Inter-Industry and Firm Size Effects on Wage Differentials and Efficiency Wages in Japan

This paper analyzes the effects of inter-industry and firm size on wage differentials,focusing on how their estimated effects vary by the introduction of elements indicating firm characteristics such as wage-experience profiles.Using the worker-establishment matched data, we find that inter-industry effects are larger than firm size ones judging from their explanatory powers and the wage distributions caused by them although the introduction of firm characteristics reduces more the effect of industry. Since this paper is based on the efficiency wage hypothesis to explain wage differentials, it is required to test for the bonding critique. Checking how steeper wage profiles affect wages of young workers, we find that even those who work at firms where wage profiles are steeply rising are not paid lower. This result supports the efficiency wage hypothesis to be a good explanation for wage differentials.

Maternity Leave Policies and Womens Employment after Childbirth: Evidence from the United States, Britain and Japan

This paper uses microdata from the United States, Britain and Japan to examine the effects of family leave coverage on women's employment after childbirth. The United States had no national family leave legislation until 1993, but many women were covered by employer policies. Britain has had maternity leave legislation since 1978, but until 1993 only about half of working women were covered. Japan has had maternity leave legislation since 1947 but not all workers were covered. We find that young children continue to have a very negative effect on women's employment, particularly in Britain. We also find that family leave coverage increases the likelihood that a woman will return to her employer after childbirth, with a particularly marked effect in Japan. This result suggests that the recent expansions in family leave coverage are likely to lead to increased employment of women after childbirth.maternity leave, womens employment

Pathogenesis and treatment of multiple myeloma bone disease

Multiple myeloma (Plasma cell myeloma), a malignancy of the plasma cells, exhibits tumor expansion preferentially in the bone marrow and the development of bone-destructive lesions. Multiple myeloma is still an incurable disease with changes in the bone marrow microenvironment in favor of the survival and proliferation of multiple myeloma cells and bone destruction. In this review, we described the recent findings on the regulators involved in the development of myeloma bone diseases, and succinctly summarize currently available therapeutic options and the development of novel bone modifying agents for myeloma treatment

Myeloma–Bone Interaction : A Vicious Cycle via TAK1–PIM2 Signaling

Myeloma cells interact with their ambient cells in the bone, such as bone marrow stromal cells, osteoclasts, and osteocytes, resulting in enhancement of osteoclastogenesis and inhibition of osteoblastogenesis while enhancing their growth and drug resistance. The activation of the TAK1–PIM2 signaling axis appears to be vital for this mutual interaction, posing it as an important therapeutic target to suppress tumor expansion and ameliorate bone destruction in multiple myeloma.Multiple myeloma (MM) has a propensity to develop preferentially in bone and form bone-destructive lesions. MM cells enhance osteoclastogenesis and bone resorption through activation of the RANKL–NF-κB signaling pathway while suppressing bone formation by inhibiting osteoblastogenesis from bone marrow stromal cells (BMSCs) by factors elaborated in the bone marrow and bone in MM, including the soluble Wnt inhibitors DKK-1 and sclerostin, activin A, and TGF-β, resulting in systemic bone destruction with loss of bone. Osteocytes have been drawn attention as multifunctional regulators in bone metabolism. MM cells induce apoptosis in osteocytes to trigger the production of factors, including RANKL, sclerostin, and DKK-1, to further exacerbate bone destruction. Bone lesions developed in MM, in turn, provide microenvironments suited for MM cell growth/survival, including niches to foster MM cells and their precursors. Thus, MM cells alter the microenvironments through bone destruction in the bone where they reside, which in turn potentiates tumor growth and survival, thereby generating a vicious loop between tumor progression and bone destruction. The serine/threonine kinases PIM2 and TAK1, an upstream mediator of PIM2, are overexpressed in bone marrow stromal cells and osteoclasts as well in MM cells in bone lesions. Upregulation of the TAK1–PIM2 pathway plays a critical role in tumor expansion and bone destruction, posing the TAK1–PIM2 pathway as a pivotal therapeutic target in MM

Corporate Finance and Human Resource Management

Corporate governance can be defined to be an institution that constrains relations between corporate managers and various stakeholders, including shareholders, creditors, workers, suppliers, and customers. Under this broad definition, corporate governance is a system of various sub-systems that are complementary to one another. This paper focuses on two sub-systems of the Japanese corporate governance: one on corporate finance and another on human resource management. After briefly documenting the characteristics of the Japanese corporate governance in these two sub-systems, the paper discusses how each sub-system has been going through substantial changes in recent years. Examining the data for 58 listed companies, we find preliminary evidence on the complementarity between the two sub-systems. The firms that have non-traditional ownership structure (especially high foreign ownership) seem to have more non-traditional human resource management practices.

コツズイ ビショウ カンキョウ ト コツズイシュ ノ シンテン

Multiple myeloma（MM）develops and expands almost exclusively in the bone marrow, and generates devastating bone destruction. MM cells produce a variety of cytokines, including MIP‐ １, to stimulate RANK ligand-mediated osteoclastogenesis and extensively resorb bone. Besides enhancing bone resorption, MM cells suppress osteoblastic differentiation from bone marrow stromal cells, leading to extensive bone destruction with rapid loss of bone. The overproduction of inhibitors for the canonical Wingless-type（Wnt）signaling pathway, including DKK‐１, sFRP‐２ and sclerostin, significantly contributes to the suppression of osteoblastogenesis and bone formation in MM. MM cells alter through bone destruction the microenvironment in bone where they colonize, which in turn favors MM tumor growth and survival, thereby forming a progressive vicious cycle between tumor expansion and bone destruction in MM. MM is still difficult to be cured despite the recent implementation of new agents, and its bone disease also remains a significant clinical problem. Further elucidation of the molecular mechanisms of the tumor-bone interactions and tumor growth in the bone microenvironment will provide us with new approaches that have a real impact on both bone disease and tumor progression in MM