bluuebunny/crossref_metadata_2025_split huggingface dataset:
Die Krise but not La Crise? The Financial Crisis and the Transformation of German and French Banking Systems
Authors: HARDIE IAIN , HOWARTH DAVID 
Published: October 2009

AbstractThis article explores what the financial crisis shows about changes in the German and French banking systems, the two largest in continental Europe. In particular, we highlight processes of financialization – defined here as the increased trading of risk. We focus on an apparent contradiction: why did the supposedly more protectionist and conservative German banking system suffer much higher losses than the more liberalized French system? This article also examines the responses of German and French banks and governments to the crisis and speculates how far these responses might limit future financialization and shape national banking systems.
The normative development of emotion regulation strategy use in children and adolescents: a 2‐year follow‐up study
Authors: Gullone Eleonora , Hughes Elizabeth K. , King Neville J. , Tonge Bruce 
Published: October 2009

Background:  Emotion regulation involves intrinsic and extrinsic processes responsible for managing one’s emotions toward goal accomplishment. Research on emotion regulation has predominantly focused on early developmental periods and the majority of emotion regulation research examining the pre‐adult years has lacked a comprehensive theoretical framework. The current study examined the use of two strategies of emotion regulation during childhood and adolescents, as conceptualised within Gross’s (1998) process‐oriented model.Methods:  To determine the use, norms and development of the Expressive Suppression and Cognitive Reappraisal strategies, the Emotion Regulation Questionnaire for Children and Adolescents (ERQ‐CA) was administered to 1,128 participants aged between 9 and 15 years. Three data collection phases, each one year apart, enabled investigation of developmental patterns in the use of the two strategies.Results:  As predicted, Suppression use was found to be lower for older participants compared to their younger peers, and over time participants reported less use of this strategy. Older participants also scored lower on Reappraisal but stability over time was found. Also as expected, males reported more Suppression use compared to females.Conclusions:  By documenting the development and norms for Cognitive Reappraisal and Expressive Suppression in a community sample of children and adolescents, the current study makes a significant contribution to our understanding of these two ER strategies during these developmental periods.
Inactivation of cytochrome c oxidase by mutant SOD1s in mouse motoneuronal NSC‐34 cells is independent from copper availability but is because of nitric oxide
Authors: Arciello Mario , Capo Concetta Rosa , Cozzolino Mauro , Ferri Alberto , Nencini Monica , Carrì Maria Teresa , Rossi Luisa 
Published: October 2009

J. Neurochem. (2010) 112, 183–192.AbstractThe copper‐enzyme cytochrome c oxidase (Cytox) has been indicated as a primary molecular target of mutant copper, zinc superoxide dismutase (SOD1) in familial amyotrophic lateral sclerosis (fALS); however, the mechanism underlying its inactivation is still unclear. As the toxicity of mutant SOD1s could arise from their selective recruitment to mitochondria, it is conceivable that they might compete with Cytox for the mitochondrial copper pool causing Cytox inactivation. To investigate this issue, we used mouse motoneuronal neuroblastoma × spinal cord cell line‐34, stably transfected for the inducible expression of low amounts of wild‐type or mutant (G93A, H46R, and H80R) human SOD1s and compared the effects observed on Cytox with those obtained by copper depletion. We demonstrated that all mutants analyzed induced cell death and decreased the Cytox activity, but not the protein content of the Cytox subunit II, at difference with copper depletion that also affected subunit II protein. Copper supplementation did not counteract mutant hSOD1s toxicity. Otherwise, the treatment of neuroblastoma × spinal cord cell line‐34 expressing G93A, H46R, or H80R hSOD1 mutants, and showing constitutive expression of iNOS and nNOS, with either a NO scavenger, or NOS inhibitors prevented the inhibition of Cytox activity and rescued cell viability. These results support the involvement of NO in mutant SOD1s‐induced Cytox damage, and mitochondrial toxicity.
Further pharmacological characterization of 5‐HT2Creceptor agonist‐induced inhibition of 5‐HT neuronal activity in the dorsal raphe nucleusin vivo
Authors: Quérée P , Peters S , Sharp T 
Published: October 2009

Background and purpose: Recent experiments using non‐selective 5‐hydroxytryptamine (5‐HT)2Creceptor agonists including WAY 161503 suggested that midbrain 5‐HT neurones are under the inhibitory control of 5‐HT2Creceptors, acting via neighbouring gamma‐aminobutyric acid (GABA) neurones. The present study extended this pharmacological characterization by comparing the actions of WAY 161503 with the 5‐HT2Creceptor agonists, Ro 60‐0275 and 1‐(3‐chlorophenyl) piperazine (mCPP), as well as the non‐selective 5‐HT agonist lysergic acid diethylamide (LSD) and the 5‐HT releasing agent 3,4‐methylenedioxymethamphetamine (MDMA).Experimental approach: 5‐HT neuronal activity was measured in the dorsal raphe nucleus (DRN) using extracellular recordings in anaesthetized rats. The activity of DRN GABA neurones was assessed using double‐label immunohistochemical measurements of Fos and glutamate decarboxylase (GAD).Key results: Ro 60‐0175, like WAY 161503, inhibited 5‐HT neurone firing, and the 5‐HT2Cantagonist SB 242084 reversed this effect. mCPP also inhibited 5‐HT neurone firing (∼60% neurones) in a SB 242084‐reversible manner. LSD inhibited 5‐HT neurone firing; however, this effect was not altered by either SB 242084 or the 5‐HT2A/Creceptor antagonist ritanserin but was reversed by the 5‐HT1Areceptor antagonist WAY 100635. Similarly, MDMA inhibited 5‐HT neurone firing in a manner reversible by WAY 100635, but not SB 242084 or ritanserin. Finally, both Ro 60‐0275 and mCPP, like WAY 161503, increased Fos expression in GAD‐positive DRN neurones.Conclusions and implications: These data strengthen the hypothesis that midbrain 5‐HT neurones are under the inhibitory control of 5‐HT2Creceptors, and suggest that the 5‐HT2Cagonists Ro 60‐0175, mCPP and WAY 161503, but not LSD or MDMA, are useful probes of the mechanism(s) involved.
Inhibition of nitric oxide‐activated guanylyl cyclase by calmodulin antagonists
Authors: James LR , Griffiths CH , Garthwaite J , Bellamy TC 
Published: October 2009

Background and purpose: Nitric oxide (NO) controls numerous physiological processes by activation of its receptor, guanylyl cyclase (sGC), leading to the accumulation of 3′‐5′ cyclic guanosine monophosphate (cGMP). Ca2+‐calmodulin (CaM) regulates both NO synthesis by NO synthase and cGMP hydrolysis by phosphodiesterase‐1. We report that, unexpectedly, the CaM antagonists, calmidazolium, phenoxybenzamine and trifluoperazine, also inhibited cGMP accumulation in cerebellar cells evoked by an exogenous NO donor, with IC50values of 11, 80 and 180 µM respectively. Here we sought to elucidate the underlying mechanism(s).Experimental approach: We used cerebellar cell suspensions to determine the influence of CaM antagonists on all steps of the NO‐cGMP pathway. Homogenized tissue and purified enzyme were used to test effects of calmidazolium on sGC activity.Key results: Inhibition of cGMP accumulation in the cells did not depend on changes in intracellular Ca2+concentration. Degradation of cGMP and inactivation of NO were both inhibited by the CaM antagonists, ruling out increased loss of cGMP or NO as explanations. Instead, calmidazolium directly inhibited purified sGC (IC50= 10 µM). The inhibition was not in competition with NO, nor did it arise from displacement of the haem moiety from sGC. Calmidazolium decreased enzymeVmaxandKm, indicating that it acts in an uncompetitive manner.Conclusions and implications: The disruption of every stage of NO signal transduction by common CaM antagonists, unrelated to CaM antagonism, cautions against their utility as pharmacological tools. More positively, the compounds exemplify a novel class of sGC inhibitors that, with improved selectivity, may be therapeutically valuable.
Role of channel activation in cognitive enhancement mediated by α7 nicotinic acetylcholine receptors
Authors: Briggs Clark A , Grønlien Jens Halvard , Curzon Peter , Timmermann Daniel B , Ween Hilde , Thorin‐Hagene Kirsten , Kerr Paige , Anderson David J , Malysz John , Dyhring Tino , Olsen Gunnar M , Peters Dan , Bunnelle William H , Gopalakrishnan Murali 
Published: October 2009

Background and purpose: Several agonists of the α7 nicotinic acetylcholine receptor (nAChR) have been developed for treatment of cognitive deficits. However, agonist efficacyin vivois difficult to reconcile with rapid α7 nAChR desensitizationin vitro; and furthermore, the correlation betweenin vitroreceptor efficacy andin vivobehavioural efficacy is not well delineated. The possibility that agonists of this receptor actually functionin vivoas inhibitors via desensitization has not been finally resolved.Experimental approach: Two structurally related α7 nAChR agonists were characterized and used to assess the degree of efficacy required in a behavioural paradigm.Key results: NS6784 activated human and rat α7 nAChR with EC50s of 0.72 and 0.88 µM, and apparent efficacies of 77 and 97% respectively. NS6740, in contrast, displayed little efficacy at α7 nAChR (<2% in oocytes, ≤8% in GH4C1 cells), although its agonist‐like properties were revealed by adding a positive allosteric modulator of α7 nAChRs or using the slowly desensitizing α7V274T receptor. In mouse inhibitory avoidance (IA) memory retention, NS6784 enhanced performance as did the 60% partial agonist A‐582941. In contrast, NS6740 did not enhance performance, but blocked effects of A‐582941.Conclusions and implications: Collectively, these findings suggest that a degree of α7 nAChR agonist efficacy is required for behavioural effects in the IA paradigm, and that such behavioural efficacy is not due to α7 nAChR desensitization. Also, a partial agonist of very low efficacy for this receptor could be used as an inhibitor, in the absence of α7 nAChR antagonists with favourable CNS penetration.
Effect of the CB1receptor antagonists rimonabant and AM251 on the firing rate of dorsal raphe nucleus neurons in rat brain slices
Authors: Mendiguren Aitziber , Pineda Joseba 
Published: October 2009

Background and purpose: Previous studies have suggested a regulation of 5‐hydroxytryptamine (5‐HT) neurons by the endocannabinoid system. The aim of our work was to examine the effect of two CB1receptor antagonists, SR141716A (rimonabant, Sanofi‐Synthélabo Recherche, Montpellier, France) and N‐(piperidin‐1‐yl)‐5‐(4‐iodophenyl)‐1‐(2,4‐dichlorophenyl)‐4‐methyl‐1H‐pyrazole‐3‐carboxamide (AM251, Tocris Cookson, Bristol, UK), on the firing rate of dorsal raphe nucleus (DRN) neurons.Experimental approach: Single‐unit extracellular recordings were performed to study the effect of CB1receptor antagonists in slices of the DRN from rat brain.Key results: Rimonabant (1 µM) and AM251 (1 µM) decreased the firing rate of about 50% of all the recorded DRN 5‐HT cells. The GABAAreceptor antagonist picrotoxin (20 µM) (Sigma) prevented and also reversed the inhibitory effect of rimonabant (1 µM) and AM251 (1 µM), suggesting that CB1receptors regulate 5‐HT neurons through the GABAergic system. However, the CB1/CB2receptor agonist R‐(+)‐[2,3‐dihydro‐5‐methyl‐3‐[(morpholinyl)‐methyl]pyrrolol[1,2,3‐de]‐1,4‐benzoxazinyl]‐(1‐naphthalenyl) methanone mesylate salt (10 µM) (WIN55212‐2, Sigma, St. Louis, MO, USA) failed to change the firing activity of non‐5‐HT (presumably GABAergic) neurons in the DRN. The endocannabinoid N‐(2‐hydroxyethyl)‐5Z,8Z,11Z,14Z‐eicosatetraenamide (anandamide, Tocris Cookson) (10 µM) also inhibited the firing activity of a number of 5‐HT neurons, but this inhibition was not blocked by rimonabant (1 µM) or AM251 (1 µM), and the stable analogue R‐(+) N‐(2‐hydroxy‐1methylethyl)‐5Z,8Z,11Z,14Z‐eicosatetraenamide (methanandamide, Tocris Cookson) (10 µM) did not mimic this effect. The selective CB1receptor agonist arachidonoyl‐2‐chloroethylamide (ACEA) (1 µM) only slightly increased the firing rate of DRN 5‐HT cells.Conclusions and implications: These results suggest a tonic/constitutive regulation of DRN 5‐HT neurons by the endocannabinoid system, which may occur through a CB1receptor‐mediated inhibition of the GABAergic system. The inhibitory effect of anandamide may be mediated through a CB1receptor‐independent mechanism.
Effects of 7,8‐dihydro‐8‐oxo‐deoxyguanosine on antigen challenge in ovalbumin‐sensitized mice may be mediated by suppression of Rac
Authors: Ro JY , Kim DY , Lee S‐H , Park JW , Chung M‐H 
Published: October 2009

Background and purpose:  Earlier we reported that 7,8‐dihydro‐8‐oxo‐deoxyguanosine (8‐oxo‐dG), an oxidatively modified guanine nucleoside, exerted anti‐inflammatory activity through inactivation of the GTP binding protein, Rac. In the present study, the effects of 8‐oxo‐dG were investigated on responses to antigen challenge in sensitized mice, as Rac is also involved at several steps of the immune process including antigen‐induced release of mediators from mast cells.Experimental approach:  Mice were sensitized and challenged with ovalbumin without or with oral administration of 8‐oxo‐dG during the challenge. Effects of 8‐oxo‐dG were assessed by measuring lung function, cells and cytokines in broncho‐alveolar lavage fluid (BALF) and serum levels of antigen‐specific IgE. Rac activity in BALF cells was also measured.Key results:  8‐oxo‐dG inhibited the increased airway resistance and decreased lung compliance of sensitized and challenged mice to the levels of non‐sensitized control mice and lowered the increased leukocytes particularly, eosinophils, in BALF. Furthermore, 8‐oxo‐dG suppressed allergy‐associated immune responses, such as raised anti‐ ovalbumin IgE antibody in serum, increased expression of CD40 and CD40 ligand in lung, increased interleukin‐4, ‐5, ‐13, interferon‐γ and tumour necrosis factor‐α in BALF and mRNA levels of these cytokines in BALF cells, dose‐dependently. The corresponding purine, 8‐oxo‐guanine, showed no effects in the same experiments. Finally, 8‐oxo‐dG, but not 8‐oxo‐guanine, inhibited the increased Rac activity in sensitized and challenged mice.Conclusion and implications:  8‐Oxo‐dG had anti‐allergic actions that might be mediated by Rac inactivation. This compound merits further evaluation of its therapeutic potential in allergic asthma.
Desensitization of endothelial P2Y1 receptors by PKC‐dependent mechanisms in pressurized rat small mesenteric arteries
Authors: Rodríguez‐Rodríguez R , Yarova P , Winter P , Dora KA 
Published: October 2009

Background and purpose: Extracellular nucleotides play a crucial role in the regulation of vascular tone and blood flow. Stimulation of endothelial cell P2Y1 receptors evokes concentration‐dependent full dilatation of resistance arteries. However, this GPCR can desensitize upon prolonged exposure to the agonist. Our aim was to determine the extent and nature of P2Y1 desensitization in isolated and pressurized rat small mesenteric arteries.Experimental approach: The non‐hydrolyzable selective P2Y1 agonist ADPβS (3 µM) was perfused through the lumen of arteries pressurized to 70 mmHg. Changes in arterial diameter and endothelial cell [Ca2+]iwere obtained in the presence and absence of inhibitors of protein kinase C (PKC).Key results: ADPβS evoked rapid dilatation to the maximum arterial diameter but faded over time to a much‐reduced plateau closer to 35% dilatation. This appeared to be due to desensitization of the P2Y1 receptor, as subsequent endothelium‐dependent dilatation to acetylcholine (1 µM) remained unaffected. Luminal treatment with the PKC inhibitors BIS‐I (1 µM) or BIS‐VIII (1 µM) tended to augment concentration‐dependent dilatation to ADPβS (0.1–3 µM) and prevented desensitization. Another PKC inhibitor, Gö 6976 (1 µM), was less effective in preventing desensitization. Measurements of endothelial cell [Ca2+]iin pressurized arteries confirmed the P2Y1 receptor but not M3muscarinic receptor desensitization.Conclusions and implications: These data demonstrate for the first time the involvement of PKC in the desensitization of endothelial P2Y1 receptors in pressurized rat mesenteric arteries, which may have important implications in the control of blood flow by circulating nucleotides.
Adenosine A1 receptor blockage mediates theophylline‐associated seizures
Authors: Fukuda Mitsumasa , Suzuki Yuka , Hino Hitomi , Kuzume Kazuyo , Morimoto Takehiko , Ishii Eiichi 
Published: October 2009

SummaryTheophylline‐associated seizures (TAS) often progress to prolonged or treatment‐resistant convulsions. Theophylline is a nonselective adenosine receptor antagonist. Adenosine is an endogenous anticonvulsant that can terminate seizures. Fever and young age have been reported to be risk factors for TAS. To elucidate the mechanism of TAS, we investigated the effect of theophylline and adenosine receptor ligands on hyperthermia‐induced seizures in juvenile rats. The treatment dose of theophylline or control saline was injected intraperitoneally 1 h before hyperthermia‐induced seizures. The seizure threshold in the theophylline group was significantly lower and seizure duration was significantly longer than those in the control group. The addition of a selective adenosine A1 receptor agonist and an adenosine kinase inhibitor completely counteracted the effects of theophylline. Moreover, a selective A1 antagonist caused a significantly longer seizure duration compared with the control. These findings suggest that blockage of the adenosine A1 receptor is the main cause of TAS.
Sequential intrarectal diazepam and intravenous levetiracetam in treating acute repetitive and prolonged seizures
Authors: Modur Pradeep N. , Milteer Warren E. , Zhang Song 
Published: October 2009

SummaryIn this retrospective study of institutionalized patients with mental retardation, we present the efficacy and safety of sequential treatment with intrarectal diazepam (IRD) gel (Diastat) and intravenous levetiracetam (IVL) in comparison with either treatment alone for acute repetitive or prolonged seizures (ARPS). We defined ARPS as ≥3 seizures of any type within 1 h or a single seizure of any type lasting ≥3 min. Eighty‐eight ARPS episodes were treated in 25 patients (14 female, age 21–72 years), with mainly symptomatic generalized epilepsy. There were no adverse events directly attributable to the administration of IRD or IVL. Seizure recurrence within 4 h of treatment, the primary outcome measure, was significantly lower after combined sequential IRD + IVL treatment (3 of 36) compared to IRD alone (6 of 24, p = 0.048) or IVL alone (10 of 28, p = 0.039). There was no statistically significant difference between the individual IRD and IVL treatments (p = 0.604). The estimated odds ratio (OR) indicated that the risk of seizure recurrence was higher after IRD or IVL monotherapy compared to combined IRD + IVL treatment. Subsequent emergency room (ER) transfers following seizure recurrence were least likely after IVL treatment (10%) compared to combined IRD + IVL (67%) or IRD (83%) treatment. These findings suggest that although IRD or IVL monotherapy is efficacious, the combination is superior in controlling ARPS in this special group of institutionalized patients. In addition, we speculate that a more reliable onset of action after IVL treatment results in rapid seizure control and fewer ER transfers, despite seizure recurrence.
The ketogenic diet in treatment of two adults with prolonged nonconvulsive status epilepticus
Authors: Wusthoff Courtney J. , Kranick Sarah M. , Morley James F. , Christina Bergqvist A. G. 
Published: October 2009

SummaryProlonged status epilepticus (SE) can be refractory to conventional interventions, with high rates of subsequent morbidity and mortality. A high fat, low protein, low carbohydrate ketogenic diet (KD) has been used successfully to treat intractable epilepsy. However, its possible role in prolonged SE has not been well described. We report successful use of the KD in two adult patients with prolonged nonconvulsive SE (NCSE) refractory to multiple other interventions. Our observations suggest induction of ketosis may be a novel strategy to safely and effectively treat status in adults even after weeks to months of refractory seizures. Although there are few data regarding the use of the ketogenic diet in the treatment of adult epilepsy syndromes, it may be an option for the treatment of adults with refractory, prolonged SE.
Innate but not adaptive immune responses contribute to behavioral seizures following viral infection
Authors: Kirkman Nikki J. , Libbey Jane E. , Wilcox Karen S. , White H. Steve , Fujinami Robert S. 
Published: October 2009

SummaryPurpose:  To examine the role of innate immunity in a novel viral infection–induced seizure model.Methods:  C57BL/6 mice, mouse strains deficient in interleukin (IL)‐1RI, IL‐6, tumor necrosis factor (TNF)‐RI, or myeloid differentiation primary response gene 88 (MyD88), or transgenic mice (OT‐I) were infected with Theiler’s murine encephalomyelitis virus (TMEV) or were mock infected. Mice were followed for acute seizures. Tissues were examined for neuron loss, the presence of virus (viral RNA and antigen), perivascular cuffs, macrophages/microglia, and gliosis, and mRNA expression of IL‐1, TNF‐α, and IL‐6.Results:  IL‐1 does not play a major role in seizures, as IL‐1RI‐ and MyD88‐deficient mice displayed a comparable seizure frequency relative to controls. In contrast, TNF‐α and IL‐6 appear to be important in the development of seizures, as only 10% and 15% of TNF‐RI‐ and IL‐6‐deficient mice, respectively, showed signs of seizure activity. TNF‐α and IL‐6 mRNA levels also increased in mice with seizures. Inflammation (perivascular cuffs, macrophages/microglia, and gliosis) was greater in mice with seizures. OT‐I mice (virus persists) had a seizure rate that was comparable to controls (no viral persistence), thereby discounting a role for TMEV‐specific T cells in seizures.Discussion:  We have implicated the innate immune response to viral infection, specifically TNF‐α and IL‐6, and concomitant inflammatory changes in the brain as contributing to the development of acute seizures. This model is a potential infection‐driven model of mesial temporal lobe epilepsy with hippocampal sclerosis.
Smith and Living Wages: Arguments in Support of a Mandated Living Wage
Authors: Clary Betsy Jane 
Published: October 2009

AbstractAdam Smith was a proponent of living wages for labor for reasons of growth and for reasons of equity. There is ample evidence in the body of Smith's work to support the thesis that Smith would support public policies that might ensure the achievement of a living wage. The argument rests, in part, on the conclusion that Smith had reservations concerning the ability of the economy to experience sufficient growth and the ability of growth, if achieved, to secure living wages. This article argues that, given Smith's views about justice and given Smith's ideas, as part of the Scottish Enlightenment, of how the rules of justice evolve, a living wage law could be one of the general rules of which Smith could approve.