Sungkyunkwan University

About: Sungkyunkwan University is a education organization based out in Seoul, South Korea. It is known for research contribution in the topics: Thin film & Graphene. The organization has 28229 authors who have published 56428 publications receiving 1352733 citations. The organization is also known as: 성균관대학교.

Ultrahigh Thermal Conductivity of Interface Materials by Silver-Functionalized Carbon Nanotube Phonon Conduits

Abstract: An ultrahigh thermal conductivity (κ = 160 W m(-1) K(-1) ) of thermal interface materials is achieved with a high enhancement factor (96). A small amount (2.3 vol%) of 1D multiwalled carbon nanotubes (MWNTs) with high κ constructs effective phonon transport pathways between microscale silver-flake islands, and a solid phonon transport junction is realized by the coalescence of silver nanoparticles pre-functionalized on the MWNTs.

Rabies Virus-Inspired Silica-Coated Gold Nanorods as a Photothermal Therapeutic Platform for Treating Brain Tumors.

Abstract: Rabies virus-inspired silica-coated gold nanorods are fabricated by mimicking size, shape, surface glycoprotein property and in vivo behavior of the rabies virus. These nanorods not only resemble the appearance of the actual rabies virus but also travel into the brain through the neuronal pathway bypassing the blood-brain barrier, and moreover respond to near-infrared laser (808 nm) irradiation, emit heat, and effectively suppress brain tumors.

The Structure of the Aluminum Fumarate Metal–Organic Framework A520

Abstract: The synthesis of the commercially available aluminum fumarate sample A520 has been optimized and its structure analyzed through a combination of powder diffraction, solid-state NMR spectroscopy, molecular simulation, IR spectroscopy, and thermal analysis A520 is an analogue of the MIL-53(Al)-BDC solid, but with a more rigid behavior The differences between the commercial and the optimized samples in terms of defects have been investigated by in situ IR spectroscopy and correlated to their catalytic activity for ethanol dehydration

UCP2-induced fatty acid synthase promotes NLRP3 inflammasome activation during sepsis

Abstract: Cellular lipid metabolism has been linked to immune responses; however, the precise mechanisms by which de novo fatty acid synthesis can regulate inflammatory responses remain unclear. The NLRP3 inflammasome serves as a platform for caspase-1–dependent maturation and secretion of proinflammatory cytokines. Here, we demonstrated that the mitochondrial uncoupling protein-2 (UCP2) regulates NLRP3-mediated caspase-1 activation through the stimulation of lipid synthesis in macrophages. UCP2-deficient mice displayed improved survival in a mouse model of polymicrobial sepsis. Moreover, UCP2 expression was increased in human sepsis. Consistently, UCP2-deficient mice displayed impaired lipid synthesis and decreased production of IL-1β and IL-18 in response to LPS challenge. In macrophages, UCP2 deficiency suppressed NLRP3-mediated caspase-1 activation and NLRP3 expression associated with inhibition of lipid synthesis. In UCP2-deficient macrophages, inhibition of lipid synthesis resulted from the downregulation of fatty acid synthase (FASN), a key regulator of fatty acid synthesis. FASN inhibition by shRNA and treatment with the chemical inhibitors C75 and cerulenin suppressed NLRP3-mediated caspase-1 activation and inhibited NLRP3 and pro–IL-1β gene expression in macrophages. In conclusion, our results suggest that UCP2 regulates the NLRP3 inflammasome by inducing the lipid synthesis pathway in macrophages. These results identify UCP2 as a potential therapeutic target in inflammatory diseases such as sepsis.

Extended release of perioperative immunotherapy prevents tumor recurrence and eliminates metastases.

Abstract: Cancer immunotherapy can confer durable benefit, but the percentage of patients who respond to this approach remains modest. The ability to concentrate immunostimulatory compounds at the site of disease can overcome local immune tolerance and reduce systemic toxicity. Surgical resection of tumors may improve the efficacy of immunotherapy by removing the concentrated immunosuppressive microenvironment; however, it also removes tumor-specific leukocytes as well as tumor antigens that may be important to establishing antitumor immunity. Moreover, surgery produces a transient immunosuppressive state associated with wound healing that has been correlated with increased metastasis. Using multiple models of spontaneous metastasis, we show that extended release of agonists of innate immunity-including agonists of Toll-like receptor 7/8 (TLR7/8) or stimulator of interferon genes (STING)-from a biodegradable hydrogel placed in the tumor resection site cured a much higher percentage of animals than systemic or local administration of the same therapy in solution. Depletion and neutralization experiments confirmed that the observed prevention of local tumor recurrence and eradication of existing metastases require both the innate and adaptive arms of the immune system. The localized therapy increased the numbers of activated natural killer (NK) cells, dendritic cells, and T cells and induced production of large amounts of type I interferons, thereby converting an immunosuppressive post-resection microenvironment into an immunostimulatory one. The results suggest that the perioperative setting may prove to be a useful context for immunotherapy, particularly when the release of the therapy is extended locally.