bluuebunny/crossref_metadata_2025_split huggingface dataset:
Incomplete Contracting, Commission Discretion and the Origins of EU Merger Control*
Authors: DOLEYS THOMAS 
Published: May 2009

AbstractCouncil Regulation 4064/89 on the Control of Concentration between Undertakings– more commonly known as the Merger Regulation – was a watershed development in the evolution of the EU's competition policy regime. In this article we seek to cast new analytical light on what, in many respects, is an established narrative. To do this we draw on insights from the new institutional economics (NIE). Specifically, we draw on the complementary concepts of incomplete contracting and delegation. We demonstrate how the Commission utilized the discretion attendant to its delegated authority to interpret and apply the indeterminate language of treaty competition articles so as to alter the economic, political and legal environment as it pertained to merger activity. It did so to such an extent that Member States, long resistant to Commission proposals for a merger control regulation, came to regard legislative action as preferable to the uncertainty represented by the evolving status quo.
Adaptive Learning and Macroeconomic Inertia in the Euro Area*
Authors: MILANI FABIO 
Published: May 2009

AbstractThis article aims to study the determinants of macroeconomic inertia in the euro area. To this end, it estimates a simple monetary DSGE model with private‐sector learning, but which also includes more structural sources of inertia, such as habit formation in consumption and inflation indexation. Economic agents are assumed to form near‐rational expectations and to learn the model parameters over time. Likelihood‐based Bayesian methods are used to estimate the agents' beliefs jointly within the system and to provide evidence on the fit of alternative learning rules. The results show that European macroeconomic inertia has only moderately changed over the sample. The evidence is consistent with a small gain coefficient and low degrees of habits and indexation, although some uncertainty remains after the estimation.
EU Identification and Endorsement in Context: The Importance of Regional Identity Salience
Authors: MOLS FRANK , JETTEN JOLANDA , HASLAM S. ALEXANDER 
Published: May 2009

AbstractPublic opinion research has increased our understanding of the variables affecting endorsement of EU integration. What is less well understood is how comparative identity processes shape EU identification. Drawing on social identity principles, we argue that EU identification is in part affected by tensions between relevant subgroup identities. To illustrate this point, two studies were conducted in UK regions (Wales and Cornwall). Findings confirm our prediction that a comparative context affects EU identity and indicate (a) that levels of EU identity were higher in contexts where regional identity was salient, and (b) that regional identity affected the bases and meaning of EU identification and EU endorsement. Discussion highlights the importance of taking context and intergroup relations into account when examining EU attitudes.
The Lisbon Treaty: De‐Constitutionalizing the European Union?*
Authors: REH CHRISTINE 
Published: May 2009

AbstractCalls to ratify the Lisbon Treaty by referendum have been countered with arguments about the Treaty's ‘non‐constitutional’ nature. Against this backdrop, this article asks how much ‘constitution’ is left in the new document. To answer this question, I assert that little is gained by classifying the Treaty in toto as a ‘European constitution’ or as the epitome of its failure. Instead, I develop an analytical framework that disaggregates the concept of constitution into its formal, material and symbolic functions, and systematically assess how far Lisbon would strengthen (or weaken) Europe's constitutional quality. The article suggests that, rather than transferring new competences to Brussels or making a constitutional saut qualitatif, Lisbon moderately bolsters the Treaties' formal functions; yet, in contrast to the Constitutional Treaty it adds little in material terms and is a decisive setback symbolically. Calls for ratification by referendum justified by the reform's extent are therefore ill‐founded.
Territorial occupancy and breeding performance in a migratory raptor do not follow ideal despotic distribution patterns
Authors: Pagán I. , Martínez J. E. , Calvo J. F. 
Published: May 2009

AbstractIt has commonly been argued that many territorial species select their breeding sites following an ideal despotic distribution model, in which the most productive, high‐quality territories are more frequently occupied. Theoretical and empirical studies have shown that this occupancy pattern may have population regulatory consequences, leading to density dependence in heterogeneous habitats. During a 9‐year research project in a forested area of south‐eastern Spain, we tested some of the predictions of the ideal despotic distribution model and the site‐dependent population regulation theory in a migratory raptor species, the booted eagle Hieraaetus pennatus. Contrary to the predictions of the despotic model, our results showed that the temporal pattern of territorial occupation did not differ from randomness, and that the territory occupancy rate was not significantly related to the reproductive parameters considered. At population level, the breeding variables were density independent, suggesting the absence of site‐dependent regulation. In addition, we were unable to find significant differences in the habitat characteristics between high‐quality and low‐quality territories, classified according to the criteria of both occupancy frequency and average productivity. Overall, our results suggest that booted eagles select their territories at random, probably due to the lack of strong environmental heterogeneity, and that occupancy rate is not a good measure of territory quality for the population studied.
Melanocortin potentiates leptin‐induced STAT3 signaling via MAPK pathway
Authors: Zhang Yan , Wu Xiaojun , He Yi , Kastin Abba J. , Hsuchou Hung , Rosenblum Charles I. , Pan Weihong 
Published: May 2009

AbstractThe co‐existence of receptors for leptin and melanocortin in cerebral microvessels suggests possible interactions between leptin and α‐melanocyte stimulating hormone (MSH) signaling. In this study, we showed that ObRb and melanocortin receptor MC3R and MC4R were present in enriched cerebral microvessels. To test the interactions between ObRb and MC3R or MC4R‐mediated cellular signaling, we over‐expressed these plasmids in RBE4 cerebral microvascular endothelial cells and HEK293 cells in culture. Activation of signal transducers and activators of transcription‐3 (STAT3) in response to leptin was determined by western blotting and luciferase reporter assays. Production of cAMP downstream to melanocortin receptors was determined with a chemiluminescent ELISA kit. αMSH, which increased intracellular cAMP, also potentiated leptin‐induced STAT3 activation. This potentiation was abolished by a specific MEK inhibitor, indicating the involvement of the mitogen‐activated kinase pathway. Reversely, the effect of leptin on αMSH‐induced cAMP production was minimal. Thus, melanocortin specifically potentiated STAT3 signaling downstream to ObRb by cross‐talk with mitogen‐activated kinase. The cooperation of ObRb and G protein‐coupled receptors in cellular signaling may have considerable biological implications not restricted to feeding and obesity.
Manganese exposure is cytotoxic and alters dopaminergic and GABAergic neurons within the basal ganglia
Authors: Stanwood Gregg D. , Leitch Duncan B. , Savchenko Valentina , Wu Jane , Fitsanakis Vanessa A. , Anderson Douglas J. , Stankowski Jeannette N. , Aschner Michael , McLaughlin BethAnn 
Published: May 2009

AbstractManganese is an essential nutrient, integral to proper metabolism of amino acids, proteins and lipids. Excessive environmental exposure to manganese can produce extrapyramidal symptoms similar to those observed in Parkinson’s disease (PD). We usedin vivoandin vitromodels to examine cellular and circuitry alterations induced by manganese exposure. Primary mesencephalic cultures were treated with 10–800 μM manganese chloride which resulted in dramatic changes in the neuronal cytoskeleton even at subtoxic concentrations. Using cultures from mice with red fluorescent protein driven by the tyrosine hydroxylase (TH) promoter, we found that dopaminergic neurons were more susceptible to manganese toxicity. To understand the vulnerability of dopaminergic cells to chronic manganese exposure, mice were given i.p. injections of MnCl2for 30 days. We observed a 20% reduction in TH‐positive neurons in the substantia nigra pars compacta (SNpc) following manganese treatment. Quantification of Nissl bodies revealed a widespread reduction in SNpc cell numbers. Other areas of the basal ganglia were also altered by manganese as evidenced by the loss of glutamic acid decarboxylase 67 in the striatum. These studies suggest that acute manganese exposure induces cytoskeletal dysfunction prior to degeneration and that chronic manganese exposure results in neurochemical dysfunction with overlapping features to PD.
Dual transgenic reporter mice as a tool for monitoring expression of glial fibrillary acidic protein
Authors: Cho Woosung , Hagemann Tracy L. , Johnson Delinda A. , Johnson Jeffrey A. , Messing Albee 
Published: May 2009

AbstractGlial fibrillary acidic protein (GFAP) is the major intermediate filament protein of astrocytes, and its expression changes dramatically during development and following injury. To facilitate study of the regulation of GFAP expression, we have generated dual transgenic mice expressing both firefly luciferase under the control of a 2.2 kb human GFAP promoter and Renilla luciferase under the control of a 0.5 kb human Glyceraldehyde 3 phosphate dehydrogenase (GAPDH) promoter for normalization of the GFAP signal. The GFAP‐fLuc was highly expressed in brain compared to other tissues, and was limited to astrocytes, whereas the GAPDH‐RLuc was more widely expressed. Normalization of the GFAP signal to the GAPDH signal reduced the inter‐individual variability compared to using the GFAP signal alone. The GFAP/GAPDH ratio correctly reflected the up‐regulation of GFAP that occurs following retinal degeneration in FVB/N mice because of the rd mutation. Following kainic acid‐induced seizures, changes in the GFAP/GAPDH ratio precede those in total GFAP protein. In knock‐in mice expressing the R236H Alexander disease mutant, GFAP promoter activity is only transiently elevated and may not entirely account for the accumulation of GFAP protein that takes place.
Impaired dopamine release and synaptic plasticity in the striatum of Parkin−/− mice
Authors: Kitada Tohru , Pisani Antonio , Karouani Maha , Haburcak Marian , Martella Giuseppina , Tscherter Anne , Platania Paola , Wu Bei , Pothos Emmanuel N. , Shen Jie 
Published: May 2009

Abstract Parkin is the most common causative gene of juvenile and early‐onset familial Parkinson’s diseases and is thought to function as an E3 ubiquitin ligase in the ubiquitin‐proteasome system. However, it remains unclear how loss of Parkin protein causes dopaminergic dysfunction and nigral neurodegeneration. To investigate the pathogenic mechanism underlying these mutations, we used parkin−/− mice to study its physiological function in the nigrostriatal circuit. Amperometric recordings showed decreases in evoked dopamine release in acute striatal slices of parkin−/− mice and reductions in the total catecholamine release and quantal size in dissociated chromaffin cells derived from parkin−/− mice. Intracellular recordings of striatal medium spiny neurons revealed impairments of long‐term depression and long‐term potentiation in parkin−/− mice, whereas long‐term potentiation was normal in the Schaeffer collateral pathway of the hippocampus. Levels of dopamine receptors and dopamine transporters were normal in the parkin−/− striatum. These results indicate that Parkin is involved in the regulation of evoked dopamine release and striatal synaptic plasticity in the nigrostriatal pathway, and suggest that impairment in evoked dopamine release may represent a common pathophysiological change in recessive parkinsonism.
Soil fertility evolution and landscape dynamics in a Mediterranean area: a case study in the Sant Llorenç Natural Park (Barcelona, NE Spain)
Authors: Nadal Jordi , Pèlachs Albert , Molina David , Soriano Joan‐Manuel 
Published: May 2009

The cartography of land covers was used to study fertility and soil evolution in a mountainous Mediterranean area during the anthropocene period (

Crutzen P J 2002

Geology of mankind Nature 415 23). The aim was to determine changes in fertility as agricultural lands were abandoned in the 14 000 hectare area that constitutes Sant Llorenç del Munt Natural Park in a pre‐coastal Catalan mountain range (north‐eastern Iberian Peninsula). The analysis of land covers using vegetation maps, orthorectified images and aerial photography has allowed us to differentiate six vegetation groups: holm‐oak wood, pine grove, oak wood, scrub, active agricultural fields and abandoned agricultural fields. The anthropic covers over the past 100 years were subdivided into five categories: active fields and those abandoned over four time periods. Study variables include field shape (concave, convex, flat), orientation (north, south) and slope (ranging from 12º to 24º). The parameters used for the physical‐chemical soil analysis included organic material, phosphorous and potassium; fertility was classified based on groups, types and classes. The results indicate that even when the visual appearance of certain landscapes is similar, the edaphic characteristics may be very different. Changes induced by human disturbance share this phenomenon. Therefore, land management should be considered globally, taking into account vegetation, soils and water as interdependent factors, since it is their interaction that produces landscape and most affects its evolution over time.
Characterization of P2Y receptor subtypes functionally expressed on neonatal rat cardiac myofibroblasts
Authors: Talasila Amarnath , Germack Renée , Dickenson John M 
Published: May 2009

Background and purpose:  Little is known about P2Y receptors in cardiac fibroblasts, which represent the predominant cell type in the heart and differentiate into myofibroblasts under certain conditions. Therefore, we have characterized the phenotype of the cells and the different P2Y receptors at the expression and functional levels in neonatal rat non‐cardiomyocytes.Experimental approach:  Non‐cardiomyocyte phenotype was determined by confocal microscopy by using discoidin domain receptor 2, α‐actin and desmin antibodies. P2Y receptor expression was investigated by reverse transcription‐polymerase chain reaction and immunocytochemistry, and receptor function by cAMP and inositol phosphate (IP) accumulation induced by adenine or uracil nucleotides in the presence or absence of selective antagonists of P2Y1 (MRS 2179, 2‐deoxy‐N6‐methyl adenosine 3′,5′‐diphosphate diammonium salt), P2Y6 (MRS 2578) and P2Y11 (NF 157, 8,8′‐[carbonylbis[imino‐3,1‐phenylenecarbonylimino(4‐fluoro‐3,1‐phenylene)carbonylimino]]bis‐1,3,5‐naphthalene trisulphonic acid hexasodium salt) receptors. Gi/o and Gq/11 pathways were evaluated by using Pertussis toxin and YM‐254890 respectively.Key results:  The cells (>95%) were α‐actin and discoidin domain receptor 2‐positive and desmin‐negative. P2Y1, P2Y2, P2Y4, P2Y6 were detected by reverse transcription‐polymerase chain reaction and immunocytochemistry, and P2Y11‐like receptors at protein level. All di‐ or tri‐phosphate nucleotides stimulated IP production in an YM‐254890‐sensitive manner. AMP, ADPβS, ATP and ATPγS increased cAMP accumulation, whereas UDP and UTP inhibited cAMP response, which was abolished by Pertussis toxin. MRS 2179 and NF 157 inhibited ADPβS‐induced IP production. MRS 2578 blocked UDP‐ and UTP‐mediated IP responses.Conclusion and implications:  P2Y1‐, P2Y2‐, P2Y4‐, P2Y6‐, P2Y11‐like receptors were co‐expressed and induced function through Gq/11 protein coupling in myofibroblasts. Furthermore, P2Y2 and P2Y4 receptor subtypes were also coupled to Gi/o. The Gs response to adenine nucleotides suggests a possible expression of a new P2Y receptor subtype.
Body weight reduction in rats by oral treatment with zinc plus cyclo‐(His‐Pro)
Authors: Song MK , Rosenthal MJ , Song AM , Uyemura K , Yang H , Ament ME , Yamaguchi DT , Cornford EM 
Published: May 2009

Background and purpose:  We have previously shown that treatment with zinc plus cyclo‐(His‐Pro) (CHP) significantly stimulated synthesis of the insulin degrading enzyme and lowered plasma insulin and blood glucose levels, alongside improving oral glucose tolerance in genetically type 2 diabetic Goto‐Kakizaki (G‐K) rats and in aged obese Sprague‐Dawley (S‐D) rats. Thus, we postulated that zinc plus CHP (ZC) treatment might also improve body weight control in these rats. We therefore determined the effects of ZC treatment on body weights in both genetically diabetic, mature G‐K rats and non‐diabetic, obese S‐D rats.Experimental approach:  G‐K rats aged 1.5–10 months and non‐diabetic overweight or obese S‐D rats aged 6–18 months were treated with 0–6 mg CHP plus 0–10 mg zinc·L−1 drinking water for 2–4 weeks, and changes in weight, serum leptin and adiponectin levels, food and water intakes were measured.Key results:  The optimal dose of CHP (in combination with zinc) to reduce weight and plasma leptin levels and to increase plasma adiponectin levels was close to 0.1 mg·kg−1·day−1, in either mature G‐K rats and aged overweight or obese S‐D rats. Food and water intake significantly decreased in ZC treated rats in both aged S‐D rats and mature G‐K rats, but not in young S‐D and G‐K rats.Conclusions and implications:  ZC treatment improved weight control and may be a possible treatment for overweight and obesity.
Oestrogen confers cardioprotection by suppressing Ca2+/calmodulin‐dependent protein kinase II
Authors: Ma Y , Cheng WT , Wu S , Wong TM 
Published: May 2009

Background and purpose: Oestrogen confers cardioprotection by down‐regulating the β1‐adrenoceptor and suppressing the expression and activity of protein kinase A. We hypothesized that oestrogen may also protect the heart by suppressing Ca2+/calmodulin‐dependent protein kinase II (CaMKII), another signalling messenger activated by the β1‐adrenoceptor, that enhances apoptosis.Experimental approach: We first determined the expression of CaMKII in the heart from sham and ovariectomized rats with and without oestrogen replacement. We then determined the effects of CaMKII inhibition (KN93, 2.5 µmol·L−1) in the presence or absence of 10−7 mol·L−1isoprenaline, a non‐selective β‐adrenoceptor agonist. We also determined the percentage apoptosis in myocytes from rats in each group with or without β‐adrenoceptor stimulation.Key results: Both CaMKIIδ and phosphorylated CaMKII were up‐regulated in the hearts from ovariectomized rats, and they were restored to normal by oestrogen replacement. The infarct size and lactate dehydrogenase release were significantly greater after ovariectomy. Similarly, cardiac contractility, the amplitude of the electrically induced intracellular Ca2+transient and the number of apoptotic cells were also greater in ovariectomized rats upon ischaemia/reperfusion in the presence or absence of isoprenaline. Most importantly, the responses to ischaemic insult in ovariectomized rats were reversed not only by oestrogen replacement, but by blockade of CaMKII with KN93.Conclusions and implications: Oestrogen confers cardioprotection at least partly by suppressing CaMKIIδ. This effect of oestrogen on CaMKII is independent of the β‐adrenoceptor and occurs in addition to down‐regulation of the receptor.
The carbon monoxide releasing molecule (CORM‐3) inhibits expression of vascular cell adhesion molecule‐1 and E‐selectin independently of haem oxygenase‐1 expression
Authors: Song H , Bergstrasser C , Rafat N , Höger S , Schmidt M , Endres N , Goebeler M , Hillebrands JL , Brigelius‐Flohé R , Banning A , Beck G , Loesel R , Yard BA 
Published: May 2009

Background and purpose:  Although carbon monoxide (CO) can modulate inflammatory processes, the influence of CO on adhesion molecules is less clear. This might be due to the limited amount of CO generated by haem degradation. We therefore tested the ability of a CO releasing molecule (CORM‐3), used in supra‐physiological concentrations, to modulate the expression of vascular cell adhesion molecule (VCAM)‐1 and E‐selectin on endothelial cells and the mechanism(s) involved.Experimental approach:  Human umbilical vein endothelial cells (HUVECs) were stimulated with tumour necrosis factor (TNF)‐α in the presence or absence of CORM‐3. The influence of CORM‐3 on VCAM‐1 and E‐selectin expression and the nuclear factor (NF)‐κB pathway was assessed by flow cytometry, Western blotting and electrophoretic mobility shift assay.Key results:  CORM‐3 inhibited the expression of VCAM‐1 and E‐selectin on TNF‐α‐stimulated HUVEC. VCAM‐1 expression was also inhibited when CORM‐3 was added 24 h after TNF‐α stimulation or when TNF‐α was removed. This was paralleled by deactivation of NF‐κB and a reduction in VCAM‐1 mRNA. Although TNF‐α removal was more effective in this regard, VCAM‐1 protein was down‐regulated more rapidly when CORM‐3 was added. CORM‐3 induced haem oxygenase‐1 (HO‐1) in a dose‐ and time‐dependent manner, mediated by the transcription factor, Nrf2. CORM‐3 was still able to down‐regulate VCAM‐1 expression in HUVEC transfected with siRNA for HO‐1 or Nrf2.Conclusions and implications:  Down‐regulation of VCAM and E‐selectin expression induced by CORM‐3 was independent of HO‐1 up‐regulation and was predominantly due to inhibition of sustained NF‐κB activation.
Mast cell degranulation – a mechanism for the anti‐arrhythmic effect of endothelin‐1?
Authors: Walsh SK , Kane KA , Wainwright CL 
Published: May 2009

Background and purpose: The aim of this study was to investigate whether the previously reported anti‐arrhythmic effect of endothelin‐1 (ET‐1) is mediated by degranulation of cardiac mast cells prior to myocardial ischaemia.Experimental approach: Male Sprague‐Dawley rats received either ET‐1 (1.6 nmol·kg−1) in the presence or absence of disodium cromoglycate (DSCG; 20 mg·kg−1·h−1) prior to coronary artery occlusion (CAO). In separate experiments rats were given compound 48/80 (50 µg·kg−1) to compare the effects of ET‐1 with those of a known mast cell degranulator. Ischaemia‐induced ventricular arrhythmias were detected through continuous monitoring of a lead I electrocardiogram. After 30 min of CAO, the hearts were removed and mast cell degranulation determined by histological analysis. A parallel series of sham groups were performed to determine the direct effects of ET‐1 and compound 48/80 on mast cell degranulation in the absence of ischaemia.Key results: ET‐1 and compound 48/80 both exerted profound anti‐arrhythmic effects, significantly reducing the total number of ventricular ectopic beats (P< 0.001) and the incidence of ventricular fibrillation (P< 0.05). These anti‐arrhythmic effects were abolished by concomitant DSCG infusion prior to CAO. In sham animals ET‐1 and compound 48/80 both induced mast cell degranulation (P< 0.001), an effect which was abolished by DSCG, confirming their ability to induce degranulation of mast cells.Conclusions and implications: These results demonstrate for the first time that when given prior to ischaemia ET‐1 mediates its anti‐arrhythmic effects, at least in part, via cardiac mast cell degranulation.