bluuebunny/crossref_metadata_2025_split huggingface dataset:
Selective adenosine A2A receptor agonist, ATL‐146e, attenuates stress‐induced gastric lesions in rats
Authors: ODASHIMA MASARU , OTAKA MICHIRO , JIN MARIO , KOMATSU KOGA , WADA ISAO , MATSUHASHI TAMOTSU , HORIKAWA YOUHEI , HATAKEYAMA NATSUMI , OYAKE JINKO , OHBA REINA , LINDEN JOEL , WATANABE SUMIO 
Published: January 2005

AbstractBackground:  Activation of adenosine A2A receptors reduces the production of various pro‐inflammatory cytokines and suppresses neutrophil activation. Water‐immersion restraint is well known to cause gastric mucosal lesions due to stress. The pathogenesis of stress‐induced gastric mucosal lesions is characterized by activation of inflammatory cells and production of inflammatory cytokines. Agonists of adenosine A2A receptors are known to be anti‐inflammatory, but the effects of these compounds on the development of gastric mucosal lesions has not been reported. In the present study, the effect of a potent and selective adenosine A2A receptor agonist, ATL‐146e, on water‐immersion stress‐induced gastric mucosal lesions was studied.Methods:  Rats were subjected to water‐immersion stress with or without pretreatment with a single intraperitoneal injection of a potent and selective agonist of the adenosine A2A receptor. The gastric concentrations of myeloperoxidase (MPO), as an index of neutrophil accumulation, and the pro‐inflammatory cytokines, tumor necrosis factor‐α (TNF‐α) and interleukin‐1β (IL‐1β), were measured.Results:  The total length of gastric erosions (ulcer index) in control rats was 21.6 ± 3.23 mm and was reduced by 86% to 3.1 ± 0.83 mm by pretreatment with 5.0 µg/kg ATL146e (P < 0.001). The gastric content of MPO, TNF‐α and IL‐1β were all increased after water‐immersion stress and reduced to near normal levels by ATL‐146e.Conclusion:  A specific adenosine A2A agonist inhibits stress‐induced gastric inflammation and damage. A2A agonist compounds may be useful for preventing ulcers and appear to act by blocking gastric inflammation.© 2004 Blackwell Publishing Asia Pty Ltd
Neutrophils enhance invasion activity of human cholangiocellular carcinoma and hepatocellular carcinoma cells: An in vitro study
Authors: IMAI YOSHIHITO , KUBOTA YOSHITSUGU , YAMAMOTO SHIN , TSUJI KAZUYUKI , SHIMATANI MASAAKI , SHIBATANI NOBUYUKI , TAKAMIDO SHOICHIROH , MATSUSHITA MASANORI , OKAZAKI KAZUICHI 
Published: January 2005

AbstractBackground and Aim:  Tumor–mesenchymal interactions are involved in the mechanism of tumor invasion in several types of carcinoma. Mutual interactions between carcinoma cells and neutrophils, however, have been poorly understood. In the present study we examined the effect of neutrophils on invasion activities of carcinoma cells in vitro. Role of hepatocyte growth factor (HGF) as a mediator was also evaluated.Methods:  Using a Matrigel invasion chamber, invasion activities of HuCC‐T1 human cholangiocellular carcinoma cells and HepG2 hepatocellular carcinoma cells in response to recombinant HGF or neutrophils were evaluated.Results:  Recombinant HGF dose‐dependently increased invasion activities of HuCC‐T1 and HepG2 cells. Neutrophils significantly enhanced invasion activities of these cells, which were suppressed to the respective basal levels with anti‐HGF antibody. The carcinoma cells did not secrete HGF. Neutrophils cultivated in tumor condition medium (TCM) of HuCC‐T1 or HepG2 cells secreted a significant level of HGF protein without increasing HGF mRNA expression. Treatment with heat or ultrafiltration of TCM of HuCC‐T1 or HepG2 cells suggested carcinoma cell‐derived HGF inducer(s) to be certain protein(s) with a molecular weight of more than 30 000.Conclusions:  The present study suggests the presence of mutual interactions between HuCC‐T1/HepG2 carcinoma cells and neutrophils in tumor invasion via paracrine regulation mediated by neutrophil‐derived HGF.
A Decomposition Analysis of Regional Poverty in Russia
Authors: Kolenikov Stanislav , Shorrocks Anthony 
Published: January 2005

AbstractThe paper applies a new decomposition technique to the study of variations in poverty across the regions of Russia. The procedure, which is based on the Shapley value in cooperative game theory, allows the deviation in regional poverty levels from the all‐Russia average to be attributed to three proximate sources: per capita income, inequality, and local prices. Contrary to expectation, regional poverty variations turn out to be due more to differences in inequality across regions than to differences in real income per capita. However, when real income per capita is split into nominal income and price components, differences in nominal incomes emerge as more important than either inequality or price effects for the majority of regions.
Fifty Years of Regional Inequality in China: a Journey Through Central Planning, Reform, and Openness
Authors: Kanbur Ravi , Zhang Xiaobo 
Published: January 2005

AbstractThe paper constructs and analyzes a long‐run time series for regional inequality in China from the Communist Revolution to the present. There have been three peaks of inequality in the last fifty years, coinciding with the Great Famine of the late 1950s, the Cultural Revolution of the late 1960s and 1970s, and finally the period of openness and global integration in the late 1990s. Econometric analysis establishes that regional inequality is explained in the different phases by three key policy variables—the ratio of heavy industry to gross output value, the degree of decentralization, and the degree of openness.
Spatial–Horizontal Inequality and the Maoist Insurgency in Nepal
Authors: Murshed S. Mansoob , Gates Scott 
Published: January 2005

AbstractThe Maoist insurgency in Nepal is one of the highest intensity internal conflicts in recent times. Investigation into the causes of the conflict would suggest that grievance rather than greed is the main motivating force. The concept of horizontal or intergroup inequality, with both an ethnic and caste dimension, is highly relevant in explaining the Nepalese civil war. There is also a spatial aspect to the conflict, which is most intense in the most disadvantaged areas in terms of human development indicators and land holdings. Using the intensity of conflict (fatalities) as the dependent variable and HDI indicators and landlessness as explanatory variables, the authors find that the intensity of conflict across the districts of Nepal is significantly explained by the degree of inequalities.
Effects of Transient Myocardial Ischemia on the Ventricular Defibrillation Threshold
Authors: ANASTASIOU‐NANA MARIA I. , TSAGALOU ELEFTHERIA P. , CHARITOS CHRISTOS , SIAFAKAS KOSTANTINOS X. , DRAKOS STAVROS , TERROVITIS JOHN V. , NTALIANIS ARGIRIOS , DOUFAS ANTONIOS , MAVRIKAKIS JOHN , NANAS JOHN N. 
Published: January 2005

Background: Acute myocardial ischemia and the mode of ventricular fibrillation (VF) induction influence the ventricular defibrillation threshold (DFT).
Objectives: The purpose of this study was to determine the effects of transient regional left ventricular (LV) ischemia on the DFT.
Methods: Ventricular effective refractory period (ERP), ventricular fibrillation threshold (VFT), and DFT were measured under nonischemic conditions (control) in 26 pigs weighing 25–35 kg. Myocardial ischemia was then induced by occlusion of the mid left anterior descending coronary artery, and measurements of ERP and VFT were repeated after 2 minutes of occlusion. The coronary artery ligation was released immediately after the onset of VF and DFT was measured.
Results: LV ERP was unchanged by ischemia (199 ± 19 ms at control vs. 200 ± 22 ms under ischemic conditions, P = 0.799), whereas VFT was significantly lower during coronary occlusion (10.7 ± 5.4 mA vs. 37.7 ± 13 mA, P = 0.000). Brief myocardial ischemia caused a significant increase in DFT (13.5 ± 12.6 J after coronary occlusion vs. 6.8 ± 6.8 J at control, P = 0.023). The duration of coronary occlusion was not correlated with the amounts of energy required to defibrillate (P = 0.526).
Conclusions: This experimental study shows that transient myocardial ischemia markedly increases the DFT, suggesting that specific defibrillation algorithms should be designed for recipients of implantable defibrillators at risk of myocardial ischemia.
Electrophysiological Characteristics of Junctional Rhythm During Ablation of the Slow Pathway in Different Types of Atrioventricular Nodal Reentrant Tachycardia
Authors: LEE SHIH‐HUANG , TAI CHING‐TAI , LEE PI‐CHANG , CHIANG CHERN‐EN , CHENG JUN‐JACK , UENG KOW‐CHANG , CHEN YI‐JEN , HSIEH MING‐HSIUNG , TSAI CHIN‐FENG , CHIOU CHUEN‐WANG , YU WEN‐CHUNG , KUO JEN‐YUAN , TSAO HSUAN‐MING , LEE KUN‐TAI , CHEN SHIH‐ANN 
Published: January 2005

Background: Junctional rhythm (JR) is commonly observed during radiofrequency (RF) ablation of the slow pathway for atrioventricular (AV) nodal reentrant tachycardia. However, the atrial activation pattern and conduction time from the His‐bundle region to the atria recorded during JR in different types of AV nodal reentrant tachycardia have not been fully defined.
Methods: Forty‐five patients who underwent RF ablation of the slow pathway for AV nodal reentrant tachycardia were included; 27 patients with slow‐fast, 11 patients with slow‐intermediate, and 7 patients with fast‐slow AV nodal reentrant tachycardia. The atrial activation pattern and HA interval (from the His‐bundle potential to the atrial recording of the high right atrial catheter) during AV nodal reentrant tachycardia (HASVT) and JR (HAJR) were analyzed.
Results: In all patients with slow‐fast AV nodal reentrant tachycardia, the atrial activation sequence recorded during JR was similar to that of the retrograde fast pathway, and transient retrograde conduction block during JR was found in 1 (4%) patient. The HAJR was significantly shorter than the HASVT (57 ± 24 vs 68 ± 21 ms, P < 0.01). In patients with slow‐intermediate AV nodal reentrant tachycardia, the atrial activation sequence of the JR was similar to that of the retrograde fast pathway in 5 (45%), and to that of the retrograde intermediate pathway in 6 (55%) patients. Transient retrograde conduction block during JR was noted in 1 (9%) patient. The HAJR was also significantly shorter than the HASVT (145 ± 27 vs 168 ± 29 ms, P = 0.014). In patients with fast‐slow AV nodal reentrant tachycardia, retrograde conduction with block during JR was noted in 7 (100%) patients. The incidence of retrograde conduction block during JR was higher in fast‐slow AV nodal reentrant tachycardia than slow‐fast (7/7 vs 1/11, P < 0.01) and slow‐intermediate AV nodal reentrant tachycardia (7/7 vs 1/27, P < 0.01).
Conclusions: In patients with slow‐fast and slow‐intermediate AV nodal reentrant tachycardia, the JR during ablation of the slow pathway conducted to the atria through the fast or intermediate pathway. In patients with fast‐slow AV nodal reentrant tachycardia, there was no retrograde conduction during JR. These findings suggested there were different characteristics of the JR during slow‐pathway ablation of different types of AV nodal reentrant tachycardia.
Twin AV Node and Induced Supraventricular Tachycardia in Fontan Palliation Patients
Authors: BAE EUN‐JUNG , NOH CHUNG‐IL , CHOI JUNG‐YUN , YUN YONG‐SOO , KIM WOONG‐HAN , LEE JEONG‐RYUL , KIM YONG‐JIN 
Published: January 2005

Introduction: The coexistence of two distinct atrioventricular (AV) nodes has been described in congenital heart disease requiring Fontan type palliation. The purpose of this study was to evaluate the occurrence of twin AV node according to anatomical subgroups, and to determine its relation to tachycardia.
Methods: From 2001 to 2003, we performed an electrophysiologic (EP) study upon 52 consecutive patients who had undergone cardiac catheterization after Fontan completion. Atrial pacing was performed at three or more different atrial sites.
Results: In 10/52 patients, two different QRS complexes were recorded at different pacing sites, suggesting twin AV node (9/20 in right isomerism, 1/8 discordance AV connections, 0/24 other complex anomalies). AV reciprocating tachycardia (AVRT), presumably involving two AV nodes and a connecting sling, was induced in 6 of 10 patients who had twin AV node (4/6 used posterior AV node as an antegrade limb, 2/6 used an anterior AV node as an antegrade limb). Heterotaxy syndrome (P < 0.001) and complete AV septal defect (P = 0.002) were found to be risk factors for twin AV node. Junctional tachycardia (JT; HR > 150/min) with either VA dissociation (7/9) or second degree VA block (2/9) were induced by pacing or isoproterenol infusion in 9/52 patients.
Conclusion: JT induction was associated with a twin AV node (P = 0.04), or a history of early postoperative junctional ectopic tachycardia (P = 0.02). A complicated AV node conduction system such as twin AV node was frequent in heterotaxy syndrome. Both AVRT and JT with VA block may be important causes of tachyarrhythmia in this patient group.
Clinical ethics, information, and communication: review of 31 cases from a clinical ethics committee: Table 1
Authors: Førde R , Vandvik I H 
Published: January 2005

Objectives:To summarise the types of case brought to the Clinical Ethics Committee of the National Hospital of Norway from 1996 to 2002 and to describe and discuss to what extent issues of information/communication have been involved in the ethical problems.Design:Systematic review of case reports.Findings:Of the 31 case discussions, (20 prospective, 11 retrospective), 19 cases concerned treatment of children. Twenty cases concerned ethical problems related to withholding/withdrawing of treatment. In 25 cases aspects of information/communication were involved in the ethical problem, either explicitly (n = 3) or implicitly (n = 22).Conclusion:Problems related to information/communication may underlie a classic ethical problem. Identification of these “hidden” problems may be important for the analysis, and hence, the solution to the ethical dilemma.
Involvement of JAM-A in Mononuclear Cell Recruitment on Inflamed or Atherosclerotic Endothelium
Authors: Ostermann Georg , Fraemohs Line , Baltus Thomas , Schober Andreas , Lietz Michael , Zernecke Alma , Liehn Elisa A. , Weber Christian 
Published: January 2005

Objective—The junctional adhesion molecule (JAM)-A on endothelium contributes to the inflammatory recruitment of mononuclear cells involving engagement of its integrin receptor lymphocyte function-associated antigen (LFA)-1. It is unknown whether these functions can be inhibited by soluble forms of JAM-A, whether JAM-A is expressed on atherosclerotic endothelium, and whether it participates in atherogenic recruitment of mononuclear cells.Methods and Results—Adhesion assays revealed that LFA-1–mediated binding of mononuclear cells to intercellular adhesion molecule (ICAM)-1 or cytokine-costimulated endothelium was dose-dependently inhibited by soluble JAM-A.Fc (sJAM-A.Fc). Similarly, sJAM-A.Fc reduced stromal cell-derived factor (SDF)-1α–triggered transendothelial chemotaxis of activated T cells and their SDF-1α–triggered arrest on cytokine-costimulated endothelium under flow conditions. Immunofluorescence analysis revealed an upregulation of JAM-A on early atherosclerotic endothelium of carotid arteries from apolipoprotein E-deficient (apoE−/−) mice fed an atherogenic diet. In ex vivo perfusion assays, pretreatment of mononuclear cells with sJAM-A.Fc inhibited their very late antigen (VLA)-4–independent accumulation on atherosclerotic endothelium of these arteries.Conclusions—Soluble forms of JAM-A can be effectively applied to inhibit distinct steps of mononuclear cell recruitment on inflamed or atherosclerotic endothelium. In conjunction with its expression on atherosclerotic endothelium, this suggests a functional contribution of JAM-A to atherogenesis.
Gudmunder Alfredsson and Katarina Tomaševski (eds.), A Thematic Guide to Documents on the Human Rights of Women: Global and Regional Standards adopted by Intergovernmental Organizations, International Non-Governmental Organizations and Professional Associations, The Raoul Wallenberg Institute Human Rights Guides, Volume 1, The Hague: Martinus Nijhoff, 1995
Authors: Thorburn  
Published: January 2005

AbstractNo Abstract
Rescue of early-stage myelodysplastic syndrome-deriving erythroid precursors by the ectopic expression of a dominant-negative form of FADD
Authors: Claessens Yann-Erick , Park Sophie , Dubart-Kupperschmitt Anne , Mariot Virginie , Garrido Carmen , Chrétien Stany , Dreyfus François , Lacombe Catherine , Mayeux Patrick , Fontenay Michaëla 
Published: January 2005

AbstractMyelodysplastic syndromes (MDSs) are characterized by peripheral blood cytopenia including anemia. We have investigated the implication of the extrinsic pathway of apoptosis in MDS-ineffective erythropoiesis by in vitro expansion of erythroid precursors from early stage (low and intermediate-1 International Prognosis Scoring System [IPSS]) MDS, advanced stage (intermediate-2 IPSS) MDS, and control bone marrow samples. We have previously shown that Fas and its ligand were overexpressed in early stage MDS erythroid cells. Here, we show that caspase-8 activity is significantly increased, whereas the expression of death receptors other than Fas, including the type 1 receptor for tumor necrosis factor α (TNF-α) and the receptors for the TNF-related apoptosis-inducing ligand (TRAIL), DR4 and DR5, was normal. We also observed that the adapter Fas-associated death domain (FADD) was overexpressed in early stage MDS erythroid cells. Transduction of early stage MDS-derived CD34+ progenitors with a FADD-encoding construct increased apoptosis of erythroid cells and dramatically reduced erythroid burst-forming unit (BFU-E) growth. Transduction of a dominant-negative (dn) mutant of FADD inhibited caspase-8 activity and cell death and rescued BFU-E growth without abrogating erythroid differentiation. These results extend the observation that Fas-dependent activation of caspase-8 accounts for apoptosis of early stage MDS erythroid cells and demonstrate for the first time that FADD is a valuable target to correct ineffective erythropoiesis in these syndromes.
SAP controls the cytolytic activity of CD8+ T cells against EBV-infected cells
Authors: Dupré Loïc , Andolfi Grazia , Tangye Stuart G. , Clementi Rita , Locatelli Franco , Aricò Maurizio , Aiuti Alessandro , Roncarolo Maria-Grazia 
Published: January 2005

AbstractThe adaptor protein SAP regulates signaling through signaling lymphocytic activation molecule (SLAM)–family receptors expressed on T and natural killer (NK) cells. In patients affected by X-linked lymphoproliferative (XLP) disease, mutations in the SH2D1A gene result in defective lytic activity. However, the mechanism by which SAP controls cytotoxic activity remains unclear. T-cell–receptor (TCR) activation of CD8+ cytotoxic T cells (CTLs) results in down-regulation of SAP, suggesting that this protein is involved in early activation events. Here, we show that SAP-deficient CTLs from patients with XLP and hemophagocytic lymphohistiocytosis (HLH) display a specific lytic defect against autologous and allogeneic Epstein-Barr virus (EBV)–positive B cells. This defect is associated with the defective polarization of 2B4, perforin, and lipid rafts at the contact area of CTLs with EBV-positive targets. Blockade of 2B4 in normal CTLs reproduces the defects in lysis and polarization observed in SAP-deficient CTLs. Expression and regulation of the SLAM-family receptors SLAM, CD84, and 2B4, as well as the lytic effectors perforin and granzyme-B are normal in SAP-deficient CTLs. In addition, TCR stimulation leads to normal proliferation and production of interleukin 2 (IL-2), IL-4, and interferon-γ (IFN-γ). These results demonstrate that the SAP/2B4 pathway plays a key role in CTL lytic activity against EBV-positive targets by promoting the polarization of the lytic machinery.
SCL/Tal-1 is essential for hematopoietic commitment of the hemangioblast but not for its development
Authors: D'Souza Sunita L. , Elefanty Andrew G. , Keller Gordon 
Published: January 2005

AbstractIn this report, we have defined the stage at which Scl functions in the establishment of the hematopoietic system and provide evidence that its primary role is in the generation of the hematopoietic lineages from a progenitor called the blast colony-forming cell (BL-CFC), a cell considered to be the in vitro equivalent of the hemangioblast. Using an embryonic stem (ES) cell line in which lacZ cDNA has been targeted to the Scl locus, we show that most of the BL-CFCs are detected in the SCL/lacZ- population, indicating that this progenitor does not express Scl. In the blast colony assay, Scl-/- cells initiate colony growth but are unable to generate endothelial and hematopoietic progeny and thus form colonies consisting of vascular smooth muscle cells only. The capacity to give rise to blast colonies can be rescued by retroviral transduction of a wild-type Scl gene into Scl-/- FLK-1+ cells, suggesting that the BL-CFC is generated in this population. Finally, we show that Scl-/- endothelial cells display a growth deficiency in monolayer cultures that can be partially overcome by maintaining this population as 3-dimensional aggregates indicating that specific cellular interactions are required for maintenance of the Scl-/- endothelial lineage in vitro.
Overexpression of transcripts originating from the MMSET locus characterizes all t(4;14)(p16;q32)-positive multiple myeloma patients
Authors: Keats Jonathan J. , Maxwell Christopher A. , Taylor Brian J. , Hendzel Michael J. , Chesi Marta , Bergsagel P. Leif , Larratt Loree M. , Mant Michael J. , Reiman Tony , Belch Andrew R. , Pilarski Linda M. 
Published: January 2005

AbstractMultiple myeloma (MM) is a B-lineage malignancy characterized by diverse genetic subtypes and clinical outcomes. The recurrent immunoglobulin heavy chain (IgH) switch translocation, t(4;14)(p16;q32), is associated with poor outcome, though the mechanism is unclear. Quantitative reverse-transcription–polymerase chain reaction (RT-PCR) for proposed target genes on a panel of myeloma cell lines and purified plasma cells showed that only transcripts originating from the WHSC1/MMSET/NSD2 gene are uniformly dysregulated in all t(4;14)POS patients. The different transcripts detected, multiple myeloma SET domain containing protein (MMSET I), MMSET II, Exon 4a/MMSET III, and response element II binding protein (RE-IIBP), are produced by alternative splicing and alternative transcription initiation events. Translation of the various transcripts, including those from major breakpoint region 4-2 (MB4-2) and MB4-3 breakpoint variants, was confirmed by transient transfection and immunoblotting. Green fluorescent protein (GFP)–tagged MMSET I and II, corresponding to proteins expressed in MB4-1 patients, localized to the nucleus but not nucleoli, whereas the MB4-2 and MB4-3 proteins concentrate in nucleoli. Cloning and localization of the Exon 4a/MMSET III splice variant, which contains the protein segment lost in the MB4-2 variant, identified a novel protein domain that prevents nucleolar localization. Kinetic studies using photobleaching suggest that the breakpoint variants are functionally distinct from wild-type proteins. In contrast, RE-IIBP is universally dysregulated and also potentially functional in all t(4;14)POS patients irrespective of fibroblast growth factor receptor 3 (FGFR3) expression or breakpoint type.
New trends in umbilical cord blood transplantation
Authors: Ballen Karen K. 
Published: January 2005

AbstractSince the first report of a successful umbilical cord blood transplantation in 1988, there has been great interest in the use of cord blood as an alternative stem cell source to treat cancer and genetic diseases. More than 4000 cord blood transplantations have been performed worldwide. In this review, the scientific rationale for this therapy, as well as related preclinical studies, cord blood banking issues, and ethical concerns, will be addressed. Results of studies in both pediatric and adult transplantation will be discussed. Finally, new indications for cord blood use and emerging technologies will be addressed.