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    <title>Repository Collection: null</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/10164</link>
    <description />
    <pubDate>Sun, 23 Aug 2026 22:31:31 GMT</pubDate>
    <dc:date>2026-08-23T22:31:31Z</dc:date>
    <item>
      <title>96-Well Format-Based Liver–Heart-on-a-Chip Platform for Facile and Parallel Testing of Drug-Induced Cardiotoxicity after Liver Metabolism</title>
      <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60611</link>
      <description>Title: 96-Well Format-Based Liver–Heart-on-a-Chip Platform for Facile and Parallel Testing of Drug-Induced Cardiotoxicity after Liver Metabolism
Author(s): Lee, Sebeen; Jin, Chaewon; Choi, Hongsoo; Kim, Jin-young
Abstract: Current preclinical drug evaluation predominantly relies on conventional two-dimensional (2D) cell cultures grown in static environments, which lack dynamic interactions and fail to recapitulate complex microenvironments. These approaches are inefficient and overly simplistic, and often require costly animal models that poorly mimic human physiology. Body-on-a-chip (BoC) technology─comprising robust and flexible three-dimensional (3D) microtissues (MTs)─has emerged to address these limitations. BoC platforms constitute microphysiological systems that mimic human organ physiology and function in vitro, enabling improved toxicity screening and personalized medicine. Here, we present a 96–well format-based microfluidic liver–heart-on-a-chip platform that supports parallel, gravity-driven perfusion to efficiently predict and assess multiorgan drug effects. We demonstrate hepatic metabolism of the cardiotoxic prodrug terfenadine (TFND) into its noncardiotoxic metabolite fexofenadine within liver MTs and the consequent physiological–pathological responses of cardiac MTs. The optimized liver–heart-on-a-chip preserves multitissue functionality, underscores the importance of continuous media circulation, and reveals intertissue interactions relevant to drug-induced cardiotoxicity after liver metabolism.</description>
      <pubDate>Sat, 28 Feb 2026 15:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholar.dgist.ac.kr/handle/20.500.11750/60611</guid>
      <dc:date>2026-02-28T15:00:00Z</dc:date>
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    <item>
      <title>Polystyrene Nanoplastics Exacerbate CCl4-Induced Liver Fibrosis by Aggravating Stretch-Induced Mechanical Stress in Hepatic Stellate Cells</title>
      <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60592</link>
      <description>Title: Polystyrene Nanoplastics Exacerbate CCl4-Induced Liver Fibrosis by Aggravating Stretch-Induced Mechanical Stress in Hepatic Stellate Cells
Author(s): Yim, Jae-Hyuk; Kim, Tae-Un; Kim, Woo Jun; Kim, Hee-Yeon; Lee, Seoung-Woo; Kang, Kyung-Ku; Seo, Min-Soo; Kim, Sung Dae; Cho, Young-Eun; Baek, Su-Min; Choi, Seong-Kyoon; Park, Jin-Kyu
Abstract: Although studies on the potential hepatotoxicity of nanoplastic depositions are being conducted, there remains a lack of research on the association between nanoplastic depositions and chronic liver disease. Therefore, this research aimed to explore the influence of polystyrene nanoparticles (PS-NPs) on the progression of liver fibrosis and the mechanisms involved in the hepatic stellate cells (HSCs) activation. Chronic exposure to PS-NPs aggravated CCl4-induced liver fibrosis, as evidenced by enhanced collagen accumulation and elevated alpha-smooth muscle actin (alpha-SMA) expression. Most PS-NPs were accumulated in non-parenchymal liver cells, with Kupffer cells exhibiting the highest uptake. This accumulation was associated with enhanced recruitment of CD68-positive macrophages. However, PS-NPs were not associated with TGF-beta expression in CD68-positive cells. Additionally, CD68-positive cells treated with PS-NPs did not affect alpha-SMA expression in HSCs. Further in vitro experiments revealed that alpha-SMA and pSmad2/3 were directly promoted by PS-NPs in both LX-2 HSCs and primary isolated HSCs, indicating a direct stimulatory effect on HSC activation. PS-NPs enhanced pTGFBR1 expression of HSCs by promoting stretch-induced mechanical stress, suggesting a novel pathway through which nanoplastics may exacerbate fibrogenesis. Our findings provide the first evidence that PS-NPs, as xenobiotic particles, can directly promote HSC activation and exacerbate liver fibrosis, indicating potential health risks associated with chronic nanoplastic exposure.</description>
      <pubDate>Wed, 31 Dec 2025 15:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholar.dgist.ac.kr/handle/20.500.11750/60592</guid>
      <dc:date>2025-12-31T15:00:00Z</dc:date>
    </item>
    <item>
      <title>Bioreducible Cu2O cluster-glutathione nanohybrids with multienzyme-mimetic ROS scavenging for cisplatin-induced acute kidney injury</title>
      <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60470</link>
      <description>Title: Bioreducible Cu2O cluster-glutathione nanohybrids with multienzyme-mimetic ROS scavenging for cisplatin-induced acute kidney injury
Author(s): Lee, Hokyung; Noh, Dahye; Lee, Kyeong-Min; Ahn, Young; Park, Shin Young; Shin, Jiyeon; Shim, Man Kyu; Kim, Sun Hwa; Noh, Tae Il; Kim, Hyun-Chul; Lee, Sangmin; Kim, Kwangmeyung; Han, Hwa Seung; Yoon, Hong Yeol
Abstract: Cisplatin (Cis)-induced nephrotoxicity remains a major clinical challenge, largely driven by reactive oxygen species (ROS)-mediated oxidative stress leading to acute kidney injury (AKI). Because effective therapies for AKI remain limited, antioxidants capable of scavenging ROS and selectively accumulating in injured kidney tissue are highly desirable. Artificial nanocatalysts have emerged as promising antioxidant therapeutics owing to their advantages over natural enzymes. Here, we developed bioreducible nanohybrids (GCuNPs) composed of copper(I) oxide (Cu2O) nanocatalysts stabilized by glutathione (GSH), synthesized via the reductive reaction of copper ions in the presence of ascorbic acid and GSH. GCuNPs exhibited enhanced broad-spectrum ROS-scavenging capacity and multi-enzyme-like activities in vitro . Following systemic administration in a Cis-induced AKI mouse model, GCuNPs preferentially accumulated in injured kidneys through an impaired glomerular filtration barrier and loosening of proximal tubular tight junctions. Immunofluorescence analysis revealed that GCuNPs significantly reduced the expression of KIM-1, a proximal tubular injury marker, while preserving HO-1 expression, indicating attenuation of tubular damage and preservation of endogenous antioxidant defense. Furthermore, GCuNP treatment significantly reduced serum creatinine and blood urea nitrogen levels, improved survival, and showed no noticeable toxicity. These findings highlight GCuNPs as a promising therapeutic strategy for mitigating Cis-induced nephrotoxicity and potentially other oxidative stress-associated kidney disorders.</description>
      <pubDate>Sun, 31 May 2026 15:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholar.dgist.ac.kr/handle/20.500.11750/60470</guid>
      <dc:date>2026-05-31T15:00:00Z</dc:date>
    </item>
    <item>
      <title>Automating population construction and parallel simulation of biophysical models for neuromuscular cells: An inverse approach</title>
      <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60365</link>
      <description>Title: Automating population construction and parallel simulation of biophysical models for neuromuscular cells: An inverse approach
Author(s): Kim, Hojeong
Abstract: Biophysical modeling and simulation help to promote a comprehensive understanding of the neuromuscular mechanisms underlying muscle force generation and control in normal and pathological states. However, this process is labor intensive and limited to special conditions due to the heterogeneity of neuromuscular cells and the variability in their organization across body parts and ages. We present a methodology to resolve this issue. First, we formulate a building-block approach with an inverse modeling framework for automated population construction and tractable hierarchical analysis under various physiological conditions. Second, we devise a network folder-based approach with a virtual environment technique for efficient parallel simulation that can operate on a multicore computer, a supercomputing system, or a computer network through the internet. Third, we implement the methodology by developing open-source command-line software called pNMS. Finally, we demonstrate that pNMS can replicate experimental and simulation results from different environments and predict the population behaviors of neuromuscular cells depending on their organization and muscle length. With an intuitive, flexible application programming interface, this software tool may offer a solution for promoting efficient investigation and an in-depth understanding of neuromuscular function at cellular resolution under realistic scenarios.</description>
      <pubDate>Tue, 31 Mar 2026 15:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholar.dgist.ac.kr/handle/20.500.11750/60365</guid>
      <dc:date>2026-03-31T15:00:00Z</dc:date>
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