A Study of Independent Practices by Japan Teachers\u27Union in the late 1950s to 60s : Through the Case of Mathematics Teaching

This paper investigates the issue of whether Japan Teachers\u27Union\u27s (JTU) independent practices of aiming to improve(Kaizen) the method of Japanese mathematics teaching in the late 1950s to 60s succeed as an school policy to include students of various abilities. Two cases are chosen. One is the teaching of Functions, and the other the teaching of Demonstration of Figures in mathematics. Results of analyses show that JTU\u27s independent practices were slightly, though not dramatically, successful when compared to worldwide trend toward higher standards of mathematical contents and greater popularization of mathematics teaching in that era. However, ""slight success"" only means that the number of students who failed mathematics did not really increase, despite the raise in standards. It is also true that, in the midst of historical conflicts between JTU and the Ministry of Education, there was an inclination to criticize some of the JTU\u27s independent practices for the sake of criticism, and to deem some practices as too radical for school implementation. While Japan has done well in past international achievement tests, there are needs to conduct new researches to historically investigate how the learning of students was enhanced by school education

Teachers\u27Images of Intelligence and Ability in Postwar Japan : Focusing on Discourses in the Movement of Japan Teachers\u27Union in 1950s

This paper probes teachers\u27images of intelligence and ability in the 1950s, with its main focus on discourses that were related to intelligence tests in the movement of Japan Teachers\u27Union (JTU). The paper suggests that intelligence tests functioned as apparatus at schools in three aspects during that time. The first function was as an apparatus for distinguishing intelligence, while the second an apparatus for measuring the correlation of academic achievement with potential ability. Finally, the third function was as an apparatus for measuring hereditary or environmental influences on learning achievement. From the viewpoint of these three functions, it can be said that teachers in the 1950s possessed images of intelligence and ability different from those in the pre-war era or after the 1960s. The uniqueness can be summarized into two points. One is that these images were constructed through examination of the teachers themselves on the educability of students, a practice which was different from the 1960s. Another point is that schools filled a major role in measuring intelligence, a phenomenon not observed in the pre-war era. In conclusion, this paper proposes hypotheses on why teachers\u27images of intelligence and ability transformed in the 1960s

COVID-19 and the Political Economy of the “September School Year Start” in Japan: Overlooked Victims and Foregone Revenues

In response to the COVID-19 pandemic, a“September School Year Start”has become a central topic of discussion in Japan. While the pros and cons of changing a conventional academic calendar have been raised, two important aspects have been largely disregarded: foregone earnings of new graduates and relevant tax revenues. We therefore analyse national statistics on the number of new graduates as overlooked victims and their expected monthly wages in conjunction with tax payment, revealing that a September Start would force new graduates to give up approximately 715.7 billion yen, which leads to 87.6 billion yen foregone tax revenues for the government. This means both individuals and the society would lose a certain amount of financial resources by merely introducing a September Start. Considering other policy options are available should national budgets equivalent to foregone tax revenues be mobilised, it is essential for policy makers to examine cost-benefit of both a September Start and alternatives so that they make a sound decision. Although the primary focus of this article is on a September Start and its consequences, the said approach with close attention to scientific evidence rather than abstract notions is now required for the effective education policy-making and beyond

Evolution of Otx paralogue usages in early patterning of the vertebrate head

AbstractTo assess evolutional changes in the expression pattern of Otx paralogues, expression analyses were undertaken in fugu, bichir, skate and lamprey. Together with those in model vertebrates, the comparison suggested that a gnathostome ancestor would have utilized all of Otx1, Otx2 and Otx5 paralogues in organizer and anterior mesendoderm for head development. In this animal, Otx1 and Otx2 would have also functioned in specification of the anterior neuroectoderm at presomite stage and subsequent development of forebrain/midbrain at somite stage, while Otx5 expression would have already been specialized in epiphysis and eyes. Otx1 and Otx2 functions in anterior neuroectoderm and brain of the gnathostome ancestor would have been differentially maintained by Otx1 in a basal actinopterygian and by Otx2 in a basal sarcopterygian. Otx5 expression in head organizer and anterior mesendoderm seems to have been lost in the teleost lineage after divergence of bichir, and also from the amniotes after divergence of amphibians as independent events. Otx1 expression was lost from the organizer in the tetrapod lineage. In contrast, in a teleost ancestor prior to whole genome duplication, Otx1 and Otx2 would have both been expressed in the dorsal margin of blastoderm, embryonic shield, anterior mesendoderm, anterior neuroectoderm and forebrain/midbrain, at respective stages of head development. Subsequent whole genome duplication and the following genome changes would have caused different Otx paralogue usages in each teleost lineage. Lampreys also have three Otx paralogues; their sequences are highly diverged from gnathostome cognates, but their expression pattern is well related to those of skate Otx cognates

Terminal axon branching is regulated by the LKB1-NUAK1 kinase pathway via presynaptic mitochondrial capture

The molecular mechanisms underlying the axon arborization of mammalian neurons are poorly understood but are critical for the establishment of functional neural circuits. We identified a pathway defined by two kinases, LKB1 and NUAK1, required for cortical axon branching in vivo. Conditional deletion of LKB1 after axon specification or knockdown of NUAK1 drastically reduced axon branching in vivo, whereas their overexpression was sufficient to increase axon branching. The LKB1-NUAK1 pathway controls mitochondria immobilization in axons. Using manipulation of Syntaphilin, a protein necessary and sufficient to arrest mitochondrial transport specifically in the axon, we demonstrate that the LKB1-NUAK1 kinase pathway regulates axon branching by promoting mitochondria immobilization. Finally, we show that LKB1 and NUAK1 are necessary and sufficient to immobilize mitochondria specifically at nascent presynaptic sites. Our results unravel a link between presynaptic mitochondrial capture and axon branching

Circadian regulation of intracellular G-protein signalling mediates intercellular synchrony and rhythmicity in the suprachiasmatic nucleus

Synchronous oscillations of thousands of cellular clocks in the suprachiasmatic nucleus (SCN), the circadian centre, are coordinated by precisely timed cell–cell communication, the principle of which is largely unknown. Here we show that the amount of RGS16 (regulator of G protein signalling 16), a protein known to inactivate Gαi, increases at a selective circadian time to allow time-dependent activation of intracellular cyclic AMP signalling in the SCN. Gene ablation of Rgs16 leads to the loss of circadian production of cAMP and as a result lengthens circadian period of behavioural rhythm. The temporally precise regulation of the cAMP signal by clock-controlled RGS16 is needed for the dorsomedial SCN to maintain a normal phase-relationship to the ventrolateral SCN. Thus, RGS16-dependent temporal regulation of intracellular G protein signalling coordinates the intercellular synchrony of SCN pacemaker neurons and thereby defines the 24 h rhythm in behaviour

Canonical Wnt signaling and its antagonist regulate anterior-posterior axis polarization by guiding cell migration in mouse visceral endoderm

The mouse embryonic axis is initially formed with a proximal-distal orientation followed by subsequent conversion to a prospective anterior-posterior (A-P) polarity with directional migration of visceral endoderm cells. Importantly, Otx2, a homeobox gene, is essential to this developmental process. However, the genetic regulatory mechanism governing axis conversion is poorly understood. Here, defective axis conversion due to Otx2 deficiency can be rescued by expression of Dkk1, a Wnt antagonist, or following removal of one copy of the beta-catenin gene. Misexpression of a canonical Wnt ligand can also inhibit correct A-P axis rotation. Moreover, asymmetrical distribution of beta-catenin localization is impaired in the Otx2-deficient and Wnt- misexpressing visceral endoderm. Concurrently, canonical Wnt and Dkk1 function as repulsive and attractive guidance cues, respectively, in the migration of visceral endoderm cells. We propose that Wnt/beta-catenin signaling mediates A-P axis polarization by guiding cell migration toward the prospective anterior in the pregastrula mouse embryo.info:eu-repo/semantics/publishedVersio

The FERM protein EPB41L5 regulates actomyosin contractility and focal adhesion formation to maintain the kidney filtration barrier

Podocytes form the outer part of the glomerular filter, where they have to withstand enormous transcapillary filtration forces driving glomerular filtration. Detachment of podocytes from the glomerular basement membrane precedes most glomerular diseases. However, little is known about the regulation of podocyte adhesion in vivo. Thus, we systematically screened for podocyte-specific focal adhesome (FA) components, using genetic reporter models in combination with iTRAQ-based mass spectrometry. This approach led to the identification of FERM domain protein EPB41L5 as a highly enriched podocyte-specific FA component in vivo. Genetic deletion of Epb41l5 resulted in severe proteinuria, detachment of podocytes, and development of focal segmental glomerulosclerosis. Remarkably, by binding and recruiting the RhoGEF ARGHEF18 to the leading edge, EPB41L5 directly controls actomyosin contractility and subsequent maturation of focal adhesions, cell spreading, and migration. Furthermore, EPB41L5 controls matrix-dependent outside-in signaling by regulating the focal adhesome composition. Thus, by linking extracellular matrix sensing and signaling, focal adhesion maturation, and actomyosin activation EPB41L5 ensures the mechanical stability required for podocytes at the kidney filtration barrier. Finally, a diminution of EPB41L5-dependent signaling programs appears to be a common theme of podocyte disease, and therefore offers unexpected interventional therapeutic strategies to prevent podocyte loss and kidney disease progression