Publications by authors named "Hoyul Lee"

mPTP is a multi-protein complex that opens in mitochondria during cell death. Cisplatin-induced hearing loss is also known to be caused by mPTP opening. Thus, our study evaluated the protective effect of a novel mPTP inhibitor named DBP-iPT against cisplatin-induced hearing loss.

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Article Synopsis
  • * It reviews current research on how elevated blood sugar levels influence immune responses differently in type 1 and type 2 diabetes and other metabolic disorders.
  • * The findings suggest that understanding the metabolic changes in immune cells under hyperglycemic conditions could lead to new therapeutic approaches for managing diabetes-related immune dysfunctions.
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The fecal microbiome is identical to the gut microbial communities and provides an easy access to the gut microbiome. Therefore, fecal microbial transplantation (FMT) strategies have been used to alter dysbiotic gut microbiomes with healthy fecal microbiota, successfully alleviating various metabolic disorders, such as obesity, type 2 diabetes, and inflammatory bowel disease (IBD). However, the success of FMT treatment is donor-dependent and variations in gut microbes cannot be avoided.

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  • * The study shows that "trained immunity" in neutrophils leads to significant metabolic changes under diabetic conditions, including increased glycolysis and fatty acid oxidation, resulting in higher levels of acetyl-coenzyme A.
  • * Inhibiting specific enzymes involved in this process can prevent the priming of neutrophils, indicating that targeting neutrophil-trained immunity could be a potential therapy to manage inflammation related to diabetes.
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Mitochondria has emerged as a critical ruler of metabolic reprogramming in immune responses and inflammation. In the context of colitogenic T cells and IBD, there has been increasing research interest in the metabolic pathways of glycolysis, pyruvate oxidation, and glutaminolysis. These pathways have been shown to play a crucial role in the metabolic reprogramming of colitogenic T cells, leading to increased inflammatory cytokine production and tissue damage.

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Emerging evidence suggest that transcription factors play multiple roles in the development of pancreatitis, a necroinflammatory condition lacking specific therapy. Estrogen-related receptor γ (ERRγ), a pleiotropic transcription factor, has been reported to play a vital role in pancreatic acinar cell (PAC) homeostasis. However, the role of ERRγ in PAC dysfunction remains hitherto unknown.

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Ca overload-induced mitochondrial dysfunction is considered as a major contributing factor in the pathogenesis of alcohol-associated liver disease (ALD). However, the initiating factors that drive mitochondrial Ca accumulation in ALD remain elusive. Here, we demonstrate that an aberrant increase in hepatic GRP75-mediated mitochondria-associated ER membrane (MAM) Ca-channeling (MCC) complex formation promotes mitochondrial dysfunction in vitro and in male mouse model of ALD.

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Article Synopsis
  • Pyruvate metabolism is essential for energy production and mitochondrial health, influencing processes like fusion/fission and mitophagy, which helps maintain cellular function.
  • Disruptions in pyruvate flow and mitochondrial quality control can lead to the accumulation of reactive oxygen species and calcium, resulting in mitochondrial dysfunction and contributing to metabolic diseases like diabetes and neurodegenerative disorders.
  • The regulation of pyruvate metabolism is crucial for immune cell function; it impacts macrophage behavior and T cell differentiation, with imbalances potentially promoting inflammation and insulin resistance.
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Background & Aims: Despite recent evidence supporting the metabolic plasticity of CD4 T cells, it is uncertain whether the metabolic checkpoint pyruvate dehydrogenase kinase (PDK) in T cells plays a role in the pathogenesis of colitis.

Methods: To investigate the role of PDK4 in colitis, we used dextran sulfate sodium (DSS)-induced colitis and T-cell transfer colitis models based on mice with constitutive knockout (KO) or CD4 T-cell-specific KO of PDK4 (Pdk4CD4). The effect of PDK4 deletion on T-cell activation was also studied in vitro.

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Background: Chronic exposure to low-dose persistent organic pollutants (POPs) can induce mitochondrial dysfunction. This study evaluated the association between serum POP concentrations and oxygen consumption rate (OCR) as a marker of mitochondrial function in humans and in vitro cells.

Methods: Serum concentrations of organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs) were measured in 323 adults.

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Background: Oxidative stress has been suggested to be a factor contributing to the disease severity of inflammatory bowel disease (IBD). BJ-1108, a derivative of 6-amino-2,4,5-trimethylpyridin-3-ol, is reported to significantly inhibit the generation of reactive oxygen species (ROS) in vitro. However, whether this molecule affects intestinal inflammation is largely unknown.

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Background: Adhesion molecules maintain the intestinal barrier function that is crucial to prevent intestinal inflammation. Dual immunoglobulin domain-containing adhesion molecule (DICAM) has been recently identified and known for the involvement in cell-cell adhesion through homophilic interaction and heterophilic interaction with integrin αVβ3. We tested whether the change of DICAM expression affects the severity of colonic inflammation.

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Inflammatory bowel diseases (IBD) are chronic inflammatory conditions of the gastrointestinal tract with multifactorial etiology. Both dietary factors and the microbe have been found to be associated with the condition. The current study examined the effects of sodium fumarate, a neutralized product of the food additives fumaric acid and monosodium fumarate when in the intestinal environment, on the growth of to determine the effects of these food additives on IBD-associated bacterial species.

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Background: Natural orifice transluminal endoscopic surgery is an emerging technique. We aimed to develop an advanced surgical robot mechanism for natural orifice surgery.

Methods: We propose the active-controlled overtube-type platform with multiple channels for an endoscopic camera and surgical tools.

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Background: We previously showed that zonula occludens toxin (Zot) encoded by Campylobacter concisus zot (808T) gene has the potential to initiate inflammatory bowel disease. This Zot protein caused prolonged intestinal epithelial barrier damage, induced intestinal epithelial and macrophage production of tumor necrosis factor-α and enhanced the responses of macrophages to other microbes. In order to understand the potential virulence of Zot proteins in other Campylobacter species, in this study we examined their presence, similarities, motifs and prophages.

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  • Campylobacter concisus is an oral bacterium linked to inflammatory bowel disease (IBD), and this study explored how pH and bile levels affect its growth.
  • The research found that exposure to highly acidic pH levels (like 2 and 3.5) significantly reduced the growth of C. concisus strains, while pH 5 had minimal impact.
  • About 55.2% of strains thrived in media with 2% bile, indicating that bile affects growth based on concentration and strain type, and suggesting that specific intestinal and gastric conditions might influence colonization of C. concisus in the digestive system.
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Campylobacter concisus is an oral bacterium that is associated with intestinal diseases. C. concisus was previously described as a bacterium that requires H2-enriched microaerobic conditions for growth.

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Investigation of the possible role of Campylobacter concisus (C. concisus) in inflammatory bowel disease (IBD) is an emerging research area. Despite the association found between C.

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Campylobacter concisus, a Gram-negative bacterium that colonizes the human oral cavity, has been shown to be associated with inflammatory bowel diseases (IBD). The effects of different C. concisus strains on intestinal epithelial expression of Toll like receptors (TLR) have not been investigated.

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