bluuebunny/crossref_metadata_2025_split huggingface dataset:
The role of sialic acid in the activation of platelets by wheat germ agglutinin
Authors: Ganguly P , Fossett NG 
Published: October 2019

Abstract
Sialic acid is believed to play a critical role in the survival of blood platelets in circulation. Wheat germ agglutinin, which shows specificity for sialic acid, N-acetylglucosamine, and N- acetylgalactosamine, strongly activates platelets. The role of sialic acid in platelet activation by this lectin was studied utilizing neuraminidase-treated platelets and the succinylated lectin that has been reported not to recognize sialic acid. The succinylated lectin had a dimeric structure similar to the native lectin, but migrated more slowly in gel electrophoresis. The modified lectin bound to about 2.8 X 10(5) sites/cell, with an apparent dissociation constant of 2 microM compared to 5 X 10(5) sites/cell and a dissociation constant of 0.4 microM for the native lectin. The succinylated lectin neither aggregated nor agglutinated platelets, but agglutination of red cells in microtiter plates was normal. Aggregation of platelets by either wheat germ agglutinin or ristocetin was not affected by the succinylated lectin. Since the native wheat germ agglutinin is a strong activator of platelets and the succinylated derivative was devoid of all activity, it appears that a sialoprotein acts as the biologic receptor of wheat germ agglutinin in human platelets. This suggestion was strengthened by the observation that platelets treated with different concentrations of neuraminidase had a decreased capacity to bind this lectin. These platelets also showed reduced aggregation and serotonin secretion when activated with the native lectin. Since sialic acid has been implicated in the removal of platelets from circulation, wheat germ agglutinin may prove to be a useful tool to explore those clinical conditions in which platelet survival is shortened.
Left shift in the peripheral blood count at diagnosis in acute lymphocytic leukemia is significantly correlated with duration of complete remission
Authors: Shen BJ , Ekert H , Tauro GP , Balderas A 
Published: October 2019

Abstract
The prognostic significance of a left shift in the peripheral blood at the time of diagnosis of acute lymphocytic leukemia was investigated by a retrospective analysis of 109 patients treated on the same protocol in a single institution. Left shift was defined as the presence of 1% or more of metamyelocytes, myelocytes, or promyelocytes. All peripheral blood films were checked at the time of diagnosis by one of the authors. It was found that the duration of complete remission at 92 mo was 74% in patients with left shift and 42% in those without left shift (p less than 0.05, log-rank test). By Cox regression analysis, only the total white cell count (p less than 0.001) and the presence or absence of left shift (p less than 0.01) were independently significant in determining the proportion of patients in complete remission. Patients with a left shift had a significantly higher granulocyte count at diagnosis (p less than 0.05). We postulate that left shift in the peripheral blood count at the time of diagnosis may be an indirect measure of the total leukemia cell load. It is a new prognostic factor of significance in determining the likely outcome of the disease.
Cytosolic free calcium changes induced by chemotactic peptide in neutrophils from patients with chronic granulomatous disease
Authors: Lew PD , Wollheim C , Seger RA , Pozzan T 
Published: October 2019

Abstract
Cytoplasmic free calcium concentration (Ca2+)i was measured in neutrophils from patients with the classical X-linked form of chronic granulomatous disease (CGD) by trapping the fluorescent calcium indicator Quin 2 in intact cells. CGD neutrophils do not produce superoxide and are only slightly depolarized upon stimulation by the chemotactic peptide. N-formyl-methionyl-leucyl-phenylalanine (FMLP). The resting levels, as well as (Ca2+)i changes induced by FMLP in CGD cells, were quantitatively and kinetically similar to those observed in normal cells. We conclude that the defect in CGD cells is distal to, or independent of, the changes in (Ca2+)i induced by FMLP stimulation and that normal membrane depolarization does not seem to be necessary for receptor-mediated rise in free cytosolic calcium in human neutrophils.
Nonspecific esterases of leukemia cell lines: evidence for activation of myeloid-associated zymogens in HL-60 by phorbol esters
Authors: Yourno J , Walsh J , Kornatowski G , O'Connor D , Kumar SA 
Published: October 2019

Abstract
Myeloid leukemia cell line HL-60 contains fluoride-sensitive, myeloid- associated isoenzymes of nonspecific esterase that increase in activity when cultures are treated with phorbol ester. These isoenzymes are not detectable in B-lymphoblast cell line KLM-2, either in control or in phorbol-ester-treated cultures. No increased de novo synthesis of the isoenzymes is detectable in HL-60 treated with phorbol ester. The data suggest stimulated conversion of a preformed, myeloid-associated zymogen in HL-60.
Clinical experience with polyelectrolyte-fractionated porcine factor VIII concentrate in the treatment of hemophiliacs with antibodies to factor VIII
Authors: Kernoff PB , Thomas ND , Lilley PA , Matthews KB , Goldman E , Tuddenham EG 
Published: October 2019

Abstract
Circulating antibodies to factor VIII (anti-VIII, “inhibitors”) occurring in patients with hemophilia neutralize porcine factor VIII less readily than human factor VIII in vitro. Over an 18-mo period, 8 patients with anti-VIII were treated with 45 courses (297 infusions) of polyelectrolyte-fractionated porcine factor VIII concentrate (PE porcine VIII). Where no anti-PE porcine VIII was detectable, mean post- infusion rise in plasma factor VIII was 1.29 U/dl/units infused/kg. Above 13 Old Oxford units of anti-PE porcine VIII and 48 Bethesda units of anti-human VIII, there were no postinfusion rises in plasma factor VIII. Where postinfusion rises were detected, clinical responses were good and conventional methods could be used to guide dosage. Ten percent of infusions were followed by febrile reactions, but these were usually mild and decreased in frequency and severity with increasing exposure. Multiple and prolonged courses of therapy were given to some patients without evidence of loss of clinical or laboratory efficacy. PE porcine VIII could provoke anamnestic rises of anti-VIII in susceptible patients, but appeared to have a lower immunogenic potential than human VIII. PE porcine VIII is a rational and effective therapeutic alternative for patients with anti-VIII, particularly those with intermediate level inhibitors who cannot be managed effectively using human factor VIII.
"Masked" Ph1 chromosome abnormalities in CML: a report of two unique cases
Authors: Bernstein R , Pinto MR , Rosendorff J , Kramer S , Mendelow B 
Published: October 2019

Abstract
Two patients with chronic myeloid leukemia (CML) showed previously undescribed variants of a “masked” Ph1 abnormality. The first patient had the karyotype 46,XY, + 21, -9, -22, +mar9,mar18 at presentation in the chronic phase. The dicentric marker 9 was interpreted as representing the usual translocation of 22q11 to 9q34, followed by translocation of the Ph1 chromosome (the deleted 22) to 9p and probable translocation of 9p to the distal long arm of the marker. The patient developed clones containing 2 and 3 copies of the “Ph1-containing” marker 9 concomitant with the metamorphosis of his disease to a more aggressive phase. The second case presented with the karyotype 46,XY,- 9,-22,+two D-group markers. A complex rearrangement of chromosomes 9 and 22 is postulated, with interstitial insertion of either 9p or distal 9q into chromosome 22q11. This patient is still in the chronic phase of his disease 9 mo after presentation. The common denominator in these unusual “masked” cases is the 22q11 breakpoint. The paucity of published reports of duplication of 9q + without concurrent duplication of the Ph1 chromosome, supported by the findings in our first case, leads us to conclude that the amplification of genes on the Ph1 chromosome are more important for the evolution of the abnormal stem cell in CML than the chromosome 9 derivative.
The number of receptors for factor VII correlates with the ability of cultured cells to initiate coagulation
Authors: Rodgers GM , Broze GJ Jr , Shuman MA 
Published: October 2019

Abstract
Previously, we showed that cells derived from nonvascular tissues initiate clotting primarily by markedly increasing the activity of coagulation factor VII. Cells derived from vascular tissue do not normally exhibit this property (tissue factor activity). In this study, we have characterized the relationship between the tissue factor activity of cultured cells derived from normal tissues and the number of receptors they possess for coagulation factor VII. Only cultured nonvascular cells expressed tissue factor activity or possessed receptors for 125I-factor VII. Fetal lung cells, the nonvascular tissue with the largest amount of procoagulant and tissue factor activity, possessed the most receptors for 125I-factor VII (880,000/cell). Bovine corneal endothelial cells, the nonvascular tissue possessing the fewest number of receptors (2,400/cell), had the least amount of procoagulant or tissue factor activity. The affinity of nonvascular cells for 125I- factor VII varied for the cells studied (Kd congruent to 1.3–90 X 10(- 10) M). Vascular cells expressed no tissue factor activity, nor did they bind 125I-factor VII. 125I-factor VII and unlabeled factor VII bound to cells had identical procoagulant activities. These results indicate that the ability of cultured cells to initiate coagulation may be regulated in part by the number of receptors they possess for factor VII.
Removal of HLA-A,B antigens from platelets
Authors: Blumberg N , Masel D , Mayer T , Horan P , Heal J 
Published: October 2019

Abstract
Recent evidence suggests that HLA-A,B antigens present on human platelets, are acquired from plasma. Using hypertonic acid chloroquine (200 mg/ml, pH 5.0, 1 hr, 4 degrees C), we demonstrate elution of most or all HLA-A2 and HLA-B7,40 immunoreactive material from platelets. Corresponding antigens on human lymphocytes were not affected by this treatment. These findings are consistent with the hypothesis that HLA- A,B antigens are adsorbed onto platelet surfaces.
Complement alternative pathway activation by chronic lymphocytic leukemia cells: its role in their hepatosplenic localization
Authors: Praz F , Karsenty G , Binet JL , Lesavre P 
Published: October 2019

Abstract
Using affinity-purified 125I-F(ab')2 anti-human C3, we have investigated the ability of various leukemic cells to activate complement. Lymphocytes from patients with chronic lymphocytic leukemia (CLL) activated the alternative pathway, but cells from patients with other forms of leukemia or normal lymphocytes did not do so. The amount of C3 deposited on the CLL cells was significantly higher in patients with organomegaly (i.e., splenomegaly and/or hepatomegaly). Activation of complement by CLL cells as assessed by C3 deposition on the membrane occurred both in vivo and in vitro and was not related to the N- acetylneuraminic acid content of the membrane.
Inhibition of the pentose phosphate shunt by lead: a potential mechanism for hemolysis in lead poisoning
Authors: Lachant NA , Tomoda A , Tanaka KR 
Published: October 2019

Abstract
Recent investigations have disclosed a decrease in pentose phosphate shunt activity in hereditary pyrimidine 5′-nucleotidase deficiency. Clinical lead poisoning is associated with an acquired decrease in pyrimidine 5′-nucleotidase activity. The current investigations were undertaken (1) to determine if pentose shunt activity was decreased in erythrocytes exposed to lead, and (2) to compare the mechanism of inhibition to that seen in hereditary pyrimidine 5′-nucleotidase deficiency. Normal erythrocytes incubated with lead acetate in vitro demonstrated increased Heinz body formation, decreased reduced glutathione, a positive ascorbate cyanide test, and a reversible suppression of pentose shunt activity in the intact erythrocyte. Lead acetate added to normal red cell hemolysates markedly inhibited the activities of glucose-6-phosphate dehydrogenase (G6PD) and phosphofructokinase. The mean Kis of lead for glucose-6-phosphate and nicotinamide adenine dinucleotide phosphate (NADP) for G6PD were 1.5 microM and 2.1 microM, respectively, which is within the range of intraerythrocytic lead concentrations found in clinical lead poisoning. Magnesium enhanced the ability of lead to inhibit G6PD. Thus, the shortened erythrocyte survival in lead poisoning appears to be due, in part, to increased oxidant sensitivity secondary to inhibition of G6PD and the pentose shunt. The mechanism of shunt inhibition is, in part, similar to that seen in hereditary pyrimidine 5′-nucleotidase deficiency.
Identification of human lymphoma cells by antisera to malignancy- associated nucleolar antigens
Authors: Ford RJ , Cramer M , Davis FM 
Published: October 2019

Abstract
The non-Hodgkin's lymphomas (NHL) are a diverse group of human lymphoid neoplasms that have long presented pathologists with formidable diagnostic challenges. These tumors of the immune system are thought to represent neoplastic transformations of most of the recognized stages in T and B lymphocyte ontogeny. Lymphoma cells, however, often simulate their normal lymphocytic counterparts both morphologically and cell surface phenotypically, creating difficulties in discriminating normal from neoplastic lymphocytes. We have used heteroantisera to the human malignancy-associated nucleolar antigen (HMNA) to prospectively evaluate its efficacy in identifying the morphologically neoplastic cells in NHL lesions. In 65 cases of T and B cell histopathologic types of NHL, the antisera reacted with nucleoli in the morphologically and cytogenetically neoplastic lymphoma cells, but not with normal- appearing lymphoid and other cell types present in the lesions. Control specimens from normal and hyperplastic lymphoid tissue also failed to react with anti-HMNA antibodies. Normal activated lymphoid cells in vitro and growth-factor-dependent normal lymphoid cell lines also failed to express the nucleolar antigen(s). These data suggest that the HMNA is a valuable tumor cell marker for neoplastic human lymphoid cell populations and can be used with other types of cell markers for a better definition of the neoplastic cells in NHL.
Deferoxamine enhances phagocytic function of human polymorphonuclear leukocytes
Authors: van Asbeck BS , Marx JJ , Struyvenberg A , van Kats JH , Verhoef J 
Published: October 2019

Abstract
Inhibition of the iron-mediated generation of toxic oxygen species by polymorphonuclear leukocytes (PMN) might prevent oxidative damage and thus enhance phagocytic function of PMN. To investigate this point, we studied the effect of the specific iron chelator, deferoxamine, on the antibacterial function of PMN. PMN were incubated for 20 hr with various concentrations of deferoxamine at 37 degrees C in medium containing 0.54 microM endogenous iron. The cells were then washed, and the phagocytic cell function was assessed. The results were compared with those for control PMN preincubated for 20 hr without deferoxamine, and those of nonincubated PMN. Compared with that of control PMN, the uptake of radiolabeled Staphylococcus aureus by PMN treated with 1 microM-1 mM deferoxamine was, on average, 10%-20% higher. This effect was not observed when iron-saturated deferoxamine (DFO) was used. Bacterial uptake was similarly increased in nonpreincubated PMN or PMN preincubated for 20 hr at 4 degrees C instead of 37 degrees C. The intracellular killing capacity of both deferoxamine-treated and control PMN exceeded 90%. PMN incubated for 20 hr at 37 degrees C with DFO not only phagocytosed more bacteria than control cells, but were also capable of killing the greater number of bacteria ingested. This increased activity of deferoxamine-treated PMN was accompanied by enhanced generation of chemiluminescence and production of superoxide during phagocytosis of S. aureus. These findings indicate that deferoxamine may enhance the antibacterial activity of PMN by protecting the cells against damage by iron-mediated generation of toxic oxygen metabolites in resting PMN.
Cobalamin (vitamin B12) and B12 binding proteins in hypereosinophilic syndromes and secondary eosinophilia
Authors: Zittoun J , Farcet JP , Marquet J , Sultan C , Zittoun R 
Published: October 2019

Abstract
Serum cobalamin (vitamin B12) and unsaturated B12 binding capacity (UBBC) have been measured in 24 cases of hypereosinophilia: 16 were cases of hypereosinophilic syndrome (HES) and 8 of secondary eosinophilia. The two groups were similar with respect to absolute eosinophil counts. Serum cobalamin and UBBC were found to be markedly increased in most cases of HES and normal in secondary eosinophilia. This elevation of UBBC was mainly related to the increase of R binders (transcobalamins I and III). The elevated serum cobalamin and R binders in HES were due neither to a higher intracellular content of R binders nor to an increased release of these binders from eosinophils of HES. Pure fractions of eosinophils obtained from HES and secondary eosinophilia did not exhibit any difference in vitamin B12 binders. On the other hand, neutrophil-rich fractions from the same patients showed a higher content of intracellular B12 binding proteins than pure eosinophil fractions, irrespective of the cause of eosinophilia. These findings suggest that the increased serum vitamin B12 and UBBC could reflect an expanded pool of both eosinophils and neutrophils in HES and, thus, provide an additional argument for the inclusion of this syndrome in the group of myeloproliferative disorders.
Inappropriately low red cell 2,3-diphosphoglycerate and p50 in transfused beta-thalassemia
Authors: Correra A , Graziano JH , Seaman C , Piomelli S 
Published: October 2019

Abstract
The relationships among hemoglobin concentration (Hb), red cell 2,3- diphosphoglycerate (2,3-DPG), and p50 were studied in 20 chronically hypertransfused patients with thalassemia major. In the nontransfused control group, which included normal individuals as well as patients with sickle cell disease or iron deficiency anemia, the Hb correlated inversely with both 2,3-DPG concentration and p50, as is well established. In contrast, however, prior to transfusion, at the nadir of Hb, patients with thalassemia major had inappropriately low 2,3-DPG concentrations and p50s. These findings occurred in all patients, regardless of whether they had received packed, leukocyte-poor, or frozen-thawed red cells. The hypothesis that the time of blood storage was a factor was excluded by repeatedly transfusing one patient with packed red cells administered within 4 hr of collection in CPDA-1. A second hypothesis, that red cell function might be impaired by the iron- overloaded thalassemic environment, was excluded by studying a newly diagnosed, newly transfused patient with aplastic anemia. In both cases, the same inability to appropriately increase 2,3-DPG and p50 as the Hb fell during the intertransfusion interval was noticed. These data suggest that red cells of chronically transfused patients are unable to adapt to the decline in Hb that occurs during the intertransfusion interval.
Elimination of high affinity heparin fractions and their anticoagulant and lipase activity
Authors: de Swart CA , Nijmeyer B , Andersson LO , Holmer E , Verschoor L , Bouma BN , Sixma JJ 
Published: October 2019

Abstract
High and low affinity heparin (HA and LA heparin) were prepared from commercial heparin by affinity chromatography to insolubilized antithrombin III. HA heparin was radiolabeled with 35S and subdivided by gel chromatography into high molecular weight (HMW, average 17,000– 26,000 daltons), intermediate molecular weight (MMW, average 12,000– 13,000 daltons), low molecular weight (LMW, average 5,000–7,000 daltons), and very low molecular weight (VLMW, average 4,600 daltons) fractions. The kinetics of lipolytic and anticoagulant activity and protein-bound radioactivity were studied after intravenous injection of these fractions. LA heparin failed to induce anticoagulant activity but released the hepatic triglyceride lipase (H-TGL) and lipoprotein lipase (LPL) activities normally. VLMW and LMW heparin failed to release both lipolytic enzymes and did not induce anticoagulant activity measurable by the activated partial thromboplastin time (APTT). A powerful anticoagulant effect was found in the anti-Xa assay, which disappeared according to a continuously concave curve in semilogarithmic plots, with elimination rates similar to those of the protein-bound radiolabel. The other heparin preparations induced all activities measured. Heparin anticoagulant activity estimated by the two assays disappeared following a convex curve, preceded by a rapid initial elimination phase in semilogarithmic plots. The disappearance rates of plasma protein-bound heparin radioactivity and heparin anticoagulant activity estimated by factor Xa inactivation were similar. Peak values of the two lipolytic activities were attained rapidly. H- TGL activity, as well as LPL activity, disappeared following convex curves in semilogarithmic plots, with elimination rates similar to those of plasma protein-bound heparin radioactivity. On the basis of these kinetics, we suggest that, after intravenous administration of heparin, the two lipolytic enzymes present in plasma are complexed with heparin, analogous to the heparin-antithrombin III complex. Finally, the kinetic data indicate that elimination of these activities is determined by the heparin part of the complexes, probably by removal of free heparin.
Viscometric and spectrophotometric measurements of hemoglobin S polymerization kinetics
Authors: Wenger GD , Balcerzak SP 
Published: October 2019

Abstract
The rates of polymerization and depolymerization of identical concentrated deoxygenated hemoglobin S (HbS) solutions following a rapid temperature change were examined by several methods. Two of these methods measured viscosity changes in either gently agitated (AGT) or nonagitated (NAGT) samples. The third method utilized a change in turbidity at 735 nm (SDT). By all three methods, a delay period, during which no observable change was detected, followed the temperature change. Gelation, as determined in nonagitated samples by a viscosity- based technique, occurred before or coincided with gelation as determined spectrophotometrically. The slope of the concentration dependence of the delay time is significantly decreased by agitation. Similar monitoring of the depolymerization reaction indicated the persistence of increased viscosity after observation of a marked decrease in turbidity.