bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hermeneutics and the Doctrine of Scripture: Why They Need Each Other
Authors: WATSON FRANCIS 
Published: March 2010

AbstractCurrent attempts to understand Scripture theologically typically appeal either to modern hermeneutics or to more traditional doctrines of Scripture – but not to both together. It is argued here that hermeneutics can help to identify and resolve certain problems bequeathed to posterity by the characteristic sixteenth‐century equation of Scripture with ‘Word of God’. The problems in question relate to the past and present modes of divine speech, the relation of text to community and the fundamental significance of the ‘Word of God’ concept itself.
Development of the State Impostor Phenomenon Scale
Authors: FUJIE RIEKO 
Published: March 2010

AbstractThe purpose of this study was to develop a State Impostor Phenomenon Scale (SIPS). Participants (344 graduate and undergraduate students) were asked to complete the SIPS, the State Self‐Esteem Scale, and the State‐Trait Anxiety Scale in three situations, followed by the Trait Self‐Esteem Scale. Results showed that the SIPS had stable factor structure, and adequate reliability. In addition, the predicted correlational patterns among the scales demonstrated the construct validity of the SIPS. Moreover, the SIPS was responsive to different situations, as evidenced by significant differences between the scores in the three situations.
Developmental changes in the effects of types of self‐corrected elaboration on incidental memory
Authors: TOYOTA HIROSHI 
Published: March 2010

AbstractThe present study investigated the developmental changes in the effects of two types of self‐corrected elaboration, namely generated correction and chosen correction, on incidental memory of words. Second and sixth graders performed an orienting task involving two types of correction followed by an unexpected recall test. They were presented with a target and its sentence, and were asked to correct the target to a congruous word in the generated‐correction condition, or to choose one of the alternative congruous words in the chosen‐correction condition. For second graders, chosen correction led to a better recall than generated correction, whereas for sixth graders the reverse relationship between the two corrections was observed. These results were interpreted as showing the developmental change in the effects of types of self‐corrected elaboration on incidental memory.
Ambiguous incorporations: microfinance and global governmentality
Authors: AITKEN ROB 
Published: March 2010

AbstractIn the spring of 2007 an event dramatically reshaped conversations relating to microfinance. This event was the Initial Public Offering (IPO) of Mexico's largest microfinance organization, Compartamos. The IPO, as this article suggests, is indicative or a broader trend through which microfinance is increasingly becoming financialized, increasingly becoming governable as a financial object. This is important at one level because it crystallizes some of the key issues at stake as microfinance becomes increasingly more reliant on global capital markets. At another level, however, the Compatarmos case is significant because of the conceptual issues it raises in relation to global finance. The main argument I put forward in this article is that the Compatarmos case – and the process of financialization it represents – is important because it allows us to glimpse global finance, and the question of global financial governance, as a decentred process in formation. Drawing on a Foucauldian notion of governmentality, I argue that the Compatarmos case orbits around two processes; processes of incorporation and differentiation. In this context, the Compartamos case implies the importance of analyses that can make global finance visible as a diverse and mundane object that is never settled in any final kind of way.
ICT and geographies of British Arab and Arab American activism
Authors: NAGEL CAROLINE , STAEHELI LYNN 
Published: March 2010

AbstractCurrent literature on migrant transnationalism highlights the role of new information and communication technologies (ICT) in facilitating lives that are situated simultaneously ‘here’ and ‘there’. Yet discussions of transnationalism and ICT obscure many complexities because of the tendency to focus on migrants' connections with ‘homeland’. In this article, we consider more broadly the spatiality of migrant activism and the different ways that ICT enters into it. Drawing on interviews conducted with Arab American and British Arab activists, we ask where is migrant activism geographically situated? How might their use of ICT factor into, or not factor into, activists' activities? In considering our respondents' diverse forms of activism, the multitude of aims and geographical orientations underpinning their activism, and their highly variable use of ICT, this article provides a variegated understanding of migrants' political subjectivities that avoids privileging any single geographical scale or location.
From doves to hawks: A spatial analysis of voting in the Monetary Policy Committee of the Bank of England
Authors: HIX SIMON , HØYLAND BJØRN , VIVYAN NICK 
Published: March 2010

AbstractThis article examines the making of monetary policy in the United Kingdom between 1997 and 2008 by analysing voting behaviour in the Bank of England's Monetary Policy Committee (MPC). It provides a new set of measures for the monetary policy preferences of individual MPC members by estimating a Bayesian item response model. The article demonstrates the usefulness of these measures by comparing the ideal points of outgoing MPC members with their successors and by looking at changes over time in the median ideal point on the MPC. The analysis indicates that the British Government has been able to move the position of the median voter on the MPC through its appointments to the Committee. This highlights the importance of central bank appointments for monetary policy.
Shikonin reduces oedema induced by phorbol ester by interfering with IκBα degradation thus inhibiting translocation of NF‐κB to the nucleus
Authors: Andújar I , Recio MC , Bacelli T , Giner RM , Ríos JL 
Published: March 2010

Background and purpose:  In the present paper we studied the effect of shikonin on ear oedema induced by 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA), and determined the mechanisms through which shikonin might exert its topical anti‐inflammatory action.Experimental approach:  Acute ear oedema was induced in mice by topical application of TPA. The in vitro assays used macrophages RAW 264.7 cells stimulated with lipopolysaccharide. Cyclooxygenase‐2, inducible nitric oxide synthase, protein kinase Cα, extracellular signal‐regulated protein kinase (ERK), phosphorylated ERK (pERK), c‐Jun N‐terminal kinase (JNK), pJNK, p38, p‐p38, p65, p‐p65, inhibitor protein of nuclear factor‐κB (NF‐κB) (IκBα) and pIκBα were measured by Western blotting, activation and binding of NF‐κB to DNA was detected by reporter gene and electrophoretic mobility shift assay, respectively, and NF‐κB p65 localization was detected by immunocytochemistry.Key results:  Shikonin reduced the oedema (inhibitory dose 50 = 1.0 mg per ear), the expression of cyclooxygenase‐2 (70%) and of inducible nitric oxide synthase (100%) in vivo. It significantly decreased TPA‐induced translocation of protein kinase Cα, the phosphorylation and activation of ERK, the nuclear translocation of NF‐κB and the TPA‐induced NF‐κB‐DNA‐binding activity in mouse skin. Moreover, in RAW 264.7 cells, shikonin significantly inhibited the binding of NF‐κB to DNA in a dose‐dependent manner and the nuclear translocation of p65.Conclusions and implications:  Shikonin exerted its topical anti‐inflammatory action by interfering with the degradation of IκBα, thus inhibiting the activation of NF‐κB.
Isoflurane protects cardiomyocytes and mitochondria by immediate and cytosol‐independent action at reperfusion
Authors: Pravdic D , Mio Y , Sedlic F , Pratt PF , Warltier DC , Bosnjak ZJ , Bienengraeber M 
Published: March 2010

Background and purpose:  The volatile anaesthetic isoflurane protects the heart from ischaemia and reperfusion (I/R) injury when applied at the onset of reperfusion [anaesthetic postconditioning (APoC)]. However, the mechanism of APoC‐mediated protection is unknown. In this study, we examined the effect of APoC on mitochondrial bioenergetics, mitochondrial matrix pH (pHm) and cytosolic pH (pHi), and intracellular Ca2+.Experimental approach:  Cardiac mitochondria from Wistar rats were isolated after in vivo I/R with or without APoC (1.4%‐vol isoflurane, 1 minimum alveolar concentration), and mitochondrial permeability transition pore (mPTP) opening, mitochondrial membrane potential (ΔΨm), and oxygen consumption were assessed. In isolated cardiomyocytes and isolated mitochondria I/R injury was produced in vitro, with or without APoC (0.5 mM isoflurane). Intracellular Ca2+, pHm, pHi and ΔΨm were monitored with SNARF‐1, TMRE and fluo‐4, respectively. Myocyte survival was assessed when APoC was induced at pH 7.4 and 7.8. In isolated mitochondria oxygen consumption and ATP synthesis were measured.Key results:  In vivo APoC protected against mPTP opening, slowed mitochondrial respiration and depolarized mitochondria. APoC decreased the number of hypercontracted cardiomyocytes at pH 7.4, but not at pH 7.8. APoC attenuated intracellular Ca2+ accumulation, maintained lower pHm, and preserved ΔΨm during reoxygenation. Isoflurane did not affect the regulation of cytosolic pH. In mitochondria, APoC preserved ATP production rate and respiration.Conclusions and implications:  At reperfusion, APoC inhibited mitochondrial respiration, depolarized mitochondria and acidified pHm. These events may lead to inhibition of mPTP opening and, consequently, to preserved ΔΨm and ATP synthesis. This reduces intracellular Ca2+ overload and cell death.This article is commented on by Moncada, pp. 217–219 of this issue. To view this commentary visit http://dx.doi.org/10.1111/j.1476‐5381.2010.00706.x and to view related papers in this issue by Puerta et al. and Kurz et al. visit http://dx.doi.org/10.1111/j.1476‐5381.2010.00663.x and http://dx.doi.org/10.1111/j.1476‐5381.2010.00656.x
Mitochondria as pharmacological targets
Authors: Moncada S 
Published: March 2010

In the last decade, mitochondria have provided a vast area of research for the pharmacologist, with a wealth of potential targets for drug action. Correct target identification and subsequent pharmacological manipulation might greatly help in the prevention and/or treatment of a number of the most prevalent diseases of our time including cancer, neurodegenerative disease and myocardial infarction. This is a commentary to accompany the publication of three papers in this issue of the BJP by Kurz et al., Pravdic et al. and Puerta et al. on different aspects of pharmacology involving mitochondria.This article is a commentary on Pravdic et al., pp. 220–232, Puerta et al., pp. 233–245 and Kurz et al. pp. 246–257 of this issue. To view these papers visit http://dx.doi.org/10.1111/j.1476‐5381.2010.00698.xhttp://dx.doi.org/10.1111/j.1476‐5381.2010.00663.x and http://dx.doi.org/10.1111/j.1476‐5381.2010.00656.x
Atomoxetine acts as an NMDA receptor blocker in clinically relevant concentrations
Authors: Ludolph Andrea G , Udvardi Patrick T , Schaz Ulrike , Henes Carolin , Adolph Oliver , Weigt Henry U , Fegert Joerg M , Boeckers Tobias M , Föhr Karl J 
Published: March 2010

Background and purpose: There is increasing evidence that not only the monoaminergic but also the glutamatergic system is involved in the pathophysiology of attention‐deficit hyperactivity disorder (ADHD). Hyperactivity of glutamate metabolism might be causally related to a hypoactive state in the dopaminergic system. Atomoxetine, a selective noradrenaline reuptake inhibitor, is the first non‐stimulant approved for the treatment of this disorder. Here we have evaluated the effects of atomoxetine on glutamate receptorsin vitro.Experimental approach: The whole‐cell configuration of the patch‐clamp technique was used to analyse the effect of atomoxetine onN‐methyl‐d‐aspartate (NMDA) receptors in cultured rodent cortical and hippocampal neurons as well as on NMDA receptors heterologously expressed in human TsA cells.Key results: Atomoxetine blocked NMDA‐induced membrane currents. Half‐maximal inhibition emerged at about 3 µM which is in the range of clinically relevant concentrations found in plasma of patients treated with this drug. The inhibition was voltage‐dependent, indicating an open‐channel blocking mechanism. Furthermore, the inhibitory potency of atomoxetine did not vary when measured on NMDA receptors from different brain regions or with different subunit compositions.Conclusions and implications: The effective NMDA receptor antagonism by atomoxetine at low micromolar concentrations may be relevant to its clinical effects in the treatment of ADHD. Our data provide further evidence that altered glutamatergic transmission might play a role in ADHD pathophysiology.
Cannabinoid‐1 receptor activation induces reactive oxygen species‐dependent and ‐independent mitogen‐activated protein kinase activation and cell death in human coronary artery endothelial cells
Authors: Rajesh Mohanraj , Mukhopadhyay Partha , Haskó György , Liaudet Lucas , Mackie Ken , Pacher Pál 
Published: March 2010

Background and purpose: Impaired endothelial activity and/or cell death play a critical role in the development of vascular dysfunction associated with congestive heart failure, diabetic complications, hypertension, coronary artery disease and atherosclerosis. Increasing evidence suggests that cannabinoid 1 (CB1) receptor inhibition is beneficial in atherosclerosis and cardiovascular inflammation both in experimental models, as well as in humans. Here, we investigated the effects of CB1receptor activation with the endocannabinoid anandamide (AEA) or synthetic agonist HU210 on cell death and interrelated signal transduction pathways in human primary coronary artery endothelial cells (HCAECs).Experimental approach: Cell death, CB1receptor expression, reactive oxygen species (ROS) generation and activation of signal transduction pathways in HCAECs were determined by flow cytometry and molecular biology tools.Key results: In HCAECs expressing CB1receptors (demonstrated by Western immunoblot and flow cytometry) AEA (5–15 µM) or HU210 (30–1000 nM) triggered concentration‐ and time‐dependent activation of p38 and c‐Jun NH2‐terminal protein kinase (JNK)–mitogen‐activated protein kinases (MAPKs), cell death and ROS generation. The AEA‐ or HU210‐induced cell death and MAPK activation were attenuated by CB1antagonists [SR141716 (rimonabant) and AM281], inhibitors of p38 and JNK–MAPKs or the antioxidantN‐acetylcysteine.N‐acetylcysteine alone prevented AEA‐ or HU210‐induced ROS generation, but only partially attenuated MAPK activation and cell death. In contrast, in combination with CB1antagonists,N‐acetylcysteine completely prevented these effects.Conclusions and implications: CB1receptor activation in endothelial cells may amplify the ROS–MAPK activation–cell death pathway in pathological conditions when the endocannabinoid synthetic or metabolic pathways are dysregulated by excessive inflammation and/or oxidative/nitrosative stress, thereby contributing to the development of endothelial dysfunction and pathophysiology of multiple cardiovascular diseases.This article is part of a themed issue on Cannabinoids. To view the editorial for this themed issue visithttp://dx.doi.org/10.1111/j.1476‐5381.2010.00831.x
Human Variation in Alcohol Response Is Influenced by Variation in Neuronal Signaling Genes
Authors: Joslyn Geoff , Ravindranathan Ajay , Brush Gerry , Schuckit Marc , White Raymond L. 
Published: March 2010

Background: Alcohol use disorders (AUD) exhibit the properties shared by common conditions and diseases classified as genetically complex. The etiology of AUDs is heterogeneous involving mostly unknown interactions of environmental and heritable factors. A person’s level of response (LR) to alcohol is inversely correlated with a family history and the development of AUDs. As an AUD endophenotype, alcohol LR is hypothesized to be less genetically complex and closer to the primary etiology of AUDs.Methods: A genome wide association study (GWAS) was performed on subjects characterized for alcohol LR phenotypes. Gene Set Enrichment Analysis (GSEA) of the GWAS data was performed to determine whether, as a group, genes that participate in a common biological function (a gene set) demonstrate greater genetic association than would be randomly expected.Results: The GSEA analysis implicated variation in neuronal signaling genes, especially glutamate signaling, as being involved in alcohol LR variability in the human population.Conclusions: These data, coupled with cell and animal model data implicating neuronal signaling in alcohol response, support the conclusion that neuronal signaling is mechanistically involved in alcohol’s cellular and behavioral effects. Further, these data suggest that genetic variation in these signaling pathways contribute to human variation in alcohol response. Finally, this concordance of the cell, animal, and human findings supports neuronal signaling, particularly glutamate signaling, as a prime target for translational studies to understand and eventually modulate alcohol’s effects.
Genome‐Wide Association Study of Alcohol Dependence Implicates a Region on Chromosome 11
Authors: Edenberg Howard J. , Koller Daniel L. , Xuei Xiaoling , Wetherill Leah , McClintick Jeanette N. , Almasy Laura , Bierut Laura J. , Bucholz Kathleen K. , Goate Alison , Aliev Fazil , Dick Danielle , Hesselbrock Victor , Hinrichs Anthony , Kramer John , Kuperman Sam , Nurnberger John I. , Rice John P. , Schuckit Marc A. , Taylor Robert , Todd Webb B. , Tischfield Jay A. , Porjesz Bernice , Foroud Tatiana 
Published: March 2010

Background:  Alcohol dependence is a complex disease, and although linkage and candidate gene studies have identified several genes associated with the risk for alcoholism, these explain only a portion of the risk.Methods:  We carried out a genome‐wide association study (GWAS) on a case–control sample drawn from the families in the Collaborative Study on the Genetics of Alcoholism. The cases all met diagnostic criteria for alcohol dependence according to the Diagnostic and Statistical Manual of Mental Disorders–Fourth Edition; controls all consumed alcohol but were not dependent on alcohol or illicit drugs. To prioritize among the strongest candidates, we genotyped most of the top 199 single nucleotide polymorphisms (SNPs) (p ≤ 2.1 × 10−4) in a sample of alcohol‐dependent families and performed pedigree‐based association analysis. We also examined whether the genes harboring the top SNPs were expressed in human brain or were differentially expressed in the presence of ethanol in lymphoblastoid cells.Results:  Although no single SNP met genome‐wide criteria for significance, there were several clusters of SNPs that provided mutual support. Combining evidence from the case–control study, the follow‐up in families, and gene expression provided strongest support for the association of a cluster of genes on chromosome 11 (SLC22A18, PHLDA2, NAP1L4, SNORA54, CARS, and OSBPL5) with alcohol dependence. Several SNPs nominated as candidates in earlier GWAS studies replicated in ours, including CPE, DNASE2B, SLC10A2, ARL6IP5, ID4, GATA4, SYNE1, and ADCY3.Conclusions:  We have identified several promising associations that warrant further examination in independent samples.
Ethanol Impairs Activation of Retinoic Acid Receptors in Cerebellar Granule Cells in a Rodent Model of Fetal Alcohol Spectrum Disorders
Authors: Kumar Ambrish , Singh Chandra K. , DiPette Donald D. , Singh Ugra S. 
Published: March 2010

Background:  Ethanol is the main addictive and neurotoxic constituent of alcohol. Ethanol exposure during embryonic development causes dysfunction of the central nervous system (CNS) and leads to fetal alcohol spectrum disorders. The cerebellum is one of the CNS regions that are particularly vulnerable to ethanol toxic effects. Retinoic acid (RA) is a physiologically active metabolite of vitamin A that is locally synthesized in the cerebellum. Studies have shown that RA is required for neuronal development, but it remains unknown if ethanol impairs RA signaling and thus induces neuronal malformations. In this study, we tested the hypothesis that ethanol impairs the expression and activation of RA receptors in cerebellum and in cerebellar granule cells.Methods:  The cerebellum of ethanol unexposed and exposed pups was used to study the expression of retinoic acid receptors (RARs or RXRs) by immunohistochemistry and by Western blot analysis. We also studied the effect of ethanol on expression of RA receptors in the cerebellar granule cells. Activation of RA receptors (DNA‐binding activities) in response to high‐dose ethanol was determined by electrophoretic mobility shift and supershift assays.Results:  Findings from these studies demonstrated that ethanol exposure reduced the expression of RARα/γ while it increased the expression of RXRα/γ in the cerebellum and in cerebellar granule neurons. Immuno‐histological studies further strengthened the expression pattern of RA receptors in response to ethanol. The DNA‐binding activity of RARs was reduced, while DNA‐binding activity of RXRs was increased in response to ethanol exposure.Conclusion:  For the first time, our studies have demonstrated that high‐dose ethanol affects the expression and activation of RA receptors, which could impair the signaling events and induce harmful effects on the survival and differentiation of cerebellar granule cells. Taken together, these findings could provide insight into the treatment options for brain defects caused by excessive ethanol exposure, such as in Fetal Alcohol Spectrum Disorders.
Effect of Intravenous Lidocaine on Manifestations of Fibromyalgia
Authors: Vlainich Roberto , Issy Adriana M. , Gerola Luis R. , Sakata Rioko K. 
Published: March 2010

AbstractBackground and Objectives:  The objective of our study was to evaluate the effect of intravenous lidocaine on the manifestations of fibromyalgia.Methods:  A randomized, double‐blind, comparative study was conducted on 30 patients. All patients received 25 mg amitriptyline. Group 1 (n = 15) received 125 mL of saline; group 2 (n = 15) received 240 mg lidocaine in 125 mL of saline once a week for 4 weeks. The following parameters were evaluated: clinical manifestations before and 4 weeks after treatment; pain intensity on a numerical scale.Results:  All patients were female, and the mean age was 44.7 ± 10.5 years in group 1 and 40.9 ± 11.6 years in group 2. No difference in pain intensity or the number of tender points was observed between groups at any time point. Both groups demonstrated a significant decrease in the two parameters after treatment. A significant reduction in sleep disorders, paresthesia, and headache was observed after treatment in the two groups, but there was no significant difference between groups. There was no significant reduction in fatigue, subjective edema or morning stiffness after treatment in either group, without a significant difference between groups.Conclusions:  The addition of 240 mg intravenous lidocaine (once a week) to 25 mg amitriptyline for 4 weeks did not modify pain intensity or manifestations in patients with fibromyalgia compared with amitriptyline alone.
Risk Management Case Project
Authors: Hoyt Robert E. , Dumm Randy E. , McCullough Kathleen A. 
Published: March 2010

AbstractCase projects are valuable tools for teaching risk management and insurance (RMI). This article describes a flexible case study approach that can be used as a comprehensive capstone project for the RMI major or in modules for graduate and undergraduate RMI courses. The project incorporates both fundamental RMI concepts and emerging trends in the field. The use of the case project provides benefits to both students and the RMI program, especially given the increasing pressure for assessment in college curricula.