Parameters of Reform and Unification in Modern Japanese Buddhist Thought: Murakami Senshō and Critical Buddhism

Reform is a word that, one might easily say, characterizes more than any other the history and development of Buddhism. Yet, it must also be said that reform movements in East Asian Buddhism have often taken on another goal—harmony or unification; that is, a desire not only to reconstruct a more worthy form of Buddhism, but to simultaneously bring together all existing forms under a single banner, in theory if not in practice. This paper explores some of the tensions between the desire for reform and the quest for harmony in modern Japanese Buddhism thought, by comparing two developments: the late 19th century movement towards ‘New Buddhism’ (shin Bukkyō) as exemplified by Murakami Senshō 村上専精 (1851–1929), and the late 20th century movement known as ‘Critical Buddhism’ (hihan Bukkyō), as found in the works of Matsumoto Shirō 松本史朗 and Hakamaya Noriaki 袴谷憲昭. In all that has been written about Critical Buddhism, in both Japanese and English, very little attention has been paid to the place of the movement within the larger traditions of Japanese Buddhist reform. Here I reconsider Critical Buddhism in relation to the concerns of the previous, much larger trends towards Buddhist reform that emerged almost exactly 100 years previous—the so-called shin Bukkyō or New Buddhism of the late-Meiji era. Shin Bukkyō is a catch-all term that includes the various writings and activities of Inoue Enryō, Shaku Sōen, and Kiyozawa Manshi, as well as the so-called Daijō-hibussetsuron, a broad term used (often critically) to describe Buddhist writers who suggested that Mahāyāna Buddhism is not, in fact, the Buddhism taught by the ‘historical’ Buddha Śākyamuni. Of these, I will make a few general remarks about Daijō-hibusseturon, before turning attention more specifically to the work of Murakami Senshō, in order to flesh out some of the similarities and differences between his attempt to construct a ‘unified Buddhism’ and the work of his late-20th century avatars, the Critical Buddhists. Though a number of their aims and ideas overlap, I argue that there remain fundamental differences with respect to the ultimate purposes of Buddhist reform. This issue hinges on the implications of key terms such as ‘unity’ and ‘harmony’ as well as the way doctrinal history is categorized and understood, but it also relates to issues of ideology and the use and abuse of Buddhist doctrines in 20th-century politics.

The Effects Of Farnesyltransferase Inhibitor Abt-100 On Murine Helper T-Cell Differentiation And Cytokine Secretion

Farnesyltransferase Inhibitors (FTIs) are a class of drugs known to prevent the farnesylation and subsequent membrane attachment of a number of intracellular proteins. In various studies, the administration of FTIs has been found to play a role in the activation and development of T-cells in the immune system. FTIs have also been found to act as immunomodulators in delaying MHC-II mismatched skin allografts in mice. This study focuses on the effect of the FTI, ABT-100, on the differentiation and cytokine secretion of Th1 and Th2 helper T-cells in BALB/C mice to better understand which immune responses are targeted by FTIs. Splenocytes were isolated from BALB/C mice, skewed towards either a Th1 or a Th2 phenotype with the addition of cytokines, and treated with various concentrations of ABT-100. Splenocytes were also isolated and immediately cultured in the presence of ABT-100 to observe differentiation trends of helper T-cells. Cytokine production was measured using intracytoplasmic flow cytometry analysis. I found that ABT-100 treatment does not block Th1 or Th2 cell differentiation. Instead, ABT-100 treatment appears to affect cytokine production from effector T-cells. I found that ABT-100 causes a decrease in IFN-¿ production in mature Th1 cells yet does not affect IL-4 production in mature Th2 cells. This decrease in cytokine production as a result of ABT-100 treatments provides a potential mechanism for how ABT-100 works to delay MHC-II mismatched allograft rejection.