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오바마 정의하기: 대통령의 정체성과 정통성에 대한 공중의 정치적 주관성
Dan B. Thomas,Larry R. Baas 한국주관성연구학회 2011 Journal of Human Subjectivity Vol.9 No.1
The issue of "presidential identity" has assumed pivotal importance in the first two years of the Obama Administration during which the president has been the target of fierce efforts by his opponents to influence his public identity. Findings from this two-part investigation reveal a range of views of the president that reflect both diverse contents and distinctive pattern of connections to individuals`` varying senses of self and their perceptions of his authenticity and his accessibility as an object of identification. Q sorts from a sample of college-age voters under a variety of conditions of instruction provide negligible evidence of the Right``s ability to affect popular narratives on the president``s character. Instead, impressions of the president found in studies conducted in two points in time reveal multifaceted yet resilient images that are at odds with the uncomplimentary caricatures advanced by his critics. 대통령의 정체성에 대한 이슈는 오바마 대통령의 정적에 의해 집중적이 포화를 맞았던 지난 임기 초 이년 동안 매우 중요했다고 할 수 있겠다. 본 연구의 두 가지 탐구로부터 발견한 것은 정체성의 대상으로서 오바마의 정통성과 접근성에 대한 개인의 자아에 대한 변화하는 의식과 그것들에 대한 지각을 연결하는 다양한 내용과 독특한 유형이 있다는 것이다. 대학생 유권자가 다양한 지시조건에 따라 소팅이 이루어 졌는데 대통령 특성에 관한 대중적 담론에 영향을 주는 우파의 능력에 있어서는 특이한 증거는 없었다. 그러나 두 시점에 실시한 본 연구를 통해 오바마의 인상은 다면적이며 그의 비판자들에 의해 만들어진 신랄한 풍자와 싸우고 있는 생기있는 이미지는 발견되었다.
Hyung Lim Elfrink,Wiep Scheper,Rob Zwart,Frank Baas 한국분자세포생물학회 2013 Molecules and cells Vol.35 No.4
Disturbances in proteostasis are observed in many neurodegenerative diseases. This leads to activation of protein quality control to restore proteostasis, with a key role for the removal of aberrant proteins by proteolysis. The unfolded protein response (UPR) is a protein quality control mechanism of the endoplasmic reticulum (ER) that is activated in several neurodegenerative diseases. Recently we showed that the major proteolytic pathway during UPR activation is via the autophagy/lysosomal system. Here we investigate UPR induction if the other major proteolytic pathway of the ER -ER associated degradation (ERAD)- is inhibited. Surprisingly, impairment of ERAD results in decreased UPR activation and protects against ER stress toxicity. Autophagy induction is not affected under these conditions, however, a striking relocalization of the lyso-somes is observed. Our data suggest that a protective UPR-modulating mechanism is activated if ERAD is inhibited, which involves lysosomes. Our data provide insight in the cross-talk between proteolytic pathways involved in ER proteostasis. This has implications for neurodegenerative diseases like Alzheimer’s disease where disturbed ER proteostasis and proteolytic impairment are early phenomena in the pathology.
Burkett, J.L.,Stalder, K.J.,Powers, W.J.,Bregendahl, K.,Pierce, J.L.,Baas, T.J.,Bailey, T.,Shafer, B.L. Asian Australasian Association of Animal Productio 2009 Animal Bioscience Vol.22 No.9
Concentrated livestock production has led to soil nutrient accumulation concerns. To reduce the environmental impact, it is necessary to understand current recommended livestock feeding practices. Two experiments were conducted to compare the effects of trace mineral supplementation on performance, carcass composition, and fecal mineral excretion of phase-fed, grow-finish pigs. Crossbred pigs (Experiment 1 (Exp. 1), (n = 528); Experiment 2 (Exp. 2), (n = 560)) were housed in totally-slatted, confinement barns, blocked by weight, penned by sex, and randomly assigned to pens at approximately 18 kg BW. Treatments were allocated in a randomized complete block design (12 replicate pens per treatment) with 9 to 12 pigs per pen throughout the grow-finish period. In Exp. 1, the control diet (Io100) contained Cu as $CuSO_{4}$, Fe as $FeSO_{4}$, and Zn (of which 25% was ZnO and 75% was $ZnO_{4}$) at concentrations of 63 and 378 mg/kg, respectively. Treatment 2 (O100) contained supplemental Cu, Fe, and Zn from organic sources (Bioplex, Alltech Inc., Nicholasville, KY) at concentrations of 19, 131, and 91 mg/kg, respectively, which are the commercially recommended dietary inclusion levels for these organic trace minerals. Organic Cu, Fe, and Zn concentrations from O100 were reduced by 25% and 50% to form treatments 3 (O75) and 4 (O50-1), respectively. In Exp. 2, treatment 5 (Io25) contained 25% of the Cu, Fe, and Zn (inorganic sources) concentrations found in Io100. Treatment 6 (O50-2) was identical to the O50-1 diet from Exp. 1. Treatment 7 (O25) contained the experimental microminerals reduced by 75% from concentrations found in O100. Treatment 8 (O0) contained no trace mineral supplementation and served as a negative control for Exp. 2. In Exp. 1, tenth-rib backfat, loin muscle area and ADG did not differ (p>0.05) between treatments. Pigs fed the control diet (Io100) consumed less feed (p<0.01) compared to pigs fed diets containing organic trace minerals, thus, G:F was greater (p = 0.03). In Exp. 2, there were no differences among treatment means for loin muscle area, but pigs fed the reduced organic trace mineral diets consumed less (p<0.05) feed and tended (p = 0.10) to have less tenth-rib backfat compared to pigs fed the reduced inorganic trace mineral diet. Considering that performance and feed intake of pigs was not affected by lower dietary trace mineral inclusion, mineral excretion could be reduced during the grow-finish phase by reducing dietary trace mineral concentration.
Yang, Seung Wook,Oh, Kyu Hee,Park, Esther,Chang, Hyun Min,Park, Jung Mi,Seong, Min Woo,Ka, Seung Hyeun,Song, Woo Keun,Park, Dong Eun,Baas, Peter W.,Jeon, Young Joo,Chung, Chin Ha Society for Neuroscience 2013 The Journal of neuroscience Vol.33 No.31
<P>Katanin is a heterodimeric enzyme that severs and disassembles microtubules. While the p60 subunit has the enzyme activity, the p80 subunit regulates the p60 activity. The microtubule-severing activity of katanin plays an essential role in axonal growth. However, the mechanisms by which neuronal cells regulate the expression of katanin-p60 remains unknown. Here we showed that USP47 and C terminus of Hsp70-interacting protein (CHIP) antagonistically regulate the stability of katanin-p60 and thereby axonal growth. USP47 was identified as a katanin-p60-specific deubiquitinating enzyme for its stabilization. We also identified CHIP as a ubiquitin E3 ligase that promotes proteasome-mediated degradation of katanin-p60. Moreover, USP47 promoted axonal growth of cultured rat hippocampal neurons, whereas CHIP inhibited it. Significantly, treatment with basic fibroblast growth factor (bFGF), an inducer of axonal growth, increased the levels of USP47 and katanin-p60, but not CHIP. Consistently, bFGF treatment resulted in a marked decrease in the level of ubiquitinated katanin-p60 and thereby in the promotion of axonal growth. On the other hand, the level of USP47, but not CHIP, decreased concurrently with that of katanin-p60 as axons reached their target cells. These results indicate that USP47 plays a crucial role in the control of axonal growth during neuronal development by antagonizing CHIP-mediated katanin-p60 degradation.</P>