• Genomics & Informatics
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• v.16 no.4
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• pp.25.1-25.5
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• 2018

Coronary artery disease (CAD) is one of the leading causes of death and disability all around the world. Recent studies have revealed that aberrantly regulated long non-coding RNA (lncRNA) as one of the main classes of cellular transcript plays a key regulatory role in transcriptional and epigenetic pathways. Recent reports have demonstrated that circulating lncRNAs in the blood can be potential biomarkers for CAD. HOTAIR is one of the most cited lncRNAs with a critical role in the initiation and progression of the gene expression regulation. Recent research on the role of the HOTAIR in cardiovascular disease lays the basis for the development of new studies considering this lncRNA as a potential biomarker and therapeutic target in CAD. In this study, we aimed to compare the expression of HOTAIR lncRNA in the blood samples of patients with CAD and control samples. The expression level was examined by semi-quantitative reverse transcriptase polymerase chain reaction technique. Our data shows that expression of HOTAIR is up-regulated in blood samples of patients with CAD.

• Molecules and Cells
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• v.42 no.1
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• pp.1-7
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• 2019

Macrophage is an important innate immune cell that not only initiates inflammatory responses, but also functions in tissue repair and anti-inflammatory responses. Regulating macrophage activity is thus critical to maintain immune homeostasis. Tyro3, Axl, and Mer are integral membrane proteins that constitute TAM family of receptor tyrosine kinases (RTKs). Growing evidence indicates that TAM family receptors play an important role in anti-inflammatory responses through modulating the function of macrophages. First, macrophages can recognize apoptotic bodies through interaction between TAM family receptors expressed on macrophages and their ligands attached to apoptotic bodies. Without TAM signaling, macrophages cannot clear up apoptotic cells, leading to broad inflammation due to over-activation of immune cells. Second, TAM signaling can prevent chronic activation of macrophages by attenuating inflammatory pathways through particular pattern recognition receptors and cytokine receptors. Third, TAM signaling can induce autophagy which is an important mechanism to inhibit NLRP3 inflammasome activation in macrophages. Fourth, TAM signaling can inhibit polarization of M1 macrophages. In this review, we will focus on mechanisms involved in how TAM family of RTKs can modulate function of macrophage associated with anti-inflammatory responses described above. We will also discuss several human diseases related to TAM signaling and potential therapeutic strategies of targeting TAM signaling.

• Journal of Urban Science
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• v.9 no.2
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• pp.45-50
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• 2020

The formation characteristics of calcium carbonates are closely related to the durability and mechanical properties of cement-based materials. In this regard, a deep understanding of the reaction pathway of calcium carbonates is critical. Recently, non-classical nucleation theory was summarized and it was presumed that prenucleation clusters are present. The formation of the prenucleation cluster at undersaturated condition (≈ 0.1 ml) in the present study was investigated via electrical characteristics of an electrolytic solution. Calcium chloride dihydrate (CaCl2·2H2O) and sodium carbonate (Na2CO3) were used as starting materials to supply calcium and carbonate sources, respectively. Furthermore, the reaction pathway of calcium carbonates was investigated by time-resolved polarization and depolarization characteristics of the electrolytic solution. The time-resolved polarization and depolarization tests were conducted by switching polarity with an interval of 20 seconds for 1 hr and by measuring the variation of electrical resistance. It can be inferred from the results obtained in the present study that the reactive constituent for the formation of calcium carbonates was mostly consumed in the period possibly associated with the prenucleation and the reaction pathways may be governed by the monomer-addition mechanism.

• BMB Reports
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• v.54 no.3
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• pp.157-163
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• 2021

The transient interactions between cellular components, particularly on membrane surfaces, are critical in the proper function of many biochemical reactions. For example, many signaling pathways involve dimerization, oligomerization, or other types of clustering of signaling proteins as a key step in the signaling cascade. However, it is often experimentally challenging to directly observe and characterize the molecular mechanisms such interactions-the greatest difficulty lies in the fact that living cells have an unknown number of background processes that may or may not participate in the molecular process of interest, and as a consequence, it is usually impossible to definitively correlate an observation to a well-defined cellular mechanism. One of the experimental methods that can quantitatively capture these interactions is through membrane reconstitution, whereby a lipid bilayer is fabricated to mimic the membrane environment, and the biological components of interest are systematically introduced, without unknown background processes. This configuration allows the extensive use of fluorescence techniques, particularly fluorescence fluctuation spectroscopy and single-molecule fluorescence microscopy. In this review, we describe how the equilibrium diffusion of two proteins, K-Ras4B and the PH domain of Bruton's tyrosine kinase (Btk), on fluid lipid membranes can be used to determine the kinetics of homodimerization reactions.

• Journal of Korean Public Health Nursing
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• v.36 no.1
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• pp.47-58
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• 2022

Purpose: This study was undertaken to present an effective plan for the development of an educational program and a strategy to promote patient safety management activities for nursing students by identifying factors that affect these activities based on the theory of planned behavior. Methods: A self-report questionnaire was distributed to 300 nursing students who had clinical practice experience at three nursing colleges in Daejeon, Gyeongbuk, and Jeonbuk. The significance of the model fit, and the path effect was confirmed by confirmatory factor analysis. Results: The hypothetical model for patient safety management activities was appropriate. Among the 5 pathways, 4 were significant. It was found that behavioral intention had a direct influence on patient safety management activities, and perceived behavioral control and attitude had an influence on behavioral intention. Conclusion: To strengthen the perceived behavioral control of nursing students' patient safety management activities, it is necessary to analyze and remove obstacles and provide education that reflects the characteristics of the subject's health problems. In addition, through self-directed learning involving simulation practice, nursing students should be exposed to patient safety accidents, so that they can recognize the risks early and solve problems through critical thinking while bringing about the necessary changes in their attitude.

• BMB Reports
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• v.54 no.12
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• pp.626-631
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• 2021

Janus kinase 2 (JAK2), a non-receptor tyrosine kinase, is a critical component of cytokine and growth factor signaling pathways regulating hematopoietic cell proliferation. JAK2 mutations are associated with multiple myeloproliferative neoplasms. Although physiological and pathological functions of JAK2 in hematopoietic tissues are well-known, such functions of JAK2 in the nervous system are not well studied yet. The present study demonstrated that JAK2 could negatively regulate neuronal differentiation of mouse embryonic stem cells (ESCs). Depletion of JAK2 stimulated neuronal differentiation of mouse ESCs and activated glycogen synthase kinase 3β, Fyn, and cyclin-dependent kinase 5. Knockdown of JAK2 resulted in accumulation of GTP-bound Rac1, a Rho GTPase implicated in the regulation of cytoskeletal dynamics. These findings suggest that JAK2 might negatively regulate neuronal differentiation by suppressing the GSK-3β/Fyn/CDK5 signaling pathway responsible for morphological maturation.

• Parasites, Hosts and Diseases
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• v.60 no.3
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• pp.155-161
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• 2022

All living organisms are destined to die. Cells, the core of those living creatures, move toward the irresistible direction of death. The question of how to die is critical and is very interesting. There are various types of death in life, including natural death, accidental death, questionable death, suicide, and homicide. The mechanisms and molecules involved in cell death also differ depending on the type of death. The dysenteric amoeba, E. histolytica, designated by the German zoologist Fritz Schaudinn in 1903, has the meaning of tissue lysis; i.e., tissue destroying, in its name. It was initially thought that the amoebae lyse tissue very quickly leading to cell death called necrosis. However, advances in measuring cell death have allowed us to more clearly investigate the various forms of cell death induced by amoeba. Increasing evidence has shown that E. histolytica can cause host cell death through induction of various intracellular signaling pathways. Understanding of the mechanisms and signaling molecules involved in host cell death induced by amoeba can provide new insights on the tissue pathology and parasitism in human amoebiasis. In this review, we emphasized on the signaling role of NADPH oxidases in reactive oxygen species (ROS)-dependent cell death by pathogenic E. histolytica.

• Journal of The Korean Society of Inherited Metabolic disease
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• v.22 no.2
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• pp.53-57
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• 2022

Congenital metabolic disorders are rare inherited disorders resulting from a defect in biochemical and metabolic pathways affecting proteins, fats, carbohydrates metabolism or impaired organelle function. Depending on the abnormality of biochemical metabolism, various precursors and their abnormal metabolites can accumulate in the body and the final products which are critical in normal physiology can be deficient, resulting in disease. Congenital metabolic disorders present complicated medical conditions involving several human organ systems, including nervous system, eyes, liver, and kidneys. Various proteins and lipids are involved in the development and homeostasis of the skin, so many congenital metabolic disorders present abnormal changes in skin and hair. In this review, congenital metabolic diseases related to amino acid and lipid metabolism accompanying skin abnormalities will be discussed.

• Molecules and Cells
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• v.46 no.3
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• pp.165-175
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• 2023

The transcription factor Nrf2 was originally identified as a master regulator of redox homeostasis, as it governs the expression of a battery of genes involved in mitigating oxidative and electrophilic stress. However, the central role of Nrf2 in dictating multiple facets of the cellular stress response has defined the Nrf2 pathway as a general mediator of cell survival. Recent studies have indicated that Nrf2 regulates the expression of genes controlling ferroptosis, an iron-and lipid peroxidation-dependent form of cell death. While Nrf2 was initially thought to have anti-ferroptotic function primarily through regulation of the antioxidant response, accumulating evidence has indicated that Nrf2 also exerts anti-ferroptotic effects via regulation of key aspects of iron and lipid metabolism. In this review, we will explore the emerging role of Nrf2 in mediating iron homeostasis and lipid peroxidation, where several Nrf2 target genes have been identified that encode critical proteins involved in these pathways. A better understanding of the mechanistic relationship between Nrf2 and ferroptosis, including how genetic and/or pharmacological manipulation of Nrf2 affect the ferroptotic response, should facilitate the development of new therapies that can be used to treat ferroptosis-associated diseases.

• Clinical Endoscopy
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• v.56 no.3
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• pp.263-267
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• 2023

Climate change is a global emergency. Consequently, current global targets to combat the climate crisis include reaching net-zero carbon emissions by 2050 and keeping global temperature increases below 1.5 ℃. In 2014, the healthcare carbon footprint was 5.5% of the total national footprint. Gastrointestinal endoscopy (GIE) has a large carbon footprint compared to other procedures performed in healthcare facilities. GIE was identified as the third largest generator of medical waste in healthcare facilities for the following reasons: (1) GIE is associated with high case volumes, (2) GIE patients and relatives travel frequently, (3) GIE involves the use of many nonrenewable wastes, (4) single-use devices are used during GIE, and (5) GIE is frequently reprocessed. Immediate actions to reduce the environmental impact of GIE include: (1) adhering to guidelines, (2) implementing audit strategies to determine the appropriateness of GIE, (3) avoiding unnecessary procedures, (4) using medication rationally, (4) digitalization, (5) telemedicine, (6) critical pathways, (7) outpatient procedures, (8) adequate waste management, and (9) minimizing single-use devices. In addition, sustainable infrastructure for endoscopy units, using renewable energy, and 3R (reduce, reuse, and recycle) programs are necessary to reduce the impact of GIE on the climate crisis. Consequently, healthcare providers need to work together to achieve a more sustainable future. Therefore, strategies must be implemented to achieve net-zero carbon emissions in the healthcare field, especially from GIE, by 2050.