https://scholar.dgist.ac.kr/handle/20.500.11750/1194 Wed, 07 Oct 2026 10:44:31 GMT 2026-10-07T10:44:31Z https://scholar.dgist.ac.kr/handle/20.500.11750/60899 Title: The insulin receptor inhibitor BMS-754807 alleviates neuroinflammation and Alzheimer's disease pathologies across human cellular and mouse models Author(s): Lee, Hyun-Ju; Seok, Jaewoo; Kang, Sora; Oh, Seokjun; Hwang, Jeong-Woo; Kim, Yu-Jin; Seo, Jinsoo; Hoe, Hyang-Sook Abstract: (Background) BMS-754807 is a dual inhibitor of insulin-like growth factor 1 receptor (IGF-1R) and insulin receptor (IR) that is in phase II clinical trials for the treatment of HR-positive and HER2-negative breast cancer. Because IGF-1R signaling regulates inflammatory responses, pharmacological modulation of IGF-1R may have therapeutic potential for Alzheimer’s disease (AD); however, the effects of BMS-754807 on neuroinflammatory responses/AD pathology and cognitive function have not been fully investigated. (Methods) We examined whether BMS-754807 modulates neuroinflammation and AD pathologies in multiple in vivo animal models and in vitro human models. BMS-754807 (20 mg/kg, i.p.) was systemically administered in wild-type mice challenged with LPS, 5xFAD mice, and PS19 transgenic mice. In addition, human-induced pluripotent stem cell (hiPSC)-derived microglia challenged with LPS and AD hiPSC-derived neurons were treated with 2.5 µM BMS-754807. For all models, the effects of BMS-754807 treatment were analyzed by real-time PCR, immunofluorescence staining, western blotting, ELISA, and/or activity assays. (Results) BMS-754807 treatment significantly decreased p-IGF-IR (on-target) levels, LPS-induced proinflammatory cytokine production, and reactive oxygen species levels; restored HO-1 expressions; and inhibited AKT/STAT3 signaling in BV2 microglial cells. Similarly, BMS-754807 treatment reduced LPS-evoked proinflammatory cytokine expressions in primary microglial cells and primary astrocytes. In addition, BMS-754807 administration mitigated LPS-stimulated gliosis, microglial/astrocyte-associated dynamics, STAT3/NF-κB phosphorylation, and potentially NLRP3 inflammasome in vitro and/or in WT mice. Moreover, BMS-754807 treatment suppressed LPS-mediated proinflammatory responses through IGF-1R and NLRP3 in BV2 microglial cells. In 5xFAD mice, BMS-754807 Thu, 30 Apr 2026 15:00:00 GMT https://scholar.dgist.ac.kr/handle/20.500.11750/60899 2026-04-30T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/60898 Title: A manifesto for Sustainability Robotics Author(s): Song, S.; Mazzolai, B.; Kovač, M. Abstract: Sustainability spans environmental, societal and economic challenges, from climate change to healthcare and education. Robotics holds substantial promise for addressing these issues, yet current developments remain fragmented and lack a unifying framework. This fragmentation risks unintended consequences, including unequal access to technology and missed opportunities for broader impact. Here we advocate for a new discipline, Sustainability Robotics, structured around three guiding principles: robots should be minimally invasive, reducing disruption to ecosystems and socio-economic systems; universally accessible, extending benefits to underserved communities and extreme environments; and symbiotic, generating mutually beneficial outcomes for humans and nature. We define two complementary dimensions. The first, sustainable robot design, focuses on minimizing environmental impact through materials, energy and manufacturing. The second, robotic solutions for sustainability, leverages robotics to address environmental, social and economic challenges. By integrating perspectives from science, engineering, economics, ethics and policy, Sustainability Robotics provides a foundation for coordinated research, education and innovation. This framework aims to align robotics development with global sustainability goals, enabling more equitable and effective technological impact. Tue, 30 Jun 2026 15:00:00 GMT https://scholar.dgist.ac.kr/handle/20.500.11750/60898 2026-06-30T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/60895 Title: Ginsenoside Rb1-Enriched Saponin Fraction Inhibits M1 Macrophage Polarization by Suppression of TLR4 Trafficking in Metabolic Dysfunction-Associated Alcoholic Liver Disease Author(s): Kim, Tae-Un; Yim, Jae-Hyuk; Kim, Woo Jun; Lee, Seoung-Woo; Kim, Hee-Yeon; Kang, Kyung-Ku; Seo, Min-Soo; Rhee, Man Hee; Baek, Su-Min; Choi, Seong-Kyoon; Park, Jin-Kyu Abstract: Background/Objectives: Metabolic dysfunction-associated alcoholic liver disease (MetALD) is a serious worldwide health concern, exhibiting metabolic dysfunction-associated lipid accumulation, alcohol-associated oxidative damage, and endotoxin-induced inflammation. Rb1-enriched red ginseng saponin fraction (RGSF) has been known to exhibit anti-inflammatory and anti-oxidative properties, but its role in MetALD remains to be fully elucidated. This study aims to investigate the specific mechanism of RGSF in the MetALD mouse model. Methods: The MetALD mouse model was administered with or without Rb1-RGSF for 7 weeks. Histopathological and molecular analyses, along with primary cell isolation, were conducted for in vivo and ex vivo investigations. M1 macrophage polarization was assessed by analyzing pro-inflammatory cytokine expression. NF-kB/p65 and TLR4 protein expression were measured before being visualized using immunofluorescence assays and confocal microscopy. Results: Histopathological examination revealed that RGSF treatment markedly reduced hepatic steatosis and attenuated inflammatory lesions in MetALD independent of oxidative stress. Notably, RGSF administration suppressed the LPS-induced internalization of surface TLR4. During the early inflammatory phase, RGSF prevented the LPS-mediated loss of the 130 kDa TLR4 form at the cell membrane, thereby limiting the generation of its 110 kDa cytoplasmic form. LPS-binding assay confirmed the direct interactions between TLR4 and RGSF. Conclusions: Collectively, these findings demonstrate that RGSF regulates TLR4 expression and trafficking, leading to the suppression of M1 macrophage polarization by inhibiting LPS-TLR4 surface interactions, thus exhibiting hepatoprotective effects. Tue, 30 Jun 2026 15:00:00 GMT https://scholar.dgist.ac.kr/handle/20.500.11750/60895 2026-06-30T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/60889 Title: Engineering extracellular vesicle biogenesis for therapeutic gene delivery: emerging genetic programming strategies and translational prospects Author(s): Preetam, Subham; Rath, Pratyasa; Al‑Enazi, Nouf M.; Sharaf, Abeer Abdullah M; Jumah, Jawaher Bin; Govindarajan, R.K.; Goud, Pavan; Thiruvengadam, Muthu; Mathivanan, Krishnamurthy Abstract: Extracellular vesicles (EVs) have emerged as promising biological nanocarriers for gene therapy due to their intrinsic ability to transport nucleic acids, proteins, and lipids between cells. Advances in EV biology have revealed complex regulatory mechanisms governing vesicle biogenesis, cargo sorting, secretion, and uptake, offering multiple opportunities for therapeutic engineering. Concurrently, modern genetic technologies, including the CRISPR-Cas9 genome editing system and synthetic biology tools, have enabled precise manipulation of EV composition and functionality. This review integrates current knowledge of EV biogenesis with emerging genetic engineering strategies to transform EVs into programmable gene delivery systems. We discuss recent advances in genetic tools for studying EV dynamics, methods for engineering EV cargo and targeting specificity, and the application of EV platforms for RNA and genome-editing therapies. Furthermore, key challenges related to vesicle heterogeneity, large-scale production, and clinical translation are examined. Finally, we highlight future perspectives on programmable EV therapeutics and their potential role in next-generation precision medicine. Tue, 30 Jun 2026 15:00:00 GMT https://scholar.dgist.ac.kr/handle/20.500.11750/60889 2026-06-30T15:00:00Z