• Title/Summary/Keyword: 임상병리학과

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Study on the Fourth Industrial Revolution and Clinical Laboratory Science Techniques (4차 산업혁명과 임상검사과학기술에 관한 연구)

  • Sung, Hyun Ho;Choi, Kwang-Mo;Jung, You Hyun;Cho, Eun Kyung
    • Korean Journal of Clinical Laboratory Science
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    • v.51 no.3
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    • pp.386-395
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    • 2019
  • The aim of this study was to introduce clinical laboratory science techniques with the core technology of the 4th Industrial Revolution. Among the core technologies of the 4th Industrial Revolution, AI, IOT, block-chain, robotics, and nanotechnology were analyzed and linked by themes. The scope of the job of clinical laboratory technologists (also known as medical laboratory technologists and medical technologists) is laboratory medicine testing, pathology testing, and clinical physiology testing. Through a number of previous papers, 73 linkages in the laboratory medicine area, 27 linkages in the pathology area, and 47 linkages in the clinical physiology area were examined. In the 4th industrial revolution and clinical laboratory science techniques, AI (4), IOT (3), block-chain (4), robotics (3) and nanotechnology (15) sectors were surveyed. The limitation of this study was the limitation in collecting and analyzing all the data and non-clinical areas were not analyzed. In addition, there was no validity test and no similar study. In conclusion, the core technologies of the 4th industrial revolution and clinical laboratory science techniques are closely related. Therefore, further research on the future and social benefits of clinical laboratory science techniques is needed.

Caspase-8 Potentiates Triglyceride (TG)-Induced Cell Death of THP-1 Macrophages via a Positive Feedback Loop (Caspase-8의 양성 피드백 방식을 통한 중성지방-유도 THP-1 대식세포 사멸 증가)

  • Jung, Byung Chul;Lim, Jaewon;Kim, Sung Hoon;Kim, Yoon Suk
    • Korean Journal of Clinical Laboratory Science
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    • v.53 no.2
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    • pp.158-164
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    • 2021
  • Hypertriglyceridemia is the main risk factor for atherosclerosis. It is reported that triglyceride (TG) induces macrophage cell death, and is involved in the formation of plaques and development of atherosclerosis. We previously reported that TG-induced cell death of macrophages is mediated via pannexin-1 activation, which increases the extracellular ATP and subsequent increase in potassium efflux, thereby activating the caspase-2/caspase-1/apoptotic caspases, including the caspase-8 pathway. Contrarily, some studies have reported that caspase-8 is an upstream molecule of caspase-1 and caspase-2 in several cellular processes. Therefore, this study was undertaken to investigate whether caspase-8 influences its upstream molecules in TG-stimulated macrophage cell death. We first confirmed that caspase-8 induces caspase-3 activation and poly ADP-ribose polymerase (PARP) cleavage in TG-treated macrophages. Next, we determined that the inhibition of caspase-8 results in reduced caspase-1 and -2 activity, which are upstream molecules of caspase-8 in TG-induced cell death of macrophages. We also found that ATP treatment restores the caspase-8 inhibitor-induced caspase-2 activity, thereby implying that caspase-8 affects the upstream molecules responsible for increasing the extracellular ATP levels in TG-induced macrophage cell death. Taken together, these findings indicate that caspase-8 potentiates the TG-induced macrophage cell death by activating its upstream molecules.

Inhibitory Effects of Esculetin Through the Down-Regulation of PI3K/MAPK Pathway on Collagen-Induced Platelets Aggregation (Esculetin이 PI3K/MAPK 경로 하향 조절을 통해 collagen 유도의 혈소판 응집 억제에 미치는 효과)

  • Park, Chang-Eun;Lee, Dong-Ha
    • Korean Journal of Pharmacognosy
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    • v.52 no.3
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    • pp.127-133
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    • 2021
  • Platelet activation plays a major role in cardiovascular disorders (CVDs). Thus, disrupting platelet activation represents an attractive therapeutic target on CVDs. Esculetin, a bioactive 6,7-dihydroxy derivative of coumarin, possesses pharmacological activities against obesity, diabetes, renal failure, and CVDs. In other report, the effect of esculetin has been examined in human platelet activation and experimental mouse models, and esculetin inhibited collagen- and arachidonic acid-induced platelet aggregation in washed human platelets. However, it had no effects on other agonists such as thrombin and U46619, and its mechanism is not also clearly known. This study investigated the effect of esculetin on collagen-induced human platelet aggregation, and we clarified the mechanism. Esuletin has effects on the down regulation of PI3K/Akt and MAPK, phosphoproteins that act in the signaling process in platelet aggregation. The effects of esculetin reduced of TXA2 production and phospholipase A2 activation, and intracellular granule secretion including ATP and serotonin, leading to inhibit platelet aggregation. These results clearly clarified the effect of esculetin in inhibiting platelet activity and thrombus formation in humans.

Anti-aggregation Effect of Artemether Through Regulation of PI3K/Akt and MAPK in U46619-induced Platelets (U46619-유도의 혈소판에서 PI3K/Akt 및 MAPK 조절을 통한 Artemether의 응집억제효과)

  • Park, Chang-Eun;Lee, Dong-Ha
    • Korean Journal of Pharmacognosy
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    • v.53 no.2
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    • pp.64-69
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    • 2022
  • When blood vessels are damaged, a rapid hemostatic response should occur in order to lower blood loss and keep normal circulation, and platelet activation and aggregation are essential. Nevertheless, abnormal or excessive platelet aggregation can be a reason of cardiovascular diseases including thrombosis, atherosclerosis, and stroke. Therefore, the screening for a substance which can regulate platelet activation and suppress aggregation reaction is very important for treatment and prevention of cardiovascular diseases. Artemether is a methyl ether derivative of artemisinin, which is isolated from the antimalarial plant Artemisia annua, but research on platelet aggregation or its mechanisms is still insufficient. This study identified the effects of artemether on U46619-induced human platelet aggregation and their granule secretion (ATP and serotonin release). In addition, the effects of artemether on the phosphorylation of PI3K/Akt or MAPK, which are related to signal transduction in platelet aggregation, were studied. As the results, artemether significantly lowered PI3K/Akt and MAPK phosphorylation, which inhibited platelet aggregation through granule secretion (ATP and serotonin release) dose-dependently. Therefore, we suggest that artemether is an antiplatelet substance that regulates PI3K/Akt and MAPK pathway and is of value as a therapeutic and preventive agent for platelet-derived cardiovascular diseases.

Over-the-counter drug records and management (일반의약품 기록 및 관리)

  • Gang, Yoo-ha;Kim, Ji-Yun;Yun, A-eun;Song, Tae-Yeong;Choi, Young
    • Proceedings of the Korean Society of Computer Information Conference
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    • 2021.07a
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    • pp.347-349
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    • 2021
  • 전문의약품은 의약품안전사용서비스(DUR)를 이용하여 병원에서 처방받은 약에서 부작용이 나타났을 때 기록하고 다음에 약을 처방받을 때 부작용이 나타난 약과 비슷한 계열의 약은 처방받지 않는다. 하지만 일반의약품은 약 구매 기록조차 남지 않아 어떤 약을 언제 처방받았는지 모르고 부작용을 관리할 수 없어 불편함을 겪는다. 이 연구를 통해 제안하는 어플은 처방내역과 복약관리, 약 추천, 약국 찾기로 구성된다. 일반의약품을 처방받은 날짜와 시간, 증상, 효과, 부작용에 대하여 기록하며, 기록을 분석하여 증상에 대한 약을 추천함으로써 치료 효과를 높일 수 있다. 환자가 스스로 투약에 관심을 가지고 기록을 관리함으로써 환자가 주체가 되어 질병을 개선할 수 있다.

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Lung Adenocarcinoma Mutation Hotspot in Koreans: Oncogenic Mutation Potential of the TP53 P72R Single Nucleotide Polymorphism (한국인의 폐선암 돌연변이 핫스팟: TP53 P72R Single Nucleotide Polymorphism의 발암성 돌연변이 가능성)

  • Jae Ha BAEK;Kyu Bong CHO
    • Korean Journal of Clinical Laboratory Science
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    • v.55 no.2
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    • pp.93-104
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    • 2023
  • This study aimed to identify new markers that cause lung adenocarcinoma by analyzing mutation hotspots for the top five genes with high mutation frequency in lung adenocarcinoma in Koreans by next generation sequencing (NGS) analysis. The association between TP53 mutation types and patterns with smoking, a major cause of lung cancer, was examined. The clinicopathological characteristics of lung adenocarcinoma patients with TP53 P72R SNPs were analyzed. In Korean lung adenocarcinoma cases, regardless of the smoking status, the TP53 P72R SNP was the most frequently occurring mutational hotspot, in which the nucleotide base was transversed from C to G, and the amino acid was substituted from proline to arginine at codon 72 of TP53. An analysis of the clinicopathological characteristics of lung adenocarcinoma cases with TP53 P72R SNP revealed no significant correlation with the patient's age, gender, smoking status, and tumor differentiation, but a significant correlation with low stage (P-value =0.026). This study confirmed an increase in TP53 rather than EGFR, which was reported as the most frequent mutations in lung adenocarcinoma in Koreans through NGS. Among them, TP53 P72R SNP is the most frequent regardless of smoking status.

MNNG-Regulated Differentially Expressed Genes that Contribute to Cancer Development in Stomach Cells (MNNG 처리에 의해 조절되는 암발생 유발 유전자의 조사)

  • Kim, Tae-Jin;Kim, Myeong-Kwan;Jung, Dongju
    • Korean Journal of Clinical Laboratory Science
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    • v.53 no.4
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    • pp.353-362
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    • 2021
  • Cancer is a global health problem. There are diverse types of cancers, but there are several common pathways which lead to the development of cancer. Changes in gene expression might be the most common similarity found in almost all cancers. An understanding of the underlying changes in gene expression during cancer progression could lay a valuable foundation for the development of cancer therapeutics and even cancer vaccines. In this study, a well-known carcinogen, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), was employed to induce changes in gene expression in normal stomach cells. MNNG is known to cause cancer by inducing damage to DNA in MNNG-treated mammalian cells and animals fed with this carcinogen. An analysis was performed by comparing the differentially expressed genes (DEGs) caused by MNNG treatment with DEGs in stomach cancer cell lines. To this end, methods of analysis for functional categorization and protein-protein interaction networks, such as gene ontology (GO), the database for annotation, visualization, and integrated discovery (DAVID), Kyoto encyclopedia of genes and genomics (KEGG) and search tool for the retrieval of interacting genes/proteins (STRING), were used. As a result of these analyses, MNNG-regulated specific genes and interaction networks of their protein products that contributed to stomach cancer were identified.

Development of TaqMan Quantitative PCR Assays for Duplex Detection of Dirofilaria immitis COI and Dog GAPDH from Infected Dog Blood (심장사상충에 감염된 개 혈액에서 Dirofilaria immitis의 COI와 개의 GAPDH를 이중 검출하기 위한 정량적 TaqMan PCR 분석법의 개발)

  • Oh, In Young;Kim, Kyung Tae;Gwon, Sun-Yeong;Sung, Ho Joong
    • Korean Journal of Clinical Laboratory Science
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    • v.51 no.1
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    • pp.64-70
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    • 2019
  • Dirofilaria immitis (D. immitis) is a filarial nematode that causes cardiopulmonary dirofilariasis in dogs. In the late stages of infection, infected dogs show one or more symptoms and advanced heart disorder with perivascular inflammation. To detect D. immitis specifically and efficiently in the early stages of infection, a duplex TaqMan qPCR assay was developed based on previous studies using primers and probes specialized to detect D. immitis cytochrome c oxidase subunit I (COI) and dog glyceraldehyde-3-phosphate dehydrogenase (GAPDH). As positive controls, plasmid DNAs were constructed from D. immitis COI or dog GAPDH and a TA-cloning vector. Simplex and duplex TaqMan qPCR assays were performed using the specific primers, probes, and genomic or plasmid DNA. The duplex reaction developed could detect D. immitis COI and dog GAPDH in the same sample simultaneously after optimization of the primer concentrations. The limit of detection was 25 copies for the simplex and duplex assays, and both showed good linearity, high sensitivity, and excellent PCR efficiency. The duplex assays for pathogen detection reduce the costs, labor, and time compared to simplex reactions. Therefore, the duplex TaqMan qPCR assay developed herein will allow efficient D. immitis detection and quantification from a large number of samples simultaneously.

Genetic Polymorphisms of SLC8A1 Are Associated with Hypertension and Left Ventricular Hypertrophy in the Korean Population (한국인에서 SLC8A1의 유전적 다형성과 고혈압 및 좌심실 비대와 연관 연구)

  • Park, Hye-Jeong;Kim, Sung-Soo;Jin, Hyun-Seok
    • Korean Journal of Clinical Laboratory Science
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    • v.51 no.3
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    • pp.286-293
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    • 2019
  • Hypertension (HTN) is one of the major chronic diseases, and HTN is defined as being in a state of continuous high blood pressure. Left ventricular hypertrophy (LVH) is a condition in which the mass of the left ventricle has increased, and HTN is a leading cause of LVH. HTN and LVH are known to be caused by the interaction of environmental factors and genetic factors. It has been reported that the polymorphisms of SLC8A1, among the genetic factors that affect high blood pressure, are related to salt sensitivity hypertension. In this study, the genetic polymorphisms of SLC8A1 were chosen based on the Korean Genome and Epidemiology data. Logistic regression analysis was then performed for HTN and LVH. Linear regression analysis was also performed for systolic blood pressure (SBP) and diastolic blood pressure (DBP). As a result, 5 SNPs showed statistically significant associations (P<0.05) with HTN, and 10 SNPs showed statistically significant associations with LVH. rs1002671 and rs9789739 showed significant correlation at the same time with HTN and LVH. These results suggest that the polymorphisms of the SLC8A1 gene are linked to the development of HTN and LVH in Koreans. We expect these results to help us understand the pathogenic mechanisms for HTN and LVH.