bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of interleukin‐2 administration on platelet function in cancer patients
Authors: Oleksowicz Leslie , Zuckerman Dina , Mrowiec Zbigniew , Puszkin Elena , Dutcher Janice P. 
Published: February 2007

AbstractPlatelet function in 16 patients with metastatlc renal cell carcinoma and melanoma was studied sequentially over the first 96 hr of treatment with moderate and highdose inter‐leukin‐2 (IL‐2). During the first 96 hr of therapy, an increased ex vivo platelet maximal aggregation (MA) response to ADP, epinephrine, and arachidonlc acld was paralleled by a decrease In the peripheral platelet count. Plasma speclmens from patients receiving the moderate dose schedule showed a significant IL‐2 induced secretory response of the platelet α‐granule components β‐thromboglobulin (BTG) and platelet factor 4 (PF4) and the eicosanoid thromboxane B2 (TBX2) as measured by RIA. The increase in TXB2 was highly correlated with MA when analyzed by bivariate regression analysls, whereas the addition of PF4 to TXB2 in a multiple regression analysls further Increased their correlation to MA. The observed decrease In peripheral platelet count correlated significantly with MA and PF4 secretion. High‐dose IL‐2‐treated patlents showed a statistically significant increase in the percentage of large platelets exceeding 12 fl in diameter and platelet responsiveness to hypotonic shock. These observations suggest that IL‐2 therapy results in a reduced peripheral platelet pool, with an increased proportion of the remaining pool of platelets larger, more viable, and actlvated. © 1994 Wiley‐Liss, Inc.
Erythropoietin in the treatment of delayed immune hemolysis of a major ABO‐incompatible bone marrow transplant
Authors: López J. , Steegmann J. L. , Pérez G. , Otero M. J. , Berberana M. , Cámara R. , Lamana M. , Villalta M. J. Fernández , Fernández‐Rañada J. M. 
Published: February 2007

AbstractDelayed immune hemolysls can be observed after major ABO‐incompatible bone marrow transplants (BMT). The management of these hemolytic eplsodes Includes transfuslofi of group O red blood cells and increases of immunosuppression. Here we report the case of a 25‐year‐old patient who developed overt immune hemolysis on day +50 after a HLA‐identical ABO‐incompatible BMT. To avoid added immunosuppression, erythropoietin was started: an Increase in reticulocytes sufficlent to maintain hemoglobin despite perslstent hemolysis was observed. We conclude that erythropoletin may have a role In the management of delayed‐onset hemolysis of major ABO‐incompatible BMT, especially when added Immunosuppresslon is undesirable. © 1994 Wiley‐Liss, Inc.
Pentosan polysulfate‐induced thrombocytopenia and thrombosis
Authors: Tardy‐Poncet Brigitte , Tardy Bernard , Grelac Françoise , Reynaud Jacqueline , Mismetti Patrick , Bertrand Jean Claude , Guyotat Denis 
Published: February 2007

AbstractPentosan polysulfate is a low‐molecular‐weight sulfated polysaccharide used as an antithrombotic drug. We present two patients who developed thrombocytopenia and venous thrombosis during treatment with pentosan polysulfate. The relationship between pentosan polysulfate and thrombocytopenia is supported by platelet aggregation and serotonin release tests. In the light of the literature and our two cases, it appears that pentosan polysulfate alone as standard heparin and low‐molecular‐weight heparin can induce thrombocytopenia and thrombosis. Platelet counts should therefore be periodically monitored during pentosan polysulfate treatment. In the case of pentosan polysulfate‐induced thrombocytopenia, it seems that heparin or low‐molecular‐weight heparin should not be instituted during the acute phase even it platelet aggregation studies are negative, because of their low sensitivity. After remission of thrombocytopenia, whether or not glycoaminoglycans can be reinstituted, at least temporarily, after antibody had disappeared is still an open question. © 1994 Wiley‐Liss, Inc.
Lineage determination of CD7+ CD5− CD2− and CD7+ CD5+ CD2− lymphoblasts: Studies on phenotype, genotype, and gene expression of myeloperoxidase, CD3ϵ, and CD3δ
Authors: Yoneda Noriko , Tatsumi Eiji , Teshigawara Keisuke , Nagata Shigekazu , Nagano Takahiro , Kishimoto Yuji , Kimura Takashi , Yasunaga Koujiro , Yamaguchi Nobuo 
Published: February 2007

AbstractThe gene expression of myeloperoxldase (MPO), CD3ϵ and CD3δ molecules, the gene rearrangement of T‐cell receptor (TCR)δ, γ, and β and Immunoglobulin heavy (IgH) chain, and the expression of cell‐surface antlgens were investigated In seven cases of CD7+ CD5− CD2− and four cases of CD7+ CD5+ CD2− acute lymphoblastic leukemia or lymphoblastic lymphoma (ALL/LBL) blasts, which were negative for cytochemical myeloperoxidase (cyMPO). More mature T‐lineage blasts were also investigated in a comparative manner. In conclusion, the CD7+ CD5− CD2− blasts included four categories: Undifferentiated blasts without lineage commitment, T‐lineage blasts, T‐/myeloid lineage blasts, and cyMPO‐negative myeioblasts. The CD7+ CD5+ CD2− blasts included two categories; T‐lineage and T‐/myeloid lineage blasts.The 11 cases were of the germ‐line gene (G) for TCRβ and IgH. Four cases were G for TCRδ and TCRγ. The others were of the monoclonally rearranged gene (R) for TCRδ and G for TCRγ or R for both TCRδ and TCRγ.The expression or In vitro induction of CD13 and/or CD33 antigens correlated with the immaturity of these neoplastic T cells, since it was observed In all 11 CD7+ CD5− CD2−and CD7+ CD5+ CD2−, and some CD7+ CD5+ CD2+ (CD3− CD4− COB‐) cases, but not in CD3± CD4+ CD8+ or CD3+ CD4+ CD8− cases.CD3ϵ mRNA, but not CD3δ mRNA, was detected in two CD7+ CD5− CD2− cases, while mRNA of neither of the two CD3 moleculea was detected In the other tested CD7+ CD5−CD2− cases. In contrast, mRNA of both CD3e and CD36 were detected in ail CD7+ CD5+ CD2− cases, indicating that CD7+ CD5+ CD2− blasts at least belong to T‐lineage.The blasts of two CD7+ CD5− CD2− cases with entire germ‐line genes and without mRNA of the three molecules (MPO, CD3ϵ, and CD3δ) were regarded as being at an undifferentiated stage prior to their commitment to either T‐ or myelold‐lineage.The co‐expression of the genes of MPO and CD3e In a CD7+ CD5− CD2− case or MPO, CD3ϵ, and CD3δ in a CD7+ CD5+ CD2− case suggested the presence of some overlapping phase for T‐ and myeloid‐lineage commitment during Immature stages of differentiation. This heips understand the conversion of some T‐ALL/LBL cases to acute myeloblastic leukemia (AML). The detection of CD3ϵ, but not CD3δ mRNA, in two CD7+ CD5− CD2−cases indicated that the gene expression of CD3ϵ occurs at a more immature stage of differentiation than that of the CD3δ chain. © 1994 Wiley‐Liss, Inc.
Myelomonocytic crisis with t(5;17) and a p53 mutation in a patient with chronic myelogenous leukemia
Authors: Nakagawa Hitoshi , Fujii Hiroshi , Nakai Hiroyuki , Inazawa Johji , Misawa Shinichi 
Published: February 2007

AbstractWe report a 64‐year‐old Japanese man with chronic myelogenous leukemia (CYL) who expired with myelomonocytlc crisis. Cytogenetic analyses of chronic phase (CP) and accelerated phase (AP) cells revealed a Philadelphia chromosome and an isochromosome for the long arm of chromosome 17, i(17q). This karyotype was replaced by another karyotype in blast crisis (BC), resulting in near triploidy with t(5;17) (p15;p11) and loss of chromosome 17pter→p11. Interphase fluorescent in situ hybridization studies with a chromosome 17 specific alpha satellite DNA probe confirmed the presence of a clonal change in BC. In addition, singie‐strand conformation polymorphism analysis and PCR‐direct sequencing of BC cells revealed a point mutation at codon 203 of the p53 gene, GAG to GAG (Val to Glu), and loss of the normal allele. In contrast, no alterations of the p53 gene were found in CP and AP cells. Therefore, progression of CML in this patient appeared to be related to loss of 17p, as well as a mutation in the p53 gene. © 1994 Wiley‐Liss, Inc.
Impact of reinduction regimens for relapsed and refractory acute lymphoblastic leukemia in adults
Authors: Welborn Jeanna L. 
Published: February 2007

AbstractThe clinical outlook for adults with acute lymphoblastic leukemia (ALL) has Improved with the use of intensive chemotherapy. Complete remissions (CR) are achieved in 80% of adults but the majority relapse on maintenance chemotherapy and a few exhibit primary resistance to induction therapy. This report compares the various salvage treatments and provides guidance in selecting a regimen with the optimum clinical outcome. Regimens using high‐dose ara‐C (HDAC) in combination with mltoxantrone, amsacrine, or idarublcin are superior to HDAC alone or with L‐asparaginase. The sequential administration of methotrexate and L‐asparaginase Is equally effective. The duration of second CR is short for all chemotherapeutic regimens. © 1994 Wiley‐Liss, Inc.
Erythropoiesis in primary (idiopathic) osteomyelofibrosis: Quantification, PCNA‐reactivity, and prognostic impact
Authors: Thiele Juergen , Windecker Roland , Kvasnicka Hans Michael , Titius Baerbel Ruth , Zankovich Rudolph , Fischer Robert 
Published: February 2007

AbstractIn 64 patients with primary (idiopathic) osteomyelofibrosis (OMF), a morphometric analysis has been performed on bone marrow trephine biopsies following sequential doubleimmunostaining with monoclonal antibodies against proliferating cell nuclear antigen (PCNA) and erythroid precursor cells (glycophorin C). The purpose of this study was to quantify erythropoiesis and its PCNA‐staining capacity and, further, to determine the impact of these parameters for the development of anemia and for prognosis. In comparison with a control group (15 patients), a significant reduction in the number of erythronormoblasts could be demonstrated, associated with an increase in PCNA‐labelling. Moreover, significant correlations between the amount of nucleated erythroid marrow cells and degree of anemia (hemoglobin level, hematocrit, erythrocyte count) and survival could be calculated. Adverse relationships were assessed between number of erythroid cells, thrombocyte count, and spleen size, and also argyrophilic (reticulin/collagen) fiber density. These interactions were thought to reflect the biological behaviour of the disease process, i.e., the progression or extent of myeloid metaplasia. Our findings support ferrokinetic studies suggesting erythroid hypoplasia as one of the major causes of anemia in OMF. The remarkable high PCNA‐labelling index of the macrocytic‐megaloblastoid appearing erythropoiesis is probably caused by an overexpression of this marker protein. A comparative evaluation of Ki‐67 antigen immunostaining in splenic tissue (myeloid metaplasia) and of the PCNA‐labelling in pernicious anemia lend support to the assumption of an undue prolongation of the S‐phase generated by secondary folate (hematinic) deficiency. © 1994 Wiley‐Liss, Inc.
Pure red cell aplasia after chemotherapy for Hodgkin's lymphoma: In vitro evidence for t cell mediated suppression of erythropoiesis and response to sequential cyclosporin and erythropoietin
Authors: Reid Thomas J. , Mullaney Mark , Burrell Linda M. , Redmond John , Mangan Kenneth F. 
Published: February 2007

AbstractAcquired pure red cell aplasia (PRCA) has been associated with various lymphoproliferative conditions but its occurrence with Hodgkin's disease is rare. We report a case of PRCA occurring immediately following the completion of induction chemotherapy in a patient with Stage IIIB nodular sclerosing Hodgkin's disease. In vitro erythroid colony studies documented evidence for T cell mediated suppression of erythropoiesis and lack of a serum inhibitor. Addition of cyclosporin to the in vitro cultures stimulated erythroid colony growth. Following in vivo treatment with cyclosporin peripheral blood CD4/CD8 ratios returned to normal. However, serum erythropoietin levels were inappropriately low. Subsequent treatment with erythropoietin induced a reticulocytosis and transfusion independence. Since discontinuing the erythropoietin, the patient has been able to maintain a hemoglobin of 100 g/L. This case illustrates that red cell aplasia occurring in the setting of Hodgkin's disease may be due to T cell mediated suppression of erythropoiesis. A response to cyclosporin may be masked by inappropriately low erythropoietin levels. © 1994 Wiley‐Liss, Inc.
Spontaneous remission of polycythemia vera: Clinical and cell culture characteristics
Authors: Cowan D. H. , Messner H. A. , Jamal N. , Aye M. T. , Smiley R. K. 
Published: February 2007

AbstractA 20‐year‐old woman presented with polycythemia vera and was treated with phlebotomy alone for eleven years, following which all clinical manifestations of the disease disappeared. The clinical remission with normal physical findings and normal peripheral blood counts has persisted for a further 11 years. Erythroid colony culture results have paralleled the clinical state. Initial bone marrow cultures revealed spontaneous growth of erythroid burst‐forming units (BFU‐E). Subsequent cultures of peripheral blood cells throughout most of the period of spontaneous clinical remission have revealed little or no spontaneous growth of BFU‐E. This suggests a suppression of the abnormal stem cell clone during the period of remission. © 1994 Wiley‐Liss, Inc.
Establishment of a human pro‐B cell line (JKB‐1) and its differentiation of preestablished bone marrow stromal cell layer
Authors: Urashima Mitsuyoshi , Hasegawa Notomi , Kamijo Makoto , Shishikura Akihiro , Kato Yoko , Hoshi Yasutaka , Akatsuka Jun‐Ichi , Maekawa Kihei 
Published: February 2007

AbstractA human pro‐B cell line, named JKB‐1, was established from the bone marrow of a 16‐year‐old girl with acute lymphoblastic leukemia (ALL) in relapse. The origin of the JKB‐1 cell line was indicated by its chromosomal and immunologic similarity to the patient's fresh leukemic cells. This cell line has been growing for more than 14 months in suspension culture medium and had a doubling time of about 24 hours. JKB‐1 expressed terminal deoxynucleotide transferase (TdT) and early antigens (HLA‐DR, CD19, CD24) of B cells, with heavy chain gene rearrangement. However, it did not express late antigens (CD10, CD20, CD21, CD22, CD23) of B cells, light chain gene rearrangement, and cytoplasmic μ‐chain. These results suggested that JKB‐1 is at the stage of “pro‐B” cell or early B‐cell precursors.This cell line was induced to differentiate after 7 days of co‐incubation with irradiated bone marrow stromal cells because of the expression of pre‐B cell antigens (CD10, CD20), cytoplasmic μ‐chain, light chain gene rearrangement, and disappearance of TdT. JKB‐1 cells adhered to a preestablished bone marrow stromal cell layer with string‐like processes under scanning electron microscope. When JKB‐1 cells were separated from the stromal layer by a cyclopore membrane with 0.45 μ pore size, they did not differentiate. Bone marrow stromal cell conditioned medium could not induce differentiation either. Thus it was suspected that direct contact between JKB‐1 cells and stromal cells was required for differentiation. In methylcellulose semisolid medium, the colony size and number of JKB‐1 cells were increased by stem cell factor (SCF), or interleukin (IL)‐3, or IL‐7, but they were decreased by IL‐6. Moreover, SCF synergized with IL‐3 or IL‐7 to stimulate the proliferation of JKB‐1 cells.Because there are very few reproducible models for examing early stages of human B‐cell differentiation, the JKB‐1 cell line would be useful for studying the relationship between human B‐cell differentiation and bone marrow microenvironment, as well as leukemogenesis. © 1994 Wiley‐Liss, Inc.
Sporotrichosis as a presenting manifestation of hairy cell leukemia
Authors: Kumar Shimareet , Kumar Dhruv , Gourley William K. , Alperin Jack B. 
Published: February 2007

AbstractAn infectious episode is the presenting manifestation of hairy cell leukemia (HCL) in approximately 30% of cases. Most often this is bacterial and only rare cases of opportunistic fungal infection are described. We report a patient who presented with sporotrichal involvement of multiple cutaneous sites and lymph nodes. The lesions resolved following antifungal therapy, but persisting pancytopenia and splenomegaly necessitated further hematological evaluation. A diagnosis of HCL was suspected based on morphologically characteristic hairy cells in the peripheral blood that contained tartrate resistant acid phosphatase. A bone marrow biopsy specimen had a normocellular marrow with an increase in interstitial lymphoid cells that stained with L26, MB2, and LN2 antibodies. On flow cytometry these cells were positive for the leukocyte common antigen, B cell markers, and the CD11c antigen confirming the diagnosis of HCL. We believe that this is the first report of sporotrichosis infection as a presenting manifestation of HCL. © 1994 Wiley‐Liss, Inc.
Acquired yon Willebrand's syndrome in association with a lupus‐like anticoagulant corrected by intravenous immunoglobulin
Authors: Hanley Debra , Arkel Yale S. , Lynch Jean , Kamiyama Mikio 
Published: February 2007

AbstractWe are reporting on a 47‐year‐old man who presented with a prolongation of the activated partial thromboplastin time (APTT) prior to orthopedic surgery. An evaluation suggested an inhibitor when his plasma prolonged a normal control APTT upon 50:50 solution of patients with normal plasma. The platelet‐neutralizing procedure (PNP), anticardiolipin antibody, and antinuclear antibody (ANA) were positive. Further studies revealed decreased von Willebrand factor ristocetin cofactor (vWF:RCoF), von Willebrand factor antigen (vWF:Ag), an inhibitor to vWF, and absent high‐molecular‐weight vWF multimeters. Assays of FVIII:C, FIX, and FXI were nonparallel to the standard curve. Intravenous immunoglobulin (IVIG) corrected the APTT, multimeric pattern, and FVIII:C by the 7th day postinfusion. This case demonstrates the efficacy of IVIG for acquired von Willebrand's syndrome (vWS) and also represents a unique combination of a lupus‐like anticoagulant and acquired vWS in a patient without the full serological requirement for systemic lupus erythematosus (SLE). Whether patients with acquired vWS and lupus inhibitors are more or less susceptible to either a thrombotic complication or hemorrhage is not established. Prospective studies for the incidence of lupus inhibitor/antiphospholipid syndromes and vWF deficiencies are needed to assess this question. © 1994 Wiley‐Liss, Inc.
Connective tissue components in serum in multiple myeloma: Analyses of propeptides of type I and type III procollagens, type I collagen telopeptide, and hyaluronan
Authors: Abildgaard Niels , Nielsen Johan Lanng , Heickendorff Lene 
Published: February 2007

AbstractThe present study was performed to evaluate whether information concerning synthesis and degradation of type I collagen in multiple myeloma (MM) as obtained by serum analyses of C‐terminal propeptide of type I procollagen (PICP) and the C‐terminal telopeptide of type I collagen (ICTP) may be useful in evaluating the development of osteolytic bone destruction. Serum N‐terminal propeptide of type III procollagen (PIIINP) may give information about marrow fibrosis in MM. No data are available about MM and serum hyaluronan, another important component of bone marrow stroma. We examined 15 consecutive patients before treatment and 15 sex‐ and age‐matched controls. We found highly significant elevations in serum ICTP (median 6.2 vs. 2.4 μg/L; P < 0.01), PIIINP (median 5.2 vs. 2.9 μ/L; P < 0.01) and hyaluronan (median 122 vs. 45 μ/L; P < 0.01). ICTP in serum correlated closely to bone morbidity (r = 0.69; P < 0.01). Furthermore, serum ICTP correlated highly significantly to serum PIIINP (P < 0.01) and serum β2‐microglobulin (P < 0.01), whereas there was no correlation between hyaluronan and any of the collagen‐derived peptides or β2‐microglobulin. The MM group was followed for 9–25 months and analysis of survival data suggested that serum ICTP may be of predictive value (P < 0.05). We conclude that important changes in connective tissue metabolism occur in MM. ICTP in serum seems to be a noninvasive marker of bone morbidity and may be of prognostic value. Furthermore, elevation of hyaluronan in serum is common in MM, the significance of which is unknown. © 1994 Wiley‐Liss, Inc.
Recombinant tissue plasminogen activator (rt‐PA) for veno‐occlusive liver disease in pediatric autologous bone marrow transplant patients
Authors: Yu Lolie C. , Malkani Indrani , Regueira Oswaldo , Ode David L. , Warrier Raj P. 
Published: February 2007

AbstractThe pathogenesis of veno‐occlusive disease (VOD) of the liver appears to be secondary to endothelial damage of terminal hepatic venules, which leads to activation of the coagulation cascade, fibrin deposition, and eventual fibrous obliteration of the hepatic venules. Patients with VOD usually present with jaundice, hepatomegaly, weight gain, and ascites. This complication is usually associated with a high mortality rate.We report here the frequency and treatment of VOD in our autologous bone marrow transplant (BMT) patient population. Three of 15 (20%) children (median age 9 years) developed VOD and were treated with recombinant tissue plasminogen activator (rt‐PA). Two of these three patients were prepared for BMT with busulfan (16 mg/kg) and cyclophosphamide (Cytoxan, 200 mg/kg), while the other child received cytosine arabinoside (ARA‐C 18 g/m2), Cytoxan (3,600 mg/m2) and total body irradiation (TBI, 1,400 r). VOD developed between days 7–24 posttransplant. Clotting studies obtained pretransplant and during VOD included prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen, fibrin‐degradation product (FDP), proteins C and S, and platelet count. There was no correlation between the incidence of VOD and coagulation status. All patients had normal pretransplant clotting studies. However, protein C levels were noted to be consistently low for those patients at the time of VOD.All three patients received rt‐PA at a dose of 0.25–0.5 mg/kg for 4 days. This dose produced increased levels of FDP but did not significantly prolong PT nor PTT. Two of the patients had dramatic responses and had complete resolution of VOD within 6–12 days from the start of therapy. The other patient died of fulminant hepatic failure. It seems that rt‐PA is effective in VOD of the liver, which may be associated with low protein C level. © 1994 Wiley‐Liss, Inc.