Fair Value, Historical Cost model, and Audit Fees: Evidence from Investment Properties

This study examines the effect of fair value model versus historical cost model for investment property on audit fees. Using China’s real state firms data from 2007-2014, controlling for other determinants of audit fees, this study finds that audit fees are higher for firms reporting investment property at the fair value model relative to those reporting investment property at the cost model. This study also finds that firm reporting investment properties at the fair value located in the cities with active markets leads to lower audit fees than those located in the remote areas with less active markets. This study does not find that investment property valued under the fair value model audited by industry specialist leads to higher audit fees than investment property audited by non-industry specialist. Finally, this study provides evidence that firms use external appraisers to monitor the fair value estimates of investment properties leads low audit fees. Overall, our result suggests that fair value measurements leads to lower audit fees in the developed regions relative to less developed regions

Spatial heterogeneity of tectonic stress and friction in the crust: new evidence from earthquake focal mechanisms in Taiwan

We performed inversions of earthquake focal mechanisms in central Taiwan to investigate the heterogeneity of the stress field and fault strength, and temporal variations of stress parameters, friction and pore pressure associated with the 1999 Chi-Chi earthquake. We divided the focal mechanism data into two groups: before and after the Chi-Chi earthquake, and analysed them separately. With the assumption of a uniform stress field, the friction coefficient is mostly within a range of 0.2–0.4 in central Taiwan, which is lower than the commonly quoted laboratory result, 0.6–0.85. The low friction coefficient is also inferred by the rotation of principal stress axes after the Chi-Chi earthquake. By contrast, if we assume that the friction is constant and failures occur on optimally oriented planes, we find that the resulting stress orientations must be spatially variable. However, a large dispersion of stress orientations is not seen in borehole breakouts and fault slip data, implying a constant friction model might be ruled out. Our analysis suggests that either the distribution of the coefficient of friction or pore pressure changed during the 1999 Chi-Chi earthquake. We infer that the pore pressure probably rose in the Chi-Chi rupture area and northern Longitudinal Valley and dropped in the areas south of the coseismic rupture area after the main shock

AMP-activated protein kinase activation mediates CCL3-induced cell migration and matrix metalloproteinase-2 expression in human chondrosarcoma

Chemokine (C-C motif) ligand 3 (CCL3), also known as macrophage inflammatory protein-1α, is a cytokine involved in inflammation and activation of polymorphonuclear leukocytes. CCL3 has been detected in infiltrating cells and tumor cells. Chondrosarcoma is a highly malignant tumor that causes distant metastasis. However, the effect of CCL3 on human chondrosarcoma metastasis is still unknown. Here, we found that CCL3 increased cellular migration and expression of matrix metalloproteinase (MMP)-2 in human chondrosarcoma cells. Pre-treatment of cells with the MMP-2 inhibitor or transfection with MMP-2 specific siRNA abolished CCL3-induced cell migration. CCL3 has been reported to exert its effects through activation of its specific receptor, CC chemokine receptor 5 (CCR5). The CCR5 and AMP-activated protein kinase (AMPK) inhibitor or siRNA also attenuated CCL3-upregulated cell motility and MMP-2 expression. CCL3-induced expression of MMP-2 and migration were also inhibited by specific inhibitors, and inactive mutants of AMPK, p38 mitogen activated protein kinase (p38 or p38-MAPK), and nuclear factor κB (NF-κB) cascades. On the other hand, CCL3 treatment demonstrably activated AMPK, p38, and NF-κB signaling pathways. Furthermore, the expression levels of CCL3, CCR5, and MMP-2 were correlated in human chondrosarcoma specimens. Taken together, our results indicate that CCL3 enhances the migratory ability of human chondrosarcoma cells by increasing MMP-2 expression via the CCR5, AMPK, p38, and NF-κB pathways

Nanoparticle conversion to biofilms: in vitro demonstration using serum-derived mineralo-organic nanoparticles

Aims: Mineralo-organic nanoparticles (NPs) detected in biological fluids have been described as precursors of physiological and pathological calcifications in the body. Our main objective was to examine the early stages of mineral NP formation in body fluids. Materials & methods: A nanomaterial approach based on atomic force microscopy, dynamic light scattering, electron microscopy and spectroscopy was used. Results: The mineral particles, which contain the serum proteins albumin and fetuin-A, initially precipitate in the form of round amorphous NPs that gradually grow in size, aggregate and coalesce to form crystalline mineral films similar to the structures observed in calcified human arteries. Conclusion: Our study reveals the early stages of particle formation and provides a platform to analyze the role(s) of mineralo-organic NPs in human tissues

Mutations in the PKM2 exon-10 region are associated with reduced allostery and increased nuclear translocation.

PKM2 is a key metabolic enzyme central to glucose metabolism and energy expenditure. Multiple stimuli regulate PKM2's activity through allosteric modulation and post-translational modifications. Furthermore, PKM2 can partner with KDM8, an oncogenic demethylase and enter the nucleus to serve as a HIF1α co-activator. Yet, the mechanistic basis of the exon-10 region in allosteric regulation and nuclear translocation remains unclear. Here, we determined the crystal structures and kinetic coupling constants of exon-10 tumor-related mutants (H391Y and R399E), showing altered structural plasticity and reduced allostery. Immunoprecipitation analysis revealed increased interaction with KDM8 for H391Y, R399E, and G415R. We also found a higher degree of HIF1α-mediated transactivation activity, particularly in the presence of KDM8. Furthermore, overexpression of PKM2 mutants significantly elevated cell growth and migration. Together, PKM2 exon-10 mutations lead to structure-allostery alterations and increased nuclear functions mediated by KDM8 in breast cancer cells. Targeting the PKM2-KDM8 complex may provide a potential therapeutic intervention

MicroRNA Expression Profiling Altered by Variant Dosage of Radiation Exposure

[[abstract]]Various biological effects are associated with radiation exposure. Irradiated cells may elevate the risk for genetic instability, mutation, and cancer under low levels of radiation exposure, in addition to being able to extend the postradiation side effects in normal tissues. Radiation-induced bystander effect (RIBE) is the focus of rigorous research as it may promote the development of cancer even at low radiation doses. Alterations in the DNA sequence could not explain these biological effects of radiation and it is thought that epigenetics factors may be involved. Indeed, some microRNAs (or miRNAs) have been found to correlate radiation-induced damages and may be potential biomarkers for the various biological effects caused by different levels of radiation exposure. However, the regulatory role that miRNA plays in this aspect remains elusive. In this study, we profiled the expression changes in miRNA under fractionated radiation exposure in human peripheral blood mononuclear cells. By utilizing publicly available microRNA knowledge bases and performing cross validations with our previous gene expression profiling under the same radiation condition, we identified various miRNA-gene interactions specific to different doses of radiation treatment, providing new insights for the molecular underpinnings of radiation injury.[[notice]]補正完畢[[incitationindex]]SCI[[incitationindex]]EI[[booktype]]電子