Problems of the “Washington Consensus” and the Road to its Overcome : Towards Application of the “Post−Washington Consensus” to Latin America.

本稿の目的は，「ワシントン・コンセンサス」をベースとした１９９０年代のIMF・世銀による途上国に対する政策が，１９９０年代後半の厳しい批判によってどのように修正されたのか，またその修正された政策は開発途上諸国の希望する改革と矛盾せず，すり合わせが可能であるのかを検討することである。本稿では，検討の対象としてラテンアメリカの国々を選んだ。IMF・世銀が，１９８０年代末から１９９０年代前半にかけてラテンアメリカをはじめとする開発途上諸国に対して要求した「新自由主義」に基づく政策の思想的ベースは「ワシントン・コンセンサス」と呼ばれる。西側政府機関，民間金融機関も初めはこの方針と共同歩調をとったが，１９９０年代後半からこの政策の問題点が頻繁に指摘されるようになった。現在，開発途上諸国では，自由化による経済成長戦略より，貧困問題などの社会問題をより重視する傾向が強まってきている。この傾向に沿ってIMF・世銀はその政策を柔軟に変化させようとしている。こうした潮流の変化の中で，IMF・世銀は「ワシントン・コンセンサス」の問題点を修正しながら開発途上諸国支援を続け，一定の成果を修めてきている。一方で，開発途上諸国においても新しいコンセンサスや経済の仕組みが提示されている。本稿では，このようなIMF・世銀内外で活発化している「ワシントン・コンセンサス」後の新しい改革を模索する動き全体を「ポスト・ワシントン・コンセンサス」と称することにする。本稿では，まずはじめに「ワシントン・コンセンサス」が形成された背景を簡単にまとめる。次に，IMF・世銀の政策変化，IMF・世銀の政策に対する批判を検討する。そして，「ワシントン・コンセンサス」に対するオルタナティブとしての性格を持つ中南米における経済再生プログラムを整理・分析し，これらが理念的・政策的にIMF・世銀の政策と対立するものなのか，または相互補完的な性格を持つものなのかを考察する。In this article, the author intends to analyze so called the “Post−Washington Consensus”, the recent economic policies after the criticism of the “Washington　Consensus”. The author defines the “Post−Washington Consensus” in the wide sense, which includes : slightly reformed policy of IMF and the World Bank, critical opinions on the policies of these international financial institutions from the liberal economists, alternative theories and policies, which are criticizing neo−liberal economics (“anti−IMF/World Bank Washington Consensus”). In the last of these groups, the author analyzes especially Latin Americans economic programs and policies as one of the “Post−Washington Consensus”. The author outlines the “solidarity economy” and the “Buenos Aires Consensus”, and analyzes that these concepts could be supplementary, not always antagonistic to the “Post−Washington Consensus” of IMF and the World Bank. In Chapter I, the author reviews the “Washington Consensus” and its problems. Chapter II shows the criticism of the “Washington Consensus” in IMF/World Bank, criticism from the liberal economists, and the “anti−IMF/ World Bank Washington Consensus” (mainly “the solidarity economy” and “the Buenos Aires Consensus” in Latin America). Chapter III compares these concepts and discusses the supplemental or antagonistic aspects of these polices

Sulforaphane induces lipophagy through the activation of AMPK-mTOR-ULK1 pathway signaling in adipocytes

Lipophagy, a form of selective autophagy, degrades lipid droplet (LD) in adipose tissue and the liver. The chemotherapeutic isothiocyanate sulforaphane (SFN) contributes to lipolysis through the activation of hormone-sensitive lipase and the browning of white adipocytes. However, the details concerning the regulation of lipolysis in adipocytes by SFN-mediated autophagy remain unclear. In this study, we investigated the effects of SFN on autophagy in the epididymal fat of mice fed a high-fat diet (HFD) or control-fat diet (CFD) and on the molecular mechanisms of autophagy in differentiated 3T3-L1 cells. Western blotting revealed that the protein expression of lipidated LC3 (LC3-II), an autophagic substrate, was induced after 3T3-L1 adipocytes treatment with SFN. In addition, SFN increased the LC3-II protein expression in the epididymal fat of mice fed an HFD. Immunofluorescence showed that the SFN-induced LC3 expression was co-localized with LDs in 3T3-L1 adipocytes and with perilipin, the most abundant adipocyte-specific protein, in adipocytes of mice fed an HFD. Next, we confirmed that SFN activates autophagy flux in differentiated 3T3-L1 cells using the mCherry-EGFP-LC3 and GFP-LC3-RFP-LC3ΔG probe. Furthermore, we examined the induction mechanisms of autophagy by SFN in 3T3-L1 adipocytes using western blotting. ATG5 knockdown partially blocked the SFN-induced release of fatty acids from LDs in mature 3T3-L1 adipocytes. SFN time-dependently elicited the phosphorylation of AMPK, the dephosphorylation of mTOR, and the phosphorylation of ULK1 in differentiated 3T3-L1 cells. Taken together, these results suggest that SFN may provoke lipophagy through AMPK-mTOR-ULK1 pathway signaling, resulting in partial lipolysis of adipocytes

Gene Expression Profiles of the Cochlea and Vestibular Endorgans: Localization and Function of Genes Causing Deafness

Objectives: We sought to elucidate the gene expression profiles of the causative genes as well as the localization of the encoded proteins involved in hereditary hearing loss. Methods: Relevant articles (as of September 2014) were searched in PubMed databases, and the gene symbols of the genes reported to be associated with deafness were located on the Hereditary Hearing Loss Honnepage using localization, expression, and distribution as keywords. Results: Our review of the literature allowed us to systematize the gene expression profiles for genetic deafness in the inner ear, clarifying the unique functions and specific expression patterns of these genes in the cochlea and vestibular endorgans. Conclusions: The coordinated actions of various encoded molecules are essential for the normal development and maintenance of auditory and vestibular function.ArticleANNALS OF OTOLOGY RHINOLOGY AND LARYNGOLOGY. 124:6S-48S (2015)journal articl

TGR 5 signalling inhibits the production of pro‐inflammatory cytokines by in vitro differentiated inflammatory and intestinal macrophages in Crohn's disease

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/97471/1/imm12045.pd

Development of a Multifunctional Lightweight Membrane with a High Specific Power Generation Capacity

As a lighter power generation system, Japan Aerospace Exploration Agency (JAXA) and Sakase Adtech Corp. are developing a demonstrator component named “Harvesting Energy with Lightweight Integrated Origami Structure” (HELIOS), which is a deployable lightweight membrane structure. HELIOS has solar arrays on its surface and demonstrates the technology which enables higher specific power generation capacity compared to the conventional solar array panels. The membrane also has communication antennas, showing the potency of lightweight membrane’s multifunctionality such as large data transmitting by 5G antennas and high-resolution observation by interferometer antennas. This paper presents the component’s concept and design, and the expected achievements

Targeting miR-223 in neutrophils enhances the clearance of Staphylococcus aureus in infected wounds

Abstract Argonaute 2 bound mature microRNA (Ago2‐miRNA) complexes are key regulators of the wound inflammatory response and function in the translational processing of target mRNAs. In this study, we identified four wound inflammation‐related Ago2‐miRNAs (miR‐139‐5p, miR‐142‐3p, miR‐142‐5p, and miR‐223) and show that miR‐223 is critical for infection control. miR‐223Y/− mice exhibited delayed sterile healing with prolonged neutrophil activation and interleukin‐6 expression, and markedly improved repair of Staphylococcus aureus‐infected wounds. We also showed that the expression of miR‐223 was regulated by CCAAT/enhancer binding protein alpha in human neutrophils after exposure to S. aureus peptides. Treatment with miR‐223Y/−‐derived neutrophils, or miR‐223 antisense oligodeoxynucleotides in S. aureus‐infected wild‐type wounds markedly improved the healing of these otherwise chronic, slow healing wounds. This study reveals how miR‐223 regulates the bactericidal capacity of neutrophils at wound sites and indicates that targeting miR‐223 might be of therapeutic benefit for infected wounds in the clinic

Reduced FOXO1 Expression Accelerates Skin Wound Healing and Attenuates Scarring

The forkhead box O (FOXO) family has been extensively investigated in aging and metabolism, but its role in tissue-repair processes remains largely unknown. Herein, we clarify the molecular aspect of the FOXO family in skin wound healing. We demonstrated that Foxo1 and Foxo3a were both up-regulated during murine skin wound healing. Partial knockout of Foxo1 in Foxo1 +/- mice throughout the body led to accelerated skin wound healing with enhanced keratinocyte migration, reduced granulation tissue formation, and decreased collagen density, accompanied by an attenuated inflammatory response, but we observed no wound phenotype in Foxo3a-/- mice. Fibroblast growth factor 2, adiponectin, and notch1 genes were significantly increased at wound sites in Foxo1+/- mice, along with markedly altered extracellular signal-regulated kinase 1/2 and AKT phosphorylation. Similarly, transient knockdown of Foxo1 at the wound site by local delivery of antisense oligodeoxynucleotides enhanced skin wound healing. The link between FOXO1 and scarring extends to patients, in particular keloid scars, where we see FOXO1 expression markedly increased in fibroblasts and inflammatory cells within the otherwise normal dermis. This occurs in the immediate vicinity of the keloid by comparison to the center of the mature keloid, indicating that FOXO1 is associated with the overgrowth of this fibrotic response into adjacent normal skin. Overall, our data indicate that molecular targeting of FOXO1 may improve the quality of healing and reduce pathological scarring