The Value of Academic Directors to Stakeholders: Evidence on Corporate Social Responsibility Reporting

This study explores the regulatory setting in Taiwan and examines the association between academic directors and corporate social responsibility (CSR) reporting. We find that firms with academic directors on the board are more likely to issue a stand-alone CSR report and obtain third-party assurance on their CSR reports. We also find a positive association between CSR reporting and academic directors with industry expertise. Further cross-sectional analyses indicate that the positive relation between academic directors (and their industry expertise) and CSR reporting is stronger in firms with higher growth, greater institutional ownership, and lower control-ownership divergence. Our findings that the presence of academic directors can promote better sustainability reporting suggest that academic directors contribute not only to shareholder value but also to wider stakeholder interests

FFTPL: An Analytic Placement Algorithm Using Fast Fourier Transform for Density Equalization

We propose a flat nonlinear placement algorithm FFTPL using fast Fourier transform for density equalization. The placement instance is modeled as an electrostatic system with the analogy of density cost to the potential energy. A well-defined Poisson's equation is proposed for gradient and cost computation. Our placer outperforms state-of-the-art placers with better solution quality and efficiency

CCN2 Enhances Resistance to Cisplatin-Mediating Cell Apoptosis in Human Osteosarcoma

Osteosarcoma (OS) is the most common form of malignant bone tumor and is an aggressive malignant neoplasm exhibiting osteoblastic differentiation. Cisplatin is one of the most efficacious antitumor drugs for osteosarcoma patients. However, treatment failures are common due to the development of chemoresistance. CCN2 (also known as CTGF), is a secreted protein that binds to integrins, modulates the invasive behavior of certain human cancer cells. However, the effect of CCN2 in cisplatin-mediated chemotherapy is still unknown. Here, we found that CCN2 was upregulated in human osteosarcoma cells after treatment with cisplatin. Moreover, overexpression of CCN2 increased the resistance to cisplatin-mediated cell apoptosis. In contrast, reduction of CCN2 by CCN2 shRNA promoted the chemotherapeutic effect of cisplatin. We also found that CCN2 provided resistance to cisplatin-induced apoptosis through upregulation of Bcl-xL and survivin. Knockdown of Bcl-xL or survivin removed the CCN2-mediated resistance to apoptosis induced by cisplatin. On the other hand, CCN2 also promoted FAK, MEK, and ERK survival signaling pathways to enhance tumor survival during cisplatin treatment. In a mouse xenograft model, overexpression of CCN2 promoted resistance to cisplatin. However, knockdown of CCN2 increased the therapeutic effect of cisplatin. Therefore, our data suggest that CCN2 might be a critical oncogene of human osteosarcoma for cisplatin-resistance and supported osteosarcoma cell growth in vivo and in vitro