bluuebunny/crossref_metadata_2025_split huggingface dataset:
Myeloid differentiation antigen defined by a monoclonal antibody IF10
Authors: Yamada K. , Okabe N. , Saito H. , Suzuki R. , Kumagai K. 
Published: February 2007

AbstractA monoclonal antibody of IgM class that defines the antigen present on human peripheral blood granulocytes was produced and characterized. This monoclonal antibody (IF10) was made from a single fusion between P3‐X63‐Ag8‐U1 (P3U1) myeloma cells and splenoctyes from a BALB/c mouse immunized against human cultured monocytoid cell line THP‐1 cells. IF10‐defined antigen(s) was expressed on the cells of granulocyte lineage such as peripheral blood granulocytes and metamyelocytes, myelocytes, promyelocytes, and a part of myeloblasts in the normal bone marrow, whereas it was not detected on resting and activated T lymphocytes, B lymphocytes, adherent monocytes, and thymocytes. The IF10‐defined antigen was also expressed on cultured monocytoid cell lines as well as myeloid and myeloid/erythroid (K‐562) cell lines. T lymphoblastoid cell lines, particularly those representing the T cells at an early thymocyte level, and a part of null cell lines were also reactive to IF10. Therefore, IF10 may be a unique monoclonal antibody that defines an antigen(s) which is expressed on almost whole stages of granulocytes and early stages of macrophages and T‐cell lineages, and possibly during very early stages of erythroid lineage.
Requirements for growth of human erythroid progenitors in nutrient agar
Authors: Januszewicz E. , Cooper I. A. , Bradley T. R. 
Published: February 2007

AbstractHuman erythroid bursts and neutrophil colonies from fetal liver, term cord blood, and adult bone marrow were grown in nutrient agar, and the colonies were scored using a fixed whole plate method. Human placental conditioned medium was shown to contain burst promoting activity, and low oxygen tension markedly enhanced growth of erythroid bursts. Morphological analysis of colonies showed that eosinophil colonies were more numerous in bone marrow than fetal liver and conversely macrophage and neutrophil‐macrophage colonies were more numerous in fetal liver. Erythroid bursts were more numerous and larger in fetal liver. Human fetal liver cells do not produce endogenous colony‐stimulating factor.
Ultrastructural studies of myeloma cells: Observations concerning the Golgi apparatus and intermediate‐size filaments
Authors: Pavelka Margit , Ludwig Heinz 
Published: February 2007

AbstractStudies on the ultrastructure of tumor cells of 22 multiple myeloma patients revealed hitherto unreported observations concerning the Golgi apparatus and intermediate‐size filaments. Various abnormalities of the Golgi apparatus including displacements of the Golgi stacks, dilatations of cisternae, and massive accumulations of vesicles as well as vacuoles in the Golgi region were found in myeloma cells of 11 patients.Intermediate‐size filaments forming a fine intracytoplasmic network were apparent in myeloma cells of all 22 patients. In five patients, in addition to this architecture, intermediate‐size filaments were gathered into thick bundles which were primarily but not exclusively located in the perinuclear region.
Intracranial myeloid metaplasia: Diagnosis by CT and Fe52 scans and treatment by cranial irradiation
Authors: Cornfield Dennis B. , Shipkin Paul , Alavi Abass , Becker Joseph , Peyster Robert 
Published: February 2007

AbstractA patient with longstanding agnogenic myeloid metaplasia developed a progressive dementia. CT scanning demonstrated multiple intracranial masses, and a Fe52 bone marrow scan demonstrated erythroid activity within the masses and confirmed the suspicion of extramedullary hematopoiesis. A potentially hazardous biopsy was avoided, and a course of cranial irradiation was administered, resulting in regression of the masses and clearing of the patient's dementia. Fe52 scintigraphy provides a specific and useful diagnostic approach which may eliminate the need for invasive procedures.
Inhibition of cold insolubility of an IgA cryoglobulin by decanedicarboxylic acid and related compounds
Authors: Lalezari Parviz , Kumar Mahendra , Kumar Kalpana M. , Lawrence Christine 
Published: February 2007

AbstractCold insolubility of a serum IgA cryoimmunoglobulin was found to be inhibited by the addition of 1.5 mM sodium decanedicarboxylate in vitro. The patient with the cryoglobulin had advanced multiple myeloma complicated by severe hyperviscosity that caused lethargy and episodic loss of consciousness. Decanedicarboxylic acid administered orally resulted in transient relief of symptoms and the loss of cryoprecipitability of the paraprotein. Further in vitro studies revealed that sodium salts of long‐chain monocarboxylic acids with a minimum of eight carbons, and dicarboxylic acids with a minimum of 12 carbons inhibited cryoprecipitation. Salts of short‐chain carboxylic acids, by contrast, enhanced cryoprecipitation. Sodium phenolate and sodium salts of benzoic acid, 2,4‐DNP, phenylpropionic acid, and salicylic acid were also inhibitory. These latter compounds, which have a ring structure, did not cause precipitation at any concentration. It was demonstrated that the presence of a free carboxylic group was required for these activities; conversion of carboxylic acid to amide resulted in the loss of both the inhibitory and cryoprecipitation‐enhancing effects. Normal plasma, or plasma from five other patients who had IgG, IgM, or mixed‐type cryoglobulinemia, were not affected by any of these compounds. It is suggested that in selected cases of hyperviscosity syndrome associated with cryoglobulinemia, some of these compounds, especially monocarboxylic acids with appropriate chain lengths, or those with a ring structure, may have therapeutic applications.
Chronic myelomonocytic leukemia with a chromosome abnormality (46,XY,20q–) in all dividing myeloid cells: Evidence for clonal origin in a multipotent stem cell common to granulocyte, monocyte, erythrocyte, and thrombocyte
Authors: Shinohara Tamiko , Takuwa Noriko , Morishita Kazuhiro , Ieki Ryuji , Yokota Jun , Nakayama Emiko , Asano Shigetaka , Miwa Shiro 
Published: February 2007

AbstractIn a typical case of chronic myelomonocytic leukemia (CMML), a chromosome abnormality, 46, XY,20q‐, was observed in all the dividing cells including up to 16‐ploid cells in the bone marrow and the blood. As the mitotic figures could be easily seen not only in myelomonocytoid cells but also in erythroblasts in the bone marrow smear, it was concluded that all the cell lineages except lymphocytes had the abnormality. The present case will support the view that the leukemic process in CMML affects a multipotent stem cell rather than a granulocyte‐monocyte committed stem cell.
Increased serum procollagen III aminoterminal peptide in myelofibrosis
Authors: Hochweiss S. , Fruchtman S. , Hahn E. G. , Gilbert H. , Donovan P. B. , Johnson J. , Goldberg J. D. , Berk P. D. 
Published: February 2007

AbstractMyelofibrosis has been shown to involve an increase in type III collagen in the marrow. The aminoterminal procollagen III (PC III) peptide fragment is released during the production of PC III by fibroblasts and its serum level is therefore a marker for type III collagen synthesis. Using a recently developed sensitive radioimmunoassay, serum levels of PC III peptide were measured in 30 patients with myeloproliferative disease and 23 normal volunteers. Levels were found to be elevated above normal values in patients with polycythemia vera, even more elevated in patients with polycythemia and evidence of secondary myelofibrosis with mycloid metaplasia, and most strikingly elevated in patients with agnogenic myeloid metaplasia and severe marrow fibrosis. There was a significant association between serum levels of PC III peptide and the extent of reticulin fibrosis in bone marrow biopsies. Serum PC III level appears to be a quantitative marker for myelofibrosis.
Analysis of transformation with epstein‐barr virus and phenotypic characteristics of lymphoblastoid cell lines established from patients with hairy cell leukemia
Authors: Sairenji Takeshi , Spiro Robert C. , Reisert Patricia S. , Paquin Louise , Sakamoto Kiyoshi , Shibuya Atsushi , Suilivan John L. , Katayama Isao , Humphreys Robert E. 
Published: February 2007

AbstractIn order to assess the role of Epstein‐Barr virus (EBV) in patients with hairy cell leukemia (HCL), we have sought to characterize 1) the ability of EBV to infect and transform hairy leukemic cells in vitro and 2) the phenotypes of cell lines putatively derived from those leukemic cells. Analysis of EBV‐induced transformation and the kinetics of Epstein‐Barr nuclear antigen (EBNA) induction in leukemic preparations indicated that most leukemic cells were not susceptible to EBV infection but that at least a small subpopulation of leukemic cells could be infected with EBV. Lymphoblastoid cells lines were established after exposure of peripheral blood or splenic cells from HCL patients to B95‐8 or QIMR‐WIL EBV. Splenic leukemic cell preparations were more sensitive targets for EBV transformation than were peripheral blood cell samples. The newly established cell lines, but not long‐established B lines such as Raji, demonstrated high levels of synthesis of p35, (a protein complex expressed abundnatly by cells of a subset of HCL patients) and high levels of tartrate‐resistant acid phosphatase (an enzyme relatively diagnostic for HCL). Lymphoblastiod lines from one patient with HCL expressed lambda light chains and no kappa chains as did the patient's leukemic cells. Virus expression in these lines showed that HCL‐derived lines had spontaneous earley antigen (EA) and viral capsid antigen (VCA) expression Tranforming EBV could be rescued from HCL‐derived cell lines but not from cord blood‐derived lines.
Change of pyruvate kinase (PK) isozymes in classical type pk deficiency and other PK deficiency cases during red cell maturation
Authors: Takegawa S. , Miwa S. 
Published: February 2007

AbstractConversion of pyruvate kinase (PK) isozymes during the maturation of erythroblasts in five cases of PK deficiency was compared with that in normal subjects using immunofluorescent antibody techniques. In normal erythroblasts, M2‐type PK was clearly seen at the proerythroblast stage, then markedly declined with cell maturation whereas L‐type PK continued to increase. In two patients with classical type PK deficiency, M2‐type PK was still clearly seen in orthochromatic erythroblast, whereas L‐type PK was hardly detected during maturation. In three patients with other types of PK deficiency, change of L‐type PK was similar to that of normal subjects whereas M2‐type PK was clearly seen even at the later stage of maturation as in classical‐type PK deficiency. The present studies indicate that compensatory M2‐type PK production occurs in the erythroblasts of patients with PK deficiency.
Analysis of T‐cell subsets in B‐cell chronic lymphocytic leukemia: A correlation with the stage of disease
Authors: Mittelman A. , Denny T. , Gebhard D. , Cirrincione C. , Kurland E. , Koziner B. 
Published: February 2007

AbstractT‐cell subsets were determined by the Leu monoclonal antibodies in the peripheral blood and/or bone marrow of 52 patients with B‐cell chronic lymphocytic leukemia (B‐CLL) not on therapy at the time of study. The diagnosis of B‐CLL required that the leukemic cells expressed surface receptors for “la‐like” antigen, Fc fragment of IgG, mouse red blood cells (MRBC), C3‐coated red cells (EAC), and low density of monoclonal surface immunoglobulin. The Leu‐3a+/2a+ ratio was applied to define the balance between the helper/suppressor subsets in the residual T‐lymphocytes. Most patients showed a decrease in the Leu‐3a+/2a+ ratios at all stages of disease. The decrease in ratio was mainly related to a decrease in the Leu‐3a+ T‐cell subset. The more advanced stages of B‐CLL were associated with lower Leu‐3a+/2a+ ratio, higher total white cell and percent lymphocyte counts. There was no correlation between the proportion of EAC or MRBC rosetting cells and stages of B‐CLL. This analysis further suggests that B‐CLL is an immunosuppressed state that becomes more pronounced in the advanced stages and is characterized by a progressive decrease in the Leu‐3a+ (helper) T‐cell subset.
Intestinal infarction caused by paroxysmal nocturnal hemoglobinuria
Authors: Doukas Michael A. , Dilorenzo Paul E. , Mohler Daniel N. 
Published: February 2007

AbstractA patient with paroxysmal nocturnal hemoglobinuria of 14 years duration presented with severe abdominal pain and fever. On admission, his hematocrit had fallen to 19% from his usual level of approximately 30%, and stools were positive for occult blood. Dilated loops of small bowel with air fluid levels were noted on radiographs, and sonography revealed free intraperitoneal fluid. Several sections of gangrenous jejunum and ileum were resected at exploratory laparotomy, and mesenteric venous thromboses were present. This is the second report of pathologically proven intestinal infarction in a patient with paroxysmal nocturnal hemoglobinuria who has survived this abdominal emergency with surgical intervention. Although abdominal pain in patients with paroxysmal nocturnal hemoglobinuria has frequently been attributed to mesenteric venous thromboses, this has rarely been documented either during life or at autopsy.
HB F‐Yamaguchi (γ75THR, γ80ASN, γ136ALA) is associated with Gγ‐thalassemia
Authors: Nakatsuji T. , Ohba Y. , Huisman T. H. J. 
Published: February 2007

AbstractRestriction endonuclease analyses of DNA from a known Hb F‐Yamaguchi heterozygote and three of his relatives have shown a deletion of about 5 kb, which includes one of the γ genes. This abnormality is similar to the Gγ‐thalassemia described recently [4] and is probably caused by an unequal crossing over between ‐Gγ‐ and ‐AγT‐genes. The abnormal ‐GγAγT‐X‐ (X = Asp→Asn at γ80) hybrid gene produces the γ‐Yamaguchi chain at a level usually seen for Gγ chains only.
Tumor interaction with hemostasis: The rationale for the use of platelet inhibitors and anticoagulants in the treatment of cancer
Authors: Al‐Mondhiry Hamid 
Published: February 2007

AbstractClinical and experimental observations have firmly established the concept of a two‐way interaction between malignancy and the hemostatic system. On the one hand, certain tumors can activate platelets and the coagulation mechanism in vivo, on the other, a convincing case has been made for the involvement of platelets and fibrin in tumor growth and metastasis. A large number of clinical and experimental studies have been conducted in order to test the efficacy of platelet inhibitors and anticoagulants as adjuvants in the treatment of cancer. Antiplatelet drugs gave variable results, depending on the drug and the tumor system tested. Prostaglandin synthetic pathways by both the host and tumor seem to be an important determinant in the response to platelet function inhibitors. Of the various anticoagulants tested, the coumarin derivatives gave somewhat consistent antitumor effect in certain human and experimental cancer. The antitumor effect of oral anticoagulants does not appear to be a primary drug effect and seems related to their role as vitamin K antagonists. It should be emphasized that although the antitumor potential of antithrombotic agents is a subject of keen interest at the present, their use in treating human cancer is still controversial.
Thalassemia‐like abnormalities of the red cell membrane in hemoglobin E trait and disease
Authors: Dorléac E. , Morlé L. , Gentilhomme O. , Jaccoud P. , Baudonnet C. , Delaunay J. 
Published: February 2007

AbstractIn recent studies, we observed a decrease of KMapp, an abnormally biphasic kinetics of the red cell membrane neutral phosphatase and an increased binding of hemoglobin to the membrane in various forms of β‐thalassemia. Since the gene encoding the β chain (βE chain) of hemoglobin E (HbE) is endowed with some thalassemic characteristics, we studied the erythrocyte membrane in 25 individuals with Hb E trait or disease. The apparent Michaelis‐Menten constant for p‐nitrophenylphosphate (the artificial substrate used) was significantly decreased, as in β‐thalassemia. However, the kinetics was monophasic in all the heterozygotes and in four of the homozygotes. It was biphasic only in the three other homozygotes. Vmax was also significantly reduced, a fact that is masked, when not reversed in β‐thalassemia, owing to the rejuvenation of the red cell population. In 5 mM phosphate buffer (pH 8.00), the binding of Hb E to the erythrocyte ghosts was increased in the homozygotes. In the heterozygotes, Hb A binding was also increased, as is the case in β‐thalassemia. This latter fact suggests that the membrane binding site(s) of hemoglobin is (are) altered. We found a highly significant increase of Hb F in EE subjects. The present study extends to the red cell membrane the β‐thalassemic phenotype associated with the βE gene.
Sideroblastic anemia: Differences in bone marrow erythroid colony (CFUe) growth responses to erythropoietin in plasma clot and methylcellulose cultures
Authors: Lutton J. D. , Ibraham N. G. , Hoffman R. , Ritchey A. K. , Levere R. D. 
Published: February 2007

AbstractBone marrow cells from three patients with idiopathic acquired sideroblastic anemia and one with X‐linked sideroblastic anemia were simultaneously cultured in plasma clot and methylcellulose cultures in order to evaluate their erythroid colony (CFUE) cloning potential in these two systems. In contrast to normals, sideroblastic anemia bone marrow cells demonstrated a marked ability to form erythropoietin (Epo)‐independent CFUE in methylcellulose culture, and were inhibited in their ability to generate CFUE in plasma clot culture even in the presence of Epo.Addition of citrated plasma to methylcellulose cultures inhibited Epo‐independent CFUE growth, but not Epo‐dependent growth, by both a normal and patients' bone marrow cells. These results demonstrate that bone marrow cells from some patients with sideroblastic anemia can undergo Epo‐independent and Epo‐dependent CFUE growth in vitro, and that there is a marked difference in CFUE growth depending on the type of clonal culture method used. It is suggested that the culture microenvironment, plasma, and sensitivity to Epo may be contributing factors which allow specific clones of sideroblastic anemia CFUE‐forming cells to proliferate in vitro.
“Leukemic” pattern of in vitro growth in a patient with Down syndrome and transient myeloproliferative disorder
Authors: Mendelow Barry , Krawitz Selma , Cohn Richard , Bernstein Renée 
Published: February 2007

AbstractPeripheral blood cells from a female infant with Down syndrome and over 60% circulating myeloblasts were cultured in soft agar. Growth was virtually restricted to cluster formation, and cluster‐forming cells resided almost exclusively in the very light density fraction (SG < 1.062). Morphological assessment of clusters revealed no evidence of cellular differentiation beyond the blast cell stage. Despite receiving no specific chemotherapy, the peripheral blood normalized within 2 months, and there was no evidence of leukemia when the patient died aged 1 year from cardiac pathology. The findings indicate that caution should be exercised when assessing prognosis on the basis of in vitro growth characteristics in such patients.
In vitro neutrophil‐erythrocyte rosette formation mediated by a serum factor (IgG)
Authors: Mirchandani Ila , Palutke Margarita , Kithier Karel , Tabaczka Pamela , Suffian Jacqueline 
Published: February 2007

AbstractIn vitro neutrophil‐erythrocyte rosette (NER) formation occurred in the peripheral blood of an elderly man. This caused problems in cross‐matching for blood transfusion initially but was resolved by performing crossmatches at 37°C because this phenomenon was temperature‐dependent. NER formation was independent of complement and of the type of anticoagulant used. NERs were induced using normal control cells with the patient's plasma, serum, and the IgG fraction of serum. The resetting factor was adsorbed by heterologous group‐specific erythrocytes, but not by leukocytes. No neutrophil antibodies were identified.
Preparation of young red cells for transfusion using the fenwal CS 3000 cell separator
Authors: Pisciotto Patricia , Kiraly Thomas , Rosen Debra , Paradis Lois , Kakaiya Ram M. , Morse Edward E. 
Published: February 2007

AbstractA pheresis procedure was devised to isolate young red cells by centrifugation using the Fenwal CS 3000 continuous flow cell separator. Young red cell enriched products were collected in a 2.5–3‐hour procedure. Large numbers of white cells and platelets were collected with the red cells, but cryopreservation and subsequent washing removed 99% of the contaminating cells. At the completion of all processing a product yielding 70% of the total hemoglobin content of a standard frozen/deglycerolized red cell unit was produced. Autologous radiochromium survival of young red cells, measured in 12 normal donors, showed an average 24‐hour recovery of 89.9% with a T50Cr of 40.8 days. In paired autologous studies (N = 4) there was a mean increase of 35% in the observed T50Cr of young red cells as compared to standard frozen red cells.
Human monocyte interaction with antibody‐coated platelets. I. General characteristics
Authors: Court Wayne S. , Christensen A. Kent , Sacks Roger W. , Lobuglio Albert F. 
Published: February 2007

AbstractThe interaction of human monocytes with antibody‐coated and normal platelets was studied using an assay system that employed rate zonal centrifugation to separate monocyte‐associated (bound) platelets from free platelets. At a monocyte:platelet ratio of 1:10, monocytes bound 21.2 ± 6.6% of antibody‐coated platelets and less than 2.2 ± 1.3% of control platelets. Monocyte binding of antibody‐coated platelets was rapid and inhibited by monomeric IgG and staphylococcal protein A. Specific binding was positively related to the number of monocytes present and the amount of IgG displayed on the platelet surface. Transmission and scanning electron micrographs illustrate the membrane binding of antibody‐coated platelets to monocytes and suggest that phagocytosis of platelet targets occurs as well. Thus, these observations indicate that monocytes can participate in Fc‐receptor binding of anti‐PLA1‐sensitized platelets. This novel assay may be useful in the analysis of monocyte‐macrophage Fc‐receptor interaction with platelets sensitized with IgG from both iso‐ and autoimmune disorders as well as in the characterization of treatment modalities which may alter monocyte Fc‐receptor recognition and binding.