Power Transition, Peaceful Change and the UN Security Council: Exploring the Role of Social Structure in International Political Change

The present study is an inquiry into power transition and how it relates to international social structure comprised of state practice, norms, international law and international organisations. It examines how the behaviour of rising powers and international political change in the context of power transition are governed and guided by international social structure through exploring the interface between three themes in International Relations scholarship: power transition, the interwar debate on peaceful change and reform of the UN Security Council. Via integration of elements of English School theory and hitherto neglected, but nevertheless valuable insights from the interwar debate on peaceful change, the study sets out the socio-structural conception of power transition—or, to be more accurate, of international political change in the context of power transition—as an institutionally governed process, presents a distinctive way of theorising power transition that radically departs from the materialistic, mechanistic and state-centric conception of power transition prevalent in the existing literature on power transition, and develops a framework for analysing actual cases of power transition from the socio-structural perspective, taking Security Council reform as a case study. The study emphasises the diversity of institutions governing change in international society, highlighting the role of international law and international organisations designed for the maintenance of international peace and security, such as the League of Nations and the UN, in managing international political change in the context of power transition, and showing the role that the Security Council as an agent of international political change plays in entrenching the institution of peaceful change in contemporary international society via exercise of its powers under Chapter VI and potentially Chapter VII of the UN Charter. From this standpoint, the study questions and reframes the existing debate on Security Council reform, specifying key issues to be addressed in future debate thereon

膵癌術後患者におけるcirculating tumour DNA検出の意義

広島大学(Hiroshima University)博士(医学)Doctor of Philosophy in Medical Sciencedoctora

Different Human Copper-Zinc Superoxide Dismutase Mutants, SOD1G93A and SOD1H46R, Exert Distinct Harmful Effects on Gross Phenotype in Mice

Amyotrophic lateral sclerosis (ALS) is a heterogeneous group of fatal neurodegenerative diseases characterized by a selective loss of motor neurons in the brain and spinal cord. Creation of transgenic mice expressing mutant Cu/Zn superoxide dismutase (SOD1), as ALS models, has made an enormous impact on progress of the ALS studies. Recently, it has been recognized that genetic background and gender affect many physiological and pathological phenotypes. However, no systematic studies focusing on such effects using ALS models other than SOD1G93A mice have been conducted. To clarify the effects of genetic background and gender on gross phenotypes among different ALS models, we here conducted a comparative analysis of growth curves and lifespans using congenic lines of SOD1G93A and SOD1H46R mice on two different genetic backgrounds; C57BL/6N (B6) and FVB/N (FVB). Copy number of the transgene and their expression between SOD1G93A and SOD1H46R lines were comparable. B6 congenic mutant SOD1 transgenic lines irrespective of their mutation and gender differences lived longer than corresponding FVB lines. Notably, the G93A mutation caused severer disease phenotypes than did the H46R mutation, where SOD1G93A mice, particularly on a FVB background, showed more extensive body weight loss and earlier death. Gender effect on survival also solely emerged in FVB congenic SOD1G93A mice. Conversely, consistent with our previous study using B6 lines, lack of Als2, a murine homolog for the recessive juvenile ALS causative gene, in FVB congenic SOD1H46R, but not SOD1G93A, mice resulted in an earlier death, implying a genetic background-independent but mutation-dependent phenotypic modification. These results indicate that SOD1G93A- and SOD1H46R-mediated toxicity and their associated pathogenic pathways are not identical. Further, distinctive injurious effects resulted from different SOD1 mutations, which are associated with genetic background and/or gender, suggests the presence of several genetic modifiers of disease expression in the mouse genome