bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differences in outcome of the interaction between Cryptococcus neoformans glucuronoxylomannan and human monocytes and neutrophils
Authors: Monari Claudia , Retini Cinzia , Casadevall Arturo , Netski Dale , Bistoni Francesco , Kozel Thomas R. , Vecchiarelli Anna 
Published: March 2003

AbstractDisseminated infections by the opportunistic yeast Cryptococcus neoformans are characterized by accumulation in tissues of glucuronoxylomannan (GXM), the major component of the capsular polysaccharide. We investigated binding, uptake, and disposal of GXM by peripheral blood neutrophils and monocytes, and the effect of GXM uptake on phagocytic cell function. GXM was efficiently bound and internalized by both types of phagocytic cells, with maximal loading at 50 μg/ml, a GXM concentration found in serum and cerebrospinal fluid of some cryptococcosis patients. However, substantial differences were noted in the kinetics for uptake by macrophages and neutrophils. Whereas neutrophils rapidly ingested limited amounts of GXM and then expelled or degraded it after 1 h of incubation, macrophages demonstrated continuous intracellular accumulation for up to 1 week of incubation. Accumulation of GXM by neutrophils was accompanied by reduced anticryptococcal activity, suggesting one more mechanism for virulence enhancement by the major capsular component of C. neoformans.
Sequential conversion of the redox status of macrophages dictates the pathological progression of autoimmune diabetes
Authors: Murata Yukie , Amao Michiko , Hamuro Junji 
Published: March 2003

AbstractThe redox status of macrophages (Mϕ), indexed by intracellular content of glutathione (icGSH), varies sequentially along with disease progression in nonobese diabetic mice. At the stage ofearly insulitis, Mϕ skew to oxidative Mϕ (OMϕ) with decreased icGSH, then to reductive Mϕ (RMϕ) with elevated icGSH and to OMϕ after the occurrence of diabetes. RMϕ or OMϕ inducing agents either delayed or accelerated the onset of diabetes in a mutually inverse manner. RMϕ or OMϕ adoptively transferred exacerbated or ameliorated the disease progression depending on the redox status of Mϕ of recipient mice. The new paradigm that the sequential conversion of redox status of Mϕ dictates the pathological progression may provide a new insight on the mechanism underlying autoimmune diabetes.
The neutrophil‐activating protein of Helicobacter pylori (HP‐NAP) activates the MAPK pathway in human neutrophils
Authors: Nishioka Hiroaki , Baesso Ilenia , Semenzato Gianpietro , Trentin Livio , Rappuoli Rino , Giudice Giuseppe Del , Montecucco Cesare 
Published: March 2003

AbstractInfection by Helicobacter pylori causes an acute inflammatory response followed by a chronic infection of the human gastric mucosa characterized by the infiltration of neutrophils andmononuclear inflammatory cells. The neutrophil‐activating protein of Helicobacter pylori (HP‐NAP) is a virulence factor that activates neutrophils, monocytes, and mast cells. However, the mechanism by which HP‐NAP activates these cells is not fully understood. Here, we show that HP‐NAP induces extracellular regulated kinase (ERK) and p38‐mitogen‐activated protein kinase (MAPK) activation in human neutrophils; c‐Jun N‐terminal kinase is not activated by HP‐NAP. A MAPK/ERK kinase inhibitor and a p38‐MAPK inhibitor suppress HP‐NAP‐mediated neutrophil oxidative burst, adhesion, andchemotaxis, but not actin polymerization. Pertussis toxin (PTX) inhibits all these neutrophil functions and the MAPK activation caused by HP‐NAP. These results demonstrate that HP‐NAP activates neutrophils through a PTX‐sensitive pathway and that ERK and p38‐MAPK are involved in many neutrophil functions stimulated by HP‐NAP.
Interleukin‐2 primes eosinophil degranulation in hypereosinophilia and Wells' syndrome
Authors: Simon Hans‐Uwe , Plötz Sabine , Simon Dagmar , Seitzer Ulrike , Braathen Lasse R. , Menz Günter , Straumann Alex , Dummer Reinhard , Levi‐Schaffer Francesca 
Published: March 2003

AbstractPatients with hypereosinophilia frequently suffer from eosinophil‐mediated damages of the heart, lungs, skin, and other organs, while some do not. The reason(s) for this difference is not known. We observed that eosinophils from most patients with hypereosinophilia express the α‐chain of the IL‐2 receptor (CD25), and that IL‐2 enhances platelet‐activating factor‐stimulated release ofeosinophil cationic protein from CD25‐expressing but not from CD25‐negative eosinophils. Such a "priming" effect has previously been described for eosinophil hematopoietins. These data suggest thatpatients with increased eosinophil surface CD25 expression are at higher risk of eosinophil degranulation and subsequent tissue damage when IL‐2 is present at inflammatory sites.
Formation of Triazinium‐Imidothioate Zwitterions and Their Role as Key Intermediates for Novel SN(ANRORC) Reaction Pathways
Authors: Wermann Kurt , Walther Martin , Günther Wolfgang , Görls Helmar , Anders Ernst 
Published: March 2003

AbstractThe formation of highly reactive zwitterionic triaziniumimidothioate intermediates 10 from bis(1,3,4‐thiadiazolo)‐1,3,5‐triazinium halides is reported. These intermediates are the first structures to be isolated from the reaction pathway between bis(1,3,4‐thiadiazolo)‐1,3,5‐triazinium halides 1 and benzylamines 2. The reaction between 1 and 2 has a very complicated hypersurface and can yield unusual bis(1,2,4‐triazolo)‐1,3,5‐triazinium halides 6, [1,2,4]triazolo[1,3,4]thiadiazolo[1,3,5]triazinium halides 7 or highly substituted guanidines 5. The formation of 6 and 7 can be understood in terms of an SN(ANRORC) process. As could be demonstrated for the tricyclic cations 6, these compounds, together with 7, could be interesting in further synthetic applications. The salts 6 react with KOH/tBuOK to give novel aminals 16 in good to excellent yields. Most of the important steps in the course of the transformation of 1 into 5, 6 and 7 are supported by B3LYP/6−311++G(d,p) calculations and the X‐ray structures of 6a, 7b, 14b and 16c. From an electronic point of view, the more important reaction steps are governed by the conformation‐controlling effect of negative hyperconjugation, accompanied by intramolecular proton‐transfer reactions. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2003)
Asymmetric Radical Synthesis of 2,5‐Diaryl‐2,3‐dihydrofurans − Application to the Preparation of (+)‐Phyltetralin
Authors: Garzino Frédéric , Méou Alain , Brun Pierre 
Published: March 2003

AbstractThe diastereoselective MnIII‐promoted radical addition of β‐oxo ester1ontoN‐cinnamoyloxazolidinone2affords, after removal of the chiral auxiliary, the enantiopure 2,5‐diaryl‐2,3‐dihydrofuran (−)‐4. Its SnCl4‐induced rearrangement leads to a 4‐aryltetralone immediate precursor of the aryltetralin lignan (+)‐phyltetralin (9). (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2003)
Domino [3+2] Cycloaddition/Annulation Reactions of β‐(2‐Aminophenyl)‐α,β‐ynones with Nitrile Oxides: Synthesis of Isoxazolo[4,5‐c]quinolines
Authors: Abbiati Giorgio , Arcadi Antonio , Marinelli Fabio , Rossi Elisabetta 
Published: March 2003

Abstractβ‐(2‐Aminophenyl)‐α,β‐ynones react with nitrile oxides by domino [3+2] cycloaddition/annulation reactions giving rise to isoxazolo[4,5‐c]quinolines in satisfactory yields. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2003)
Ectyoceramide, the First Natural Hexofuranosylceramide from the Marine Sponge Ectyoplasia ferox
Authors: Costantino Valeria , Fattorusso Ernesto , Imperatore Concetta , Mangoni Alfonso 
Published: March 2003

AbstractEctyoceramide (1a), a unique monoglycosylceramide with a galactose in the furanose form, was isolated from Ectyoplasia ferox, and its structure was determined by NMR spectroscopy, multiple tandem mass spectrometry, and chemical degradation. Ectyoceramide is the first example of a monohexofuranosylceramide and, more generally, the first natural glycosphingolipid with its first sugar in the furanose form. (Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2003)
The Direct Metalation and Subsequent Functionalization of Trifluoromethyl‐Substituted Pyridines and Quinolines
Authors: Schlosser Manfred , Marull Marc 
Published: March 2003

AbstractDepending on the choice of the reagent, 2‐(trifluoromethyl)pyridine can be selectively metalated and subsequently carboxylated or otherwise functionalized either at the 3‐ or at the 6‐position. “Optional site selectivity” can also be achieved with 4‐(trifluoromethyl)pyridine, which may be deprotonated either at the 2‐ or at the 3‐position. In contrast, 3‐(trifluoromethyl)pyridine undergoes nucleophilic addition and ensuing decomposition whatever the base. Depending on the reaction conditions, 2‐(trifluoromethyl)quinoline displays reactivity toward lithium reagents at its 3‐, 4‐, or 8‐positions, 3‐(trifluoromethyl)quinolines at the 2‐ or 4‐positions, and 4‐(trifluoromethyl)quinoline at the 2‐ or 3‐positions. It was therefore possible to prepare four trifluoromethyl‐substituted pyridinecarboxylic acids (1, 4, 9, and 10) and six trifluoromethyl‐substituted quinolinecarboxylic acids (11, 13, 14, 15, 17, and 18) regioisomerically uncontaminated and in a most straightforward way. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2003)
Thermal kinetics of color degradation of mulberry fruit extract
Authors: Suh Hyung Joo , Noh Dong Ouk , Kang Chang Soo , Kim Jin Man , Lee Seog Won 
Published: March 2003

AbstractThe effects of temperature and pH on color degradation kinetics of the mulberry fruit extract were investigated. The absorbance at 510 nm was decreased with increase of heating time, but that at 420 nm was increased with the increase of heating time at 100°C. The change of the browning index (A510/A420) was increased with increase of pH and was lower at pH 2.0 than that at pH 5.0. The browning index variation was adequately described by both the first‐order and the zero‐order kinetic. However, the zero‐order kinetic model was proposed because of the better fit. According to the Arrhenius model, the activation energies for the browning index in the range of 80–100°C for the four different pH values were 30.68 kJ/mol for pH 2.0, 35.87 kJ/mol for pH 3.0, 42.67 kJ/mol for pH 4.0, and 43.49 kJ/mol for pH 5.0.
Modelling trends in central England temperatures
Authors: Harvey David I. , Mills Terence C. 
Published: March 2003

AbstractTrends are extracted from the central England temperature (CET) data available from 1723, using both annual and seasonal averages. Attention is focused on fitting non‐parametric trends and it is found that, while there is no compelling evidence of a trend increase in the CET, there have been three periods of cooling, stability, and warming, roughly associated with the beginning and the end of the Industrial Revolution. There does appear to have been an upward shift in trend spring temperatures, but forecasting of current trends is hazardous because of the statistical uncertainty surrounding them. Copyright © 2003 John Wiley & Sons, Ltd.
A novel cryptic translocation t(12;17)(p13;p12–p13) in a secondary acute myeloid leukemia results in a fusion of the ETV6 gene and the antisense strand of the PER1 gene
Authors: Penas Eva Maria Murga , Cools Jan , Algenstaedt Petra , Hinz Kristina , Seeger Doris , Schafhausen Philippe , Schilling Georgia , Marynen Peter , Hossfeld Dieter K. , Dierlamm Judith 
Published: March 2003

AbstractThe ETV6 gene is a member of the ETS family of transcription factors and the main target of chromosomal rearrangements affecting chromosome band 12p13. To date, more than 15 fusion partners of ETV6 have been characterized at the molecular level. Most of these fusions encode chimeric proteins with oncogenic properties. However, some of the translocations do not produce a functional fusion protein, but may induce ectopic expression of oncogenes located close to the breakpoint. We herein report the characterization and cloning of a novel cryptic translocation, t(12;17)(p13;p12–p13), occurring in a patient with an acute myeloid leukemia evolving from a chronic myelomonocytic leukemia. Cytogenetic analysis suggested the presence of a deletion of the short arm of chromosome 12, del(12)(p13), in three of the five metaphase cells analyzed. However, fluorescence in situ hybridization (FISH) with the ETV6‐specific cosmid clones 179A6, 50F4, 163E7, and 148B6 as well as probes hybridizing to the TP53 gene on 17p13 and the subtelomeric region of 17p revealed the presence of a translocation between 12p and 17p. By FISH, the breakpoints could be localized in intron 1 of ETV6 and centromeric to TP53. By 3′ rapid amplification of cDNA ends–polymerase chain reaction (3′ RACE‐PCR), a fusion transcript between exon 1 of ETV6 and the antisense strand of PER1 (period homolog 1, Drosophila), a circadian clock gene, could be identified. This ETV6‐PER1 (antisense PER1 strand) fusion transcript does not produce a fusion protein, and no other fusion transcripts could be detected. We hypothesize that in the absence of a fusion protein, the inactivation of PER1 or deregulation of a gene in the neighborhood of PER1 may contribute to the pathogenesis of leukemias with a t(12;17)(p13;p12–p13). © 2003 Wiley‐Liss, Inc.
Fusion of ALK to the Ran‐binding protein 2 (RANBP2) gene in inflammatory myofibroblastic tumor
Authors: Ma Zhigui , Hill D. Ashley , Collins Margaret H. , Morris Stephan W. , Sumegi Janos , Zhou Ming , Zuppan Craig , Bridge Julia A. 
Published: March 2003

AbstractInflammatory myofibroblastic tumor (IMT) is a rare mesenchymal proliferation of transformed myofibroblasts, with a prominent inflammatory cell component, that can mimic other spindle cell processes such as nodular fasciitis, desmoid tumor, and gastrointestinal stromal tumor. Genetic analyses have recently demonstrated rearrangements of anaplastic lymphoma kinase (ALK), located at 2p23, in a subset of IMTs. Molecular characterizations have identified ALK fusions involving tropomyosin‐3 and ‐4 (TPM‐3 and ‐4), the clathrin heavy chain (CLTC), and the cysteinyl‐tRNA synthetase (CARS) genes as fusion partners. Here we describe two IMTs with a novel ALK fusion that involves the Ran‐binding protein 2 (RANBP2) gene at 2q13, which normally encodes a large (358‐kDa) nucleopore protein localized at the cytoplasmic side of the nuclear pore complex. The N‐terminal 867 residues of RANBP2 are fused to the cytoplasmic segment of ALK in the 1,430–amino acid RANBP2‐ALK chimeric protein. Myofibroblasts that express RANBP2‐ALK exhibit nuclear membrane‐associated ALK staining that is unique compared to the subcellular localization observed with other ALK fusions in IMT, presumably attributable to heteroassociation of the fusion with normal RANBP2 at the nuclear pore. These findings expand the spectrum of ALK abnormalities observed in IMT and further confirm the clonal, neoplastic nature of these lesions. © 2003 Wiley‐Liss, Inc.
Mutations of CEBPA in acute myeloid leukemia FAB types M1 and M2
Authors: Snaddon Jennifer , Smith Matthew L. , Neat Michael , Cambal‐Parrales Maxine , Dixon‐McIver Amanda , Arch Rachael , Amess John A. , Rohatiner Ama Z. , Lister T. Andrew , Fitzgibbon Jude 
Published: March 2003

AbstractCEBPA encodes the transcription factor C/EBPα and is specifically up‐regulated during granulocytic differentiation. The gene is mutated in approximately 20% of patients with acute myeloid leukemia (AML) FAB type M2 and occurs in the absence of the t(8;21). In much the same way as specific translocations are associated with a particular AML FAB type, the identification of non‐random associations of gene mutation with karyotype or FAB type may be helpful in elucidating the molecular basis of certain forms of leukemia. To confirm these initial findings, 99 patients with AML FAB type M1 or M2 were screened for CEBPA mutations by use of a PCR–single‐strand conformational polymorphism and sequencing approach. Nine CEBPA mutations were identified in eight patients. The mutations were clustered toward the COOH terminal of the protein and occurred exclusively in the intermediate cytogenetic risk group (8/64, 12.5%). Two patients with biallelic mutation, one homozygous for 1137Ins (57 bp) and another with two CEBPA mutations, 1096Ins (27 bp) and 363Ins (GGCC), were observed. There was no evidence for deletion of this region in the other six mutated samples analyzed by fluorescence in situ hybridization with a BAC clone spanning the CEBPA locus. CEBPA mutation status was not demonstrated to be of prognostic importance in this patient group, although this may reflect the selection and size of the AML population studied. In conclusion, mutation of CEBPA is a recurrent finding in AML and appears specific to the intermediate cytogenetic risk group patients. © 2003 Wiley‐Liss, Inc.
High expression of B‐cell receptor inducible gene BIC in all subtypes of Hodgkin lymphoma
Authors: van den Berg Anke , Kroesen Bart‐Jan , Kooistra Klaas , de Jong Debora , Briggs Jane , Blokzijl Tjasso , Jacobs Susan , Kluiver Joost , Diepstra Arjan , Maggio Ewerton , Poppema Sibrand 
Published: March 2003

AbstractIn a search for genes specifically expressed in Reed–Sternberg (RS) cells of Hodgkin lymphoma (HL), we applied the serial analysis of gene expression (SAGE) technique on the HL‐derived cell line DEV. Genes highly expressed in DEV were subjected to an RT‐PCR analysis to confirm the SAGE results. For one of the genes, a high expression was observed in DEV and other HL‐derived cell lines but not in non‐Hodgkin lymphoma (NHL)–derived cell lines and normal controls, suggesting an HL‐specific expression. This gene corresponds to the human BIC gene, a member of the noncoding mRNA‐like molecules. RNA in situ hybridization (ISH) indicated an exclusive nucleolar localization of BIC transcripts in all RS cells in 91% of HL cases, including nodular lymphocyte predominance (NLP) HL and classical HL. Analyses of normal human tissues revealed BIC transcripts in only a small number of CD20‐positive B‐cells in lymph node and tonsil tissue, albeit at a much lower level compared to that of RS cells. BIC RT‐PCR in the Burkitt lymphoma–derived cell line Ramos demonstrated a significant up‐regulation upon cross‐linking of the B‐cell receptor (BcR). IκBα‐mediated blocking of NF‐κB translocation in Ramos did not effect the up‐regulation of BIC expression upon BcR triggering, suggesting that activation of NF‐κB is not involved in regulation of BIC expression. In summary, our data show that expression of BIC is specific for RS cells of HL. In normal tissue, BIC is expressed weakly in a minority of germinal center B cells. Expression of BIC can be modified/influenced by BcR triggering, indicating that BIC might play a role in the selection of B cells. © 2003 Wiley‐Liss, Inc.
CDKN2A, CDKN2B, and MTAP gene dosage permits precise characterization of mono‐ and bi‐allelic 9p21 deletions in childhood acute lymphoblastic leukemia
Authors: Bertin Raphaëlle , Acquaviva Cécile , Mirebeau Delphine , Guidal‐Giroux Christine , Vilmer Etienne , Cavé Hélène 
Published: March 2003

AbstractDeletion of the 9p21 chromosomal region is frequently found in childhood acute lymphoblastic leukemia (ALL). The target of these deletions is CDKN2A, a gene encoding both p16INK4a and p14ARF. However, contiguous genes such as CDKN2B, encoding p15INK4b, or MTAP, encoding methylthioadenosine phosphorylase, can be included in the deletions. Gene dosage by use of real‐time PCR has recently been proposed as a promising technical option for the diagnosis of deletions. However, its reliability and its capacity to detect mono‐allelic deletions in tumor samples are controversial. To evaluate the frequency and extent of deletions in 284 children with ALL, we devised a real‐time PCR assay for CDKN2A, CDKN2B exons 1β and 3, and MTAP gene dosage and validated it by comparison with loss‐of‐heterozygosity analysis. We show that, if several controls and adjustments are performed, real‐time PCR can provide a reliable test for mono‐ and bi‐allelic deletions in ALL. We propose a strategy that overcomes the major caveats of such a dosage in tumor samples: aneuploidy and contamination by normal cells. By use of this assay, we found bi‐allelic deletions in 58 and 17% of T‐ and B‐lineage ALL, respectively. Mono‐allelic deletion was observed in about 15% of cases, stressing the importance of their detection in ALL. CDKN2B and/or MTAP co‐deletions were highly variable in both T‐ and B‐lineage ALL, making ALL with 9p21 a rather heterogeneous group. Because proteins encoded by these genes might influence the response to treatment, the prognosis of 9p21‐deleted ALL could vary according to the extent of the deletion. © 2003 Wiley‐Liss, Inc.
Role of short telomeres in inducing preferential chromosomal aberrations in human ovarian surface epithelial cells: A combined telomere quantitative fluorescence in situ hybridization and whole‐chromosome painting study
Authors: Deng Wen , Tsao Sai Wah , Guan Xin‐Yuan , Lucas Joe N. , Cheung Annie L. M. 
Published: March 2003

AbstractIt is well established that specific cancers and immortalized cells have nonrandom chromosome aberrations. However, little is understood about the underlying mechanism that initiates these aberrations in human cells. To examine whether human chromosomes with the shortest telomeres initiate the preferential chromosomal aberrations before cellular immortalization, we simultaneously applied telomere quantitative fluorescence in situ hybridization and specific whole‐chromosome painting on chromosomes 1, 5, 8, 17, 19, and 20 in human ovarian surface epithelial (HOSE 6‐3) cells expressing human papilloma viral oncogenes (HPV16 E6E7). The HPV16 E6E7–expressing cells, with extended in vitro life span and telomerase‐negative status, were previously identified as having nonrandom chromosomal imbalances and high frequencies of dicentrics. Our analyses showed that among six pairs of targeted chromosomes, chromosomes 8 and 20 showed critically short telomeres with an undetectable telomere signal in more than 50% of cells analyzed. These chromosomes with the critically short telomeres were preferentially involved in various types of chromosomal aberrations including dicentrics, translocations, breaks, insertions, and losses or gains of chromosomal elements. Our findings suggest that nonrandom chromosome aberrations in HOSE cells occurring before cellular immortalization could be caused by the telomere length heterogeneity. © 2003 Wiley‐Liss, Inc.
Activation of HOX11L2 by juxtaposition with 3′‐BCL11B in an acute lymphoblastic leukemia cell line (HPB‐ALL) with t(5;14)(q35;q32.2)
Authors: MacLeod Roderick A.F. , Nagel Stefan , Kaufmann Maren , Janssen Johannes W.G. , Drexler Hans G. 
Published: March 2003

AbstractCytogenetic analysis of a pediatric T‐cell acute lymphoblastic leukemia (ALL) cell line (HPB‐ALL) revealed the cryptic t(5;14)(q35;q32.2), recently found in 15–20% pediatric T‐ALL patients, with 5q35 and 14q32.2 breakpoints at 5′‐HOX11L2 and 3′‐BCL11B, respectively. Expression of both BCL11B, which is hematologically restricted to T cells, and HOX11L2 was detected, whereas adjacent genes at 5q35 (RANBP17) and 14q32 (VRK1, HSU88895) were not dysregulated. Apparently, t(5;14)(q35;q32.2) serves to activate HOX11L2 by juxtaposition with elements downstream of BCL11B, implying a novel dysregulatory mechanism comparable to TCRA/D or IGH juxtaposition. As well as providing molecular cytogenetic documentation of t(5;14) ALL, this report validates HPB‐ALL cells for investigating this important new disease entity in vitro. © 2003 Wiley‐Liss, Inc.