• Applied Chemistry for Engineering
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• v.29 no.2
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• pp.138-146
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• 2018

Photodynamic therapy (PDT) is a great potential approach for the localized tumor removal with fewer metastatic potentials and side effects in treating the disease. In the treatment process, a photosensitizer (PS) that absorbs a light energy to generate reactive oxygen is essential. In general, a visible light is used as a light source of PDT, so that side effects from the light source are inevitable. For this reason, upconversion nanoparticles (UCNPs) using near-infrared (NIR) as an excitation source are attracting attention in the field of disease diagnosis and treatment. UCNPs have the low cytotoxicity and phototoxicity, and also advantages such as deep tissue penetration and low background autofluorescence. For PDT, UCNPs should be combined with a PS which absorbs the light energy from UCNPs and transfers it to the surrounding oxygen to produce reactive oxygen. In addition, the therapeutic efficacy can be improved by modifying nanoparticle surfaces, adding anti-cancer drugs, or combining with photothermal therapy (PTT). In this review, we summarize the recent research to improve the efficiency of PDT using UCNPs.

• Therapeutic Science for Rehabilitation
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• v.1 no.1
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• pp.29-38
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• 2012

Introduction : This study reviews the main areas of cognitive rehabilitation including executive dysfunction, memory dysfunction, perceptual dysfunction, attention deficit, and dysfunctions in activities of daily living in order to apply to the adaptation of occupational therapy. Body : Cognition programs based on the virtual reality are being used not only to evaluate but to train the overall components of human's cognition. Because the cognitive program is concentrating on the real environment, it is known to bring a remarkable transitional effect to the actual environment, compared to the basic computer-based evaluation and training. Applying virtual reality to the rehabilitation program can develop and advance the high technology and can result in a major effect on the innovative treatment technology. Conclusions : In this process, virtual reality is expected to be researched more in the near future. Particularly in the cognitive realm, it is imperative for researchers to pay attention to the improved transitional effect of the virtual reality toward the actual environment, rather than the already existing method of evaluations. Therefore, application of the virtual reality for the cognitive training should be researched for various types of subjects in the diverse aspects of congnitive function. Application of the virtual reality in the cognitive function has its unlimited potential, thus the rehabilitation program integrated with not only evaluation but training and education is expected extensively in the future.

• The Journal of Internal Korean Medicine
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• v.41 no.1
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• pp.1-13
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• 2020

Objectives: Osteoarthritis (OA) is a chronic and degenerative joint disease characterized by progressive degeneration of articular cartilage. Inflammation is a recognized and important factor of OA progression. The present study was designed to investigate the protective effect of Corni Fructus water extract (CFW) on a monosodium iodoacetate (MIA)-induced rat model of OA. Methods: Osteoarthritis was induced by injection of MIA (50 µL; 80 mg/mL) into the knee joint cavity of rats. After an adaptation period for seven days, the rats were divided into 4 groups (n=8/group): normal, control, indomethacin-treated (5 mg/kg), and CFW-treated (200 mg/kg) groups. The rats were treated orally for 14 days. Pain was evaluated by determining hind paw weight distribution. For biochemical analyses, we measured the changes in reactive oxygen species (ROS) and peroxynitrite (ONOO^-) in the knee joint. The presence of anti-oxidant proteins and inflammatory proteins was determined by western blotting. Results: The administration of CFW significantly improved the hind paw weight distribution. The ROS and ONOO^- levels of knee joint were significantly decreased in the CFW group. CFW inhibited the production of inflammatory mediators, such as COX-2, and inflammatory cytokines, including IL-6 and IL-1β, via the NF-κB signaling pathway. The expression of anti-oxidant enzymes, such as catalase and GPx-1/2 also increased significantly. Conclusions: The findings indicate that CFW has a therapeutic and protective effect on OA by suppression of inflammation. Therefore, CFW could represent a potential and effective candidate for OA treatment.

• Journal of the Korean Society of Radiology
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• v.11 no.2
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• pp.87-94
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• 2017

Monte Carlo simulations were used to assess dose enhancement effects for 60-, 90-, 120-, and 150-kV X-rays, and for 6- and 15-MV X-rays. The MCNPX code was used for a computer simulation of the ICRU slab phantom, and gold, gadolinium, and iron oxide (Fe2O3) were employed as dose enhancement agents. In consideration of the buildup region of the incident energy, agent concentrations of 5, 10, 15, and 20 mg/g were inserted on the surface of the phantom at a depth of 5 cm. Based on baseline values obtained in the absence of dose enhancement agents, a quantitative analysis was performed by evaluating depth-dependent changes in the absorbed energy and the dose enhancement factor (DEF). A higher concentration of dose enhancement agents led to a greater dose enhancement effect with iron oxide, gadolinium, and gold in descending order. For kilovoltage (kV) X-rays, as the incident energy was decreased and as the energy became closer to the ionization potential of the atoms in the enhancement agent, the dose enhancement effect increased. In the megavoltage (MV) X-ray range, dose enhancement was higher at 6 MV compared with 15 MV. However, the overall dose enhancements were significantly lower compared to the results obtained with kV X-rays.

• Journal of Chest Surgery
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• v.31 no.7
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• pp.692-696
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• 1998

For the management of a secondary spontaneous pneumothorax, videothoracoscopic surgery may offer the potential therapeutic benefits of a minimally invasive approach. We report on a series of 36 patients(33 men and 3 women) with a mean age of 56.3 years(range, 31 to 80 years) who underwent thoracoscopic surgical procedures for the treatment of secondary spontaneous pneumothorax. Twenty-one patients had emphysema and 20 patients had old pulmonary tuberculosis. Nineteen patients presented a persistent severe air leak more than 3 days preoperatively and 15 patients had more than one recurrence. Bullectomy or exclusion of the lesion was performed in 33 patients. Mechanical pleurodesis was performed in the entire patients, talc was sprayed in 22 and vibramycin in 14. Mild pleural adhesion at the upper lobe was shown in 10 patients and severe pleural adhesion in 7 patients. One patient with persistent air leak died of persistent air leak and respiratory failure. The mean postoperative stay was 7.0 days(range, 2 to 17 days). At a mean follow-up of 15.8 months (range, 5 to 45 months), no pneumothorax had recurred. In comparison with the result of the treatment for 112 patients with primary spontaneous pneumothorax, the operating time was not significantly longer and there were no more primary treatment failures, but the duration of postoperative chest drainage and hospital stay was longer. Videothoracoscopic surgery has proved to be an effective treatment for secondary spontaneous pneumothorax in elderly patients who represent high-risk candidates for thoracotomy.

• Korean Journal of Clinical Laboratory Science
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• v.52 no.3
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• pp.253-260
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• 2020

Alzheimer's disease (AD) is a chronic and progressive neurodegenerative disease that can be described by the occurrence of dementia due to a decline in cognitive function. The disease is characterized by the formation of extracellular and intracellular amyloid plaques. Amyloid beta (Aβ) is a hallmark of AD, and microglia can be activated in the presence of Aβ. Activated microglia secrete pro-inflammatory cytokines. Furthermore, S100A9 is an important innate immunity pro-inflammatory contributor in inflammation and a potential contributor to AD. This study examined the effects of metformin and α-LA on the inflammatory response and NLRP3 inflammasome activation in Aβ- and S100A9-induced BV-2 microglial cells. Metformin and α-LA attenuated inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). In addition, metformin and α-LA inhibited the phosphorylation of JNK, ERK, and p38. They activated the nuclear factor kappa B (NF-κB) pathway and the NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome. Moreover, metformin and α-LA reduced the marker levels of the M1 phenotype, ICAM1, whereas the M2 phenotype, ARG1, was increased. These findings suggest that metformin and α-LA are therapeutic agents against the Aβ- and S100A9-induced neuroinflammatory responses.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.12
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• pp.5089-5094
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• 2015

FADS1 (fatty acid desaturase 1) plays a crucial role in fatty acid metabolism, and it was recently reported to be involved in tumorigenesis. However, the role of FADS1 expression in esophageal squamous cell carcinoma (ESCC) remains unknown. In the current study, we investigated the expression and clinical pathologic and prognostic significance of FADS1 in ESCC. Immunohistochemical analyses revealed that 58.2% (146/251) of the ESCC tissues had low levels of FADS1 expression, whereas 41.8% (105/251) exhibited high levels of FADS1 expression. In positive cases, FADS1 expression was detected in the cytoplasm of cells. Correlation analyses demonstrated that FADS1 expression was significantly correlated with tumor location (p=0.025) but not with age, gender, histological grade, tumor status, nodal status or TNM staging. Furthermore, patients with tumors expressing high levels of FADS1had a longer disease-free survival time (p<0.001) and overall survival time (p <0.001). Univariate and multivariate analyses revealed that, along with nodal status, FADS1 expression was an independent and significant predictive factor (p<0.001). In conclusion, our study suggested that FADS1 might be a valuable biomarker and potential therapeutic target for ESCC.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.8
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• pp.3651-3657
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• 2014

Hepatocellular carcinoma (HCC) has a relatively higher incidence in many countries of Asia. Globally, HCC has a high fatality rate and short survival. Epirubicin, a doxorubicin analogue, may be administered alone or in combination with other agents to treat primary liver cancer and metastatic diseases. However, the toxic effects of epirubicin to normal tissues and cells have been one of the major obstacles to successful cancer chemotherapy. Here, we investigated the effects of epirubicin in combination with kappa-selenocarrageenan on mice with H22 implanted tumors and HepG-2 cell proliferation, immune organ index, morphology, cell cycle and related protein expressions in vivo and in vitro with sequential drug exposure. The inhibitory rate of tumor growth in vivo was calculated. Drug sensitivity was measured by MTT assay, and the King's principle was used to evaluate the interaction of drug combination. Morphological changes were observed by fluorescent microscopy. Cell cycle changes were analyzed by flow cytometry. Expression of cyclin A, Cdc25A and Cdk2 were detected by Western blotting. In vivo results demonstrated that the inhibitory rate of EPI combined with KSC was higher than that of KSC or EPI alone, and the Q value indicated an additive effect. In addition, KSC could significantly raise the thymus and spleen indices of mice with H22 implanted tumors. In the drug sensitivity assay in vitro, exposure to KSC and EPI simultaneously was more effective than exposure sequentially in HepG-2 cells, while exposure to KSC prior to EPI was more effective than exposure to EPI prior to KSC. Q values showed an additive effect in the simultaneous group and antagonistic effects in the sequential groups. Morphological analysis showed similar results to the drug sensitivity assay. Cell cycle analysis revealed that exposure to KSC or EPI alone arrested the cells in S phase in HepG-2 cells, exposure to KSC and EPI simultaneously caused accumulation in the S phase, an effect caused by either KSC or EPI. Expression of cyclin A, Cdc25A and Cdk2 protein was down-regulated following exposure to KSC and EPI alone or in combination, exposure to KSC and EPI simultaneously resulting in the lowest values. Taken together, our findings suggest that KSC in combination with EPI might have potential as a new therapeutic regimen against HCC.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.5
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• pp.1961-1970
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• 2014

Pyruvate kinase isozyme type M2 (PKM2) was first found in hepatocellular carcinoma (HCC), and its expression has been thought to correlate with prognosis. A large number of studies have demonstrated that epithelial-mesenchymal transition (EMT) is a crucial event in hepatocellular carcinoma (HCC) and associated metastasis, resulting in enhanced malignancy of HCC. However, the roles of PKM2 in HCC EMT and metastasis remain largely unknown. The present study aimed to determine the effects of PKM2 in EGF-induced HCC EMT and elucidate the molecular mechanisms in vitro. Our results showed that EGF promoted EMT in HCC cell lines as evidenced by altered morphology, expression of EMT-associated markers, and enhanced invasion capacity. Furthermore, the present study also revealed that nuclear translocation of PKM2, which is regulated by the ERK pathway, regulated ${\beta}$-catenin-TCF/LEF-1 transcriptional activity and associated EMT in HCC cell lines. These discoveries provide evidence of novel roles of PKM2 in the progression of HCC and potential therapeutic target for advanced cases.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.13
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• pp.5181-5186
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• 2014

Tumors have evolved numerous mechanisms by which they can escape from immune surveillance. One of these is to produce immunosuppressive cytokines. Transforming growth factor-${\beta}$(TGF-${\beta}$) is a pleiotropic cytokine with a crucial function in mediating immune suppression, especially in the tumor microenvironment. TGF-${\beta}$ produced by T cells has been demonstrated as an important factor for suppressing antitumor immune responses, but the role of tumor-derived TGF-${\beta}$ in this process is poorly understood. In this study, we demonstrated that knockdown of tumor-derived TGF-${\beta}$ using shRNA resulted in dramatically reduced tumor size, slowing tumor formation, prolonging survival rate of tumor-bearing mice and inhibiting metastasis. We revealed possible underlying mechanisms as reducing the number of myeloid-derived suppressor cells (MDSC) and $CD4^+Foxp3^+$ Treg cells, and consequently enhanced IFN-${\gamma}$ production by CTLs. Knockdown of tumor-derived TGF-${\beta}$ also significantly reduced the conversion of na$\ddot{i}$ve $CD4^+$ T cells into Treg cells in vitro. Finally, we found that knockdown of TGF-${\beta}$ suppressed cell migration, but did not change the proliferation and apoptosis of tumor cells in vitro. In summary, our study provided evidence that tumor-derived TGF-${\beta}$ is a critical factor for tumor progression and evasion of immune surveillance, and blocking tumor-derived TGF-${\beta}$ may serve as a potential therapeutic approach for cancer.