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995 results on '"Han, Young-Min"'

259. Synthesis, modeling, and crystallographic study of 3,4-disubstituted-1,2,5-oxadiazoles and evaluation of their ability to decrease STAT3 activity

Author

Shin Dae, S, Masciocchi, D, Gelain, A, Villa, S, Barlocco, D, Meneghetti, F, Pedretti, A, Han Young, M, Han Dong, C, Kwon Byoung, M, Legnani, L, Toma, L, Shin Dae Seop, Masciocchi Daniela, Gelain Arianna, Villa Stefania, Barlocco Daniela, Meneghetti Fiorella, Pedretti Alessandro, Han Young Min, Han Dong Cho, Kwon Byoung Mog, LEGNANI, LAURA, TOMA, LUCIO, Shin Dae, S, Masciocchi, D, Gelain, A, Villa, S, Barlocco, D, Meneghetti, F, Pedretti, A, Han Young, M, Han Dong, C, Kwon Byoung, M, Legnani, L, Toma, L, Shin Dae Seop, Masciocchi Daniela, Gelain Arianna, Villa Stefania, Barlocco Daniela, Meneghetti Fiorella, Pedretti Alessandro, Han Young Min, Han Dong Cho, Kwon Byoung Mog, LEGNANI, LAURA, and TOMA, LUCIO

Abstract

STAT3 (Signal Transducer and Activator of Transcription 3) is a transcription factor constitutively activated by aberrant upstream tyrosine kinase activities in a broad spectrum of human solid and blood tumors, thus suggesting that its inhibition could represent an interesting molecular target for cancer therapy. With the aim to disclose novel scaffolds for compounds active on STAT3 the potential of the 1,2,5-oxadiazole ring was explored and several new compounds substituted at positions 3 and 4 of the heterocycle were synthesized. When tested in a dual-luciferase assay, using HCT-116 cells, some compounds showed a significant inhibition value towards STAT3. So, to give support to the biological results, modeling and crystallographic studies of representative terms of the new series were performed.

Published
2010

276. Tracking controls of torque and force of 4-degree-of-freedom haptic master featuring smart electrorheological fluid.

Author

Han, Young-Min, Choi, Seung-Bok, and Oh, Jong-Seok

Subjects
TRACKING control systems, TORQUE control, FORCE & energy, DEGREES of freedom, ELECTRORHEOLOGICAL fluids, HAPTIC devices, ROTATIONAL motion
Abstract

This study presents a new type of haptic master device using electrorheological fluid for minimally invasive surgery application. The proposed haptic master consists of an electrorheological spherical haptic device for 3-degree-of-freedom rotational motion and an electrorheological linear haptic device for 1-degree-of-freedom translational motion. The principal design variables of the haptic master are determined using the Bingham characteristic of electrorheological fluid and geometrical constraints. After designing an organ model, control performances are evaluated in a virtual environment using a sliding mode controller. It is demonstrated that the proposed haptic master can track well both torque and force which are required (or desired) ones for surgical operation using the robot-assisted minimally invasive surgery. [ABSTRACT FROM AUTHOR]

Published
2016
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277. The role of chronic inflammation in the development of gastrointestinal cancers: reviewing cancer prevention with natural anti-inflammatory intervention.

Author

Lee, Ho-Jae, Park, Jong-Min, Han, Young Min, Gil, Hong Kwon, Kim, Jinhyung, Chang, Ji Young, Jeong, Migyeong, Go, Eun-Jin, and Hahm, Ki Baik

Subjects
GASTROINTESTINAL cancer, INFLAMMATION, CANCER prevention, OXIDATIVE stress, PROTON pump inhibitors, MONOCLONAL antibodies, CANCER risk factors
Abstract

Inflammatory mediators alter the local environment of tumors, known as the tumor microenvironment. Mechanistically, chronic inflammation induces DNA damage, but understanding this hazard may help in the search for new chemopreventive agents for gastrointestinal (GI) cancer which attenuate inflammation. In the clinic, GI cancer still remains a major cause of cancer-associated mortality, chemoprevention with anti-inflammatory agents is thought to be a realistic approach to reduce GI cancer. Proton pump inhibitors, monoclonal antibodies targeting tumor necrosis factor-alpha, anti-sense targeted smad7 and non-steroidal anti-inflammatory agents have been investigated for their potential to prevent inflammation-based GI cancer. Besides these, a wide variety of natural products have also shown potential for the prevention of GI cancer. In this review, the authors will provide insights to explain the mechanistic connection between inflammation and GI cancer, as well as describe a feasible cancer prevention strategy based on anti-inflammatory treatments. [ABSTRACT FROM PUBLISHER]

Published
2016
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297. A Pilot Study for the Neuroprotective Effect of Gongjin-dan on Transient Middle Cerebral Artery Occlusion-Induced Ischemic Rat Brain

Author

Sunwoo, Yun-Young, primary, Park, Sang In, additional, Chung, Yong-An, additional, Lee, Jisoo, additional, Park, Moon-Seo, additional, Jang, Kyung-Sool, additional, Maeng, Lee-So, additional, Jang, Dong-Kyu, additional, Im, Ruth, additional, Jung, Yu Jin, additional, Park, Soon A., additional, Kang, Eun-Sun, additional, Kim, Min-Wook, additional, and Han, Young-Min, additional

Published
2012
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299. Emerging Targets to Relieve Fat Stress-Induced Liver Diseases: UDCA, Tocotrienol, ω-3 PUFAs, and IgY Targeted NPC1L1 Cholesterol Transporter

Author

Cha, Ji-Young, Park, Jong-Min, Lee, Ho-Jae, Bae, Jin-Sik, Han, Young-Min, Oh, Byung-Chul, Hyun Ko, Kwang, and Hahm, Ki-Baik

Abstract

Fat stress-induced liver disease is a hepatic manifestation of metabolic syndrome initiated by excess fat accumulation and encompasses a wide spectrum of diseases from non-alcoholic fatty liver disease to nonalcoholic steatohepatitis, a precursor lesion progressing to more aggressive liver cirrhosis and hepatocellular carcinoma. Although the incidence of these fat stress-induced liver diseases is rapidly increasing worldwide in parallel with the growing epidemics of obesity and metabolic diseases, its exact pathogenesis is not well defined. Although obesity, sedentary life-style, altered dietary pattern, insulin resistance, altered intestinal barrier function, inflammatory cytokines, and oxidative stress have been acknowledged as contributing factors because of the indefinite pathogenesis of metabolic diseases, the only reliable treatment is lifestyle intervention composed of restrictive diet and exercise. Additionally, some existing medications such as pioglitazone and antioxidants such as vitamin E were reported to be effective; in this review, several novel agents especifically targeting nonalcoholic fatty liver disease pathogenesis under clinical trial will be introduced. These include an NPC1L1 blocker (ezetimibe), which significantly improved histological and symptomatic scores associated with steatohepatitis and fibrosis; clofibrate, phentoxyfylline, ursodeoxycholic acid, and tocopherol, all of which are prescribed to relieve fat stress; and additional IgY targeted NPC1L1, tocotrienol, ursodeoxycholic acid, and ω-3 polyunsaturated fatty acids, which are actively under investigation to confirm the safety of long-term use.

Published
2017
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300. Deletion of PRKAAtriggers mitochondrial fission by inhibiting the autophagy-dependent degradation of DNM1L

Author

Wang, Qilong, Wu, Shengnan, Zhu, Huaiping, Ding, Ye, Dai, Xiaoyan, Ouyang, Changhan, Han, Young-min, Xie, Zhonglin, and Zou, Ming-Hui

Abstract

ABSTRACTPRKAA (protein kinase, AMP-activated, α catalytic subunit) regulates mitochondrial biogenesis, function, and turnover. However, the molecular mechanisms by which PRKAA regulates mitochondrial dynamics remain poorly characterized. Here, we report that PRKAA regulated mitochondrial fission via the autophagy-dependent degradation of DNM1L (dynamin 1-like). Deletion of Prkaa1/AMPKα1 or Prkaa2/AMPKα2 resulted in defective autophagy, DNM1L accumulation, and aberrant mitochondrial fragmentation in the mouse aortic endothelium. Furthermore, autophagy inhibition by chloroquine treatment or ATG7small interfering RNA (siRNA) transfection, upregulated DNM1L expression and triggered DNM1L-mediated mitochondrial fragmentation. In contrast, autophagy activation by overexpression of ATG7 or chronic administration of rapamycin, the MTOR inhibitor, promoted DNM1L degradation and attenuated mitochondrial fragmentation in Prkaa2-deficient (prkaa2−/−) mice, suggesting that defective autophagy contributes to enhanced DNM1L expression and mitochondrial fragmentation. Additionally, the autophagic receptor protein SQSTM1/p62, which bound to DNM1L and led to its translocation into the autophagosome, was involved in DNM1L degradation by the autophagy-lysosome pathway. Gene silencing of SQSTM1markedly reduced the association between SQSTM1 and DNM1L, impaired the degradation of DNM1L, and enhanced mitochondrial fragmentation in PRKAA-deficient endothelial cells. Finally, the genetic (DNM1LsiRNA) or pharmacological (mdivi-1) inhibition of DNMA1L ablated mitochondrial fragmentation in the mouse aortic endothelium and prevented the acetylcholine-induced relaxation of isolated mouse aortas. This suggests that aberrant DNM1L is responsible for enhanced mitochondrial fragmentation and endothelial dysfunction in prkaaknockout mice. Overall, our results show that PRKAA deletion promoted mitochondrial fragmentation in vascular endothelial cells by inhibiting the autophagy-dependent degradation of DNM1L.

Published
2017
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