bluuebunny/crossref_metadata_2025_split huggingface dataset:
Studies on the effects of primary therapy for DIC following circulatory arrest
Authors: Takemoto Yoshinobu , Tanaka Shigeru , Tanabe Jun , Nakamura Yoshihiro , Kohama Akitsugu , Shibata Susumu 
Published: February 2007

AbstractComparative studies in early treatment for DIC caused by circulatory arrest were carried out on three groups of dogs during 300 min from the recovery of circulatory arrest: a heparin group, a FOY (gabexate mesilate) group, and a FUT‐175 (nafamostat mesilate) group. The parameters employed were platelet count, prothrombin time (PT), activated partial prothrombin time (APTT), fibrinogen, antithrombin‐III (AT‐III), and fibrin or fibrinogen degradation products (FDP).In the heparin group, there was less of a drop in the platelet count and the level of AT‐III than in the control group, but the FDP levels were the same as in the control group. The PT and APTT remained within normal limits in the FOY group and no decrease was observed in either platelet count or AT‐III levels. In addition, FDP levels were kept within normal limits. In the FUT‐175 group, prolongation of APTT, no decline in the platelet count and AT‐III levels, and normal levels of FDP were observed.The results of these experiments indicate the importance of early treatment for DIC. Judging from the parameters, better results were obtained in the FOY and FUT‐175 group than in the heparin group.
Teardrop‐shaped red cells in autoimmune hemolytic anemia
Authors: Farolino Deborah L. , Rustagi Pradip K. , Currie Mark S. , Doeblin Thomas D. , Logue Gerald L. 
Published: February 2007

AbstractThe presence of teardrop‐shaped red cells in peripheral blood has traditionally been felt to reflect altered marrow architecture, namely myelofibrosis. We evaluated two patients with splenomegaly, moderately severe hemolytic anemia due to warm‐reactive IgG anti‐red cell autoantibody, and bone marrow erythroid hyperplasia without myelofibrosis. A striking predominance of teardrop‐shaped red cells was noted upon examination of their blood films. Removal of a spleen containing extramedullary hematopoiesis in one and resolution of splenomegaly in the other were accompanied by disappearance of these cells. Our observations support a role for the spleen and for extramedullary hematopoiesis in the pathogenesis of this distinctive red cell morphologic abnormality.
Immunoregulatory abnormalities in myelodysplastic disorders
Authors: Baumann Michael A. , Milson Thomas J. , Patrick Catherine W. , Libnoch Joseph A. , Keller Robert H. 
Published: February 2007

AbstractImmunoregulation was assessed in a group of patients with myelodysplasia (MDS) by flow cytometric analysis of peripheral blood lymphocyte subsets and in vitro studies of mitogen‐stimulated T‐lymphocyte blastogenesis. Mitogenesis was significantly depressed in MDS patients compared to controls (p < .001) and a similar defect was found in a small group of patients with untreated acute nonlymphocytic leukemia (ANLL) (p < .005). The impaired mitogenic response ability of T‐cells in these patients did not appear to be the result of alteration in lymphocyte subpopulation ratios. The observed defect might result from defective cooperation between Tlymphocytes and abnormal myeloid elements. Alternatively, the lymphocytes themselves could be derived from the abnormal clone and thus be functionally abnormal.
Protein C levels in nephrotic syndrome: Use of a new enzyme‐linked immunoadsorbent assay for protein C antigen
Authors: Soff Gerald A. , Sica Domenic A. , Marlar Richard A. , Evans Herbert J. , Qureshi G. Dastgir 
Published: February 2007

AbstractActivated protein C is a potent, physiologic anticoagulant that inactivates the activated forms of factors V and VIII as well as facilitates in vivo fibrinolysis. We developed a competitive protein‐binding enzyme‐linked immunoadsorbent assay (ELISA) for protein C that was utilized to investigate if the hypercoagulability of the nephrotic syndrome is related to a deficiency of circulating plasma protein C. Protein C was measured in plasma of 11 patients with nephrotic syndrome (24 hr protein 8.4 ± 1.6 g, SEM; serum creatinine 4.2 ± .74 mg/dl, SEM). Ten azotemic nonnephrotic patients were employed as controls (serum creatinine 6.0 ± 1.25 mg/dl, SEM). No significant reduction of protein C values was observed (mean 108%, range 65–200%) in nephrotic patients when compared with the controls (mean 127%, range 100–200%) even though protein C antigen was present in all nephrotic urine samples tested. Also, no correlation existed between blood levels of urea nitrogen, creatinine, albumin, total protein, or 24‐hr urine protein excretion and the observed protein C values. These results suggest that in patients with the nephrotic syndrome, a hyper‐coagulable state may not be related to a deficiency of protein C and that the level of this zymogen in nephrotic syndrome reflects a dynamic balance between urinary losses and systemic production.
A patient with the inability to maintain in vivo levels of bound cobalamin (Cbl) and manifestations of tissue deficiency of Cbl
Authors: Begley James A. , Burkart Peter T. , Hall Charles A. 
Published: February 2007

AbstractA 39‐year‐old woman presented with mild anemia, glossitis, an increased MCV, a low serum cobalamin (Cbl) (vitamin B12), mild tissue deficiency of Cbl, but with neither malabsorption of Cbl, impaired intake, nor deficiency of or inactivity of transcobalamin II (TC II). Because of a persistently low holo‐TC II (TC II carrying Cbl as the circulating complex of TC II‐Cbl), much of the evaluation was focused on the patient's TC II. Her TC II promoted the uptake of Cbl, reacted with anti‐TC II, and bound Cbl in vitro. A test dose of 200 μg of cyanocobalamin (CN‐Cbl) i.m. increased her holo TC II to levels higher than those in healthy persons, but with a much more abrupt fall to a subnormal level. Two milligrams of CN‐Cbl i.m. followed by 100 μg i.m. monthly failed to maintain normal amounts of circulating TC II‐Cbl or to overcome the tissue deficiency of Cbl. One milligram i.m. weekly or daily p.o. corrected both. The low holo TC II was considered to be responsible for the clinical expression and may have been primary to the reduced amounts of total and holo R binder of Cbl in the circulation. This study of a newly recognized defect points out the need for circulating holo TC II, a rational use of pharmacologic amounts of Cbl, and a possible interrelationship between TC II and the R binder of Cbl.
The effect of acute and chronic leukapheresis on the natural killer (NK) cell function of normal human volunteers
Authors: Stevenson Henry C. , Beman Joann S. , Crisp Beth , Coggin David , Kanapa D. J. , Miller Paul , Herberman Ronald B. , Maluish Annette E. 
Published: February 2007

AbstractTwenty‐two normal volunteers had approximately eight, 2‐hr‐long leukapheresis procedures over a 2‐year period and their natural killer (NK) cell function was prospectively measured. The NK activity of the preprocedure peripheral blood (pre‐PB) was found to correlate well with the NK activity of the inital leukocytes removed by leukapheresis (I‐Leuk). When the I‐Leuk specimens were compared with the leukapheresis specimens removed at the termination of leukapheresis (T‐Leuk), T‐Leuk showed a consistent 10% increase in NK activity. When the pre‐PB and the I‐Leuk values were analyzed for each donor over the 2 years of the study, 18 donors revealed no significant change from their baseline NK activity, two donors showed a minimal increase in NK cell activity, and two donors displayed a minimal decrease in NK cell activity. We conclude that although leukapheresis appears acutely to boost NK cell activity, this increase is transient and small in magnitude. Most importantly, repeated leukapheresis does not appear adversely to effect this important effector function in normal donors.
Changes in platelet β‐thromboglobulin, fibrinogen, albumin, 5‐hydroxytryptamine, ATP, and ADP during and after surgery with extracorporeal circulation in man
Authors: Mezzano Diego , Aranda Eduardo , Urzúa Jorge , Lema Guillermo , Habash Jeanette , Irarrázabal Manuel J. , Pereira Jaime 
Published: February 2007

AbstractSurgery with extracorporeal circulation (ECC) is associated with transient alterations of platelet function whose pathogenic mechanisms are not completely understood. To define further the platelet abnormalities, we determined the changes in platelet content of several granule‐associated substances during and after ECC in patients subjected to aortocoronary bypass surgery.Platelet β‐thromboglobulin (β‐TG) decreased to 79.8% of the preoperative level at the end of ECC (p < 0.01) and, as expected, did not recover 1 hr after the end of surgery. Platelet fibrinogen and albumin decreased to 67.9% (p < 0.01) and to 29.8% (p < 0.01) of baseline, respectively. However, 1 hr after surgery, platelet fibrinogen rose to 92% and albumin to 55.5% of baseline, denoting that during the recovery from ECC, platelets incorporate some plasma proteins.During ECC, platelet 5‐hydroxytryptamine (5‐HT) and total ATP and ADP decreased to 50.8% (p < 0.01), 63.2% (p < 0.01), and 69.9% (p < 0.01) of their respective preoperative values, indicating dense body release. One hour after surgery, ATP recovered to 83.8%, suggesting that previous depletion compromised also the metabolic pool of adenine nucleotides.In summary, 1) Our results confirm and extend previous observations demonstrating α‐granule release during ECC. 2) Platelets undergoing ECC can incorporate plasma proteins as evidenced by the rapid increase of platelet fibrinogen and albumin after bypass. Although the mechanisms of this increase and site of storage of the exogenous substances are unknown, this observation justifies further studies to determine if internalization of plasma proteins, especially fibrinogen, may take place in physiological conditions. 3) Dense body depletion with transient storage pool deficiency appears to be a component of the reduced platelet function during ECC. 4) Consumption of metabolic ATP with alteration of platelet energy metabolism may further impair platelet function, contributing to the bleeding episodes observed during surgery with ECC.
Burkitt's cells can be triggered by teleocidin to secrete interferon‐γ
Authors: Benjamin David , Hartmann Dan P. , Bazar Leonard S. , Jacobson Robert J. 
Published: February 2007

AbstractThe secretion of interferon (IFN)‐γ by T lymphocytes is mediated by the synthesis of interleukin 2 (IL‐2) and the availability of IL‐2 receptors. Since some Burkitt's lymphoma lines express Tac antigen and can be triggered to secrete IL‐2 following activation with the new tumor promoter teleocidin, we addressed the question of whether the induction of IL‐2 by B lymphocytes is accompanied by the induction of IFN‐γ. IFN‐γ has not been detected in any of the 25 cell lines studied, and following stimulation with teleocidin, we triggered the synthesis of IFN‐γ in JLP(C), a pre‐Burkitt's cell line.The mechanism of IFN‐γ secretion by B lymphocytes is not clear. Our findings demonstrate that the synthesis of IL‐2 by B cells is not accompanied by IFN‐γ and suggest that the synthesis of IFN‐γ is not mediated by IL‐2 or IL‐1 or B‐cell growth factor. Neutralization studies have shown that IFN‐γ secretion is not accompanied by the induction of IFN‐α or IFN‐β.Our data imply that B cells can be triggered to secrete IFN‐γ under certain circumstances. Whether similar function occurs in vivo is not known.
Terminal deoxynucleotidyl transferase activity in acute leukemia: A study of 100 cases comparing an immunoperoxidase (PAP) vs immunofluorescent method
Authors: Krause John R. , Brody Judith P. , Kaplan Sandra S. , Penchansky Lila 
Published: February 2007

AbstractA comparison between the immunofluorescent (IF) method for terminal deoxynucleotidyl transferase (TdT) activity and the immunoperoxidase (IP) method by peroxidase‐anti‐peroxidase (PAP) technique was done for 100 cases of acute leukemia. For the acute lymphoblastic leukemias (ALL) there was agreement in 93% of the cases. However, the IP method detected 51/55 (93%) TdT+ cases versus 47/55 (85%) by the IF method. For the acute nonlymphocytic leukemias (ANLL), there was an agreement in 89% of the cases. The IP method detected 8/36 (22%) TdT‐positive cases while IF detected 4/36 (11%) positive cases. If a figure of 10% TdT+ cells is considered significant in the marrow of the ANLLs, then the IP method would detect eight additional cases for a total of 16/36 (44%) TdT+ cases. This latter figure questions the ability of the IP TdT assay as a single test adequately to determine the lineage of a cell line. It may be rather that TdT is a marker that is expressed in a stem cell.
The β0‐thalassemia in an American black family is due to a single nucleotide substitution in the acceptor splice junction of the second intervening sequence
Authors: Padanilam B. J. , Huisman T. H. J. 
Published: February 2007

AbstractAn AG dinucleotide is an invariant feature of all acceptor splice sites, and deletion or substitution of (one of) these nucleotides will result in abnormal processing of the β‐globin mRNA. Restriction endonuclease mapping of DNA from an American black patient with Hb S‐β0‐thalassemia failed to detect any deletion in the β0‐globin gene region, but cloning and sequencing of the β0‐globin gene showed a point mutation (A → C) in the highly conserved dinucleotide AG of the acceptor splice junction of the IVS‐2. Blot hybridization analysis of RNA prepared from the erythroid cells of the patient showed only RNA of normal size. The patient and her daughter, who has the same condition, have high levels of Hb F (27%–35%); the mechanism responsible for the greatly increased γ chain production remains unclear.
Acute lymphocytic leukemia in children presenting with bone marrow necrosis
Authors: Macfarlane S. D. , Tauro G. P. 
Published: February 2007

AbstractBone marrow necrosis has been regarded as an indicator of very poor prognosis in malignant disease. The cause and incidence are unknown, and reports of treatment response are few. We describe four children with marrow necrosis at presentation with acute lymphocytic leukemia (ALL), all of whom entered remission with standard treatment showing complete marrow healing. The bleak outlook for patients with marrow necrosis based on early experience in adults with disseminated malignancy does not appear to apply to children with ALL. The incidence of marrow necrosis at diagnosis of childhood ALL is 1%.
Zinc inhibits FPA release and increases fibrin turbidity
Authors: Marx Gerard , Hopmeier Pierre 
Published: February 2007

AbstractPhysiologic concentrations of Zn(II) (4–40 μM) can increase the rate of thrombin‐induced fibrin clot formation (decreased clotting time, CT) and increase the turbidity of the fibrin gel. Both the initial and ultimate turbidity (Abs600 mm) of fibrin gels are increased in the presence of Zn(II). Two techniques were used to elaborate the mechanisms of Zn+2 procoagulant effect. Analytical ultracentrifugation indicates that Zn(II) does not induce the formation of fibrinogen multimers. Radioimmunoassay for FPA indicates that thrombin activation of fibrinogen is decreased by Zn(II), with 50% inhibition of FPA release observed at 35 μM Zn(II). These experiments indicate that the critical feature of Zn(II) procoagulant effect is not due to the induction of fibrinogen proteolysis by thrombin, which is actually decreased. Rather, it appears that Zn(II) accelerates the polymerization step of fibrin assembly and concomitantly modifies fibrin gel structure.
Complete recovery of pure red cell aplasia by intramuscular gammaglobulin therapy in a child with hypoparathyroidism
Authors: Etzioni A. , Atias D. , Pollack S. , Levy J. , Vardi P. , Hazani H. , Benderly A. 
Published: February 2007

AbstractA 10‐year‐old girl with multiple endocrinopathies, hypoparathyroidism, and pernicious anemia subsequently developed pure red cell aplasia, which responded only temporarily to cytotoxic therapy. Because of transfusion dependency, resistance to steroids, plasmapheresis, and Cytoxan, she was given injections of intramuscular gammaglobulin. The injections caused a prompt and sustained rise in the child's erythropoiesis.
Lymphoblastic transformation of myelodysplastic syndrome
Authors: Ascensao Joao L. , Kay Neil E. , Wright John J. , Arthur Diane , Finkel Barbara , Rydell Robert , Kaplan Manuel E. 
Published: February 2007

AbstractAcute myeloblastic leukemia occurs as a complication of myelodysplastic syndromes, but the appearance of an acute lymphoblastic leukemia (ALL) has only been reported once. We describe a case in which lymphoblastic transformation occurred in the setting of a dysmyelopoietic syndrome. This leukemia was characterized by lymphoid morphology, terminal deoxynucleotidyl transferase (TdT) positivity, cytogenetic abnormalities, and immunoglobulin gene rearrangements. The patient responded to conventional therapy for this leukemia (vincristine and prednisone). Our case supports the hypothesis of a common lymphohemopoietic progenitor and suggests that in vitro tests may help identify a subset of these patients and be important in selecting appropriate therapy.
Suppression of chemotactic activity of human polymorphonuclears by monoclonal IgMs with and without biological activity
Authors: Pruzanski W. , Nitzan D. W. , Saito S. 
Published: February 2007

AbstractThe influence of monoclonal IgMs on migration of human polymorphonuclears was studied at various temperatures by the use of 19 sera with monoclonal IgMs from patients with macroglobulinemia of Waldenstrom (MW) without obvious biological activity, 29 sera with monoclonal IgM cold agglutinins (18 with anti‐I and 11 with anti‐i IgMs) and 3 sera with monoclonal IgM rheumatoid factor (RF). Under‐agarose migration method and modified Boyden chamber method with double filters and 51Cr‐PMNs were used. In under‐agarose method, chemotactic differentials for controls, MW, anti‐I, and anti‐i groups were, respectively, 57 ± 8 mm, 39 ± 9 mm, 44 ± 14 mm, and 32 ± 16 mm at 37°C and 47 ± 18 mm, 22 ± 11 mm, 17 ± 9 mm, and 15 ± 12 mm at 24°C. All three sera with IgM RF inhibited chemotaxis. The differences between all groups and controls were significant at p < 0.01. Random migration was inhibited at 24°C (p < 0.01) but not at 37°C. Inhibitory concentrations of IgM in the sera tested were equal or less than 0.5 mg/ml. Thirteen sera were tested by the modified Boyden chamber method. At 37°C 8 of 13 sera and at 24°C 11 of 13 sera inhibited significantly chemotaxis at a concentration of IgM of 1 mg/ml. The lowest inhibitory concentration of IgM was 25 μg/ml.Eleven chromatographically pure IgMs were tested in the under‐agarose assay. At concentrations of 0.4‐3.7 mg/ml, eight IgMs inhibited chemotactic differential at 37°C and nine inhibited it at 24°C. At concentrations of 0.6‐2.0 mg/ml, all seven pure IgMs tested by the Boyden chamber method significantly inhibited chemotaxis at 24°C and 37°C. Some IgMs inhibited chemotaxis at concentrations as low as 25 μ/ml. Ten IgM CA were eluted from the red blood cells. Eluates inhibited strongly chemotaxis at 24°C and 37°C. Heat inactivation did not alter inhibitory activity of IgM, however pepsin digestion or reduction and alkylation of purified IgMs did abolish their inhibitory activity. Inhibition of chemotaxis was not related to the light chain type, the titre, or the thermoamplitude of cold agglutination. However, monoclonal IgMs with anti‐i cold agglutinin activity were stronger inhibitors than anti‐I. Since 75% of IgMs tested inhibited chemotaxis at 37°C, it is possible that monoclonal IgMs, especially those with anti‐i cold agglutinin activity, inhibit PMN migration in vivo.
Disseminated intravascular coagulation in lupus erythematosus responding to prednisone therapy
Authors: Riddell Stanley R. , Shojania A. Majid 
Published: February 2007

AbstractA 48‐year‐old man with systemic lupus erythematosus (SLE) developed disseminated intravascular coagulation (DIC) with clinical bleeding. Since no other cause for DIC could be demonstrated, he was treated with prednisone, which rapidly corrected his DIC.This case demonstrates the need for a complete hematological investigation of patients with SLE who present with hemostatic abnormalities.
Comparative activity of erythrocyte adenosine deaminase and orotidine decarboxylase in Diamond‐Blackfan anemia
Authors: Glader Bertil E. , Backer Karen 
Published: February 2007

AbstractIt previously has been reported that red blood cells (RBC) of patients with Diamond‐Blackfan syndrome (DBS) have increased activity of orotidine decarboxylase (ODC) and adenosine deaminase (ADA). The studies reported here compared the activity of these two enzymes in DBS erythrocytes, cord blood, and reticulocytes. The activity of ODC, although increased in some DBS erythrocytes, was not significantly different from that seen in cord RBC or reticulocytes. In contrast, RBC‐ADA activity was increased in 23 of 26 DBS patients; and this enzyme elevation was distinct from that seen in cord blood and reticulocytes. Moreover, ADA activity was normal in 26 of 27 patients with transient erythroblastopenia of childhood (TEC). Taken together, these data indicate RBC‐ADA activity is more sensitive than ODC as a marker of DBS. In addition, RBC‐ADA activity continues to be useful for distinguishing DBS and TEC in most patients with RBC hypoplasia.
A serum ferritin assay for prevalence studies of iron deficiency
Authors: Flowers Carol A. , Kuizon Miriam , Beard John L. , Skikne Barry S. , Covell M. , Cook James D. 
Published: February 2007

AbstractA specialized serum ferritin assay has been developed for the detection of iron deficiency in epidemiologic studies. An enzyme immunoassay (EIA) was employed to climinate the need for radioisotopes. The problem of low sensitivity inherent with the EIA for serum ferritin was eliminated by the use of monoclonal immunologic reagents. The working range of the assay is 1–100 μg/L with a sensitivity of 0.5 μg/ L. Excellent agreement in serum ferritin levels was observed between the present method and the two‐site immunoradiometric assay (IRMA), while the variability at low ferritin concentrations was significantly less with the EIA. Because only 10 μl of serum is required for each assay, duplicate measurements can be performed on a single capillary tube of blood. When an automatic microtiter plate reader for optical density measurements is used, 80‐100 duplicate determinations can be completed by one technologist in a single working day.
Autoreactive erythroid progenitor‐T suppressor cells in the pure red cell aplasia associated with thymoma and panhypogammaglobulinemia
Authors: Mangan Kenneth F. , Volkin Robert , Winkelstein Alan 
Published: February 2007

AbstractIn vitro erythroid culture studies and lymphocyte markers were performed in a patient with a spindle cell thymoma who developed red cell aplasia, panhypogammaglobulinemia, and multiple opportunistic infections. At the time of presentation, erythroid progenitor cells (CFUe, BFUe) were markedly reduced when cultured from marrow mononuclear cells. Removal of T cells from bone marrow mononuclear cells by Erosetting or complement‐mediated lysis with OKT3 pan T cell monoclonal antibody increased growth of erythroid progenitor cells in vitro. Readdition of bone marrow or pleural fluid T cells derived from the thymoma suppressed autologous, but not allogenic, erythroid progenitor cell (CFUe, BFUe) proliferation in vitro. The erythroid progenitor suppressor T cells were predominantly OKTH +, OKT3 +, OKT8 + and Ia + consistent with activated suppressor T cells. Treatment of the patient with cyclophsphamide and corticosteroids reduced marrow lymphocytes fourfold, and a prompt reticulocytosis ensued. After recovery, erythroid progenitor cells were easily detectable. These studies provide new evidence for T cell‐mediated suppression of erythropoiesis in a unique subset of patients with red cell aplasia associated with thymoma and hypogammaglobulinemia.