• 대한임상검사과학회지
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• 제55권1호
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• pp.1-8
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• 2023

본 연구의 목적은 임상병리사의 전공과 직업에 정체성을 부여할 수 있는 용어를 찾는 것이다. 임상병리학이라는 용어는 병리학의 모든 분야, 즉 해부병리학, 화학병리학, 혈액학, 미생물학 및 이들의 모든 하위 전문 분야를 포함하도록 의도되었다. 불행히도, 많은 나라에서 임상병리학이라는 용어는 해부병리학을 배제하는 것으로 생각되었는데, 이는 이름이 영어 이외의 언어로 번역되었을 때 문제가 복잡해졌다. 임상병리학(미국, 영국)은 의학의 한 전문 분야이다. 유사한 용어로는 검사의학(독일, 폴란드), 의료/임상생물학(프랑스, 네덜란드) 또는 임상분석학(스페인)이 있다. 의료기술은 개인, 회사 및 기관과 같이 질문하는 사람에 따라 약간 다르게 정의된다. 물론, 질문하는 언어에 따라 다르다. 의료기술은 임상검사기술학, 지원보건과학, 의료기기, 의생명공학, 보건기술로도 번역될 수 있다. 지원보건과학에서는 '임상병리기술학·병리기술학'이라는 용어를 사용하지 않는다. '보건계열 임상병리학 및 임상병리사'의 명칭은 '의생명검험과학·의생명검험사' 또는 '임상검사분석학·임상검사분석사'로 대체할 수 있다. 본 연구에서는 학문과 자격의 명칭을 '의생명'이 결합된 용어로 '의료생물학·의료생물사'로 변경할 것을 제안해 본다.

• BMB Reports
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• 제45권8호
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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.

• 한국원자력학회:학술대회논문집
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• 한국원자력학회 2004년도 추계학술발표회 발표논문집
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• pp.1138-1139
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• 2004

• Asian Pacific Journal of Cancer Prevention
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• 제14권7호
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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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• 제46권8호
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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.

• 한국원자력학회:학술대회논문집
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• 한국원자력학회 2004년도 추계학술발표회 발표논문집
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• pp.1211-1211
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• 2004

• 한국동물번식학회:학술대회논문집
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• 한국동물번식학회 2002년도 춘계학술발표대회 발표논문초록집
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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)

• 한국동물번식학회:학술대회논문집
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• 한국동물번식학회 2002년도 춘계학술발표대회 발표논문초록집
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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)

• 한국임상수의학회:학술대회논문집
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• 한국임상수의학회 2007년도 춘계학술대회
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• pp.110-110
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• 2007

• BMB Reports
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• 제52권8호
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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.