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    <title>ScholarWorks Community:</title>
    <link>https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/792</link>
    <description />
    <pubDate>Mon, 13 Apr 2026 05:16:14 GMT</pubDate>
    <dc:date>2026-04-13T05:16:14Z</dc:date>
    <item>
      <title>Aspacochioside C from Asparagus cochinchinensis attenuates eumelanin synthesis via inhibition of TRP2 expression</title>
      <link>https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/89482</link>
      <description>Title: Aspacochioside C from Asparagus cochinchinensis attenuates eumelanin synthesis via inhibition of TRP2 expression
Authors: Yunmam, Silvia; Lee, Hae Ran; Hong, Seong Min; Kim, Ji-Young; Kang, Tong Ho; Lee, Ai Young; Jang, Dae Sik; Kim, Sun Yeou
Abstract: Aspacochioside C (ACC) is a steroidal saponin isolated from Asparagus cochinchinensis. Steroidal saponins, such as pseudoprotodioscin and dioscin, are known to inhibit melanogenesis, but the role of ACC in melanogenesis remains unknown. Due to the toxic effect of the commonly used skin whitening agents like arbutin, kojic acid and a-lipoic acid alternative plant products are recentlybeen studied for their anti-hypergmentation effect. This study explores the role of ACC in melanogenesis in both in vivo and in vitro models. Here, we for the first time demonstrate that ACC attenuated a-MSH- and UVB-induced eumelanin production by inhibiting tyrosinase-related protein (TRP)-2 protein expression in both murine B16F10 and human melanoma MNT1 cells. However, ACC had no significant effect on pheomelanin concentration. ACC also decreased the pigmentation density in zebrafish embryos, which indicates that ACC targets TRP2 and inhibits eumelanin synthesis. Our results demonstrate that ACC inhibits TRP2, thereby attenuating eumelanin synthesis both in in vitro and in vivo zebrafish model. Therefore, ACC can potentially be used as an anti-melanogenic agent for both aesthetic and pharmaceutical purposes.</description>
      <pubDate>Fri, 01 Sep 2023 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/89482</guid>
      <dc:date>2023-09-01T00:00:00Z</dc:date>
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    <item>
      <title>Hypersensitivity Reactions to Anticancer Monoclonal Antibodies</title>
      <link>https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/89424</link>
      <description>Title: Hypersensitivity Reactions to Anticancer Monoclonal Antibodies
Authors: 장하영; 최보윤; 강혜련; 오정미
Abstract: Therapeutic monoclonal antibodies (TmAbs) are new treatment options for cancer. While their use is more common, hypersensitivity reactions (HSRs) to these drugs have been increased, preventing the use of first-line therapies. The aim of this review is to update and discuss the HSRs to TmAbs in their clinical features and management. Type 1 hypersensitivity is the most common type of the HSRs to TmAbs, followed by cytokine release reactions (CRRs) and type 4 hypersensitivity. Mixed reactions of various types might also occur. TmAbs can have different immunogenicity depending on their non-human epitope contents, target proteins, and solubilizing additives. It may be also affected by the patient’s baseline condition and the number of administrations. When HSRs occur, it is recommended to classify the mechanism into type 1/type 4 hypersensitivity and CRRs. A skin test and desensitization are generally the most useful management for type 1 hypersensitivity but there is no standardized protocol for TmAbs yet. Readministration is contraindicated in type 4 hypersensitivity reactions and supportive care is effective in CCRs. Understanding the characteristics and measures for each HSRs may be helpful to ensure the safe use of anticancer monoclonal antibodies. (PeRM 2023;15:1-10)</description>
      <pubDate>Wed, 01 Mar 2023 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/89424</guid>
      <dc:date>2023-03-01T00:00:00Z</dc:date>
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    <item>
      <title>Aerobic Exercise Ameliorates Muscle Atrophy Induced by Methylglyoxal via Increasing Gastrocnemius and Extensor Digitorum Longus Muscle Sensitivity</title>
      <link>https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/89417</link>
      <description>Title: Aerobic Exercise Ameliorates Muscle Atrophy Induced by Methylglyoxal via Increasing Gastrocnemius and Extensor Digitorum Longus Muscle Sensitivity
Authors: Hong, Seong-Min; Lee, Eun Yoo; Park, Jinho; Kim, Jiyoun; Kim, Sun Yeou
Abstract: Muscle atrophy is characterized by the loss of muscle function. Many efforts are being made to prevent muscle atrophy, and exercise is an important alternative. Methylglyoxal is a well-known causative agent of metabolic diseases and diabetic complications.
This study aimed to evaluate whether methylglyoxal induces muscle atrophy and to evaluate the ameliorative effect of moderateintensity aerobic exercise in a methylglyoxal-induced muscle atrophy animal model. Each mouse was randomly divided into three groups: control, methylglyoxal-treated, and methylglyoxal-treated within aerobic exercise. In the exercise group, each mouse was trained on a treadmill for 2 weeks. On the last day, all groups were evaluated for several atrophic behaviors and skeletal muscles, including the soleus, plantaris, gastrocnemius, and extensor digitorum longus were analyzed. In the exercise group, muscle mass was restored, causing in attenuation of muscle atrophy. The gastrocnemius and extensor digitorum longus muscles showed improved fiber cross-sectional area and reduced myofibrils. Further, they produced regulated atrophy-related proteins (i.e., muscle atrophy F-box, muscle RING-finger protein-1, and myosin heavy chain), indicating that aerobic exercise stimulated their muscle sensitivity to reverse skeletal muscle atrophy. In conclusion, shortness of the gastrocnemius caused by methylglyoxal may induce the dynamic imbalance of skeletal muscle atrophy, thus methylglyoxal may be a key target for treating skeletal muscle atrophy. To this end, aerobic exercise may be a powerful tool for regulating methylglyoxal-induced skeletal muscle atrophy.</description>
      <pubDate>Fri, 01 Sep 2023 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/89417</guid>
      <dc:date>2023-09-01T00:00:00Z</dc:date>
    </item>
    <item>
      <title>Cremastranone-Derived Homoisoflavanes Suppress the Growth of Breast Cancer Cells via Cell Cycle Arrest and Caspase-Independent Cell Death</title>
      <link>https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/89416</link>
      <description>Title: Cremastranone-Derived Homoisoflavanes Suppress the Growth of Breast Cancer Cells via Cell Cycle Arrest and Caspase-Independent Cell Death
Authors: Choi, Yeram; Park, Sangkyu; Lee, Seul; Shin, Ha-Eun; Kwon, Sangil; Choi, Jun-Kyu; Lee, Myeong-Heon; Seo, Seung-Yong; Lee, Younghee
Abstract: Breast cancer is the most common cancer and a frequent cause of cancer-related deaths among women wordlwide. As therapeutic strategies for breast cancer have limitations, novel chemotherapeutic reagents and treatment strategies are needed. In this study, we investigated the anti-cancer effect of synthetic homoisoflavane derivatives of cremastranone on breast cancer cells.
Homoisoflavane derivatives, SH-17059 and SH-19021, reduced cell proliferation through G2/M cell cycle arrest and induced caspase-independent cell death. These compounds increased heme oxygenase-1 (HO-1) and 5-aminolevulinic acid synthase 1 (ALAS1), suggesting downregulation of heme. They also induced reactive oxygen species (ROS) generation and lipid peroxidation.
Furthermore, they reduced expression of glutathione peroxidase 4 (GPX4). Therefore, we suggest that the SH-17059 and SH-19021 induced the caspase-independent cell death through the accumulation of iron from heme degradation, and the ferroptosis might be one of the potential candidates for caspase-independent cell death.</description>
      <pubDate>Fri, 01 Sep 2023 00:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/89416</guid>
      <dc:date>2023-09-01T00:00:00Z</dc:date>
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