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  <channel rdf:about="https://ir.ymlib.yonsei.ac.kr/handle/22282913/168742">
    <title>DSpace Community:</title>
    <link>https://ir.ymlib.yonsei.ac.kr/handle/22282913/168742</link>
    <description />
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        <rdf:li rdf:resource="https://ir.ymlib.yonsei.ac.kr/handle/22282913/210210" />
        <rdf:li rdf:resource="https://ir.ymlib.yonsei.ac.kr/handle/22282913/211445" />
        <rdf:li rdf:resource="https://ir.ymlib.yonsei.ac.kr/handle/22282913/211298" />
        <rdf:li rdf:resource="https://ir.ymlib.yonsei.ac.kr/handle/22282913/211299" />
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    </items>
    <dc:date>2026-04-18T18:05:00Z</dc:date>
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  <item rdf:about="https://ir.ymlib.yonsei.ac.kr/handle/22282913/210210">
    <title>Impact of gut microbiota on host stem cells across the gastrointestinal tract</title>
    <link>https://ir.ymlib.yonsei.ac.kr/handle/22282913/210210</link>
    <description>Title: Impact of gut microbiota on host stem cells across the gastrointestinal tract
Authors: Jeong, Haengdueng; Lee, Yura; Nam, Ki Taek; 이유라
Abstract: The gut microbiota plays a pivotal role in maintaining gastrointestinal (GI) homeostasis by influencing epithelial integrity, immunity, and metabolism. Recent studies have uncovered that gut microbiota can directly or indirectly modulate the behavior and function of adult stem cells across the GI tract, which are essential for tissue regeneration and disease prevention. Moreover, key microbial metabolites including short-chain fatty acids (SCFAs), tryptophan-derived indoles, succinate, secondary bile acids, and retinoic acid exert diverse effects on stem cell quiescence, proliferation, and differentiation. This review provides current knowledge on the interaction between gut microbiota and host stem cells in the stomach, intestine, and colon.</description>
    <dc:date>2026-12-01T00:00:00Z</dc:date>
  </item>
  <item rdf:about="https://ir.ymlib.yonsei.ac.kr/handle/22282913/211445">
    <title>Design, synthesis and biological evaluation of symmetric thiadiazole carboxamide derivative as glutaminase inhibitor</title>
    <link>https://ir.ymlib.yonsei.ac.kr/handle/22282913/211445</link>
    <description>Title: Design, synthesis and biological evaluation of symmetric thiadiazole carboxamide derivative as glutaminase inhibitor
Authors: Cyriac, Rajath; Lee, Eun Ji; Kwon, Yeongju; Yun, Mi Ran; Jung, Myoung Eun; Ahn, Sunjoo; Chae, Chang Hak; Choi, Gildon; Cho, Byoung Chul; Lee, Kwangho; 윤미란
Abstract: Metabolic reprogramming toward glutamine anaplerosis is a well-established vulnerability in tumors harboring co-occurring KRAS and KEAP1 mutations, creating a dependency on glutaminase (GLS)-mediated glutaminolysis for survival and growth. Although allosteric GLS inhibitors such as BPTES (Bis-2-(5-phenylacetamido-1,3,4thiadiazol-2-yl)ethyl sulfide) and later-generation analogs such as CB-839 (Telaglenastat) have pharmacologically validated this target, their clinical utility has been constrained by suboptimal drug-like properties, including poor solubility and bioavailability. To overcome these limitations, we developed TRG-192, a novel symmetric amidothiadiazole derivative engineered with a distinct chemical scaffold to enhance physicochemical and pharmacokinetic profiles. In vitro characterization revealed that TRG-192 is a potent GLS inhibitor (IC50 = 68 nM). This biochemical potency translated to a functional effect in a cellular model of glutamine dependence, as evidenced by a significant depletion of intracellular glutamate pools in LDK378-resistant (LR) cells. Furthermore, TRG-192 demonstrated a favorable preclinical safety profile in initial toxicological assessments. Collectively, these data-encompassing potent target engagement, functional on-target activity, and preliminary safety-provide a compelling rationale for the advancement of TRG-192 into in vivo efficacy studies.</description>
    <dc:date>2026-07-01T00:00:00Z</dc:date>
  </item>
  <item rdf:about="https://ir.ymlib.yonsei.ac.kr/handle/22282913/211298">
    <title>Engineered atopic dermatitis models for recreating hypoxic conditions in atopic dermatitis microenvironments</title>
    <link>https://ir.ymlib.yonsei.ac.kr/handle/22282913/211298</link>
    <description>Title: Engineered atopic dermatitis models for recreating hypoxic conditions in atopic dermatitis microenvironments
Authors: Na, Kyeong Seok; Park, Jooyoung; Kim, Su Min; Lee, Jina; Lee, Eunji; Woo, Wonjin; Choi, Jungmin; Kim, Lark Kyun; Park, Kyung Min
Abstract: Atopic dermatitis (AD) is a chronic inflammatory condition with severe itching. The complex physiology and diverse pathogenesis of AD complicate the prediction of clinical outcomes. Therefore, it is essential to develop preclinical models closely mimicking features of AD. Herein, gelatin-based in situ crosslinkable hydrogel AD models are engineered replicating the characteristics of AD tissue. First, public data of patients with AD is used to confirm the following, using single-cell RNA sequencing analysis: (1) collagen type VI alpha 5 chain (COL6A5+) fibroblast expression in patient tissues, (2) cell interaction with dorsal root ganglions that induce itching, and (3) overexpression of hypoxia-related factors in AD tissues. Based on these characteristics, an artificial AD model is developed using gelatin-based in situ crosslinked hydrogels. 3D cell culture systems are fabricated by encapsulating cells within hydrogels, supporting 3D cell survival and growth. These models exhibit a hypoxic (pO2 &lt; 5 %) environment within the hydrogels, with upregulated expression of hypoxia-related genes. In these hydrogelbased skin models, the AD microenvironment is recreated, inducing immune responses and chronic hypoxia through IL-4 treatment and controlled oxygen concentration. Overexpression of itch-related factors, evaluation of drug response to treatment, and gene upregulation under hypoxic and immune conditions are also analyzed in the models. Our platforms are potential preclinical models for drug screening and fundamental research.</description>
    <dc:date>2026-05-01T00:00:00Z</dc:date>
  </item>
  <item rdf:about="https://ir.ymlib.yonsei.ac.kr/handle/22282913/211299">
    <title>A large puncture closer of aortic wall by multi-memory actions with thrombo-hemodynamic control</title>
    <link>https://ir.ymlib.yonsei.ac.kr/handle/22282913/211299</link>
    <description>Title: A large puncture closer of aortic wall by multi-memory actions with thrombo-hemodynamic control
Authors: Cho, Sungwoo; Ha, Hyun-Su; Lee, Sangmin; Kim, Hyunjae; Lee, Seok Joon; Kim, Jueun; Lee, Yerin; Lee, Kang Suk; Joo, Hyun-Chel; Sung, Hak-Joon; 하현수; 이예린
Abstract: The vascular wall regulates the pattern and pressure of blood flow. In cardiovascular interventions, catheters are deployed by puncturing the vessel wall, without exception. Despite continuous progress, the outcomes remain highly operator-dependent, and large punctures with high-pressure bleeding continue to pose clinical challenges. As a translatable solution, this study introduces a shape memory vascular wall plug (VWP) that automates both the Body and Wing functions within a single component, supported by a Ring assembly to maximize pressure resistance. The VWP is deployed into a 6-mm puncture in a porcine thoracic aorta under peak blood pressure, and shape recovery is triggered by a 45 degrees C saline flush to enable automated activation. Upon recovery, Body expansion combined with Ring compression tightly seals the puncture tract. The curved Wing induces hemostatic sealing and then flattens to maintain healthy blood flow and physiologic pressures. The VWP achieves suturinglevel performance in aortic puncture closure, demonstrating effective hemostasis, patency, and endothelialization. The flow-blockage ratio required to balance hemostasis with hemodynamics is computationally modeled and validated using whole-blood microfluidics. Pressure resistance is maximized by tuning Ring strain through polymer blending, indicating multi-level strategies in polymer, device design, and memory function to advance the vascular closure technology.</description>
    <dc:date>2026-05-01T00:00:00Z</dc:date>
  </item>
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