• 생명과학회지
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• 제30권9호
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• pp.772-782
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• 2020

골격근의 분화 또는 근육 분화는 근육량과 신진대사 항상성을 유지하기 위해 중요하다. 근육 특이적 microRNAs (miRNAs)는 골격근 분화에 중요한 역할을 한다. 본 연구에서는 rat miRNAs 마이크로어레이를 사용하여 rat L6 근아세포의 근육 분화 과정에서의 miRNAs 발현 양상을 조사했다. 우리는 miR-128의 발현 증가를 발견했고, 동시에 이미 알려진 근육 분화 조절 miRNAs인 miR-1, miR-133b와 mi-206의 발현 증가를 확인했다. 이 microarray 결과를 확인하기위해 우리는 Quantitative RT-PCR 기술을 사용하였고, microarray 결과와 유사하게 발현 초기 mRNAs와 발현 후 성숙 miRNAs에서 모두 miR-128의 발현 증가를 확인했다. 또한 Rat L6 근아세포로의 miR-128 발현 향상은 muscle creatine kinase (MCK), myogenin, myosin heavy chain (MHC)와 같은 근육분화 표지 유전자 발현을 유발했고, 또한 MHC의 단백질 발현을 증가시켰다. 억제 PNAs를 사용한 miR-128의 작용 억제는 이러한 근육 분화 표지 유전자들의 발현을 차단했다. 또한, miR-128 발현 향상은 Erk와 Akt 단백질의 인슐린 자극에 의한 인산화를 증가시켰고, 고인슐린혈증과 고혈당증으로 인해 유도된 인슐린 저항성으로 인한 Erk와 Akt의 억제된 인산화를 회복했다. 이러한 발견은 miR-128이 근육분화와 인슐린 작용에 중요한 역할을 할 수 있다는 것을 시사한다.

• 한국지능시스템학회논문지
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• 제19권1호
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• pp.128-132
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• 2009

Sostak개념의 intuitionistic fuzzy topological space에서 fuzzy S-weakly (r,s)-continuous mapping의 개념과 연산을 소개하며 기본적인 성질을 조사한다.

• Asian Pacific Journal of Cancer Prevention
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• 제15권7호
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• pp.3247-3252
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• 2014

Background: Genetic factors have been shown to play an important role in the development of cancers. However, individual studies may fail to completely demonstrate complicated genetic relationships because of small sample size. Therefore, we performed a meta-analysis to evaluate the association of E-selectin Ser128Arg (S128R) with cancer risk. Materials and Methods: A literature search in PubMed, Embase, Web of Science, Science Direct, SpringerLink, EBSCO, Wanfang, and Chinese National Knowledge Infrastructure databases was carried out to identify studies of the association between E-selectin S128R polymorphism and cancer risk. The odds ratio (OR) with 95% confidence intervals (95%CIs) were used to assess the strength of association. Results: A total of eight studies involving 1,675 cancer cases and 2,285 controls were included in the meta-analysis. In overall populations, S128R polymorphism seemed to be associated with cancer risk (Arg allele vs Ser allele: OR=1.65, 95%CI =1.33-2.04, p<0.01; Arg/Arg+Arg/Ser vs Ser/Ser: OR=1.87, 95%CI =1.48-2.36, p<0.01; Arg/Ser vs Ser/Ser: OR=1.80, 95%CI =1.51-2.14, p<0.01). Similarly, subgroup analysis by ethnicity and source of control also revealed that this polymorphism was related to cancer risk. Conclusions: Our meta-analysis revealed that there was association between the E-selectin S128R polymorphism and the risk of cancer. Further large and well-designed studies are needed to confirm this association.

• Yonsei Medical Journal
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• 제59권9호
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• pp.1096-1106
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• 2018

Purpose: Alzheimer's disease (AD) is the sixth most common cause of death in the United States. MicroRNAs have been identified as vital players in neurodegenerative diseases, including AD. microRNA-128 (miR-128) has been shown to be dysregulated in AD. This study aimed to explore the roles and molecular mechanisms of miR-128 in AD progression. Materials and Methods: Expression patterns of miR-128 and peroxisome proliferator-activated receptor gamma ($PPAR-{\gamma}$) messenger RNA in clinical samples and cells were measured using RT-qPCR assay. $PPAR-{\gamma}$ protein levels were determined by Western blot assay. Cell viability was determined by MTT assay. Cell apoptotic rate was detected by flow cytometry via double-staining of Annexin V-FITC/PI. Caspase 3 and $NF-{\kappa}B$ activity was determined by a Caspase 3 Activity Assay Kit or $NF-{\kappa}B$ p65 Transcription Factor Assay Kit, respectively. Bioinformatics prediction and luciferase reporter assay were used to investigate interactions between miR-128 and $PPAR-{\gamma}$ 3'UTR. Results: MiR-128 expression was upregulated and $PPAR-{\gamma}$ expression was downregulated in plasma from AD patients and $amyloid-{\beta}$ $(A{\beta})-treated$ primary mouse cortical neurons (MCN) and Neuro2a (N2a) cells. Inhibition of miR-128 decreased $A{\beta}-mediated$ cytotoxicity through inactivation of $NF-{\kappa}B$ in MCN and N2a cells. Moreover, $PPAR-{\gamma}$ was a target of miR-128. $PPAR-{\gamma}$ upregulation attenuated $A{\beta}-mediated$ cytotoxicity by inactivating $NF-{\kappa}B$ in MCN and N2a cells. Furthermore, $PPAR-{\gamma}$ downregulation was able to abolish the effect of anti-miR-128 on cytotoxicity and $NF-{\kappa}B$ activity in MCN and N2a cells. Conclusion: MiR-128 inhibitor decreased $A{\beta}-mediated$ cytotoxicity by upregulating $PPAR-{\gamma}$ via inactivation of $NF-{\kappa}B$ in MCN and N2a cells, providing a new potential target in AD treatment.

• Journal of Korean Neurosurgical Society
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• 제63권5호
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• pp.550-558
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• 2020

To perform a systematic review of the data collected from case-control studies conducted earlier to investigate the correlation between E-selectin S128R polymorphism and ischemic stroke (IS) risk among the Chinese population. The PubMed, Web of Science, Chinese biomedical literature database (CBM), Chinese databases China National Knowledge Infrastructure (CNKI), WanfangData knowledge service platform (Wanfang Data), and information resource integration service platform (VIP) Databases were searched to retrieve case-control studies on the correlation between E-selectin gene S128R polymorphism and IS from the inception of the database till June 2019. The literature was screened, data were extracted, the risk of bias was reviewed, and the studies included were assessed independently by two reviewers. Stata ver. 12.0 software (Stata Corp LLC, College Station, TX, USA) was used to perform the meta-analysis. A total of 2907 cases from eight case-control studies involving 1478 IS patients and 1429 controls were included in this study. The R allele and RS genotype in E-selectin were found to be associated with the risk of IS as per the results of the meta-analysis (R vs. S : odds ratio [OR], 2.75; 95% confidence interval [CI], 2.15-3.51; p<0.00001; RS vs. SS : OR, 2.50; 95% CI, 1.95-3.19; p<0.00001; RR+RS vs. SS : OR, 2.85, 95% CI, 2.21-3.67; p<0.00001). The E-selectin gene S128R polymorphism is likely related to IS based on the results of a meta-analysis in the Chinese population, and the R allele and RS genotype of E-selectin may be IS risk factors.

• 한국자기학회:학술대회 개요집
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• 한국자기학회 2008년도 Asian Magnetics Conference
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• pp.128.1-128.1
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• 2008

• 한국정밀공학회:학술대회논문집
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• 한국정밀공학회 2010년도 춘계학술대회 논문집
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• pp.127-128
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• 2010

• Elastomers and Composites
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• 제55권2호
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• pp.128-136
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• 2020

The hydrolysis mechanisms as well as the hydrolysis measurement technique and its practical applications in material manufacturing fields are revised. This chapter, Part 1, elaborates the theoretical aspects of the hydrolysis mechanism. Acid-catalyzed and base-catalyzed hydrolysis mechanisms are reviewed. The quantitative analysis method based on the SIM technique using py-GC-MS is reviewed. Examples of hydrolysis of alkoxysilane in elastomer composites currently used in the industry and hydrolysis of amine in plastic composites are shown. Moreover, Part 2 discusses the mechanical property changes in elastomer and plastic composites after hydrolysis.

• Advances in Traditional Medicine
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• 제7권2호
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• pp.128-132
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• 2007

Diarun plus, a polyherbal formulation containing herbal ingredients of folkloric Antidiabetic effect, was investigated for its effect on glycemic status in rats and mice. In contrast to conventional chemical induced diabetic animal models, changes in glycemic states were induced by physiological maneuvers. Results revealed that in euglycemic animals Diarun plus elicited little change (-10 to +10%), which was insignificant. In food deprivation/swim exercise induced hypoglycemia, Diarun plus reduced the degree of hypoglycemia in both rats and mice (from 38% to 27% in rats and 45% to 32% in mice). Similarly, the marked hyperglycemia induced by dextrose (70% in rats and 95% in mice) was reduced markedly to 8% and 25% respectively. The findings of the present study suggests that the ingredients of Diarun plus have the unique property of maintaining near euglycemic state irrespective of the altered glycemic state, and that have no significant effect in euglycemic condition.

• 한국기술혁신학회:학술대회논문집
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• 한국기술혁신학회 2014년도 추계 학술대회 논문집
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• pp.189-203
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• 2014

Silicon Valley's legal foundation in recent years has surfaced on the radar of policy planners who model Silicon Valley's ICT industry. Precisely, the prohibition of covenants not to compete is linked to firm to firm knowledge spillovers by way of mobile workers positioned as nodes in a system of innovation. Meanwhile, traditional frameworks support enforcement of covenants not to compete as a way to encourage R&D into the worker and to prevent the worker's tacit knowledge and know-how from fleeing. This article examines the ICT industry in Silicon Valley and Route 128 to argue that California's unique law is a key factor in the success of Silicon Valley firms. Theoretically, we reconcile the ostensible strife between enforcement and prohibition frameworks by presenting an industrial approach. We contend that selective enforcement by industry can maximize the policy tools of discorded planners.