of pain crisis serum on autologous and homologous neutrophil migration; but pain crisis plasma did not.Chemotactic effect of sera of Hb SS children in steady state or pain crisis and control children on neutrophils of eight adults with normal Hb were similar and comparable to that of pooled normal serum. Thus, children with sickle cell disease develop chemotactic inhibitor(s) in their circulation during pain crisis. This may lead to defective leucotaxis and enhanced susceptibility to infection.
Antibody‐dependent Cell‐mediated Cytotoxicity (ADCC) of Penicillin‐treated Human Red Blood Cells
Authors: Yust Israel , Frisch B. , Goldsher Naomi 
Published: March 2008

Summary. Penicillin‐treated human red blood cells (RBC) were lysed by the cooperation of autologous nonsensitized peripheral blood mononuclear cells and human anti‐penicillin serum. Using a rapid (3 h) assay of antibody‐dependent cell‐mediated cytotoxicity (ADGC), lysis was proportional to serum (anti‐penicillin antibody) concentration, to incubation time and to the concentration of attacking cells, which were obtained from normal human peripheral blood by Ficoll‐Hypaque separation. Incubation of these lymphoid effector cells on a nylon column prior to the tests depleted the number of phagocytic (latex positive) cells in the effluent; there was a concomitant drop in cytotoxic activity. Enrichment of mononuclear phagocytes in the attacking cell population by albumin gradient separation led to an increase in cytotoxicity. Granulocytes separated by Ficoll‐Hypaque were not active in this system. Using specific antisera the antibody was found to be of the IgG1 sub‐class. Anti‐penicillin antibody activated the complement system in vitro, but failed to induce lysis of penicillin‐treated RBC in the presence of complement without attacking cells.These results suggest that ADCC may participate in the destruction of RBC in penicillin‐induced haemolysis in vivo.
Racial Differences in Ristocetin‐induced Platelet Aggregation
Authors: Buchanan George R. , Holtkamp Christine A. , Levy Eric N. 
Published: March 2008

Summary. Several investigators have reported defective ristocetin‐induced platelet aggregation (RIPA) in individuals whose red blood cells contain sickle haemoglobin, but the race of control subjects in these studies was not stated. Therefore, maximal amplitude of RIPA was examined in 75 normal whites and blacks, 16 of whom had sickle trait defined by haemoglobin electrophoresis and sickle prep. Final ristocetin concentrations in platelet rich plasma were 1·1,1·2 and 1·5 mg/ml. Mean aggregation at 1·1 mg/ml was significantly less in blacks (mean 31%) than in whites (mean 72%) (P < 0·001). 60% of blacks but only 11% of whites had less than 50% RIPA at 1·1 mg/ml. RIPA was entirely absent in 19% of blacks. Differences in RIPA between black and white subjects were also present at ristocetin concentrations of 1·2 and 1·5 mg/ml but were less striking. RIPA in 25 children with homozygous sickle cell anaemia was similar to that in the normal AA and AS blacks. Differences in RIPA could not be explained by age, sex, presence of sickle haemoglobin, or medications. Addition of normal plasma or platelets did not correct reduced RIPA in seven blacks, and their plasma inhibited normal RIPA responses.Reduced platelet aggregation to low concentrations of ristocetin is a normal finding in many blacks, is not related to the presence of sickle haemoglobin, and appears to be due to a plasma inhibitor against RIPA.
Ferritin Polymers and the Formation of Haemosiderin
Authors: Hoy T. G. , Jacobs A. 
Published: March 2008

Summary. When ferritin is isolated from Chang liver cells in culture iron loading is found to be associated with changes in the surface of the protein shell characterized by a change in immunoreactivity to anti ‘heart’and anti ‘spleen’antibodies at each specific pI and an overall shift in isoferritins to a lower pI range (Hoy & Jacobs, 1981). Ferritin polymers have been isolated from human tissues and their biochemical properties assessed in terms of these surface changes and the iron/protein ratio of the molecules.The results suggest that changes in the surface of ferritin molecules are associated with the formation of stable polymers. These are precursors of clumps of ferritin and eventually haemosiderin. Changes in the surface of the molecule may provide a signal for polymerization and incorporation of the protein within the lysosomes.
Collagen synthesis by bone marrow stromal cells: a quantitative study
Authors: Bentley S. A. 
Published: March 2008

Collagen‐producing, marrow‐derived adherent cells (MDAC) provide a microenvironment which supports haemopoietic stem cell (HSC) proliferation in vitro. To investigate the relationship between collagen‐producing cells in intact marrow and in MDAC cultures, quantitative studies of collagen synthesis were performed.Collagen synthesis by fresh murine bone marrow cells was 0.22% of total protein synthesis and collagen types I and III were synthesized in a ratio of approximately 5:1. During MDAC cultivation, the collagen synthesis fraction increased to 2.3%. The relative amounts of type I and type III remained more or less constant. The MDAC monolayers showed characteristic pleomorphism, and were shown to support HSC proliferation in continuous bone marrow culture for periods of at least 5 weeks.These results suggest that MDAC culture, under the conditions reported, selects a specific type of bone marrow connective tissue cell, probably a reticulum cell, which synthesizes collagen types I and III in a ratio of approximately 5:1.
Effects of human serum on the release of haemopoietic growth factors
Authors: Nissen Catherine , Moser Yolanda , Speck Bruno 
Published: March 2008

Summary.Unstimulated peripheral blood cells incubated without serum release unexpectedly high amounts of colony‐stimulating activity (CSA) and burst‐promoting activity (BPA). This ‘basal’release of haemopoietic growth factor activity is strongly reduced by the presence of normal human serum. Serum from patients with aplastic anaemia partly lacks this inhibitory activity on the release of CSA and BPA.
The role of the cellular sodium pump in human granulopoiesis in vitro
Authors: Steed A. J. , Boardman K. M. , Delamore I. W. 
Published: March 2008

Summary.The specific sodium pump antagonist ouabain was used to study the effect of sodium pump inhibition on granulopoietic colony formation by normal human bone marrow cells cultured in soft agar for 7 d. Suppression of colony formation was dose‐dependent and occurred at a low and reproducible concentration. The use of an extended range of concentrations (1 × 10−19m to 1 × 10−4m) revealed no additional effect. Inhibition occurred when colony formation was stimulated by either normal human white blood cells in a soft agar underlayer, or the inclusion of pre‐formed colony‐stimulating activity. Sensitivity to inhibition was similar under either set of conditions, the 50% inhibitory concentrations being 2.70 ± 0.43 (SE) × 10−8m and 2.83 ± 0.21 (SE) × 10−8m respectively. This is interpreted as showing an effect primarily on the colony‐forming cells rather than on the cellular production of colony‐stimulating activity. Inhibition of colony formation by ouabain was opposed by the addition of extra potassium to the culture medium, confirming that the inhibition was mediated via a perturbation of monovalent cation exchange. Inhibition by 2 × 10−7m ouabain appeared to be reversible by simple washing after exposure for up to 24 h, suggesting that the inhibitory effect of ouabain is not primarily cytotoxic.
Lithium enhances growth of human leukaemia cells in vitro
Authors: Gauwerky C. E. , Golde D. W. 
Published: March 2008

Summary.Lithium is known to cause leucocytosis in normal humans, and lithium salts have been used therapeutically in attenuating leucopenia in patients undergoing chemotherapy. Recent reports also described leukaemia development during lithium treatment. We have investigated the effect of lithium chloride on the proliferation of human myeloid, erythroblastic, and T‐ and B‐lymphoblast leukaemia cells in vitro. Colony formation by cells of the myeloid leukaemia lines HL‐60 and KG‐1 was enhanced by lithium chloride, and maximal stimulation was seen at 5 x 10−4 M. Lithium also increased the proliferation of KG‐1a cells, a subline of KG‐1 cells that does not respond to colony‐stimulating factor, indicating a direct growth‐promoting effect on myeloid leukaemia cells. Lithium was found to enhance colony formation by the T‐lymphoblast cell line MOLT 4 and the B‐lymphoblast line IM‐9 at concentrations between 10−6 and 10−3 M. The addition of lithium chloride to murine Friend or human K‐562 erythroleukaemia cells also caused an augmentation in colony formation. These observations may have relevance to the therapeutic use of lithium in patients with haematological malignancies.
Subnormal platelet response to thromboxane A2 in a patient with chronic myeloid leukaemia
Authors: Okuma Minoru , Takayama Hiroshi , Uchino Haruto 
Published: March 2008

Summary.A new type of acquired platelet dysfunction was found in a chronic myeloid leukaemia patient with petechiae and thrombocytosis. Platelet aggregation induced by arachidonic acid (AA), collagen and A23187 was decreased, secondary aggregation by ADP and epinephrine was defective and ristocetin‐induced aggregation was completely reversible. No platelet ATP was released by AA and collagen. Only high concentrations of AA (≤ 2 mM) induced minimal reversible aggregation. 14C‐serotonin uptake by the platelet and platelet adenine nucleotide contents were normal. Normal AA metabolism was demonstrated by thin‐layer radiochromatographic analysis of the metabolites of 14C‐AA and the determination of thiobarbituric acid reactive substances produced by the incubation of AA or thrombin with the platelets. Minimal reversible aggregation was observed when patient's platelet‐rich plasma was added to a reaction mixture in which thromboxane A2 (TXA2) had been generated. TXA2 produced by patient's platelets showed normal platelet‐aggregating activity. These results suggest that a subnormal platelet response to TXA2 is included as a mechanism for this acquired hypofunction of the platelet.
IS TRANSFERRIN NORMAL IN IDIOPATHIC HAEMOCHROMATOSIS?
Authors: Jenkins T. , Bothwell T. H. , Maier G. , Laidler Avril 
Published: March 2008

Summary.Family studies were done to ascertain whether there is linkage between the transferrin locus and the HLA loci on chromosome 6. The findings in four families in which there was variation at the transferrin locus did not demonstrate any linkage, with 17 of the 30 offspring of heterozygous parents being recombinants and 13 non‐recombinants. These results indicate that the HLA linked defect responsible for increased iron absorption in idiopathic haemochromatosis is not a consequence of any abnormality in the primary structure of transferrin.
Monoester lipase activity in the red cells of patients with various blood disordrs
Authors: Gastaut J. A. , Vérine A. , Crcassonne Y. , Boyer J. 
Published: March 2008

Summary. Membrane‐bound monoester lipase (MEL) activity was measured by a radiochemical assay in intact red blood cells (RBC) from 77 patients with various blood disorders. MEL activity levels in their RBC were compared with levels in normal subjects. The increase in MEL activity was greatest in RBC of regenerative anaemias (N=8) and blastic crisis of chronic granulocytic leukaemias (7) whereas a lesser, although significant, increase was found in acute non‐lymphoblastic leukaemias (14). MEL activity was markedly decreased in RBC of erythroleukaemias (N=5) and decreased to a lesser extent in acute lymphoblastic leukaemias (10) and in chronic myeloproliferative disorders other than chronic granulocytic leukaemias (8). MEL activity levels were roughly correlated with reticulocyte counts, but the relationship was not of predictive value in individual cases. Further exploration of the possible diagnostic or prognostic implications of these variations in enzyme levels seems warranted.A monoester lipase (MEL) activity has been recently identified and characterized as a membrane‐bound enzyme in red blood cell (RBC) from rats (Arnaud et al, 1979) and human subjects (Boyer et al, 1981). No attempt has been made so far to search for abnormalities of this enzyme. We have therefore measured MEL activity in RBC of 77 patients with various blood disorders.