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Search Results: 1 - 10 of 772 matches for " Ikuyo Kou "
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Effects of the Chinese Innovation System on Regional Innovation Performance  [PDF]
Kou Kou
Technology and Investment (TI) , 2018, DOI: 10.4236/ti.2018.91003
Abstract: This paper presents the influence of innovation systems on regional innovation performance in China for the period 1998-2008. It places special emphasis on the effects of institutional factors, namely marketization level. The findings indicate that the innovation system contributes greatly to increasing the level of innovation. Among the factors of innovation systems, the openness of the region and government expenditure on education plays key roles. Market-oriented institutional arrangements also increase innovation performance.
Asporin expression is highly regulated in human chondrocytes
Elise Duval,Nicolas Bigot,Magalie Hervieu,Ikuyo Kou,Sylvain Leclercq,Philippe Galéra,Karim Boumediene,Catherine Baugé
Quantitative Biology , 2015, DOI: 10.2119/molmed.2011.00052
Abstract: A significant association between a polymorphism in the D repeat of the gene encoding asporin and osteoarthritis, the most frequent of articular diseases, has been recently reported. The goal of the present study was to investigate the expression of this new class I small leucine-rich proteoglycan (SLRP) in human articular chondrocytes. First, we studied the modulation of asporin (ASPN) expression by cytokines by Western blot and reverse transcription-polymerase chain reaction. Interleukin-1$\beta$ and tumor necrosis factor-$\alpha$ downregulated ASPN, whereas transforming growth factor-$\beta$1 (when incubated in a serum-free medium) upregulated it. Similarly to proinflammatory cytokines, chondrocyte dedifferentiation induced by a successive passages of cells was accompanied by a decreased asporin expression, whereas their redifferentiation by three-dimensional culture restored its expression. Finally, we found an important role of the transcription factor Sp1 in the regulation of ASPN expression. Sp1 ectopic expression increased ASPN mRNA level and promoter activity. In addition, using gene reporter assay and electrophoretic mobility shift assay, we showed that Sp1 mediated its effect through a region located between -473 and -140 bp upstream of the transcription start site in ASPN gene. In conclusion, this report is the first study on the regulation of asporin expression by different cytokines in human articular chondrocytes. Our data indicate that the expression of this gene is finely regulated in cartilage and suggest a major role of Sp1.
FOXC2 Mutations in Familial and Sporadic Spinal Extradural Arachnoid Cyst
Yoji Ogura, Shoji Yabuki, Aritoshi Iida, Ikuyo Kou, Masahiro Nakajima, Hiroki Kano, Masaaki Shiina, Shinichi Kikuchi, Yoshiaki Toyama, Kazuhiro Ogata, Masaya Nakamura, Morio Matsumoto, Shiro Ikegawa
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0080548
Abstract: Spinal extradural arachnoid cyst (SEDAC) is a cyst in the spinal canal that protrudes into the epidural space from a defect in the dura mater. Most cases are sporadic; however, three familial SEDAC cases have been reported, suggesting genetic etiological factors. All familial cases are associated with lymphedema-distichiasis syndrome (LDS), whose causal gene is FOXC2. However, FOXC2 mutation analysis has been performed in only 1 family, and no mutation analysis has been performed on sporadic (non-familial) SEDACs. We recruited 17 SEDAC subjects consisting of 2 familial and 7 sporadic cases and examined FOXC2 mutations by Sanger sequencing and structural abnormalities by TaqMan copy number assay. We identified 2 novel FOXC2 mutations in 2 familial cases. Incomplete LDS penetrance was noted in both families. Four subjects presented with SEDACs only. Thus, SEDAC caused by the heterozygous FOXC2 loss-of-function mutation should be considered a feature of LDS, although it often manifests as the sole symptom. Seven sporadic SEDAC subjects had no FOXC2 mutations, no symptoms of LDS, and showed differing clinical characteristics from those who had FOXC2 mutations, suggesting that other gene(s) besides FOXC2 are likely to be involved in SEDAC.
Functional Investigation of a Non-coding Variant Associated with Adolescent Idiopathic Scoliosis in Zebrafish: Elevated Expression of the Ladybird Homeobox Gene Causes Body Axis Deformation
Long Guo?,Hiroshi Yamashita?,Ikuyo Kou,Aki Takimoto?,Makiko Meguro-Horike?,Shin-ichi Horike?,Tetsushi Sakuma?,Shigenori Miura?,Taiji Adachi?,Takashi Yamamoto
PLOS Genetics , 2016, DOI: 10.1371/journal.pgen.1005802
Abstract: Previously, we identified an adolescent idiopathic scoliosis susceptibility locus near human ladybird homeobox 1 (LBX1) and FLJ41350 by a genome-wide association study. Here, we characterized the associated non-coding variant and investigated the function of these genes. A chromosome conformation capture assay revealed that the genome region with the most significantly associated single nucleotide polymorphism (rs11190870) physically interacted with the promoter region of LBX1-FLJ41350. The promoter in the direction of LBX1, combined with a 590-bp region including rs11190870, had higher transcriptional activity with the risk allele than that with the non-risk allele in HEK 293T cells. The ubiquitous overexpression of human LBX1 or either of the zebrafish lbx genes (lbx1a, lbx1b, and lbx2), but not FLJ41350, in zebrafish embryos caused body curvature followed by death prior to vertebral column formation. Such body axis deformation was not observed in transcription activator-like effector nucleases mediated knockout zebrafish of lbx1b or lbx2. Mosaic expression of lbx1b driven by the GATA2 minimal promoter and the lbx1b enhancer in zebrafish significantly alleviated the embryonic lethal phenotype to allow observation of the later onset of the spinal curvature with or without vertebral malformation. Deformation of the embryonic body axis by lbx1b overexpression was associated with defects in convergent extension, which is a component of the main axis-elongation machinery in gastrulating embryos. In embryos overexpressing lbx1b, wnt5b, a ligand of the non-canonical Wnt/planar cell polarity (PCP) pathway, was significantly downregulated. Injection of mRNA for wnt5b or RhoA, a key downstream effector of Wnt/PCP signaling, rescued the defective convergent extension phenotype and attenuated the lbx1b-induced curvature of the body axis. Thus, our study presents a novel pathological feature of LBX1 and its zebrafish homologs in body axis deformation at various stages of embryonic and subsequent growth in zebrafish.
A case of superior segmental optic hypoplasia accompanied by a glaucomatous optic neuropathy
Ikuyo Ohguro,Hiroshi Ohguro
Clinical Ophthalmology , 2008,
Abstract: Ikuyo Ohguro, Hiroshi OhguroDepartment of Ophthalmology, Sapporo Medical University School of Medicine, Sapporo, Hokkaido, JapanAbstract: This is the first case report of a bilateral superior segmental optic hypoplasia (SSOH) accompanied by a glaucomatous optic neuropathy (GON). A 47-year-old man incidentally diagnosed as having bilateral SSOH, simultaneously disclosed glaucomatous optic disc appearances, including enlargements of the cup of the optic nerve heads and a thinning of the infero-temporal neuroretinal rim with laminar dot sign accompanied by a retinal nerve fiber layer (RNFL) local defect of infero-temporal region in the right eye. The visual field examination revealed that the corresponding nasal step, arcuate scotoma and RNFL field defects in the right eye.Keyword: retinal nerve fiber layer
Common Variants in a Novel Gene, FONG on Chromosome 2q33.1 Confer Risk of Osteoporosis in Japanese
Ikuyo Kou,Atsushi Takahashi,Tomohiko Urano,Naoshi Fukui,Hideki Ito,Kouichi Ozaki,Toshihiro Tanaka,Takayuki Hosoi,Masataka Shiraki,Satoshi Inoue,Yusuke Nakamura,Naoyuki Kamatani,Michiaki Kubo,Seijiro Mori,Shiro Ikegawa
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0019641
Abstract: Osteoporosis is a common disease characterized by low bone mass, decreased bone quality and increased predisposition to fracture. Genetic factors have been implicated in its etiology; however, the specific genes related to susceptibility to osteoporosis are not entirely known. To detect susceptibility genes for osteoporosis, we conducted a genome-wide association study in Japanese using ~270,000 SNPs in 1,747 subjects (190 cases and 1,557 controls) followed by multiple levels of replication of the association using a total of ~5,000 subjects (2,092 cases and 3,114 controls). Through these staged association studies followed by resequencing and linkage disequilibrium mapping, we identified a single nucleotide polymorphism (SNP), rs7605378 associated with osteoporosis. (combined P = 1.51×10?8, odds ratio = 1.25). This SNP is in a previously unknown gene on chromosome 2q33.1, FONG. FONG is predicted to encode a 147 amino-acid protein with a formiminotransferase domain in its N-terminal (FTCD_N domain) and is ubiquitously expressed in various tissues including bone. Our findings would give a new insight into osteoporosis etiology and pathogenesis.
Advances in Research on the Pathogenesis of Type 2 Diabetes Complicated with Gallstone  [PDF]
Jianchu Tan, Jiguang Kou
International Journal of Clinical Medicine (IJCM) , 2019, DOI: 10.4236/ijcm.2019.103016
Abstract: At present, the incidence of diabetes complicated with gallstones is increasing rapidly, and there are still many problems in the pathogenesis of the disease. Diabetes complicated with gallstones is a chronic complication of diabetes, with diabetes-induced hyperinsulinemia and insulin resistance, gallbladder emptying disorders, Oddis sphincter dysfunction, gastrointestinal hormone disorders, gastrointestinal dyskinesia, fat metabolism disorders, bile Bacterial infection and other factors are related. In recent years, it has been found that in diabetic patients, Telocytes (TC) and Cajal interstitial cells (ICC) are reduced in the biliary system. In addition, the contact between ICC cells and smooth muscle cells and nerve endings is significantly reduced, so it is considered that bile Stone formation has a certain relationship with TC and ICC reduction. This article reviews recent research progress.
New Sequence Variants in HLA Class II/III Region Associated with Susceptibility to Knee Osteoarthritis Identified by Genome-Wide Association Study
Masahiro Nakajima,Atsushi Takahashi,Ikuyo Kou,Cristina Rodriguez-Fontenla,Juan J. Gomez-Reino,Tatsuya Furuichi,Jin Dai,Akihiro Sudo,Atsumasa Uchida,Naoshi Fukui,Michiaki Kubo,Naoyuki Kamatani,Tatsuhiko Tsunoda,Konstantinos N. Malizos,Aspasia Tsezou,Antonio Gonzalez,Yusuke Nakamura,Shiro Ikegawa
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0009723
Abstract: Osteoarthritis (OA) is a common disease that has a definite genetic component. Only a few OA susceptibility genes that have definite functional evidence and replication of association have been reported, however. Through a genome-wide association study and a replication using a total of ~4,800 Japanese subjects, we identified two single nucleotide polymorphisms (SNPs) (rs7775228 and rs10947262) associated with susceptibility to knee OA. The two SNPs were in a region containing HLA class II/III genes and their association reached genome-wide significance (combined P = 2.43×10?8 for rs7775228 and 6.73×10?8 for rs10947262). Our results suggest that immunologic mechanism is implicated in the etiology of OA.
Identification of a Susceptibility Locus for Severe Adolescent Idiopathic Scoliosis on Chromosome 17q24.3
Atsushi Miyake, Ikuyo Kou, Yohei Takahashi, Todd A. Johnson, Yoji Ogura, Jin Dai, Xusheng Qiu, Atsushi Takahashi, Hua Jiang, Huang Yan, Katsuki Kono, Noriaki Kawakami, Koki Uno, Manabu Ito, Shohei Minami, Haruhisa Yanagida, Hiroshi Taneichi, Naoya Hosono, Taichi Tsuji, Teppei Suzuki, Hideki Sudo, Toshiaki Kotani, Ikuho Yonezawa, Michiaki Kubo, Tatsuhiko Tsunoda, Kota Watanabe, Kazuhiro Chiba, Yoshiaki Toyama, Yong Qiu, Morio Matsumoto, Shiro Ikegawa
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0072802
Abstract: Adolescent idiopathic scoliosis (AIS) is the most common spinal deformity, affecting around 2% of adolescents worldwide. Genetic factors play an important role in its etiology. Using a genome-wide association study (GWAS), we recently identified novel AIS susceptibility loci on chromosomes 10q24.31 and 6q24.1. To identify more AIS susceptibility loci relating to its severity and progression, we performed GWAS by limiting the case subjects to those with severe AIS. Through a two-stage association study using a total of ~12,000 Japanese subjects, we identified a common variant, rs12946942 that showed a significant association with severe AIS in the recessive model (P = 4.00×10?8, odds ratio [OR] = 2.05). Its association was replicated in a Chinese population (combined P = 6.43×10?12, OR = 2.21). rs12946942 is on chromosome 17q24.3 near the genes SOX9 and KCNJ2, which when mutated cause scoliosis phenotypes. Our findings will offer new insight into the etiology and progression of AIS.
Metastatic sarcomatoid renal cell carcinoma to the mandible treated with Sorafenib  [PDF]
Kazuhiro Murakami, Kazuhiko Yamamoto, Kumiko Aoki, Ikuyo Fukumoto, Tsutomu Sugiura, Tadaaki Kirita
Open Journal of Stomatology (OJST) , 2012, DOI: 10.4236/ojst.2012.23039
Abstract: A case of metastatic sarcomatoid renal cell carcinoma to the mandible treated with Sorafenib is reported. A 76-year-old man consulted us for hyposthesia of the right lower lip. Panorama X-ray film showed a ra-diolucent lesion in the right mandibular body. A diagnosis of metastatic tumor to the mandible from the left kidney was made after evaluation by computed tomography and positron emission tomography, which also revealed multiple bone metastases. After radiotherapy for mandibular and thoracic lesions, nephrectomy was performed. Histological diagnosis was sarcomatoid renal cell carcinoma. Interferon therapy was performed but was not effective; therefore, a molecular targeted drug, Sorafenib, was administered. Sorafenib effectively inhibited the growth of oral and other metastatic lesions for 10 months. Quality of life was relatively well maintained with tolerable adverse effects. The patient survived for as long as 2 years after appearance of the first symptom.
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