• Journal of Korean Clinical Nursing Research
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• v.26 no.2
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• pp.198-206
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• 2020

Purpose: The rapid response team is a patient safety system that detects symptoms and signs of deteriorating inpatients and provides intervention and treatment. This study analyzed the factors influencing the activation time of the team. Methods: This is a descriptive correlation study that analyzed the electronic medical records of patients activated by the rapid response team. The collection period was from January 2014 to December 2017. We analyzed 278 pieces of data activated by the rapid response team for patients aged 16 years or older at C University S Hospital in Seoul. We employed the SPSS 23.0 program for data analysis. Results: The reasons for activation of the rapid response team were oxygen saturation of less than 90.0%, other causes, and change in consciousness. The most common diagnosis of activated patients was respiratory failure (32.4%). The average activation time was 153.43±286.05 min. The activation time was shortest during convulsions (13.29±7.32 min). For patients with a history of kidney disease (B=0.58, p=.008), in case of surgery (B=0.55, p<.001), if the first symptom is mediated by the physician (B=0.53, p=.007) the active time is often extended. On the other hand, activation time is reduced when consciousness changes (B=-0.51, p=.002), especially when oxygen saturation is below 90.0% (B=-0.64, p<.001). Conclusion: Based on the results of the study, it is expected that patients deteriorating in the general ward would be recognized early, which will help in the effective activation of the rapid response team.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.14
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• pp.5883-5887
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• 2015

Despite recent advances in therapeutic strategies for lung cancer, mortality still is increasing. In the present study, we investigated the anti-cancer effects of KMU-193, 2-(4-Ethoxy-phenyl)-N-{5-[2-fluoro-4-(4-methylpiperazine-1-carbonyl)-phenylamino]-1H-indazol-3-yl}-acetamide in a human non-small cell lung cancer cell line A549. KMU-193 strongly inhibited the proliferation of A549 cells, but it did not have anti-proliferative effect in other types of cancer cell lines. KMU-193 further induced apoptosis in association with activation of caspase-3 and cleavage of PLC-${\gamma}1$. However, KMU-193 had no apoptotic effect in untransformed cells such as TMCK-1 and BEAS-2B. Interestingly, pretreatment with z-VAD-fmk, a pan-caspase inhibitor, strongly abrogated KMU-193-induced apoptosis. KMU-193 treatment enhanced the expression levels of p53 and PUMA. Importantly, p53 siRNA transfection attenuated KMU-193-induced apoptosis. Collectively, these results for the first time demonstrate that KMU-193 has strong apoptotic effects on A549 cells and these are largely mediated through caspase-3- and p53-dependent pathways.

• Toxicological Research
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• v.23 no.3
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• pp.231-238
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• 2007

Evaluation of potentials of chemicals to alter expression of genes that are involved in carcinogenesis may serve useful tools in toxicological research. In this investigation, we developed reporter cell lines that expressed luciferase in response to transactivation of hypoxia inducible factor-1, P53 tumor suppressor and Nur77 of which roles have been well established in cancer development and progression. Whereas these reporter cell lines displayed low constitutive backgrounds, the reporter activities were significantly enhanced in response to $desferriosamine/CoCl_2$, adriamycin or 6-mercaptopurine, which are hypoxia mimicking chemicals, P53 activator or Nur77 inducer, respectively. The activation of the reporter was time- and dose-dependent. Known tumor initiators and promoters, such as phorbol 12-myristate 13-acetate and phorbol 12, 13-dicaprinate induced the reporter activity at as low as 10nM in these stable cell lines. Further, known anti-tumor promoters, such as ascorbic acid and ${\beta}-carotene$ repressed the reporter activities. These results indicate that our stable reporter cell lines could serve as a useful system for rapid assessment of carcinogenicity of toxic chemicals.

• BMB Reports
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• v.53 no.8
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• pp.425-430
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• 2020

Tumor necrosis factor-inducible gene 6 protein (TSG-6) is a cytokine secreted by mesenchymal stem cells (MSCs) and regulates MSC stemness. We previously reported that TSG-6 changes primary human hepatic stellate cells (pHSCs) into stem-like cells by activating yes-associated protein-1 (YAP-1). However, the molecular mechanism behind the reprogramming action of TSG-6 in pHSCs remains unknown. Cluster of differentiation 44 (CD44) is a transmembrane protein that has multiple functions depending on the ligand it is binding, and it is involved in various signaling pathways, including the Wnt/β-catenin pathway. Given that β-catenin influences stemness and acts downstream of CD44, we hypothesized that TSG-6 interacts with the CD44 receptor and stimulates β-catenin to activate YAP-1 during TSG-6-mediated transdifferentiation of HSCs. Immunoprecipitation assays showed the interaction of TSG-6 with CD44, and immunofluorescence staining analyses revealed the colocalization of TSG-6 and CD44 at the plasma membrane of TSG-6-treated pHSCs. In addition, TSG-6 treatment upregulated the inactive form of phosphorylated glycogen synthase kinase (GSK)-3β, which is a negative regulator of β-catenin, and promoted nuclear accumulation of active/nonphosphorylated β-catenin, eventually leading to the activation of YAP-1. However, CD44 suppression in pHSCs following CD44 siRNA treatment blocked the activation of β-catenin and YAP-1, which inhibited the transition of TSG-6-treated HSCs into stem-like cells. Therefore, these findings demonstrate that TSG-6 interacts with CD44 and activates β-catenin and YAP-1 during the conversion of TSG-6-treated pHSCs into stem-like cells, suggesting that this novel pathway is an effective therapeutic target for controlling liver disease.

• Tuberculosis and Respiratory Diseases
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• v.40 no.6
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• pp.653-658
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• 1993

Background: Recent advancement of molecular genetics has revealed that malignant transformation of a cell may be a complex multistep process and this process is grouped, in general, into two distinct categories, activation of protooncogenes and inactivation of tumor suppressor genes. This study was focused on the mutation of p53 tumor suppressor gene, because p53 gene mutation is now generally accepted to be one of the most frequent genetic changes in a variety of human cancers. Although lung cancer is one of the common cancers in Korea, the genetic change in the carcinogenesis process is not yet known clearly. To investigate the role of p53 gene mutation in lung cancer, we examined the mutations of exon 4-8 of the p53 gene in humna lung cancer cell lines, because most of the mutations of p53 gene have been reported to develop in exon 4-8. Method: Genomic DNA was obtained by the digestion of proteinase K and the extraction by phenol-chloroform-ethanol method from two human pulmonary adenocarcinoma cell lines, PC-9 and PC-14, and one human small cell lung cancer cell line, H69. To detect the mutations of exon 4-8 of the p53 gene, polymerase chain reaction single-strand conformation polymorphism(PCR-SSCP) analysis was performed with the DNA extracted from the cells. Results: The mutation of p53 gene was present in all three cell lines tested. In PC-9, PC-14 and H69, the altered mobility was detected in exon 7, 7 and 5, respectively. Conclusion: These results suggest that p53 gene mutation plays an important role in certain steps of the carcinogenesis of human non-small cell and small cell lung cancer.

• Journal of Korean Neurosurgical Society
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• v.30 no.sup1
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• pp.5-12
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• 2001

This study was designed to investigate the mechanism of cell death after cisplatin treatment in human glioblastoma A172 cells. Cis-diamminedichloroplatinum(Cisplatin) demonstrated cytostatic or cytotoxic effects on A172 cells in a dosedependent manner. Cisplatin-mediated cytotoxity in A172 cells was revealed as an apoptosis characterized by high molecular weight DNA fragmentation by agarose electrophoresis as well as nuclear fragmentation by Hoechst staining. Cisplatin also resulted in the activation of caspase 3-like protease as well as poly(ADP-ribose) polymerase(PARP) cleavage. Interestingly, the anti-apoptotic Bcl2 protein was degraded and furthermore, expression of p53 protein was increased by cisplatin in a time-dependent manner. Taken together, these results suggest that anticancer drug, cisplatin induces the apoptotic death of human glioblastoma A172 cells via the activations of caspase 3-like protease, degradation of anti-apoptotic Bcl2 protein and increase in the expression of p53.

• The Korean Journal of Physiology and Pharmacology
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• v.26 no.5
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• pp.377-387
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• 2022

Benzimidazole anthelmintic agents have been recently repurposed to overcome cancers resistant to conventional therapies. To evaluate the anti-cancer effects of benzimidazole on resistant cells, various cell death pathways were investigated in 5-fluorouracil-resistant colorectal cancer cells. The viability of wild-type and 5-fluorouracil-resistant SNU-C5 colorectal cancer cells was assayed, followed by Western blotting. Flow cytometry assays for cell death and cell cycle was also performed to analyze the anti-cancer effects of benzimidazole. When compared with albendazole, fenbendazole showed higher susceptibility to 5-fluorouracil-resistant SNU-C5 cells and was used in subsequent experiments. Flow cytometry revealed that fenbendazole significantly induces apoptosis as well as cell cycle arrest at G2/M phase on both cells. When compared with wild-type SNU-C5 cells, 5-fluorouracil-resistant SNU-C5 cells showed reduced autophagy, increased ferroptosis and ferroptosis-augmented apoptosis, and less activation of caspase-8 and p53. These results suggest that fenbendazole may be a potential alternative treatment in 5-fluorouracil-resistant cancer cells, and the anticancer activity of fenbendazole does not require p53 in 5-fluorouracil-resistant SNU-C5 cells.

• The Journal of Korean Society for Neurotherapy
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• v.22 no.3
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• pp.31-36
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• 2018

Purpose The purpose of this study was to investigate the effects of contact handorientation response(CHOR) during sit-to-stand(STS) in people with stroke. Methods The subjects of the study were Thirty hemiplegia participated (Rt. hemiplegia/Lt. hemiplegia: 15/15, mean age: $65.82{\pm}8.53$) in this study. The analysis of muscles activation (rectus femoris, biceps femoris, tibialis anterior, gastrocnemius) distribution was conducted by the EMG, and the analysis of foot pressure distribution was conducted by the resistive pressure sensor. Hemiplegic stroke patients were instructed to perform STS three times with the non-affected side hand and affected side hand on the table. Results There was a significant positive correlation between rectus femoris, tibialis anterior muscle activation and affected side hand contact during STS(p<0.05). The STS correlated with the foot pressure in the affected side hand contact(p<0.05). Conclusion AS a result, CHOR during STS is related to muscle activation and the characteristics of foot pressure. This information was observed in the affected side hand contact on the table, suggestion that rehabilitation programs should be implemented.

• PNF and Movement
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• v.9 no.3
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• pp.19-24
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• 2011

Purpose : The purpose of this study was to analyze the effect of PNF lower extremity flexion pattern on the eletromyographic (EMG) activity in rectus abdominis, internal oblique abdominal, external oblique abdominal, erector spinae. Methods : Twenty-six healthy adults volunteered to participate in this study. Subjects were required complete following two PNF lower extremity patterns; flexion-adduction-external rotation with knee flexion (D1) and flexion-abduction-internal rotation with knee flexion (D2). A paired t-test was used to determine the influence of the PNF two patterns on muscle activity for each muscle and descriptive statistics was used to determine local/global muscle ratio. Results : The D1 pattern was showed significant rectus abdominis (p<.05) and Median of internal oblique/rectus abdominis ratio was 2.23 and internal oblique/external oblique ratio was 1.53. The D2 pattern showed significant erector spinae (p<.05) and Median of internal oblique/rectus abdominis ratio was 3.06 and internal oblique/external oblique ratio was 1.72. Conclusion : The D1 pattern made rectus abdominis activation increase. The D2 pattern made erector spinae activation increase. As compared D1 and D2 pattern on trunk muscle activation, it's will be useful decision making for the trunk muscle strength and stabilization.

• Asian-Australasian Journal of Animal Sciences
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• v.20 no.5
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• pp.718-724
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• 2007

Considerable attention has been focused on the cloning of mammalian embryos, as a consequence of poor development, in order to enhance the application of genetic engineering. Experiments were conducted to compare the developmental competence of parthenotes and reconstructed (NT) rabbit eggs with fetal fibroblasts (FFs) following various activation regimens. Oocytes and NT eggs were exposed to: electric stimulation (EST, Group 1) and EST followed by 6-dimethylaminopurine (DMAP, Group 2), cycloheximide (CHX, Group 3) or DMAP/CHX (Group 4). Pronuclear (PN) status, cleavage, blastocyst development and the ploidy were assessed. In parthenote groups 1, 2, 3 and 4, the PN formation differed significantly. And, the cleavage and blastocyst rates were 41.7 and 5%, 75.6 and 53.7%, 68 and 36%, 82.1 and 52.6%, respectively, among treatments. Polyploidy was observed in 17.2% of EST plus DMAP and 44.9% of EST plus DMAP/CHX groups. In SCNT groups (Group 1, 2, 3 and 4), the cleavage and blastocyst rates were 28.6 and 7.1%, 58.3 and 29.2%, 56.8 and 24.1%, 64.5 and 27.8%, respectively. The chromosomal composition differed significantly (p<0.05) among treatments. In Group 2 and 3, 53.8% and 81.8% of embryos revealed diploid chromosomal sets, respectively. However, in Group 4, 53.3% of embryos showed abnormal ploidy (mixoploid). Although DMAP or combination with DMAP/CHX resulted in higher in vitro development of rabbit SCNT embryos, higher incidence of chromosomal abnormality may induce problems related to fetal loss of at late stage of development.