1,457 research outputs found

    Trade And Structural Adjustment Policies In Selected Developing Countries

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    The experience of the five examined industries (agro-food in Chile, cut flowers in Kenya,garment in Lesotho and in Mauritius and seafood in Thailand) demonstrates that non-traditional industries can emerge and achieved strong growth rates in very diverse settings in terms of geography and initial economic and social conditions. In most of these cases, the government adopted a relatively export-oriented, business- friendly attitude and adapted its policies as the industries developed. Hence, a key factor for successful structural adjustment has been the pro-active role of government in establishing an enabling economic and policy environment that allows local firms to operate on a level-playing field and strengthen their competitive edge in international markets. This highlights the importance of implementing trade policies in the framework of comprehensive development strategies and establishing a consultative national policy-making process for ensuring a coherent approach to trade and structural adjustment. The case studies also underscore that countries (government and industry) are compelled to constantly adapt in light of new sources of competition, growing wage levels, environmental constraints, technological advances and demanding product and process standards. Policy-makers in most countries under review are aware of this challenge. As a consequence, some of them have taken the initiative to set up specific mechanisms or programmes for further enhancing the competitiveness of existing export sectors and/or promoting emerging non-traditional export industries.Trade and structural adjustment, export diversification, trade capacity building

    Employers Liability for Damages Suffered by Employee in the Performance of his Work

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    Sas-Ptp10D shapes germ-line stem cell niche by facilitating JNK-mediated apoptosis

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    卵幹細胞ニッチの形づくりが卵幹細胞の数と卵産生能を決めることを解明. 京都大学プレスリリース. 2023-04-04.The function of the stem cell system is supported by a stereotypical shape of the niche structure. In Drosophila ovarian germarium, somatic cap cells form a dish-like niche structure that allows only two or three germ-line stem cells (GSCs) reside in the niche. Despite extensive studies on the mechanism of stem cell maintenance, the mechanisms of how the dish-like niche structure is shaped and how this structure contributes to the stem cell system have been elusive. Here, we show that a transmembrane protein Stranded at second (Sas) and its receptor Protein tyrosine phosphatase 10D (Ptp10D), effectors of axon guidance and cell competition via epidermal growth factor receptor (Egfr) inhibition, shape the dish-like niche structure by facilitating c-Jun N-terminal kinase (JNK)-mediated apoptosis. Loss of Sas or Ptp10D in gonadal apical cells, but not in GSCs or cap cells, during the pre-pupal stage results in abnormal shaping of the niche structure in the adult, which allows excessive, four to six GSCs reside in the niche. Mechanistically, loss of Sas-Ptp10D elevates Egfr signaling in the gonadal apical cells, thereby suppressing their naturally-occurring JNK-mediated apoptosis that is essential for the shaping of the dish-like niche structure by neighboring cap cells. Notably, the abnormal niche shape and resulting excessive GSCs lead to diminished egg production. Our data propose a concept that the stereotypical shaping of the niche structure optimizes the stem cell system, thereby maximizing the reproductive capacity

    Fukuyama-type congenital muscular dystrophy and defective glycosylation of α-dystroglycan

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    Fukuyama-type congenital muscular dystrophy (FCMD) is a severe form of muscular dystrophy accompanied by abnormalities in the eye and brain. The incidence of FCMD is particularly high in the Japanese population. Mutations in the fukutin gene have been identified in patients with FCMD. Fukutin is predicted to be a Golgi apparatus resident protein and to be involved in the post-translational modification of cell-surface proteins. Recently, progress has been made in our understanding of the molecular mechanisms by which the mutation of fukutin leads to the phenotype of FCMD. Loss of function of fukutin results in defective glycosylation of α-dystroglycan, a central component of the dystrophin-glycoprotein complex, leading to disruption of the linkage between basal lamina and cytoskeleton. This disruption is implicated in the pathogenesis of both the MD and brain anomalies in FCMD. Furthermore, genetic analyses have revealed that the spectrum of the FCMD phenotype is much wider than originally thought. In this review, we summarize the diverging clinical phenotype of FCMD and its molecular pathomechanisms

    Biological Role of Dystroglycan in Schwann Cell Function and Its Implications in Peripheral Nervous System Diseases

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    Dystroglycan is a central component of the dystrophin-glycoprotein complex (DGC) that links extracellular matrix with cytoskeleton, expressed in a variety of fetal and adult tissues. Dystroglycan plays diverse roles in development and homeostasis including basement membrane formation, epithelial morphogenesis, membrane stability, cell polarization, and cell migration. In this paper, we will focus on biological role of dystroglycan in Schwann cell function, especially myelination. First, we review the molecular architecture of DGC in Schwann cell abaxonal membrane. Then, we will review the loss-of-function studies using targeted mutagenesis, which have revealed biological functions of each component of DGC in Schwann cells. Based on these findings, roles of dystroglycan in Schwann cell function, in myelination in particular, and its implications in diseases will be discussed in detail. Finally, in view of the fact that understanding the role of dystroglycan in Schwann cells is just beginning, future perspectives will be discussed
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