Auditor choice, audit fees and internal governance in family firms

I study the role of auditing in mitigating agency concerns in family firms. Family firms face less severe agency problems due to the separation of ownership and control (Type 1) but more severe agency problems between controlling and noncontrolling shareholders (Type 2). As family firms make up a large part of most free enterprise economies it is important to examine these two agency problems with respect to auditor choice and audit effort. I find that family firms are more likely to choose a specialist auditor than nonfamily firms, consistent with the argument that family firms need to signal their non-expropriating behaviors by choosing specialist auditors. I further find that audit fees are lower in family firms compared to nonfamily firms, consistent with the hypothesis that the Type 1 agency conflict dominates the Type 2 agency conflict in the determination of audit effort and pricing. Moreover, consistent with prior literature that states that effective internal governance demands a quality auditor and more audit effort irrespective of ownership structure, I find that the positive association between family ownership and specialist auditor choice is stronger when internal governance is strong and the negative relation between audit fees and family ownership is weaker when the internal governance is strong. I find that these results on audit fees are robust to the use of alternative measures of concentrated influence such as CEO ownership, inside director ownership, and the presence of one or more founder directors. I also find that the effect of internal governance on audit fees is not limited to one or a few components of internal governance

Formation of Rotational Discontinuities in Compressive three-dimensional MHD Turbulence

Measurements of solar wind turbulence reveal the ubiquity of discontinuities. In this study, we investigate how the discontinuities, especially rotational discontinuities (RDs), are formed in magnetohydrodynamic (MHD) turbulence. In a simulation of the decaying compressive three-dimensional (3-D) MHD turbulence with an imposed uniform background magnetic field, we detect RDs with sharp field rotations and little variations of magnetic field intensity as well as mass density. At the same time, in the de Hoffman-Teller (HT) frame, the plasma velocity is nearly in agreement with the Alfv\'{e}n speed, and is field-aligned on both sides of the discontinuity. We take one of the identified RDs to analyze in details its 3-D structure and temporal evolution. By checking the magnetic field and plasma parameters, we find that the identified RD evolves from the steepening of the Alfv\'{e}n wave with moderate amplitude, and that steepening is caused by the nonuniformity of the Alfv\'{e}n speed in the ambient turbulence.Comment: Five figures enclosed. Submitted to Astrophys. J., Under referrin

Line bisection performance in patients with generalized anxiety disorder and treatment-resistant depression

Background and Objectives The line bisection error to the left of the true center has been interpreted as a relative right hemisphere activation, which might relate to the subject's emotional state. Considering that patients with generalized anxiety disorder (GAD) or treatment-resistant depression (TRD) often have negative emotions, we hypothesized that these patients would bisect lines significantly leftward. Methods We tried the line bisection task in the right-handed healthy volunteers (n = 56), GAD (n = 47) and TRD outpatients (n = 52). Subjects also completed the Zuckerman - Kuhlman Personality Questionnaire, the Zuckerman Sensation Seeking Scales, and the Plutchik-van Praag Depression Inventory. Results GAD patients scored highest on the Neuroticism-Anxiety trait, TRD patients scored highest on depression, and both patients scored lower on the Sociability trait. Patients with GAD also bisected lines significantly leftward compared to the healthy subjects. The Frequency of the bisection error was negatively correlated with Disinhibition-Seeking in the healthy subjects, and with Total sensation-seeking and Experience-Seeking in GAD patients, while the Magnitude of the line bisection error was negatively correlated with depression in TRD patients. Conclusions The study suggests a stronger right hemispheric activation, a weaker left activation, or both in the GAD, instead of TRD patients

Dissecting order amidst chaos of programmed cell deaths: construction of a diagnostic model for KIRC using transcriptomic information in blood-derived exosomes and single-cell multi-omics data in tumor microenvironment

BackgroundKidney renal clear cell carcinoma (KIRC) is the most frequently diagnosed subtype of renal cell carcinoma (RCC); however, the pathogenesis and diagnostic approaches for KIRC remain elusive. Using single-cell transcriptomic information of KIRC, we constructed a diagnostic model depicting the landscape of programmed cell death (PCD)-associated genes, namely cell death-related genes (CDRGs).MethodsIn this study, six CDRG categories, including apoptosis, necroptosis, autophagy, pyroptosis, ferroptosis, and cuproptosis, were collected. RNA sequencing (RNA-seq) data of blood-derived exosomes from the exoRBase database, RNA-seq data of tissues from The Cancer Genome Atlas (TCGA) combined with control samples from the GTEx databases, and single-cell RNA sequencing (scRNA-seq) data from the Gene Expression Omnibus (GEO) database were downloaded. Next, we intersected the differentially expressed genes (DEGs) of the KIRC cohort from exoRBase and the TCGA databases with CDRGs and DEGs obtained from single-cell datasets, further screening out the candidate biomarker genes using clinical indicators and machine learning methods and thus constructing a diagnostic model for KIRC. Finally, we investigated the underlying mechanisms of key genes and their roles in the tumor microenvironment using scRNA-seq, single-cell assays for transposase-accessible chromatin sequencing (scATAC-seq), and the spatial transcriptomics sequencing (stRNA-seq) data of KIRC provided by the GEO database.ResultWe obtained 1,428 samples and 216,155 single cells. After the rational screening, we constructed a 13-gene diagnostic model for KIRC, which had high diagnostic efficacy in the exoRBase KIRC cohort (training set: AUC = 1; testing set: AUC = 0.965) and TCGA KIRC cohort (training set: AUC = 1; testing set: AUC = 0.982), with an additional validation cohort from GEO databases presenting an AUC value of 0.914. The results of a subsequent analysis revealed a specific tumor epithelial cell of TRIB3high subset. Moreover, the results of a mechanical analysis showed the relatively elevated chromatin accessibility of TRIB3 in tumor epithelial cells in the scATAC data, while stRNA-seq verified that TRIB3 was predominantly expressed in cancer tissues.ConclusionsThe 13-gene diagnostic model yielded high accuracy in KIRC screening, and TRIB3high tumor epithelial cells could be a promising therapeutic target for KIRC

Chronic Arsenic Exposure and Angiogenesis in Human Bronchial Epithelial Cells via the ROS/miR-199a-5p/HIF-1α/COX-2 Pathway.

Background: Environmental and occupational exposure to arsenic is a major public health concern. Although it has been identified as a human carcinogen, the molecular mechanism underlying the arsenic-induced carcinogenesis is not well understood.Objectives: We aimed to determine the role and mechanisms of miRNAs in arsenic-induced tumor angiogenesis and tumor growth.Methods: We utilized an in vitro model in which human lung epithelial BEAS-2B cells were transformed through long-term exposure to arsenic. A human xenograft tumor model was established to assess tumor angiogenesis and tumor growth in vivo. Tube formation assay and chorioallantoic membranes assay were used to assess tumor angiogenesis.Results: We found that miR-199a-5p expression levels were more than 100-fold lower in arsenic-transformed cells than parental cells. Re-expression of miR-199a-5p impaired arsenic-induced angiogenesis and tumor growth through its direct targets HIF-1α and COX-2. We further showed that arsenic induced COX-2 expression through HIF-1 regulation at the transcriptional level. In addition, we demonstrated that reactive oxygen species are an upstream event of miR-199a-5p/ HIF-1α/COX-2 pathway in arsenic-induced carcinogenesis.Conclusion: The findings establish critical roles of miR-199a-5p and its downstream targets HIF-1/COX-2 in arsenic-induced tumor growth and angiogenesis.Citation: He J, Wang M, Jiang Y, Chen Q, Xu S, Xu Q, Jiang BH, Liu LZ. 2014. Chronic arsenic exposure and angiogenesis in human bronchial epithelial cells via the ROS/miR-199a-5p/HIF-1α/COX-2 Pathway. Environ Health Perspect 122:255-261; http://dx.doi.org/10.1289/ehp.1307545