記述言語：日本語   出版者・発行元：一般社団法人 日本聴覚医学会  

DOI： 10.4295/audiology.65.443

CiNii Research

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記述言語：日本語   出版者・発行元：日本耳鼻咽喉科免疫アレルギー感染症学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Quantifying proliferative virus particles is one of the most important experimental procedures in virology. Compared with classical overlay materials, newly developed cellulose derivatives enable a plaque-forming assay to produce countable clear plaques easily. HEp-2 cells are widely used in plaque assays for human respiratory syncytial virus (RSV). It is crucial to use an overlay material to keep HEp-2 cell proliferation and prevent RSV particles from spreading over the fluid. Among four cellulose derivatives, carboxymethyl cellulose sodium salt (CMC), hydroxypropyl methylcellulose (HPMC), microcrystalline cellulose (MCC), and hydroxyethyl cellulose (HEC), we found that HPMC was the optimal overlay material because HPMC maintained HEp-2 cell proliferation and RSV infectivity. Although MCC was unsuitable for RSV, it assisted the plaque-forming by human metapneumovirus in TMPRSS2-expressing cells. Therefore, depending on the cells and viruses, it is necessary to use different overlay materials at varying concentrations.

DOI： 10.1016/j.jviromet.2022.114528

PubMed

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記述言語：日本語   出版者・発行元：日本耳鼻咽喉科免疫アレルギー感染症学会  

医中誌

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記述言語：日本語   出版者・発行元：(有)科学評論社  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本聴覚医学会  

その他リンク： https://search-tp.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2021&ichushi_jid=J00125&link_issn=&doc_id=20211001350123&doc_link_id=%2Fdm7audio%2F2021%2F006405%2F124%2F0467-0467%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fdm7audio%2F2021%2F006405%2F124%2F0467-0467%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：MDPI AG  

The airway epithelium of the human nasal mucosa acts as a physical barrier that protects against inhaled substances and pathogens via bicellular and tricellular tight junctions (bTJs and tTJs) including claudins, angulin-1/LSR and tricellulin. High mobility group box-1 (HMGB1) increased by TGF-β1 is involved in the induction of nasal inflammation and injury in patients with allergic rhinitis, chronic rhinosinusitis, and eosinophilic chronic rhinosinusitis. However, the detailed mechanisms by which this occurs remain unknown. In the present study, to investigate how HMGB1 affects the barrier of normal human nasal epithelial cells, 2D and 2.5D Matrigel culture of primary cultured human nasal epithelial cells were pretreated with TGF-β type I receptor kinase inhibitor EW-7197 before treatment with HMGB1. Knockdown of angulin-1/LSR downregulated the epithelial barrier. Treatment with EW-7197 decreased angulin-1/LSR and concentrated the expression at tTJs from bTJs and increased the epithelial barrier. Treatment with a binder to angulin-1/LSR angubindin-1 decreased angulin-1/LSR and the epithelial barrier. Treatment with HMGB1 decreased angulin-1/LSR and the epithelial barrier. In 2.5D Matrigel culture, treatment with HMGB1 induced permeability of FITC-dextran (FD-4) into the lumen. Pretreatment with EW-7197 prevented the effects of HMGB1. HMGB1 disrupted the angulin-1/LSR-dependent epithelial permeability barriers of HNECs via TGF-β signaling in HNECs.

DOI： 10.3390/ijms22168390

PubMed

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記述言語：日本語   出版者・発行元：日本耳鼻咽喉科免疫アレルギー感染症学会  

医中誌

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記述言語：日本語   出版者・発行元：日本耳鼻咽喉科免疫アレルギー感染症学会  

医中誌

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記述言語：日本語   出版者・発行元：日本耳鼻咽喉科免疫アレルギー感染症学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本耳鼻咽喉科頭頸部外科学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

In human head and neck squamous cell carcinoma (HNSCC), the invasion and metastatic properties of cancer cells are promoted by junctional adhesion molecule‑A (JAM‑A) and claudin‑1; these are epithelial tight junction molecules regulated by histone deacetylases (HDACs) and transcription factor p63. HDAC expression is reportedly upregulated in HNSCC, and HDAC inhibitors suppress cancer cell proliferation by initiating proliferative arrest or apoptosis. However, little is known of the anti‑cancer mechanisms of HDAC inhibitors in HNSCC. Thus, in the present study, the HNSCC Detroit 562 cell line and primary cultured HNSCC cells were treated with HDAC inhibitors to investigate their effects in HNSCC. Higher expression of p63, HDAC1, JAM‑A and claudin‑1 was observed in HNSCC tissues compared with the adjacent dysplastic regions. In Detroit 562 cells, treatment with trichostatin A (TSA), an inhibitor of HDAC1 and 6, downregulated the expression of p63, JAM‑A and claudin‑1, and upregulated that of acetylated tubulin; conversely, p63 knockdown resulted in the downregulation of JAM‑A and claudin‑1. Collectively, inhibiting HDAC suppressed the migration and invasiveness of cancer cells. In addition, treatment with TSA suppressed cancer cell proliferation via G2/M arrest, as well as upregulating p21 and downregulating cyclin D1 expression. TSA also downregulated the expression of epidermal growth factor receptor (EGFR) and phospho‑ERK1/2. p63 knockdown and treatment with an EGFR inhibitor induced G1 arrest and downregulated EGFR and phospho‑ERK1/2 levels, respectively. HDAC inhibition also suppressed the migration and invasiveness of primary cultured HNSCC cells. Collectively, the results of the present study indicate that HDAC inhibitors suppress the proliferation, migration and invasiveness of HNSCC by downregulating the p63‑mediated tight junction molecules JAM‑A and claudin‑1, and inducing p63 or p21‑mediated growth arrest.

DOI： 10.3892/or.2021.7997

PubMed

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記述言語：日本語   出版者・発行元：(一社)日本耳鼻咽喉科頭頸部外科学会  

医中誌

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記述言語：日本語   出版者・発行元：日本耳鼻咽喉科免疫アレルギー学会  

医中誌

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記述言語：日本語   出版者・発行元：日本耳鼻咽喉科免疫アレルギー学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本聴覚医学会  

その他リンク： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2020&ichushi_jid=J00125&link_issn=&doc_id=20200917530031&doc_link_id=10.4295%2Faudiology.63.326&url=https%3A%2F%2Fdoi.org%2F10.4295%2Faudiology.63.326&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本聴覚医学会  

その他リンク： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2020&ichushi_jid=J00125&link_issn=&doc_id=20200917530133&doc_link_id=10.4295%2Faudiology.63.428&url=https%3A%2F%2Fdoi.org%2F10.4295%2Faudiology.63.428&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

医中誌

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記述言語：日本語   出版者・発行元：(NPO)日本頭頸部外科学会  

その他リンク： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2020&ichushi_jid=J04210&link_issn=&doc_id=20200720160007&doc_link_id=10.5106%2Fjjshns.30.35&url=https%3A%2F%2Fdoi.org%2F10.5106%2Fjjshns.30.35&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

医中誌

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記述言語：英語  

TNF receptor II is expressed on ILC2s and TNF is able to induce production of type 2 cytokines in human ILC2s. TNF may play a role in causing or amplifying type 2 immunity contributing to health and disease.

DOI： 10.1016/j.jaci.2019.09.001

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Chronic rhinosinusitis with nasal polyps (CRSwNP) is characterized by type 2 inflammation with accumulation of activated group 2 innate lymphoid cells (ILC2s) and elevation of thymic stromal lymphopoietin (TSLP). A member of the TNF superfamily (TNFSF), TNFSF15, is known to induce the production of type 2 cytokines in ILC2s. Although ILC2s have been implicated in CRSwNP, the presence and role of TNFSFs in ILC2-mediated type 2 inflammation in CRSwNP has not been elucidated. Here, we investigate the involvement of TNFSFs in ILC2-mediated type 2 inflammation in CRSwNP. We found that receptor activator of NF-κB (RANK) ligand (RANK-L (TNFSF11)) was significantly elevated in nasal polyps (NPs), and that the receptor of RANK-L, RANK, was expressed on ILC2s in human peripheral blood and NPs. An agonistic antibody against RANK induced production of type 2 cytokines in human ILC2s, and TSLP significantly enhanced this reaction. The membrane-bound RANK-L was detected mainly on CD45 + immune cells, including TH2 cells in NPs. The co-culture of NP-derived ILC2s and TH2 cells significantly enhanced production of type 2 cytokines, and anti-RANK-L monoclonal antibody suppressed this enhancement. In conclusion, RANK-L, together with TSLP, may play an inductive role in the ILC2-mediated type 2 inflammation in CRSwNP.

DOI： 10.1038/s41385-019-0215-8

PubMed

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記述言語：日本語   出版者・発行元：(一社)日本聴覚医学会  

その他リンク： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2019&ichushi_jid=J00125&link_issn=&doc_id=20191015460045&doc_link_id=10.4295%2Faudiology.62.392&url=https%3A%2F%2Fdoi.org%2F10.4295%2Faudiology.62.392&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本聴覚医学会  

その他リンク： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2019&ichushi_jid=J00125&link_issn=&doc_id=20191015460157&doc_link_id=10.4295%2Faudiology.62.504&url=https%3A%2F%2Fdoi.org%2F10.4295%2Faudiology.62.504&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本聴覚医学会  

その他リンク： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2019&ichushi_jid=J00125&link_issn=&doc_id=20191015460202&doc_link_id=10.4295%2Faudiology.62.549&url=https%3A%2F%2Fdoi.org%2F10.4295%2Faudiology.62.549&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Rho-kinase inhibitor Y27632, which is a factor in conditional reprogramming culture, induces airway progenitor clone formation. To investigate whether Y27632 enhances airway progenitor cells in nasal epithelium, primary cultures of HNECs transfected with human telomerase reverse transcriptase (hTERT-HNECs) were treated with Y27632. In TERT-HNECs treated with Y27632 for 5 days, upregulation of p63, gap junction molecules Cx26, Cx30, Cx43, cytochrome P450 enzymes CYP2C9, CYP2C18, CYP39A1, CYP4B1, CYP2G1P, CYP4Z1, and KLF families KLF10 and KLF11 were observed compared to the control. Downregulation of tight junction molecules claudin-4, -7, and -23 was observed. Circumfential submembrane F-actin was also induced. The functions of gap junctional intercellular communication (GJIC) and the epithelial barrier were upregulated. Knockdown of p63 by siRNAs of TAp63 or ΔNp63 inhibited Cx26, Cx43 and CYP2C18, and induced claudin-1, and -4. Knockdown of KLF11 prevented p63 expression and enhancement of the epithelial barrier function by Y27632. In nasal mucosal tissues from patients with allergic rhinitis (AR), localized alteration of p63, KLF11, RhoA, Cx30 and claudin-4 was observed. Treatment with Y27632 in long-term culture induced airway progenitor cells via KLF11 in p63-positive human nasal epithelium. Airway progenitor cells of nasal epithelium induced by Y27632 is important in understanding upper airway disease-specific characteristics.

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Guanylate-binding protein-1 (GBP-1) is an interferon-inducible large GTPase involved in the epithelial barrier at tight junctions. To investigate the role of GBP-1 in the epithelial barrier, primary human salivary gland duct epithelial cells were treated with the the proinflammatory cytokines IFNγ, IL-1β, TNFα and the growth factor TGF-β. Treatment with IFNγ, IL-1β, or TNFα markedly enhanced GBP-1 and the epithelial barrier function, and induced not only CLDN-7 but also the tricellular tight junction molecule lipolysis-stimulated lipoprotein receptor (LSR). Knockdown of GBP-1 by its siRNA induced endocytosis of tight junction molecules, and prevented the increases of CLDN-7 and LSR with the upregulation of the epithelial barrier function induced by treatment with IFNγ or TNFα. Treatment with a PKCα inhibitor induced expression of GBP-1, CLDN-7 and LSR and enhanced the epithelial barrier function. In almost intact salivary gland ducts from patients with IgG4-related disease (IgG4-RD) indicated significant infiltration of IgG-positive plasma cells, expression of GBP-1, CLDN-7 and LSR was increased. These findings indicated that GBP-1 might play a crucial role in barrier function of normal human salivary gland duct epithelium and perform a preventive role in the duct epithelium of IgG4-RD disease.

DOI： 10.1016/j.yexcr.2018.07.033

PubMed

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記述言語：日本語   出版者・発行元：(一社)日本耳鼻咽喉科学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

The plaque-forming assay is the standard technique for determining viral titer, and a critical measurement for investigating viral replication. However, this assay is highly dependent on experimental technique and conditions. In the case of human respiratory syncytial virus (RSV) in particular, it can be difficult to objectively confirm the accuracy of plaque-forming assay because the plaques made by RSV are often small and unclear. In recent studies, RT-qPCR methods have emerged as a supportive procedure for assessment of viral titer, yielding highly sensitive and reproducible results. In this report, we compare the viral replication, as determined by plaque-forming assay, and the copy numbers of RSV genes NS1, NS2, N, and F, as determined by RT-qPCR. Two real-time PCR systems, SYBR Green and TaqMan probe, gave highly similar results for measurement of copy numbers of RSV N genes of virus subgroups A. We determined the RSV gene copy numbers in the culture cell supernatant and cell lysate measured at various multiplicities of infection. We found that copy number of the RSV N gene in the culture supernatant and cell lysate was highly correlated with plaque-forming units. In conclusion, RT-qPCR measurement of RSV gene copy number was highly dependent on viral titer, and the detailed comparison between each gene copy number and virus titer should be useful and supportive in confirming RSV plaque-forming assay and virus dynamics. The technique may also be used to estimate the amount of RSV present in clinical specimens.

DOI： 10.1111/1348-0421.12563

PubMed

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記述言語：日本語   出版者・発行元：(株)東京医学社  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.4049/jimmunol.1601507

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

P63 is a regulator of cell-cell junction complexes in the epidermis. Claudin-4 is regulated via various factors in normal epithelial cells and diseases. We found that claudin-4 was directly regulated via p63 (TAp63 and ΔNp63) in human keratinocytes and nasal epithelial cells. In the epidermis of atopic dermatitis (AD), which contains ΔNp63-deficient keratinocytes, high expression of claudin-4 was observed. In primary keratinocytes, downregulation of ΔNp63 by treatment with short interfering RNA (siRNA)-p63 induced claudin-4 expression. In nasal epithelial cells in the context of rhinitis or nasal polyps, upregulation of TAp63 and downregulation of claudin-4 were observed. In primary nasal epithelial cells transfected with the human telomerase reverse transcriptase gene, knockdown of p63 by siRNAs induced claudin-4 expression. Taken together, these findings indicate that p63 is a negative regulator of claudin-4 expression. Understanding the regulation of claudin-4 via p63 in human epithelial cells may be important for developing therapies for allergies and drug delivery systems.

DOI： 10.1111/nyas.13456

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Disruption of nasal epithelial tight junctions (TJs) and ciliary dysfunction are found in patients with chronic rhinosinusitis (CRS) and nasal polyps (NPs), along with an increase of p63-positive basal cells and histone deacetylase (HDAC) activity. To investigate these mechanisms, primary cultures of HNECs transfected with human telomerase reverse transcriptase (hTERT-HNECs) were transfected with siRNAs of TAp63 and ΔNp63, treated with the NF-kB inhibitor curucumin and inhibitors of HDACs, and infected with respiratory syncytial virus (RSV). In TERT-HNECs, knockdown of p63 by siRNAs of TAp63 and ΔNp63, induced claudin-1 and -4 with Sp1 activity and enhanced barrier and fence functions. The knockdown of p63 enhanced the number of microvilli with the presence of cilia-like structures. Treatment with curcumin and inhibitors of HDACs, or infection with RSV prevented expression of p63 with an increase of claudin-4 and the number of microvilli. The knockdown or downregulation of p63 inhibited phospho-p38MAPK, and the p38MAPK inhibitor downregulated p63 and upregulated the barrier function. Thus, epithelial barrier and ciliogenesis of nasal epithelium are regulated in a p63-negative manner in normal and upper airway diseases. Understanding of the regulation of p63/p38 MAPK/NF-κB may be important in the therapy for airway allergy and its drug delivery system.

DOI： 10.1038/s41598-017-11481-w

PubMed

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記述言語：日本語   出版者・発行元：(一社)日本鼻科学会  

医中誌

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記述言語：日本語   出版者・発行元：日本耳鼻咽喉科感染症・エアロゾル学会  

医中誌

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記述言語：日本語   出版者・発行元：日本耳鼻咽喉科免疫アレルギー学会  

医中誌

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記述言語：日本語   出版者・発行元：日本耳鼻咽喉科免疫アレルギー学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

CONCLUSION: This is the first report to investigate the correlation between ear anomalies related to the development of specific ear structures and chorda tympani dysfunction (CTD) in congenital microtia. CTD is not always consistent with the severity of the ear anomaly or the presence of facial nerve paralysis (FNP). OBJECTIVES: To investigate the relationship between the severity of ear anomalies and CTD as well as FNP in congenital microtia. METHODS: A retrospective assessment was performed for all patients with microtia over the period 2010-2016. All ears were graded based on the severity of ear deformity using the Jahrsdoerfer system, based on findings on computed tomography of the temporal bone. Electrogustometry (EGM) was performed to evaluate CTD. RESULTS: The group included 110 male and 62 female patients. The right ear was the most commonly affected (right 106, left 47). Eighteen patients (10.5%) had abnormal EGM thresholds. The mean (± SD) Jahrsdoerfer scores in the without CTD and positive for CTD groups were 6.53 ± 0.32 and 7.06 ± 0.37, respectively. In terms of sub-total points, there was no significant correlation between anatomic structure and CTD. There was no significant correlation between CTD and the presence of FNP.

DOI： 10.1080/00016489.2016.1278306

PubMed

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記述言語：日本語   出版者・発行元：(株)医学書院  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本耳鼻咽喉科学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本病理学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Macrolide antibiotics have immunomodulatory activities, including suppression of cytokine production, cell adhesion molecule expression, and mucin production. These immunomodulatory activities improve the symptoms of respiratory diseases associated with chronic inflammation. However, the underlying molecular mechanism(s) is not well understood yet. To address this, we prepared clarithromycin (CAM)-conjugated Sepharose and examined bound cellular proteins by proteome analysis. We identified mitochondrial proteins 4-nitrophenylphosphatase domain and non-neuronal synaptosomal associated protein 25-like protein homolog (NIP-SNAP)-1 and -2 and very long-chain acyl-CoA dehydrogenase (VLCAD) as CAM-binding proteins. Production of proinflammatory cytokines (IL-8 and IL-6) induced by lipopolysaccharides (LPSs) and Pam3-CSK4 in human epithelial cell lines BEAS-2B and T24 were suppressed by knockdown of NIP-SNAP-1 or -2, and partly by knockdown of VLCAD. Also, knockdown of NIP-SNAP-1 or -2 in various cell lines suppressed LPS-induced expression of IL-8 and IL-6 mRNA and NF-κB activity. Thus, CAM suppresses NF-κB-mediated proinflammatory cytokine production by interacting with mitochondrial proteins, NIP-SNAP-1 and -2.

DOI： 10.1016/j.bbrc.2016.12.100

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

NIP-SNAP-1 and -2 are ubiquitous proteins thought to be associated with maintenance of mitochondrial function, neuronal transmission, and autophagy. However, their physiological functions remain largely unknown. To elucidate their functional importance, we screened for proteins that interact with NIP-SNAP-1 and -2, resulting in identification of HSP60 and P62/SQSTM1 as binding proteins. NIP-SNAP-1 and -2 localized in the mitochondrial inner membrane space, whereas HSP60 localized in the matrix. Native gel electrophoresis and filter trap assays revealed that human HSP60 prevented aggregation of newly synthesized NIP-SNAP-2 in an in vitro translation system. Moreover, expression levels of NIP-SNAP-1 and -2 in cells were decreased by knockdown of HSP60, but not HSP10. These findings indicate that HSP60 promotes folding and maintains the stability of NIP-SNAP-1 and -2.

DOI： 10.1016/j.bbrc.2016.12.133

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.anl.2016.05.011

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Lipid mediators such as leukotrienes and lipoxines broadly regulate innate and acquired immunity, and their dysfunction causes various immune-mediated disorders. We previously reported a salient feature of arachidonate 5-lipoxyganase (Alox5), which is responsible for the production of such lipid mediators, in the regulation of high affinity antibodies in vivo. The aim of this study was to determine the functional significance of Alox5-related lipid mediators during the processes of acquired humoral responses. The results of in vitro experiments using lymphocytes in tonsils and blood specimens showed that lipoxin A4 (LXA4) and leukotriene B4 (LTB4) have the capacity to differentiate naïve CD4+ T cells into T follicular helper (Tfh) cells, which activate naïve B cells to form germinal centers. Such a function of LXA4 was further supported by results of in vitro studies using BML-111 and BOC-2, which are an agonist and an antagonist, respectively, of FPR2 of an LXA4-specific cell-surface receptor. The results suggest that such lipid mediators have a potential role in the development of lymphoid follicles through the regulation of Tfh cell differentiation.

DOI： 10.1016/j.imlet.2016.11.006

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1038/srep37049

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Tricellular tight junctions (tTJs) are specialized structures that occur where the corners of three cells meet to seal adjacent intercellular space. The molecular components of tTJs include tricellulin (TRIC) and lipolysis-stimulated lipoprotein receptor (LSR) which recruits TRIC, are required for normal hearing. Although loss of TRIC causes hearing loss with degeneration of cochlear cells, the detailed mechanisms remains unclear. In the present study, by using temperature-sensitive mouse cochlear cells, US/VOT-E36 cell line, we investigated the changes of TRIC and LSR during cochlear cell differentiation and the effects of histone deacetylase (HDAC) inhibitors against cell degeneration induced by loss of TRIC and LSR. During cell differentiation induced by the temperature change, expression of TRIC and LSR were clearly induced. Treatment with metformin enhanced expression TRIC and LSR via AMPK during cell differentiation. Loss of TRIC and LSR by the siRNAs induced cell death in differentiated cells. Treatment with HDAC inhibitors trichostatin A and HDAC6 inhibitor prevented the cell death induced by loss of TRIC and LSR. Collectively, these findings suggest that both tTJ proteins TRIC and LSR have crucial roles for the differentiated cochlear cell survival, and that HDAC inhibitors may be potential therapeutic agents to prevent hearing loss.

DOI： 10.1371/journal.pone.0182291

PubMed

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記述言語：日本語   掲載種別：研究論文（学術雑誌）  

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.21873/anticanres.11176

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.3109/10717544.2015.1050530

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.phrs.2016.07.033

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1097/MAO.0000000000001048

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

OBJECTIVE: Patients with multiple sensory deficits, including hearing loss and visual impairment, present a unique problem. We evaluated the clinical outcomes of cochlear implantation in patients with severe to profound sensorineural hearing loss and visual impairment. METHODS: We retrospectively reviewed eight patients with severe sensorineural hearing loss and visual impairment who underwent cochlear implantation at our institution between 1993 and 2014. The follow-up period was between 2 and 20 years. We evaluated the case histories, etiologies of hearing loss and visual impairment, pre- and postoperative pure-tone thresholds, speech perception rates after CI using the Japanese CD speech discrimination scoring system (CI-2004 test) for words and sentences, and pre- and postoperative communication means. Postoperative speech discrimination scores were compared between patients with and without visual impairment who underwent cochlear implantation. RESULTS: The outcomes of cochlear implantation were good in all patients, with seven showing the ability to hold a conversation with others. The average proportion of correct answers for words and sentences in the CI-2004 test was 72.3 ± 19.1% and 86.0 ± 16.1%, respectively, for the patients with visual impairment and 62.1 ± 21.7% and 78.5 ± 20.9%, respectively, for those without visual impairment (based on auditory senses only). There were no significant differences in results between the patients with and without visual impairment. CONCLUSIONS: Cochlear implantation is important for the rehabilitation of patients with severe auditory loss and visual impairment. Medical staff members require additional skills to perform auditory evaluations and rehabilitate patients with multiple sensory deficits.

DOI： 10.1016/j.anl.2015.08.005

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1002/eji.201545499

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.18632/oncotarget.8432

PubMed

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記述言語：日本語   出版者・発行元：(一社)日本細胞生物学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本細胞生物学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Medquest Communications LLC  

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

The human noggin (NOG) gene is responsible for a broad spectrum of clinical manifestations of NOG-related symphalangism spectrum disorder (NOG-SSD), which include proximal symphalangism, multiple synostoses, stapes ankylosis with broad thumbs (SABTT), tarsal-carpal coalition syndrome, and brachydactyly type B2. Some of these disorders exhibit phenotypes associated with congenital stapes ankylosis. In the present study, we describe a Japanese pedigree with dactylosymphysis and conductive hearing loss due to congenital stapes ankylosis. The range of motion in her elbow joint was also restricted. The family showed multiple clinical features and was diagnosed with SABTT. Sanger sequencing analysis of the NOG gene in the family members revealed a novel heterozygous nonsense mutation (c.397A>T; p.K133*). In the family, the prevalence of dactylosymphysis and hyperopia was 100% while that of stapes ankylosis was less than 100%. Stapes surgery using a CO2 laser led to a significant improvement of the conductive hearing loss. This novel mutation expands our understanding of NOG-SSD from clinical and genetic perspectives.

DOI： 10.1038/hgv.2016.23

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

More than 20 years have passed since cochlear implantation (CI) was first introduced in Japan. We began CI at the Sapporo Medical University Hospital in 1988; since then, up to the first half of 2015, we have performed CI on 280 ears. In patients aged less than and those aged over 18 years, 121 and 159 ears, respectively, have undergone surgery. This report presents typical cases of CI, such as an adult case, a bilateral case, a case where both hearing and vision were impaired, a pediatric case, a case with multiple handicaps, a case with a genetic mutation leading to severe hearing loss, and a complicated case. In addition, complications with CI cases experienced during extended follow-up periods are also summarized.

DOI： 10.1159/000441858

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

Cochlear implantation (CI) has proven to be an effective treatment for severe bilateral sensorineural hearing loss (SNHL). Inner ear malformation is a rare anomaly and occurs in approximately 20% of cases with congenital SNHL. In cases with cochlear malformation, CI can be successfully performed in nearly all patients, the exceptions being those with complete labyrinthine and cochlear aplasia. It is important to evaluate the severity of inner ear deformity and other associated anomalies during the preimplantation radiological assessment in order to identify any complication that may potentially occur during the surgery and subsequent patient management.

DOI： 10.1159/000441859

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：S. Karger AG  

DOI： 10.1159/000441868

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：S. Karger AG  

DOI： 10.1159/000441861

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：S. Karger AG  

DOI： 10.1159/000441867

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：S. Karger AG  

DOI： 10.1159/000441881

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.ejphar.2015.04.031

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.clim.2015.02.016

PubMed

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記述言語：日本語   出版者・発行元：(一社)日本アレルギー学会  

医中誌

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記述言語：日本語   出版者・発行元：日本小児耳鼻咽喉科学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1007/s00232-015-9774-0

PubMed

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記述言語：日本語   出版者・発行元：顎顔面口腔育成研究会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本耳科学会  

その他リンク： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2015&ichushi_jid=J02471&link_issn=&doc_id=20150306240009&doc_link_id=10.11289%2Fotoljpn.25.51&url=https%3A%2F%2Fdoi.org%2F10.11289%2Fotoljpn.25.51&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_3.gif

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1016/j.amjoto.2014.02.011

PubMed

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記述言語：日本語   出版者・発行元：(一社)日本細胞生物学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1186/1465-9921-15-21

PubMed

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記述言語：英語  

DOI： 10.1155/2013/947072

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.3109/00016489.2011.562537

PubMed

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記述言語：英語  

DOI： 10.3109/00016489.2010.520022

PubMed

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記述言語：英語   掲載種別：研究論文（国際会議プロシーディングス）  

DOI： 10.1159/000324590

PubMed

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1007/s00418-009-0674-1

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1007/s00795-009-0470-y

PubMed

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記述言語：日本語   出版者・発行元：日本耳鼻咽喉科免疫アレルギー学会  

その他リンク： https://search.jamas.or.jp/default/link?pub_year=2009&ichushi_jid=J01987&link_issn=&doc_id=20091028360002&doc_link_id=%2Fch6menek%2F2009%2F002702%2F023%2F0082-0083%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fch6menek%2F2009%2F002702%2F023%2F0082-0083%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

医中誌

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記述言語：日本語   出版者・発行元：耳鼻咽喉科展望会  

医中誌

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記述言語：日本語   掲載種別：研究論文（学術雑誌）  

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記述言語：日本語   出版者・発行元：(一社)日本耳鼻咽喉科頭頸部外科学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本炎症・再生医学会  

医中誌

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1007/s10735-008-9162-5

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記述言語：英語   出版者・発行元：The Japanese Society of Inflammation and Regeneration  

Thymic stromal lymphopoietin (TSLP) is an interleukin 7-like cytokine that triggers dendritic cell (DC)-mediated T helper 2-type inflammatory responses and is considered to be a master switch for allergic inflammation such as that in asthma and atopic dermatitis. Furthermore, proinflammatory cytokines and Toll-like receptor ligands can induce TSLP production in human bronchial epithelial cells and human keratinocytes. We first found high expression of endogenous TSLP in the epithelium of allergic rhinitis with recruitment and infiltration of DCs. In culture, the TSLP production in human nasal epithelial cells was markedly and significantly increased by treatment with the proinflammatory cytokines interleukin 1β/tumor necrosis factor-α and a Toll-like receptor 2 ligand, P<SUB>3</SUB>CSK<SUB>4</SUB>. Since it is also thought that TSLP expression not only activates DCs but also affects the epithelial barrier in allergic rhinitis, we investigated the effects of TSLP on tight junctions of human nasal epithelial cells and DCs <I>in vitro</I>. Treatment with TSLP enhanced the barrier function of human nasal epithelial cells <I>in vitro</I> together with an increase of the tight junction proteins claudin-1,-4,-7, and occludin. Furthermore, TSLP could exclusively induce claudin-7 expression in mouse DC line XS52, which expressed tight junction molecules claudin-1,-3,-4,-6,-7,-8, occludin and tricellulin.<BR>These findings suggest that nasal epithelial-derived TSLP plays an important role in allergic rhinitis as well as asthma and atopic dermatitis and may control tight junctions of epithelial cells and DCs to preserve the epithelial barrier and promote direct sampling of antigens by DCs.

その他リンク： https://jlc.jst.go.jp/DN/JALC/00314785334?from=CiNii

DOI： 10.2492/inflammregen.28.160

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記述言語：日本語   出版者・発行元：一般社団法人 日本アレルギー学会  

DOI： 10.15036/arerugi.57.1396_2

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記述言語：日本語   出版者・発行元：(一社)日本細胞生物学会  

医中誌

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記述言語：日本語   出版者・発行元：耳鼻咽喉科臨床学会  

医中誌

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記述言語：日本語   出版者・発行元：耳鼻咽喉科臨床学会  

医中誌

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J-GLOBAL

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記述言語：日本語   出版者・発行元：日本耳鼻咽喉科感染症・エアロゾル学会  

その他リンク:： http://search.jamas.or.jp/link/ui/2016286725

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記述言語：日本語   出版者・発行元：(一社)日本鼻科学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本鼻科学会  

医中誌

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記述言語：日本語   出版者・発行元：(一社)日本細胞生物学会  

医中誌

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記述言語：日本語   掲載種別：記事・総説・解説・論説等（その他）  

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記述言語：日本語   出版者・発行元：日本小児耳鼻咽喉科学会  

DOI： 10.11374/shonijibi.34.360

医中誌

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記述言語：日本語   掲載種別：記事・総説・解説・論説等（その他）  

DOI： 10.11453/orltokyo.56.162

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DOI： 10.11374/shonijibi.34.239

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）  

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記述言語：英語   掲載種別：研究発表ペーパー・要旨（国際会議）  

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記述言語：日本語  

DOI： 10.11374/shonijibi.31.244

J-GLOBAL

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記述言語：日本語  

DOI： 10.11453/orltokyo.51.s32

J-GLOBAL

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記述言語：日本語   出版者・発行元：(株)北隆館  

医中誌

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記述言語：日本語   出版者・発行元：耳鼻咽喉科臨床学会  

71歳女。拍動性耳鳴と左聴力低下を主訴とした。左鼓膜に拍動性腫瘤を透見し、純音聴力検査では左中等度の混合性難聴を認めた。側頭骨CT検査では蝸牛岬角に接し左鼓室内に突出する軟部組織を認め、この軟部組織は内側へ走行し頸動脈管の水平部に連続していた。また、ツチ骨柄への接触を認め、中耳伝音系の障害が示唆され、拍動性耳鳴、伝音障害の原因と考えられた。さらに、左の頸動脈管垂直部は認められず、下鼓室神経小管の拡張がみられ、拡張した下鼓室神経小管から鼓室内の軟部組織へと連続している像を認めた。また、頭部造影MRI、MRA検査では左内頸動脈の外側への偏位を認め、左内頸動脈の走行異常が確認された。中耳腔内Aberrant internal carotid arteryと診断し、その発生起源を確認するため頸部造影3DT検査を施行した。右内頸動脈の正常な分岐点に対し、左の内頸動脈分岐部が高位であり、左内頸動脈の狭小化を認めた。このことから、先天的な血管の異常が発生起源と考えられた。現在、外来経過観察中である。

その他リンク:： https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2007&ichushi_jid=J00580&link_issn=&doc_id=20070731350007&doc_link_id=10.5631%2Fjibirin.100.643&url=https%3A%2F%2Fdoi.org%2F10.5631%2Fjibirin.100.643&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_2.gif

医中誌

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記述言語：日本語   出版者・発行元：耳鼻咽喉科臨床学会  

医中誌

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記述言語：日本語  

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記述言語：英語  

DOI： 10.1016/j.anl.2004.01.003

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J-GLOBAL

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