bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nematodes of the order Dorylaimida from Andalucía Oriental, Spain: Discolaimus Cobb, 1913. 1. Description of two new species
Authors: Torres Baltasar , Abolafia Joaquín , Peña-Santiago Reyes , Liébanas Gracia 
Published: October 2002

AbstractTwo new species of the genus Discolaimus Cobb, 1913 are described from southeastern Spain. D. mariae sp. n. is distinguished by its large size (L = 2.4-3.3 mm), lip region diameter 29-35 μm, odontostyle 23-25 μm, pharyngeal expansion occupying two-thirds of the total neck length, presence of dorsal cell bodies close to cardia, V = 46-53, female genital system didelphicamphidelphic, tail conical with rounded terminus (33-39 μm, c = 72-88, c′ = 0.9-1.0) and with a terminal gap in the inner cuticle, and males absent. D. labiatus sp. n. is characterised by being medium sized (L = 0.99-1.20 mm), lip region diameter 14-17 μm wide, labial disc with no radial but six longitudinal grooves, inner (perioral) labial portion forming well developed liplets, odontostyle 10.0-12.5 μm, vulva relatively anterior (V = 39-43), female tail conical with rounded terminus (26-27 μm, c = 37-46, c′ = 1.5-1.7), and male unknown. Scanning electron microscope observations of the species are also presented.
The discursive position of religious studies in Japan: Masaharu Anesaki and the origins of religious studies
Authors: Isomae Jun'ichi 
Published: October 2002

AbstractIn Japan today, the issue of religious cults is a frequent topic of discussion, particularly in the aftermath of the Aum Shinrikyo incident. However, at the time of the Aum incident, the views of scholars in religious studies were scarcely heeded. This can be attributed to the fact that for many people, religious studies was thought to lean too much toward a defense of religion. Focusing upon Masaharu Anesaki, the founder of religious studies in Japan, this article explores the fundamental characteristics of the discourse of religious studies as it has come down to the present day. It seeks to elucidate the close relationship of religious studies to the political situation in Japanese society during the Meiji period (1868-1912), and how this contributed to the development of the field. It further maintains that in conjunction with state policies for national education, the discourse of religious studies helped instantiate religion as an integral component of modern society, one defined particularly by the vacillation between individualism and nationalism. After World War II, there were few in Japan who would openly express admiration for nationalist ideology, but in religious studies a tendency toward nationalism remained evident in its yearning for the solidarity of religious groups and other kinds of communal bodies. Thus, even as its outward form underwent change, this tendency toward nationalism not only served as a defense of religion, but it also continued to uphold the existing discursive positionality of religious studies.
Characterization and crystal chemistry of an Fe-rich montmorillonite from Ölberg, Germany
Authors: Petit S. , Caillaud J . , Righi D. , Madejová J . , Elsass F. , Köster H. M. 
Published: October 2002

AbstractAn Fe-rich smectite from Ölberg (Germany) was characterized using X-ray diffraction, infrared spectroscopy and analytical electron microscopy. Progressive reduction of the octahedral charge was performed through the Hofmann & Klemen effect at increasing temperatures. The sample was heterogeneous, consisting of two smectite populations. One population, which comprises a minor portion of the sample, is an ‘Fe3+-montmorillonite’ with little or no tetrahedral charge and Fe3+as the major octahedral cation. The other population, a major constituent of the sample, contains less Mg and more Al than the first one and exhibits some tetrahedral charge. This fraction may be considered as an inter-grade between nontronite (dominant tetrahedral charge) and Fe3+-montmorillonite (dominant octahedral charge). These two populations may occur as separate particles but also as interstratified layers.
Factor VIII expression in azoxymethane-induced murine fulminant hepatic failure
Authors: Doering Christopher B. , Josephson Cassandra D. , Craddock Heather N. , Lollar Pete 
Published: October 2002

AbstractFulminant hepatic failure (FHF) in humans produces a bleeding diathesis due in large part to a reduction in the biosynthesis of liver-derived coagulation factors. Remarkably, factor VIII procoagulant activity is elevated in most of these patients despite widespread liver cell death. FHF can be modeled in mice by administration of azoxymethane, the active ingredient found in cycad palm nuts. We compared the expression of factor VIII to other hepatic hemostatic factors in azoxymethane-induced murine FHF. Mice displayed dose-dependent decreases in all coagulation factor activities measured, including factors V, VII, VIII, and IX. At the highest dose of azoxymethane (50 μg/g body weight), factor VIII activity in plasma decreased by 98% within 36 hours after treatment, which was associated with an 80% reduction in hepatic factor VIII messenger RNA (mRNA). In contrast, factor VIII mRNA levels in spleen, kidney, and lung tissue of azoxymethane-treated mice were unchanged. Cellular damage in these mice appeared to be limited to hepatocytes as evident by histologic examination. This finding is supported by 2 observations. First, hepatic mRNA levels of von Willebrand factor, which is synthesized by liver sinusoidal endothelial cells but not hepatocytes, were unchanged. Second, von Willebrand factor was detected antigenically in liver sections of azoxymethane-treated mice by immunofluorescence. These results indicate that the contribution of the liver to factor VIII biosynthesis is not replaced or significantly supplemented by other tissues in this model of FHF.
Circulating and binding characteristics of wild-type factor IX and certain Gla domain mutants in vivo
Authors: Gui Tong , Lin Hui-Feng , Jin Da-Yun , Hoffman Maureane , Straight David L. , Roberts Harold R. , Stafford Darrel W. 
Published: October 2002

AbstractResidue K5 in factor IX γ-carboxyglutamic acid (Gla) domain participates in binding endothelial cells/collagen IV. We injected recombinant factor IX containing mutations at residue 5 (K5A, K5R) into factor IX–deficient mice and compared their behavior with that of wild-type factor IX. The plasma concentration of factor IX that binds to endothelial cells/collagen IV (recombinant wild type and K5R) was consistently lower than that of the one that does not bind (K5A). Mice treated with wild type or K5R had 79% of the injected factor IX in the liver after 2 minutes, whereas 17% remained in circulation. In mice injected with K5A, 59% of the injected factor IX was found in liver and 31% was found in plasma. When we blocked the liver circulation before factor IX injection, 74% of K5A and 64% of K5R remained in the blood. When we treated the mouse with EDTA after injecting exogenous factor IX, the blood levels of factor IX that bind to endothelial cells/collagen IV increased, presumably because of release from endothelial cell/collagen IV binding sites. In contrast, the levels of the mutants that do not bind were unaffected by EDTA. In immunohistochemical studies, factor IX appears on the endothelial surfaces of mouse arteries after factor IX injection and of human arteries from surgical specimens. Thus, we have demonstrated that factor IX binds in vivo to endothelial cell–collagen IV surfaces. Our results suggest that factor IX Gla-domain mediated binding to endothelial cells/collagen IV plays a role in controlling factor IX concentration in the blood.
Band 3 is an anchor protein and a target for SHP-2 tyrosine phosphatase in human erythrocytes
Authors: Bordin Luciana , Brunati Anna Maria , Donella-Deana Arianna , Baggio Bruno , Toninello Antonio , Clari Giulio 
Published: October 2002

AbstractTyr phosphorylation of the multifunctional transmembrane protein band 3 has been implicated in several erythrocyte functions and disorders. We previously demonstrated that pervanadate treatment of human erythrocytes induces band-3 Tyr phosphorylation, which is catalyzed by the sequential action of tyrosine kinase Syk and tyrosine kinase(s) belonging to the Src family. In this study, we show that Tyr phosphorylation of band 3, elicited by pervanadate, N-ethylmaleimide, or diamide, greatly increases band-3 interaction with the tyrosine phosphatase SHP-2 in parallel with the translocation of SHP-2 to erythrocyte membranes. These events seem to be mediated by Src-like catalyzed phosphorylation of band 3 because both SHP-2 translocation to cellular membranes and its interaction with Tyr-phosphorylated protein are greatly counteracted by PP2, a specific inhibitor of Src kinases. Binding-competition experiments demonstrate that SHP-2 recruitment to band 3 occurs via its SH2 domain(s). In particular, our data support the view that SHP-2 docks specifically with P-Y359 of band 3. Experiments performed with intact erythrocytes in the presence of the SHP-2 inhibitor calpeptin suggest that, once recruited to Tyr-phosphorylated band 3, the tyrosine phosphatase dephosphorylates the protein. P-Y8, 21, and 904 are the residues affected by SHP-2, as judged by 32P-peptide mapping of band 3 digested with trypsin. These results indicate that in treated erythrocytes, recruitment of cytosolic SHP-2 to band 3 is a prerequisite for the subsequent dephosphorylation of the transmembrane protein.
High numbers of active caspase 3–positive Reed-Sternberg cells in pretreatment biopsy specimens of patients with Hodgkin disease predict favorable clinical outcome
Authors: Dukers Danny F. , Meijer Chris J. L. M. , ten Berge Rosita L. , Vos Wim , Ossenkoppele Gert J. , Oudejans Joost J. 
Published: October 2002

Abstract
In vitro studies suggest that resistance to the apoptosis-inducing effect of chemotherapy might explain poor responses to therapy in fatal instances of Hodgkin disease (HD). Execution of apoptosis depends on proper functioning of effector caspases, in particular caspase 3, which is activated on the induction of apoptosis through either the stress-induced pathway or the death receptor–mediated pathway. Thus, high levels of caspase 3 activation should reflect proper functioning of one or both identified apoptosis pathways, resulting in chemotherapy-sensitive neoplastic cells and thus a favorable clinical response to chemotherapy. We tested this hypothesis by quantifying active caspase 3–positive tumor cells in primary biopsy specimens of HD and compared these numbers to clinical outcomes. Using an immunohistochemical assay, activation of caspase 3 was detected in 0% to 13% of neoplastic cells. High numbers of active caspase 3–positive tumor cells (5% or more) correlated with excellent clinical prognosis; 0 of 22 patients with 5% or more active caspase 3–positive cells died compared with 11 of 41 patients with less than 5% positive cells (P = .007). Proper functioning of active caspase 3 was demonstrated by the detection of one of its cleaved substrates, PARP-1/p89, in similar percentages of neoplastic cells. High levels of active caspase 3–positive neoplastic cells were associated with the expression of p53 and its downstream effector molecule p21, suggesting proper functioning of the stress-induced apoptosis pathway. In conclusion, high numbers of active caspase 3–positive neoplastic cells predict a highly favorable clinical outcome in HD patients, supporting the notion that an (at least partially) intact apoptosis cascade is essential for the cell killing effect of chemotherapy.
Persistence of HTLV-I in blood components after leukocyte depletion
Authors: Pennington Joanne , Taylor Graham P. , Sutherland Janet , Davis Ricardo E. , Seghatchian Jerhard , Allain Jean-Pierre , Williamson Lorna M. 
Published: October 2002

Abstract
The human T-cell leukemia virus HTLV-I is a transfusion-transmissible retrovirus targeting T lymphocytes for which screening is not currently undertaken in United Kingdom blood donors. The introduction of universal leukocyte depletion (LD) of the United Kingdom blood supply raises the question as to the degree of protection afforded by this procedure against HTLV-I transmission by blood components. HTLV-I viral DNA removal by leukocyte-depleting filters was assessed in units of whole blood and platelets by real-time quantitative polymerase chain reaction (PCR) and by nested PCR for HTLV-I Tax DNA. We examined HTLV-I removal by LD filters using a model system of blood units containing exogenous spiked HTLV-I–positive MT-2 cells at a relevant concentration and whole blood donations from asymptomatic HTLV-I carriers. T-lymphocyte removal was assessed in parallel by measurement of endogenous subset-specific CD3 mRNA. In the MT-2 model system we observed 3.5 log10 to 4 log10 removal of HTLV-I Tax DNA by filtration of whole blood and 2 log10 to 3 log10 removal across platelet filters with 13 of 16 whole blood and 8 of 8 platelet units still positive after filtration. Despite 3 log10 to 4 log10 viral removal, HTLV-I Tax DNA could be detected after whole blood filtration in asymptomatic carriers with viral loads above 108 proviral DNA copies/L. T-lymphocyte removal was also between 3.5 log10 and 4.5 log10. HTLV-I provirus removal was incomplete in the model system and in asymptomatic carriers with viral loads greater than 108 copies/L. These results suggest that LD alone may not provide complete protection from HTLV-I transmission by transfusion.
Keratinocyte growth factor preserves normal thymopoiesis and thymic microenvironment during experimental graft-versus-host disease
Authors: Rossi Simona , Blazar Bruce R. , Farrell Catherine L. , Danilenko Dimitry M. , Lacey David L. , Weinberg Kenneth I. , Krenger Werner , Holländer Georg A. 
Published: October 2002

AbstractThymus-dependent reconstitution of the peripheral T-cell compartment is critical for the successful outcome of bone marrow transplantation. However, graft-versus-host disease (GVHD) affects thymic stromal function and thus prevents normal T-cell maturation and selection. To determine whether cytoprotection of thymic epithelial cells (TECs) by keratinocyte growth factor (KGF) averts GVHD-related injury to the thymus, a nonirradiated murine parent→F1 transplantation model was investigated. Administration of KGF between days −3 and +3 of GVHD induction preserved normal thymic size, cellularity, and thymocyte phenotype when measured 2 weeks after transplantation and compared with saline-treated parent→F1 mice that received allogeneic transplants. Moreover, the characteristic GVHD-induced impairment in cell cycle progression of pro- and pre-T cells was prevented by KGF. However, the normal phenotypic and functional status of the thymus did not correlate with the higher number of GVHD-inducing mature donor T cells in thymi of KGF-treated mice. Importantly, extensive analysis of the different TEC populations within the thymic cortex and medulla revealed an almost normal stromal architecture and composition in GVHD mice treated with KGF. These observations are likely to reflect an indirect effect of KGF on thymopoiesis as KGF-receptor expression was demonstrated to be restricted to TECs. Thus, pharmacologic doses of KGF appear to exert a potent effect on TEC function, which in turn allows for normal T lymphopoiesis to occur during acute GVHD.
Novel mutation in ferroportin1 is associated with autosomal dominant hemochromatosis
Authors: Wallace Daniel F. , Pedersen Palle , Dixon Jeannette L. , Stephenson Peter , Searle Jeffrey W. , Powell Lawrie W. , Subramaniam V. Nathan 
Published: October 2002

Abstract
Hemochromatosis is a common disorder characterized by excess iron absorption and accumulation of iron in tissues. Usually hemochromatosis is inherited in an autosomal recessive pattern and is caused by mutations in the HFE gene. Less common non-HFE–related forms of hemochromatosis have been reported and are caused by mutations in the transferrin receptor 2 gene and in a gene localized to chromosome 1q. Autosomal dominant forms of hemochromatosis have also been described. Recently, 2 mutations in theferroportin1 gene, which encodes the iron transport protein ferroportin1, have been implicated in families with autosomal dominant hemochromatosis from the Netherlands and Italy. We report the finding of a novel mutation (V162del) in ferroportin1 in an Australian family with autosomal dominant hemochromatosis. We propose that this mutation disrupts the function of the ferroportin1 protein, leading to impaired iron homeostasis and iron overload.
Processing of the lipocalin α1-microglobulin by hemoglobin induces heme-binding and heme-degradation properties
Authors: Allhorn Maria , Berggård Tord , Nordberg Jonas , Olsson Martin L. , Åkerström Bo 
Published: October 2002

Abstractα1-Microglobulin is a 26-kd protein, widespread in plasma and tissues and well-conserved among vertebrates. α1-Microglobulin belongs to the lipocalins, a protein superfamily with highly conserved 3-dimensional structures, forming an internal ligand binding pocket. The protein, isolated from urine, has a heterogeneous yellow-brown chromophore bound covalently to amino acid side groups around the entrance of the lipocalin pocket. α1-Microglobulin is found in blood both in free form and complex-bound to immunoglobulin A (IgA) via a half-cystine residue at position 34. It is shown here that an α1-microglobulin species, which we name t–α1-microglobulin (t = truncated), with a free Cys34 thiol group, lacking its C-terminal tetrapeptide, LIPR, and with a more polar environment around the entrance of the lipocalin pocket, is released from IgA–α1-microglobulin as well as from free α1-microglobulin when exposed to the cytosolic side of erythrocyte membranes or to purified oxyhemoglobin. The processed t–α1-microglobulin binds heme and the α1-microglobulin–heme complex shows a time-dependent spectral rearrangement, suggestive of degradation of heme concomitantly with formation of a heterogeneous chromophore associated with the protein. The processed t–α1-microglobulin is found in normal and pathologic human urine, indicating that the cleavage process occurs in vivo. The results suggest that α1-microglobulin is involved in extracellular heme catabolism.
Prognostic significance and modalities of flow cytometric minimal residual disease detection in childhood acute lymphoblastic leukemia
Authors: Dworzak Michael N. , Fröschl Gertraud , Printz Dieter , Mann Georg , Pötschger Ulrike , Mühlegger Nora , Fritsch Gerhard , Gadner Helmut 
Published: October 2002

AbstractDetection of minimal residual disease (MRD) in acute lymphoblastic leukemia (ALL) predicts outcome. Previous studies were invariably based on relative quantification and did not investigate sample-inherent parameters that influence test accuracy, which makes comparisons and clinical conclusions cumbersome. Hence, we conducted a prospective, population-based MRD study in 108 sequentially recruited children with ALL uniformly treated with the ALL-Berlin-Frankfurt-Münster (ALL-BFM) 95 protocol in Austria (median follow-up of 40 months). Using sensitive, limited antibody panel flow cytometry applicable to 97% of patients, we investigated 329 bone marrow samples from 4 treatment time points. MRD was quantified by blast percentages among nucleated cells (NCs) and by absolute counts (per microliter). Covariables such as NC count, normal B cells, and an estimate of the test sensitivity were also recorded. Presence and distinct levels of MRD correlated with a high probability of early relapse at each of the time points studied. Sequential monitoring at day 33 and week 12 was most useful for predicting outcome independently from clinical risk groups: patients with persistent disease (≥ 1 blast/μL) had a 100% probability of relapse, compared to 6% in all others. Absolute MRD quantification was more appropriate than relative, due to considerable variations in total NC counts between samples. Regeneration of normal immature B cells after periods of rest from treatment limited the test sensitivity. In conclusion, MRD detection by flow cytometry is a strong and independent outcome indicator in childhood ALL. Standardization regarding absolute quantification on the basis of NCs and assessment during periods of continuous treatment promise to increase the accuracy, simplicity, and cost efficiency of the approach.
Infant hypervitaminosis A causes severe anemia and thrombocytopenia: evidence of a retinol-dependent bone marrow cell growth inhibition
Authors: Perrotta Silverio , Nobili Bruno , Rossi Francesca , Criscuolo Maria , Iolascon Achille , Di Pinto Daniela , Passaro Irene , Cennamo Lucia , Oliva Adriana , Della Ragione Fulvio 
Published: October 2002

Abstract
Vitamin A is a pivotal biochemical factor required for normal proliferation and differentiation as well as for specialized functions, such as vision. The dietary intake of 1500 IU/day is recommended in the first year of life. Here, we report the case of an infant who had been given 62 000 IU/day for 80 days. The infant showed several clinical signs of retinol intoxication, including severe anemia and thrombocytopenia. Bone marrow showed a remarkably reduced number of erythroid and megakaryocytic cells. The interruption of vitamin A treatment was immediately followed by clinical and biochemical recovery. To clarify whether the effects of retinol are due to a direct action on bone marrow cell proliferation, we investigated the activity of retinol (both the drug and the pure molecule) on the growth of K-562, a multipotent hematopoietic cell line, and on bone marrow mesenchymal stem cells. We observed that vitamin A strongly inhibited the proliferation of the cells at concentrations similar to those reached in vivo. Subsequent biochemical analyses of the cell cycle suggested that the effect was mediated by the up-regulation of cyclin-dependent kinase inhibitors, p21Cip1 and p27Kip1. These are the first findings to demonstrate that infant hypervitaminosis A causes a severe anemia and thrombocytopenia and that this is probably due to the direct effect of the molecule on the growth of all bone marrow cellular components. Our data also suggest potential bone marrow functional alterations after excessive vitamin A intake because of emerging social habits.
Expression of C/EBPβ from the C/ebpα gene locus is sufficient for normal hematopoiesis in vivo
Authors: Jones Letetia C. , Lin Meng-Liang , Chen Shih-Shun , Krug Utz , Hofmann Wolf-K. , Lee Stephen , Lee Ying-Hue , Koeffler H. Phillip 
Published: October 2002

Abstract
CCAAT/enhancer-binding proteins (C/EBPs) are critical transcriptional regulators of differentiation of hematopoietic cells. Previous studies have shown that targeted disruption of theC/ebpα gene results in a lack of granulocytic differentiation with an arrest at the stage of immature myeloblasts. By using a gene replacement strategy in which C/EBPβ was expressed from the C/ebpα gene locus of C/EBPα-null mice, we have evaluated the ability of C/EBPβ to function for C/EBPα in directing differentiation along the granulocytic pathway. We show that the morphology and the differential cell counts of the bone marrow and peripheral blood cells from C/EBPβ knockin mice are indistinguishable from those of their wild-type littermates, indicating that hematopoiesis occurs normally in these animals. Additionally, we analyzed expression of 21 myeloid-specific genes, including markers for distinct stages of granulocytic differentiation, and found no significant differences in their levels of expression in the bone marrow of C/EBPβ knockin and wild-type mice. These results imply that C/EBPβ can substitute for C/EBPα during hematopoiesis when expressed from the C/ebpα gene locus.