bluuebunny/crossref_metadata_2025_split huggingface dataset:
Morphologic characteristics of acute lymphoblastic leukemia (ALL) with abnormalities of chromosome 8, band q24
Authors: Davey F. R. , Lawrence D. , Maccallum J. , Varney J. , Hutchison R. , Wurster‐Hill D. , Schiffer C. , Sobol R. E. , Ciminelli N. , le Beau M. , Bloomfield C. D. 
Published: February 2007

AbstractThe CALGB prospectively studied 140 adult acute lymphoblastic leukemia (ALL) patients for cytogenetic abnormalities. Seven (5%) patients with adequate cytogenetic preparations had t(8;14)(q24;q32) or t(8;22)(q24;q11). Patients were compared with non‐8q24 patients for clinical and laboratory characteristics, response to therapy, and survival. The median age of patients with translocations involving 8q24 (71% males) was 40 years. Forty‐three percent had lymphadenopathy, 29% splenomegaly, and 29% hepatomegaly. None exhibited central nervous system (CNS), skin, or gum involvement. These features did not differ significantly from non‐8q24 ALLs. Patients with 8q24 translocations had higher hemoglobins (11.5 vs. 9.8 g/dl; P = 0.04) and lower percentage of blasts in the peripheral blood (8.5% vs. 69%; P = 0.007). Although all seven were finally categorized as ALL‐L3, a marked variation in the proportion of typical L3 blasts was observed that initially resulted in the diagnoses of ALL‐L2 in three cases and prolymphocytic leukemia in one. In five of five patients, the blasts typed as B cells (Slg+ and CD19+). Complete remission rates for patients with 8q24 translocations were 43%, whereas they were 68% for non‐8q24 ALLS (P = 0.22). Furthermore, patients with 8q24 abnormalities exhibited significantly shorter survival (4.8 vs. 18.4 mo; P < 0.001). We conclude that ALL with translocations of 8q24 in adults shows a mature B‐cell immunophenotype (Slg+), poor prognosis and morphology ranging from classical ALL‐L3 to ALL with a subpopulation of L3 cells. Thus, the diagnosis of ALL‐L3 should be made when blastic cells possess a mature B‐cell immunophenotype (SIg+) and an 8q24 translocation, even though the number of L3 cells is low. © 1992 Wiley‐Liss, Inc.
Role of splenectomy in the management of hemophilic patients with human immunodeficiency virus‐associated immunopathic thrombocytopenic purpura
Authors: Leissinger Cindy A. , Andes W. Abe 
Published: February 2007

AbstractImmunopathic thrombocytopenic purpura (ITP) can be a life‐threatening complication of human immunodeficiency virus (HIV) infection in patients with hemophilia and can seriously compromise quality of life if not managed effectively. We report here complete response to splenectomy in four severe hemophiliacs with HIV‐associated ITP. All patients were symptomatic, had platelet counts less than 25,000/mm3, and had failed at least one non‐surgical therapy prior to splenectomy. All patients tolerated surgery well and obtained an immediate and durable complete response. In addition to our experience, a review of the literature shows that splenectomy is well tolerated and provides the most effective long‐term solution for hemophiliacs with HIV‐ITP. © 1992 Wiley‐Liss, Inc.
Phorbol ester‐induced hairy cell features on chronic lymphocytic leukemia cells in vitro
Authors: Ai‐Katib Ayad , Wang Chang Yi , McKenzie Susan , Clarkson Bayard D. , Koziner Benjamin 
Published: February 2007

AbstractLeukemic cells from eight patients with chronic lymphocytic leukemia were isolated and cultured in the continuous presence of 12‐O‐tetradecanoylphorbol 13‐acetate (TPA) at a concentration of 1.6 × 10−9 M for 4–10 days. Aliquots of cells were then analyzed at intervals of 24–72 hr for changes in morphology, acid phosphatase staining (AP), and expression of two hairy cell‐associated surface antigens, HCL1 (CD22, Leu 14) and HCL3 (CD11c, Leu M5). All cases studied showed typical B‐CLL phenotype, and only a small proportion of cells expressed CD22 and CD11c (mean 7% and 4.9%, respectively). TPA treatment induced the coexpression of CD22 (mean 49%) and CD11c (mean 48%) and tartrate‐resistant acid phosphatase in seven of eight cases. Morphologically, cells in TPA cultures expressed hairy cell features that were evident in light and electron microscopic studies. Collectively these changes indicate that TPA can induce hairy cell features on CLL cells in vitro, suggesting the later maturational stage of HCL compared with CLL. © 1992 Wiley‐Liss, Inc.
Laboratory and clinical aspects of inherited thrombotic disorders
Authors: Rodgers George M. , Chandler Wayne L. 
Published: February 2007

AbstractThe laboratory evaluation of patients with recurrent thrombosis is frequently frustrating, with a low diagnostic yield obtained despite extensive testing. The likelihood of reaching a diagnosis in these patients can be increased by considering diagnostic possibilities usually overlooked and by using assays optimal for their detection. This review summarizes clinical and laboratory issues important in inherited thrombotic disease and discusses practical aspects and a strategy for laboratory testing. New information is provided on the fibrinolytic disorders that may be a common cause of recurrent thrombosis. © 1992 Wiley‐Liss, Inc.
A new case of acute lymphoblastic leukemia B‐cell type with chromosomal rearrangements involving the T‐cell receptor breakpoint at band 14q11
Authors: Cigudosa J. C. , Calasanz M. J. , Gullón A. , Prósper F. , Cuesta B. , Rifón J. , Rocha E. 
Published: February 2007

AbstractA patient with B‐cell acute lymphoblastic leukemia (ALL) and a translocation t(8;14) (q24;q11) is described. Translocation t(8;14)(q24;q32) is commonly associated with B‐cell leukemia; nevertheless, translocations affecting chromosome 14 at band q11 are associated with T‐cell malignancies, since the locus 14q11 contains genes that encode for the α and δ chains of the T‐cell receptor (TCR). This finding points to the idea that the association between 14q11 rearrangements and T‐cell neoplasia is less than complete. © 1992 Wiley‐Liss, Inc.
Influence of calcium permeabilization and membrane‐attached hemoglobin on erythrocyte deformability
Authors: Friederichs E. , Farley R. A. , Meiselman H. J. 
Published: February 2007

AbstractThe present study was designed to evaluate the influence of intracellular calcium [Ca]1 regulated membrane attached hemoglobin (Hbm) on the deformability of human RBC and ghosts. [Ca]1 of RBC was elevated via the Ionophore A23187 (10 μM); the deformability of RBC and resealed ghosts was determined via measuring RBC and ghost transit times through 5 μm diameter pores with the Cell Transit Analyzer (CTA). Salient results included: (1) significantly increased RBC levels of Hbm following ionophore treatment; (2) elevated Hbm with increasing lysing medium calcium concentration (0–5 mM); (3) decreased deformability of both intact RBC and ghosts with increasing Hbm and significant (P < 0.02 or better) linear relationships between Hbm and RBC or ghost transit times; and (4) an increased sensitivity to ionophore treatment/membrane attached hemoglobin for the higher percentiles of the CTA transit time distribution (i.e., for more rigid subpopulations). Our results thus indicate that calcium‐induced interaction of hemoglobin with the RBC membrane produces cellular rheological changes; in addition, they demonstrate the usefulness of the CTA system in measuring both average RBC rheologic behavior and the distribution of cellular rheologic properties within an erythrocyte population. © 1992 Wiley‐Liss, Inc.
Treatment of acute myeloid leukemia in the elderly with low‐dose cytarabine, hydroxyurea, and calcitriol
Authors: Slapak Christopher A. , Desforges Jane F. , Fogaren Terry , Miller Kenneth B. 
Published: February 2007

AbstractTwenty‐nine patients aged 62–82 years with acute myeloid leukemia (AML) were treated with a 21‐day course of continuous infusion cytarabine, oral hydroxyurea, and 1,25‐dihydroxyvitamin D3 (calcitriol). Ten patients had an antecedent myelodysplastic syndrome. Calcitriol was continued as the only postremission therapy. Thirteen patients (45%) obtained a complete remission, and 10 patients (34%) had a partial response for an overall 79% response rate. There were three early deaths. The median remission duration was 9.8 months. Overall median survival was 12 months for all patients and 14 months for responding patients. All responding patients had marked bone marrow hypoplasia. Twenty patients received part or all of their chemotherapy as outpatients. This regimen has acceptable toxicity and can result in prolonged remissions in elderly, high‐risk patients with AML. The favorable results may be related to the synergistic effect of hydroxyurea, cytarabine, and calcitriol. © 1992 Wiley‐Liss, Inc.
Serum granulocyte colony‐stimulating factor in patients with repeated infections
Authors: Kawakami Mutsumi , Tsutsumi Hisashi , Kumakawa Toshiro , Hirai Makiko , Kurosawa Shinichiro , Mori Mayumi , Fukushima Masafumi 
Published: February 2007

AbstractWe have already reported significant elevation of serum granulocyte colony‐stimulating factor (G‐CSF) in the acute phase of infection. In this study, we compared the responses to infection between patients with frequently repeated infection (repeaters) and others (non‐repeaters). We examined the clinical data and serum G‐CSF levels in 48 patients with acute infections. Serum G‐CSF levels were significantly lower in repeaters than in non‐repeaters (197.7 ± 370.0 vs. 1014.1 ± 924.4 pg/ml. P < 0.001). There were no significant differences in age, serum total protein, or cholinesterase between the groups, but serum albumin was significantly lower in repeaters than in non‐repeaters (2.87 ± 0.5 vs. 3.31 ± 0.4 g/dl. P < 0.005). It is suggested that administration of recombinant G‐CSF may be useful for patients with repeated infections. © 1992 Wiley‐Liss, Inc.
Reduced erythropoietin secretion in senile anemia
Authors: Kario Kazuomi , Kodama Kazuya , Matsuo Takefumi , Nakao Kazukiyo , Asada Reiko 
Published: February 2007

AbstractTo investigate the etiology of the age‐related decrease in hemoglobin (Hb) concentration, we measured serum erythropoietin (EPO), serum iron, total iron binding capacity, and serum feritin levels in 247 elderly subjects aged 60–99 years. EPO levels were determined by radioimmunoassay. An age‐related increase in the serum EPO concentration (r = 0.220; P < 0.01) and a significant inverse relationship between EPO and Hb concentrations were found in normal elderly subjects without anemia (r = –0.302; P < 0.001), but not in 111 younger controls. Serum EPO levels were slightly higher in elderly subjects with preanemic iron deficiency than in the normal elderly subjects (P < 0.05). These results suggest that the EPO secretion is accelerated in the elderly even though the Hb remains above 12.0 g/dl, probably as a compensatory mechanism for peripheral tissue hypoxia. An inverse relationship between the EPO and Hb concentrations was found in the elderly subjects with iron deficiency anemia, but not in those with unexplained senile anemia. The changes of EPO levels were also assessed in 20 elderly subjects who had developed anemia when reviewed after 12 months. Serum EPO levels increased in relation to the decrease in Hb concentration in those with iron deficiency anemia, but not in those with unexplained senile anemia. Reduced EPO secretion thus seems to play a role in the progression of unexplained senile anemia, and recombinant human EPO may possibly be effective for treating this type of anemia by mobilizing excess iron. © 1992 Wiley‐Liss, Inc.
Hereditary hemolytic disease with increased red blood cell phosphatidylcholine and dehydration: One, two, or many disorders?
Authors: Clark Margaret R. , Shohet Stephen B. , Gottfried Eugene L. 
Published: February 2007

AbstractWe have compared characteristics of red cells from patients who were originally diagnosed as having two different disorders, high phosphatidyl choline hemolytic anemia (HPCHA) and hereditary xerocytosis (HX). Both types of cells had reduced intracellular potassium, with attendant cell dehydration and an increase in the relative amount of membrane phosphatidyl choline. Neither these observations nor a review of previous studies of HX and HPCHA revealed any means of distinguishing between the two disorders. Measurements of chloride‐dependent potassium transport revealed flux characteristics in both HX and HPCHA red cells that were different from those in simultaneously run control samples. HX and HPCHA red cells did not show the same kinds of deviations from the normal pattern. However, extensive characterization of transport behavior under a variety of controlled conditions will be required to determine whether these differences represent intrinsic differences in chloride‐dependent transport properties. It appears likely that HX and HPCHA both represent a spectrum of disorders resulting from a variety of defects that produce the same general pattern of abnormalities in cation content and membrane phospholipid composition © 1993 Wiley‐Liss, Inc.
Acute episodic hemolysis in the African black rhinoceros as an analogue of human glucose‐6‐phosphate dehydrogenase deficiency
Authors: Paglia Donald E. 
Published: February 2007

AbstractSudden episodes of massive hemolysis have become the most common cause of death among captive black rhinoceroses, and there is evidence that they occur in the wild as well. We have observed radically unique enzyme and metabolite profiles in normal rhinoceros erythrocytes compared to humans and other mammals, including marked deficiencies of intracellular adenosine triphosphate (ATP), catalase, adenosine deaminase, and other enzymes involved in glycolysis, glutathione cycling, and nucleotide metabolism. Minimal concentrations of ATP appear to impair effective acceleration of hexosemono‐phosphate shunt activity in response to oxidants by restricting substrate generation at the hexokinase step. Antioxidant defenses are further compromised by catalase deficiency, which may be a general characteristic of rhinoceros erythrocytes, perhaps related to the common occurrence of severe mucocutaneous ulcerative disease. It is proposed that erythrocyte ATP deficiency in rhinoceroses may be an evolutionary adaptation conferring selective advantage against common hemic parasites, comparable to the role of human glucose‐6‐phosphate dehydrogenase (G‐6‐PD) deficiency in falciparum malaria. © 1993 Wiley‐Liss, Inc.
Study of glucose‐6‐phosphate dehydrogenase: History and molecular biology
Authors: Beutler Ernest 
Published: February 2007

AbstractGlucose‐6‐phosphate dehydrogenase (G6PD) deficiency was discovered in the 1950s. The history of the development of knowledge about G6PD deficiency is reviewed here. In the first decade after its discovery, the clinical manifestations of G6PD deficiency began to be understood. In the second decade, attention was focused on the degree of variability of this enzyme and the distinction of the various biochemical variants from one another. In the last decade, it has been possible to understand the mutations that effect this enzyme at the DNA level. Some 40 different mutations have now been characterized. Analysis of these mutations indicates that, while diversity sometimes exists within a mutation considered biochemical homogeneous, more often variants thought to be distinct prove to be identical. The study of G6PD mutations is beginning to provide insight into structurefunction relationships. © 1993 Wiley‐Liss, Inc.
A concise review: Iron absorption—The mucin‐mobilferrin‐integrin pathway. A competitive pathway for metal absorption
Authors: Conrad Marcel E. , Umbreit Jay N. 
Published: February 2007

AbstractNewly identified iron binding proteins isolated from rat duodenal homogenates permit better understanding of iron absorption. Mucins bind iron at acid pH to keep iron soluble and available for absorption at the more alkaline pH of the duodenum; this explains iron deficiency following prolonged achlorhydria. Integrin (90/150 kD) was identified on the absorptive surface of enterocytes in association with radioiron and is believed to facilitate transit of iron through the microvillous membrane. Mobilferrin, a 56 kD iron binding protein, was isolated from enterocyte cytosol. It coprecipitates with integrin and appears in close association with integrins in the apical cytoplasm. We postulate it accepts dietary iron from integrin and acts as the shuttle protein for iron in the cytoplasm. Since iron in enterocytes remains in equilibrium with body stores, we postulate mucosal iron uptake is regulated by the number of iron binding sites either occupied or unoccupied by iron on mobilferrin. Iron repletion of enterocytes from body stores is accomplished via transferrin receptors on the posterolateral membranes of enterocytes. Increased transfer of iron from blood into absorptive enterocytes occurs in iron replete animals to inhibit mucosal uptake of dietary iron. Little transfer of iron from plasma to enterocytes occurs in iron deficiency. Enhanced mucosal transfer of iron into the body occurs with increased body need for iron. The exact mechanism for mucosal transfer of iron into the plasma has not been defined but may also be mediated by an integrin. © 1993 Wiley‐Liss, Inc.
Antisense suppression of transferrin receptor gene expression in a human hepatoma cell (HuH‐7) line
Authors: Sasaki Katsunori , Zak Olga , Aisen Philip 
Published: February 2007

AbstractA recombinant plasmid carrying human transferrin receptor cDNA in reverse orientation downstream from the human cytomegalovirus immediate early promoter/enhancer element was introduced into the HuH‐7 human hepatoma cell line by lipofection. Cell surface transferrin binding and iron uptake from transferrin each decreased by about 50% in stable transfectants bearing integrated antisense DNA expression vector. Northern blot analysis indicated that the abundance of target transferrin receptor message was not altered by antisense RNA. These results suggest that the antisense transcript interferes with expression of the endogenous transferrin receptor gene at the level of translation. © 1993 Wiley‐Liss, Inc.
Agranulocytosis during antibiotic therapy: Drug sensitivity or sepsis?
Authors: Pisciotta Anthony V. 
Published: February 2007

AbstractForty‐three patients reviewed from the literature and five cases of agranulocytosis during antibiotic therapy studied by the author are presented. Time required to develop agranulocytosis with antibiotics was <19 days in comparison to >40 days required with nonantibiotic drugs. In all, agranulocytosis occurred concomitantly with drug treatment and became normal as treatment was discontinued. Retrospective rechallenge studies suggest that agranulocytosis may be dose related. In all cases PMNs were almost completely deleted and marrows were devoid of granulocyte precursors. In contrast, leukopenia secondary to overwhelming sepsis displayed persisting granulocytes in peripheral blood and marrow. While leukagglutinins were not found in nine cited cases, four serums were toxic to test PMNs as measured by suppression of postphagocytosis respiratory burst. Clindamycin directly suppressed development of CFU‐G in one sensitive patient but not in 16 normal controls. The hazard of antibiotics in suppressing granulocytopoiesis is emphasized by these observations. © 1993 Wiley‐Liss, Inc.
Inhibition of the activation of hageman factor (factor XII) by eosinophils and eosinophilic constituents
Authors: Ratnoff Oscar D. , Gleich Gerald J. , Shurin Susan B. , Kazura James , Everson Barbara , Embury Paula 
Published: February 2007

AbstractSeveral syndromes characterized by striking eosinophilia may be complicated by thrombosis. The experiments described indicate that, paradoxically, eosinophils and certain of their constituents inhibit the activation of Hageman factor (HF, factor XII). In earlier studies, suspensions of mixed types of granulocytes, other nucleated peripheral blood cells, and platelets inhibited activation of Hageman factor by ellagic acid, glass, and sulfatides. After these cells were sedimented by centrifugation, the supernatant fluids were also inhibitory. No attempt had been made earlier to distinguish among different granulocytic species. In the present study, suspensions of eosinophils and the supernatant fluid after eosinophils had been separated by centrifugation inhibited activation of Hageman factor by ellagic acid. The protein concentration of that amount of supernatant fluid that inhibited activation by about half was 16 μg/ml, approximately the same as had been described for suspensions of peripheral blood mononuclear cells. Activation of Hageman factor by ellagic acid was also inhibited by certain constituents of eosinophils, including eosinophil peroxidase, eosinophil major basic protein and eosinophil cationic protein. Inhibition was not specific for ellagic acid‐induced activation of Hageman factor, as inhibition was also observed with sulfatide‐induced activation. Inhibition was presumably related to neutralization of the negative charge of activators of Hageman factor. Thus, bismuth subgallate, a particulate activator of Hageman factor, was no longer effective after it had been exposed to eosinophil cationic protein. The observations reported here raise the question of whether in vivo eosinophils modulate certain of the defense reactions ascribed to Hageman factor. © 1993 Wiley‐Liss, Inc.
Flow cytometric analysis of the ploidy of normoblasts in the peripheral blood of patients with beta‐thalassemia
Authors: Fibach Eitan , Rachmilewitz Eliezer A. 
Published: February 2007

AbstractThe chronic severe anemia of patients with β‐thalassemia major stimulates extensive erythropoiesis, which results in circulating nucleated normoblasts. We devised a dual staining flow cytometric procedure in order to analyse the cell cycle and ploidy of these normoblasts. Peripheral blood cells of O blood‐group type were first stained with Fluorescein Isothiocyanate (FITC)‐conjugated anti‐H lectin which labels erythroid cells (RBC and normoblasts) by green fluorescence, and then with propidium iodide (PI) which binds to ONA and thereby labels nucleated cells (leukocytes and normoblasts) by red fluorescence. The leukocytes and normoblasts present in the blood sample of thalassemic patients could be distinguished and “gated” based on their green fluorescence. The PI (red) fluorescence, i.e., the DNA histogram of each population, was thus obtained. The results indicated no statistically significant difference in the PI fluorescence of these two populations. Thus, in spite of the abnormal erythropoiesis in β‐thalassemia, the resultant orthochromatic normoblasts are normal with respect to their DNA content © 1993 Wiley‐Liss, Inc.
Triclonal gammopathy (IgAk, IgGk, and IgMk) in a patient with plasmacytoid lymphoma derived from a monoclonal origin
Authors: Murata Takashi , Fujita Hiroyuki , Harano Hiroshi , Hukawa Masaya , Kanamori Heiwa , Matsuzaki Michio , Mohri Hiroshi , Kudoh Jun , Shimizu Nobuyoshi , Okubo Takao 
Published: February 2007

AbstractWe report the case of a 64‐year‐old woman with plasma cytoid lymphoma of the ileum and gastric wall. Serum protein electrophoresis and immunoelectrophoresis showed a triclonal IgGk, IgAk, and IgMk gammopathy. Biopsy of the tumor revealed three different cell types, which were stained with antibodies specific for IgG, IgA, and IgM. However, DNA analysis of immunoglobulin gene rearrangements using JH, Cμ, and Ck gene probes showed a monoclonal pattern. These results suggest that the three types of malignant cells producing different classes of immunoglobulins were derived from a single clone of B‐cells that had undergone a “class switch”. © 1993 Wiley‐Liss, Inc.