Director Networks and Cost of Equity Capital: Based on “Busy Director Hypothesis” Analysis

This paper uses the data of Shanghai and Shenzhen A-share-listed companies from 2008 to 2018 to construct the director networks as an indicator to explore the relationship between the company’s director networks and the cost of equity capital and the influence of nature of property rights and the ownership structure on the aforementioned relationship. The research results demonstrate that director networks cannot effectively reduce the cost of equity capital. This conclusion verifies the “busy director hypothesis.” With the increase in the director networks centrality, the increase in the cost of equity capital in non-state-owned listed companies is more significant compared with state-owned listed companies; equity concentration plays a significant negative regulatory role in the director networks centrality and affects the cost of equity capital. Compared with the networks centrality of independent director, the networks centrality of nonindependent director has a stronger negative effect on the cost of equity capital. This article broadens the perspective of corporate governance research and provides new ideas for listed companies to make financing decisions.

The Complex Impact of Relational Embeddedness on Enterprise Value: The Moderating Effect of Environmental Dynamics

Based on social network theory and dynamic capability theory, a theoretical model is constructed that specifies the process through which relational embeddedness affects enterprise value. The authors selected 612 Shenzhen and Shanghai A-share manufacturing enterprises in the CSMAR database as sample enterprises, and a multiple regression analysis method was used to test hypotheses. The results show that (1) there is an inverted “U” relationship between relational embeddedness and enterprise value; that is, the enterprises’ relational embeddedness has an “inflection point” effect on the enterprise value; (2) the enterprises’ resource integration capability plays an intermediate role in the impact of relational embeddedness on enterprise value; (3) the market environmental dynamics and technology environmental dynamics play negative regulatory roles in the inverted “U” relationship between relational embeddedness and enterprise value, and they play different regulatory roles before and after the enterprise relational embeddedness reaches the “inflection point”; that is, before the relational embeddedness reaches the inflection point, the technology environmental dynamics plays a major negative regulatory role, while after the relational embeddedness reaches the inflection point, the market environmental dynamics plays a major negative regulatory role. Compared with the market environmental dynamics, the impact of technology environmental dynamics on the relationship between relational embeddedness and enterprise value is more significant; that is, the effect of relational embeddedness on enterprises value is more sensitive to the technology environmental dynamics.

TNF Is Partially Required for Cell-Death-Triggered Skin Inflammation upon Acute Loss of cFLIP

cFLIP is required for epidermal integrity and skin inflammation silencing via protection from TNF-induced keratinocyte apoptosis. Here, we generated and analyzed cFLIP epidermal KO mice with additional TNF deficiency. Intriguingly, the ablation of TNF rescued the pathological phenotype of epidermal cFLIP KO from characteristic weight loss and increased mortality. Moreover, the lack of TNF in these animals strongly reduced and delayed the epidermal hyperkeratosis and the increased apoptosis in keratinocytes. Our data demonstrate that TNF signaling in cFLIP-deficient keratinocytes is the critical factor for the regulation of skin inflammation via modulated cytokine and chemokine expression and, thus, the attraction of immune cells. Our data suggest that autocrine TNF loop activation upon cFLIP deletion is dispensable for T cells, but is critical for neutrophil attraction. Our findings provide evidence for a negative regulatory role of cFLIP for TNF-dependent apoptosis and partially for epidermal inflammation. However, alternative signaling pathways may contribute to the development of the dramatic skin disease upon cFLIP deletion. Our data warrant future studies of the regulatory mechanism controlling the development of skin disease upon cFLIP deficiency and the role of cFLIP/TNF in a number of inflammatory skin diseases, including toxic epidermal necrolysis (TEN).

The Emerging Potentials of Human Regulatory B Cells Mediated Therapies in Myasthenia Gravis

Regulatory B cells (Bregs) with immunosuppressive function are critical in maintaining immune tolerance. In recent years, Bregs is an essential part of the study due to its therapeutic relevance and function in immune tolerance. The positive and negative regulatory role of human Bregs in immune tolerance is being discussed in several pathologies, including in autoimmune diseases, cancers, chronic infections, strokes in multiple reports. The negative regulatory roles of human Bregs are associated with lesser numbers and functional abnormalities in most of these studies, including myasthenia gravis (MG). In this review, the potential findings regarding human Bregs in MG, and Bregs mediated potential therapeutic strategies with its pros and cons have been discussed based on previous and current reports.

Interleukin-2 Family Members and their Role in Demyelinating Disease

Interleukin-2 (IL-2) has a family which includes IL-2, IL-4, IL-7, IL-9, IL-15 and IL-21 cytokines. This family group of an IL-2 cytokine plays important, but different roles in neurologically related demyelinating disease studied in multiple sclerosis (MS) and it’s experimentally induced rodent models. IL-2 play role in strong T-cell expansion and participates in the maintenance of T-regs cells, but also keep in the stimulation and proliferation of pathogenic T cells. IL-4 induces differentiation of naïve helper T cells (Th0) to Th2 cells. IL-7 promotes Th1 cell differentiation. IL-9 is a hematopoietic growth factor for major pathogenic Th17 cells in EAE. IL-15 is necessary for memory CD8+ T cells and plays a negative regulatory role through CD8+ CD122+ T cells in reducing Th17-mediated inflammation. IL-21 has potent regulatory effects on the natural killer (NK) cells and cytotoxic T cells. IL-21 activates CD4+ and up-regulates the Th2 and Th17 subsets of T helper cells. Based on different roles of each family member in demyelinating disease, bio-agents and therapeutic agents have been attempted in an experimental model to study their role in demyelinating disease is described in the present review.