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《만물진원》의 간행과 17∼18세기 유교 지식인의 반응 ―제10편 창조설을 중심으로
최정연 ( Choi¸ Jeongyeon ) 한국중국어문학회 2021 中國文學 Vol.108 No.-
This article compares and examines the responses of Chinese and Joseon Confucian intellectuals to the theory of Creation in Wanwu zhenyuan. Wanwu zhenyuan is an exclamation book written by Aleni, a Jesuit in China, that proves that the ‘true origin of all things’ is God and introduces the process of Creation. It has exerted considerable influence in China since its publication in Beijing in 1628. The doctrines of Wanwu zhenyuan caused animosity among local intellectuals. The reasons were many, but one of the main ones was the aggressive and exclusive attitude of the Jesuit missionaries toward the Confucian tradition and cultural authority. In particular, the notion of the Hell that even the ancient kings, the creators of Confucian civilization and bearers of truth, can not ascend to heaven seems to reinforce the resistance of Confucian intellectuals such as Huangzhen and Xudashou. In the 18th century, Joseon intellectuals who viewed Wanwu zhenyuan showed a different aspect from Chinese intellectuals in that they criticized it academically. After the Jinsan Incident in 1791, while the problem of Seohak became publicly debated at the national level and negative perceptions about it were strengthened, Nam Geukgwan and Hong Jeongha approached it carefully and dealt with it in the context of traditional knowledge. Their attitude can be said to be different from other anti-Seohak intellectuals who exclusively rejected Seohak before and after the Jinsan incident, and it can be said that they were far from the rigid atmosphere of the 19th century intellectual circle that completely denied Seohak and reproduced crude criticism.
FcγRIIb mediates amyloid-β neurotoxicity and memory impairment in Alzheimer's disease.
Kam, Tae-In,Song, Sungmin,Gwon, Youngdae,Park, Hyejin,Yan, Ji-Jing,Im, Isak,Choi, Ji-Woo,Choi, Tae-Yong,Kim, Jeongyeon,Song, Dong-Keun,Takai, Toshiyuki,Kim, Yong-Chul,Kim, Key-Sun,Choi, Se-Young,Choi, American Society for Clinical Investigation 2013 The Journal of clinical investigation Vol.123 No.7
<P>Amyloid-β (Aβ) induces neuronal loss and cognitive deficits and is believed to be a prominent cause of Alzheimer's disease (AD); however, the cellular pathology of the disease is not fully understood. Here, we report that IgG Fcγ receptor II-b (FcγRIIb) mediates Aβ neurotoxicity and neurodegeneration. We found that FcγRIIb is significantly upregulated in the hippocampus of AD brains and neuronal cells exposed to synthetic Aβ. Neuronal FcγRIIb activated ER stress and caspase-12, and Fcgr2b KO primary neurons were resistant to synthetic Aβ-induced cell death in vitro. Fcgr2b deficiency ameliorated Aβ-induced inhibition of long-term potentiation and inhibited the reduction of synaptic density by naturally secreted Aβ. Moreover, genetic depletion of Fcgr2b rescued memory impairments in an AD mouse model. To determine the mechanism of action of FcγRIIb in Aβ neurotoxicity, we demonstrated that soluble Aβ oligomers interact with FcγRIIb in vitro and in AD brains, and that inhibition of their interaction blocks synthetic Aβ neurotoxicity. We conclude that FcγRIIb has an aberrant, but essential, role in Aβ-mediated neuronal dysfunction.</P>
Choi, Kwanhoon,Yoon, Jeongyeon,Lim, Hyun Kyo,Ryoo, Sungwoo The Korean Society of Pharmacology 2014 The Korean Journal of Physiology & Pharmacology Vol.18 No.2
Cardiovascular disease is the prime cause of morbidity and mortality and the population ages that may contribute to increase in the occurrence of cardiovascular disease. Arginase upregulation is associated with impaired endothelial function in aged vascular system and thus may contribute to cardiovascular disease. According to recent research, Korean Red Ginseng water extract (KRGE) may reduce cardiovascular disease risk by improving vascular system health. The purpose of this study was to examine mechanisms contributing to age-related vascular endothelial dysfunction and to determine whether KRGE improves these functions in aged mice. Young ($10{\pm}3$ weeks) and aged ($55{\pm}5$ weeks) male mice (C57BL/6J) were orally administered 0, 10, or 20 mg/mouse/day of KRGE for 4 weeks. Animals were sacrificed and the aortas were removed. Endothelial arginase activity, nitric oxide (NO) generation and reactive oxygen species (ROS) production, endothelial nitric oxide synthase (eNOS) coupling, vascular tension, and plasma peroxynitrite production were measured. KRGE attenuated arginase activity, restored nitric oxide (NO) generation, reduced ROS production, and enhanced eNOS coupling in aged mice. KRGE also improved vascular tension in aged vessels, as indicated by increased acetylcholine-induced vasorelaxation and improved phenylephrine-stimulated vasoconstriction. Furthermore, KRGE prevented plasma peroxynitrite formation in aged mice, indicating reduced lipid peroxidation. These results suggest KRGE exerts vasoprotective effects by inhibiting arginase activity and augmenting NO signaling and may be a useful treatment for age-dependent vascular diseases.
Amygdala depotentiation ex vivo requires mitogen-activated protein kinases and protein synthesis
Kim, Jeongyeon,Park, Sungmo,Lee, Sukwon,Choi, Sukwoo Lippincott Williams Wilkins, Inc. 2009 NEUROREPORT - Vol.20 No.5
We have recently characterized a form of ex vivo depotentiation (depotentiationex vivo), which correlates tightly with fear extinction, at thalamic input synapses onto the lateral amygdala. Here, we examined the effects of learning-attenuating drugs, reported to impair fear extinction when microinjected into the basolateral amygdala, on depotentiationex vivo. U0126, a mitogen-activated protein kinase inhibitor, and cycloheximide, a protein synthesis inhibitor, blocked depotentiationex vivo. However, ifenprodil, an NR2B-containing NMDA receptor inhibitor, did not alter depotentiationex vivo, although it blocked amygdala long-term potentiation. These findings indicate that amygdala depotentiation shares some molecular processes with learning and further suggest that different forms of synaptic plasticity in the basolateral amygdala mediate fear extinction.
Reactivation of fear memory renders consolidated amygdala synapses labile.
Kim, Jeongyeon,Song, Beomjong,Hong, Ingie,Kim, Jihye,Lee, Junuk,Park, Sungmo,Yong Eom, Jae,Lee, C Justin,Lee, Sukwon,Choi, Sukwoo The Society 2010 The Journal of neuroscience Vol.30 No.28
<P>It is believed that memory reactivation transiently renders consolidated memory labile and that this labile or deconsolidated memory is reconsolidated in a protein synthesis-dependent manner. The synaptic correlate of memory deconsolidation upon reactivation, however, has not been fully characterized. Here, we show that 3,5-dihydroxyphenylglycine (DHPG), an agonist for group I metabotropic glutamate receptors (mGluRI), induces synaptic depotentiation only at thalamic input synapses onto the lateral amygdala (T-LA synapses) where synaptic potentiation is consolidated, but not at synapses where synaptic potentiation is not consolidated. Using this mGluRI-induced synaptic depotentiation (mGluRI-depotentiation) as a marker of consolidated synapses, we found that mGluRI-depotentiation correlated well with the state of memory deconsolidation and reconsolidation in a predictable manner. DHPG failed to induce mGluRI-depotentiation in slices prepared immediately after reactivation when the reactivated memory was deconsolidated. DHPG induced mGluRI-depotentiation 1 h after reactivation when the reactivated memory was reconsolidated, but it failed to do so when reconsolidation was blocked by a protein synthesis inhibitor. To test the memory-specificity of mGluRI-depotentiation, conditioned fear was acquired twice using two discriminative tones (2.8 and 20 kHz). Under this condition, mGluRI-depotentiation was fully impaired in slices prepared immediately after reactivation with both tones, whereas mGluRI-depotentiation was partially impaired immediately after reactivation with the 20 kHz tone. Consistently, microinjection of DHPG into the LA 1 h after reactivation reduced fear memory retention, whereas DHPG injection immediately after reactivation failed to do so. Our findings suggest that, upon memory reactivation, consolidated T-LA synapses enter a temporary labile state, displaying insensitivity to mGluRI-depotentiation.</P>