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Natalia Kim 중동유럽한국학회 2016 중동유럽한국학회지 Vol.16 No.-
이 연구는 한국 사회에서 여성 이민자들이 직면하고 있는 사회문화적 적응 문제에 초점을 맞추고 있다. 연구의 목적은 문화변용 이론을 바탕으로 한국국민과 결혼한 여성 이민자들이 직면하는사회문화적 적응에 있어 주요한 문제점을 조사하고, 이들 여성들이 문화적응에 관련된 문제들에 대처하기 위해 사용하는 행동전략을 규명해내는 것이다. 결혼이민여성들이 정서적, 사회문화적으로 한국 문화에 적응하는 과정에서 이들의 문화 적응전략의 선택에 연관된 요소와 사안들에 대해서 통계적 방법과 각종 분석 데이터들을 적극 이용하여 연구하였다. 연구의 예비결과로는 문화적응 전략의 선택은 결혼 이민자들의 소속 민족과 본인들의 교육 배경이라는 두가지 요인에 크게 의존하는 것으로 나타났다. 유럽 출신의 비교적 높은 교육을 받은 결혼이민자들은 주로 통합전략을 수행한다. 반면에 주로 동남아지역 출신의 교육받지 못한 여성 결혼이민자들은 새로운 환경에 잘 적응하여 동화되거나 아니면 한국사회에서 소외되는 상황에 처하기도 한다. 하지만 어떤 경우에서던지 아직은 다민족 사회가 아닌 한국이 가지고 있는 결혼이민여성들에 대한 각종 편견들은 결혼이민여성들이 한국사회로의 원활한 통합과 문화적응을 크게 방해하고 있는 실정이다. This research focuses on current problems of sociocultural adaptation facing women immigrants in South Korean society. The goal of the present study is to investigate, through the lens of acculturation theory, the major problems in sociocultural adaptation facing women immigrants married to Korean nationals, and to define the strategies they use for coping with the problems involved in cultural adjustment. Statistical data and analytical reports were used to determine the issues and factors influencing the choice of acculturation strategies for women marriage immigrants during their process of psychological and sociocultural adaptation to the host culture. The preliminary results of the research showed that the choice of acculturation strategy is strongly dependent both on ethnic origin and educational background of marriage immigrants. The integration strategy is mainly practiced by the marriage immigrants of European origins with high professional qualifications while the immigrants with low educational background from Southeast Asia have to be either assimilated to better adjust to a new social environment or else face being marginalized. In any case, a smooth integration and acculturation of marriage immigrants is significantly hampered by the existing racial prejudices towards foreigners in South Korea, which is yet cannot be called a multicultural society.
Kim, H.G.,Kim, H.T.,Leach, Natalia T.,Lan, F.,Ullmann, R.,Silahtaroglu, A.,Kurth, I.,Nowka, A.,Seong, I.,Shen, Y.,Talkowski, Michael E.,Ruderfer, D.,Lee, J.H.,Glotzbach, C.,Ha, K.,Kjaergaard, S.,Levin University of Chicago Press [etc.] 2012 American journal of human genetics Vol.91 No.1
Potocki-Shaffer syndrome (PSS) is a contiguous gene disorder due to the interstitial deletion of band p11.2 of chromosome 11 and is characterized by multiple exostoses, parietal foramina, intellectual disability (ID), and craniofacial anomalies (CFAs). Despite the identification of individual genes responsible for multiple exostoses and parietal foramina in PSS, the identity of the gene(s) associated with the ID and CFA phenotypes has remained elusive. Through characterization of independent subjects with balanced translocations and supportive comparative deletion mapping of PSS subjects, we have uncovered evidence that the ID and CFA phenotypes are both caused by haploinsufficiency of a single gene, PHF21A, at 11p11.2. PHF21A encodes a plant homeodomain finger protein whose murine and zebrafish orthologs are both expressed in a manner consistent with a function in neurofacial and craniofacial development, and suppression of the latter led to both craniofacial abnormalities and neuronal apoptosis. Along with lysine-specific demethylase 1 (LSD1), PHF21A, also known as BHC80, is a component of the BRAF-histone deacetylase complex that represses target-gene transcription. In lymphoblastoid cell lines from two translocation subjects in whom PHF21A was directly disrupted by the respective breakpoints, we observed derepression of the neuronal gene SCN3A and reduced LSD1 occupancy at the SCN3A promoter, supporting a direct functional consequence of PHF21A haploinsufficiency on transcriptional regulation. Our finding that disruption of PHF21A by translocations in the PSS region is associated with ID adds to the growing list of ID-associated genes that emphasize the critical role of transcriptional regulation and chromatin remodeling in normal brain development and cognitive function.
Functional role of serotonin in insulin secretion in a diet-induced insulin-resistant state.
Kim, Kyuho,Oh, Chang-Myung,Ohara-Imaizumi, Mica,Park, Sangkyu,Namkung, Jun,Yadav, Vijay K,Tamarina, Natalia A,Roe, Michael W,Philipson, Louis H,Karsenty, Gerard,Nagamatsu, Shinya,German, Michael S,Kim The Endocrine Society 2015 Endocrinology Vol.156 No.2
<P>The physiological role of serotonin, or 5-hydroxytryptamine (5-HT), in pancreatic β-cell function was previously elucidated using a pregnant mouse model. During pregnancy, 5-HT increases β-cell proliferation and glucose-stimulated insulin secretion (GSIS) through the Gαq-coupled 5-HT2b receptor (Htr2b) and the 5-HT3 receptor (Htr3), a ligand-gated cation channel, respectively. However, the role of 5-HT in β-cell function in an insulin-resistant state has yet to be elucidated. Here, we characterized the metabolic phenotypes of β-cell-specific Htr2b(-/-) (Htr2b βKO), Htr3a(-/-) (Htr3a knock-out [KO]), and β-cell-specific tryptophan hydroxylase 1 (Tph1)(-/-) (Tph1 βKO) mice on a high-fat diet (HFD). Htr2b βKO, Htr3a KO, and Tph1 βKO mice exhibited normal glucose tolerance on a standard chow diet. After 6 weeks on an HFD, beginning at 4 weeks of age, both Htr3a KO and Tph1 βKO mice developed glucose intolerance, but Htr2b βKO mice remained normoglycemic. Pancreas perfusion assays revealed defective first-phase insulin secretion in Htr3a KO mice. GSIS was impaired in islets isolated from HFD-fed Htr3a KO and Tph1 βKO mice, and 5-HT treatment improved insulin secretion from Tph1 βKO islets but not from Htr3a KO islets. Tph1 and Htr3a gene expression in pancreatic islets was not affected by an HFD, and immunostaining could not detect 5-HT in pancreatic islets from mice fed an HFD. Taken together, these results demonstrate that basal 5-HT levels in β-cells play a role in GSIS through Htr3, which becomes more evident in a diet-induced insulin-resistant state.</P>
Extensive Mammalian Ancestry of Pandemic (H1N1) 2009 Virus
Ilyushina, Natalia A.,Kim, Jeong-Ki,Negovetich, Nicholas J.,Choi, Young-Ki,Lang, Victoria,Bovin, Nicolai V.,Forrest, Heather L.,Song, Min-Suk,Pascua, Philippe Noriel Q.,Kim, Chul-Joong,Webster, Robert Centers for Disease Control and Prevention 2010 Emerging infectious diseases Vol.16 No.2
<P>We demonstrate that the novel pandemic influenza (H1N1) viruses have human virus–like receptor specificity and can no longer replicate in aquatic waterfowl, their historic natural reservoir. The biological properties of these viruses are consistent with those of their phylogenetic progenitors, indicating longstanding adaptation to mammals.</P>
Therapeutic Potential of Induced Neural Stem Cells for Spinal Cord Injury
Hong, Jin Young,Lee, Sung Ho,Lee, Seung Chan,Kim, Jong-Wan,Kim, Kee-Pyo,Kim, Sung Min,Tapia, Natalia,Lim, Kyung Tae,Kim, Jonghun,Ahn, Hong-Sun,Ko, Kinarm,Shin, Chan Young,Lee, Hoon Taek,Schö,ler, American Society for Biochemistry and Molecular Bi 2014 The Journal of biological chemistry Vol.289 No.47
<P>The spinal cord does not spontaneously regenerate, and treatment that ensures functional recovery after spinal cord injury (SCI) is still not available. Recently, fibroblasts have been directly converted into induced neural stem cells (iNSCs) by the forced expression defined transcription factors. Although directly converted iNSCs have been considered to be a cell source for clinical applications, their therapeutic potential has not yet been investigated. Here we show that iNSCs directly converted from mouse fibroblasts enhance the functional recovery of SCI animals. Engrafted iNSCs could differentiate into all neuronal lineages, including different subtypes of mature neurons. Furthermore, iNSC-derived neurons could form synapses with host neurons, thus enhancing the locomotor function recovery. A time course analysis of iNSC-treated SCI animals revealed that engrafted iNSCs effectively reduced the inflammatory response and apoptosis in the injured area. iNSC transplantation also promoted the active regeneration of the endogenous recipient environment in the absence of tumor formation. Therefore, our data suggest that directly converted iNSCs hold therapeutic potential for treatment of SCI and may thus represent a promising cell source for transplantation therapy in patients with SCI.</P>
Kim, Yoo Seok,Yuniarti, Ana R.,Song, Kwang-Soup,Trayanova, Natalia A.,Shim, Eun Bo,Lim, Ki Moo Springer Berlin Heidelberg 2018 Medical & biological engineering & computing Vol.56 No.5
<P>Valvular insufficiency affects cardiac responses and the pumping efficacy of left ventricular assist devices (LVADs) when patients undergo LVAD therapy. Knowledge of the effect of valvular regurgitation on the function of LVADs is important when treating heart failure patients. The goal of this study was to examine the effect of valvular regurgitation on the ventricular mechanics of a heart under LVAD treatment and the pumping efficacy of an LVAD using a computational model of the cardiovascular system. For this purpose, a 3D electromechanical model of failing ventricles in a human heart was coupled with a lumped-parameter model of valvular regurgitation and an LVAD-implanted vascular system. We used the computational model to predict cardiac responses with respect to the severity of valvular regurgitation in the presence of LVAD treatment. An LVAD could reduce left ventricle (LV) pressure (up to 34%) and end-diastolic ventricular volume (up to 80%) and maintain cardiac output at the estimated flow rate from the LVAD under the condition of mitral regurgitation (MR); however, the opposite would occur under the condition of aortic regurgitation (AR). Considering these physiological responses, we conclude that AR, and not MR, diminishes the pumping function of LVADs.</P>
Kim, Chang-Hyun,Song, Kwang-Soup,Trayanova, Natalia A.,Lim, Ki Moo Springer Berlin Heidelberg 2018 Medical & biological engineering & computing Vol.56 No.5
<P>Intra-aortic balloon pump (IABP) is normally contraindicated in significant aortic regurgitation (AR). It causes and aggravates pre-existing AR while performing well in the event of mitral regurgitation (MR). Indirect parameters, such as the mean systolic pressure, product of heart rate and peak systolic pressure, and pressure–volume are used to quantify the effect of IABP on ventricular workload. However, to date, no studies have directly quantified the reduction in workload with IABP. The goal of this study is to examine the effect of IABP therapy on ventricular mechanics under valvular insufficiency by using a computational model of the heart. For this purpose, the 3D electromechanical model of the failing ventricles used in previous studies was coupled with a lumped parameter model of valvular regurgitation and the IABP-treated vascular system. The IABP therapy was disturbed in terms of reducing the myocardial tension generation and contractile ATP consumption by valvular regurgitation, particularly in the AR condition. The IABP worsened the problem of ventricular expansion induced as a result of the regurgitated blood volume during the diastole under the AR condition. The IABP reduced the LV stroke work in the AR, MR, and no regurgitation conditions. Therefore, the IABP helped the ventricle to pump blood and reduced the ventricular workload. In conclusion, the IABP partially performed its role in the MR condition. However, it was disturbed by the AR and worsened the cardiovascular responses that followed the AR. Therefore, this study computationally proved the reason for the clinical contraindication of IABP in AR patients.</P>