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    <title>Repository Collection: null</title>
    <link>https://scholar.dgist.ac.kr/handle/20.500.11750/1194</link>
    <description />
    <pubDate>Thu, 04 Jun 2026 14:36:27 GMT</pubDate>
    <dc:date>2026-06-04T14:36:27Z</dc:date>
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      <title>Comprehensive Insights into Prion Diseases: Classification, Mechanisms of Action, Detection Methods, and Preventive Strategies</title>
      <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60406</link>
      <description>Title: Comprehensive Insights into Prion Diseases: Classification, Mechanisms of Action, Detection Methods, and Preventive Strategies
Author(s): Bora, Jutishna; Kumari, Pallavi; Tripathi, Anjali; Mondal, Sagar; Pandey, Vinay Kumar; Malik, Sumira M.; Rustagi, Sarvesh; Ramniwas, Seema; Talukder, Nayan; Preetam, Subham
Abstract: Health concerns have become increasingly prominent in society, with even minor injuries demonstrating an exaggerated potential for complications. This phenomenon parallels an unrelated yet historically significant observation from the 18th century, wherein Merino sheep exhibited abnormal behavioural manifestations indicative of a mysterious ailment. Upon further scientific investigation, this condition was identified as the first recorded instance of a novel class of neurodegenerative disorders now classified as prion diseases, or transmissible spongiform encephalopathies (TSEs), which are brought on by aberrant folding of the brain&amp;apos;s cellular prion protein (PrPc). Rapidly progressive neurodegenerative disorders due to prion disease can be seen that can be tough to analyse and are transmissible under certain circumstances. Transmissible spongiform encephalopathies, sometimes known as prion diseases, are a fatal class of inherited, spontaneous, and epidemic neurodegenerative illnesses that affect both humans and animals. Prion disease arises in three ways: acquired or sporadic, inherited, or causal. Many pharmacological techniques and therapies aimed at various stages of the illness progression have been developed and assessed over an extended period, with a select number making progress in clinical trials. As yet, there are no helpful treatment medications authorised for prion illnesses. This paper contains a comprehensive study of the prion protein, prion disease, and different types of prion disease found in animals and humans. The mechanism of this disease, as well as its detection, diagnosis, treatment, and prevention, is discussed in this article. © 2025 Elsevier B.V., All rights reserved.</description>
      <pubDate>Mon, 30 Jun 2025 15:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholar.dgist.ac.kr/handle/20.500.11750/60406</guid>
      <dc:date>2025-06-30T15:00:00Z</dc:date>
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    <item>
      <title>Bioactive Coatings for Cardiovascular Stents: Modulating Immune Response for Enhanced Performance</title>
      <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60405</link>
      <description>Title: Bioactive Coatings for Cardiovascular Stents: Modulating Immune Response for Enhanced Performance
Author(s): Preetam, Subham; Mishra, Richa; Thapliyal, Shailendra; Rustagi, Sarvesh; Deshwal, Ravi Kumar; Ramniwas, Seema; Dhasmana, Archna; S. Rajab, Bodour; Alghamdi, Saad; Malik, Sumira
Abstract: Cardiovascular disorders remain a leading cause of death worldwide, and the use of contemporary stents is paving the way for a profound shift in the field of cardiology. In the surgical process postimplantation, the graft or stent and host-immune interaction play a significant role in the healing process, thus it is a major challenge in healthcare. To address these challenges, recent advancements have introduced bioactive coatings with specialized modifications in stents to enhance their interaction with surrounding environment. These next-generation coatings are emphasizing strategies that reduce immune responses, that achieve up to similar to 45% decrease in TNF-alpha expression and similar to 60% reduction in IL-1 beta release in vitro, as well as similar to 2.5-fold increase in M2/M1 macrophage ratio in animal models and promote vascular healing. In this review, we explore a range of coating materials, such as bioactive peptides, polymers, and composite systems, that have demonstrated the ability to elicit favorable biological responses while mitigating complications like inflammation, thrombosis, and restenosis. We explored the recent in vitro and in vivo research that shows the clinical potential of these coatings over times. Emerging innovations in this field highlight promising strategies for reducing inflammation and promoting endothelial healing in future cardiovascular stent designs.</description>
      <pubDate>Tue, 30 Sep 2025 15:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholar.dgist.ac.kr/handle/20.500.11750/60405</guid>
      <dc:date>2025-09-30T15:00:00Z</dc:date>
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      <title>Exosome-driven biohybrid nanorobots: bridging nature and nanotechnology in biomedical innovation</title>
      <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60404</link>
      <description>Title: Exosome-driven biohybrid nanorobots: bridging nature and nanotechnology in biomedical innovation
Author(s): Preetam, Subham; Lata, Smita; Bora, Jutishna; Thapliyal, Shailendra; Mehta, Shalini; Ramniwas, Seema; Deshwal, Ravi; Rustagi, Sarvesh; Talukdar, Nayan; Malik, Sumira
Abstract: Exosome- and extracellular vesicle (EV)-based biohybrid nanorobots represent a cutting-edge approach in nanomedicine, combining the natural targeting, immune tolerance, and molecular transport capabilities of EVs with the functional versatility of engineered nanomaterials. These hybrid systems can be designed for guided or autonomous navigation, enabling site-specific drug delivery with minimal cytotoxicity. Recent advances have integrated magnetic, photothermal, or drug-loaded components into EVs, transforming them into innovative nanoscale delivery systems. As naturally secreted vesicles from most cell types, EVs facilitate intercellular communication and are increasingly recognized for their clinical potential in treating conditions like Crohn&amp;apos;s disease, type 1 diabetes, and COVID-19. Biohybrid EV nanorobots offer enhanced biodistribution, stability, and cellular uptake compared to traditional nanoparticles. Key design challenges include ensuring reproducibility, size control, and functional stability. This next-generation drug delivery platform holds promise for overcoming limitations of conventional systems while advancing targeted therapy and personalized medicine.</description>
      <pubDate>Sun, 31 Aug 2025 15:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholar.dgist.ac.kr/handle/20.500.11750/60404</guid>
      <dc:date>2025-08-31T15:00:00Z</dc:date>
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      <title>Down-regulation of HSPA9 reduces tyrosine hydroxylase-positive neurons in mouse substantia nigra and induces Parkinson&amp;apos;s disease-like motor impairments</title>
      <link>https://scholar.dgist.ac.kr/handle/20.500.11750/60403</link>
      <description>Title: Down-regulation of HSPA9 reduces tyrosine hydroxylase-positive neurons in mouse substantia nigra and induces Parkinson&amp;apos;s disease-like motor impairments
Author(s): Hyung, Hyejin; Jang, Soyoung; Kim, Si-Yong; Bae, Ji-Eun; Park, Ji Yeong; Lim, Su-Geun; Ko, Jiwon; Jang, Soyeon; Kim, Joon Bum; Chae, Hee Young; Park, Song; Yi, Junkoo; Choi, Dong Kyu; Kim, Myoung Ok; Lee, Hyun-Shik; Cho, Dong-Hyung; Young Ryoo, Zae
Abstract: Parkinson&amp;apos;s disease (PD) is a progressive neurological disorder characterized by the degeneration of midbrain dopaminergic neurons and disabling motor impairments. Heat shock protein family A member 9 (HSPA9) play a crucial role in neuronal homeostasis by regulating the import of various mitochondrial proteins. HSPA9 is down-regulated in neurodegenerative diseases such as Alzheimer&amp;apos;s disease and PD, and its loss leads to excessive mitochondrial fragmentation with oxidative stress, which subsequently causes damage to dopaminergic neurons. Moreover, HSPA9 interacts with multiple PD-associated proteins, including Pink1, DJ-1, and alpha-synuclein, however precise roles of HSPA9 in PD pathophysiology remain unclear. To further explore the contributions of HSPA9 in PD pathogenesis, we developed an HSPA9 knockout mouse. Haploinsufficiency of Hspa9 (Hspa9+/-) was associated with the loss of tyrosine hydroxylase-positive neurons in the striatum and substantia nigra. Furthermore, Hspa9 haploinsufficiency induced excessive mitochondrial fission, enhanced apoptotic signaling, and resulted in diminished motor performance during the rotarod test. Administration of the mitochondrial neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in Hspa9+/- mice further exacerbated the loss of dopaminergic neurons, aggravated motor impairments, and enhanced activation of apoptosis effector caspase-3. These results suggest that down-regulation of HSPA9 may contribute to the development and progression of PD, potentially offering a new therapeutic strategy for PD treatment.</description>
      <pubDate>Sun, 30 Nov 2025 15:00:00 GMT</pubDate>
      <guid isPermaLink="false">https://scholar.dgist.ac.kr/handle/20.500.11750/60403</guid>
      <dc:date>2025-11-30T15:00:00Z</dc:date>
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