119 research outputs found

    Determinants Of The Use Of Special Purpose Companies (SPCs) On Pre- And Post-IFRS: Empirical Evidence From Korea

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    We investigate which factors determine the use of a special purpose company (SPC) by a sponsoring company and whether those determinants differ before and after IFRS (International Financial Reporting Standards) adoption. Using financial data from Korean listed companies, our results indicate that use of an SPC is associated with financial reporting incentives (e.g., lowering leverage) and economic benefits (e.g., fundraising). However, the effect of leverage on the use of SPCs is not significant after the adoption of the IFRS. These results suggest that, although companies are generally motivated to use SPCs for both financial reporting and economic purposes, only economic motivation influences the use of SPCs after IFRS adoption. This implies that the regulation for reporting an SPC’s consolidated financial statement under IFRS plays a role in decreasing the use of SPCs for financial reporting discretion. We extend the prior literature on SPCs by documenting the effects of IFRS adoption on the determinants of the use of SPCs

    Organ-specific regulation of ATP7A abundance is coordinated with systemic copper homeostasis

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    Copper (Cu) is an essential cofactor for various enzymatic activities including mitochondrial electron transport, iron mobilization, and peptide hormone maturation. Consequently, Cu dysregulation is associated with fatal neonatal disease, liver and cardiac dysfunction, and anemia. While the Cu transporter ATP7A plays a major role in both intestinal Cu mobilization to the periphery and prevention of Cu over-accumulation, it is unclear how regulation of ATP7A contributes to Cu homeostasis in response to systemic Cu fluctuation. Here we show, using Cu-deficient mouse models, that steadystate levels of ATP7A are lower in peripheral tissues (including the heart, spleen, and liver) under Cu deficiency and that subcutaneous administration of Cu to these animals restore normal ATP7A levels in these tissues. Strikingly, ATP7A in the intestine is regulated in the opposite manner - low systemic Cu increases ATP7A while subcutaneous Cu administration decreases ATP7A suggesting that intestinespecific non-autonomous regulation of ATP7A abundance may serve as a key homeostatic control for Cu export into the circulation. Our results support a systemic model for how a single transporter can be inversely regulated in a tissue-specific manner to maintain organismal Cu homeostasis

    Distinct Mechanisms for Ctr1-mediated Copper and Cisplatin Transport

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    The Ctr1 family of integral membrane proteins is necessary for high affinity copper uptake in eukaryotes. Ctr1 is also involved in cellular accumulation of cisplatin, a platinum-based anticancer drug. Although the physiological role of Ctr1 has been revealed, the mechanism of action of Ctr1 remains to be elucidated. To gain a better understanding of Ctr1-mediated copper and cisplatin transport, we have monitored molecular dynamics and transport activities of yeast Saccharomyces cerevisiae Ctr1 and its mutant alleles. Co-expression of functional Ctr1 monomers fused with either cyan or yellow fluorescent protein resulted in fluorescence resonance energy transfer (FRET), which is consistent with multimer assembly of Ctr1. Copper near the Km value of Ctr1 enhanced FRET in a manner that correlated with cellular copper transport. In vitro cross-linking of Ctr1 confirmed that copper-induced FRET reflects conformational changes within pre-existing Ctr1 complexes. FRET assays in membrane-disrupted cells and protein extracts showed that intact cell structure is necessary for Ctr1 activity. Despite Ctr1-dependent cellular accumulation, cisplatin did not change Ctr1 FRET nor did it attenuate copper-induced FRET. A Ctr1 allele defective in copper transport enhanced cellular cisplatin accumulation. N-terminal methionine-rich motifs that are dispensable for copper transport play a critical role for cisplatin uptake. Taken together, our data reveal functional roles for structural remodeling of the Ctr1 multimeric complex in copper transport and suggest distinct mechanisms employed by Ctr1 for copper and cisplatin transport

    IFRS adoption and investor perceptions of earnings quality: evidence from Korea

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    This study examines the consequences of International Financial Reporting Standards (IFRS) adoption in terms of the investor perception of earnings quality in the Korean stock market. Building on evidence from Ecker et al. (2006) suggesting that return-based earnings quality (E-loading), as captured by the sensitivity of stock returns to accounting information risk, accurately represents investor perceptions of earnings information risk, the authors examine whether E-loading is different between the pre- and post-IFRS adoption periods. Using KSE-listed firms from 2006 to 2014, the authors find the evidence that the extent of stock return sensitivity to information risk embedded in financial statements is greater in the period of post-IFRS adoption than in the period of pre-IFRS adoption. This finding indicates that even though accounting-based earnings quality improves after the adoption of IFRS, investors perceive earnings information after the adoption of IFRS as riskier than before. In addition, the difference in investor perception is more pronounced for firms with low accruals quality as captured by discretionary accruals, indicating that the effect of IFRS adoption on return-based earnings quality is distinctive from that on accounting-based earnings quality. The paper contributes to the literature on IFRS by exploring the effect of IFRS adoption through a new perspective on earnings quality in capital market

    Rydberg-atom graphs for quadratic unconstrained binary optimization problems

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    There is a growing interest in harnessing the potential of the Rydberg-atom system to address complex combinatorial optimization challenges. Here we present an experimental demonstration of how the quadratic unconstrained binary optimization (QUBO) problem can be effectively addressed using Rydberg-atom graphs. The Rydberg-atom graphs are configurations of neutral atoms organized into mathematical graphs, facilitated by programmable optical tweezers, and designed to exhibit many-body ground states that correspond to the maximum independent set (MIS) of their respective graphs. We have developed four elementary Rydberg-atom subgraph components, not only to eliminate the need of local control but also to be robust against interatomic distance errors, while serving as the building blocks sufficient for formulating generic QUBO graphs. To validate the feasibility of our approach, we have conducted a series of Rydberg-atom experiments selected to demonstrate proof-of-concept operations of these building blocks. These experiments illustrate how these components can be used to programmatically encode the QUBO problems to Rydberg-atom graphs and, by measuring their many-body ground states, how their QUBO solutions are determined subsequently.Comment: 13 pages, 6 figure

    Arsenite exposure suppresses adipogenesis, mitochondrial biogenesis and thermogenesis via autophagy inhibition in brown adipose tissue

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    Arsenite, a trivalent form of arsenic, is an element that occurs naturally in the environment. Humans are exposed to high dose of arsenite through consuming arsenite-contaminated drinking water and food, and the arsenite can accumulate in the human tissues. Arsenite induces oxidative stress, which is linked to metabolic disorders such as obesity and diabetes. Brown adipocytes dissipating energy as heat have emerging roles for obesity treatment and prevention. therefore, understanding the pathophysiological role of brown adipocytes can provide effective strategies delineating the link between arsenite exposure and metabolic disorders. Our study revealed that arsenite significantly reduced differentiation of murine brown adipocytes and mitochondrial biogenesis and respiration, leading to attenuated thermogenesis via decreasing UCP1 expression. Oral administration of arsenite in mice resulted in heavy accumulation in brown adipose tissue and suppression of lipogenesis, mitochondrial biogenesis and thermogenesis.Mechanistically, arsenite exposure significantly inhibited autophagy necessary for homeostasis of brown adipose tissue through suppression of Sestrin2 and ULK1. These results clearly confirm the emerging mechanisms underlying the implications of arsenite exposure in metabolic disorders

    Evaluation of the Clinical Usefulness of Critical Patient Severity Classification System and Glasgow Coma Scale for Neurological Patients in Intensive Care Units

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    Keywords: critical illness Glasgow Coma Scale intensive care units neurology s u m m a r y Purpose: The purpose of this study was to evaluate the clinical usefulness of the Critical Patient Severity Classification System (CPSCS) and Glasgow Coma Scale (GCS) for critically ill neurological patients and to determine the applicability of CPSCS and GCS in predicting their mortality. Methods: Data were collected from the medical records of 187 neurological patients who were admitted to the intensive care unit of C university hospital. The data were analyzed through chi-square test, t test, MannWhitney, Kruskal-Wallis, goodness-of-fit test, and receiver operating characteristic curve. Results: In accordance with patients' general and clinical characteristics, patient mortality turned out to be significantly different depending on intensive care unit stay, endotracheal intubation, central venous catheter, and severity by CPSCS. Hosmer-Lemeshow goodness-of-fit tests were applied to CPSCS and GCS. The results of the discrimination test using the receiver operating characteristic curve were CPSCS 0 , .743, GCS 0 .583, CPSCS 24 , .734, GCS 24 .612, CPSCS 48 , .591, GCS 48 .646, CPSCS 72 , .622, and GCS 72 .623. Logistic regression analysis showed that each point on the CPSCS score signifies a 1.034 higher likelihood of dying. Conclusion: Applied to neurologically ill patients, early CPSCS scores can be regarded as a useful tool

    Oma1 Links Mitochondrial Protein Quality Control and TOR Signaling To Modulate Physiological Plasticity and Cellular Stress Responses

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    ACKNOWLEDGMENTS We thank Dennis Winge (University of Utah) and the members of the Khalimonchuk laboratory for critical comments. We also thank Christoph Schuller (University of Natural Resources, Austria) and Paul Herman (Ohio State University) for reagents. We acknowledge the expert technical assistance of Nataliya Zahayko. We also thank Donna MacCallum for help with the Candida virulence assays. This research was supported by grants from the NIH (P30GM103335 and 5R01GM108975 [O.K.], GM071775-06 and GM105781-01 [A.B.], DK079209 [J.L.]), the U.K. Biotechnology and Biological Research Council (BB/K017365/1 [A.J.P.B.]), the U.K. Medical Research Council (MR/ M026663/1 [A.J.P.B.]), and the European Research Council (C-2009- AdG-249793 [A.J.P.B.]). We declare that we have no competing financial interests. FUNDING INFORMATION This work, including the efforts of Alistair J. P. Brown, was funded by Biotechnology and Biological Research Counsil (BB/K017365/1). This work, including the efforts of Oleh Khalimonchuk, was funded by HHS | National Institutes of Health (NIH) (5R01GM108975). This work, including the efforts of Oleh Khalimonchuk, was funded by HHS | National Institutes of Health (NIH) (P30GM103335).This work, including the efforts of Antoni Barrientos, was funded by HHS | National Institutes of Health (NIH) (GM071775-06). This work, including the efforts of Antoni Barrientos, was funded by HHS | National Institutes of Health (NIH) (GM105781-01). This work, including the efforts of Jaekwon Lee, was funded by HHS | National Institutes of Health (NIH) (DK079209). This work, including the efforts of Alistair J. P. Brown, was funded by Medical Research Council (MRC) (MR/M026663/1). This work, including the efforts of Alistair J. P. Brown, was funded by EC | European Research Council (ERC) (C-2009-AdG-249793).Peer reviewedPublisher PD

    Cadmium and Secondary Structure-dependent Function of a Degron in the Pca1p Cadmium Exporter

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    Protein turnover is a critical cellular process regulating biochemical pathways and destroying terminally misfolded or damaged proteins. Pca1p, a cadmium exporter in the yeast Saccharomyces cerevisiae, is rapidly degraded by the endoplasmic reticulum-associated degradation (ERAD) system via a cis-acting degron that exists at the 250–350 amino acid region of Pca1p and is transferable to other proteins to serve as a degradation signal. Cadmium stabilizes Pca1p in a manner dependent on the degron. This suggested that cadmium-mediated masking of the degron impedes its interaction with the molecular factors involved in the ERAD. The characteristics and mechanisms of action of the degron in Pca1p and most of those in other proteins however remain to be determined. The results presented here indicate that specific cysteine residues in a degron of Pca1p sense cadmium.Anunbiased approach selecting non-functional degrons indicated a critical role of hydrophobic amino acids in the degron for its function.Asecondary structure modeling predicted the formation of an amphipathic helix. Site-directed mutagenesis confirmed the functional significance of the hydrophobic patch. Last, hydrophobic amino acids in the degron- and cadmium-binding region affected the interaction of Pca1p with the Ssa1p molecular chaperone, which is involved in ERAD. These results reveal the mechanism of action of the degron, which might be useful for the identification and characterization of other degrons
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