Publications by authors named "Su Ji Han"

In this paper, we explore the development of a multi-functional surface designed to tackle the challenges posed by (), a common opportunistic pathogen. Infections caused by during surgical procedures highlight the need for effective strategies to inhibit its adhesion, growth, and colonization, particularly on the surfaces of invasive medical devices. Until now, most existing research has focused on nanopillar structures (positive topographies).

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The inability of adult human cardiomyocytes to proliferate is an obstacle to efficient cardiac regeneration after injury. Understanding the mechanisms that drive postnatal cardiomyocytes to switch to a non-regenerative state is therefore of great significance. Here we show that Arid1a, a subunit of the switching defective/sucrose non-fermenting (SWI/SNF) chromatin remodeling complex, suppresses postnatal cardiomyocyte proliferation while enhancing maturation.

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Arrhythmogenic cardiomyopathy (ACM) is an inherited progressive cardiac disease. Many patients with ACM harbor mutations in desmosomal genes, predominantly in plakophilin-2 (). Although the genetic basis of ACM is well characterized, the underlying disease-driving mechanisms remain unresolved.

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Arrhythmogenic cardiomyopathy (ACM) is an inherited progressive disease characterized by electrophysiological and structural remodeling of the ventricles. However, the disease-causing molecular pathways, as a consequence of desmosomal mutations, are poorly understood. Here, we identified a novel missense mutation within desmoplakin in a patient clinically diagnosed with ACM.

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Arrhythmogenic cardiomyopathy (ACM) is an inherited heart disease involving arrhythmia in young adults accompanied by structural changes at later stages. In this issue of EMBO Molecular Medicine, Sommariva et al (2021) identified a positive correlation between circulating levels of oxidized low-density lipoproteins (oxLDL) and ACM disease penetrance, which contributes to fibro-fatty cardiac remodeling via the oxLDL/CD36/PPARγ axis. These data identify oxidized low-density lipoproteins as a risk factor for ACM and uncover a novel therapeutic intervention option to block disease pathogenesis.

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In studying the mechanisms underlying the susceptibility of the kidney to candidal infection, we previously reported that the reduced production of cytokines [i.e. tumour necrosis factor-alpha (TNF-alpha)] via platelet-activating factor (PAF)-induced activation of nuclear factor-kappaB (NF-kappaB) renders the organ susceptible to the fungal burden.

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The development of novel 'new generation' vaccine systems that is based on proteins, peptides or DNA is of great current interest. However, due to the lower efficiencies of these new generation vaccines, they are seldomly used alone. Rather, their formulations often contain adjuvants, either to enhance the immune responses or to reduce dosing.

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Porphyromonas gingivalis is one of the suspected periodontopathic bacteria. The lipopolysaccharide (LPS) of P. gingivalis is a key factor in the development of periodontitis.

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A novel and improved vaccine delivery system and/or adjuvant is actively sought to enhance the potency of vaccines. Previously, we reported that strong antitumor immunity could be generated when a peptide antigen was incorporated into LPD (cationic liposome-polycation-pDNA) nanoparticles. In this study, we found that both the cationic liposome and DNA are required for the full immunostimulation activity of LPD.

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Purpose: Previously, our laboratory has reported that liposome-protamine-DNA (LPD) nanoparticle is an effective delivery system for tumor-associated antigens. Mannan, which potentially targets antigen-presenting cells, was coated on LPD to further enhance its antitumor activity.

Methods: Cholesterol-conjugated mannan was coated on LPD.

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The nuclear factor-kappaB (NF-kappaB) is an important transcription factor necessary for initiating and sustaining inflammatory and immune reactions. The inducers of NF-kappaB are well characterized, but the molecular mechanisms underlying multiple in vivo NF-kappaB activation processes are poorly understood. The injection of lipopolysaccharide resulted in a biphasic activation of NF-kappaB during the 18-h observation period in various organs of mice.

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This study investigated the mechanisms of platelet-activating factor (PAF)-induced angiogenesis in a mouse model of Matrigel implantation. PAF induced a dose- and time-dependent angiogenic response. Inhibitors of nuclear factor (NF) kappaB expression or action, including antisense oligonucleotides to the p65 subunit of NFkappaB (p65 antisense) and antioxidants such as alpha-tocopherol and N-acetyl-L-cysteine, significantly reduced PAF-induced angiogenesis.

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