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- 저자 : ( Jaeku Kang (검색결과 18 건)
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Kang Jaeku,Choi Seung Yong,Oh Sejong,조경진 대한의학레이저학회 2023 MEDICAL LASERS Vol.12 No.4
Background: To assess an improved machine learning model for calculation of intraocular lens (IOL) power during cataract surgery.Methods: We reviewed 346 medical records of cataract surgery patients from the Dankook University Hospital and developed a machine regression model to calculate IOL power. Well-known machine learning algorithms such as random forest, gradient boosting machine, support vector machine (SVM), and eXtreme Gradient Boosting were tested to develop the best prediction model. The model accuracy was judged by comparing the difference between the predicted refractory powers and the actual postoperative refractory ones based on ±0.25, ±0.5, ±0.75, and ±1 D. The prediction error was also evaluated by statistical measures. The proposed model was compared with existing formulas, such as SRK/T, Barrett Universal II, Hill-RBF, and Kane.Results: The proposed SVM model produced an accuracy of 43.3%, 77.2%, 87.0%, and 95.4% for refraction powers based on ±0.25, ±0.5, ±0.75, and ±1 D, respectively. In contrast, the Barrett Universal II formula produced an accuracy of 34.3%, 60.8%, 83.2%, and 93.0% for refraction powers.Conclusion: The proposed machine learning prediction model showed better performance than the current formulas. This improved machine learning model using machine learning calculations could thus be used in IOL power calculations.
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Jaeku Kang,Yu Kyung Ko,Hye Kyung Lee,Kyung Hee Kang,Year Hur,Keum Ho Lee 한국간호과학회 정신간호학회 2013 정신간호학회지 Vol.22 No.1
Purpose: The purposes of this study were to identify factors affecting depression in college students and the corre-lation of depression with self-esteem and academic stress, and to identify differences among student self-esteem, academic stress, and general characteristics and the relation ship of these variables to depression. Methods: The study was done in April 2011 with 852 students in health-related majors (medicine, nursing science, and dental hygiene) of a medical college in Korea. A self-rating survey containing 10 items from the Rosenberg Self-esteem Scale, 20 items from the Self-rating Depression Scale, and 22 items on academic stress was used. Data were analyzed using descriptive statistics, t-tests, one0way ANOVA, and logistic regression. Results: Medical students‘ scores for self-esteem were significantly higher than dental hygiene students, but for academic stress scores, the result was the opposite. Logistic regression showed that self-esteem, academic stress, academic major and satisfaction with it (positive affect), and home income level (negative affect) significantly affected the level of depression. Conclusion: Designing and implementing realistic programs tailored to students‘ academic majors to enhance their self-esteem and implementing realistic programs tailored to students‘ academic majors to enhance their self-esteem and provide practical knowledge in dealing with academic stress will help these stu-dents obtain a healthier school life emotionally as well as academically.
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Kang, Jaeku,Lee, Soo Young,Lee, Sun Young,Kim, Young Jin,Park, Jae Yong,Kwon, Sun Jung,Na, Moon Jun,Lee, Eun Jin,Jeon, Hyo Sung,Son, Ji Woong Spandidos Pub.] 2012 Experimental and therapeutic medicine Vol.3 No.1
<P>microRNAs (miRNAs) play a significant role in cancer development and progression by regulating the expression of proto-oncogenes or tumor suppressor genes. Our previous study using microarrays demonstrated that miR-99b was downregulated in patients with lung cancer. To assess whether or not miR-99b has a functional role in lung cancer, we determined the expression of miR-99b and fibroblast growth factor receptor 3 (FGFR3), which is a predicted target of miR-99b in public algorithms in human lung cancer tissues. miR-99b was downregulated and FGFR3 was upregulated in lung cancer patients. We demonstrated that the overexpression of miR-99b induced a reduction in FGFR3 expression and confirmed the target specificity between miR-99b and the FGFR3 3'-untranslated region by luciferase reporter assay. In addition, the growth rate in miR-99b precursor-treated cells was lower compared to the negative controls. Taken together, these results suggest that miR-99b may be a tumor suppressor through the downregulation of FGFR3. miR-99b may be a potent tumor suppressor and may be a potential therapeutic tool for patients with lung cancer.</P>
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Park, Soon Young,Kang, Joo Hee,Jeong, Kang Jin,Lee, Jangsoon,Han, Jeong Whan,Choi, Wahn Soo,Kim, Yong Kee,Kang, Jaeku,Park, Chang Gyo,Lee, Hoi Young Wiley Subscription Services, Inc., A Wiley Company 2011 International journal of cancer: Journal internati Vol.128 No.10
<P><B>Abstract</B></P><P>A growing number of studies have demonstrated that physiological factors can influence the progression of several cancers <I>via</I> cellular immune function, angiogenesis and metastasis. Recently, stress‐induced catecholamines have been shown to increase the expression of various cancer progressive factors, including vascular endothelial growth factor (VEGF), matrix metalloproteinases and interleukins. However, a detailed mechanism remains to be identified. In this study, we investigated the role of adrenergic receptors and hypoxia‐inducible factor (HIF)‐1α protein in catecholamine‐induced VEGF expression and angiogenesis. Treatment of the cells with norepinephrine (NE) or isoproterenol induced VEGF expression and HIF‐1α protein amount in a dose‐dependent manner. Induction of VEGF expression by NE was abrogated when the cells were transfected with HIF‐1α–specific siRNA. Similarly, adenylate cyclase activator forskolin and cyclic AMP‐dependent protein kinase A inhibitor H‐89 enhanced and decreased HIF‐1α protein amount, respectively. More importantly, conditioned medium of NE‐stimulated cancer cells induced angiogenesis in a HIF‐1α protein–dependent manner. In addition, pretreatment of cells with propranolol, a β‐adrenergic receptor (AR) blocker, completely abolished induction of VEGF expression and HIF‐1α protein amount by NE in all of the tested cancer cells. However, treatment with the α1‐AR blocker prazosin inhibited NE‐induced HIF‐1α protein amount and angiogenesis in SK‐Hep1 and PC‐3 but not MDA‐MB‐231 cells. Collectively, our results suggest that ARs and HIF‐1α protein have critical roles in NE‐induced VEGF expression in cancer cells, leading to stimulation of angiogenesis. These findings will help to understand the mechanism of cancer progression by stress‐induced catecholamines and design therapeutic strategies for cancer angiogenesis.</P>
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( Minhyeok Lee ),( Ji Woong Son ),( Chang Ryul Park ),( Daeun Kang ),( Su Yel Lee ),( Se Jin Park ),( Wan Jin Hwang ),( Gwan Woo Ku ),( Seong Lan Yu ),( In Beom Jeong ),( Sun Jung Kwon ),( Jaeku Kang 대한결핵 및 호흡기학회 2021 대한결핵 및 호흡기학회 추계학술대회 초록집 Vol.129 No.-
Purpose Cancer stem cells (CSCs) identified in lung cancer exhibit resistance to chemotherapy, radiotherapy, and targeted therapy. Therefore, a technology to control of CSCs is needed to overcome such resistance to cancer therapy. Various evidences about the association between epithelial-mesenchymal transition related transcriptomic alteration and acquisition of CSC phenotype have been proposed recently. In our previous research, down-regulated miR-26a-5p is closely related to mesenchymal-like lung cancer cell lines. These findings suggest that miR-26a-5p might be involved in lung cancer stemness. Methods RNA polymerase III subunit G (POLR3G) was selected as a candidate target of miR-26a-5p related to cancer stemness. its quantitative relationship was investigated by polymerase chain reaction, western blot after transfection of miR-26a-5p. luciferase assay were done for investigating the direct regulation of miR-26a-5p on POLR3G expression. After transfection of miR-26a-5p, colony formation assay and sphere formation assay were performed to evaluate the effect on cancer stemness. By treating cancer cell by miR-26a-5p and paclitaxel, cell viability was checked by 3-(4,5-dimethylthiazol-2-yl)-5-(3- carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay and Muse cell analyzer. Expression level of each gene and its impact on survival were revealed by the cancer genome atlas pancancer database. Results miR-26a-5p regulated the expression of POLR3G directly. Overexpression of miR-26a-5p induced down regulation of POLR3G and a marked reduction of colony formation and sphere formation. Co-treatment of miR-26a-5p with paclitaxel decreased cell growth, suggesting that miR-26a-5p might play a role as a chemotherapy sensitizer. In the cancer genome atlas data, downregulated miR-26a-5p and up-regulated POLR3G were shown compared to adjacent normal tissue. High miR-26a-5p and low POLR3G expression were also related to higher survival rate of patients with lung adenocarcinoma. Conclusions Overexpression of miR-26a-5p can suppress lung cancer stemness and make cancer cell become sensitive to chemotherapy. This finding provides a novel insight into a potential lung cancer treatment by regulating stemness.
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Kim, Jong-Yeup,Cha, Min-Ji,Park, Young-Seon,Kang, Jaeku,Choi, Jong-Joong,In, Seung Min,Kim, Dong-Kyu Korean Society for Molecular and Cellular Biology 2019 Molecules and cells Vol.42 No.4
Eosinophilic chronic rhinosinusitis with nasal polyps (CRSwNP) is one of the most challenging problems in clinical rhinology. FZD5 is a receptor for Wnt5A, and its complex with Wnt5A contributes to activating inflammation and tissue modification. Nasal polyps and eosinophil/non-eosinophil counts are reported to be directly correlated. This study investigated the expression and distribution of FZD5, and the role of eosinophil infiltration and FZD5 in eosinophilic CRSwNP pathogenesis. The prognostic role of eosinophil levels was evaluated in seven patients with CRSwNP. Fifteen patients with CRS were classified based on the percentage of eosinophils in nasal polyp tissue. Methylated genes were detected using methylCpG-binding domain sequencing, and qRT-PCR and immunohistochemistry were used to detect FZD5 expression in nasal polyp tissue samples. The results showed that mRNA expression of FZD5 was upregulated in nasal polyps. FZD5 expression was significantly higher in nasal polyp samples from patients with eosinophilic CRSwNP than in those from patients with non-eosinophilic CRSwNP, as indicated by immunohistochemistry. Furthermore, inflammatory cytokine levels were higher in eosinophilic CRSwNP-derived epithelial cells than in normal tissues. In conclusion, FZD5 expression in nasal mucosal epithelial cells is correlated with inflammatory cells and might play a role in the pathogenesis of eosinophilic CRSwNP.
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Identification of mTOR inhibitor-resistant genes in cutaneous squamous cell carcinoma
Yu, Seong-Lan,Lee, Dong Chul,Baek, Seung Woo,Cho, Do Yeun,Choi, Jong Gwon,Kang, JaeKu Dove Medical Press 2018 Cancer management and research Vol.10 No.-
<P><B>Purpose</B></P><P>The PI3K/AKT/mTOR pathway is frequently activated in various squamous cell carcinomas (SCCs). Although mTOR inhibitors are suggested as effective treatments in immunosuppressed patients with metastatic SCC, they are still not proven to be favorable in treating skin SCC patients not undergoing immunosuppressive therapy. Moreover, the exact mechanism of the mTOR signaling pathway in SCC has not yet been identified. In this study, we aimed to determine the genes associated with mTOR inhibitors in skin SCC.</P><P><B>Materials and methods</B></P><P>The identification of cell viability according to concentration of everolimus and Western blot was done. To analyze the global gene expression profiles, A431 and HSC-1 cells were treated with dimethyl sulfoxide (DMSO) or 100 nM of everolimus for 72 hours. Furthermore, differentially expressed genes (DEGs) were identified using Affymetrix analysis. To identify the gene network associated with everolimus resistance in SCC cells, pathway analysis was performed using the Ingenuity Pathway Analysis (IPA) tool.</P><P><B>Results</B></P><P>The effects of cell death with respect to the mTOR inhibitor concentration were observed in the HSC-1 cell line; however, the mTOR inhibitor did not show effective cytotoxic activity in the A431 cell line. p-mTOR concentration also diminished with respect to everolimus concentrations in the HSC-1 cell line. Moreover, the microarray results showed that the <I>MYC/CCND1/TP73/NUPR1/SBD/ERBB2/CDKN2B</I> genes were related to mTOR inhibitor resistance. However, CCND1 gene overexpression was most closely related to mTOR inhibitor resistance.</P><P><B>Conclusion</B></P><P>We identified mTOR inhibitor resistance genes, and our findings may help select therapeutic targets in skin SCC.</P>
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YU, SEONG-LAN,LEE, DONG CHUL,SON, JI WOONG,PARK, CHANG GYO,LEE, HOI YOUNG,KANG, JAEKU Spandidos Publications 2013 Oncology reports Vol.30 No.3
<P>Histone deacetylases (HDACs) have been shown to play important roles in the regulation of chromatin remodeling by histone deacetylation, and their expression is induced in several types of cancer. In addition, they are known to be associated with resistance to anticancer drugs. However, the relevance of HDAC4 in chemoresistance remains unclear. Therefore, we investigated the interaction between HDAC4 expression and chemoresistance in breast cancer cells. We found that increased HDAC4 expression in MDA-MB-231 cells was associated with resistance to the anticancer drug 5-fluorouracil (5-FU). To verify these results, a cell line stably overexpressing HDAC4 was generated using MCF-7 cells (HDAC4OE). This cell line displayed increased 5-FU resistance, and HDAC4 knockdown in HDAC4OE cells restored 5-FU sensitivity. Consequently, we concluded that HDAC4 is a critical gene associated with 5?FU chemoresistance. Further investigation using a microarray approach revealed that 355 genes were differentially expressed following HDAC4 overexpression. Based on functional annotation of the array results, HDAC4 overexpression was found to downregulate genes related to the transforming growth factor (TGF) β signaling pathway, including SMAD4, SMAD6, bone morphogenetic protein 6, inhibitor of DNA binding 1 and TGFβ2. We also found that HDAC4 expression regulates SMAD4 expression by inducing deacetylation of histone H3 in the SMAD4 promoter region. In addition, SMAD4 knockdown in MCF?7 cells increased 5-FU resistance. In summary, our data suggest that HDAC4?mediated deacetylation of the SMAD4 promoter may lead to 5-FU resistance in breast cancer cells.</P>
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