bluuebunny/crossref_metadata_2025_split huggingface dataset:
EIN UNERKANNTER QUAESTIONESKOMMENTAR (EXC.THEOD. 4F) UND DIE DEUTUNG DER VERKLÄRUNG CHRISTI IN FRÜHCHRISTLICHEN TEXTEN
Authors: Scholten Clemens 
Published: January 2004

AbstractThere are traces of attempts at a methodical explanation of biblical texts before the appearance of full-scale commentaries on Holy Scripture. The use of exegetical technical forms arose in Christian schools from the necessity to understand the contents of the Bible as coherent. In Clement of Alexandria, exc. Theod. 4f, a hitherto overlooked fragment of an early Christian Quaestiones-commentary has been preserved. The specific interest in Christ's transfiguration concerns his identity with God and the comprehension of his disciples. The differences between heretical and orthodox exegesis do not depend on the choice of methods, as Marc the Magician and Clement demonstrate. The narrative of the transfiguration in the apocryphal Acts of the Apostles testifies to exegetical expertise. Origen considers his own scholarly exegesis as basically debatable.
L'UTILISATION DES PARABOLES DANS L'INTERPRÉTATION DE LA GNOSE (NH XI,1)
Authors: Painchaud Louis 
Published: January 2004

AbstractOf all the various Nag Hammadi texts that use parables drawn from the New Testament, the Interpretation of Knowledge (NHC XI,1) has attracted the least scholarly attention, no doubt due to the text's extremely lacunous state of conservation. But despite the fact that two thirds of the work have been lost, it is still possible to identify references to the parable of the Sower (IntKnow 5,16-19 ; cf. Mt 13,3b-9 and parallels) and the parable of the Good Samaritan (6,19-23 ; cf. Lk 10,29-35), as well as an amalgamation of allusions to the parable of the Lost Sheep (Mt 18,10-14 and parallels), that of the lamb which must be rescued on the Sabbath (Mt 12,11-12) and the tale of the Good Shepherd ( Jn 10,1-21), at IntKnow 10,20a-38. In this article, the function of this material in the Interpretation of Knowledge will be examined and its use will be situated within the wider context of both gnostic and non-gnostic exegesis in early Christianity.
VALENTINIAN VARIATIONS ON LK 12,8-9/MT 10,32
Authors: Löhr Winrich 
Published: January 2004

AbstractClement of Alexandria has preserved a fragment of Herakleon, disciple of Valentinus, which comments on Lk 12,8-9 (11) par. The article interprets Herakleon's fragment as a piece of subtle second century Gospel exegesis, considers it in the context of the early Christian exegesis of Lk 12,8-9 par. and compares it with another Valentinian exegesis of the same verse which is related by Tertullian. Some conjectures as to the form of Herakleon's commentary are attempted: Apparently he first quoted the lemma and then commented on it, carefully discussing verse after verse. Method and form of the fragment are close to Herakleon's 'hypomnemata' on the Gospel of John. Our piece, however, probably formed no part of these 'hypomnemata'—Herakleon being the first known Christian exegete who commented both on the Gospel of Luke (taking into account the Synoptic parallels) and the Gospel of John.
Homing of in vitro expanded Stro-1- or Stro-1+ human mesenchymal stem cells into the NOD/SCID mouse and their role in supporting human CD34 cell engraftment
Authors: Bensidhoum Morad , Chapel Alain , Francois Sabine , Demarquay Christelle , Mazurier Christelle , Fouillard Loic , Bouchet Sandrine , Bertho Jean Marc , Gourmelon Patrick , Aigueperse Jocelyne , Charbord Pierre , Gorin Norbert Claude , Thierry Dominique , Lopez Manuel 
Published: January 2004

AbstractThe Stro-1 antigen potentially defines a mesenchymal stem cell (MSC) progenitor subset. We here report on the role of human ex vivo-expanded selected Stro-1+ or Stro-1- MSC subsets on the engraftment of human CD34+ cord blood cells in the nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mouse model. The data show that cotransplantation of expanded Stro-1- cells with CD34+ cells resulted in a significant increase of human CD45, CD34, CD19, and CD11b cells detected in blood or in bone marrow (BM) and spleen as compared with the infusion of CD34+ cells alone. Infusion into mice of expanded Stro-1+ and Stro-1- cells (without CD34+ cells) showed that the numbers of Stro-1+-derived (as assessed by DNA analysis of human β-globin with quantitative polymerase chain reaction [PCR]) were higher than Stro-1--derived cells in spleen, muscles, BM, and kidneys, while more Stro-1--derived than Stro-1+-derived cells were found in lungs. The transduction of expanded Stro-1+ cells with an enhanced green fluorescent protein (eGFP) gene did not modify their cytokine release and their homing in NOD/SCID mouse tissues. The difference between the hematopoietic support and the homing capabilities of expanded Stro-1+ and Stro-1- cells may be of importance for clinical therapeutic applications: Stro-1+ cells may rather be used for gene delivery in tissues while Stro-1- cells may rather be used to support hematopoietic engraftment. (Blood. 2004;103:3313-3319)
CD45-associated protein inhibits CD45 dimerization and up-regulates its protein tyrosine phosphatase activity
Authors: Takeda Akiko , Matsuda Akio , Paul Rachelle M. J. , Yaseen Nabeel R. 
Published: January 2004

AbstractCD45, a receptor-like protein tyrosine phosphatase (PTP), plays an essential role in lymphocyte development and immune responses. Recent evidence suggests that dimerization of CD45 down-regulates its function. However, the mechanisms by which CD45 dimerization is regulated remain unclear, and there is no direct evidence that the PTP activity of CD45 dimers is less than that of monomers. CD45 in lymphocytes associates with CD45-AP (CD45-associated protein). Here we show that T cells from CD45-AP-null mice have a much higher level of CD45 dimers than those of wild-type mice, suggesting that CD45-AP inhibits CD45 dimer formation. This was confirmed with the use of a novel CD45-AP-null T-cell line, ALST-1, that we established from a spontaneous thymic tumor found in a CD45-AP-null mouse. Transfected CD45-AP inhibited CD45 dimer formation in ALST-1 cells in proportion to the amount of CD45-AP expressed. Finally, with the use of microsomal fractions from both mouse thymocytes and ALST-1 transfectants, the PTP activity of CD45 was found to be significantly lower in CD45-AP-negative cells than in CD45-AP-positive cells. Therefore, our results support a model in which binding of CD45-AP to inactive CD45 dimers converts them to active monomers. (Blood. 2004;103:3440-3447)
Unexpectedly, induction of cytotoxic T lymphocytes enhances the humoral response after DNA immunization
Authors: Dyer Christopher M. , Zhan Yifan , Brady Jamie L. , Carbone Francis R. , Smyth Mark J. , Lew Andrew M. 
Published: January 2004

AbstractAlthough there are many examples (eg, immune deviation) in which enhanced cellular responses correspond with lower humoral responses, here we demonstrate for the first time 2 models in which cytotoxic T-lymphocyte (CTL) activity is associated with an enhanced antibody response. First, C57BL/6 mice generate a stronger antibody response to ovalbumin DNA immunization than congenic bm1 mice. The latter differ from C57BL/6 mice in that the H-2Kb molecule is mutated so that the immunodominant CTL epitope of ovalbumin is no longer presented. Second, pre-existing CTLs (induced by ovalbumin peptide-priming) increased the antibody response to a second unrelated antigen (β-galactosidase) co-immunized with ovalbumin. One possible mechanism is that CTLs may release antigen from DNA-transfected cells by killing or damaging them, and this freed antigen is then accessible to dendritic cells and B cells. Our finding of CTL-mediated antibody enhancement has important implications for tumor and viral immunobiology and vaccination. (Blood. 2004;103:3073-3075)
Clonality analysis of alveolar B lymphocytes contributes to the diagnostic strategy in clinical suspicion of pulmonary lymphoma
Authors: Zompi Simona , Couderc Louis-Jean , Cadranel Jacques , Antoine Martine , Epardeau Bernard , Fleury-Feith Jocelyne , Popa Natalia , Santoli François , Farcet Jean-Pierre , Delfau-Larue Marie-Hélène 
Published: January 2004

AbstractThe diagnostic procedure of chronic pulmonary opacities may envisage the search for non-Hodgkin lymphoma (NHL). Previous retrospective studies have shown that clonality analysis of bronchoalveolar B lymphocytes could reflect the clonality of pulmonary lymphocytes. Our objective was to define the diagnostic usefulness of bronchoalveolar lavage (BAL) B-lymphocyte clonality analysis in the setting of a clinical suspicion of both primary and secondary pulmonary lymphoma. A prospective BAL fluid B-cell clonality analysis was performed by polymerase chain reaction (PCR) in 106 consecutive patients presenting with a clinical suspicion of pulmonary NHL. Diagnosis was pulmonary B-cell lymphoma for 22 patients (13 primary and 9 secondary). When compared, pulmonary biopsy and BAL fluid have clonal identity. The detection of a strong B-cell clonal population in BAL fluid was associated with the diagnosis of pulmonary NHL (P &lt; .0001), with a 97% specificity and a 95% negative predictive value. Thus, the absence of a dominant B-cell clone detection in BAL fluid could help to dismiss invasive investigations of pulmonary lesions. The detection of a dominant B-cell clone would lead to the performance of a pulmonary biopsy to get histologic diagnosis in primary pulmonary lymphoma and, by contrast, would avoid the need for biopsy in the setting of a secondary pulmonary lymphoma. (Blood. 2004;103: 3208-3215)
Light-chain only multiple myeloma is due to the absence of functional (productive) rearrangement of the IgH gene at the DNA level
Authors: Magrangeas Florence , Cormier Marie-Laure , Descamps Géraldine , Gouy Nadège , Lodé Laurence , Mellerin Marie-Paule , Harousseau Jean-Luc , Bataille Régis , Minvielle Stéphane , Avet-Loiseau Hervé ,   for the Intergroupe Francophone du Myélome
Published: January 2004

AbstractAlthough most multiple myeloma (MM) cases are characterized by the detection of a monoclonal immunoglobulin in the serum, about 15% of the patients present only immunoglobulin light chains, detected either in the urine or serum or both. These patients are designated as having light-chain (LC) MM. Using fiber-fluorescent in situ hybridization, and in contrast to patients and myeloma cell lines secreting heavy chains (who presented a legitimate functional IgH rearrangement in every case), LC MM never displayed a functional IgH recombination. Interestingly, most LC MM cases presented one IgH allele with a germline configuration (including the DJ region), the second allele being usually involved in an illegitimate recombination. Of note, most of these translocations occurred close to (or at) switch regions, even though in some cases, breakpoints involving nonswitch regions were observed. Thus, this study clearly showed that LC MM is due to the absence of legitimate IgH rearrangement at the DNA level, reflecting possible abnormalities in the IgH gene recombinations during B-cell maturation. Furthermore, it showed that this defect did not prevent the activation of the switch process because most of 14q32 translocations observed in LC MM occurred at switch regions.
Thrombophilic dysfibrinogen Tokyo V with the amino acid substitution of γ Ala327Thr: formation of fragile but fibrinolysis-resistant fibrin clots and its relevance to arterial thromboembolism
Authors: Hamano Akiei , Mimuro Jun , Aoshima Motonori , Itoh Takeyoshi , Kitamura Noboru , Nishinarita Susumu , Takano Katsuhiro , Ishiwata Akira , Kashiwakura Yuji , Niwa Kazuki , Ono Tomoko , Madoiwa Seiji , Sugo Teruko , Matsuda Michio , Sakata Yoichi 
Published: January 2004

AbstractThrombophilic dysfibrinogen Tokyo V was identified in a 43-year-old man with recurrent thromboembolism. Based on analyses of the patient fibrinogen genes, the amino acid sequence of the aberrant fibrinogen peptide, and deglycosylation experiments, fibrinogen Tokyo V was shown to have an amino acid substitution of γ Ala327Thr and possibly extra glycosylation at γ Asn325 because the mutation confers the N-linked glycosylation consensus sequence Asn-X-Thr. The mutation resulted in impaired function and hypofibrinogenemia (hypodysfibrinogen). Polymerization of fibrin monomers derived from patient fibrinogen was severely impaired with a partial correction in the presence of calcium, resulting in very low clottability. Additionally, a large amount of soluble cross-linked fibrin was formed upon thrombin treatment in the presence of factor XIII and calcium. However, Tokyo V–derived fibrin was resistant to degradation by tissue plasminogen activator (tPA)–catalyzed plasmin digestion. The structure of Tokyo V fibrin appeared severely perturbed, since there are large pores inside the tangled fibrin networks and fiber ends at the boundaries. Taken together, these data suggest that Tokyo V fibrin clots are fragile, so that fibrinolysis-resistant insoluble fibrin and soluble fibrin polymers may be released to the circulation, partly accounting for the recurrent embolic episodes in the patient. (Blood. 2004;103:3045-3050)
Involvement of casein kinase Iϵ in cytokine-induced granulocytic differentiation
Authors: Okamura Atsuo , Iwata Nobuko , Nagata Aki , Tamekane Akira , Shimoyama Manabu , Gomyo Hiroshi , Yakushijin Kimikazu , Urahama Norinaga , Hamaguchi Miyuki , Fukui Chie , Chihara Kazuo , Ito Mitsuhiro , Matsui Toshimitsu 
Published: January 2004

AbstractTwo closely related casein kinase I (CKI) isoforms, CKIδ and CKIϵ, are ubiquitously expressed in many human tissues, but their specific biologic function remains to be clarified. Here, we provide the first evidence that CKIϵ is involved in hematopoietic cell differentiation. CKIϵ, but not CKIδ, was down-regulated along with human granulocytic differentiation. The specific down-regulation was observed in granulocyte colony-stimulating factor (G-CSF)–induced cell differentiation of murine interleukin-3 (IL-3)–dependent myeloid progenitor 32D cells. Introduction of wild-type (WT)–CKIϵ into 32D cells inhibited the G-CSF–induced cell differentiation, whereas kinase-negative (KN)–CKIϵ promoted the differentiation. Neither WT- nor KN-CKIϵ affected IL-3–dependent cell growth. Moreover, introduction of WT- or KN-CKIδ did not affect the cytokine-induced cell growth and differentiation. While G-CSF–induced activation of signal transducers and activators of transcription 3 (STAT3) was sustained by KN-CKIϵ, STAT3 activation was attenuated by WT-CKIϵ. This may be explained by the fact that the suppressor of cytokine signaling 3 (SOCS3) was stabilized by its physical association with CKIϵ. Such stabilization by CKIϵ was also seen in IL-3–induced β-catenin. The stabilization of downstream components of cytokine and Wnt signaling by CKIϵ might be critical for integration of several intracellular signaling pathways to a cell-specific biologic response in hematopoietic cell self-renewal. (Blood. 2004;103: 2997-3004)
Environmental guidance of normal and tumor cell plasticity: epithelial mesenchymal transitions as a paradigm
Authors: Prindull Gregor , Zipori Dov 
Published: January 2004

AbstractEpithelial mesenchymal transitions are a remarkable example of cellular plasticity. These transitions are the hallmark of embryo development, are pivotal in cancer progression, and seem to occur infrequently in adult organisms. The reduced incidence of transitions in the adult could result from restrictive functions of the microenvironment that stabilizes adult cell phenotypes and prevents plastic behavior. Multipotential progenitor cells exhibiting a mesenchymal phenotype have been derived from various adult tissues. The ability of these cells to differentiate into all germ layer cell types, raises the question as to whether mesenchymal epithelial transitions occur in the adult organism more frequently than presently appreciated. A series of cytokines are known to promote the transitions between epithelium and mesenchyme. Moreover, several transcription factors and other intracellular regulator molecules have been conclusively shown to mediate these transitions. However, the exact molecular basis of these transitions is yet to be resolved. The identification of the restrictive mechanisms that prevent cellular transitions in adult organisms, which seem to be unleashed in cancerous tissues, may lead to the development of tools for therapeutic tissue repair and effective tumor suppression. (Blood. 2004; 103:2892-2899)
Defective fetal liver erythropoiesis and T lymphopoiesis in mice lacking the phosphatidylserine receptor
Authors: Kunisaki Yuya , Masuko Sadahiko , Noda Mayuko , Inayoshi Ayumi , Sanui Terukazu , Harada Mine , Sasazuki Takehiko , Fukui Yoshinori 
Published: January 2004

Abstract
Clearance of apoptotic cells by macrophages is considered important for prevention of inflammatory responses leading to tissue damage. The phosphatidylserine receptor (PSR), which specifically binds to phosphatidylserine (PS) exposed on the surface of apoptotic cells, mediates uptake of apoptotic cells in vitro, yet the physiologic relevance of PSR remains unknown. This issue was addressed by generating PSR-deficient (PSR-/-) mice. PSR-/- mice exhibited severe anemia and died during the perinatal period. In the PSR-/- fetal livers, erythroid differentiation was blocked at an early erythroblast stage. In addition, PSR-/- embryos exhibited thymus atrophy owing to a developmental defect of T-lymphoid cells. Clearance of apoptotic cells by macrophages was impaired in both liver and thymus of PSR-/- embryos. However, this did not induce up-regulation of inflammatory cytokines. These results indicate that during embryonic development, PSR-mediated apoptotic cell uptake is required for definitive erythropoiesis and T lymphopoiesis, independently of the prevention of inflammatory responses. (Blood. 2004;103:3362-3364)
Transcriptional profiling of IKK2/NF-κB— and p38 MAP kinasedependent gene expression in TNF-α—stimulated primary human endothelial cells
Authors: Viemann Dorothee , Goebeler Matthias , Schmid Sybille , Klimmek Kerstin , Sorg Clemens , Ludwig Stephan , Roth Johannes 
Published: January 2004

AbstractInflammatory stimulation of endothelial cells by tumor necrosis factor α (TNF-α) involves activation of nuclear factor κB (NF-κB) and p38 mitogen-activated protein (MAP) kinase signaling pathways. A reliable analysis of the gene expression program elicited by TNF-α and its assignment to distinct signaling pathways is not available. A sophisticated analysis of oligonucleotide microarrays covering more than 13 000 genes allowed definition of the TNF-α-regulated endothelial gene expression profile and novel TNF-α-induced genes. Virtually all TNF-α-inducible genes were dependent on IκB kinase 2 (IKK2)/NF-κB activation, whereas a minor number was additionally modulated by p38. Furthermore, genes suppressed by IKK2/NF-κB were newly identified. Real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and flow cytometry confirmed reliability of data. Thus, these results define a list of primary candidates for targeted modulation of endothelial functions during inflammation. (Blood. 2004;103:3365-3373)
Phase III Study of N,N-Diethyl-2-[4-(Phenylmethyl) Phenoxy]Ethanamine (BMS-217380-01) Combined With Doxorubicin Versus Doxorubicin Alone in Metastatic/Recurrent Breast Cancer: National Cancer Institute of Canada Clinical Trials Group Study MA.19
Authors: Reyno Leonard , Seymour Lesley , Tu Dongsheng , Dent Susan , Gelmon Karen , Walley Barbara , Pluzanska Anna , Gorbunova Vera , Garin Avgust , Jassem Jacek , Pienkowski Tadeusz , Dancey Janet , Pearce Laura , MacNeil Mary , Marlin Susan , Lebwohl David , Voi Maurizio , Pritchard Kathleen 
Published: January 2004

Purpose N,N-diethyl-2-[4-(phenylmethyl)phenoxy]ethanamine (DPPE; tesmilifene) is a novel agent that augments chemotherapy cytotoxicity in vitro and in vivo. A phase II trial combining DPPE and doxorubicin (DOX) in metastatic breast carcinoma showed increased response over that expected with DOX. We report a phase III trial comparing DOX with DPPE plus DOX in metastatic or recurrent breast cancer. Patients and Methods Anthracycline-naive women with measurable metastatic disease were randomly assigned to receive, every 21 days, either DOX 60 mg/m2 intravenously or DOX during the last 20 minutes of an 80-minute infusion of DPPE (5.3 mg/kg), in both cases to cumulative DOX doses of 450 mg/m2. Patients receiving DPPE were aggressively premedicated to ameliorate toxicity. End points included progression-free survival (PFS), response rate (RR), and response duration (RD), quality of life (QOL), toxicity, and overall survival (OS). Results A planned interim analysis failed to detect an RR difference more than 5%. The study was closed to additional accrual and all DPPE was discontinued. The final analysis was conducted as planned after 256 progression events (median follow-up, 20.5 months). There was no significant difference in RR, RD, or PFS between arms. DPPE plus DOX was statistically superior to DOX in OS (hazard ratio, 0.66; 95% CI, 0.48 to 0.91; P = .021). DPPE plus DOX was associated with more gastrointestinal and CNS toxicity. No consistent influence on QOL was detected. Conclusion This study demonstrated no advantage in RR, RD, or PFS but significantly superior OS for DPPE plus DOX. Additional studies of DPPE are warranted.
Clinical Cardiac Tolerability of Trastuzumab
Authors: Perez Edith A. , Rodeheffer Richard 
Published: January 2004

Purpose This review provides an update on the current understanding of the clinical cardiac tolerability of trastuzumab, a humanized monoclonal antibody effective in the treatment of patients with advanced breast cancer overexpressing or amplifying HER2. Methods and Results We produced a summary of currently available information regarding the incidence and natural history of trastuzumab-associated cardiac dysfunction. Data from new, prospective clinical studies that incorporate close cardiac monitoring and standardized follow-up in patients with either advanced or earlier stages of breast cancer are also presented, and hypotheses regarding potential mechanisms of trastuzumab-related cardiotoxicity are discussed. Patients treated with trastuzumab in the pivotal trials were found to have increased risk for cardiac dysfunction, mostly when used concurrent with anthracyclines. Recent trials have required more stringent and consistent cardiac monitoring criteria and excluded patients with abnormal cardiac function, pre-existing heart disease, and/or high cumulative doses of anthracyclines. Decreases of ejection fraction and a few cases of congestive heart failure (CHF) requiring medical therapy have been detected. Improvements in ejection fraction and the symptoms of CHF have been subsequently noted in a significant number of these patients. Conclusion Trastuzumab is associated with an increased risk of asymptomatic decreases in ejection fraction, and, in a small number of patients, CHF that is almost always responsive to medical management. This risk is greatest in patients receiving concurrent anthracyclines. More data are needed to help elucidate the pathophysiology of this syndrome.