bluuebunny/crossref_metadata_2025_split huggingface dataset:
Non‐reactive metal/oxide interfaces: from model calculations towards realistic simulations
Authors: Goniakowski Jacek , Mottet Christine , Noguera Claudine 
Published: June 2006

AbstractIn the last decade two principal factors have stimulated the progressive regain of interest for non‐reactive metal/oxide interfaces. On one hand, the efforts invested by the community of model catalysis in analyzing the reactivity properties of supported metal nano‐clusters have resulted in an abundance of high quality experimental data. They have also risen several precise questions on the direct and indirect role played by the substrate in the determination of catalytic properties of deposited metal particles, and have thus reiterated the interrogations concerning the nature of interactions at the metal/oxide interfaces. On the other hand, conceptual improvements of first‐principles calculations, such as implementations of various GGA functionals, have added enormously to the reliability of these methods, and have enlarged considerably their field of application. However, most ab initio simulations are sooner or later confronted to the constrains on the computational cost, inherent of this kind of approaches. It concerns principally the limited size of systems which can be treated in practice, a factor which turns out to be particularly limiting in realistic studies of interfaces, where the mismatch of lattice parameters is at the origin of incommensurate interface structures, long‐range reconstructions, or/and complex structural deformations and dislocations.In this context, the goal of this paper is two‐fold. First, we give an overview of essential metal/oxide interface characteristics as obtained from ab initio calculations on model systems, with a special focus on late transition metals, such as Pd, and on a highly ionic oxide substrate, such as MgO. It includes results on the relation between the strength of interfacial interaction and the type of deposited metal (transition, noble), the nature of metal deposit (isolated atoms, constituted interface), and the character of the substrate (non‐polar, polar). We also comment on effects due to defects at the oxide surface. Secondly, we describe an effective approach to simulate non‐reactive deposition of nano‐scale metal objects on a surface of highly ionic oxide. The core of this approach is a many‐body potential energy surface (PES) constructed on the basis of results of ab initio calculations for model metal/oxide interface structures. We present its application to studies on the deposition of late transition metals (Pd, Ag) on the MgO(100) surface, including the determination of substrate‐induced change of equilibrium atomic structure and morphology of metal nano‐clusters, the analysis of stress release at the interface, and the investigation of the role of the oxide substrate on the melting properties of supported clusters. (© 2006 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)
Isolation and Molecular Characterization of Makal (Xanthosoma yucatanensis) Starch
Authors: Torruco‐Uco Juan G. , Chel‐Guerrero Luis A. , Betancur‐Ancona David 
Published: June 2006

AbstractStarch was isolated from a non‐conventional source: makal (Xanthosoma yucatanensis) and molecular characteristics were determined using X‐ray diffraction, light scattering and chain length determination. The granules had an oval shape with sizes between 8 and 20 μm, with an average size of 12.4 μm. Amylose content was 22.4% and amylopectin content 77.6%. The granules presented a C‐type X‐ray diffraction pattern, with a degree of polymerization (DP) of 5–19 for branch chain lengths and an average molar mass of 5.4×106 g/mol. The RH and the RG was 61.7 and 92.7 nm, respectively. Gelatinization temperature was 72.6 to 84.2°C and transition enthalpy was 15 J/g, which may be related to the X‐ray diffraction pattern and to the small granule size of makal starch. The retrogradation of makal starch increased during storage.
Profiles of adolescent stress: The development of the adolescent stress questionnaire (ASQ)
Authors: Byrne D.G. , Davenport S.C. , Mazanov J. 
Published: June 2006

ABSTRACTThe importance of stress in the understanding of adolescent health and well‐being is widely documented. The measurement of adolescent stress has however been subjected to sufficient methodological and conceptual criticism in recent times to warrant a concerted re‐evaluation of the exercise. This study sought information on the nature of adolescent stressors, building on a previous instrument developed by the first author to ask adolescents themselves to inform the development of a pool of new items reflecting stressor experience and to advise on the wording of these items to comprehensively assess that experience. This pool of items was then administered as a self‐reported questionnaire to a large sample of school‐age adolescents (N>1000) together with a scale to assess the intensity of distress arising from stressor occurrence. Principal components analysis of the questionnaire yielded 10 internally reliable dimensions of adolescent stress, the nature of which were consistent with the available literature on adolescent stressor experience. Scales constructed from this PCA related positively to measures of anxiety and depression, and negatively to a measure of self‐esteem, suggesting that they were valid measures of adolescent stress. Test–retest reliability was good for all scales. The resultant Adolescent Stress Questionnaire (ASQ) is therefore suggested to have potential for the measurement of adolescent stress in both research and clinical contexts.
Aetiology‐specific patterns in end‐stage heart failure patients identified by functional annotation and classification of microarray data
Authors: Beisvag Vidar , Lehre Per Kristian , Midelfart Herman , Aass Halfdan , Geiran Odd , Sandvik Arne Kristian , Lægreid Astrid , Komorowski Jan , Ellingsen Øyvind 
Published: June 2006

AbstractBackground:The objective of the present study was to use gene expression profiling, functional annotations and classification to identify aetiology‐specific biological processes and potential molecular markers for different aetiologies of end‐stage heart failure.Methods and results:Individual left ventricular myocardial samples from eleven coronary artery disease and nine dilated cardiomyopathy transplant patients were co‐hybridized with pooled RNA from four non‐failing hearts on custom‐made arrays of 7000 human genes. Significance analysis identified differential expression of 153 and 147 genes, respectively, in coronary artery disease or dilated cardiomyopathy versus non‐failing hearts. Analysis of Gene Ontology biological process annotations indicated aetiology‐specific patterns, primarily related to genes involved in catabolism and in regulation of protein kinase activity. Gene expression classifiers were obtained and used for class prediction of random samples of coronary artery diseased and dilated cardiomyopathic hearts. Best classifiers frequently included matrix metalloproteinase 3, fibulin 1, ATP‐binding cassette, sub‐family B member 1 and iroquois homeobox protein 5.Conclusion:Combining functional annotation from microarray data and classification analysis constitutes a potent strategy to identify disease‐specific biological processes and gene expression markers in e.g. end‐stage coronary artery disease and dilated cardiomyopathy.
VIOLENCE AND CIVILITY IN EARLY MODERN EUROPE
Authors: SHEPARD ALEXANDRA 
Published: June 2006

Violence in early modern Europe, 1500–1800. By Julius R. Ruff. Cambridge: Cambridge University Press, 2001. Pp. xii+269. ISBN 0-521-59119-8. £13.95.The London mob: violence and disorder in eighteenth-century England. By Robert Shoemaker. London: Hambledon and London, 2004. Pp. xvi+393. ISBN 1-85285-389-1. £25.00.Outlaws and highwaymen: the cult of the robber in England from the middle ages to the nineteenth century. By Gillian Spraggs. London: Pimlico, 2001. Pp. x+372. ISBN 0-7126-6479-3. £12.50.The duel in early modern England: civility, politeness and honour. By Markku Peltonen. Cambridge: Cambridge University Press, 2003. Pp. x+355. ISBN 0-521-82062-6. £45.00.Swordsmen: the martial ethos in the three kingdoms. By Roger B. Manning. Oxford: Oxford University Press, 2003. Pp. xvi+272. ISBN 0-19-926121-0. £47.00.Rebellion, community and custom in early modern Germany. By Norbert Schindler, translated by Pamela E. Selwyn. Cambridge: Cambridge University Press, 2002. Pp. xiv+311. ISBN 0-521-65010-0. £55.00.The history of violence appears to hold a particular fascination for scholars of the early modern period. This is not least because it is so often deemed integral to the differences between modern and pre-modern culture and politics, despite the fact that this particular difference is becoming increasingly difficult to sustain. The progressive decline and containment of violence – or at least certain forms of violence – has been central to narratives of state formation, the transition from courtesy to civility, a shift from aristocratic to bourgeois cultural hegemony, and the ‘civilizing process’ first theorized by Norbert Elias. Despite Michel Foucault's complication (if not rejection) of their teleological assumptions, such celebratory accounts of modernization have proved remarkably tenacious, albeit in a fragmented fashion. As the selection of books under review here illustrates, with the exception of Manning and, most notably, Peltonen, current scholarship is more likely to uphold, or to modify subtly, rather than to reject entrenched views of a gradual abeyance of violence in early modern Europe in response to imperatives of civility and politeness and to emergent state control.
In vivo evidence for a role of protein kinase C in peripheral nociceptive processing
Authors: Souza Adriano L S , Moreira Fabrício A , Almeida Karine R , Bertollo Caryne M , Costa Karina A , Coelho Márcio M 
Published: June 2006

The present study was designed to characterize the nociceptive response induced by protein kinase C (PKC) peripheral activation and to investigate if this biochemical event is important for the nociceptive response induced by formaldehyde, and bradykinin (BK).
Intraplantar injection of phorbol‐12,13‐didecanoate (PDD; 0.01, 0.1 or 1 μg), a PKC activator, but not of 4α‐PDD (inactive analogue), dose‐dependently induced thermal hyperalgesia in rats. This response was not observed at the contralateral hindpaw. Intraplantar injection of PDD (0.01, 0.1 or 1 μg) also induced mechanical allodynia. In mice, injection of PDD (0.1 or 1 μg) into the dorsum of the hindpaw induced a spontaneous licking behaviour.
Intraplantar co‐injection of chelerythrine (10 or 50 μg), a PKC inhibitor, attenuated the thermal hyperalgesia induced by PDD (0.1 μg) in rats.
The second phase of the nociceptive response induced by the injection of formaldehyde (0.92%, 20 μl) into the dorsum of mice hindpaws was inhibited by ipsi‐, but not contralateral, pre‐treatment with chelerythrine (1 μg).
Intraplantar injection of BK (10 μg) induced mechanical allodynia in rats. Ipsi‐ but not contralateral injection of bisindolylmaleimide I (10 μg), a PKC inhibitor, inhibited BK‐induced mechanical allodynia.
In conclusion, this study demonstrates that PKC activation at peripheral tissues leads to the development of spontaneous nociceptive response, thermal hyperalgesia and mechanical allodynia. Most importantly, it also gives in vivo evidence that peripheral PKC activation is essential for the full establishment of the nociceptive response induced by two different inflammatory stimuli.

British Journal of Pharmacology (2002) 135, 239–247; doi:10.1038/sj.bjp.0704434
Effect of NXY‐059 on infarct volume after transient or permanent middle cerebral artery occlusion in the rat; studies on dose, plasma concentration and therapeutic time window
Authors: Sydserff S G , Borelli A R , Green A R , Cross A J 
Published: June 2006

The efficacy of the free radical trapping agent NXY‐059 in reducing the infarct volume following both transient and permanent focal ischaemia has been examined in rats.
In the transient ischaemia model, rats were subjected to a 2 h occlusion of the middle cerebral artery (MCA). Intravenous infusion of NXY‐059 (1, 10 and 30 mg kg−1 h) for 21.75 h starting 2.25 h after the occlusion, produced a dose‐dependent decrease in both neurological impairment and the histologically measured infarct volume (a mean 59% decrease at 10 mg kg−1 h).
In the permanent ischaemia model, animals were injected (s.c.) with a loading dose of NXY‐059 of 32.5, 53.8 or 75.4 mg kg−1 and osmotic minipumps were implanted which had been primed to deliver respectively 30, 50 or 70 mg kg−1 h. When treatment was initiated 5 min after MCA occlusion there was a dose dependent protection of both cortical and sub‐cortical tissue (cortex: 63% at the mid‐range dose). Protection was related linearly to plasma concentration (plasma unbound NXY‐059 concentration at 1 h: 37±16 μmol l−1 at the mid‐range dose).
When the mid range dose was administered between 5 min – 4 h after MCA occlusion, a marked and statistically significant protection was seen at all time points (44% protection in cortex at 4 h).
These data demonstrate the substantial neuroprotective efficacy of NXY‐059 at plasma concentrations that can be achieved clinically and indicate that NXY‐059 also has a therapeutic window of opportunity that is clinically relevant.

British Journal of Pharmacology (2002) 135, 103–112; doi:10.1038/sj.bjp.0704449
HMG CoA reductase inhibitors affect the fibrinolytic system of human vascular cells in vitro: a comparative study using different statins
Authors: Wiesbauer Franz , Kaun Christoph , Zorn Gerlinde , Maurer Gerald , Huber Kurt , Wojta Johann 
Published: June 2006

The results of several clinical studies investigating the effect of statin therapy on the fibrinolytic system in vivo are inconclusive. We compared the effect of six different statins (atorvastatin, cerivastatin, fluvastatin, lovastatin, pravastatin, simvastatin) on components of the fibrinolytic system expressed by human vascular endothelial cells and smooth muscle cells and by the human hepatoma cell line HepG2.
All statins used except pravastatin significantly decreased PAI‐1 production in human endothelial and smooth muscle cells. This effect was also seen in the presence of IL‐1α and TNF‐α. All statins except pravastatin increased t‐PA production in human smooth muscle cells. On a molar basis cerivastatin was the most effective HMG CoA reductase inhibitor used. Only simvastatin and lovastatin increased t‐PA production in endothelial cells. The effects on the fibrinolytic system were reversed by mevalonate. Statins decreased mRNA levels for PAI‐1 in endothelial and smooth muscle cells and increased mRNA levels for t‐PA in smooth muscle cells. Statins did not affect PAI‐1 expression in HepG2 cells. Cell viability was not influenced by statins in endothelial cells and HepG2 cells whereas in smooth muscle cells a cytotoxic effect was seen at high concentrations.
If the effects on the fibrinolytic system of vascular cells in vitro shown in this study are also operative in vivo one could speculate that by increasing t‐PA and decreasing PAI‐1 at sites of vascular lesions statins might reduce fibrin formation and thrombus development. Such an effect might contribute to the clinically proven benefits of statin therapy.

British Journal of Pharmacology (2002) 135, 284–292; doi:10.1038/sj.bjp.0704454
Magnolol attenuates VCAM‐1 expression in vitro in TNF‐α‐treated human aortic endothelial cells and in vivo in the aorta of cholesterol‐fed rabbits
Authors: Chen Yung‐Hsiang , Lin Shing‐Jong , Chen Jaw‐Wen , Ku Hung‐Hai , Chen Yuh‐Lien 
Published: June 2006

In a previous study, we showed that magnolol, a potent antioxidant derived from a Chinese herb, attenuates monocyte chemotactic protein‐1 (MCP‐1) expression and intimal hyperplasia in the balloon‐injured aorta of cholesterol‐fed rabbits. Expression of cell adhesion molecules by the arterial endothelium and the attachment of leukocytes to the endothelium may play a major role in atherosclerosis. In the present study, the effects of magnolol on the expression of endothelial‐leukocyte adhesion molecules and the activation of nuclear factor kappa B (NF‐κB) in tumour necrosis factor‐α (TNF‐α)‐treated human aortic endothelial cells (HAECs) were investigated.
Pretreatment of HAECs with magnolol (5 μM) significantly suppressed the TNF‐α‐induced expression of vascular cell adhesion molecule‐1 (VCAM‐1) (64.8±1.9%), but had no effect on the expression of intercellular cell adhesion molecule‐1 and endothelial cell selectin.
Magnolol (5 and 10 μM) significantly reduced the binding of the human monocytic cell line, U937, to TNF‐α‐stimulated HAECs (58.4 and 56.4% inhibition, respectively). Gel shift assays using the 32P‐labelled NF‐κB consensus sequence as probe showed that magnolol pretreatment reduced the density of the shifted bands seen after TNF‐α‐induced activation. Immunoblot analysis and immunofluorescence staining of nuclear extracts demonstrated a 58% reduction in the amount of NF‐κB p65 in the nuclei in magnolol‐treated HAECs. Magnolol also attenuated intracellular H2O2 generation in both control and TNF‐α treated HAECs.
Furthermore, in vivo, magnolol attenuates the intimal thickening and TNF‐α and VCAM‐1 protein expression seen in the thoracic aortas of cholesterol‐fed rabbits.
Taken together, these data demonstrate that magnolol inhibits TNF‐α‐induced nuclear translocation of NF‐κB p65 and thereby suppresses expression of VCAM‐1, resulting in reduced adhesion of leukocytes. These results suggest that magnolol has anti‐inflammatory properties and may play important roles in the prevention of atherosclerosis and inflammatory responses in vivo.

British Journal of Pharmacology (2002) 135, 37–47; doi:10.1038/sj.bjp.0704458
Role of P1 residues Arg336 and Arg562 in the activated-Protein-C-catalysed inactivation of Factor VIIIa
Authors: Varfaj Fatbardha , Neuberg Julie , Jenkins P. Vincent , Wakabayashi Hironao , Fay Philip J. 
Published: June 2006

APC (activated Protein C) inactivates human Factor VIIIa following cleavage at residues Arg336 and Arg562 within the A1 and A2 subunits respectively. The role of the P1 arginine in APC-catalysed inactivation of Factor VIIIa was examined by employing recombinant Factor VIIIa molecules where residues 336 and 562 were replaced with alanine and/or glutamine. Stably expressed Factor VIII proteins were activated by thrombin and resultant Factor VIIIa was reacted at high concentration with APC to minimize cofactor inactivation due to A2 subunit dissociation. APC cleaved wild-type Factor VIIIa at the A1 site with a rate ∼25-fold greater than that for the A2 site. A1 mutants R336A and R336Q were inactivated ∼9-fold slower than wild-type Factor VIIIa, whereas the A2 mutant R562A was inactivated ∼2-fold slower. No cleavage at the mutated sites was observed. Taken together, these results suggested that cleavage at the A1 site was the dominant mechanism for Factor VIIIa inactivation catalysed by the proteinase. On the basis of cleavage at Arg336, a Km value for wild-type Factor VIIIa of 102 nM was determined, and this value was significantly greater than Ki values (∼9–18 nM) obtained for an R336Q/R562Q Factor VIIIa. Furthermore, evaluation of a series of cluster mutants in the C-terminal region of the A1 subunit revealed a role for acidic residues in segment 341–345 in the APC-catalysed proteolysis of Arg336. Thus, while P1 residues contribute to catalytic efficiency, residues removed from these sites make a primary contribution to the overall binding of APC to Factor VIIIa.
Training-induced energy balance mismatch in Standardbred mares
Authors: Gordon ME , McKeever KH , Bokman S , Betros CL , Manso-Filho HC , Liburt NR , Streltsova JM 
Published: June 2006

AbstractThis study tested the hypothesis that exercise training would alter feed intake (FI), body composition (BC) and plasma concentrations of active ghrelin, leptin, cortisol, insulin and glucose. Eight Standardbred mares (12±2 years, 509±36 kg body weight (BW), mean±SD) were trained (EX) in an equine Equi-ciser (initially 3 days per week at 60% maximal heart rate (HRmax) for 20 min and gradually increased to 5 days per week at 70% HRmaxfor 30 min, with a 10-min warm-up and 10-min cool-down period at the walk). Six mares (12±2 years, 537±45 kg) served as non-exercise controls (CON). All mares were unfit and had not been subjected to conditioning for 3 years before the experiment. Pre- and post-training incremental exercise tests (GXT) were run to determine HRmaxand maximal oxygen uptake (VO2max). A total mixed ration (TMR) of hay cubes was fed free choice for 16 h day-1with the primary experiment following a 6-week diet adaptation period. Mares' FI was measured daily and reported in grams per kilogram BW of feed eaten per week. Changes in BC were assessed using BW (electronic scale) and percentage fat calculated using rump fat thickness and the Westervelt equation. Blood samples were taken every 2 weeks at 15:25, before mares were given their allotment of hay cubes on a day when they did not exercise, to measure plasma hormone and glucose concentrations. Gastroscopy for gastric ulcers was performed before, during and after the trial. VO2maxincreased by 7.0% (P<0.03) in EX, but did not change (P>0.05) in CON. FI decreased (P<0.001) in both groups, but was only different (P<0.02) between EX and CON at week 3. Digestible energy (DE) intake (Mcal day-1) was initially higher (P<0.001) than calculated DE requirements in EX. However, over time, DE only matched and then fell below (P<0.03) the DE intake required for training. In CON horses, DE intake was higher (P<0.001) than calculated requirements. BW and percentage body fat increased (P<0.001) over time in EX and CON. Plasma leptin concentration increased (P<0.001) over time in both groups, but was 60% higher (P<0.04) in CON compared to EX at weeks 4–8. There were no differences (P>0.05) in active ghrelin, glucose, insulin or cortisol between the groups and over time. Five out of seven EX mares developed gastric ulcers. No CON mares developed gastric ulcers. Training was associated with changes in plasma leptin concentration, an increased incidence of gastric ulcers and a disruption of the balance between required DE and actual intake.