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  <title>ScholarWorks Community:</title>
  <link rel="alternate" href="https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/1238" />
  <subtitle />
  <id>https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/1238</id>
  <updated>2026-04-04T00:52:09Z</updated>
  <dc:date>2026-04-04T00:52:09Z</dc:date>
  <entry>
    <title>Pet Ownership Increases the Exhaled Nitric Oxide and Asthma Severity in Children With Atopic Asthma</title>
    <link rel="alternate" href="https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/27691" />
    <author>
      <name>Song, Kun-Baek</name>
    </author>
    <author>
      <name>Kim, Jeong-Hoon</name>
    </author>
    <author>
      <name>Choi, Eom Ji</name>
    </author>
    <author>
      <name>Lee, Seung Won</name>
    </author>
    <author>
      <name>Kim, Jin Tack</name>
    </author>
    <author>
      <name>Lim, Dae Hyun</name>
    </author>
    <author>
      <name>Kim, Woo Kyung</name>
    </author>
    <author>
      <name>Song, Dae Jin</name>
    </author>
    <author>
      <name>Yoo, Young</name>
    </author>
    <author>
      <name>Suh, Dong In</name>
    </author>
    <author>
      <name>Baek, Hey-Sung</name>
    </author>
    <author>
      <name>Shin, Meeyong</name>
    </author>
    <author>
      <name>Kwon, Ji-Won</name>
    </author>
    <author>
      <name>Jang, Gwang Cheon</name>
    </author>
    <author>
      <name>Yang, Hyeon-Jong</name>
    </author>
    <author>
      <name>Lee, Eun</name>
    </author>
    <author>
      <name>Kim, Hwan Soo</name>
    </author>
    <author>
      <name>Seo, Ju-Hee</name>
    </author>
    <author>
      <name>Woo, Sung-Il</name>
    </author>
    <author>
      <name>Kim, Hyung Young</name>
    </author>
    <author>
      <name>Shin, Youn Ho</name>
    </author>
    <author>
      <name>Lee, Ju Suk</name>
    </author>
    <author>
      <name>Yu, Jinho</name>
    </author>
    <id>https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/27691</id>
    <updated>2025-11-22T05:39:27Z</updated>
    <published>2025-05-01T00:00:00Z</published>
    <summary type="text">Title: Pet Ownership Increases the Exhaled Nitric Oxide and Asthma Severity in Children With Atopic Asthma
Authors: Song, Kun-Baek; Kim, Jeong-Hoon; Choi, Eom Ji; Lee, Seung Won; Kim, Jin Tack; Lim, Dae Hyun; Kim, Woo Kyung; Song, Dae Jin; Yoo, Young; Suh, Dong In; Baek, Hey-Sung; Shin, Meeyong; Kwon, Ji-Won; Jang, Gwang Cheon; Yang, Hyeon-Jong; Lee, Eun; Kim, Hwan Soo; Seo, Ju-Hee; Woo, Sung-Il; Kim, Hyung Young; Shin, Youn Ho; Lee, Ju Suk; Yu, Jinho
Abstract: Exposure to pets can trigger symptoms in asthmatic children sensitized to pets. However, little is known about the association between pet ownership and asthma morbidity in children who are not sensitized to pets. We aimed to investigate the effect of pets on lung function, airway inflammation, and morbidity in children with asthma, and to determine whether the effect of exposure to pets vary based on pet sensitization status. A total of 975 asthmatic children, aged 5-15 years, were enrolled in the Korean Childhood Asthma Study. Pet ownership and asthma morbidity were evaluated by questionnaires or pediatrician evaluations. Pulmonary function, fractional exhaled nitric oxide (FeNO), and atopic status were assessed. FeNO levels were significantly higher in children with pets than in those without pets. Pet ownership significantly increased FeNO levels in atopic asthmatic children, irrespective of pet sensitization status. In children sensitized to pets, the geometric mean was 46.6 (range of 1 standard deviation, 26.9-81.5) for those with pets vs. 27.2 (13.8-53.6) for those without pets (P &amp;lt; 0.001). In children without sensitization to pets, the geometric mean was 37.3 (15.0-53.6) for pet owners vs. 25.2 (12.9-49.2) for non-owners (P = 0.014). The multiple regression analysis also revealed that pet ownership was significantly associated with increased FeNO levels and asthma severity in atopic asthmatic children. Pet ownership increased the FeNO levels and asthma severity, regardless of pet sensitization status, in children with atopic asthma. Exposure to pets could increase airway inflammation and disease severity even in atopic asthmatic children who are not sensitized to pets.</summary>
    <dc:date>2025-05-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Identification of topological alterations using microstate dynamics in patients with infantile epileptic spasms syndrome</title>
    <link rel="alternate" href="https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/28149" />
    <author>
      <name>Ahn, Seong-Ho</name>
    </author>
    <author>
      <name>Jang, Han Na</name>
    </author>
    <author>
      <name>Kim, Seeun</name>
    </author>
    <author>
      <name>Kim, Min-Jee</name>
    </author>
    <author>
      <name>Yum, Mi-Sun</name>
    </author>
    <author>
      <name>Jeong, Dong-Hwa</name>
    </author>
    <id>https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/28149</id>
    <updated>2026-03-11T05:02:54Z</updated>
    <published>2025-03-01T00:00:00Z</published>
    <summary type="text">Title: Identification of topological alterations using microstate dynamics in patients with infantile epileptic spasms syndrome
Authors: Ahn, Seong-Ho; Jang, Han Na; Kim, Seeun; Kim, Min-Jee; Yum, Mi-Sun; Jeong, Dong-Hwa
Abstract: Infantile epileptic spasm syndrome (IESS) is characterized by clustered epileptic spasms and hypsarrhythmia on electroencephalography (EEG). This study aimed to investigate the temporal dynamics and dynamic synchronization of neural networks in IESS using EEG microstate analysis of interictal recordings from 49 healthy controls (HC) and 42 patients with IESS. Five microstate maps were identified, and features including the global explained variance (GEV), mean correlation, occurrence, time coverage, mean time duration, and transition probabilities were extracted. Significant differences were observed in patients with IESS compared to HCs, with increased microstate features and transition probabilities in microstates A and B, and reduced values in microstates D and E. Furthermore, in patients with structural/metabolic etiologies, microstate A demonstrated heightened microstate features and transition probabilities compared to genetic/unknown etiologies. These microstate characteristics enabled accurate classification of IESS versus HCs and differentiation between structural/metabolic and genetic/unknown etiologies. The altered microstate topologies in IESS reflect disruptions in brain network dynamics, suggesting that specific microstate features and transition probabilities could serve as potential diagnostic biomarkers. This study underscores the potential of EEG microstate analysis in understanding neural dysfunction, particularly in structural/metabolic subtypes of IESS.</summary>
    <dc:date>2025-03-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Growth Prediction Model for Prepubertal Children With Idiopathic Growth Hormone Deficiency: An Analysis of LG Growth Study Data</title>
    <link rel="alternate" href="https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/27945" />
    <author>
      <name>Jeong, Hwal Rim</name>
    </author>
    <author>
      <name>Lee, Hae Sang</name>
    </author>
    <author>
      <name>Hwang, Jin Soon</name>
    </author>
    <id>https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/27945</id>
    <updated>2026-03-11T01:32:47Z</updated>
    <published>2025-03-01T00:00:00Z</published>
    <summary type="text">Title: Growth Prediction Model for Prepubertal Children With Idiopathic Growth Hormone Deficiency: An Analysis of LG Growth Study Data
Authors: Jeong, Hwal Rim; Lee, Hae Sang; Hwang, Jin Soon
Abstract: BackgroundGrowth hormone (GH) treatment is effective in restoring normal growth in children with GH deficiency (GHD). However, individual responses to GH treatment vary, necessitating predictive models to estimate growth outcomes. This study aimed to develop and validate a predictive model for GH treatment response during the first 2 years in patients with idiopathic GHD using the LG growth study (LGS) database.MethodsThis observational study included 669 prepubertal patients with idiopathic GHD from the LGS registry who received GH treatment for at least 2 years. Clinical and laboratory data were collected at baseline and every 6 months thereafter. Stepwise multivariate regression analysis was performed to develop prediction models for the treatment period.ResultsThe mean age of patients with GDH was 6.0 +/- 1.8 years. Height standard deviation score (SDS) significantly increased from -2.50 +/- 0.71 to -1.66 +/- 0.71 in the first year and -1.35 +/- 0.71 in the second year. The first-year growth velocity was 9.06 +/- 1.51 cm, decreasing to 7.42 +/- 1.37 cm in the second year. The prediction models incorporated variables such as age, birth weight, bone age, initial height SDS, body mass index SDS, mid-parental height, GH dose and first year of height after GH treatment, explaining 76.9% and 84.1% of the variability in height SDS changes in the first and second years, respectively.ConclusionsGH treatment significantly improves height outcomes in prepubertal children with GHD. The developed predictive models demonstrated accuracy, facilitating personalized GH therapy. Future research should focus on refining these models and exploring the long-term effects of GH treatment in pubertal patients.Trial Registration identifier: NCT01604395.</summary>
    <dc:date>2025-03-01T00:00:00Z</dc:date>
  </entry>
  <entry>
    <title>Developmental trajectories of atopic dermatitis with multiomics approaches in the infant gut: COCOA birth cohort</title>
    <link rel="alternate" href="https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/27690" />
    <author>
      <name>Lee, Eun</name>
    </author>
    <author>
      <name>Kim, Jeong-Hyun</name>
    </author>
    <author>
      <name>Lee, So-Yeon</name>
    </author>
    <author>
      <name>Lee, Si Hyeon</name>
    </author>
    <author>
      <name>Park, Yoon Mee</name>
    </author>
    <author>
      <name>Oh, Hea Young</name>
    </author>
    <author>
      <name>Yeom, Jeonghun</name>
    </author>
    <author>
      <name>Ahn, Hee-Sung</name>
    </author>
    <author>
      <name>Yoo, Hyun Ju</name>
    </author>
    <author>
      <name>Kim, Bong-Soo</name>
    </author>
    <author>
      <name>Yun, Sun Mi</name>
    </author>
    <author>
      <name>Choi, Eom Ji</name>
    </author>
    <author>
      <name>Song, Kun Baek</name>
    </author>
    <author>
      <name>Park, Min Jee</name>
    </author>
    <author>
      <name>Ahn, Kangmo</name>
    </author>
    <author>
      <name>Kim, Kyung Won</name>
    </author>
    <author>
      <name>Shin, Youn Ho</name>
    </author>
    <author>
      <name>Suh, Dong In</name>
    </author>
    <author>
      <name>Song, Joo Young</name>
    </author>
    <author>
      <name>Hong, Soo-Jong</name>
    </author>
    <id>https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/27690</id>
    <updated>2025-11-22T05:39:23Z</updated>
    <published>2025-02-01T00:00:00Z</published>
    <summary type="text">Title: Developmental trajectories of atopic dermatitis with multiomics approaches in the infant gut: COCOA birth cohort
Authors: Lee, Eun; Kim, Jeong-Hyun; Lee, So-Yeon; Lee, Si Hyeon; Park, Yoon Mee; Oh, Hea Young; Yeom, Jeonghun; Ahn, Hee-Sung; Yoo, Hyun Ju; Kim, Bong-Soo; Yun, Sun Mi; Choi, Eom Ji; Song, Kun Baek; Park, Min Jee; Ahn, Kangmo; Kim, Kyung Won; Shin, Youn Ho; Suh, Dong In; Song, Joo Young; Hong, Soo-Jong
Abstract: Background: An understanding of the phenotypes and endotypes of atopic dermatitis (AD) is essential for developing precision therapies. Recent studies have demonstrated evidence for the gut-skin axis in AD . Objective: We sought to determine the natural course and clinical characteristics of AD phenotypes and investigate their mechanisms on the basis of multiomics analyses. Methods: Latent class trajectory analysis was used to classify AD phenotypes in 2247 children who were followed until age 9 years from the COhort for Childhood Origin of Asthma and allergic diseases birth cohort study. Multiomics analyses (microbiome, metabolites, and gut epithelial cell transcriptome) using stool samples collected at age 6 months were performed to elucidate the underlying mechanisms of AD phenotypes. Results: Five AD phenotypes were classified as follows: never/ infrequent, early-onset transient, intermediate transient, late- onset, and early-onset persistent. Early-onset persistent and late-onset phenotypes showed increased risks of food allergy and wheezing treatment ever, with bronchial hyperresponsiveness evident only in the early-onset persistent phenotype. Multiomics analyses revealed a significantly lower relative abundance of Ruminococcus gnavus and a decreased gut acetate level in the early-onset persistent phenotype, with potential associations to ACSS2, Janus kinase-signal transducer and activator of transcription signaling, and systemic TH2 inflammation. The early-onset transient phenotype was associated with adenosine monophosphate-activated protein kinase (AMPK) and/or chemokine signaling regulation, whereas the late-onset phenotype was linked with IL-17 and barrier dysfunction. Conclusions: Multiomics profiling in early life may offer insights into different mechanisms underlying AD phenotypes in children. (J Allergy Clin Immunol 2025;155:557-68.)</summary>
    <dc:date>2025-02-01T00:00:00Z</dc:date>
  </entry>
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