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This paper illustrates the historical process of the prevalence of upper secondary education in Japan focusing on the public and private relationships. After reviewing high school policy at the central administration, actual high school supply at local government levels is examined and the harmonious relationship between public and private sectors is introduced. Japanese private schools must fulfill the same standards of school facilities, teachers' licenses, and curriculum as those of public schools, under the control of school education laws with a few exceptions. The universal upper secondary education in Japan has been managed with diversities between local prefectures. Japanese education succeeded in the wave of industrialization and constructed a cooperation between public and private high schools. This educational system has supported Japanese development to achieve competent human resources. However, Japan is now facing a new difficulty of determining what further steps to take in the pursuit of top school education in a post-industrialized global world.

This paper addresses the following two research questions: What role does senior high school choice play, in terms of the choices between public and private and between academic and vocational education in Japan and Taiwan? How do senior high school students matriculate to tertiary education in Japan and Taiwan? Japan and Taiwan have both experienced a rapid expansion of upper secondary education in the process of late industrialization. In these two societies, senior high school tracking decides students' educational careers. In addition, people living in these two societies have been inclined toward the belief that national and public schools are more prestigious than private schools. Therefore, the role of private senior high schools is different in these societies than in Europe or America. In both Japan and Taiwan students with higher grades tend to attend public academic senior high schools, whereas students with lower grades tend to enroll in private senior high schools. During the educational expansion in both societies, private senior high schools have provided opportunities for students of lower grades as well as lower social status. This research confirms the existence of a new trend in private school education: the rise of private academic education in the younger cohort. We need to continue to monitor this trend not only in these two societies but also in other East Asian countries. Keywords: senior high school; tracking; private schools

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2010.08.028 Byline: Yusuke Sakurai, Daisuke Kurokawa, Hiroshi Kiyonari, Eriko Kajikawa, Yoko Suda, Shinichi Aizawa Keywords: Otx2; Otx1; Enhancer; Forebrain; Midbrain; Isthmus Abstract: Otx2 is expressed in each step and site of head development. To dissect each Otx2 function we have identified a series of Otx2 enhancers. The Otx2 expression in the anterior neuroectoderm is regulated by the AN enhancer and the subsequent expression in forebrain and midbrain later than E8.5 by FM1 and FM2 enhancers; the Otx1 expression takes place at E8.0. In telencephalon later than E9.5 Otx1 continues to be expressed in the entire pallium, while the Otx2 expression is confined to the most medial pallium. To determine the Otx functions in forebrain and midbrain development we have generated mouse mutants that lack both FM1 and FM2 enhancers (DKO: Otx2.sup.[DELTA]FM1[DELTA]FM2/[DELTA]FM1[DELTA]FM2) and examined the TKO (Otx1.sup.-/- Otx2.sup.[DELTA]FM1[DELTA]FM2/[DELTA]FM1[DELTA]FM2) phenotype. The mutants develop normally until E8.0, but subsequently by E9.5 the diencephalon, including thalamic eminence and prethalamus, and the mesencephalon are caudalized into metencephalon consisting of isthmus and rhombomere 1; the caudalization does not extend to rhombomere 2 and more caudal rhombomeres. In rostral forebrain, neopallium, ganglionic eminences and hypothalamus in front of prethalamus develop; we propose that they become insensitive to the caudalization with the switch from the Otx2 expression under the AN enhancer to that under FM1 and FM2 enhancers. In contrast, the medial pallium requires Otx1 and Otx2 for its development later than E9.5, and the Otx2 expression in diencepalon and mesencephalon later than E9.5 is also directed by an enhancer other than FM1 and FM2 enhancers. Article History: Received 18 June 2010; Revised 24 August 2010; Accepted 25 August 2010

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2010.03.013 Byline: Daisuke Kurokawa (a)(b), Tomomi Ohmura (a), Hajime Ogino (c), Masaki Takeuchi (a), Ai Inoue (a), Fumitaka Inoue (a), Yoko Suda (a), Shinichi Aizawa (a) Keywords: Otx2; Head organizer; Anterior visceral endoderm; Anterior mesendoderm; Cis-element; Evolution Abstract: In the mouse, the Otx2 gene has been shown to play essential roles in the visceral endoderm during anterior-posterior axis formation and head induction. While these are primary processes in vertebrate embryogenesis, the visceral endoderm is a tissue unique to mammals. Two enhancers (VE and CM) have been previously found to direct Otx2 expression during early embryogenesis. This study demonstrates that in anterior visceral endoderm the CM enhancer does not have an activity by itself, but enhances the activity of the VE enhancer. These two enhancers also cooperate for the activities in anterior mesendoderm and cephalic mesenchyme. Comparative studies suggest that VE enhancer function was most likely established before the divergence of sarcopterygians into Actinistia, Dipnoi and tetrapods, while the nucleotide sequence corresponding to the VE enhancer was already present in the last common ancestor of bony fishes. The CM enhancer sequence and function would have been also established in ancestral sarcopterygians. The VE/CM enhancers and their gene cascades in the ancestral sarcopterygian head organizer would then have been co-opted by amphibian deep endoderm cells and mammalian visceral endoderm cells for the head development. Author Affiliation: (a) Laboratory for Vertebrate Body Plan, Center for Developmental Biology, RIKEN Kobe, 2-2-3 Minatojima Minamimachi, Chuou-ku, Kobe 650-0047, Japan (b) Misaki Marine Biological Station, Graduate School of Science, The University of Tokyo, Miura 238-0225, Japan (c) Graduate School of Biological Sciences, Nara Institute of Science and Technology (NAIST), Ikoma 630-0192, Japan Article History: Received 1 December 2009; Revised 15 March 2010; Accepted 16 March 2010

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2009.05.543 Byline: Masaki Takeuchi (a), Maiko Takahashi (a), Masataka Okabe (b), Shinichi Aizawa (a) Keywords: Bichir; Lamprey; Holoblastic cleavage; Primary germ layer; Endoderm; Extraembryonic; vegetal cell mass; VegT Abstract: Amphibian holoblastic cleavage in which all blastomeres contribute to any one of the three primary germ layers has been widely thought to be a developmental pattern in the stem lineage of vertebrates, and meroblastic cleavage to have evolved independently in each vertebrate lineage. In extant primitive vertebrates, agnathan lamprey and basal bony fishes also undergo holoblastic cleavage, and their vegetal blastomeres have been generally thought to contribute to embryonic endoderm. However, the present marker analyses in basal ray-finned fish bichir and agnathan lamprey embryos indicated that their mesoderm and endoderm develop in the equatorial marginal zone, and their vegetal cell mass is extraembryonic nutritive yolk cells, having non-cell autonomous meso-endoderm inducing activity. Eomesodermin (eomes), but not VegT, orthologs are expressed maternally in these animals, suggesting that VegT is a maternal factor for endoderm differentiation only in amphibian. The study raises the viewpoint that the lamprey/bichir type holoblastic development would have been ancestral to extant vertebrates and retained in their stem lineage; amphibian-type holoblastic development would have been acquired secondarily, accompanied by the exploitation of new molecular machinery such as maternal VegT. Author Affiliation: (a) Laboratory for Vertebrate Body Plan, Center for Developmental Biology (CDB), RIKEN Kobe, 2-2-3 Minatojima Minamimachi, Chuo-ku, Hyogo 650-0047, Japan (b) Department of Anatomy, The Jikei University School of Medicine, 3-25-8 NishiShinbashi, Minatoku, Tokyo 105-8461, Japan Article History: Received 28 January 2009; Revised 21 April 2009; Accepted 5 May 2009

Phosphoinositide 3-kinase (PI3K) p85[alpha]-deficient mice exhibit hypoglycemia as a result of increased insulin sensitivity and glucose uptake in peripheral tissues. Although PI3K is central to the metabolic actions of insulin, its mechanism of action in liver is not well understood. In the present study, we investigated hepatic insulin signaling and glucose homeostasis in p85[alpha]-deficient and wild-type mice. In the livers of p85[alpha]-deficient mice, p50[alpha] played a compensatory role in insulin-stimulated PI3K activation by binding to insulin receptor substrate (IRS)-1/2. In p85[alpha]-deficient mice, the ratio of p50[alpha] over p110 catalytic subunit of PI3K in the liver was higher than in the muscles. PI3K activity associated with IRS-1/2 was not affected by the lack of p85[alpha] in the liver. Insulin-stimulated Akt and phosphatase and tensin homologue deleted on chromosome 10 (PTEN) activities in the liver were similar in p85[alpha]-deficient and wild-type mice. A hyperinsulinemic-euglycemic clamp study revealed that the glucose infusion rate and the rate of disappearance were higher in p85[alpha]-deficient mice than in wild-type mice but that endogenous glucose production tended to be higher in p85[alpha]-deficient mice than in wild-type mice. Consistent with this finding, the expression of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase in livers after fasting was higher in p85[alpha]-deficient mice than in wild-type mice. After mice were fasted, the intrahepatic glucose-6-phosphate level was almost completely depleted in p85[alpha]-deficient mice. The glycogen content fell to nearly zero as a result of glycogenolysis shortly after the initiation of fasting in p85[alpha]-deficient mice. The absence of an increase in insulin-stimulated PI3K activation in the liver of p85[alpha]-deficient mice, unlike the muscles, may be associated with the molecular balance between the regulatory subunit and the catalytic subunit of PI3K. Gluconeogenesis was rather elevated in p85[alpha]-deficient mice, compared with in wild-type mice, and the liver seemed to partially compensate for the increase in glucose uptake in peripheral tissues. phosphoinositide 3-kinase; regulatory subunit; catalytic subunit

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2008.09.018 Byline: Yoko Suda (a), Daisuke Kurokawa (a)(c), Masaki Takeuchi (a), Eriko Kajikawa (a), Shigeru Kuratani (b), Chris Amemiya (d), Shinichi Aizawa (a) Keywords: Otx; Fugu; Bichir; Skate; Lamprey; Head development; Organizer; Anterior mesendoderm; Anterior neuroectoderm; Brain Abstract: To 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. Author Affiliation: (a) Laboratory for Vertebrate Body Plan, Center for Developmental Biology, RIKEN Kobe, 2-2-3 Minatojima Minamimachi, Chuo-ku, Kobe 650-0047, Japan (b) Evolutionary Morphology, Center for Developmental Biology, RIKEN Kobe, 2-2-3 Minatojima Minamimachi, Chuo-ku, Kobe 650-0047, Japan (c) Misaki Marine Biological Station, Graduate School of Science, The University of Tokyo, 1024 Koajiro, Misaki, Miura, Kanagawa 238-0225, Japan (d) Molecular Genetics Program, Benaroya Research Institute at Virginia Mason, 1201 Ninth Avenue, Seattle, WA 98101, USA Article History: Received 15 May 2008; Revised 10 September 2008; Accepted 12 September 2008

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2008.05.054 Byline: Sayaka Sugiyama (1)(6), Ariel A. Di Nardo (2), Shinichi Aizawa (3), Isao Matsuo (4), Michel Volovitch (2), Alain Prochiantz (2)(5), Takao K. Hensch (1)(6)(7) Keywords: MOLNEURO; SYSNEURO; SIGNALING Abstract: Neural circuits are shaped by experience in early postnatal life. Distinct GABAergic connections within visual cortex determine the timing of the critical period for rewiring ocular dominance to establish visual acuity. We find that maturation of the parvalbumin (PV)-cell network that controls plasticity onset is regulated by a selective re-expression of the embryonic Otx2 homeoprotein. Visual experience promoted the accumulation of non-cell-autonomous Otx2 in PV-cells, and cortical infusion of exogenous Otx2 accelerated both PV-cell development and critical period timing. Conversely, conditional removal of Otx2 from non-PV cells or from the visual pathway abolished plasticity. Thus, the experience-dependent transfer of a homeoprotein may establish the physiological milieu for postnatal plasticity of a neural circuit. Author Affiliation: (1) Lab for Neuronal Circuit Development, RIKEN Brain Science Institute, 2-1 Hirosawa, Wako-shi, Saitama 351-0198, Japan (2) CNRS UMR 8542, Ecole Normale Superieure, 46 rue d'Ulm, 75230 Paris Cedex 05, France (3) RIKEN Center for Developmental Biology, 2-2-3 Minatojima-minamimachi, Chuo-ku, Kobe 650-0047, Japan (4) Department of Molecular Embryology, Osaka Medical Center and Research Institute for Maternal and Child Health, 840 Murodo-cho, Izumi, Osaka 594-1101, Japan (5) College de France, Paris, France (6) Department of Neurology, Children's Hospital Boston, Harvard Medical School, 300 Longwood Avenue Boston, MA 02115, USA (7) Department of Molecular & Cellular Biology, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA Article History: Received 22 June 2007; Revised 22 April 2008; Accepted 5 May 2008 Article Note: (miscellaneous) Published: August 7, 2008

Glucokinase (Gck) functions as a glucose sensor for insulin secretion, and in mice fed standard chow, haplo-insufficiency of [beta] cell-specific Gck (Gc[k.sup.+/-]) causes impaired insulin secretion to glucose, although the [...]

A novel antagonist against Wnt and FGF signaling for head formation, Shisa, which functions cell autonomously in the endoplasmic reticulum (ER) was identified. Shisa is specifically expressed in the prospective head ectoderm and the Spemann organizer of Xenopus gastrulae and it is indicated that Shisa controls head formation by regulating the establishment of the receptors for caudalizing factors.

Previous analysis employing chimeric and transgenic rescue experiments has suggested that Otx2 is required in the neuroectoderm for development of the forebrain region. In order to elucidate the precise role of Otx2 in forebrain development, we attempted to generate an allelic series of Otx2 mutations by Flp- and Cre-mediated recombination for the production of conditional knock-out mice. Unexpectedly, the neo-cassette insertion created a hypomorphic Otx2 allele; consequently, the phenotype of compound mutant embryos carrying both a hypomorphic and a null allele ([Otx2.sup.frt-neo/-]) was analyzed. [Otx2.sup.frt-neo/-] mutant mice died at birth, displaying rostral head malformations. Molecular marker analysis demonstrated that [Otx2.sup.frt-neo/-] mutant embryos appeared to undergo anterior-posterior axis generation and induction of anterior neuroectoderm normally; however, these mutants subsequently failed to correctly specify the forebrain region. As the rostral margin of the neural plate, termed the anterior neural ridge (ANR), plays crucial roles with respect to neural plate specification, we examined expression of molecular markers for the ANR and the neural plate; moreover, neural plate explant studies were performed. Analyses revealed that telencephalic gene expression did not occur in mutant embryos due to defects of the neural plate; however, the mutant ANR bore normal induction activity on gene expression. These results further suggest that Otx2 dosage may be crucial in the neural plate with respect to response to inductive signals primarily from the ANR for forebrain specification. Key Words: forebrain; neural plate; anterior neural ridge; regionalization; hypomorphic allele; Otx2.