Details of a Researcher - OGASAWARA Noriko

Papers - OGASAWARA Noriko

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COVID-19における嗅裂閉鎖所見と嗅覚障害の検討

山本圭佑, 藤谷好弘, 山直也, 黒沼幸治, 小笠原徳子, 横田伸一, 高橋聡, 高野賢一

日本耳鼻咽喉科免疫アレルギー感染症学会誌 ( 日本耳鼻咽喉科免疫アレルギー感染症学会 ) 2 ( 2 ) 49 - 54 2022.06

A Hydroxypropyl Methylcellulose Plaque Assay for Human Respiratory Syncytial Virus.

Yuka Takumi-Tanimukai, Soh Yamamoto, Noriko Ogasawara, Sayaka Nakabayashi, Katsumi Mizuta, Keisuke Yamamoto, Ryo Miyata, Takuya Kakuki, Sumito Jitsukawa, Toyotaka Sato, Hiroyuki Tsutsumi, Takashi Kojima, Kenichi Takano, Shin-Ichi Yokota

Journal of virological methods 304 114528 - 114528 2022.03 [International journal]

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.

[ROLE OF GROUP 2 INNATE LYMPHOID CELLS IN ALLERGIC INFLAMMATION OF THE UPPER RESPIRATORY TRACT].

Noriko Ogasawara, Atsushi Kato

Arerugi = [Allergy] 71 ( 3 ) 195 - 199 2022 [Domestic journal]

Self-reported Smell and Taste Disorders in Patients With COVID-19: A Japanese Single-center Study.

Keisuke Yamamoto, Yoshihiro Fujiya, Koji Kuronuma, Noriko Ogasawara, Tsuyoshi Ohkuni, Shin-Ichi Yokota, Satoshi Takahashi, Kenichi Takano

In vivo (Athens, Greece) 36 ( 2 ) 918 - 924 2022 [International journal]

BACKGROUND/AIM: Smell and taste disorders are among the most common symptoms of COVID-19. However, the relationship between smell and taste disorders and systemic symptoms is not fully understood in Japan. PATIENTS AND METHODS: Questionnaires were mailed to 105 of 111 COVID-19 patients who were hospitalized at our hospital between March and July 2020 in Japan. RESULTS: A total of 74 patients (response rate: 70.5%) completed the survey. Of these, six patients (8.1%) presented with smell disorders only, 16 (21.6%) presented with taste disorders only, and 17 (23.0%) presented with both smell and taste disorders. The mean Visual Analog Scale for smell and taste was 0.5 and 20, respectively, at the time of the most severe symptoms. CONCLUSION: Among COVID-19 patients in Japan, smell and taste disorders are often followed by fever and may not be the first symptoms. Sense of smell is particularly impaired. These symptoms often improve, although they sometimes persist for a long time as sequelae.

Reduction of susceptibility to azoles and 5-fluorocytosine and growth acceleration in Candida albicans in glucosuria.

Yoshiki Hiyama, Toyotaka Sato, Satoshi Takahashi, Soh Yamamoto, Noriko Ogasawara, Naoya Masumori, Shin-Ichi Yokota

Diagnostic microbiology and infectious disease 102 ( 1 ) 115556 - 115556 2021.09 [International journal]

Diabetes mellitus is a chronic metabolic disease characterized by hyperglycemia and glucosuria, and is a risk factor for Candida infections. To reveal the potential effects of glucosuria on Candida spp., we investigated their growth and antifungal susceptibilities in normal human urine to which glucose was added. The viable cell numbers of Candida spp. were more than 10 fold higher in the urine added 3000 mg/dL glucose than in plain urine. In antifungal susceptibility, more than 80% of Candida albicans clinical isolates increased minimum inhibitory concentrations of azoles and 5-fluorocytosine with the addition of glucose, and exceeded their breakpoints. In most of the C. albicans clinical isolates, the mRNA expression of the azole resistance genes ERG11, CDR1, CDR2, and MDR1 in the presence of glucose in urine. These observations provide valuable information about the clinical course and therapeutic effects of azoles against C. albicans infections in patients with diabetes mellitus and hyperglucosuria.

A nationwide epidemiologic, clinical, genetic study of Usher syndrome in Japan

Hidekane Yoshimura, Shin ya Nishio, Yuichi Isaka, Toru Kurokawa, Shin ichi Usami, Katada Akihiro, Noriko Ogasawara, Tomoko Shintani, Yumiko Kobayashi, Hiroaki Sato, Seiji Kakehata, Daisuke Kikuchi, Tetsuo Ikezono, Kotaro Ishikawa, Kyoko Shirai, Masahiro Takahashi, Satoshi Iwasaki, Yasuhiro Arai, Hajime Sano, Mayuri Okami, Hiroshi Nakanishi, Tomoko Esaki, Michihiko Sone, Jun Nakayama, Takayuki Okano, Yumi Ota, Hiroshi Nishimura, Yasushi Naito, Yuko Kataoka, Akiko Sugaya, Yukihide Maeda, Shin Masuda, Kazuma Sugawara, Hiroshi Yamashita, Naoto Hato, Takashi Nakagawa, Akira Ganaha, Tetsuya Tono, Ikuyo Miyanohara, Mikio Suzuki

Acta Oto-Laryngologica 141 ( 9 ) 841 - 846 2021

Background: Usher syndrome (USH) typically leads to deaf-blindness, requiring the provision of extensive education and rehabilitation services. Therefore, investigating the prevalence is crucial to requests for proper government support for USH patients. Objective: The aim was to perform a nationwide epidemiologic survey of USH in Japan to estimate the prevalence of USH and reveal the relative frequency and characteristics of the three USH subtypes. Methods: To estimate the number of USH patients visiting hospitals over a 1-year period, 1,628 hospitals were randomly selected from all Departments of Otorhinolaryngology and Ophthalmology in Japan. Subsequently, we collected data regarding the clinical characteristics of each patient treated and the results of genetic testing, if performed. Results: We found that the prevalence of USH was at least 0.4 per 100,000 population. The frequency of clinical subtypes and causal genes for USH were consistent with previous reports. Also, we demonstrated the feasibility of genetic counseling for USH patients based on the results of genetic testing. Conclusion: USH is a rare disease, but requires social support due to the severity of symptoms. To minimize these issues, understanding the clinical characteristics and performing comprehensive genetic testing could allow early and accurate diagnosis as well as medical intervention.

The Prevalence and Clinical Characteristics of TECTA-Associated Autosomal Dominant Hearing Loss.

Rika Yasukawa, Hideaki Moteki, Shin-Ya Nishio, Kotaro Ishikawa, Satoko Abe, Yohei Honkura, Misako Hyogo, Ryota Mihashi, Tetsuo Ikezono, Tomoko Shintani, Noriko Ogasawara, Kyoko Shirai, Hiroshi Yoshihashi, Takashi Ishino, Koshi Otsuki, Tsukasa Ito, Kazuma Sugahara, Shin-Ichi Usami

Genes 10 ( 10 ) 2019.09 [Refereed] [International journal]

TECTA is well known as a causative gene for autosomal dominant mid-frequency hearing loss observed in various populations. In this study, we performed next-generation sequencing analysis of a large Japanese hearing loss cohort, including eight hundred and twelve (812) subjects from unrelated autosomal dominant hearing loss families, to estimate the prevalence and phenotype-genotype correlations in patients with TECTA mutations. The prevalence of TECTA mutations in Japanese autosomal dominant sensorineural hearing loss families was found to be 3.2%. With regard to the type of hearing loss, the patients with mutations in the nidogen-like domain or ZA domain of TECTA showed varied audiograms. However, most of the patients with mutations in the ZP domain showed mid-frequency hearing loss. The rate of hearing deterioration in TECTA-associated hearing loss patients and in the normal hearing Japanese control population were the same and regression lines for each group were parallel. We carried out haplotype analysis for four families which had one recurring missense variant, c.5597C>T (p.Thr1866Met). Our results revealed four different haplotypes, suggesting that this mutation occurred independently in each family. In conclusion, TECTA variants represent the second largest cause of autosomal dominant sensorineural hearing loss in Japan. The hearing loss progression observed in the patients with TECTA mutations might reflect presbycusis. The c.5597C>T mutation occurred in a mutational hot spot and is observed in many ethnic populations.

Cutting Edge: A Critical Role of Lesional T Follicular Helper Cells in the Pathogenesis of IgG4-Related Disease.

Ryuta Kamekura, Kenichi Takano, Motohisa Yamamoto, Koji Kawata, Katsunori Shigehara, Sumito Jitsukawa, Tomonori Nagaya, Fumie Ito, Akinori Sato, Noriko Ogasawara, Chieko Tsubomatsu, Hiroki Takahashi, Hiroshi Nakase, Tetsuo Himi, Shingo Ichimiya

Journal of immunology (Baltimore, Md. : 1950) ( AMER ASSOC IMMUNOLOGISTS ) 199 ( 8 ) 2624 - 2629 2017.10 [Refereed] [International journal]

IgG4-related disease (IgG4-RD) is a newly recognized systemic chronic fibroinflammatory disease. However, the pathogenesis of IgG4-RD remains unknown. To determine the pathophysiologic features of IgG4-RD, we examined T follicular helper (Tfh) cells in lesions and blood from patients with IgG4-RD. Patients with IgG4-related dacryoadenitis and sialadenitis (IgG4-DS) showed increased infiltration of Tfh cells highly expressing programmed death 1 and ICOS in submandibular glands. Tfh cells from IgG4-DS submandibular glands had higher expression of B cell lymphoma 6 and a greater capacity to help B cells produce IgG4 than did tonsillar Tfh cells. We also found that the percentage of programmed death 1hi circulating Tfh cells in IgG4-DS patients was higher than that in healthy volunteers and was well correlated with clinical parameters. Our findings indicate that anomalous Tfh cells in tissue lesions of IgG4-RD have features distinct from those in lymphoid counterparts or blood and potentially regulate local IgG4 production in IgG4-RD.

Regulation of claudin-4 via p63 in human epithelial cells.

Takashi Kojima, Takayuki Kohno, Terufumi Kubo, Yakuto Kaneko, Takuya Kakuki, Akito Kakiuchi, Makoto Kurose, Ken-Ichi Takano, Noriko Ogasawara, Kazufumi Obata, Kazuaki Nomura, Ryo Miyata, Takumi Konno, Shingo Ichimiya, Tetsuo Himi

Annals of the New York Academy of Sciences ( WILEY ) 1405 ( 1 ) 25 - 31 2017.10 [Refereed] [International journal]

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.

The role of transcriptional factor p63 in regulation of epithelial barrier and ciliogenesis of human nasal epithelial cells.

Yakuto Kaneko, Takayuki Kohno, Takuya Kakuki, Ken-Ichi Takano, Noriko Ogasawara, Ryo Miyata, Shin Kikuchi, Takumi Konno, Tsuyoshi Ohkuni, Ryoto Yajima, Akito Kakiuchi, Shin-Ichi Yokota, Tetsuo Himi, Takashi Kojima

Scientific reports ( NATURE PUBLISHING GROUP ) 7 ( 1 ) 10935 - 10935 2017.09 [Refereed] [International journal]

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.

Chorda tympani nerve dysfunction associated with congenital microtia.

Kenichi Takano, Nozomi Takahashi, Noriko Ogasawara, Takatoshi Yotsuyanagi, Tetsuo Himi

Acta oto-laryngologica ( TAYLOR & FRANCIS LTD ) 137 ( 7 ) 686 - 689 2017.07 [Refereed] [International journal]

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.

Tigecycline Nonsusceptibility Occurs Exclusively in Fluoroquinolone-Resistant Escherichia coli Clinical Isolates, Including the Major Multidrug-Resistant Lineages O25b:H4-ST131-H30R and O1-ST648.

Toyotaka Sato, Yuuki Suzuki, Tsukasa Shiraishi, Hiroyuki Honda, Masaaki Shinagawa, Soh Yamamoto, Noriko Ogasawara, Hiroki Takahashi, Satoshi Takahashi, Yutaka Tamura, Shin-Ichi Yokota

Antimicrobial agents and chemotherapy ( AMER SOC MICROBIOLOGY ) 61 ( 2 ) 2017.02 [Refereed] [International journal]

Tigecycline (TGC) is a last-line drug for multidrug-resistant Enterobacteriaceae We investigated the mechanism(s) underlying TGC nonsusceptibility (TGC resistant/intermediate) in Escherichia coli clinical isolates. The MIC of TGC was determined for 277 fluoroquinolone-susceptible isolates (ciprofloxacin [CIP] MIC, <0.125 mg/liter) and 194 fluoroquinolone-resistant isolates (CIP MIC, >2 mg/liter). The MIC50 and MIC90 for TGC in fluoroquinolone-resistant isolates were 2-fold higher than those in fluoroquinolone-susceptible isolates (MIC50, 0.5 mg/liter versus 0.25 mg/liter; MIC90, 1 mg/liter versus 0.5 mg/liter, respectively). Two fluoroquinolone-resistant isolates (O25b:H4-ST131-H30R and O125:H37-ST48) were TGC resistant (MICs of 4 and 16 mg/liter, respectively), and four other isolates of O25b:H4-ST131-H30R and an isolate of O1-ST648 showed an intermediate interpretation (MIC, 2 mg/liter). No TGC-resistant/intermediate strains were found among the fluoroquinolone-susceptible isolates. The TGC-resistant/intermediate isolates expressed higher levels of acrA and acrB and had lower intracellular TGC concentrations than susceptible isolates, and they possessed mutations in acrR and/or marR The MICs of acrAB-deficient mutants were markedly lower (0.25 mg/liter) than those of the parental strain. After continuous stepwise exposure to CIP in vitro, six of eight TGC-susceptible isolates had reduced TGC susceptibility. Two of them acquired TGC resistance (TGC MIC, 4 mg/liter) and exhibited expression of acrA and acrB and mutations in acrR and/or marR In conclusion, a population of fluoroquinolone-resistant E. coli isolates, including major extraintestinal pathogenic lineages O25b:H4-ST131-H30R and O1-ST648, showed reduced susceptibility to TGC due to overexpression of the efflux pump AcrAB-TolC, leading to decreased intracellular concentrations of the antibiotics that may be associated with the development of fluoroquinolone resistance.

HIV-associated cystic lesions of the parotid gland

Noriko Ogasawara, Ken-ichi Takano, Hajime Kobayashi, Keisuke Kikuchi, Hiroshi Matsumiya, Iwao Yoshioka, Tetsuo Himi

AURIS NASUS LARYNX ( ELSEVIER SCI LTD ) 44 ( 1 ) 126 - 130 2017.02 [Refereed]

We present two cases of an HIV-associated parotid gland cyst. One case was a 36-year-old HIV infected woman. She was diagnosed with HIV infection and presented with slowly enlarged parotid gland cysts together with elevation of HIV viral RNA copies/mL in her serum. She was performed parotid gland biopsy under the general anesthesia. The histopathologic analysis revealed negative HIV p24-antigen in her parotid gland tissue. The other case was a 43-year-old man found his parotid gland swelling shortly after highly active antiretroviral therapy (HAART). He was diagnosed with HIV infection 2 years previously. He had started HAART several days before. He showed exceeding elevation of IgE in his serum. We treated him with medication using anti-histamic drugs for his cyst. A computed tomography scan revealed a complete response of his parotid gland cyst 4 weeks after the medication. His serum IgE level was decreased to half of the level before the medication. These findings suggested that the parotid gland swelling associated with HIV was due to various factors including immune reconstitution inflammatory syndrome (IRIS). In case such a parotid gland swelling, we could avoid invasive treatments. (C)2016 Elsevier Ireland Ltd. All rights reserved.

Lipid mediators foster the differentiation of T follicular helper cells.

Tomonori Nagaya, Koji Kawata, Ryuta Kamekura, Sumito Jitsukawa, Terufumi Kubo, Motonari Kamei, Noriko Ogasawara, Ken-Ichi Takano, Tetsuo Himi, Shingo Ichimiya

Immunology letters ( ELSEVIER SCIENCE BV ) 181 51 - 57 2017.01 [Refereed] [International journal]

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.

Mechanism of Reduced Susceptibility to Fosfomycin in Escherichia coli Clinical Isolates.

Yasuo Ohkoshi, Toyotaka Sato, Yuuki Suzuki, Soh Yamamoto, Tsukasa Shiraishi, Noriko Ogasawara, Shin-Ichi Yokota

BioMed research international ( HINDAWI LTD ) 2017 5470241 - 5470241 2017 [Refereed] [International journal]

In recent years, multidrug resistance of Escherichia coli has become a serious problem. However, resistance to fosfomycin (FOM) has been low. We screened E. coli clinical isolates with reduced susceptibility to FOM and characterized molecular mechanisms of resistance and reduced susceptibility of these strains. Ten strains showing reduced FOM susceptibility (MIC ≥ 8 μg/mL) in 211 clinical isolates were found and examined. Acquisition of genes encoding FOM-modifying enzyme genes (fos genes) and mutations in murA that underlie high resistance to FOM were not observed. We examined ability of FOM incorporation via glucose-6-phosphate (G6P) transporter and sn-glycerol-3-phosphate transporter. In ten strains, nine showed lack of growth on M9 minimum salt agar supplemented with G6P. Eight of the ten strains showed fluctuated induction by G6P of uhpT that encodes G6P transporter expression. Nucleotide sequences of the uhpT, uhpA, glpT, ptsI, and cyaA shared several deletions and amino acid mutations in the nine strains with lack of growth on G6P-supplemented M9 agar. In conclusion, reduction of uhpT function is largely responsible for the reduced sensitivity to FOM in clinical isolates that have not acquired FOM-modifying genes or mutations in murA. However, there are a few strains whose mechanisms of reduced susceptibility to FOM are still unclear.

Pathogenic Lineage of mcr-Negative Colistin-Resistant Escherichia coli, Japan, 2008-2015.

Toyotaka Sato, Akira Fukuda, Yuuki Suzuki, Tsukasa Shiraishi, Hiroyuki Honda, Masaaki Shinagawa, Soh Yamamoto, Noriko Ogasawara, Masaru Usui, Hiroki Takahashi, Satoshi Takahashi, Yutaka Tamura, Shin-Ichi Yokota

Emerging infectious diseases ( CENTERS DISEASE CONTROL ) 22 ( 12 ) 2223 - 2225 2016.12 [Refereed] [International journal]

Outcomes of visually impaired patients who received cochlear implantations.

Kenichi Takano, Aya Kaizaki, Etsuko Saikawa, Ayami Konno, Noriko Ogasawara, Tetsuo Himi

Nihon Jibiinkoka Gakkai kaiho ( Oto-Rhino-Laryngological Society of Japan Inc. ) 119 ( 12 ) 1551 - 2 2016.12 [Refereed] [Domestic journal]

The Association of External and Middle Ear Anomaly and Mandibular Morphology in Congenital Microtia

Kenichi Takano, Nozomi Takahashi, Noriko Ogasawara, Tetsuo Himi

OTOLOGY & NEUROTOLOGY ( LIPPINCOTT WILLIAMS & WILKINS ) 37 ( 7 ) 889 - 894 2016.08 [Refereed]

Objective: To investigate the relationship between the severity of ear anomaly and mandibular dysplasia in congenital microtia. Study Design: Retrospective case review. Setting: Sapporo Medical University Hospital. Patients: Congenital microtia: 44 patients over a period of 4 years. Interventions: The height of the condylar process of the mandible was assessed by three-dimensional computed tomography (CT), and the patients were divided into three groups based on the ratio of the condylar process height on the affected side to that on the unaffected side: Group A, >= 1.00; Group B, 0.99 to 0.85; Group C, <0.85. Developmental abnormalities of the ear were evaluated using Jahrsdoerfer's scoring system on high-resolution CT scans. Main Outcome Measures: Nonparametric statistical tests were used to determine correlations between the height of the condylar process of the mandible and Jahrsdoerfer's score. Results: The total Jahrsdoerfer's score for each group was 7.36 +/- 2.23, 7.28 +/- 0.10, and 4.52 +/- 0.30, respectively; this value was significantly lower in Group C than in the other groups. In terms of subtotal points, oval window open, middle ear aeration, and mastoid pneumatization correlated significantly with mandibular dysplasia. Patients in Group C tended to have grade III microtia, by Marx's classification. Facial nerve weakness was not significantly correlated with mandibular dysplasia. Conclusions: In congenital microtia, mandibular development correlated significantly with aeration of the middle ear space, pneumatization of the mastoid, and formation of the oval window, but not with the presence of a bony part of the external auditory canal or with ossicular development.

Bob1 limits cellular frequency of T-follicular helper cells (vol 46, pg 1361, 2016)

Yamashita Keiji, Kawata Koji, Matsumiya Hiroshi, Kamekura Ryuta, Jitsukawa Sumito, Nagaya Tomonori, Ogasawara Noriko, Takano Ken-ichi, Kubo Terufumi, Kimura Sachiko, Shigehara Katsunori, Himi Tetsuo, Ichimiya Shingo

EUROPEAN JOURNAL OF IMMUNOLOGY 46 ( 8 ) 2054 2016.08 [Refereed]

Measles Virus Genotype D Wild Strains Suppress Interferon-Stimulated Gene Expression More Potently than Laboratory Strains in SiHa Cells

Masaru Jinushi, Soh Yamamoto, Noriko Ogasawara, Hideki Nagano, Shin Hashimoto, Hiroyuki Tsutsumi, Tetsuo Himi, Shin-ichi Yokota

VIRAL IMMUNOLOGY ( MARY ANN LIEBERT, INC ) 29 ( 5 ) 296 - 306 2016.06 [Refereed]

Changes in interferon (IFN)-stimulated gene (ISG) expression in cells infected with measles virus (MeV), four wild strains (belonging to different genotypes), and the laboratory strain Edmonston were examined. ISGs [MxA, 2'-5'-oligoadenylate synthetase, and interferon regulatory factor-1] were upregulated in an MeV-infection- induced manner and in an IFN-induced manner. In MeV-infected SiHa cell lines, the MeV infection-induced expression levels were in the order of A>H1>D8>D5>D3. On the other hand, all infected cell lines abolished type I and III IFN-induced ISG expression. However, partial type II IFN-mediated induction was observed in the MeV-infected cells. The wild strain of genotype D3 was the most potent inhibitor of MeV infection-induced and IFN-induced ISG expression and generated the highest titer of infectious viral particles. Edmonston triggered the highest levels of MeV infection-induced ISG expression in SiHa cells and produced the lowest titer of infectious particles. Expression of the viral C protein was associated with suppression of MeV infection-induced and type II IFN-induced ISG expression.

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