bluuebunny/crossref_metadata_2025_split huggingface dataset:
A follow up model for patients with atrophic chronic gastritis and intestinal metaplasia
Authors: Dinis-Ribeiro M , Lopes C , da Costa-Pereira A , Guilherme M , Barbosa J , Lomba-Viana H , Silva R , Moreira-Dias L 
Published: January 2004

Aim:To devise a follow up model for patients with gastric cancer associated lesions, such as atrophic chronic gastritis (ACG) and intestinal metaplasia (IM).Methods:Cohort study of 144 patients, followed for a minimum of one year, in whom at least two upper gastrointestinal endoscopic biopsies in flat gastric mucosa provided a diagnosis of ACG, IM, or low grade dysplasia (LGD).Results:Of those diagnosed with ACG at first endoscopic biopsy (entry biopsy), 12% progressed to LGD in outcome biopsy, as did 8% of those with type I IM, 38% with type II or III IM, and 32% with LGD. Type of IM at entry independently predicted progression to LGD and cancer. Type II and III IM had a higher rate of progression to LGD than type I IM, which showed an indolent behaviour similar to ACG. Patients with type II or III IM were at higher risk for development of dysplasia, and 7% of patients with type III IM at first biopsy progressed to high grade dysplasia (HGD), whereas no cases of ACG or type I/II IM progressed to HGD during the first three years.Conclusion:Patients with ACG or IM could possibly be allocated to different management schedules, based on differences in rate and proportion of progression to LGD or HGD. Less intensive follow up (two/three yearly with “serological evaluation” (pepsinogen)) may suit those with ACG or type I IM. Patients with type III IM may benefit from six to 12 monthly improved endoscopic examination (magnification chromoendoscopy).
The immunohistochemical expression of calcitonin receptor-like receptor (CRLR) in human gliomas
Authors: Benes L , Kappus C , McGregor G P , Bertalanffy H , Mennel H D , Hagner S 
Published: January 2004

Background:Gliomas are the most common primary tumours of the central nervous system and exhibit rapid growth that is associated with neovascularisation. Adrenomedullin is an important tumour survival factor in human carcinogenesis. It has growth promoting effects on gliomas, and blockade of its actions has been experimentally shown to reduce the growth of glioma tissues and cell lines. There is some evidence that the calcitonin receptor-like receptor (CRLR) mediates the tumorigenic actions of adrenomedullin.Aim:To determine whether CRLR is expressed in human gliomas and the probable cellular targets of adrenomedullin.Methods:Biopsies from 95 human gliomas of varying grade were processed for immunohistochemical analysis using a previously developed and characterised antibody to CRLR.Results:All tumour specimens were positive for CRLR. As previously found in normal peripheral tissues, CRLR immunostaining was particularly intense in the endothelial cells. This was evident in all the various vascular conformations that were observed, and which are typical of gliomas. In addition, clear immunostaining of tumour cells with astrocyte morphology was observed. These were preferentially localised around vessels.Conclusions:This study has shown for the first time that the CRLR protein is present in human glioma tissue. The expression of the receptor in endothelial cells and in astrocytic tumour cells is consistent with the evidence that its endogenous ligand, adrenomedullin, may influence glioma growth by means of both direct mitogenic and indirect angiogenic effects. CRLR may be a valuable target for effective therapeutic intervention in these malignant tumours.
The effect of a symptom related “gating policy” on ANCA requests in routine clinical practice
Authors: Sinclair D , Saas M , Stevens J M 
Published: January 2004

Background:Most positive antineutrophil cytoplasmic antibody (ANCA) results are associated with non-vasculitic conditions, and guidelines have been proposed for the judicious use of this test. The outcome of applying similar guidelines in a routine laboratory is reported.Methods:All immunology requests (6500) over six months were selected, and those requesting ANCA were studied for the appropriateness of the clinical data supporting the request, the presence of ANCA in those samples tested, and the final diagnosis. Antibodies were detected by indirect immunofluorescence.Results:ANCA testing was requested in 287 samples. Application of a “gating policy”, which refuses analysis on requests that are not supported by clinical data suggestive of systemic vasculitis, made clinicians more selective about the patients for whom they requested ANCA testing. The percentage of “appropriate” screens for systemic vasculitis was relatively high (212 of 287 requests: 72.5%). Only one of the remainder, for whom ANCA testing was initially refused, developed an ANCA related systemic vasculitis in the two years after the study, but the delay in reporting her positive ANCA was only two days. Most of the samples tested were negative (155 of 212), but most (42 of 57) of the patients with positive ANCA results were found to have a systemic vasculitis.Conclusions:A gating policy to select requests supported by clinical data suggestive of systemic vasculitis makes ANCA testing more clinically relevant and cost effective. Studies where guidelines can be proposed and their effects measured are important in the light of clinical governance and evidence based medicine.
SIMPLICITY IN COMPACT ABSTRACT THEORIES
Authors: BEN-YAACOV ITAY 
Published: January 2004

We continue [2], developing simplicity in the framework of compact abstract theories. Due to the generality of the context we need to introduce definitions which differ somewhat from the ones use in first order theories. With these modified tools we obtain more or less classical behaviour: simplicity is characterized by the existence of a certain notion of independence, stability is characterized by simplicity and bounded multiplicity, and hyperimaginary canonical bases exist.
SYSTEMIC LUPUS ERYTHEMATOSUS IN AFRICAN-AMERICAN WOMEN: COGNITIVE PHYSIOLOGICAL MODULES, AUTOIMMUNE DISEASE, AND STRUCTURED PSYCHOSOCIAL STRESS
Authors: WALLACE RODRICK 
Published: January 2004

Examining elevated rates of systemic lupus erythematosus in African-American women from perspectives of immune cognition suggests the disease constitutes an internalized physiological image of external patterns of structured psychosocial stress, a 'pathogenic social hierarchy' involving the synergism of racism and gender discrimination, in the context of policy-driven social disintegration which has particularly affected ethnic minorities in the USA. The disorder represents the punctuated resetting of 'normal' immune self-image to a self-attacking 'excited' state, a process formally analogous to models of punctuated equilibrium in evolutionary theory.Thus disease onset takes place in the context of a particular immunological 'cognitive module' similar to what has been proposed by evolutionary psychologists for the human mind. Disease progression involves interaction of the hypothalamic-pituitary-adrenal axis, which we also treat as a cognitive physiological submodule, with both immune cognition and an embedding pathogenic social hierarchy, a structured psychosocial stress which literally writes an image of itself on the course of the disorder. Both onset and progression may be stratified by a relation to cyclic physiological responses which are long in comparison with heartbeat period: circadian, hormonal, and annual light/temperature cycles.The high rate of lupus in African-American women suggests existence of a larger dynamic which entrains powerful as well as subordinate population subgroups, implying that the wide ranging programs of social and economic reform required to cause declines in disease among African-American women will bring significant benefit to all.
Efficient lentiviral gene transfer to canine repopulating cells using an overnight transduction protocol
Authors: Horn Peter A. , Keyser Kirsten A. , Peterson Laura J. , Neff Tobias , Thomasson Bobbie M. , Thompson Jesse , Kiem Hans-Peter 
Published: January 2004

Abstract
The use of lentiviral vectors for the transduction of hematopoietic stem cells has evoked much interest owing to their ability to stably integrate into the genome of nondividing cells. However, published large animal studies have reported highly variable gene transfer rates of typically less than 1%. Here we report the use of lentiviral vectors for the transduction of canine CD34+ hematopoietic repopulating cells using a very short, 18-hour transduction protocol. We compared lentiviral transduction of hematopoietic repopulating cells from either stem cell factor (SCF)– and granulocyte-colony stimulating factor (G-CSF)–primed marrow or mobilized peripheral blood in a competitive repopulation assay in 3 dogs. All dogs engrafted rapidly within 9 days. Transgene expression was detected in all lineages (B cells, T cells, granulocytes, and red blood cells as well as platelets) indicating multilineage engraftment of transduced cells, with overall long-term marking levels of up to 12%. Gene transfer levels in mobilized peripheral blood cells were slightly higher than in primed marrow cells. In conclusion, we show efficient lentiviral transduction of canine repopulating cells using an overnight transduction protocol. These results have important implications for the design of stem cell gene therapy protocols, especially for those diseases in which the maintenance of stem cells in culture is a major limitation.
Autoimmune anemia in macaques following erythropoietin gene therapy
Authors: Chenuaud Pierre , Larcher Thibaut , Rabinowitz Joseph E. , Provost Nathalie , Cherel Yan , Casadevall Nicole , Samulski Richard J. , Moullier Philippe 
Published: January 2004

Abstract
We delivered the homologous erythropoietin (Epo) cDNA driven from a doxycycline-regulated promoter via recombinant adeno-associated virus in skeletal muscle of 9 cynomolgus macaques. Upon induction, rapid supraphysiologic levels of Epo were obtained. Unexpectedly, some individuals developed a profound anemia that correlated with the appearance of neutralizing antibodies against the endogenous Epo. Both the endogenous erythropoietin and vector sequences were identical. This is the first example of the inadvertent development of an autoimmune disease in primates as a result of gene transfer of a gene expressing a self-antigen. It raises some concerns when a therapeutic protein is produced at high levels from an ectopic site. (Blood. 2004;103:3303-3304)
Rituximab and ICE as second-line therapy before autologous stem cell transplantation for relapsed or primary refractory diffuse large B-cell lymphoma
Authors: Kewalramani Tarun , Zelenetz Andrew D. , Nimer Stephen D. , Portlock Carol , Straus David , Noy Ariela , O'Connor Owen , Filippa Daniel A. , Teruya-Feldstein Julie , Gencarelli Alison , Qin Jing , Waxman Alyson , Yahalom Joachim , Moskowitz Craig H. 
Published: January 2004

Abstract
Patients with relapsed or primary refractory diffuse large B-cell lymphoma (DLBCL) who achieve complete response (CR) before autologous stem cell transplantation (ASCT) generally have better outcomes than those who achieve only partial response (PR). We investigated whether adding rituximab to the ifosfamide-carboplatin-etoposide (ICE) chemotherapy regimen (RICE) could increase the CR rate of patients with DLBCL under consideration for ASCT. Thirty-six eligible patients were treated with RICE, and 34 received all 3 planned cycles. The CR rate was 53%, significantly better than the 27% CR rate (P = .01) achieved among 147 similar consecutive historical control patients with DLBCL treated with ICE; the PR rate was 25%. Febrile neutropenia was the most frequent grade 3 or 4 nonhematologic toxicity; it occurred in 7.5% of delivered cycles. No patient had RICE-related toxicity that precluded ASCT. The median number of CD34+ cells per kilogram mobilized was 6.3 × 106. Progression-free survival rates of patients who underwent transplantation after RICE were marginally better than those of 95 consecutive historical control patients who underwent transplantation after ICE (54% vs 43% at 2 years; P = .25). RICE appears to induce very high CR rates in patients with relapsed and refractory DLBCL; however, further studies are necessary to determine whether this treatment regimen will improve outcomes after ASCT.
A fungal multicopper oxidase restores iron homeostasis in aceruloplasminemia
Authors: Harris Z. Leah , Davis-Kaplan Sandra R. , Gitlin Jonathan D. , Kaplan Jerry 
Published: January 2004

Abstract
Mutations that lead to a loss of the copper-containing plasma enzyme ceruloplasmin disrupt mammalian iron homeostasis. The mechanism by which ceruloplasmin mobilizes iron from cell stores has been controversial. We demonstrate that injection of a soluble copper-containing yeast protein Fet3p can restore iron homeostasis in phlebotomized mice with a deletion of the ceruloplasmin gene. These results show the conservation of function of copper-containing proteins in eukaryotic iron metabolism. (Blood. 2004;103:4672-4673)
PU.1 determines the self-renewal capacity of erythroid progenitor cells
Authors: Back Jonathan , Dierich Andrée , Bronn Corinne , Kastner Philippe , Chan Susan 
Published: January 2004

AbstractPU.1 is a hematopoietic-specific transcriptional activator that is absolutely required for the differentiation of B lymphocytes and myeloid-lineage cells. Although PU.1 is also expressed by early erythroid progenitor cells, its role in erythropoiesis, if any, is unknown. To investigate the relevance of PU.1 in erythropoiesis, we produced a line of PU.1-deficient mice carrying a green fluorescent protein reporter at this locus. We report here that PU.1 is tightly regulated during differentiation—it is expressed at low levels in erythroid progenitor cells and down-regulated upon terminal differentiation. Strikingly, PU.1-deficient fetal erythroid progenitors lose their self-renewal capacity and undergo proliferation arrest, premature differentiation, and apoptosis. In adult mice lacking one PU.1 allele, similar defects are detected following stress-induced erythropoiesis. These studies identify PU.1 as a novel and critical regulator of erythropoiesis and highlight the versatility of this transcription factor in promoting or preventing differentiation depending on the hematopoietic lineage.
Low-molecular-weight heparin versus low-dose aspirin in women with one fetal loss and a constitutional thrombophilic disorder
Authors: Gris Jean-Christophe , Mercier Eric , Quéré Isabelle , Lavigne-Lissalde Géraldine , Cochery-Nouvellon Eva , Hoffet Médéric , Ripart-Neveu Sylvie , Tailland Marie-Laure , Dauzat Michel , Marès Pierre 
Published: January 2004

Abstract
The prospective evaluation of the effect of thromboprophylaxis in women with one unexplained pregnancy loss from the 10th week of amenorrhea was performed. A total of 160 patients with heterozygous factor V Leiden mutation, prothrombin G20210A mutation, or protein S deficiency were given 5 mg folic acid daily before conception, to be continued during pregnancy, and low-dose aspirin 100 mg daily or low-molecular-weight heparin enoxaparin 40 mg was taken from the 8th week. Twenty-three of the 80 patients treated with low-dose aspirin and 69 of the 80 patients treated with enoxaparin had a healthy live birth (odds ratio [OR], 15.5; 95% confidence interval [CI], 7-34, P &lt; .0001). Enoxaparin was superior to low-dose aspirin in each subgroup defined according to the underlying constitutional thrombophilic disorder. An associated protein Z deficiency and/or positive antiprotein Z antibodies were associated with poorer outcomes. The neonate weight was higher in the women successfully treated with enoxaparin, and neonates small for gestational age were more frequent in patients treated with low-dose aspirin. No significant side effects of the treatments could be evidenced in patients or newborns. As there is no argument to prove that low-dose aspirin may have been deleterious, these results support enoxaparin use during such at-risk pregnancies.
Activation of phosphatidylinositol 3-kinase and c-Jun-N-terminal kinase cascades enhances NF-κB-dependent gene transcription in BCG-stimulated macrophages through promotion of p65/p300 binding
Authors: Darieva Zoulfia , Lasunskaia Elena B , Campos Mariana N N , Kipnis Thereza L , da Silva Wilmar D 
Published: January 2004

AbstractThe proinflammatory response of infected macrophages is an important early host defense mechanism against mycobacterial infection. Mycobacteria have been demonstrated to induce proinflammatory gene transcription through the Toll-like receptors, (TLR)2 and TLR 4, which initiate signaling cascades leading to nuclear factor (NF)-κB activation. The main transduction pathway responsible for NF-κB activation has been established and involves the MyD88, interleukin-1 receptor-associated kinase, tumor necrosis factor receptor-associated factor-6, NF-κB-inducing kinase, and inhibitor of κB kinase complex. The role of other kinase cascades triggered by mycobacteria in the NF-κB activation is less clear. We herein examine the role of the mitogen-activated protein kinases (MAPKs) and phosphatidylinositol 3-kinase (PI-3K) cascades in the expression of the bacillus Calmette-Guerin (BCG) mycobacteria-induced NF-κB-dependent genes, macrophage-inflammatory protein-2 (MIP-2) and inducible nitric oxide (NO) synthase. Specific pharmacological inhibition of the PI-3K, c-jun-N-terminal kinase (JNK), and to a smaller extent, p38 MAPK but not extracellular-regulated kinase (ERK), suppressed NF-κB-dependent reporter gene transcription and MIP-2 and NO secretion in BCG-induced RAW264.7 macrophages. A similar effect was obtained following molecular inhibition of JNK via JNK-interacting protein-1 overexpression. In addition, a kinase-dead mutant of MEK kinase-1, the up-stream regulator of JNK, also proved to be a potent inhibitor of NF-κB-reporter activity. The effect of inhibitors was mediated by the down-regulation of NF-κB transcription activity and without effecting its nuclear translocation. These data suggest an indirect mechanism of the NF-κB regulation by these kinases, probably through p65 phosphorylation and improved binding to the p300 transcription coactivator. The data obtained demonstrate that PI-3K, JNK, and p38 MAPK activation by mycobacteria enhance NF-κB-driven gene expression contributing to the proinflammatory macrophage response.
Soluble Jagged-1 is able to inhibit the function of its multivalent form to induce hematopoietic stem cell self-renewal in a surrogate in vitro assay
Authors: Vas Virág , Szilágyi László , Pálóczi Katalin , Uher Ferenc 
Published: January 2004

AbstractStem cells reside in customized microenvironments (niches) that contribute to their unique ability to divide asymmetrically to give rise to self and to a daughter cell with distinct properties. Notch receptors and their ligands are highly conserved and have been shown to regulate cell-fate decisions in multiple developmental systems through local cell interactions. To assess whether Notch signaling may regulate hematopoiesis to maintain cells in an immature state, we examined the functional role of the recombinant, secreted form of the Notch ligand Jagged-1 during mouse hematopoietic stem cell (HSC) and progenitor cell proliferation and maturation. We found that ligand immobilization on stromal layer or on Sepharose-4B beads is required for the induction of self-renewing divisions of days 28–35 cobblestone area-forming cell. The free, soluble Jagged-1, however, has a dominant-negative effect on self-renewal in the stem-cell compartment. In contrast, free as well as immobilized Jagged-1 promotes growth factor-induced colony formation of committed hematopoietic progenitor cells. Therefore, we propose that differences in Jagged-1 presentation and developmental stage of the Notch receptor-bearing cells influence Notch ligand-binding results toward activation or inhibition of downstream signaling. Moreover, these results suggest potential clinical use of recombinant Notch ligands for expanding human HSC populations in vitro.
Characterization of branchial lead-calcium interaction in the freshwater rainbow trout Oncorhynchus mykiss
Authors: Rogers Joseph T. , Wood Chris M. 
Published: January 2004

SUMMARY
The mechanism of branchial lead uptake and interplay with Ca2+transport was investigated in the freshwater rainbow trout Oncorhynchus mykiss. Lead significantly reduced Ca2+ influx by approximately 40% and 30% after exposure to 2.3±0.1 and 1.4±0.2μmol l-1 dissolved lead, respectively, for 0-48 h. Acute inhibition of Ca2+ influx by lead exhibited typical Michaelis-Menten kinetics with an approximate 16-fold increase in Km, whereas Jmax values did not significantly change, yielding an inhibitor constant(Ki,Pb) of 0.48 μmol l-1. Alternative analyses suggest the possibility of a mixed competitive/non-competitive interaction at the highest lead concentration tested (4.8 μmol l-1). Branchial lead accumulation was reduced with increasing waterborne Ca2+ concentrations, suggesting a protective effect of Ca2+ against lead uptake at the gill. The apical entries of Ca2+ and lead were both inhibited (55% and 77%, respectively) by the addition of lanthanum (1 μmol l-1) to the exposure water. The use of cadmium (1 μmol l-1) and zinc (100 μmol l-1) as voltage-independent calcium channel competitors also reduced branchial lead uptake by approximately 56% and 47%, respectively. Nifedipine and verapamil (up to 100 μmol l-1), both voltage-dependent calcium channel blockers, had no effect on gill lead accumulation. CaCl2 injection reduced both Ca2+ and lead uptake by the gills. This suggests transport of lead through apical voltage-independent calcium channels, similar to the entry of Ca2+. High-affinity Ca2+-ATPase activity was not acutely affected by lead, but a significant 80% reduction in activity occurred during exposure for 96 h to 5.5±0.4 μmol l-1 dissolved lead, indicating a possible non-competitive component to lead-induced Ca2+ disruption. The effect of lead on Ca2+ efflux was investigated and found to be insignificant. We conclude that uptake of lead occurs, at least in part, by the same mechanism as Ca2+, which results in disruption of Ca2+ influx and ultimately Ca2+ homeostasis.
Synthesis of Dialkyl Dithiophosphate Surface-Capped Copper Nanoclusters
Authors: Wang Xiaobo , Liu Weimin , Yan Fengyuan , Zhang Zhijun , Xu Binshi 
Published: January 2004

Abstract
Dialkyl dithiophosphate-capped lyophobic copper nanoclusters of a mean size of 4.0 ± 1.1 nm were synthesized by a novel method. The method was characterized by the generation of small copper clusters through aqueous reduction and the extraction of the clusters into organic solvent using dialkyldithiophosphate.
Selective Oxidation of Cycloalkanes over Iron-substituted Hexagonal Mesoporous Aluminophosphate Molecular Sieves
Authors: Mohapatra Susanta K , Selvam Parasuraman 
Published: January 2004

Abstract
Iron-substituted hexagonal mesoposours aluminiphosphate (FeHMA) molecular sieves oxidize cycloalkanes into cycloalkanols and cycloalkanones with excellent yield in the presence of molecular oxygen or air under mild reaction conditions. The catalyst showed higher activity as compared to mesoporous FeMCM-41 as well as microporous FeS-1 and FeAPO-5 molecular sieves, and that FeHMA can be recycled without much loss in activity.
Catalytic Oxidation of Cyclohexene by Molecular Oxygen over Isopolyoxometalates
Authors: Liu Yanyong , Murata Kazuhisa , Inaba Megumu , Nakajima Hitoshi , Koya Masahiko , Tomokuni Keizou 
Published: January 2004

Abstract
Isopolyoxomolybdates exhibited high selectivities for the industrially useful products (cyclohexene oxide and 2-cyclohexen-1-ol) catalyzing effectively the reaction of initial product cyclohexenyl hydroperoxide with cyclohexene in the oxidation of cyclohexene by molecular oxygen.