Publications by authors named "Seong Eun Hong"

The potential of multi-layer nanoemulsions (NEs) for improving the cellular uptake, antioxidant activity, and in vitro bioaccessibility of α-tocopherol (ToC) was examined. ToC-loaded multi-layer NEs were prepared using lecithin (primary-NEs, P-NEs), chitosan (secondary-NEs, S-NEs), and dextran sulfate (tertiary-NEs, T-NEs) as wall materials. The bioadhesion, cellular permeability, and uptake of the multi-layer NEs were significantly higher than that of the free coumarin 6 (C6).

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  • - Cinchonine (CN) has demonstrated various health benefits, including antimalarial and antiobesity effects, and was found to inhibit specific kinases (TAK1 and AKT) linked to bone metabolism, although its role in this area was previously unclear.
  • - The study showed that CN inhibits the differentiation of osteoclasts (cells that break down bone) by reducing NFATc1 expression, which is crucial for osteoclast formation, while also affecting key signaling pathways involving TAK1 and AKT.
  • - Moreover, CN not only reduces the harmful effects of mature osteoclasts but also promotes the formation of osteoblasts (cells that build bone) and offers protective effects against bone loss in mouse models
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  • Bone diseases like osteoporosis and periodontitis are linked to high levels of osteoclast activity and inflammation.
  • Benzydamine (BA) is a non-steroidal anti-inflammatory drug that reduces pro-inflammatory cytokines, but its effects on osteoclasts were previously unclear.
  • This study found that BA inhibits osteoclast differentiation by suppressing IL-1 production and enhances osteoblast differentiation, indicating its potential as a treatment for inflammation-related bone diseases and postmenopausal osteoporosis.
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  • The study focuses on skullcapflavone II (SFII), a flavonoid known for its anti-inflammatory effects, and its role in controlling osteoclasts, which are cells that contribute to bone diseases like osteoporosis and rheumatoid arthritis.
  • SFII was found to inhibit osteoclast formation and activity by affecting key signaling pathways, decreasing reactive oxygen species (ROS), and modulating the integrin pathway, which governs cell survival and function.
  • The findings suggest that SFII has potential as a therapeutic agent for treating and preventing bone diseases linked to excessive osteoclast activity by targeting specific cellular mechanisms.
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Concurrent presentation of acute hepatitis A virus (HAV) infection and Graves' disease has not been reported in literature worldwide. Although there is no well-established mechanism that explains the induction of Graves' disease by HAV to date, our case suggests that HAV infection may be responsible for inducing Graves' disease. A healthy 27-year-old female presented fever, palpitation, and diarrhea, and she was subsequently diagnosed as acute HAV infection.

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  • Excessive osteoclast activity leads to bone diseases like osteoporosis and rheumatoid arthritis, prompting research into therapies that inhibit osteoclast formation and function.* -
  • Euphorbia factor L1 (EFL1), a compound from Euphorbia lathyris, has been shown to hinder the formation of osteoclasts, promote their apoptosis, and decrease bone resorption by affecting certain signaling pathways.* -
  • EFL1 also demonstrated effectiveness in preventing bone loss in inflammatory conditions and in ovariectomized mice, suggesting its potential as a treatment for diseases caused by excessive osteoclast activity.*
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Background: Hip fracture is a common health problem in the elderly that is associated with increased mortality. Acute kidney injury (AKI) is a frequent complication in elderly patients undergoing surgery and is associated with the clinical outcome. We evaluated the incidence and risk factors of AKI in elderly patients undergoing hip fracture surgery and the impact of AKI on short- and long-term clinical outcomes.

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  • - Cancer cells are more reliant on antioxidant activities than normal cells, making them vulnerable to oxidative damage, which can be exploited for treatment.
  • - The study introduces a new Srx inhibitor, K27, which increases oxidative stress in cancer cells by causing the accumulation of sulfinylated peroxiredoxins, leading to cell death and mitochondrial damage.
  • - K27 selectively kills tumor cells while sparing non-tumor cells and effectively inhibits tumor growth in vivo without causing acute toxicity, indicating that targeting Srx could be a promising cancer therapy approach.
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Recent studies have shown that many types of cancer cells have increased levels of reactive oxygen species (ROS) and enhance antioxidant capacity as an adaptation to intrinsic oxidative stress, suggesting that cancer cells are more vulnerable to oxidative insults and are more dependent on antioxidant systems compared with normal cells. Thus, disruption of redox homeostasis caused by a decline in antioxidant capacity may provide a method for the selective death of cancer cells. Here we show that ROS-mediated selective death of tumor cells can be caused by inhibiting sulfiredoxin (Srx), which reduces hyperoxidized peroxiredoxins, leading to their reactivation.

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In cases with metastatic invasion of the heart, electrocardiographic abnormalities are commonly seen. However, most of these electrocardiographic changes are nonspecific; certain findings may be highly suggestive of myocardial involvement of the tumor. We report a patient with lung cancer who presented with persistent ST-segment elevation with coexisting reciprocal changes on electrocardiography due to myocardial invasion of the lung cancer.

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A 51-year-old highly fit man presented for dyspnea with strenuous aerobic exercise. The patient was asymptomatic and all tests were normal at rest. With increasing exercise intensity, he suddenly complained of dyspnea and showed a severe exercise-induced hypoxemia with an excessive alveolar-arterial oxygen tension difference.

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