Narrow band imaging accentuates differences in contrast between cartilage and perichondrium in the elevation of the muco-perichondrium flap during septoplasty and open septorhinoplasty

鼻中隔矯正術において区別が難しい軟骨と軟骨膜を白色光（White light; WL）と狭帯域光観察（Narrow band imaging; NBI）で観察した．軟骨と軟骨膜の間の輝度の差はWLよりNBIで有意に大きかった．得られた画像を赤・緑・青に分光すると，赤では有意に輝度の差がみられた．以上からNBIを用いると軟骨と軟骨膜の間のコントラストが強調されることが示された．また，このコントラストの強調はNBIの赤色の処理によることが示された

A hydroxypropyl methylcellulose plaque assay for human respiratory syncytial virus

ウイルスの研究において感染性のあるウイルス粒子を正確に定量することは，病原性の評価のみならずウイルスに対する新規治療薬の効果を客観的に評価するために極めて重要な手技である．プラークアッセイ法はウイルス粒子を定量するために不可欠な技術であるが，Respiratory syncytial virus（RSV）において，プラークアッセイ法を安定して行うことはしばしば困難である．今回我々は，overlay material（充填化合物）が細胞増殖に与える影響を中心にRSVおよびhuman metapneumovirus（hMPV）におけるプラークアッセイ法の最適化の検討を行った

The Effects of Utilizing Cartilage Conduction Hearing Aids among Patients with Conductive Hearing Loss

The cartilage-conduction hearing aid (CC-HA) is a new hearing device that is suitable for use in patients with conductive hearing loss. It has been 5 years since the introduction of the CC-HA. Although the number of users has increased, the CC-HA is not yet widely known. This study examines the effects of CC-HA on patients with conductive hearing loss and investigates factors that affect the willingness to use the device by comparing purchasers and non-purchasers of CC-HA in patients with unilateral conductive hearing loss. Eight patients had bilateral conductive hearing loss, and 35 had unilateral conductive hearing loss. Each patient underwent sound field tests and speech audiometry, and the effects of the CC-HA were compared with those of conventional bone conduction hearing aids (BC-HA). In patients with bilateral conductive hearing loss, the CC-HA was non-inferior to BC-HA. The CC-HA improved the hearing thresholds and speech recognition in patients with unilateral conductive hearing loss. Moreover, in patients with unilateral conductive hearing loss, experiencing the effect of wearing the CC-HA under conditions such as putting noise in the better ear could affect patients’ willingness to use the CC-HA

Effects of HMGB1 on Tricellular Tight Junctions via TGF-β Signaling in Human Nasal Epithelial Cells

様々な組織の炎症性疾患と密接な関係があるHigh mobility group box-1（HMGB1）は，主に核内に局在して転写の制御を行うとともに，細胞死や炎症性の刺激によって細胞外に放出され細胞障害性のシグナルを誘導するとされている．アレルギー性鼻炎や慢性副鼻腔炎の病態においてHMGB1が密接な関連があり，今回われわれはHMGB1 がTGF-βシグナリングを介して3細胞間接着分子であるangulin-1/LSRの発現を低下させることでバリア機能を低下させることを明らかとした

Histone deacetylase inhibition prevents cell death induced by loss of tricellular tight junction proteins in temperature-sensitive mouse cochlear cells

<div><p>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.</p></div

Trichostatin A (TSA) and histone deacetylase 6 inhibitor (iHDAC6) treatment induced LSR, TRIC, and acetylated-tubulin (Ac-tubulin) expression in differentiated cochlear cells.

<p>(A) Immunocytochemical staining for LSR, TRIC, and Ac-tubulin after TSA and iHDAC6 treatment. Scale bar: 20 μm. (B) Scanning electron microscopy (SEM) of differentiated cochlear cells after treatment with TSA and iHDAC6. Arrow heads indicate the sealing elements between two adjacent cells. Scale bars: 20 μm.</p

Histone deacetylase inhibition prevents cell death induced by loss of tricellular tight junction proteins in temperature-sensitive mouse cochlear cells - Fig 3

<p>(A) Western blotting for TRIC, LSR, HDAC1, HDAC6, and Ac-tubulin in differentiated cochlear cells after treatment with 0.1 or 1 μM TSA and 0.1 or 1 μM iHDAC6. (B) RT-PCR for LSR and TRIC after treatment with 0.1 or 1 μM TSA and 0.1 or 1 μM iHDAC6. (C) Western blotting for LSR, TRIC, acetylated lysine (Ac-Lysine), Ac-tubulin, α-tubulin, β-tubulin in LSR, TRIC, or Ac-Lysine immunoprecipitates (IP) from cochlear cells treated with 1 μM TSA and 1 μM iHDAC6. (D) Transendothelial resistance (TER) analysis in cochlear cells treated with 1 μM TSA and 1 μM iHDAC6. *<i>P</i> < 0.05 and **<i>P</i> < 0.01 vs. control.</p

ZO-1 expression was unchanged following treatment with TSA and iHDAC6.

<p>(A) Immunocytochemical staining for ZO-1, LSR, TRIC, and Ac-tubulin in differentiated cochlear cells after TSA and iHDAC6 treatment. Scale bar: 20 μm. (B) Double-immunocytochemistry for ZO-1 and LSR in differentiated hair cells after TSA. Scale bar: 20 μm. (C) Western blotting for ZO-1 after treatment with 0.1 or 1 μM TSA and 0.1 or 1 μM iHDAC6.</p