Publications by authors named "Youjin Jo"
Background: An automated web-based assessment and monitoring system ( www.psynary.com ) has been developed to assist non-specialist clinicians in managing common mood and anxiety disorders.
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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
Article Synopsis
- 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.
Article Synopsis
- 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.
Article Synopsis
- 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.*
Effective killing of cancer cells and regression of tumor growth by K27 targeting sulfiredoxin.
Free Radic Biol Med
December 2016
Article Synopsis
- - 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.
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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