start-ver=1.4
cd-journal=joma
no-vol=19
cd-vols=
no-issue=1
article-no=
start-page=103
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2023
dt-pub=20231205
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Successful use of dupilumab for egg-induced eosinophilic gastroenteritis with duodenal ulcer: a pediatric case report and review of literature
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background Non-esophageal eosinophilic gastrointestinal disorder (non-EoE-EGID) is a rare disease in which eosinophils infiltrate parts of the gastrointestinal tract other than the esophagus; however, the number of patients with non-EoE-EGID has been increasing in recent years. Owing to its chronic course with repeated relapses, it can lead to developmental delays due to malnutrition, especially in pediatric patients. No established treatment exists for non-EoE-EGID, necessitating long-term systemic corticosteroid administration. Although the efficacy of dupilumab, an anti-IL-4/13 receptor monoclonal antibody, for eosinophilic esophagitis, has been reported, only few reports have demonstrated its efficacy in non-EoE EGIDs.<br>
Case presentation A 13-year-old boy developed non-EoE-EGID with duodenal ulcers, with chicken eggs as the trigger. He was successfully treated with an egg-free diet, proton pump inhibitors, and leukotriene receptor antagonists. However, at age 15, he developed worsening upper abdominal pain and difficulty eating. Blood analysis revealed eosinophilia; elevated erythrocyte sedimentation rate; and elevated levels of C-reactive protein, total immunoglobulin E, and thymic and activation-regulated chemokines. Upper gastrointestinal endoscopy revealed a duodenal ulcer with marked mucosal eosinophilic infiltration. Gastrointestinal symptoms persisted even after starting systemic steroids, making it difficult to reduce the steroid dose. Subcutaneous injection of dupilumab was initiated because of comorbid atopic dermatitis exacerbation. After 3 months, the gastrointestinal symptoms disappeared, and after 5 months, the duodenal ulcer disappeared and the eosinophil count decreased in the mucosa. Six months later, systemic steroids were discontinued, and the duodenal ulcer remained recurrence-free. The egg challenge test result was negative; therefore, the egg-free diet was discontinued. Blood eosinophil count and serum IL-5, IL-13, and eotaxin-3 levels decreased after dupilumab treatment. The serum levels of IL-5 and eotaxin-3 remained within normal ranges, although the blood eosinophil counts increased again after discontinuation of oral prednisolone.<br>
Conclusions Suppression of IL-4R/IL-13R-mediated signaling by dupilumab may improve abdominal symptoms and endoscopic and histologic findings in patients with non-EoE-EGID, leading to the discontinuation of systemic steroid administration and tolerance of causative foods.
en-copyright=
kn-copyright=

en-aut-name=TsugeMitsuru
en-aut-sei=Tsuge
en-aut-mei=Mitsuru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=ShigeharaKenji
en-aut-sei=Shigehara
en-aut-mei=Kenji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=UdaKazuhiro
en-aut-sei=Uda
en-aut-mei=Kazuhiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KawanoSeiji
en-aut-sei=Kawano
en-aut-mei=Seiji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=IwamuroMasaya
en-aut-sei=Iwamuro
en-aut-mei=Masaya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SaitoYukie
en-aut-sei=Saito
en-aut-mei=Yukie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=YashiroMasato
en-aut-sei=Yashiro
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=TsukaharaHirokazu
en-aut-sei=Tsukahara
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

affil-num=1
en-affil=Department of Pediatric Acute Diseases, Okayama University Academic  Field of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Pediatrics, Okayama  University Hospital
kn-affil=

affil-num=3
en-affil=Department of Pediatrics, Okayama  University Hospital
kn-affil=

affil-num=4
en-affil=Department of Gastroenterology and Hepatology, Okayama University Hospital
kn-affil=

affil-num=5
en-affil=Department of Gastroenterology and Hepatology, Okayama University Hospital
kn-affil=

affil-num=6
en-affil=Department of Pediatrics, Okayama University Hospital
kn-affil=

affil-num=7
en-affil=Department of Pediatrics, Okayama University Hospital
kn-affil=

affil-num=8
en-affil=Department of Pediatrics, Okayama University Hospital
kn-affil=

affil-num=9
en-affil=Department of Pediatrics, Okayama University Academic Field of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=Duodenal ulcer
kn-keyword=Duodenal ulcer
en-keyword=Dupilumab
kn-keyword=Dupilumab
en-keyword=Eosinophilic gastroenteritis
kn-keyword=Eosinophilic gastroenteritis
en-keyword=Eotaxin-3
kn-keyword=Eotaxin-3
en-keyword=Food allergy
kn-keyword=Food allergy
en-keyword=Interleukin-5
kn-keyword=Interleukin-5
en-keyword=Interleukin-13
kn-keyword=Interleukin-13
en-keyword=Non-esophageal eosinophilic gastrointestinal disorder
kn-keyword=Non-esophageal eosinophilic gastrointestinal disorder
END

start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=8
article-no=
start-page=1253
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220819
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Novel Lung Growth Strategy with Biological Therapy Targeting Airway Remodeling in Childhood Bronchial Asthma
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Anti-inflammatory therapy, centered on inhaled steroids, suppresses airway inflammation in asthma, reduces asthma mortality and hospitalization rates, and achieves clinical remission in many pediatric patients. However, the spontaneous remission rate of childhood asthma in adulthood is not high, and airway inflammation and airway remodeling persist after remission of asthma symptoms. Childhood asthma impairs normal lung maturation, interferes with peak lung function in adolescence, reduces lung function in adulthood, and increases the risk of developing chronic obstructive pulmonary disease (COPD). Early suppression of airway inflammation in childhood and prevention of asthma exacerbations may improve lung maturation, leading to good lung function and prevention of adult COPD. Biological drugs that target T-helper 2 (Th2) cytokines are used in patients with severe pediatric asthma to reduce exacerbations and airway inflammation and improve respiratory function. They may also suppress airway remodeling in childhood and prevent respiratory deterioration in adulthood, reducing the risk of COPD and improving long-term prognosis. No studies have demonstrated a suppressive effect on airway remodeling in childhood severe asthma, and further clinical trials using airway imaging analysis are needed to ascertain the inhibitory effect of biological drugs on airway remodeling in severe childhood asthma. In this review, we describe the natural prognosis of lung function in childhood asthma and the risk of developing adult COPD, the pathophysiology of allergic airway inflammation and airway remodeling via Th2 cytokines, and the inhibitory effect of biological drugs on airway remodeling in childhood asthma.
en-copyright=
kn-copyright=

en-aut-name=TsugeMitsuru
en-aut-sei=Tsuge
en-aut-mei=Mitsuru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=TsukaharaHirokazu
en-aut-sei=Tsukahara
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

affil-num=1
en-affil=Department of Pediatric Acute Diseases, Okayama University Academic Field of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Okayama University School of Medicine
kn-affil=

affil-num=3
en-affil=Department of Pediatrics, Okayama University Academic Field of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=bronchial asthma
kn-keyword=bronchial asthma
en-keyword=chronic obstructive pulmonary disease
kn-keyword=chronic obstructive pulmonary disease
en-keyword=lung function trajectory
kn-keyword=lung function trajectory
en-keyword=type 2 inflammation
kn-keyword=type 2 inflammation
en-keyword=airway remodeling
kn-keyword=airway remodeling
en-keyword=omalizumab
kn-keyword=omalizumab
en-keyword=mepolizumab
kn-keyword=mepolizumab
en-keyword=benralizumab
kn-keyword=benralizumab
en-keyword=dupilumab
kn-keyword=dupilumab
END

start-ver=1.4
cd-journal=joma
no-vol=50
cd-vols=
no-issue=1
article-no=
start-page=03000605211070492
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2022
dt-pub=20220107
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Severe pediatric asthma with a poor response to omalizumab: a report of three cases and three-dimensional bronchial wall analysis
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Omalizumab is used for the treatment of persistent severe allergic asthma in adults and children. However, some patients remain symptomatic even after omalizumab treatment. In bronchial asthma, chronic inflammation of the bronchial wall causes thickening of the airway wall, resulting from irreversible airway remodeling. Progression of airway remodeling causes airflow obstruction, leading to treatment resistance. We report three Japanese children with severe asthma who had a poor response to omalizumab treatment. They had a long period of inadequate management of asthma before initiating omalizumab. Even after omalizumab treatment, their symptoms persisted, and the parameters of spirometry tests did not improve. We hypothesized that omalizumab was less effective in these patients because airway wall remodeling had already progressed. We retrospectively evaluated the bronchial wall thickness using a three-dimensional bronchial wall analysis with chest computed tomography. The bronchial wall thickness was increased in these cases compared with six responders. Progressed airway wall thickness caused by airway remodeling may be associated with a poor response to omalizumab in children with severe asthma.
en-copyright=
kn-copyright=

en-aut-name=TsugeMitsuru
en-aut-sei=Tsuge
en-aut-mei=Mitsuru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=KondoYoichi
en-aut-sei=Kondo
en-aut-mei=Yoichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=TsukaharaHirokazu
en-aut-sei=Tsukahara
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

affil-num=1
en-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Pediatrics, Okayama University Hospital
kn-affil=

affil-num=3
en-affil=Department of Pediatrics, Matsuyama Red Cross Hospital
kn-affil=

affil-num=4
en-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
en-keyword=Bronchial asthma
kn-keyword=Bronchial asthma
en-keyword=omalizumab
kn-keyword=omalizumab
en-keyword=bronchial wall thickness
kn-keyword=bronchial wall thickness
en-keyword=child
kn-keyword=child
en-keyword=computed tomography
kn-keyword=computed tomography
en-keyword=airway
kn-keyword=airway
END

start-ver=1.4
cd-journal=joma
no-vol=8
cd-vols=
no-issue=11
article-no=
start-page=1067
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2021
dt-pub=20211119
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Current Insights into Atopic March
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=The incidence of allergic diseases is increasing, and research on their epidemiology, pathophysiology, and the prevention of onset is urgently needed. The onset of allergic disease begins in infancy with atopic dermatitis and food allergy and develops into allergic asthma and allergic rhinitis in childhood; the process is defined as "atopic march ". Atopic march is caused by multiple immunological pathways, including allergen exposure, environmental pollutants, skin barrier dysfunction, type 2 inflammation, and oxidative stress, which promote the progression of atopic march. Using recent evidence, herein, we explain the involvement of allergic inflammatory conditions and oxidative stress in the process of atopic march, its epidemiology, and methods for prevention of onset.
en-copyright=
kn-copyright=

en-aut-name=TsugeMitsuru
en-aut-sei=Tsuge
en-aut-mei=Mitsuru
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=MatsumotoNaomi
en-aut-sei=Matsumoto
en-aut-mei=Naomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=YorifujiTakashi
en-aut-sei=Yorifuji
en-aut-mei=Takashi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=TsukaharaHirokazu
en-aut-sei=Tsukahara
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=Department of Pediatric Acute Diseases, Okayama University Academic Field of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Pediatrics, Okayama University Academic Field of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Epidemiology, Okayama University Academic Field of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Epidemiology, Okayama University Academic Field of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Pediatrics, Okayama University Academic Field of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=atopic march
kn-keyword=atopic march
en-keyword=atopic dermatitis
kn-keyword=atopic dermatitis
en-keyword=food allergy
kn-keyword=food allergy
en-keyword=allergic asthma
kn-keyword=allergic asthma
en-keyword=allergic rhinitis
kn-keyword=allergic rhinitis
en-keyword=skin barrier dysfunction
kn-keyword=skin barrier dysfunction
en-keyword=alarmin
kn-keyword=alarmin
en-keyword=group 2 innate lymphoid cells
kn-keyword=group 2 innate lymphoid cells
en-keyword=type 2 inflammation
kn-keyword=type 2 inflammation
en-keyword=oxidative stress
kn-keyword=oxidative stress
en-keyword=specific biomarker
kn-keyword=specific biomarker
en-keyword=epidemiology
kn-keyword=epidemiology
en-keyword=phenotype
kn-keyword=phenotype
en-keyword=early intervention
kn-keyword=early intervention
en-keyword=emollient
kn-keyword=emollient
END

start-ver=1.4
cd-journal=joma
no-vol=13
cd-vols=
no-issue=10
article-no=
start-page=100463
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=202010
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Evaluation of oral immunotherapy efficacy and safety by maintenance dose dependency: A multicenter randomized study
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Background</br>
Generally, oral immunotherapy (OIT) aims for daily administration. Recently, the efficacy of treatment with OIT at a low dose has been reported. However, the optimal dose and the evaluation of dose-dependent OIT outcome have not been described.</br>
Methods</br>
A multicenter, parallel, open-labeled, prospective, non-placebo controlled, randomized study enrolled 101 Japanese patients for treatment with OIT. We hypothesized that target dose OIT would induce short-term unresponsiveness (StU) earlier than reduced dose OIT. StU was defined as no response to 6200 mg whole egg, 3400 mg milk, and 2600 mg wheat protein, as evaluated by oral food challenge after 2-week ingestion cessation. To compare the two doses of OIT efficacy, the maximum ingestion doses during the maintenance phase of OIT were divided into 100%-dose or 25%-dose groups against their target StU dose, respectively. A total of 51 patients were assigned to the 100%-dose group [hen's egg (HE) = 26, cow's milk (CM) = 13, wheat = 12] and 50 to the 25%-dose group (HE = 25, CM = 13, wheat = 12). Primary outcome was established by comparing StU at 1 year. Secondary outcome was StU at 2 years and established by comparing allergic symptoms and immunological changes.</br>
Results</br>
The year 1 StU rates (%) for the 100%- and 25%-dose groups were 26.9 vs. 20.0 (HE), 7.7 vs. 15.4 (CM), and 50.0 vs. 16.7 (wheat), respectively. The year 2 StU rates were 30.8 vs. 36.0 (HE), 7.7 vs. 23.1 (CM), and 58.3 vs. 58.3 (wheat), respectively. There were no statistically significant differences in StU between years 1 and 2. The total allergic symptom rate in the 25%-dose group was lower than that in the 100%-dose group for egg, milk, and wheat. Antigen-specific IgE levels for egg-white, milk, and wheat decreased at 12 months.</br>
Conclusions</br>
Reduced maintenance dose of egg OIT showed similar therapeutic efficacy to the target dose. However, we were not able to clearly demonstrate the efficacy, particularly for milk and wheat. Reducing the maintenance dose for eggs, milk, and wheat may effectively lower the symptoms associated with their consumption compared to the target OIT dose. Furthermore, aggressive reduction of the maintenance dose might be important for milk and wheat, compared to the 25%-dose OIT.
en-copyright=
kn-copyright=

en-aut-name=OguraKiyotake
en-aut-sei=Ogura
en-aut-mei=Kiyotake
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YanagidaNoriyuki
en-aut-sei=Yanagida
en-aut-mei=Noriyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=SatoSakura
en-aut-sei=Sato
en-aut-mei=Sakura
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=ImaiTakanori
en-aut-sei=Imai
en-aut-mei=Takanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=ItoKomei
en-aut-sei=Ito
en-aut-mei=Komei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=KandoNaoyuki
en-aut-sei=Kando
en-aut-mei=Naoyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=ShibataRumiko
en-aut-sei=Shibata
en-aut-mei=Rumiko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MurakamiYoko
en-aut-sei=Murakami
en-aut-mei=Yoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=FujisawaTakao
en-aut-sei=Fujisawa
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=NagaoMizuho
en-aut-sei=Nagao
en-aut-mei=Mizuho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=KawamotoNorio
en-aut-sei=Kawamoto
en-aut-mei=Norio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=KondoNaomi
en-aut-sei=Kondo
en-aut-mei=Naomi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=UrisuAtsuo
en-aut-sei=Urisu
en-aut-mei=Atsuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=TsugeIkuya
en-aut-sei=Tsuge
en-aut-mei=Ikuya
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=KondoYasuto
en-aut-sei=Kondo
en-aut-mei=Yasuto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=SugaiKazuko
en-aut-sei=Sugai
en-aut-mei=Kazuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

en-aut-name=UchidaOsamu
en-aut-sei=Uchida
en-aut-mei=Osamu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=18
ORCID=

en-aut-name=UrashimaMitsuyoshi
en-aut-sei=Urashima
en-aut-mei=Mitsuyoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=19
ORCID=

en-aut-name=TaniguchiMasami
en-aut-sei=Taniguchi
en-aut-mei=Masami
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=20
ORCID=

en-aut-name=EbisawaMotohiro
en-aut-sei=Ebisawa
en-aut-mei=Motohiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=21
ORCID=

affil-num=1
en-affil=Department of Pediatrics, National Hospital Organization, Sagamihara National Hospital
kn-affil=

affil-num=2
en-affil=Department of Pediatrics, National Hospital Organization, Sagamihara National Hospital
kn-affil=

affil-num=3
en-affil=Course of Allergy and Clinical Immunology, Juntendo University Graduate School of Medicine
kn-affil=

affil-num=4
en-affil=Department of Pediatrics, Showa University School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Allergy, Aichi Children's Health and Medical Center
kn-affil=

affil-num=6
en-affil=Department of Allergy, Aichi Children's Health and Medical Center
kn-affil=

affil-num=7
en-affil=Department of Pediatric Acute Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=8
en-affil=Department of Pediatrics, National Hospital Organization, Fukuoka National Hospital
kn-affil=

affil-num=9
en-affil=Department of Pediatrics, National Hospital Organization, Fukuoka National Hospital
kn-affil=

affil-num=10
en-affil=Institute for Clinical Research, National Hospital Organization, Mie National Hospital
kn-affil=

affil-num=11
en-affil=Institute for Clinical Research, National Hospital Organization, Mie National Hospital
kn-affil=

affil-num=12
en-affil=Department of Pediatrics, Graduate School of Medicine, Gifu University
kn-affil=

affil-num=13
en-affil=Department of Pediatrics, Graduate School of Medicine, Gifu University
kn-affil=

affil-num=14
en-affil=Department of Pediatrics, Fujita Health University, The Second Teaching Hospital
kn-affil=

affil-num=15
en-affil=Department of Pediatrics, Fujita Health University, The Second Teaching Hospital
kn-affil=

affil-num=16
en-affil=Department of Pediatrics, Fujita Health University, The Second Teaching Hospital
kn-affil=

affil-num=17
en-affil=Department of Pediatrics, National Hospital Organization, Yokohama Medical Center
kn-affil=

affil-num=18
en-affil=Department of Pediatrics, National Hospital Organization, Yokohama Medical Center
kn-affil=

affil-num=19
en-affil=Division of Molecular Epidemiology, The Jikei University School of Medicine
kn-affil=

affil-num=20
en-affil=Course of Allergy and Clinical Immunology, Juntendo University Graduate School of Medicine
kn-affil=

affil-num=21
en-affil=Course of Allergy and Clinical Immunology, Juntendo University Graduate School of Medicine
kn-affil=
en-keyword=Food hypersensitivity
kn-keyword=Food hypersensitivity
en-keyword=Immunotherapy
kn-keyword=Immunotherapy
en-keyword=Dose-response relationship
kn-keyword=Dose-response relationship
en-keyword=Desensitization
kn-keyword=Desensitization
END

start-ver=1.4
cd-journal=joma
no-vol=69
cd-vols=
no-issue=3
article-no=
start-page=356
end-page=369
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200404
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Japanese guidelines for atopic dermatitis 2020.
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Atopic dermatitis (AD) is a disease characterized by relapsing eczema with pruritus as a primary lesion, which is frequently encountered in clinical practice. Skin barrier dysfunction leads to enhanced skin irritability to non-specific stimuli and epicutaneous sensitization. In the lesion site, a further inflammation-related reduction in skin barrier function, enhanced irritability and scratching-related stimuli deteriorate eczema, leading to vicious cycle of inflammation. The current strategies to treat AD in Japan from the perspective of evidence-based medicine consist of three primary measures: (i) the use of topical corticosteroids and tacrolimus ointment as the main treatment for the inflammation; (ii) topical application of emollients to treat the cutaneous barrier dysfunction; and (iii) avoidance of apparent exacerbating factors, psychological counseling and advice about daily life. The guidelines present recommendations to review clinical research articles, evaluate the balance between the advantages and disadvantages of medical activities, and optimize medical activity-related patient outcomes with respect to several important points requiring decision-making in clinical practice. 
en-copyright=
kn-copyright=

en-aut-name=KatohNorito
en-aut-sei=Katoh
en-aut-mei=Norito
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=OhyaYukihiro
en-aut-sei=Ohya
en-aut-mei=Yukihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=EbiharaTamotsu
en-aut-sei=Ebihara
en-aut-mei=Tamotsu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KatayamaIchiro
en-aut-sei=Katayama
en-aut-mei=Ichiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SaekiHidehisa
en-aut-sei=Saeki
en-aut-mei=Hidehisa
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ShimojoNaoki
en-aut-sei=Shimojo
en-aut-mei=Naoki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=TanakaAkio
en-aut-sei=Tanaka
en-aut-mei=Akio
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=NakaharaTakeshi
en-aut-sei=Nakahara
en-aut-mei=Takeshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=NagaoMizuho
en-aut-sei=Nagao
en-aut-mei=Mizuho
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

en-aut-name=HideMichihiro
en-aut-sei=Hide
en-aut-mei=Michihiro
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=11
ORCID=

en-aut-name=FujitaYuji
en-aut-sei=Fujita
en-aut-mei=Yuji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=12
ORCID=

en-aut-name=FujisawaTakao
en-aut-sei=Fujisawa
en-aut-mei=Takao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=13
ORCID=

en-aut-name=FutamuraMasaki
en-aut-sei=Futamura
en-aut-mei=Masaki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=14
ORCID=

en-aut-name=MasudaKoji
en-aut-sei=Masuda
en-aut-mei=Koji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=15
ORCID=

en-aut-name=MurotaHiroyuki
en-aut-sei=Murota
en-aut-mei=Hiroyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=16
ORCID=

en-aut-name=Yamamoto-HanadaKiwako
en-aut-sei=Yamamoto-Hanada
en-aut-mei=Kiwako
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=17
ORCID=

affil-num=1
en-affil=Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science
kn-affil=

affil-num=2
en-affil=Allergy Center, National Center for Child Health and Development
kn-affil=

affil-num=3
en-affil=Department of Pediatric Acute Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Dermatology, Keio University School of Medicine
kn-affil=

affil-num=5
en-affil=Department of Dermatology, Graduate School of Medicine, Osaka University
kn-affil=

affil-num=6
en-affil=Department of Dermatology, Graduate School of Medicine, Nihon Medical School
kn-affil=

affil-num=7
en-affil=Department of Pediatrics, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=8
en-affil=Department of Dermatology, Hiroshima University Graduate School of Biomedical Sciences
kn-affil=

affil-num=9
en-affil=Division of Skin Surface Sensing, Department of Dermatology, Graduate School of Medical Sciences, Kyushu University
kn-affil=

affil-num=10
en-affil=Division of Clinical Research, National Hospital Organization Mie National Hospital
kn-affil=

affil-num=11
en-affil=Department of Dermatology, Hiroshima University Graduate School of Biomedical Sciences
kn-affil=

affil-num=12
en-affil=Department of Pediatrics, Graduate School of Medicine, Chiba University
kn-affil=

affil-num=13
en-affil=Division of Allergy, National Hospital Organization Mie National Hospital
kn-affil=

affil-num=14
en-affil=Division of Pediatrics, National Hospital Organization Nagoya Medical Center
kn-affil=

affil-num=15
en-affil=Department of Dermatology, Kyoto Prefectural University of Medicine Graduate School of Medical Science
kn-affil=

affil-num=16
en-affil=Department of Dermatology, Nagasaki University Graduate School of Biomedical Sciences
kn-affil=

affil-num=17
en-affil=Allergy Center, National Center for Child Health and Development
kn-affil=
en-keyword=Atopic dermatitis
kn-keyword=Atopic dermatitis
en-keyword=Clinical practice guidelines
kn-keyword=Clinical practice guidelines
en-keyword=Eczema
kn-keyword=Eczema
en-keyword=Evidence-based medicine
kn-keyword=Evidence-based medicine
en-keyword=Treatment
kn-keyword=Treatment
END

start-ver=1.4
cd-journal=joma
no-vol=
cd-vols=
no-issue=
article-no=
start-page=2380179
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2018
dt-pub=20180314
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Serum Procalcitonin Levels in Acute Encephalopathy with Biphasic Seizures and Late Reduced Diffusion
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Procalcitonin (PCT) is used as a biomarker in severe infections. Here, we retrospectively investigated levels of serum PCT, C-reactive protein (CRP), and inflammatory cytokines (IL-6, TNF-alpha, and IFN-gamma) in the second phase of patients with acute encephalopathy with biphasic seizures and late reduced diffusion (AESD). Nine AESD pediatric patients (4 men, 5 women; AESD group) admitted to Okayama University Hospital from 2010 to 2016 were compared with 10 control patients with febrile seizures (FS) (3 men, 7 women; FS group). Mean PCT concentrations (ng/mL) in the AESD and FS groups were significantly different, at 9.8 +/- 6.7 and 0.8 +/- 0.9, respectively (p = 0 0006). CRP (mg/dL) were 0.79 +/- 0.89 and 1.4 +/- 1.0 (p = 0 94), respectively; IL-6 (pg/mL) were 449.7 +/- 705.0 and 118.3 +/- 145.4 (p = 0 20), respectively; TNF-alpha (pg/mL) were 18.6 +/- 12.5 and 16.6 +/- 6.0 (p = 0 67), respectively; and IFN-gamma (pg/mL) were 79.6 +/- 158.5 and 41.9 +/- 63.7 (p = 0 56), respectively. Ratios of PCT to CRP were 27.5 +/- 34.2 and 3.2 +/- 6.8 (p < 0 0001), respectively. The sensitivity and specificity in the diagnosis of AESD using a cutoff of PCT/CRP ratio of 1.0 were 79% and 100%, respectively. These results suggest that PCT and the PCT/CRP ratio are useful in auxiliary diagnosis of the second stage of AESD, and in AESD, PCT is likely to increase through a different mechanism.
en-copyright=
kn-copyright=

en-aut-name=FujiiYosuke
en-aut-sei=Fujii
en-aut-mei=Yosuke
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=YashiroMasato
en-aut-sei=Yashiro
en-aut-mei=Masato
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=YamadaMutsuko
en-aut-sei=Yamada
en-aut-mei=Mutsuko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=KikkawaTomonobu
en-aut-sei=Kikkawa
en-aut-mei=Tomonobu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=NosakaNobuyuki
en-aut-sei=Nosaka
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=SaitoYukie
en-aut-sei=Saito
en-aut-mei=Yukie
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=TsukaharaKohei
en-aut-sei=Tsukahara
en-aut-mei=Kohei
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

en-aut-name=MorishimaTsuneo
en-aut-sei=Morishima
en-aut-mei=Tsuneo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=9
ORCID=

en-aut-name=TsukaharaHirokazu
en-aut-sei=Tsukahara
en-aut-mei=Hirokazu
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=10
ORCID=

affil-num=1
en-affil=Department of Pediatric Acute Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=4
en-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=6
en-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=7
en-affil=Department of Emergency and Critical Care Medicine, Okayama University Graduate School of Medicine, Dentistry and
kn-affil=

affil-num=8
en-affil=Department of Pediatric Acute Medicine, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=9
en-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=

affil-num=10
en-affil=Department of Pediatrics, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
kn-affil=
END

start-ver=1.4
cd-journal=joma
no-vol=430
cd-vols=
no-issue=2
article-no=
start-page=592
end-page=597
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2013
dt-pub=20130111
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=PML tumor suppressor protein is required for HCV production
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=PML tumor suppressor protein, which forms discrete nuclear structures termed PML-nuclear bodies, has been associated with several cellular functions, including cell proliferation, apoptosis and antiviral defense. Recently, it was reported that the HCV core protein colocalizes with PML in PML-NBs and abrogates the PML function through interaction with PML. However, role(s) of PML in HCV life cycle is unknown. To test whether or not PML affects HCV life cycle, we examined the level of secreted HCV core and the infectivity of HCV in the culture supernatants as well as the level of HCV RNA in HuH-7-derived RSc cells, in which HCV-JFH1 can infect and efficiently replicate, stably expressing short hairpin RNA targeted to PML. In this context, the level of secreted HCV core and the infectivity in the supernatants from PML knockdown cells was remarkably reduced, whereas the level of HCV RNA in the PML knockdown cells was not significantly affected in spite of very effective knockdown of PML. In fact, we showed that PML is unrelated to HCV RNA replication using the subgenomic HCV-JFH1 replicon RNA, JRN/3-5B. Furthermore, the infectivity of HCV-like particle in the culture supernatants was significantly reduced in PML knockdown JRN/3-5B cells expressing core to NS2 coding region of HCV-JFH1 genome using the trans-packaging system. Finally, we also demonstrated that INI1 and DDX5, the PML-related proteins, are involved in HCV production. Taken together, these findings suggest that PML is required for HCV production.
en-copyright=
kn-copyright=

en-aut-name=KurokiMisao
en-aut-sei=Kuroki
en-aut-mei=Misao
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=AriumiYasuo
en-aut-sei=Ariumi
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=HijikataMakoto
en-aut-sei=Hijikata
en-aut-mei=Makoto
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=DansakoHiromichi
en-aut-sei=Dansako
en-aut-mei=Hiromichi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=WakitaTakaji
en-aut-sei=Wakita
en-aut-mei=Takaji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=ShimotohnoKunitada
en-aut-sei=Shimotohno
en-aut-mei=Kunitada
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

en-aut-name=KatoNobuyuki
en-aut-sei=Kato
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=8
ORCID=

affil-num=1
en-affil=
kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci

affil-num=2
en-affil=
kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci

affil-num=3
en-affil=
kn-affil=Kyoto Univ, Dept Viral Oncol, Inst Virus Res

affil-num=4
en-affil=
kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci

affil-num=5
en-affil=
kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci

affil-num=6
en-affil=
kn-affil=Natl Inst Infect Dis, Dept Virol 2

affil-num=7
en-affil=
kn-affil=Natl Ctr Global Hlth & Med, Res Ctr Hepatitis & Immunol

affil-num=8
en-affil=
kn-affil=Okayama Univ, Dept Tumor Virol, Sch Med Dent & Pharmaceut Sci
en-keyword=Hepatitis C virus
kn-keyword=Hepatitis C virus
en-keyword=PML
kn-keyword=PML
en-keyword=INI1
kn-keyword=INI1
en-keyword=DDX5
kn-keyword=DDX5
en-keyword=Tumor suppressor
kn-keyword=Tumor suppressor
en-keyword=Lipid droplet
kn-keyword=Lipid droplet
END

start-ver=1.4
cd-journal=joma
no-vol=409
cd-vols=
no-issue=4
article-no=
start-page=663
end-page=668
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2011
dt-pub=20110617
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Plural assay systems derived from different cell lines and hepatitis C virus strains are required for the objective evaluation of anti-hepatitis C virus reagents
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=Persistent hepatitis C virus (HCV) infection causes chronic liver diseases and is a global health problem. HuH-7 hepatoma-derived cells are widely used as the only cell-based HCV replication system for HCV research, including drug assays. Recently, using different hepatoma Li23-derived cells, we developed an HCV drug assay system (ORL8), in which the genome-length HCV RNA (O strain of genotype 1b) encoding renilla luciferase replicates efficiently. In this study, using the HuH-7-derived OR6 assay system that we developed previously and the ORL8 assay system, we evaluated 26 anti-HCV reagents, which other groups had reported as anti-HCV candidates using HuH-7-derived assay systems other than ORB. The results revealed that more than half of the reagents showed different anti-HCV activities from those in the previous studies, and that anti-HCV activities evaluated by the ORB and ORL8 assays were also frequently different. In further evaluation using the HuH-7-derived AH1R assay system, which was developed using the AH1 strain of genotype 1b, several reagents showed different anti-HCV activities in comparison with those evaluated by the OR6 and ORL8 assays. These results suggest that the different activities of anti-HCV reagents are caused by the differences in cell lines or HCV strains used for the development of assay systems. Therefore, we conclude that plural HCV assay systems developed using different cell lines or HCV strains are required for the objective evaluation of anti-HCV reagents.
en-copyright=
kn-copyright=

en-aut-name=UedaYouki
en-aut-sei=Ueda
en-aut-mei=Youki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=MoriKyoko
en-aut-sei=Mori
en-aut-mei=Kyoko
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=AriumiYasuo
en-aut-sei=Ariumi
en-aut-mei=Yasuo
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=KatoNobuyuki
en-aut-sei=Kato
en-aut-mei=Nobuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

affil-num=1
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=2
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=3
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=4
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences

affil-num=5
en-affil=
kn-affil=Department of Tumor Virology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
en-keyword=HCV
kn-keyword=HCV
en-keyword=HCV RNA replication system
kn-keyword=HCV RNA replication system
en-keyword=Li23 cells
kn-keyword=Li23 cells
en-keyword=Reporter assay for anti-HCV reagents
kn-keyword=Reporter assay for anti-HCV reagents
END

start-ver=1.4
cd-journal=joma
no-vol=122
cd-vols=
no-issue=1
article-no=
start-page=9
end-page=16
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2010
dt-pub=20100401
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=The DNA damage sensors ataxia-telangiectasia mutated kinase and checkpoint kinase 2 are required for hepatitis C virus RNA replication
kn-title=DNA 損傷センサーATMキナーゼとChk2はＣ型肝炎ウイルスのRNA複製に必要である
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=AriumiYasuo
en-aut-sei=Ariumi
en-aut-mei=Yasuo
kn-aut-name=有海康雄
kn-aut-sei=有海
kn-aut-mei=康雄
aut-affil-num=1
ORCID=

en-aut-name=KurokiMisao
en-aut-sei=Kuroki
en-aut-mei=Misao
kn-aut-name=黒木美沙緒
kn-aut-sei=黒木
kn-aut-mei=美沙緒
aut-affil-num=2
ORCID=

en-aut-name=DansakoHiromichi
en-aut-sei=Dansako
en-aut-mei=Hiromichi
kn-aut-name=團迫浩方
kn-aut-sei=團迫
kn-aut-mei=浩方
aut-affil-num=3
ORCID=

en-aut-name=AbeKenichi
en-aut-sei=Abe
en-aut-mei=Kenichi
kn-aut-name=阿部健一
kn-aut-sei=阿部
kn-aut-mei=健一
aut-affil-num=4
ORCID=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=池田正徳
kn-aut-sei=池田
kn-aut-mei=正徳
aut-affil-num=5
ORCID=

en-aut-name=WakitaTakaji
en-aut-sei=Wakita
en-aut-mei=Takaji
kn-aut-name=脇田隆字
kn-aut-sei=脇田
kn-aut-mei=隆字
aut-affil-num=6
ORCID=

en-aut-name=KatoNobuyuki
en-aut-sei=Kato
en-aut-mei=Nobuyuki
kn-aut-name=加藤宣之
kn-aut-sei=加藤
kn-aut-mei=宣之
aut-affil-num=7
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学

affil-num=2
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学

affil-num=3
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学

affil-num=4
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学

affil-num=5
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学

affil-num=6
en-affil=
kn-affil=国立感染症研究所　ウイルス第二部

affil-num=7
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　腫瘍ウイルス学
en-keyword=HCV
kn-keyword=HCV
en-keyword=ATM
kn-keyword=ATM
en-keyword=Chk2
kn-keyword=Chk2
en-keyword=宿主因子
kn-keyword=宿主因子
en-keyword=DNA 損傷センサー
kn-keyword=DNA 損傷センサー
END

start-ver=1.4
cd-journal=joma
no-vol=120
cd-vols=
no-issue=1
article-no=
start-page=29
end-page=34
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2008
dt-pub=20080501
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=Statins inhibit hepatitis C virus RNA replication in human hepatoma cells
kn-title=培養肝細胞を用いたスタチン剤のＣ型肝炎ウイルス抑制効果について
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=
en-copyright=
kn-copyright=

en-aut-name=IkedaMasanori
en-aut-sei=Ikeda
en-aut-mei=Masanori
kn-aut-name=池田正徳
kn-aut-sei=池田
kn-aut-mei=正徳
aut-affil-num=1
ORCID=

affil-num=1
en-affil=
kn-affil=岡山大学大学院医歯薬学総合研究科　分子生物学
en-keyword=HCV
kn-keyword=HCV
en-keyword=レプリコン
kn-keyword=レプリコン
en-keyword=スタチン
kn-keyword=スタチン
en-keyword=HMG-CoA reductase
kn-keyword=HMG-CoA reductase
en-keyword=ゲラニルゲラニル化
kn-keyword=ゲラニルゲラニル化
END