bluuebunny/crossref_metadata_2025_split huggingface dataset:
The horse has bolted: revisiting the market reaction to going concern modifications of audit reports
Authors: Herbohn Kathleen , Ragunathan Vanitha , Garsden Robert 
Published: September 2007

AbstractThis paper examines what value is added by an audit report through an investigation of the information content for first‐time going concern modifications (GCMs). Consistent with prior research, we find no evidence of a short‐term market reaction to the public announcement of a first‐time GCM. We document a significant adverse medium‐term market reaction in the 12 months prior to a first‐time GCM announcement, but find no evidence of a persistent market underreaction in the 12 months following the announcement. These results are consistent with an audit opinion fulfilling an attestation function and confirming the deteriorating financial condition of a firm.
Use of loan loss provisions for capital, earnings management and signalling by Australian banks
Authors: Anandarajan Asokan , Hasan Iftekhar , McCarthy Cornelia 
Published: September 2007

AbstractThis study examines whether and to what extent Australian banks use loan loss provisions (LLPs) for capital, earnings management and signalling. We examine if there were changes in the use of LLPs as a result of the implementation of banking regulations consistent with the Basel Accord of 1988, which made loan loss reserves no longer part of Tier I capital in the numerator of the capital adequacy ratio. We find some evidence to indicate that Australian banks use LLPs for capital management, but we find no evidence of a change in this behaviour after the implementation of the Basel Accord. Our results indicate that banks in Australia use LLPs to manage earnings. Furthermore, listed commercial banks engage more aggressively in earnings management using LLPs than unlisted commercial banks. We also find that earnings management behaviour is more pronounced in the post‐Basel period. Overall, we find a significant understating of LLPs in the post‐Basel period relative to the pre‐Basel period. This indicates that reported earnings might not reflect the true economic reality underlying those numbers. Finally, Australian banks do not appear to use LLPs for signalling future intentions of higher earnings to investors.
A Dynamic Model of Cracks Development Based on a 3D Discrete Shrinkage Volume Propagation
Authors: Valette Gilles , Prévost Stéphanie , Lucas Laurent , Léonard Joël 
Published: September 2007

ABSTRACT We attempt to model and visualize the main characteristics of cracks produced on the surface of a desiccating crusted soil: their patterns, their different widths and depths and their dynamics of creation and evolution. In this purpose we propose a method to dynamically produce three‐dimensional (3D) quasi‐static fractures, which takes into account the characteristics of the soil. The main originality of this method is the use of a 3D discrete propagation of ‘shrinkage volumes’ with respect to 2D precalculated paths. In order to get realistic cracks, we newly propose to take into account a possibly inhomogeneous thickness of the shrinking layer by using a watershed transformation to compute these paths. Moreover, we use the waterfall algorithm in order to introduce in our simulation a hierarchy notion in the cracks appearance, which is therefore linked with the initial structure of the surface. In this paper, this method is presented in detail and a validation of the cracks patterns by a comparison with real ones is given.
Differential regulation of the Cdk5‐dependent phosphorylation sites of inhibitor‐1 and DARPP‐32 by depolarization
Authors: Nguyen Chan , Hosokawa Tomohisa , Kuroiwa Mahomi , Ip Nancy Y. , Nishi Akinori , Hisanaga Shin‐ichi , Bibb James A. 
Published: September 2007

AbstractWhile cyclin‐dependent kinase 5 (Cdk5) is of growing importance to neuronal signaling, its regulation remains relatively unexplored. Examination of the mechanism by which NMDA modulates the phosphorylation of protein phosphatase inhibitor‐1 at Ser6 and Ser67 and dopamine‐ and cAMP‐regulated phosphoprotein Mr 32 000 at Thr75 revealed that generalized depolarization, rather than specific activation of NMDA receptors, was sufficient to induce decreases in these Cdk5 sites. Although no evidence for the involvement of the Cdk5 cofactors p35 or p39, or for L‐ and T‐type voltage‐gated Ca2+ channels, was found, evaluation of the role of phosphatases and extracellular cations revealed differential regulation of the three sites. NMDA‐induced decreases in the phosphorylation of Thr75 of dopamine‐ and cAMP‐regulated phosphoprotein Mr 32 000 required protein phosphatase 1/2A activity and extracellular Ca2+. In contrast, the effects on Ser6 and Ser67 of inhibitor‐1 were not cation specific; either Na+ or Ca2+ sufficed. Furthermore, while the decrease in phosphorylation of Ser6 was partially dependent on protein phosphatase 2B, that of Ser67 was independent of the major protein serine/threonine phosphatases, likely indicating the presence of a pathway by which NMDA inhibits Cdk5 activity. Thus, in the striatum the regulation of phosphorylation of Cdk5‐dependent sites by NMDA occurs through multiple distinct pathways.
P2Y2 nucleotide receptors inhibit trauma‐induced death of astrocytic cells
Authors: Burgos Michelle , Neary Joseph T. , González Fernando A. 
Published: September 2007

AbstractNucleotides as well as other neurotransmitters are known to be released to the extracellular space upon injury. To determine whether nucleotides acting on P2Y2 nucleotide receptors promote protective or degenerative events after trauma in astrocytic cells, a well‐established model of in vitro brain trauma was applied to 1321N1 cells expressing recombinant P2Y2 nucleotide receptors (P2Y2R‐1321N1). Cellular death was examined by measuring DNA fragmentation and caspase activation. Fragmented DNA was observed 48 h post‐injury in 1321N1 cells, while P2Y2 nucleotide receptor expressing cells did not show DNA fragmentation. A laddering pattern of fragmented DNA following injury was observed upon inhibition of P2Y2 nucleotide receptors with suramin. Time‐dependent increases of cleaved caspase‐9, a mitochondrial‐associated caspase, correlated with injury‐induced cellular death. A decreased bax/bcl‐2 gene expression ratio was observed in P2Y2R‐1321N1 cells after traumatic injury, while untransfected 1321N1 cells showed a significant time‐dependent increase of the bax/bcl‐2 gene expression ratio. Activation of protein kinases was assessed to determine the signaling pathways involved in cell death and survival responses following traumatic injury. In P2Y2R‐1321N1 and 1321N1 cells p38 phosphorylation was stimulated in a time‐dependent manner but the phosphatidylinositol 3‐kinase‐dependent activation of extracellular signal‐regulated kinase 1/2 and protein kinase B (PKB)/Akt was only observed in P2Y2R‐1321N1 cells after injury. The stress‐activated protein kinase/c‐Jun NH2‐terminal kinase (SAPK/JNK) signaling pathway was not activated by traumatic injury in either astrocytic cell line. Inhibition of p38 kinase signaling pathway by treatment with PD1693, a MKK3/6 inhibitor, abolished the expression of cleaved caspase‐9, the increase in the bax/bcl‐2 gene expression ratio, as well as the fragmentation of DNA that followed injury of 1321N1 cells. Taken together, our results demonstrate a novel role for P2Y2 nucleotide receptors and extracellular nucleotides in mediating survival responses to glial cells undergoing cellular death induced by trauma.
Constitutive endocytosis and recycling of the neuronal glutamate transporter, excitatory amino acid carrier 1
Authors: González Marco I. , Susarla Bala T. S. , Fournier Keith M. , Sheldon Amanda L. , Robinson Michael B. 
Published: September 2007

AbstractThe neuronal glutamate transporter, excitatory amino acid carrier 1 (EAAC1), has a diverse array of physiologic and metabolic functions. There is evidence that there is a relatively large intracellular pool of EAAC1 both in vivo and in vitro, that EAAC1 cycles on and off the plasma membrane, and that EAAC1 cell surface expression can be rapidly regulated by intracellular signals. Despite the possible relevance of EAAC1 trafficking to both physiologic and pathologic processes, the cellular machinery involved has not been defined. In the present study, we found that agents that disrupt clathrin‐dependent endocytosis or plasma membrane cholesterol increased steady‐state levels of biotinylated EAAC1 in C6 glioma cells and primary neuronal cultures. Acute depletion of cholesterol increased the Vmax for EAAC1‐mediated activity and had no effect on Na+‐dependent glycine transport in the same system. These agents also impaired endocytosis as measured using a reversible biotinylating reagent. Co‐expression with dominant‐negative variants of dynamin or the clathrin adaptor, epidermal growth factor receptor pathway substrate clone 15, increased the steady‐state levels of biotinylated myc‐EAAC1. EAAC1 immunoreactivity was found in a subcellular fraction enriched in early endosome antigen 1 (EEA1) isolated by differential centrifugation and partially co‐localized with EEA1. Co‐expression of a dominant‐negative variant of Rab11 (Rab11 S25N) reduced steady‐state levels of biotinylated myc‐EAAC1 and slowed constitutive delivery of myc‐EAAC1 to the plasma membrane. Together, these observations suggest that EAAC1 is constitutively internalized via a clathrin‐ and dynamin‐dependent pathway into early endosomes and that EAAC1 is trafficked back to the cell surface via the endocytic recycling compartment in a Rab11‐dependent mechanism. As one defines the machinery required for constitutive trafficking of EAAC1, it may be possible to determine how intracellular signals regulate EAAC1 cell surface expression.
Brain‐to‐blood elimination of 24S‐hydroxycholesterol from rat brain is mediated by organic anion transporting polypeptide 2 (oatp2) at the blood–brain barrier
Authors: Ohtsuki Sumio , Ito Shingo , Matsuda Akihiro , Hori Satoko , Abe Takaaki , Terasaki Tetsuya 
Published: September 2007

Abstract24S‐Hydroxycholesterol (24S‐OH‐chol), a major cerebral cholesterol metabolite, is an endogenous ligand for the liver X receptor and is a potential stimulant of cholesterol release from glial cells. The elimination mechanism of 24S‐OH‐chol from the brain is one of the key issues for understanding cerebral cholesterol homeostasis. The purpose of the present study was to clarify the molecular mechanism of the elimination process of 24S‐OH‐chol across the blood–brain barrier (BBB). After an intracerebral injection in rats, [3H]24S‐OH‐chol was eliminated from the brain and the radioactivity derived from [3H]24S‐OH‐chol was detected in the plasma, while [3H]cholesterol was not significantly eliminated from the brain. Co‐administration of unlabeled 24S‐OH‐chol significantly inhibited the [3H]24S‐OH‐chol elimination, while no inhibitory effect was seen at the same concentration of cholesterol. The [3H]24S‐OH‐chol elimination was inhibited by co‐administration of probenecid, but not by benzylpenicillin. Pre‐administration of digoxin completely inhibited the elimination.Xenopus laevisoocytes expressing rat oatp2 exhibited significant transport of [3H]24S‐OH‐chol, and this was inhibited by unlabeled 24S‐OH‐chol and digoxin, indicating that rat oatp2 transports 24S‐OH‐chol. These results are the first direct demonstration that 24S‐OH‐chol undergoes elimination from the brain to blood across the BBB via a carrier‐mediated process, which involves oatp2 expressed at the BBB in rats.
Cellular prion protein expression in astrocytes modulates neuronal survival and differentiation
Authors: Lima Flavia R. S. , Arantes Camila P. , Muras Angelita G. , Nomizo Regina , Brentani Ricardo R. , Martins Vilma R. 
Published: September 2007

AbstractThe functions of cellular prion protein (PrPC) are under intense debate and PrPC loss of function has been implicated in the pathology of prion diseases. Neuronal PrPC engagement with stress‐inducible protein‐1 and laminin (LN) plays a key role in cell survival and differentiation. The present study evaluated whether PrPC expression in astrocytes modulates neuron‐glia cross‐talk that underlies neuronal survival and differentiation. Astrocytes from wild‐type mice promoted a higher level neuritogenesis than astrocytes obtained from PrPC‐null animals. Remarkably, neuritogenesis was greatly diminished in co‐cultures combining PrPC‐null astrocytes and neurons. LN secreted and deposited at the extracellular matrix by wild‐type astrocytes presented a fibrillary pattern and was permissive for neuritogenesis. Conversely, LN coming from PrPC‐null astrocytes displayed a punctate distribution, and did not support neuronal differentiation. Additionally, secreted soluble factors from PrPC‐null astrocytes promoted lower levels of neuronal survival than those secreted by wild‐type astrocytes. PrPC and stress‐inducible protein‐1 were characterized as soluble molecules secreted by astrocytes which participate in neuronal survival. Taken together, these data indicate that PrPC expression in astrocytes is critical for sustaining cell‐to‐cell interactions, the organization of the extracellular matrix, and the secretion of soluble factors, all of which are essential events for neuronal differentiation and survival.
Superoxide dismutase/catalase mimetics but not MAP kinase inhibitors are neuroprotective against oxygen/glucose deprivation‐induced neuronal death in hippocampus
Authors: Zhou Miou , Dominguez Reymundo , Baudry Michel 
Published: September 2007

AbstractAlthough oxygen/glucose deprivation (OGD) has been widely used as a model of ischemic brain damage, the mechanisms underlying acute neuronal death in this model are not yet well understood. We used OGD in acute hippocampal slices to investigate the roles of reactive oxygen species and of the mitogen‐activated protein kinases (MAPKs) in neuronal death. In particular, we tested the neuroprotective effects of two synthetic superoxide dismutase/catalase mimetics, EUK‐189 and EUK‐207. Acute hippocampal slices prepared from 2‐month‐old or postnatal day 10 rats were exposed to oxygen and glucose deprivation for 2 h followed by 2.5 h reoxygenation. Lactate dehydrogenase (LDH) release in the medium and propidium iodide (PI) uptake were used to evaluate cell viability. EUK‐189 or EUK‐207 applied during the OGD and reoxygenation periods decreased LDH release and PI uptake in slices from 2‐month‐old rats. EUK‐189 or EUK‐207 also partly blocked OGD‐induced ATP depletion and extracellular signal‐regulated kinases 1 and 2 (ERK1/2) dephosphorylation, and completely eliminated reactive oxygen species generation. The MEK inhibitor U0126 applied together with EUK‐189 or EUK‐207 completely blocked ERK1/2 activation, but had no effect on their protective effects against OGD‐induced LDH release. U0126 alone had no effect on OGD‐induced LDH release. EUK‐207 had no effect on OGD‐induced p38 or c‐Jun N‐terminal kinase dephosphorylation, and when the p38 inhibitor SB203580 was applied together with EUK‐207, it had no effect on the protective effects of EUK‐207. SB203580 alone had no effect on OGD‐induced LDH release either. In slices from p10 rats, OGD also induced high‐LDH release that was partly reversed by EUK‐207; however, neither OGD nor EUK‐207 produced significant changes in ERK1/2 and p38 phosphorylation. OGD‐induced spectrin degradation was not modified by EUK‐189 or EUK‐207 in slices from p10 or 2‐month‐old rats, suggesting that their protective effects was not mediated through inhibition of calpain activation. Thus, both EUK‐189 and EUK‐207 provide neuroprotection in acute ischemic conditions, and this effect is related to elimination of free radical formation and partial reversal of ATP depletion, but not mediated by the activation or inhibition of the MEK/ERK or p38 pathways, or inhibition of calpain activation.
Catecholamine exocytosis is diminished in R6/2 Huntington’s disease model mice
Authors: Johnson Michael A. , Villanueva Melissa , Haynes Christy L. , Seipel Andrew T. , Buhler Leah A. , Wightman R. Mark 
Published: September 2007

AbstractIn this work, the mechanisms responsible for dopamine (DA) release impairments observed previously in Huntington’s disease model R6/2 mice were evaluated. Voltammetrically measured DA release evoked in striatal brain slices from 12‐week old R6/2 mice by a single electrical stimulus pulse was only 19% of wild‐type (WT) control mice. Iontophoresis experiments suggest that the concentration of released DA is not diluted by a larger striatal extracellular volume arising from brain atrophy, but, rather, that striatal dopaminergic terminals have a decreased capacity for DA release. This decreased capacity was not due to an altered requirement for extracellular Ca2+, and, as in WT mice, the release in R6/2 mice required functioning vesicular transporters. Catecholamine secretion from individual vesicles was measured during exocytosis from adrenal chromaffin cells harvested from R6/2 and WT mice. While the number of exocytotic events was unchanged, the amounts released per vesicle were significantly diminished in R6/2 mice, indicating that vesicular catecholamines are present in decreased amounts. Treatment of chromaffin cells with 3‐nitropropionic acid decreased the vesicular release amount from WT cells by 50%, mimicking the release observed from untreated R6/2 cells. Thus, catecholamine release from tissues isolated from R6/2 mice is diminished because of impaired vesicle loading.
Expression level and activity profile of membrane bound guanylate cyclase type 2 in rod outer segments
Authors: Helten Andreas , Säftel Werner , Koch Karl‐Wilhelm 
Published: September 2007

AbstractRod and cone cells of the mammalian retina harbor two types of a membrane bound guanylate cyclase (GC), rod outer segment guanylate cyclase type 1 (ROS‐GC1) and ROS‐GC2. Both enzymes are regulated by small Ca2+‐binding proteins named GC‐activating proteins that operate as Ca2+ sensors and enable cyclases to respond to changes of intracellular Ca2+after illumination. We determined the expression level of ROS‐GC2 in bovine ROS preparations and compared it with the level of ROS‐GC1 in ROSs. The molar ratio of a ROS‐GC2 dimer to rhodopsin was 1 : 13 200. The amount of ROS‐GC1 was 25‐fold higher than the amount of ROS‐GC2. Heterologously expressed ROS‐GC2 was differentially activated by GC‐activating protein 1 and 2 at low free Ca2+ concentrations. Mutants of GC‐activating protein 2 modulated ROS‐GC2 in a manner different from their action on ROS‐GC1 indicating that the Ca2+ sensitivity of the Ca2+ sensor is controlled by the mode of target–sensor interaction.
PERMANENT GENETIC RESOURCES: Development of polymorphic microsatellite loci for the common vampire bat, Desmodus rotundus (Chiroptera: Phylostomidae)
Authors: PIAGGIO ANTOINETTE J. , JOHNSTON JOHN J. , PERKINS SUSAN L. 
Published: September 2007

AbstractThe common vampire bat (Desmodus rotundus) is one of three haematophagous species of bats and the only species in this genus. These New World bats prey on mammals and create significant economic impacts through transmission of rabies in areas where livestock are prevalent. Furthermore, in some portions of their range, it is not uncommon for them to prey upon humans. It is critical to the management of this species and for understanding the spread of bat rabies that detailed studies of D. rotundus population structure be conducted. To further such studies, we have characterized 12 microsatellite loci for this species.
PERMANENT GENETIC RESOURCES: Development of microsatellite markers for the ecosystem bioengineer mussel Perumytilus purpuratus and cross‐priming testing in six Mytilinae genera
Authors: PÉREZ M. , GUIÑEZ R. , LLAVONA A. , TORO J. E. , ASTORGA M. , PRESA P. 
Published: September 2007

AbstractEight microsatellite markers have been characterized from the Perumytilus purpuratus genome. Their gene diversity ranged from 0.057 to 0.873 and significant interpopulation genic heterogeneity was observed between two populations of southeastern Pacific (Chile) and southwestern Atlantic (Argentine). Distinct cross‐priming amplification rates were recovered on nine additional species belonging to six Mytilinae genera. The microsatellites developed herein would likely be a powerful intraspecific genetic tool to undertake fine population studies in the intertidal ecosystem bioengineer P. purpuratus along the South American shoreline.
PERMANENT GENETIC RESOURCES: Identification of microsatellite loci for parentage analysis in roach Rutilus rutilus and eight other cyprinid fish by cross‐species amplification, and a novel test for detecting hybrids between roach and other cyprinids
Authors: HAMILTON P. B. , TYLER C. R. 
Published: September 2007

AbstractIn order to identify microsatellite loci for parentage analysis in roach Rutilus rutilus, 59 published primer sets were tested on roach and eight other cyprinid fish. Twenty polymorphic loci were identified for roach, of which the polymerase chain reaction products of seven could be pooled for sequencer analysis. Together, these seven loci have an exclusion probability of 0.997 for parentage, when no parents are known. We also describe a novel test for hybrids between roach and four other cyprinids, based on intraspecies length differences of internal transcribed spacer region 1.
Unemployment and Psychological Well‐being*
Authors: CARROLL NICK 
Published: September 2007

Who records the largest drops in life satisfaction when they move into unemployment? Do men experience a larger drop in life satisfaction? Do Australians and Americans record a larger drop than Europeans? Using panel data, this paper finds that the unemployed in Australia report lower life satisfaction than observationally equivalent employed people (holding current income constant). Being unemployed is estimated to be equivalent to the loss of $A42 100 annual income for men and even more for women. It is found that unemployment is less painful for men in Australia than for men in Germany and the UK.