• Korean Journal of Clinical Laboratory Science
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• v.55 no.1
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• pp.1-8
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• 2023

The purpose of this study is to find terms that can give identity to the major and occupation of clinical laboratory technologist (also known as medical technologist). The term clinical pathology includes all branches of pathology, namely anatomical pathology, chemical pathology, hematology, microbiology, and all respective subspecialties. Unfortunately, several countries exclude anatomical pathology from the term clinical pathology, a problem that gets compounded when the title is translated into languages other than English. Clinical pathology (US, UK) is a medical specialty. Similar terms are laboratory medicine (Germany, Poland), medical/clinical biology (France, Netherlands) or clinical analysis (Spain). Depending on the person questioned, medical technology is defined slightly differently by individuals, companies, and institutions. The definition also depends on the language in which the question is asked. Medical technology can be translated to define clinical laboratory technology, allied health sciences, medical equipment, biomedical engineering, and health technology. The terms 'clinical pathology technology and pathological technology' are not used in allied health sciences. The names of 'medical technology·medical technologist' can be replaced by 'biomedical laboratory science·biomedical laboratory technologist' or 'clinical laboratory analysis·clinical laboratory analyst'. In this study, it is proposed to change the name of academic and occupation to 'medical biology·medical biology technologist' that combines the term biomedical.

• BMB Reports
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• v.45 no.8
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• pp.470-475
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• 2012

Protein arginine methyltransferase 1 (PRMT1), a type-I arginine methyltransferase, has been implicated in diverse cellular events. We have focused on the role of PRMT1 in gliomagenesis. In this study, we showed that PRMT1 expression was up-regulated in glioma tissues and cell lines compared with normal brain tissues. The knock-down of PRMT1 resulted in an arrest in the G1-S phase of the cell cycle, proliferation inhibition and apoptosis induction in four glioma cell lines (T98G, U87MG, U251, and A172). Moreover, an in vivo study confirmed that the tumor growth in nude mouse xenografts was significantly decreased in the RNAi-PRMT1 group. Additionally, we found that the level of the asymmetric dimethylated modification of H4R3, a substrate of PRMT1, was higher in glioma cells than in normal brain tissues and decreased after PRMT1 knock-down. Our data suggest a potential role for PRMT1 as a novel biomarker of and therapeutic target in gliomas.

• Proceedings of the Korean Nuclear Society Conference
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• 2004.10a
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• pp.1138-1139
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• 2004

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.7
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• pp.4243-4247
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• 2013

The relationship between the X-ray repair cross-complementing group 3 (XRCC3) Thr241Met polymorphism and gliomas remains inclusive or controversial. For better understanding of the effect of XRCC3 Thr241Met polymorphism on glioma risk, a meta-analysis was performed. All eligible studies were identified through a search of PubMed, Elsevier Science Direct, Excerpta Medica Database (Embase) and Chinese Biomedical Literature Database (CBM) before May 2013. The association between the XRCC3 Thr241Met polymorphism and gliomas risk was conducted by odds ratios (ORs) and 95% confidence intervals (95% CIs). A total of nine case-control studies including 3,533 cases and 4,696 controls were eventually collected. Overall, we found that XRCC3 Thr241Met polymorphism was significantly associated with the risk of gliomas (T vs. C: OR=1.10, 95%CI=1.01-1.20, P=0.034; TT vs. CC: OR=1.30, 95%CI=1.03-1.65, P=0.027; TT vs. TC/CC: OR=1.29, 95%CI=1.01-1.64, P=0.039). In the subgroup analysis based on ethnicity, the significant association was found in Asian under four models (T vs. C: OR=1.17, 95%CI=1.07-1.28, P=0.00; TT vs. CC: OR=1.79, 95%CI=1.36-2.36, P=0.00; TT vs. TC/CC: OR=1.75, 95%CI=1.32-2.32, P=0.00; TT/TC vs. CC: OR=1.11,95% CI=1.02-1.20). This meta-analysis suggested that the XRCC3 Thr241Met polymorphism is a risk factor for gliomas, especially for Asians. Considering the limited sample size and ethnicities included in the meta-analysis, further large scale and well-designed studies are needed to confirm our results.

• BMB Reports
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• v.46 no.8
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• pp.422-427
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• 2013

Although BMP9 is highly capable of promoting osteogenic differentiation of mesenchymal stem cell (MSCs), the molecular mechanism involved remains to be fully elucidated. Here, we explore the possible involvement and detail role of JNKs (c-Jun N-terminal kinases) in BMP9-induced osteogenic differentiation of MSCs. It was found that BMP9 stimulated the activation of JNKs in MSCs. BMP9-induced osteogenic differentiation of MSCs was dramatically inhibited by JNKs inhibitor SP600125. Moreover, BMP9-activated Smads signaling was decreased by SP600125 treatment in MSCs. The effects of inhibitor are reproduced with adenoviruses expressing siRNA targeted JNKs. Taken together, our results revealed that JNKs was activated in BMP9-induced osteogenic differentiation of MSCs. What is most noteworthy, however, is that inhibition of JNKs activity resulted in reduction of BMP9-induced osteogenic differentiation of MSCs, implying that activation of JNKs is essential for BMP9 osteoinductive activity.

• Proceedings of the Korean Nuclear Society Conference
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• 2004.10a
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• pp.1211-1211
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• 2004

• Proceedings of the KSAR Conference
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• 2002.06a
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• pp.93-93
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• 2002

The utility of transgenic animal for studying the function of a particular gene in the breast system has been limited because transgenic typically occurs constitutively throughout development and in most tissue. So we use the inducible gene expression system. Several inducible gene expression system have been developed in vitro in recent years to overcome limitation with transgenic mice. (omitted)

• Proceedings of the KSAR Conference
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• 2002.06a
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• pp.68-68
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• 2002

Positional cloning of hereditary deafness genes is a direct approach to identify molecules and mechanisms underlying auditory function. Nowadays many deafness genes are newly identified by finding the locus for the causative genes. Mutations at many different loci in humans and mice are known to cause hearing impairment. Mouse mutants exhibiting deafness may be useful in identifying some of genes involved. (omitted)

• Proceedings of the Korean Society of Veterinary Clinics Conference
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• 2007.05a
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• pp.110-110
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• 2007

• BMB Reports
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• v.52 no.8
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• pp.520-525
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• 2019

Dihydroartemisinin (DHA) has been reported to possess anti-cancer activity against many cancers. However, the pharmacologic effect of DHA on HBV-positive hepatocellular carcinoma (HCC) remains unknown. Thus, the objective of the present study was to determine whether DHA could inhibit the proliferation of HepG2.2.15 cells and uncover the underlying mechanisms involved in the effect of DHA on HepG2.2.15 cells. We found that DHA effectively inhibited HepG2.2.15 HCC cell proliferation both in vivo and in vitro. DHA also reduced the migration and tumorigenicity capacity of HepG2.2.15 cells. Regarding the underlying mechanisms, results showed that DHA induced cellular senescence by up-regulating expression levels of proteins such as p-ATM, p-ATR, ${\gamma}-H_2AX$, P53, and P21 involved in DNA damage response. DHA also induced autophagy (green LC3 puncta gathered together and LC3II/LC3I ratio increased through AKT-mTOR pathway suppression). Results also revealed that DHA-induced autophagy was not linked to senescence or cell death. TPP1 (telomere shelterin) overexpression could not rescue DHA-induced anticancer activity (cell proliferation). Moreover, DHA down-regulated TPP1 expression. Gene knockdown of TPP1 caused similar phenotypes and mechanisms as DHA induced phenotypes and mechanisms in HepG2.2.15 cells. These results demonstrate that DHA might inhibit HepG2.2.15 cells proliferation through inducing cellular senescence and autophagy.