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Taro Suzuki,Yoshiharu Amano,Jun-ichi Takiguchi,Takumi Hashizume,Shinji Suzuki,Atsushi Yamaba 제어로봇시스템학회 2009 제어로봇시스템학회 국제학술대회 논문집 Vol.2009 No.8
This paper describes a low-cost and flexible vegetation monitoring system and compares it with traditional remote sensing systems usch as airplanes and staellites. We have developed a small unmanned aerial vehicle(UAV) equipped with visible and infrared cameras for vegetation obsevation. This system can automatically generate widespread high-resolution mosaic image and calculate the vegetation index from the multiple aerial images collected by an autonomous flight of the UAV. We performed monitoring experiments at Yawata moor in Hiroshima Prefectrue. From the experimental results, we conclued that the small UAV system was effective and useful for carrying out low-cost and flexible vegetation monitoring.
Enzyme Sensors Modified with Avidin/Biotin Systembased Protein Multilayers
Anzai, Jun-Ichi,Du, Xiao-Yan,Hoshi, Tomonori,Suzuki, Yasuhiro,Takeshita, Hiroki,Osa, Tetsuo 한국분석과학회 1995 분석과학 Vol.8 No.4
Enzyme multilayers composed of avidin and biotin-labeled enzymes were prepared on the surface of electrode, through a strong affinity between avidin and biotin (binding constant: ca $10^{15} M^{-1}$). The enzyme multilayers were useful for the improvement of the performance characteristies of enzyme sensors. The output current of the enzyme sensors depended linearly on the number of enzyme layers deposited. Thus, lactate oxidase (LOx) and alcohol oxidase (AlOx) were deposited after being modified with biotin for constructing enzyme sensors sensitive to L-lactate and ethanol respectively. It was also possible to deposit two different kinds of enzymes successively in a single multilayer. The glucose oxidase (GOx) and ascorbate oxidase (AsOx) were built into a multilayer structure on a Platinum electrode. The GOx, AsOx multilayer-modified electrode was useful for the elimination of ascorbic acid interference of the glucose sensor.
Park, Seong Bin,Hikima, Jun-ichi,Suzuki, Yoshiaki,Ohtani, Maki,Nho, Seong Won,Cha, In Seok,Jang, Ho Bin,Kondo, Hidehiro,Hirono, Ikuo,Aoki, Takashi,Jung, Tae Sung Elsevier 2012 DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY Vol.36 No.4
<P><B>Highlights</B></P><P>► The gene encoding nucleotide-binding oligomerization domain 1 (NOD1) was cloned in olive flounder. ► NOD1 was expressed in all fish tissues examined. ► NOD1 mRNA levels was elevated in fish infected with <I>Edwardsiella tarda</I>, <I>Streptococcus iniae</I>, or VHSV. ► The inhibition of <I>E. tarda</I> and the increase of IL-1β levels were observed in NOD1 over-expressing cells.</P> <P><B>Abstract</B></P><P>The gene encoding nucleotide-binding oligomerization domain 1 (NOD1) was cloned from olive flounder (<I>Paralichthys olivaceus</I>) and the role played by NOD1 during <I>Edwardsiella tarda</I> infection was evaluated. The complete open reading frame of NOD1 was 2820bp in length, encoding a 939-amino acid polypeptide. The NOD1 protein contains three conserved domain structures including C-terminal LRRs, a central NACHT motif, and an N-terminal CARD domain, which show similarities of 49–74% to those of other vertebrate counterpart proteins. NOD1 expression was observed in all fish tissues examined, and the levels increased in olive flounder infected with <I>E. tarda</I>, <I>Streptococcus iniae</I>, or viral hemorrhagic septicemia virus (VHSV). When hirame natural embryo (HINAE) cells over-expressing NOD1 were infected with <I>E. tarda</I>, bacterial growth was inhibited, and the IL-1β transcript level increased compared to that of the control. These findings imply that NOD1 plays an important role in response to <I>E. tarda</I> infection of olive flounder.</P>
Novel Concept of a Heart-Gut Axis in the Pathophysiology of Heart Failure
Takehiro Kamo,Hiroshi Akazawa,Jun ichi suzuki,Issei Komuro 대한심장학회 2017 Korean Circulation Journal Vol.47 No.5
Patients with heart failure (HF) have structural and functional changes of the gut as a result of microcirculatory disturbances. A disrupted gut epithelial barrier may lead to translocation of microbial products into systemic circulation, possibly aggravating HF by inducing inflammatory responses. Gut microbiota play an essential role in the maintenance of host homeostasis because large quantities of their gene products complement host physiological processes. Emerging evidence has suggested the potential clinical significance of gut microbiota in the pathophysiology of HF. Imbalances of gut microbe-derived metabolites can contribute to cardiac dysfunction and other morbidities in patients with HF. Therapeutic research for HF through targeting microbiota is under way. Thus, the novel concept of a heart-gut axis may lead to breakthroughs in the development of innovative diagnostics and therapeutic approaches for HF.
BALDUCCI-SILANO, PINA L.,SUZUKI, KOICHI,OHTA, MASANORI,SAITO, JUN,OHMORI, MASAYUKI,MONTANI, VALERIA,NAPOLITANO, GIORGIO,SHONG, MINHO,TANIGUCHI, SHIN-ICHI,PIETRARELLI, MICHELE,LAVARONI, STEFANO,MORI, A 충남대학교 생물공학연구소 1999 생물공학연구지 Vol.7 No.-
The single strand binding protein (SSBP-1) is a positive regulator of TSH receptor gene expression and binds to an element with a GXXXXG motif. The S box of the mouse major histocompatibility classⅡ gene has multiple GXXXXG motifs and can also bind SSBP-1. The S box is one of four highly conserved elements on the 5'-flanking region of classⅡ genes that are necessary for interferon-γ (IFNγ) to overcome the normally suppressed state of the gene and induce aberrant classⅡ expression. In this report we show that SSBP-1, when overexpressed in FRTL-5 thyroid cells, is a positive regulator of human leukocyte antigen (HLA)-DRα classⅡ gene expression, as is IFNγ or the classⅡ trans-activator (CIITA). This is evidenced by increased exogenous promoter activity, increased endogenous RNA levels, and increased endogenous antigen expression after transfecting full-length SSBP-1 complementary DNA together with a HLA-DRα promoter-reporter gene chimera into TSH-treated FRTL-5 thyroid cells whose endogenous SSBP-1 levels are low. IFNγ reverses the ability of TSH to decrease endogenous SSBP-1 RNA levels. Also, whereas SSBP-1 transfection does not cause any increase in IFNγ-induced exogenous promoter activity, transfection of SSBP-1 and CIITA additively increases endogenous classⅡ RNA levels to levels measured in cells treated with IFNγ. Further, competition studies show that SSBP-1 binding is necessary for formation of the double strand protein/DNA complexes that are seen in electrophoretic mobility shift assays when the classⅡ 5'-flanking region is incubated with extracts from IFNγ-treated FRTL-5 cells and that have been previously associated with IFNγ-induced aberrant classⅡ expression. These data suggest that SSBP-1 is involved in the action of IFNγ to overcome the normally suppressed state of the classⅡ gene; it functions together with CIITA, whose expression is independently increased by IFNγ. The effect of SSBP-1 as a positive regulator of classⅡ promoter activity is lost in cells maintained without TSH, in which endogenous SSBP-1 RNA levels are already high in the absence of aberrant classⅡ gene expression. These data suggest that high levels of endogenous SSBP-1 are insufficient to cause aberrant classⅡ expression, but, rather, TSH or IFNγ treatment additionally modulates the cell, albeit differently, such that transfected or endogenous SSBP-1, respectively, can express its positive regulatory activity. The effect of TSH is consistent with reports indicating that TSH enhances the ability of IFNγ to increase classⅡ gene expression despite the fact IFNγ increases endogenous SSBP-1 to only the same levels as in cells untreated with TSH. Finally, the effect of SSBP-1 as a positive regulator is lost when GXXXXG motifs, which exist on both the coding and noncoding strands of the S box, are mutated. Consistent with this, mutation and oligonucleotide competition studies show that GXXXXG motifs are necessary for either strand of the S box to bind protein/DNA complexes containing SSBP-1 in FRTL-5 cell extracts or to bind to recombinant SSBP-1. They also suggest that the SSBP-1-binding sites on either strand of the HLA-DRα S box are functionally distinct. We conclude from these data that the positive regulatory action of SSBP-1 on classⅡ gene expression involves GXXXXG motifs on each strand of the highly conserved S box of the classⅡ 5'-flanking region. As SSBP-1 is modulated by IFNγ and is involved in classⅠ and TSH receptor as well as classⅡ gene expression in FRTL-5 cells, the sum of the data supports the hypotheses that common transcription factors regulate all three genes, and their altered activities may contribute to the development of autoimmunity. (Endocrinology 139: 2300-2313, 1998)
Ohtani, Maki,Hikima, Jun-ichi,Hwang, Seong Don,Morita, Takahiro,Suzuki, Yoshiaki,Kato, Goshi,Kondo, Hidehiro,Hirono, Ikuo,Jung, Tae-Sung,Aoki, Takashi Elsevier 2012 DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY Vol.36 No.4
<P><B>Highlights</B></P><P>► Japanese flounder type I IFN gene was cloned and clustered with Acanthopterygii. ► The poly I:C-responsible region (−634 to −179bp) was found in IFN promoter. ► Transcriptional activity of IFN promoter was enhanced by the flounder IRF3. ► The activity of IFN promoter was induced by RLRs after poly I:C-stimulation.</P> <P><B>Abstract</B></P><P>Type I interferon (IFN) induces the antiviral response in innate immunity. The type I IFN gene cloned from Japanese flounder (<I>Paralichthys olivaceus</I>) has a length of 1189bp and consisting of 5 exons and 4 introns. In a phylogenetic tree of type I IFNs, Japanese flounder grouped with other Acanthopterygii. To gain insight into the transcriptional regulation of IFN gene, the 1.36kb 5′-upstream region including numerous canonical motifs to bind transcription factors [for example, IFN regulatory factor (IRF)] was analyzed. In HINAE cells using a luciferase reporter assay, poly I:C-responsive transcriptional activity was found in the region from −634 to −179bp. This region includes several IRF motifs. In the presence of poly I:C, overexpression of IRF3 and RLR strongly enhanced transcriptional activity. These results suggest that the transcriptional regulation of Japanese flounder type I IFN is regulated by IRF3 after triggering with dsRNA sensors.</P>