Japan's new central banking law: A critical view

Japan's new central banking law, enacted in June 1997 with effect from April 1, 1998, takes several steps in the direction of assuring greater transparency, independence, and accountability for the Bank of Japan's conduct of monetary policy. But with respect to the other functions of a central bank, it does no such thing. Instead, the approach has been to leave these traditional banking functions which are at least important as monetary policy narrowly defined - as much as practicable under the control of the government's finance ministry. Most disappointing has been the opaque and haphazard process by which the new law was drafted and passed. This reflects badly on the maturity of Japan's democratic institutions, and represents a discouraging start to the government's "Big Bang" program of financial reform. However, the law does not, in itself, preclude the emergence of an independent and successful central bank: That outcome will depend much more on actions taken by BoJ officials over the next few years

THE DEVELOPMENT OF THE EFFICIENT CELLULAR AND BIOCHEMICAL ASSAY SYSTEM OF APOPTOSIS REGULATING CHEMICALS

Abstract Programmed cell death is genetic and biochemical process caused by specific chemicals and stress stimulation like UV-irradiation. Using Hela cell line, we have developed efficient assay system for determining apoptotic (and anti-apoptotic) properties of a number of chemical substances. Cell death inducing activities are assessed by measuring cell viability (WST-8) and cytotoxicity (LDH) using 96-well plates. Further characterization of cell death inducing chemicals was performed by one dish-based Annexin-V and DNA ladder formation assay. Additionally, activation of the cell death executing caspase-3 was detected by western blot analysis using the protein extracted from the same cell population as Annexin-V and DNA ladder formation assay. As for the initial test chemicals, we used staurosporine, TRAIL+IFNγ, tunicamycin, and brefeldin-A. External apoptotic stimuli (staurosporine) and death receptor-mediated inducer (TRAIL+IFNγ) showed rapid apoptosis induction 4-8 hr after treatment in Annexin-V, DNA ladder formation, and caspase-3 assay. In contrast, ER stress inducers (tunicamycin, brefeldin-A) showed rather slow and modest apoptosis induction activities in all the three assays. Cell nuclear and mitochondrial morphological investigation further supports the distinct properties of these acute and modest apoptosis inducers. Taken together, the apoptosis assay system established here would be strong tools to evaluate a number of chemicals including dioxins

Analysis of the piggyBac transposase reveals a functional nuclear targeting signal in the 94 c-terminal residues

<p>Abstract</p> <p>Background</p> <p>The <it>piggyBac</it> transposable element is a popular tool for germ-line transgenesis of eukaryotes. Despite this, little is known about the mechanism of transposition or the transposase (TPase) itself. A thorough understanding of just how <it>piggyBac</it> works may lead to more effective use of this important mobile element. A PSORTII analysis of the TPase amino acid sequence predicts a bipartite nuclear localization signal (NLS) near the c-terminus, just upstream of a putative ZnF (ZnF).</p> <p>Results</p> <p>We fused the <it>piggyBac</it> TPase upstream of and in-frame with the enhanced yellow fluorescent protein (EYFP) in the <it>Drosophila melanogaster</it> inducible metallothionein protein. Using Drosophila Schneider 2 (S2) cells and the deep red fluorescent nuclear stain Draq5, we were able to track the pattern of <it>piggyBac</it> localization with a scanning confocal microscope 48 hours after induction with copper sulphate.</p> <p>Conclusion</p> <p>Through n and c-terminal truncations, targeted internal deletions, and specific amino acid mutations of the <it>piggyBac</it> TPase open reading frame, we found that not only is the PSORTII-predicted NLS required for the TPase to enter the nucleus of S2 cells, but there are additional requirements for negatively charged amino acids a short length upstream of this region for nuclear localization.</p

Nuclear Importation of Mariner Transposases among Eukaryotes: Motif Requirements and Homo-Protein Interactions

Mariner-like elements (MLEs) are widespread transposable elements in animal genomes. They have been divided into at least five sub-families with differing host ranges. We investigated whether the ability of transposases encoded by Mos1, Himar1 and Mcmar1 to be actively imported into nuclei varies between host belonging to different eukaryotic taxa. Our findings demonstrate that nuclear importation could restrict the host range of some MLEs in certain eukaryotic lineages, depending on their expression level. We then focused on the nuclear localization signal (NLS) in these proteins, and showed that the first 175 N-terminal residues in the three transposases were required for nuclear importation. We found that two components are involved in the nuclear importation of the Mos1 transposase: an SV40 NLS-like motif (position: aa 168 to 174), and a dimerization sub-domain located within the first 80 residues. Sequence analyses revealed that the dimerization moiety is conserved among MLE transposases, but the Himar1 and Mcmar1 transposases do not contain any conserved NLS motif. This suggests that other NLS-like motifs must intervene in these proteins. Finally, we showed that the over-expression of the Mos1 transposase prevents its nuclear importation in HeLa cells, due to the assembly of transposase aggregates in the cytoplasm

Effects of Hormone Agonists on Sf9 Cells, Proliferation and Cell Cycle Arrest

Methoxyfenozide and methoprene are two insecticides that mimic the action of the main hormones involved in the control of insect growth and development, 20-hydroxyecdysone and juvenile hormone. We investigated their effect on the Spodoptera frugiperda Sf9 cell line. Methoxyfenozide was more toxic than methoprene in cell viability tests and more potent in the inhibition of cellular proliferation. Cell growth arrest occurred in the G2/M phase after a methoprene treatment and more modestly in G1 after methoxyfenozide treatment. Microarray experiments and real-time quantitative PCR to follow the expression of nuclear receptors ultraspiracle and ecdysone receptor were performed to understand the molecular action of these hormone agonists. Twenty-six genes were differentially expressed after methoxyfenozide treatment and 55 genes after methoprene treatment with no gene in common between the two treatments. Our results suggest two different signalling pathways in Sf9 cells

Reimagining Development 3.0 for a Changing Planet

This working paper argues we need to reimagine development tactics to fashion Development 3.0, to match what business analysts now call World 3.0, a global system characterized by high turbulence and new threats. It begins by contrasting our former classification of countries spatially into First, Second and Third worlds with a new division of development epochs in sequence since the end of World War II. World 1.0 emphasized industrialization, urbanization, and modernization, lasting from 1945 to 1980. World 2.0 emphasized global trade, and a shift to private actors doing the work of development, from 1980 to the early 2000s. World 3.0 can be seen as superceding globalization by concern with emergent threats. World 1.0 privileged state actions to accelerate “nation building” within former colonies, whereas World 2.0 privileged private capital and free trade as engines for economic growth. Now, following wars, disasters, and the near meltdown of the global financial system in 2007/08, we enter World 3.0 as depicted by Ghemawat and others. We review thirteen major changes not recognized within World 2.0 or its accompanying Development 2.0 regime. The major changes include the rise of homeless capital, the Conservative counter-revolution of the 1980s, the implosion of the USSR, rise of modern China, emergence of BRIC nations, a pan-urban world, rise of identity politics, reemergence of Africa, shift to non-state warfare, growing threat of climate change, MENA nations experience Arab Spring, digital worlds expand, and velocity increases. They suggest coming turbulence and unexpected outcomes, or “mashups” (Ramo). These changes suggest a different emergent system, becoming World 3.0 which has profound differences from how we view our planet’s political economy (World 2.0). If so, the paper outlines implications which suggest the time has come to “take on board” our changed planetary circumstances, and thus begin crafting Development 3.0. “Where the wild things are”, introduces metaphors to change the ‘meta-narratives’ used for viewing World 3.0: “herding elephants,” “taming feral capital”, “swimming with tides” and “avoiding mashups”. They help us realize that long recognized problems (or “elephants”) may show unexpected behaviors to pose new threats within World 3.0. The main argument of the paper then lays out a baker’s dozen changes needed if we hope to fashion more effective ways to promote development for us all. We must “rebalance society” (ala Mintzberg), refashion aid, privilege sustainability, emphasize fair trade, tame feral capital, devise better metrics, include all nations & peoples, seat G-20 not G-8, recognize semi-sovereigns, focus on a pan-urban world, build coalitions in networks, involve women & youth, and rebuild community leadership. All of which assumes we can offset a strong tide towards return to the excesses of World 2.0