<?xml version="1.0" encoding="UTF-8"?>
<rss xmlns:dc="http://purl.org/dc/elements/1.1/" version="2.0">
  <channel>
    <title>ScholarWorks Collection:</title>
    <link>https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/396</link>
    <description />
    <pubDate>Fri, 24 Jul 2026 08:07:40 GMT</pubDate>
    <dc:date>2026-07-24T08:07:40Z</dc:date>
    <item>
      <title>Smartwatch-Based Unobtrusive Continuous Anxiety Tracker for Evaluating Post-Stroke Patients’ Quality of Life</title>
      <link>https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/219369</link>
      <description>Title: Smartwatch-Based Unobtrusive Continuous Anxiety Tracker for Evaluating Post-Stroke Patients’ Quality of Life
Authors: Choi, Sanghoon; Seo, Woo-Keun; Jung, Jin-Man; Park, Seongho; Seo, Hyo-Chang
Abstract: Post-stroke anxiety (PSA) affects 20–30% of stroke survivors and significantly impacts quality of life (QoL) and rehabilitation outcomes. Traditional emotion assessment relies on subjective self-reports, limiting to capture real-time fluctuations in emotional states. This study proposes a self-supervised learning (SSL) framework combined with a transformer-based emotion classifier to enable continuous anxiety tracking in patients with stroke using smartwatch-derived photoplethysmography (PPG). The SSL model was pretrained on the VitalDB dataset using R-peak-to-peak intervals (RRIs) extracted from electrocardiography (ECG) signals. The pretrained encoder is then integrated into a transformer-based classifier trained on the Psychophysiology of Positive and Negative Emotions (POPANE) dataset with labeled emotional responses. The trained model was applied to smartwatch-derived pulse peak intervals (PPI) from patients with stroke, and evaluated against Generalized Anxiety Disorder-7 (GAD-7) scores and we evaluated it against GAD-7 scores using both group-level and 90-day longitudinal analyses, along with on-device feasibility on a Galaxy Watch6. Over the 30 days preceding the second survey, between-group differences were significant by Welch’s t-test (p = 0.0086), and discrimination reached an AUC of 0.859 with a 95% confidence interval of 0.664–0.992. In 90-day monitoring, generalized estimating equations showed persistent divergence when groups were defined by the second survey, with significant differences across multiple weeks preceding the survey, consistent with the retrospective GAD-7 window. These findings indicate that ECG-pretrained cardiac representations can be translated to smartwatch PPG for unobtrusive, continuous anxiety tracking in stroke. The results provide feasibility-level evidence and motivate larger, multi-site prospective validation toward clinical deployment.</description>
      <pubDate>Wed, 01 Jul 2026 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/219369</guid>
      <dc:date>2026-07-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Regional amyloid PET asymmetry and long-term clinical trajectory in mild cognitive impairment</title>
      <link>https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/218201</link>
      <description>Title: Regional amyloid PET asymmetry and long-term clinical trajectory in mild cognitive impairment
Authors: Lee, Yunjin; Kang, Sungwoo; Kim, Yong Sung; Kim, June Sic; Kim, Hee-Jin
Abstract: INTRODUCTION: Hemispheric amyloid positron emission tomography(PET) asymmetry may capture prognostic information beyond binary amyloid status in amnestic mild cognitive impairment (aMCI). METHODS: We retrospectively studied 158 aMCI patients with baseline 18F-florbetaben PET and magnetic resonance imaging acquired within 12 months and a mean follow-up of 6.89 +/- 2.63 years. Participants were classified as amyloid beta (Aj3)-stable (n = 67), Aj3-progressor (n =18), Aj3+ stable (n = 33), or Aj3+ progressor (n = 40). Vertex-wise cortical standardized uptake value ratio (SUVR) asymmetry (|AI|) was analyzed using surface-based general linear models adjusted for age, sex, education years, apolipoprotein E E4 carrier status, global cortical SUVR, and clinical follow-up duration. RESULTS: Aj3-MCI progressors showed higher |AI| in the lateral orbitofrontal cortex (790 vertices, cluster-wise p = 0.0002). Aj3+ MCI progressors showed lower |AI| in the lingual gyrus (478 vertices, cluster-wise p = 0.0001). No cross-status contrast yielded a significant cluster in the covariate-adjusted model. DISCUSSION: Amyloid PET asymmetry reflects prognostic heterogeneity in aMCI, with distinct distributional patterns according to amyloid status.</description>
      <pubDate>Mon, 01 Jun 2026 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/218201</guid>
      <dc:date>2026-06-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Functional impact of the ATP1A3-p.A813V variant: insights into a calcium-driven hyperexcitability cascade in rapid-onset dystonia-Parkinsonism</title>
      <link>https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/212896</link>
      <description>Title: Functional impact of the ATP1A3-p.A813V variant: insights into a calcium-driven hyperexcitability cascade in rapid-onset dystonia-Parkinsonism
Authors: Lim, Su Min; Kim, Suhyun; Park, Jinseok; Kim, Young-Eun; Na, Ok Cho; Nahm, Minyeop; Noh, Min-Young; Oh, Ki-Wook; Ki, Chang-Seok; Shin, Woong-Hee; Park, Hae-Chul; Kim, Seung Hyun
Abstract: Background Mutations in the neuronal Na+/K+-ATPase subunit ATP1A3 are linked to a spectrum of neurological disorders, including rapid-onset dystonia-parkinsonism (RDP), yet their pathogenic mechanisms remain incompletely understood. We describe the complex clinical characteristics of a patient with early-onset movement disorders and a likely pathogenic de novo variant in ATP1A3(c &amp;amp; centerdot;2438C&amp;gt;T, p.A813V). Methods We identified a de novo heterozygous ATP1A3 p.A813V variant in a patient with clinically confirmed RDP and employed an integrative approach combining molecular dynamics (MD) simulations, zebrafish models, and patient-derived induced neurons (iNeurons) to delineate its pathogenesis. Results MD simulations revealed that the p.A813V substitution structurally distorts transmembrane helix packing, reduces structural stability, and diminishes water accessibility at the cation-binding site, predicting impaired Na+/K+-ATPase function. In vivo, atp1a3b knockout zebrafish developed pronounced neuronal hyperexcitability-reflected by elevated c-fos and pERK expression-that emerged before overt neurodegeneration, motor axonopathy, and neuromuscular junction defects. Complementarily, neurons expressing ATP1A3-p.A813V displayed significantly prolonged calcium transient decay times, suggesting a potential mechanism of altered Ca2+ handling and delayed clearance mechanisms compatible with ATP1A3 dysfunction. Consistent with these findings, patient-derived iNeurons exhibited markedly reduced ATP1A3 protein abundance and Na+/K+-ATPase activity. Conclusions Together, these findings lead us to propose a mechanistic model in which ATP1A3 dysfunction disrupts Ca2+ homeostasis, triggers neuronal hyperexcitability, and culminates in progressive neurodegeneration. This work provides a molecular and functional framework for targeting ionic and calcium homeostasis as a promising therapeutic strategy for ATP1A3-related disorders.</description>
      <pubDate>Fri, 01 May 2026 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/212896</guid>
      <dc:date>2026-05-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Physical frailty and MRI markers of structural brain integrity in the community-dwelling late middle-aged and old adults (vol 15, 40464, 2025)</title>
      <link>https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/212792</link>
      <description>Title: Physical frailty and MRI markers of structural brain integrity in the community-dwelling late middle-aged and old adults (vol 15, 40464, 2025)
Authors: Lee, Dong Yoon; Kim, Young Seo; Kim, Mi Kyung; Shin, Min-Ho; Koh, Sang Baek; Kim, Hyeon Chang; Chung, Insung; Lee, Jong-Min; Kang, Yeonwook; Kim, Yu-Mi
Abstract: Correction to: Scientific Reportshttps://doi.org/10.1038/s41598-025-24208-z, published online 18 November 2025 The original version of this Article contained errors. In the original version of this Article, a dataset contained a coding error, in which the code was mis-specified as ‘-5’ instead of ‘5’. Although this didn’t alter the study’s findings, some of the values are incorrect. (Table presented.) Furthermore, the values presented in Figs. 2 and 3 have been corrected. The Original, incorrect Figures and their accompanying legends are present in this Correction Note. And finally, some values in the Supplementary information file have been corrected. The Original Incorrect Supplementary information file is provided below. The original version of this Article has been corrected.</description>
      <pubDate>Wed, 01 Apr 2026 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/212792</guid>
      <dc:date>2026-04-01T00:00:00Z</dc:date>
    </item>
  </channel>
</rss>

