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Tumor necrosis factor-α converting enzyme is a key mediator of abdominal aortic aneurysm development
Kaneko, Hidehiro,Anzai, Toshihisa,Horiuchi, Keisuke,Kohno, Takashi,Nagai, Toshiyuki,Anzai, Atsushi,Takahashi, Toshiyuki,Sasaki, Aya,Shimoda, Masayuki,Maekawa, Yuichiro,Shimizu, Hideyuki,Yoshikawa, Tsu Elsevier 2011 Atherosclerosis Vol.218 No.2
<P><B>Abstract</B></P><P><B>Objective</B></P><P>Tumor necrosis factor (TNF)-α is known to be elevated in plasma and the aorta in abdominal aortic aneurysm (AAA) patients. We sought to clarify the role of TNF-α converting enzyme (Tace), which cleaves the transmembrane precursor of TNF-α, in AAA development.</P><P><B>Methods</B></P><P>We obtained aortic sample of AAA during surgical operation to assess the histological features and protein expression of human AAA. AAA was induced in mice with temporal systemic deletion of Tace by the inducible Mx-1 Cre transgene (TaceMx1) and in wild-type littermates (CON) by periaortic application of CaCl<SUB>2</SUB> (AAA/TaceMx1, AAA/CON).</P><P><B>Results</B></P><P>Tace expression was increased in human AAA samples as compared with normal aorta. Six weeks postoperatively, aortic diameter in AAA/TaceMx1 was decreased than in AAA/CON in association with attenuated TNF-α expression and extracellular matrix disruption. Increased activities of matrix metalloproteinase (MMP)-9 and MMP-2, numbers of Mac-2-positive macrophages, CD3-positive T lymphocytes and CD31-positive vessels in periaortic tissues, mRNA expression of CD68, monocyte chemotactic protein-1, TNF-α, vascular endothelial growth factor-A, p47 and glutathione peroxidases, and protein expression of phospho-c-Jun N-terminal kinase in AAA were all attenuated by Tace deletion. Protein expression of transforming growth factor (TGF)-β1 was upregulated by Tace deletion in sham-operated mice. TGF-β1 expression was further increased in AAA/TaceMx1.</P><P><B>Conclusions</B></P><P>Tace was overexpressed in the aortic wall in human and experimental AAA. Temporal systemic deletion of Tace prevented AAA development in association with attenuating inflammation, oxidative stress, neoangiogenesis and extracellular matrix disruption, suggesting a crucial role of Tace in AAA development.</P>
Mechanism for the Differentiation of EoL-1 Cells into Eosinophils by Histone Deacetylase Inhibitors
Kaneko, Motoko,Ishihara, Kenji,Takahashi, Aki,Hong, JangJa,Hirasawa, Noriyasu,Zee, OkPyo,Ohuchi, Kazuo S.Karger 2007 International archives of allergy and immunology Vol.143//SUP1 No.-
<P><I>Background:</I> EoL-1 cells have a <I>FIP1L1-PDGFRA</I> fusion gene which causes the transformation of eosinophilic precursor cells into leukemia cells. Recently, we suggested that the induction of differentiation of EoL-1 cells into eosinophils by the HDAC inhibitors apicidin and n-butyrate is due to the continuous inhibition of HDACs. However, neither apicidin nor n-butyrate inhibited the expression of FIP1L1-PDGFRA mRNA, although both these inhibitors suppressed cell proliferation. Therefore, in this study, we analyzed whether the levels of FIP1L1-PDGFRα protein and phosphorylated-Stat5 involved in the signaling for the proliferation of EoL-1 cells are attenuated by HDAC inhibitors. <I>Methods:</I> EoL-1 cells were incubated in the presence of apicidin, TSA or n-butyrate. FIP1L1-PDGFRα and phosphorylated-Stat5 were detected by Western blotting. <I>Results:</I> Treatment of EoL-1 cells with apicidin at 100 n<I>M</I> or n-butyrate at 500 μ<I>M</I> decreased the levels of FIP1L1-PDGFRα protein and phosphorylated-Stat5, while that with trichostatin A at 30 n<I>M</I> did not. <I>Conclusions:</I> The decrease in the level of FIP1L1-PDGFRα protein caused by apicidin and n-butyrate might be one of the mechanisms by which EoL-1 cells are induced to differentiate into eosinophils by these HDAC inhibitors.</P><P>Copyright © 2007 S. Karger AG, Basel</P>
Clinical Characteristics of Esophageal Motility Disorders in Patients With Heartburn
( Satsuki Takahashi ),( Tomoaki Matsumura ),( Tatsuya Kaneko ),( Mamoru Tokunaga ),( Hirotaka Oura ),( Tsubasa Ishikawa ),( Ariki Nagashima ),( Wataru Shiratori ),( Naoki Akizue ),( Yuki Ohta ),( Atsu 대한소화기기능성질환·운동학회 2021 Journal of Neurogastroenterology and Motility (JNM Vol.27 No.4
Background/Aims Esophageal motility disorders (EMDs) contribute to the pathophysiology of gastroesophageal reflux disease. However, the causes of EMDs and their impact on gastroesophageal reflux disease-associated symptoms remain unknown. This study aims to elucidate clinical features associated with various types of EMDs in patients with heartburn symptoms. Methods Of the 511 patients who underwent high-resolution manometry, 394 who were evaluated for heartburn symptoms were examined. Patients subjected to high-resolution manometry were classified into 4 groups: outflow obstruction group, hypermotility group, hypomotility group, and normal motility group. Symptoms were evaluated using 3 questionnaires. Patient characteristics and symptoms for each EMD type were compared with those of the normal motility group. Results Of the 394 patients, 193 (48.9%) were diagnosed with EMDs, including 71 with outflow obstruction, 15 with hypermotility, and 107 with hypomotility. The mean dysphagia score was significantly higher in each of the 3 EMD groups compared with those with normal motility. The mean acid reflux and dyspepsia scores were significantly lower in the outflow obstruction group (P < 0.05). The mean body mass index and median Brinkman index were significantly higher in the hypermotility group (P = 0.001 and P = 0.018, respectively), whereas the mean diarrhea and constipation scores were significantly lower in the hypomotility group (P < 0.05). Conclusions The results of our study indicate that different EMDs have distinct characteristics. Cigarette smoking and high body mass index were associated with esophageal hypermotility. Assessment of the dysphagia symptom scores may help identify patients with EMDs. (J Neurogastroenterol Motil 2021;27:545-554)
Enami Kaneko,Naoki Sato,Tae Sugawara,Aya Noto,Kazue Takahashi,Kenichi Makino,Yukihiro Terada 대한부인종양학회 2021 Journal of Gynecologic Oncology Vol.32 No.6
Objective: The antitumor effects of anti-PD-1 antibody against mismatch repair deficiency (MMR-D)-associated cancers have been reported. MMR-D is found in approximately20%–30% of endometrial carcinomas (ECs) and frequently occurs due to promoter hypermethylation ( -PHM). ECs with -PHM are classified according to the molecular screening of Lynch syndrome (LS), but few detailed reports are available. The purpose of this study was to clarify the clinical features of EC with -PHM. Methods: Immunohistochemistry of MMR proteins (MLH1, MSH2, MSH6, and PMS2) was performed on specimens from 527 ECs treated at our university hospital from 2003 to 2018. methylation analysis was added to cases with MLH1/PMS2 loss. ECs were classified as follows: cases that retained MMR proteins as “MMR-proficient;” cases with MLH1/PMS2 loss and -PHM as “met-EC;” and cases with other MMR protein loss and MLH1/PMS2 loss without -PHM as “suspected-LS.” The clinical features, including long-term prognosis, of each group, were analyzed. Results: Accordingly, 419 (79.5%), 65 (12.3%), and 43 (8.2%) cases were categorized as “MMR-proficient,” “suspected-LS,” and “met-EC,” respectively. Significantly, “met-EC” had a lower proportion of grade 1 tumors (37.5%) and a higher proportion of stage III/IV tumors (37.2%) than the other groups. The overall and progression-free survival of “met-EC” were significantly worse than those of “suspected-LS” in all cases. Conclusion: In ECs with MMR-D, “met-ECs” were a subgroup with a poorer prognosis than “suspected-LS.” “Met-ECs” would be the main target for anti-PD-1 antibody treatment, and its clinical susceptibility should be verified individually.
Ishikawa, Taro,Kaneko, Masahiro,Shin, Hee-Sup,Takahashi, Tomoyuki Wiley (The Physiological Society) 2005 The Journal of physiology Vol.568 No.1
<P>At the nerve terminal, both N- and P/Q-type Ca2+ channels mediate synaptic transmission, with their relative contribution varying between synapses and with postnatal age. To clarify functional significance of different presynaptic Ca2+ channel subtypes, we recorded N-type and P/Q-type Ca2+ currents directly from calyces of Held nerve terminals in alpha1A-subunit-deficient mice and wild-type (WT) mice, respectively. The most prominent feature of P/Q-type Ca2+ currents was activity-dependent facilitation, which was absent for N-type Ca2+ currents. EPSCs mediated by P/Q-type Ca2+ currents showed less depression during high-frequency stimulation compared with those mediated by N-type Ca2+ currents. In addition, the maximal inhibition by the GABAB receptor agonist baclofen was greater for EPSCs mediated by N-type channels than for those mediated by P/Q-type channels. These results suggest that the developmental switch of presynaptic Ca2+ channels from N- to P/Q-type may serve to increase synaptic efficacy at high frequencies of activity, securing high-fidelity synaptic transmission.</P>
Keizo Kato,Kazuki Takahashi,Keisuke Suzuki,Takayuki Sato,Kazunari Shinbo,Futao Kaneko,Hidehiko Shimizu,Nozomu Tsuboi,Toyoyasu Tadokoro,Shinichi Ohta 한국물리학회 2005 Current Applied Physics Vol.5 No.4
Organic light emitting diodes (OLEDs) with nanostructured ultrathin layers inserted at the interface between electron- and hole-transport layers were investigated. The fundamental structure of the OLEDs fabricated by a vacuum evaporation method wasindium-tin-oxide (ITO) anode/copper phthalocyanine (CuPc)/N,N0-diphenyl-N,N0-bis(3-methylphenyl)-1,10-diphenyl-4,40-diamine(TPD)/8-hydroxyquinoline aluminum (Alq3)/LiF/Al cathode. Fullerene (C60) and rhodamine B (RhB) molecules were used as thenanosutructured ultrathin layers inserted at the interface between the Alq3 and TPD layers. The electroluminescent (EL) propertieshave been measured for the OLEDs with C60 and RhB ultrathin layers and the dependences on the thickness and the position of theinserted layers were examined. For the OLEDs with the C60 ultrathin layer, the improvements of the drive voltage and EL eciencywere observed. The OLED with the inserted C60 ultrathin lm of a monolayer thickness showed the highest eciency, which wastwice as large as that without C60 layer. On the contrary, the improvements were not observed for the OLEDs with the RhB ul-trathin layer..