http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Ahnak deficiency attenuates high-fat diet-induced fatty liver in mice through FGF21 induction
Kim Yo Na,Shin Jae Hoon,Kyeong Dong Soo,Cho Soo Young,김미영,Lim Hee Jung,Jimenez Maria Raquel Rojas,Kim Il Yong,Lee Mi-Ock,Bae Yun Soo,Seong Je Kyung 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-
The AHNAK nucleoprotein has been determined to exert an anti-obesity effect in adipose tissue and further inhibit adipogenic differentiation. In this study, we examined the role of AHNAK in regulating hepatic lipid metabolism to prevent diet-induced fatty liver. Ahnak KO mice have reportedly exhibited reduced fat accumulation in the liver and decreased serum triglyceride (TG) levels when provided with either a normal chow diet or a high-fat diet (HFD). Gene expression profiling was used to identify novel factors that could be modulated by genetic manipulation of the Ahnak gene. The results revealed that fibroblast growth factor 21 (FGF21) was markedly increased in the livers of Ahnak KO mice compared with WT mice fed a HFD. Ahnak knockdown in hepatocytes reportedly prevented excessive lipid accumulation induced by palmitate treatment and was associated with increased secretion of FGF21 and the expression of genes involved in fatty acid oxidation, which are primarily downstream of PPARα. These results indicate that pronounced obesity and hepatic steatosis are attenuated in HFD-fed Ahnak KO mice. This may be attributed, in part, to the induction of FGF21 and regulation of lipid metabolism, which are considered to be involved in increased fatty acid oxidation and reduced lipogenesis in the liver. These findings suggest that targeting AHNAK may have beneficial implications in preventing or treating hepatic steatosis.
Kang Na Ri,Ahn Yo Han,박유진,Lee Keum Hwa,Baek Hee Sun,Kim Seong Heon,Cho Heeyeon,Cho Min Hyun,Shin Jae Il,Lee Joo Hoon,Cheong Hae Il,Kang Hee Gyung,Park Young Seo,Ha Il-Soo,Moon Duk-Soo,Han Kyoung Hee 대한의학회 2021 Journal of Korean medical science Vol.36 No.20
Background: Chronic kidney disease (CKD) has a negative impact on growth and development in children and is a risk factor for neurocognitive impairment; however, there is limited research on the cognitive function of children and adolescents with CKD. This study therefore aimed to investigate the mean intelligence and risk factors for low intelligence in children and adolescents with CKD. Methods: Eighty-one patients with CKD under 18 years old were included in the KoreaN cohort study for Outcomes in patients With Pediatric Chronic Kidney Disease (KNOW-Ped CKD). Participants completed either the Wechsler Intelligence Scale for Children (6–16 years), or Wechsler Adult Intelligence Scale (> 16 years). Results: The mean full-scale intelligence quotient (IQ) was 91 ± 19; 24.7% of participants scored a full-scale IQ below 80. Participants with a short stature (height Z scores < −1.88), failure to thrive (weight Z scores < −1.65), more severe CKD stage (≥ IIIb), longer duration of CKD (≥ 5 years), and those who were Medicare or Medicaid beneficiaries, had significantly lower mean full-scale IQs. Conclusion: On linear regression analysis, the association between the full-scale IQ, and longer duration of CKD and growth failure, remained significant after controlling for demographic and clinical variables. It is therefore necessary to investigate cognitive impairment in pediatric patients with CKD who exhibit growth failure or for a longer postmorbid period. It is believed that early interventions, such as kidney transplantation, will have a positive effect on IQ in children with CKD, as the disease negatively affects IQ due to poor glomerular filtration rate over time.
조영재 ( Young Jae Cho ),이상우 ( Sang Woo Lee ),임성택 ( Seung Taek Lim ),김종근 ( Jong Keun Kim ),김영호 ( Young Ho Kim ),이찬우 ( Chan Woo Lee ),오동호 ( Dong Ho Oh ),민복기 ( Pok Kee Min ),나건연 ( Gun Yoen Na ),박지영 ( Ji Yo 대한류마티스학회 2004 대한류마티스학회지 Vol.11 No.3
Sweet`s syndrome is an uncommon reactive dermatosis characterized by fever, poly-morphonuclear leukocytosis, painful erythematous cutaneous plaques and dense dermal infiltrate of neutrophils at the skin lesions. Unlike Sweet`s syndrome associated with patients with malignancies, autoimmune diseases, antecedent infectons-most commonly the upper respiratory infections, it is reported to be rarely associated with systemic lupus erythematosus (SLE). Here we report a rare case of young female with Sweet`s syndrome and SLE presenting with high fever.
Kim, Eunjin,Kang, Jeongwoo,Cho, Minchul,Lee, Sojung,Seo, Eunhee,Choi, Heesook,Kim, Yumi,Kim, Junghee,Kang, Kum Yong,Kim, Kwang Pyo,Han, Jaeyong,Sheen, Yhunyhong,Yum, Young Na,Park, Sue-Nie,Yoon, Do-Yo D. A. Spandidos 2009 MOLECULAR MEDICINE REPORTS Vol.2 No.1
<P>The E6 and E7 oncoproteins of human papilloma virus (HPV) type 16 have been known to cooperatively induce the immortalization and transformation of primary keratinocytes. We established an E7 transgenic mouse model to screen HPV-related biomakers using the omics approach. The methods used to identify HPV-modulated factors were genomics analysis by microarray using the Affymetrix 430 2.0 array to screen E7-modulated genes, and proteomics analysis using nano-LC-ESI-MS/MS to screen E7-modulated proteins with the lung tissue of E7 transgenic mice. According to omics data, cyclin B1, cyclin E2, topoisomerase IIα, calnexin, activated leukocyte cell adhesion molecule CD166, actinin α1, diaphorase 1, gelsolin, platelet glycoprotein, and annexin A2 and A4 were up-regulated in the E7-Tg mice, while proteoglycan 4, sarcolipin, titin, vimentin, drep 1, troponin and cofilin-1 were down-regulated. We further confirmed the significance of differences between the expression levels of the selected factors in E7-Tg and non-Tg mice by real-time PCR. Genes related to cancer cell adhesion, cell cycle and migration, proliferation and apoptosis, as well as to the intermediate filament network and to endoplasmic reticulum proteins, were selected. Taken together, the results suggest that the E7 oncogene modulates the expression levels of cell cycle-related (cyclin B1, cyclin E2) and cell adhesion- and migration-related (actinin α1, CD166) factors, which may play important roles in cellular transformation in cancer. In addition, the solubilization of the rigid intermediate filament network by specific proteolysis mediated via up-regulating gelsolin and down-regulating cofilin-1, as well as increased levels of endoplasmic reticulum protein calnexin with chaperone functions, might also be involved in E7-lung epithelial cells.</P>
인상우 ( Sang Woo In ),조선미 ( Sun Mi Cho ),나영일 ( Young Il Na ),이요한 ( Yo Han Lee ) 한국체육사학회 2014 체육사학회지 Vol.19 No.2
본 연구의 목적은 학문으로서의 체육사학의 연구경향을 파악하고 이를 통해 체육사학의 지식체계를 탐색하는데 있다. 이를 위해 1996년에서 2013년 12월까지 발행되었던 연구논문 전체인 373건을 대상으로 모든 연구물의 초록을 수집하였으며 수집된 자료는 디지털화 작업을 거쳐 텍스트로 변환하였다. 텍스트로 변환된 초록으로부터 빈도색인어를 추출하였으며 이를 색인어 군집에 따라 시계열적으로 분석하였다. 연구결과를 연구목적별, 연구방법별, 빈도색인어별로 제시하였으며 연구의 경향을 살펴본 결과 상대적으로 연구의 다양성에서는 크게 성장하였으나 그 연구방법의 다양성에는 한계를 보임을 확인할 수 있었다. 또한 연구초창기에는 학사연구 등 거시적인 관점과 서양사에 대한 빈도색인어가 많이 추출되었던 반면 최근에는 한국사나 인물, 종목 등 미시적인 관점에서의 연구가 이루어졌으며 연구의 영역과 관련된 새로운 용어의 등장을 확인하였다. 연구결과를 토대로 현재 체육사 연구의 특징과 함께 향후 발전방향이 논의되었다. The purpose of this study was to examine current research trend of Korean sport history and explore the knowledge frame of the research. This paper analysed the abstracts of all 373 papers published in the Korean Journal of History for Physical Education, Sport, and Dance from year 1996 to 2013. The abstracts were digitalized and textualized for frequency indexing. The index were clustered by its research purpose, historical research scope, and overall frequencies. From the time-series analysis, we found the increase of variety in the research topics but limit to the research methods. In the early stage of researches had focused relatively macro topics such as the history of sport, and western sport history and these research trends have moved toward more micro topics such as Korean sport history, sport person, and specific sports. Furthermore the new terms has been increased recently. From the analysis of the research trend the research characteristics of the Korean sport history researches and the future directions were discussed.
Correlation between Acupuncture Stimulation and Cortical Activation - Further Evidence
조장희,김경요,김형균,이병렬,강창기,나창수,Cho, Zang-Hee,Kim, Kyung-Yo,Kim, Hyeong-Kyun,Lee, Byung-Ryul,Wong, E.K.,Kang, Chang-Ki,Na, Chang-Su The Korean Acupuncture Moxibustion Medicine Societ 2001 대한침구의학회지 Vol.18 No.3
목적 : 이 실험의 목적은 경혈에 대한 침자극이 대뇌피질에 어떠한 영향을 미치는가에 대하여 체계적이고 객관적으로 증명하는 것이다. 방법 : 시각과 관련이 있는 광명(GB37), 청각과 관련이 있는 협계(GB43) 및 외관(SJ5)을 자극하고 fMRI를 통하여 대뇌피질의 활성정도를 관찰하였다. 결과 : 이들 경혈의 자극으로 시각과 청각과 관련된 피질의 활성이 나타났다. 자극에 의한 대뇌피질 활성을 fMRI를 통하여 고찰한 결과 특정한 경혈의 자극이 대뇌피질을 활성화시킨다는 사실을 알 수 있었다. 결론 : 치료 효과는 그 경혈의 자극에 의한 대뇌피질의 활성과 관련이 있음을 말하는 것으로, 경혈지극과 대뇌와의 상관성을 증명하는 것이다.
Kim, Kook Hwan,Jeong, Yeon Taek,Oh, Hyunhee,Kim, Seong Hun,Cho, Jae Min,Kim, Yo-Na,Kim, Su Sung,Kim, Do Hoon,Hur, Kyu Yeon,Kim, Hyoung Kyu,Ko, TaeHee,Han, Jin,Kim, Hong Lim,Kim, Jin,Back, Sung Hoon,Ko Nature Publishing Group, a division of Macmillan P 2013 Nature medicine Vol.19 No.1
Despite growing interest and a recent surge in papers, the role of autophagy in glucose and lipid metabolism is unclear. We produced mice with skeletal muscle–specific deletion of Atg7 (encoding autophagy-related 7). Unexpectedly, these mice showed decreased fat mass and were protected from diet-induced obesity and insulin resistance; this phenotype was accompanied by increased fatty acid oxidation and browning of white adipose tissue (WAT) owing to induction of fibroblast growth factor 21 (Fgf21). Mitochondrial dysfunction induced by autophagy deficiency increased Fgf21 expression through induction of Atf4, a master regulator of the integrated stress response. Mitochondrial respiratory chain inhibitors also induced Fgf21 in an Atf4-dependent manner. We also observed induction of Fgf21, resistance to diet-induced obesity and amelioration of insulin resistance in mice with autophagy deficiency in the liver, another insulin target tissue. These findings suggest that autophagy deficiency and subsequent mitochondrial dysfunction promote Fgf21 expression, a hormone we consequently term a 'mitokine', and together these processes promote protection from diet-induced obesity and insulin resistance.