Decision Engineering Analysis of Fraud Information Disclosure after China's Share-Splitting Reform

AbstractThis paper outlines a dynamic game model to analyze the fraud information disclosure by listed companies in China since the share-splitting reform in 2005. By analyzing the conditions of coalition-proof Nash equilibrium between large shareholders and the manager, exogenous variables’ effects on the equilibrium as well as the first-order condition of the maximum utility of the supervisory department, it is concluded that efficient capital markets require a high supervising probability and intensity of penalty to the “insider” and shortened the intervals between supervising conducts as well. Moreover, there exists a unique optimum incentive stock option ratio over which fraud information disclosure becomes more rampant. This results in a higher intensity of penalty to the manager given more stock option incentive and, in contrast, a higher intensity of penalty to large shareholders of a well managed and efficiently capital-structured company once fraud information disclosure is detected. The model's conclusions are consistent with the facts of listed companies in China. Finally, the model makes sharp suggestions for the mechanism design of stock option incentive as well as suggestions for the supervisory department to achieve efficiency of capital markets in China

Structural characterization of an α-1, 6-linked galactomannan from natural Cordyceps 2 sinensis

An α-1, 6-linked galactomannan was isolated and purified from natural Cordyceps sinensis. The fine structure analysis of this polysaccharide was elucidated based on partial acid hydrolysis, monosaccharide composition, methylation and 1D/2D nuclear magnetic resonance (NMR) spectroscopy. Monosaccharide composition analysis revealed that this polysaccharide was mainly composed of galactose (68.65%), glucose (6.65%) and mannose (24.02%). However, after partial acid hydrolysis the percentages of galactose, glucose and mannose were changed to 3.96%, 13.82% and 82.22%, respectively. The molecular weight of this polysaccharide was 7207. Methylation and NMR analysis revealed that this galactomannan had a highly branched structure, mainly consisted of a mannan skeleton and galactofuranosyl chains. The structure of galactofuranosyl part was formed by alternating (1 → 5)-lined β-Galf and (1 → 6)-liked β-Galf or a single (1 → 6)-liked β-Galf, attaching to the O-2 and O-4 of the mannose chain, and terminated at β-T-Galf. The mannan core was revealed by analyzing the partial acid hydrolysate of the galactomannan and the structure was composed of (1 → 6)-linked α-Manp backbone, with substituted at C-2 by short chains of 2-substituted Manp or Galf branches

A Joint Positioning and Attitude Solving Method for Shearer and Scraper Conveyor under Complex Conditions

In a fully mechanized coal-mining face, the positioning and attitude of the shearer and scraper conveyor are inaccurate. To overcome this problem, a joint positioning and attitude solving method that considers the effect of an uneven floor is proposed. In addition, the real-time connection and coupling relationship between the two devices is analyzed. Two types of sensors, namely, the tilt sensor and strapdown inertial navigation system (SINS), are used to measure the shearer body pitch angle and the scraper conveyor shape, respectively. To improve the accuracy, two pieces of information are fused using the adaptive information fusion algorithm. It is observed that, using a marking strategy, the shearer body pitch angle can be reversely mapped to the real-time shape of the scraper conveyor. Then, a virtual-reality (VR) software that can visually simulate this entire operation process under different conditions is developed. Finally, experiments are conducted on a prototype experimental platform. The positioning error is found to be less than 0.38 times the middle trough length; moreover, no accumulated error is detected. This method can monitor the operation of the shearer and scraper conveyor in a highly dynamic and precise manner and provide strong technical support for safe and efficient operation of a fully mechanized coal-mining face

YY1 directly interacts with myocardin to repress the triad myocardin/SRF/CArG box-mediated smooth muscle gene transcription during smooth muscle phenotypic modulation

Yin Yang 1 (YY1) regulates gene transcription in a variety of biological processes. In this study, we aim to determine the role of YY1 in vascular smooth muscle cell (VSMC) phenotypic modulation both in vivo and in vitro. Here we show that vascular injury in rodent carotid arteries induces YY1 expression along with reduced expression of smooth muscle differentiation markers in the carotids. Consistent with this finding, YY1 expression is induced in differentiated VSMCs in response to serum stimulation. To determine the underlying molecular mechanisms, we found that YY1 suppresses the transcription of CArG box-dependent SMC-specific genes including SM22α, SMα-actin and SMMHC. Interestingly, YY1 suppresses the transcriptional activity of the SM22α promoter by hindering the binding of serum response factor (SRF) to the proximal CArG box. YY1 also suppresses the transcription and the transactivation of myocardin (MYOCD), a master regulator for SMC-specific gene transcription by binding to SRF to form the MYOCD/SRF/CArG box triad (known as the ternary complex). Mechanistically, YY1 directly interacts with MYOCD to competitively displace MYOCD from SRF. This is the first evidence showing that YY1 inhibits SMC differentiation by directly targeting MYOCD. These findings provide new mechanistic insights into the regulatory mechanisms that govern SMC phenotypic modulation in the pathogenesis of vascular diseases

Altered FGF Signaling Pathways Impair Cell Proliferation and Elevation of Palate Shelves

In palatogenesis, palatal shelves are patterned along the mediolateral axis as well as the anteroposterior axis before the onset of palatal fusion. Fgf10 specifically expressed in lateral mesenchyme of palate maintains Shh transcription in lateral epithelium, while Fgf7 activated in medial mesenchyme by Dlx5, suppressed the expansion of Shh expression to medial epithelium. How FGF signaling pathways regulate the cell behaviors of developing palate remains elusive. In our study, we found that when Fgf8 is ectopically expressed in the embryonic palatal mesenchyme, the elevation of palatal shelves is impaired and the posterior palatal shelves are enlarged, especially in the medial side. The palatal deformity results from the drastic increase of cell proliferation in posterior mesenchyme and decrease of cell proliferation in epithelium. The expression of mesenchymal Fgf10 and epithelial Shh in the lateral palate, as well as the Dlx5 and Fgf7 transcription in the medial mesenchyme are all interrupted, indicating that the epithelial-mesenchymal interactions during palatogenesis are disrupted by the ectopic activation of mesenchymal Fgf8. Besides the altered Fgf7, Fgf10, Dlx5 and Shh expression pattern, the reduced Osr2 expression domain in the lateral mesenchyme also suggests an impaired mediolateral patterning of posterior palate. Moreover, the ectopic Fgf8 expression up-regulates pJak1 throughout the palatal mesenchyme and pErk in the medial mesenchyme, but down-regulates pJak2 in the epithelium, suggesting that during normal palatogenesis, the medial mesenchymal cell proliferation is stimulated by FGF/Erk pathway, while the epithelial cell proliferation is maintained through FGF/Jak2 pathway

Comparative analysis of novel and conventional Hsp90 inhibitors on HIF activity and angiogenic potential in clear cell renal cell carcinoma: implications for clinical evaluation

<p>Abstract</p> <p>Background</p> <p>Perturbing Hsp90 chaperone function targets hypoxia inducible factor (HIF) function in a von Hippel-Lindau (VHL) independent manner, and represents an approach to combat the contribution of HIF to cell renal carcinoma (CCRCC) progression. However, clinical trials with the prototypic Hsp90 inhibitor 17-AAG have been unsuccessful in halting the progression of advanced CCRCC.</p> <p>Methods</p> <p>Here we evaluated a novel next generation small molecule Hsp90 inhibitor, EC154, against HIF isoforms and HIF-driven molecular and functional endpoints. The effects of EC154 were compared to those of the prototypic Hsp90 inhibitor 17-AAG and the histone deacetylase (HDAC) inhibitor LBH589.</p> <p>Results</p> <p>The findings indicate that EC154 is a potent inhibitor of HIF, effective at doses 10-fold lower than 17-AAG. While EC154, 17-AAG and the histone deacetylase (HDAC) inhibitor LBH589 impaired HIF transcriptional activity, CCRCC cell motility, and angiogenesis; these effects did not correlate with their ability to diminish HIF protein expression. Further, our results illustrate the complexity of HIF targeting, in that although these agents suppressed HIF transcripts with differential dynamics, these effects were not predictive of drug efficacy in other relevant assays.</p> <p>Conclusions</p> <p>We provide evidence for EC154 targeting of HIF in CCRCC and for LBH589 acting as a suppressor of both HIF-1 and HIF-2 activity. We also demonstrate that 17-AAG and EC154, but not LBH589, can restore endothelial barrier function, highlighting a potentially new clinical application for Hsp90 inhibitors. Finally, given the discordance between HIF activity and protein expression, we conclude that HIF expression is not a reliable surrogate for HIF activity. Taken together, our findings emphasize the need to incorporate an integrated approach in evaluating Hsp90 inhibitors within the context of HIF suppression.</p