The Impact of the Asset Impairment Standard on the Choice of Earnings Management

本文探討《財務會計準則公報》第35號〈資產減損之會計處理準則〉，是否會影響企業的盈餘管理方法選擇，以及盈餘管理工具間的替代關係。雖然實證結果未能證實〈資產減損會計處理準則〉對應計項目盈餘管理及實質盈餘管理有影響，但是實證結果仍顯示，當企業利用應計項目盈餘管理受限，會增加實質盈餘管理程度，亦即，應計項目盈餘管理與實質盈餘管理間存在替代關係。此外，資產減損損失公報會削弱了應計項目與實質盈餘管理間的替代關係。This study examines how Statement Financial Accounting Standards (SFAS) No. 35, ＂Accounting for the Impairment of Assets,＂ has the effect on the choice of earnings management and the substitution among accruals-based earnings management, real earnings management and asset write-downs. The results reveal that accruals-based earnings management and real earnings management are in effect substitutive. Moreover, the substitutive relationships between accruals-based earnings management and real earnings management was decreased after Accounting Research and Development Foundation in Taiwan issued SFAS No.35

Managerial Overconfidence and Earnings Quality

本研究以2005年至2014年台灣上市櫃電子工業公司為樣本，檢測經理人過度自信傾向與盈餘穩健性之關係。本研究以當年度持股增加達10%以上做為經理人過度自信之衡量，以應計數及裁決性應計數做為盈餘穩健性之代理變數。結果顯示當經理人具過度自信傾向，公司負值的應計盈餘數愈少，表示經理人過度自信使盈餘報導較不穩健。本研究進一步探討裁決性應計數與經理人過度自信之關係，結果發現經理人過度自信與正裁決性應計數呈顯著正相關，表示過度自信經理人會有從事正向盈餘管理的現象，導致盈餘穩健程度降低。整體 而言，本研究證實具過度自信心理特質之經理人會有樂觀的盈餘報導及正向的盈餘管理，因而減少盈餘穩健性，不利影響盈餘品質。Overconfident managers tend to overestimate future returns from their firms' investment. Thus, this study predicts that overconfident managers will tend to delay loss recognition and use less conservative accounting. Based on a sample of Taiwanese listed companies in the electronics industry from 2005 to 2014, this study investigates the relationship between managerial overconfidence and earnings quality. This study classifies managers as overconfident using a dichotomous variable where OverCon is set equal to 1 if managers increase their ownership in the firm by 10% during the fiscal year. This study uses accruals and discretionary accruals as proxies to measure earnings conservatism. The empirical results show that managerial overconfidence is significantly and negatively associated with negative accruals, indicating that overconfident managers use less conservative accounting. This study further finds that managerial overconfidence is positively associated with positive discretionary accruals, suggesting that overconfident managers tend to manage their earnings upward. Thus, this study suggests a negative association between managerial overconfidence and earning equality

Stimulation phosphatidylinositol 3-kinase/protein kinase B signaling by Porphyromonas gingivalis lipopolysacch aride mediates interleukin-6 and interleukin-8 mRNA/protein expression in pulpal inflammation

Background/purpose: The signaling mechanisms for Porphyromonas gingivalis lipopolysaccharide (PgLPS)-induced inflammation in human dental pulp cells are not fully clarified. This in vitro study aimed to evaluate the involvement of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway in PgLPS-induced pulpal inflammation. Methods: Human dental pulp cells (HDPCs) were challenged with PgLPS with or without pretreatment and coincubation with a PI3K/Akt inhibitor (LY294002). The gene or protein levels of PI3K, Akt, interleukin (IL)-6, IL-8, alkaline phosphatase (ALP), osteocalcin and osteonectin were analyzed by reverse transcription polymerase chain reaction (PCR), real-time PCR, western blotting, and immunofluorescent staining. In addition, an enzyme-linked immunosorbent assay was used to analyze IL-6 and IL-8 levels in culture medium. Results: In response to 5 μg/ml PgLPS, IL-6, IL-8, and PI3K, but not Akt mRNA expression of HDPCs, was upregulated. IL-6, IL-8, PI3K, and p-Akt protein levels were stimulated by 10–50 μg/ml of PgLPS in HDPCs. PgLPS also induced IL-6 and IL-8 secretion at concentrations higher than 5 μg/ml. Pretreatment and co-incubation by LY294002 attenuated PgLPS-induced IL-6 and IL-8 mRNA expression in HDPCs. The mRNA expression of ALP, but not osteocalcin and osteonectin, was inhibited by higher concentrations of PgLPS in HDPCs. Conclusion: P. gingivalis contributes to pulpal inflammation in HDPCs by dysregulating PI3K/Akt signaling pathway to stimulate IL-6 and IL-8 mRNA/protein expression and secretion. These results are useful for understanding the pulpal inflammation and possible biomarkers of inflamed pulp diagnosis and treatment

The pregnancy health and birth outcomes of women who underwent assisted reproductive technology: Results of a national survey

Background: There is an upward trend for parents to resort to assisted reproductive technology (ART) treatment due to delayed childbirth or birth difficulties. Objective: This study investigates the pregnancy health and birth outcomes of women who underwent ART and analyzes the factors that influence birth weight to become<10 percentile when undergoing ART. Materials and Methods: This study analyzed results of the first wave of the Taiwan Birth Cohort study. Through stratified systematic sampling, 24,200 mother-and-child sampling pairs were obtained from a total of 206,741 live births in Taiwan in 2005; 366 of the babies were born with the use of ART. Results: During pregnancy, mothers who used ART suffered from higher risks of complication than the natural conception counterparts, including gestational diabetes mellitus (GDM), pregnancy induced hypertension (PIH), and placenta previa. Additionally, babies born through ART had poorer outcomes than the natural conception groups: the low birth weight (<2500g) was 33.1% compared to 6.4% for babies born naturally. Conclusion: Pregnancy health and birth outcomes of women who underwent ART were worse than those who got natural conception. Types of maternal complication among ART women included GDM, PIH, and placenta previa. Having multiple births was the most important factor that causes low birth weight in babies. The results of this study can be used as a reference for the health and care of mothers and babies who use ART

Endothelial angiogenesis is directed by RUNX1T1-regulated VEGFA, BMP4 and TGF-β2 expression

<div><p>Tissue angiogenesis is intimately regulated during embryogenesis and postnatal development. Defected angiogenesis contributes to aberrant development and is the main complication associated with ischemia-related diseases. We previously identified the increased expression of RUNX1T1 in umbilical cord blood-derived endothelial colony-forming cells (ECFCs) by gene expression microarray. However, the biological relevance of RUNX1T1 in endothelial lineage is not defined clearly. Here, we demonstrate RUNX1T1 regulates the survival, motility and tube forming capability of ECFCs and EA.hy926 endothelial cells by loss-and gain-of function assays, respectively. Second, embryonic vasculatures and quantity of bone marrow-derived angiogenic progenitors are found to be reduced in the established <i>Runx1t1</i> heterozygous knockout mice. Finally, a central RUNX1T1-regulated signature is uncovered and VEGFA, BMP4 as well as TGF-β2 are demonstrated to mediate RUNX1T1-orchested angiogenic activities. Taken together, our results reveal that RUNX1T1 serves as a common angiogenic driver for vaculogenesis and functionality of endothelial lineage cells. Therefore, the discovery and application of pharmaceutical activators for RUNX1T1 will improve therapeutic efficacy toward ischemia by promoting neovascularization.</p></div

The decreased quantity of bone marrow-derived angiogenic progenitor cells and impaired aorta are observed in <i>Runx1t1</i> deficient mice.

<p>(A) A schematic representation of the gene-targeting strategy. The P1, P2 and P3 primers were used for the genotyping. The <i>loxP</i> sequence and a FRT-floxed neomycin cassette was introduced into intron 2 and another <i>loxP</i> sequence was inserted into intron 4 to allow Cre-ceconbinase-mediated removal of exons 2 and exon 3. E, exon; Kb, kilobase; Cre, cre-recombinase. (B) A Western blot showing the expression of Runx1t1 in the aorta of 6-month-old wild-type (+/+) and heterozygous <i>Runx1t1</i> knockout (+/-) mice. The band intensity was quantified and normalized to control cells. (C) The histograms for showing percentage of bone marrow-derived CD34 (+)/KDR (+) angiogenic precursor cells of indicated mice. *, <i>p</i><0.05 (Student’s t-test); **, <i>p</i><0.01 (Student’s t-test). Data represent mean ± S.D. n = 4 for each group (D) The quantification of thickness for aorta wall at indicated mice. n = 4 for each group, 6-month-old mice.*, <i>p</i><0.05 (Student’s t test). (E) The histological images of aortas from indicated mice by hematoxylin and eosin staining. n = 4 for each group. Scale bar = 100 μm. (F). Representative pictures for Evans blue extravasation assay in the 6-month-old wild-type (+/+) and heterozygous <i>Runx1t1</i> knockout (+/-) mice. Arrows indicated relative location of extravasation observed in heterozygous <i>Runx1t1</i> knockout (+/-) mice. Star indicated the location of liver. (G) The histogram for showing percentage of aberrant vessel permeability in <i>Runx1t1</i> deficient mice. n (total mice number used for analysis) = 9 and 8 for 6-month-old wild-type mice (+/+) and <i>Runx1t1</i> heterozygous mice (+/-), respectively. *, <i>p</i><0.05, (Fisher’s exact test). (H) The histogram for showing quantification of Evans blue extravasation in liver (upper panel) and heart (lower panel) of <i>Runx1t1</i> deficient mice (+/-).*, <i>p</i><0.05; **, <i>p</i><0.01 (Student’s t-test).</p

RUNX1T1 is sufficient to enhance angiogenic activity of endothelial cells.

<p>(A) Western blots showing for RUNX1T1 expression levels in 926-EC. VEC, vector control cells; ROV, ectopically <i>RUNX1T1</i>-expressing cells. The band intensity was quantified and normalized to control cells. (B) A histogram showing the relative viability of 926-EC measured by MTT assay. **, <i>p</i><0.01 (Student’s t test). Data represent mean ± S.D. n = 3 independent experiments. (C) A histogram showing the relative motility of 926-EC. ***, <i>p</i><0.001 (Student’s t test). (D) Representative images of transwell migration assays. Scale bar = 50 μm. (E) A histogram showing relative capillary formation ability of 926-EC. ***, <i>p</i><0.001 (Student’s t test). (F) Representative images for the tube formation assays. Scale bar = 50 μm. (G) A histogram showing the relative capillary branch number of 926-ECs. (H) A histogram for showing the relative capillary formation capacity of the ECFCs (left panel) and the HUVECs (right panel) of different passage numbers. P4, the fourth passaged cells; P6, the sixth passaged cells. *, <i>p</i><0.05; **, <i>p</i><0.01 (Student’s t test). (I) A histogram for showing the relative capillary branch number of the ECFCs (left panel) and the HUVECs (right panel) of different passage numbers. *, <i>p</i><0.05; **, <i>p</i><0.01 (Student’s t test). (J) RT-qPCR results for showing the relative expression levels of <i>RUNX1T1</i> in ECFCs (left panel) and HUVECs (right panel) of different passage numbers. ***, <i>p</i><0.001 (Student’s t test).</p

VEGFA, BMP4 and TGF-β2 mediate RUNX1T1-directed growth, motility and capillary-forming capacity in endothelial cells.

<p>(A) The connectivity network of RUNX1T1-regulated genes created by Ingenuity Pathway Analysis. Yellow, secreted or membranic proteins; Green, cytosolic proteins; Red, nuclear proteins. (B-C) RT-qPCR results for validating expression levels of selected genes marked in yellow in panel A in 926-ECs (B) and <i>Runx1t1</i> deficient mice (C) **, <i>p</i><0.01; ***, <i>p</i><0.001 (Student’s t test). Data represent mean ± S.D. n = 3 independent experiments. (D) Western blotting for showing the expression levels of VEGF-A, TGF-β2 and BMP4 at the indicated models. The band intensity was quantified and normalized to corresponding control cells. (E) The immunoreactivity of VEGFA of heart vessel. n = 2 for each group, 6-month-old mice. Scale bar = 50 μm. (F) The immunoreactivity of BMP4 of heart vessel. n = 2 for each group, 6-month-old mice. Scale bar = 50 μm. (G) The immunoreactivity of TGF-β2 of heart vessel. n = 2 for each group, 6-month-old mice. Scale bar = 50 μm. (H) A histogram for showing the relative viability at the indicated conditions (VEC-CM, the conditional medium from 926ECs-vector control cells; ROV-CM, the conditional medium from RUNX1T1-expressing 926ECs; nAb, neutralizing antibody). *, <i>p</i><0.05 and **, <i>p</i><0.01 (one-way ANOVA). (I) A histogram for showing the relative capillary formation ability at indicated conditions. N.D, none detected. **, <i>p</i><0.01, (one-way ANOVA). (J) A histogram for showing the relative cell migration ability at indicated conditions. *, <i>p</i><0.05 and **, <i>p</i><0.01, (one-way ANOVA).</p

RUNX1T1 is required for angiogenic activity of ECFCs and HUVECs.

<p>(A) Representative pictures for illustrating the tube formation capacity of indicated cells. Scale bar = 50 μm (B) A histogram for showing endothelial tube lengths formed from the tube formation assay. N.D, none detected. Data represent mean± S.D. n = 3 independent experiments. (C) The RT-qPCR results for showing the relative expression levels of <i>RUNX1T1</i> at indicated cells. ***, <i>p</i><0.001 (one-way ANOVA). (D) A Western blot showing the expression level of RUNX1T1. The band intensity was quantified and normalized to control cells. Scr, scramble control cells; shT1, <i>RUNX1T1-</i>knockdowned cells. (E) A histogram for showing the relative viability of ECFCs measured by MTT assay. **, <i>p</i><0.01 (Student’s t test). (F) Representative images of the migration assay (upper panel) and the tube formation assay (lower panel). Scale bar = 50 μm. (G) A histogram for showing the relative motility of ECFCs. *, <i>p</i><0.05 (Student’s t test). (H) A histogram showing the relative capillary formation ability of ECFCs. *, <i>p</i><0.05 (Student’s t test). (I) A histogram for showing endothelial tube branch number from the tube formation assay. ***, <i>p</i><0.001 (Student’s t test). (J) RT-qPCR results for showing the relative expression levels of <i>RUNX1T1</i> in HUVECs. **, <i>p</i><0.001 (Student’s t test). (K) A histogram for showing the relative viability of HUVECs measured by MTT assay. *, <i>p</i><0.05 (Student’s t test). (L). A histogram for showing the relative motility of HUVECs. **, <i>p</i><0.01 (Student’s t test). (M). A histogram showing the relative capillary formation ability of HUVECs. **, <i>p</i><0.01 (Student’s t test). (N). A histogram showing the relative capillary branch number of HUVECs. **, <i>p</i><0.01 (Student’s t test). (O). The GSEA result showing a correlation between the core RUNX1T1 signature and the KSHV-infection signature (GSE16354). ES: enrichment score, FDR: false discovery rate.</p