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Liu, Hong Feng,Zhao, ZhengLin,Zhang, Jie,Wu, Yi Yan,Jiao, Yu,Wu, Tong,Kim, Sang Chan,Lee, Bong Hyo,Fan, Yu,Lee, Chul Won,Kim, Young Woo,Yang, Chae Ha,Zhu, Xiao Dong,Zhao, Rong Jie Elsevier 2019 Neuroscience Letters Vol.705 No.-
<P><B>Abstract</B></P> <P>Noradrenergic projections from the nucleus tractus solitarius (NTS) to the hypothalamic paraventricular nucleus (PVN) are involved in nicotine (Nic) dependence. Nic induces hypothalamic norepinephrine (NE) release through <I>N</I>-methyl-<SMALL>D</SMALL>-aspartate receptors (NMDARs) and nitric oxide in the NTS. However, acupuncture attenuates Nic withdrawal-induced anxiety. Therefore, this study investigated the effects of acupuncture on Nic-induced hypothalamic NE release. Rats received an intravenous infusion of Nic (90 μg/kg, over 60 s) and extracellular NE levels in the PVN were determined by in vivo microdialysis. Immediately after Nic administration, the rats were bilaterally treated with acupuncture at acupoint HT7 (Shen-Men) or PC6 (Nei-Guan), or a non-acupoint (tail) for 60 s. Acupuncture at HT7, but not at PC6 or the tail, significantly reduced Nic-induced NE release. However, this was abolished by a post-acupuncture infusion of either NMDA or sodium nitroprusside into the NTS. Additionally, acupuncture at HT7, but not the control points, prevented Nic-induced plasma corticosterone secretion and inhibited Nic-induced increases in the phosphorylation of neuronal nitric oxide synthase (nNOS) and endothelial NOS in the NTS. These findings suggest that acupuncture at HT7 reduces Nic-induced NE release in the PVN via inhibition of the solitary NMDAR/NOS pathway.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Acupuncture inhibited nicotine-induced hypothalamic norepinephrine release. </LI> <LI> Acupuncture diminished nicotine-induced plasma corticosterone secretion. </LI> <LI> Acupuncture reversed nicotine-induced phosphorylation of solitary nNOS and eNOS. </LI> <LI> NMDA abolished acupunctural effects on nicotine-induced norepinephrine release. </LI> <LI> NO abolished acupunctural effects on nicotine-induced norepinephrine release. </LI> </UL> </P>
Targeting Non-proteolytic Protein Ubiquitination for the Treatment of Diffuse Large B Cell Lymphoma
Yang, Y.,Kelly, P.,Shaffer, A.L.,Schmitz, R.,Yoo, H.M.,Liu, X.,Huang, D.W.,Webster, D.,Young, R.M.,Nakagawa, M.,Ceribelli, M.,Wright, G.W.,Yang, Y.,Zhao, H.,Yu, X.,Xu, W.,Chan, W.C.,Jaffe, E.S.,Gascoy Cell Press 2016 CANCER CELL Vol.29 No.4
Chronic active B cell receptor (BCR) signaling, a hallmark of the activated B cell-like (ABC) subtype of diffuse large B cell lymphoma (DLBCL), engages the CARD11-MALT1-BCL10 (CBM) adapter complex to activate IκB kinase (IKK) and the classical NF-κB pathway. Here we show that the CBM complex includes the E3 ubiquitin ligases cIAP1 and cIAP2, which are essential mediators of BCR-dependent NF-κB activity in ABC DLBCL. cIAP½ attach K63-linked polyubiquitin chains on themselves and on BCL10, resulting in the recruitment of IKK and the linear ubiquitin chain ligase LUBAC, which is essential for IKK activation. SMAC mimetics target cIAP½ for destruction, and consequently suppress NF-κB and selectively kill BCR-dependent ABC DLBCL lines, supporting their clinical evaluation in patients with ABC DLBCL.
A decade of liver organoids: Advances in disease modeling
Yue Liu,Jian-Ying Sheng,Chun-Fang Yang,Junjun Ding,Yun-Shen Chan 대한간학회 2023 Clinical and Molecular Hepatology(대한간학회지) Vol.29 No.3
Liver organoids are three-dimensional cellular tissue models in which cells interact to form unique structures in culture. During the past 10 years, liver organoids with various cellular compositions, structural features, and functional properties have been described. Methods to create these advanced human cell models range from simple tissue culture techniques to complex bioengineering approaches. Liver organoid culture platforms have been used in various research fields, from modeling liver diseases to regenerative therapy. This review discusses how liver organoids are used to model disease, including hereditary liver diseases, primary liver cancer, viral hepatitis, and nonalcoholic fatty liver disease. Specifically, we focus on studies that used either of two widely adopted approaches: differentiation from pluripotent stem cells or epithelial organoids cultured from patient tissues. These approaches have enabled the generation of advanced human liver models and, more importantly, the establishment of patient-tailored models for evaluating disease phenotypes and therapeutic responses at the individual level.
PANM DB ver 5.0 : An update of PANM, Database for invertebrate NGS data analysis
Jun Yang Jeong,Jie Eun Park,Dae Kwon Song,Chan-Eui Hong,Yong Tae Kim,Hyeonjun Shin,Ziwei Liu,Hyeyoon Jo,Min Kyu Sang,Hongray Howrelia Patnaik,Bharat Bhusan Patmaik,Se Won Kang,So Young Park,Jun Sang L 한국수산과학회 양식분과 2022 한국수산과학회 양식분과 학술대회 Vol.2022 No.10
Genmeng Yang,Juan Li,Yanxia Peng,Baoyu Shen,Yuanyuan Li,Liu Liu,Chan Wang,Yue Xu,Shucheng Lin,Shuwei Zhang,Yi Tan,Huijie Zhang,Xiaofeng Zeng,Qi Li,Gang Lu 고려인삼학회 2022 Journal of Ginseng Research Vol.46 No.3
This study investigates the effects of ginsenoside Rb1 (GsRb1) on methamphetamine (METH)-induced toxicity in SH-SY5Y neuroblastoma cells and METH-induced conditioned place preference (CPP)in adult Sprague-Dawley rats. It also examines whether GsRb1 can regulate these effects through theNR2B/ERK/CREB/BDNF signaling pathways. Methods: SH-SY5Y cells were pretreated with GsRb1 (20 mM and 40 mM) for 1 h, followed by METHtreatment (2 mM) for 24 h. Rats were treated with METH (2 mg/kg) or saline on alternating days for 10days to allow CPP to be examined. GsRb1 (5, 10, and 20 mg/kg) was injected intraperitoneally 1 h beforeMETH or saline. Western blot was used to examine the protein expression of NR2B, ERK, P-ERK, CREB, PCREB, and BDNF in the SH-SY5Y cells and the rats' hippocampus, nucleus accumbens (NAc), and prefrontal cortex (PFC). Results: METH dose-dependently reduced the viability of SH-SY5Y cells. Pretreatment of cells with 40mM of GsRb1 increased cell viability and reduced the expression of METH-induced NR2B, p-ERK, p-CREBand BDNF. GsRb1 also attenuated the expression of METH CPP in a dose-dependent manner in rats. Further, GsRb1 dose-dependently reduced the expression of METH-induced NR2B, p-ERK, p-CREB, andBDNF in the PFC, hippocampus, and NAc of rats. Conclusion: GsRb1 regulated METH-induced neurotoxicity in vitro and METH-induced CPP through theNR2B/ERK/CREB/BDNF regulatory pathway. GsRb1 could be a therapeutic target for treating METHinduced neurotoxicity or METH addiction.