On Linking National Econometric Models of Japan, U.S.A., and the East and Southeast Asia Countries

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What Lessons Do the Lost Two Decades of the Japanese Economy Give to the Other Economies?

During the recent three decades, 1980~2010, the Japanese economy has experienced a period of rapid growth followed by two stagnant decades with serious financial distress and continuous deflation. In this process, Japan established a strong base for manufacturing industries in the world but could not handle the external shocks—the Plaza Accord, the rise of China, the Asian financial Crisis and the 2008 Financial Crisis—and adjust its economy to the dramatic changes in the energy/resources and financial markets. This paper sums up the representative views of Japanese economists on these problems and then presents the author‘s own opinions. A sharp and continuous decline of economic growth was caused not only by external events but also aggravated by the mismanagement of private and public agencies, particularly in the financial sector. The author relies on a number of outstanding works by Japanese and foreign economies like Mitsuo Saito (1927-2010), The Japanese Economy, WSPC, 2000; 3 volumes edited by Fumio Hayashi, Positive Analysis and Design of Economic Institutions (J). Keiso Shobo, 2007, besides his own studies: Political Economy of Japanese and Asian Development, Springer-Verlag and Sobun-sha, 2003, and other essays. One important work is Tadao Kagono, The Spirit of Management (J), Japan Productivity Center Pub. Co., 2010 which pointed out that the Japanese government made a mistake in reforming the Corporation law, at the suggestion of the US government, to change the behavior patterns of Japanese entrepreneurs toward less risk-taking when more out-ward-looking behaviors are required in this uncertain world nowadays, and lost the precious traditional spirit of Japanese-style management. All other important references are given at the end of the paper with a statistical appendix

Silenced Expression of NFKBIA in Lung Adenocarcinoma Patients with a Never-smoking History

Nuclear factor of κ-light polypeptide gene enhancer in B cells inhibitor α (NFKBIA), which is a tumor suppressor gene, was found to be silenced in lung adenocarcinomas. We examined NFKBIA expression, mutations in the EGFR and K-ras genes, and EML4-ALK fusion in 101 resected lung adenocarcinoma samples from never-smokers. NFKBIA expression was evaluated using immunohistochemistry. NFKBIA expression was negative in 16 of the 101 samples (15.8%). EGFR and K-ras mutations and EML4-ALK fusion were detected in 61 (60.5%), 1 (1.0%), and 2 (2.0%) of the 101 samples, respectively, in a completely mutually exclusive manner. Negative NFKBIA expression was observed significantly more frequently among the tumors with none of the three genetic alterations compared to those with such alterations (p＝0.009). In addition, negative NFKBIA expression was significantly more frequent among the EGFR-wild type samples compared to the EGFR-mutant samples (p＝0.013). In conclusion, NFKBIA expression was silenced in adenocarcinomas without EGFR/K-ras mutations or EML4-ALK fusion, suggesting that the silencing of NFKBIA may play an important role in the carcinogenesis of adenocarcinomas independent of EGFR/K-ras mutations or EML4-ALK fusion

Kerja Sama selaku Penasihat Ekonomi Jepang di Indonesia

Short Biography Shinichi Ichimura lahir di Kyoto, pada 1925. Seusai lulus dari Fakultas Ekonomi Universitas Kyoto (1949), beliau menempuh studi di Amerika Serikat tahun 1950, dan mendapat gelar Ph.D. dari MIT tahun 1953. Beliau pernah menjabat sebagai associate professor di UniversitasWakayama, profesor di Institute of Social and Economic Research, Universitas Osaka, lalu tahun 1968 menjabat sebagai dosen di Centre for Southeast Asian Studies di Universitas Kyoto (1969–1979 sebagai direktur). Setelah pensiun pada Maret 1988, beliau mendapat gelar Profesor Emeritus dan diangkat sebagaiWakil Rektor Osaka International University per April 1988, lalu menjadi Presiden International Centre for the Study of East Asian Development (ICSEAD) di Kitakyushu pada 1995. Kemudian menjabat sebagai penasihat ICSEAD tahun 2002–2005. Selain itu, pada 1961 terpilih sebagai Fellow dari The Econometric Society. Beliau juga pernah menjabat sebagai Ketua East Asian Economic Association tahun 1992–1996 dan Ketua Editor Asian Economic Journal pada 1988–1996. Kontribusi kepada dunia dilakukan dengan cara aktif menyusun dan menerapkan tabel input-output, serta model ekonometrik makro untuk Jepang dan negara-negara Asia yang dituangkan dalam banyak publikasi yang berbahasa Inggris

Tumor-specific exon creation of the HELLS/SMARCA6 gene in non-small cell lung cancer

In an attempt to identify tumor suppressor genes on chromosome 10 in non-small cell lung cancers, we isolated 10 types of splicing variants of the HELLS/ SMARCA6 gene transcripts. HELLS/SMARCA6 is a novel member of SNF2 family, which is implicated in cellular function like chromatin remodeling. Variant 1 was an alternatively spliced isoform containing an insertion of a 44-ntd intronic sequence between exons 3 and 4, giving rise to a premature termination of translation. The expression of the variant 1 was detected exclusively in the lung cancer specimens (11 of 43 cases, 26%), but was not detected in corresponding normal tissues. D10S520 marker in the proximity of the HELLS/SMARCA6 gene showed prevalent allelic loss (41%) as compared with flanking markers (25-31%). These results suggest that loss of function of HELLS/SMARCA6 by allelic loss and aberrant proteins by tumor-specific exon creation may result in epigenetic deregulation, leading the lung cells to malignancy or its progression

Impact of GLUT1 and Ki-67 expression on early-stage lung adenocarcinoma diagnosed according to a new international multidisciplinary classification

High expression levels of glucose transporter isoform 1 (GLUT1) and Ki-67 are reportedly associated with malignancy-related clinicopathological factors in malignant tumors. Recently, a new histological IASLC/ATS/ERS classification for lung adenocarcinoma was proposed. In this study, we investigated the clinicopathological impact of GLUT1 and Ki-67 expression on early-stage lung adenocarcinoma classified according to the IASLC/ATS/ERS classification. One hundred and five patients with completely resected stage IA lung adenocarcinoma were retrospectively classified into two groups, a 'non-invasive type' (n=31) or an 'invasive type' (n=74), based on the IASLC/ATS/ERS classification. GLUT1 and Ki-67 expression status was evaluated using immunohistochemistry. The epidermal growth factor receptor (EGFR) and KRAS mutation status was determined using PCR-based assays. Positive GLUT1 and Ki-67 expression and EGFR and KRAS mutations were detected in 28 (27%), 33 (31%), 51 (49%) and 5 (8%) cases, respectively. Positive GLUT1 expression was significantly associated with a wild-type EGFR and mutant KRAS status. A multivariate analysis revealed that positive GLUT1 expression was independently associated with the 'invasive type'. In multivariate analyses for overall survival (OS) and disease-free survival (DFS), positive Ki-67 and GLUT1 expression was the only independent factor for a poor OS (P=0.012) and DFS (P=0.040), respectively. In addition, when stratified according to the GLUT1 and Ki-67 status, double-positive cases had the poorest DFS and OS times, compared with the other categories. Positive GLUT1 expression is associated with the invasive character of early-stage lung adenocarcinoma and with early disease relapse. Our results strongly suggest that GLUT1 and Ki-67 play important roles in acquiring biological malignant potential in early-stage lung adenocarcinoma

Triple-negative pleomorphic lobular carcinoma and expression of androgen receptor: Personal case series and review of the literature

Pleomorphic lobular carcinoma (PLC) is a histological variant of invasive lobular carcinoma (ILC) and is associated with worse prognosis than classical ILC. It exhibits a greater degree of cellular atypia and pleomorphism and is occasionally accompanied with apocrine morphology. We investigated the immunohistochemical characteristics of samples from 31 Japanese patients with PLC to elucidate the clinicopathological characteristics of PLC including androgen receptor (AR) immunoreactivity. The surrogate molecular subtypes were luminal A-like, luminal B-like, luminal B-like/HER2, HER2-type, and triple-negative in 5, 4, 3, 5, and 14 cases, respectively. AR was positive in 92.8% (13/14) of the triple-negative PLC cases and 100% (10/10) of the non-triple-negative PLC cases. Disease-specific survival was worse in patients with histological grade 3 PLCs than in those with histological grade 2 PLCs (p = 0.007). However, there was no significant difference in the progression-free survival between the two groups (p = 0.152). No other clinicopathological characteristics were associated with prognosis. These results reveal that PLC exhibits various surrogate molecular subtypes and that the triple-negative subtype frequently expresses AR. The observed molecular apocrine differentiation implicates that triple-negative PLC can be categorized into the luminal AR subtype. Furthermore, AR-targeted therapy might be useful for patients with triple-negative PLC

Multiple routes of hepatitis C virus transmission among injection drug users in Hai Phong, Northern Vietnam

金沢大学医薬保健研究域医学系To identify hepatitis C virus (HCV) transmission routes among injection drug users in Northern Vietnam, plasma samples were collected from 486 drug users in Hai Phong. Plasma viral RNA was extracted from 323 (66.5%) samples that were positive for anti-HCV antibodies. Portions of the HCV 5′- untranslated (5′UTR)-Core and NS5B genes were amplified by reverse-transcriptase polymerase chain reaction, sequenced directly, and genotyped in 194 and 195 specimens, respectively. Both regions were genotyped in 137 specimens. In the 5′UTR-Core region, genotype 6a was predominant (32.5%), followed by genotype 1a (23.7%), genotype 1b (20.6%), and genotype 6e (14.4%). In the NS5B region, genotype 1a was predominant (42.6%), followed by genotype 1b (24.1%), genotype 6a (14.4%), genotype 3b (7.2%), and genotype 6e (5.1%). Of the 137 specimens with both regions genotyped, 23 (16.8%) showed discordant genotyping results between the two regions, suggesting possible recombination and/or dual infection. Phylogenetic analysis revealed close associations between Hai Phong strains and strains from Southern China: the Yunnan province for genotype 3b; the Guangxi province for genotype 6e; the USA for genotype 1a; and Southern Vietnam for genotypes 1a and 6e. The human immunodeficiency virus (HIV) infection rate among HCV-infected injection drug users was 52.6-55.4% and did not differ significantly by HCV genotype. Most drug users infected with HIV-1 [98.8% (171/173)] were co-infected with HCV. These results suggest multiple routes of HCV transmission among injection drug users in Northern Vietnam that may also be HIV transmission routes. © 2010 Wiley-Liss, Inc

A Possible Contribution of Altered Cathepsin B Expression to the Development of Skin Sclerosis and Vasculopathy in Systemic Sclerosis

Cathepsin B (CTSB) is a proteolytic enzyme potentially modulating angiogenic processes and extracellular matrix remodeling. While matrix metalloproteinases are shown to be implicated in tissue fibrosis and vasculopathy associated with systemic sclerosis (SSc), the role of cathepsins in this disease has not been well studied. The aim of this study is to evaluate the roles of CTSB in SSc. Serum pro-CTSB levels were determined by enzyme-linked immunosorbent assay in 55 SSc patients and 19 normal controls. Since the deficiency of transcription factor Fli1 in endothelial cells is potentially associated with the development of SSc vasculopathy, cutaneous CTSB expression was evaluated by immunostaining in Fli1+/− and wild type mice as well as in SSc and control subjects. The effects of Fli1 gene silencing and transforming growth factor-β (TGF-β) on CTSB expression were determined by real-time PCR in human dermal microvascular endothelial cells (HDMECs) and dermal fibroblasts, respectively. Serum pro-CTSB levels were significantly higher in limited cutaneous SSc (lcSSc) and late-stage diffuse cutaneous SSc (dcSSc) patients than in healthy controls. In dcSSc, patients with increased serum pro-CTSB levels showed a significantly higher frequency of digital ulcers than those with normal levels. CTSB expression in dermal blood vessels was increased in Fli1+/− mice compared with wild type mice and in SSc patients compared with healthy controls. Consistently, Fli1 gene silencing increased CTSB expression in HDMECs. In cultured dermal fibroblasts from early dcSSc, CTSB expression was decreased compared with normal fibroblasts and significantly reversed by TGF-β1 antisense oligonucleotide. In conclusion, up-regulation of endothelial CTSB due to Fli1 deficiency may contribute to the development of SSc vasculopathy, especially digital ulcers, while reduced expression of CTSB in lesional dermal fibroblasts is likely to be associated with skin sclerosis in early dcSSc