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Lim S.-N.,Inje University | Han H.-S.,Chungbuk National University | Lee K.-H.,Chungbuk National University | Lee S.-C.,Soonchunhyang University | And 10 more authors.
Journal of Palliative Medicine | Year: 2015

Background: Pain is one of the most common and distressing symptoms in patients with cancer, with a high prevalence of 90%. Appropriate pain assessment is very important in managing cancer pain. Objective: The aims of this study were to (1) evaluate patient satisfaction with pain control therapy using a self-reporting pain assessment tool, (2) explore the usefulness of a self-reporting assessment tool for patients and physicians, and (3) evaluate patient perception of pain management and opioid analgesics. Methods: We enrolled a total of 587 South Korean adult cancer patients hospitalized for five days or more. Pain assessment using a self-reporting pain assessment tool was performed by patients themselves from Day 1 to Day 5. The average pain intensity on a numeric rating scale (NRS) and the frequency of breakthrough pain between Day 1 and Day 5 were recorded with a self-reporting pain assessment tool. We evaluated patient satisfaction with pain control and the usefulness of a self-reporting pain assessment tool for patients and physicians on Day 5. Results: Among the 587 enrolled patients, 551, excluding 36 patients who violated inclusion criteria, were analyzed. The pain satisfaction rate was 79.5%, and only 6.2% of assessed patients had a negative pain management index (PMI). However, symmetry analysis for pain intensity between patient and physician showed low agreement (kappa=0.21). The patients with dissatisfaction for cancer pain control expressed negative attitudes toward using opioid analgesics and misconceptions regarding pain management. The satisfaction for using a self-reporting pain assessment tool was 79.2% in patients and 86.4% in physicians, respectively. Conclusion: The use of a self-reporting pain assessment tool as a communication instrument provides an effective foundation for evaluating pain intensity in cancer pain management. A more individualized approach to patient education about pain management may improve patient outcome. © Mary Ann Liebert, Inc. 2015. Source


Shin D.Y.,Dongnam Institute of Radiological and Medicine science | Choi Y.H.,Korea University
Journal of the Korean Society of Food Science and Nutrition | Year: 2013

Cancer cells exhibit increased demand for glutamine-derived carbons to support anabolic processes. Indeed, the spectrum of glutamine-dependent tumors and the mechanisms through which glutamine supports cancer metabolism remain areas of active investigation. In the present study, we investigated the effects of glutamine deprivation on the correlation between tightening of tight junctions (TJs) and anti-invasive activity in human prostate carcinoma LnCap cells. Glutamine deprivation markedly inhibited cell motility and invasiveness in a time-dependent manner. The anti-invasive activity of glutamine deprivation was associated with an increased tightness of the TJ, which was demonstrated by an increase in transepithelial electrical resistance (TER). The activities of matrix metalloproteinase (MMP)-2 and MMP-9 were inhibited in a time-dependent fashion by glutamine deprivation, which was correlated with a decrease in expression of their mRNA and proteins and up-regulation of tissue inhibitors of metalloproteinases (TIMPs) expression. Furthermore, glutamine deprivation repressed the levels of the claudin family members, which are major components of TJs that play a key role in the control and selectivity of paracellular transport. Moreover, the levels of E-cadherin, a type I transmembrane glycoprotein, and snail, an epithelial to mesenchymal transition regulator and zinc finger transcription factor, were markedly modulated by glutamine deprivation. Taken together, these findings suggest that TJs and MMPs are critical targets of glutamine deprivation-induced anti-invasion in human prostate carcinoma LnCap cells. © 2013 by The Korean Society of Food Science and Nutrition. All rights reserved. Source


Shin D.Y.,Dongnam Institute of Radiological and Medicine science | Cha H.-J.,Kosin University | Kim G.-Y.,Jeju National University | Kim W.-J.,Chungbuk National University | Choi Y.H.,Korea University
International Journal of Molecular Sciences | Year: 2013

Diallyl trisulfide (DATS), an organosulfur compound in garlic, possesses pronounced anti-cancer potential. However, the anti-invasive mechanism of this compound in human bladder carcinoma is not fully understood. In this study, we evaluated the anti-invasive effects of DATS on a human bladder carcinoma (5637) cell line and investigated the underlying mechanism. The results indicated that DATS suppressed migration and invasion of 5637 cells by reducing the activities and expression of matrix metalloproteinase (MMP)-2 and MMP-9 at both the protein and mRNA levels. DATS treatment up-regulated expression of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 in 5637 cells. The inhibitory effects of DATS on invasiveness were associated with an increase in transepithelial electrical resistance and repression of the levels of claudin family members. Although further studies are needed, our data demonstrate that DATS exhibits anti-invasive effects in 5637 cells by down-regulating the activity of tight junctions and MMPs. DATS may have future utility in clinical applications for treating bladder cancer. © 2013 by the authors; licensee MDPI, Basel, Switzerland. Source


Shin D.Y.,Dongnam Institute of Radiological and Medicine science | Kim G.-Y.,Jeju National University | Lee J.H.,Chemistry and Biotechnology Examination Bureau | Choi B.T.,Pusan National University | And 2 more authors.
International Journal of Molecular Sciences | Year: 2012

Diallyl disulfide (DADS), a sulfur compound derived from garlic, has various biological properties, such as anticancer, antiangiogenic and anti-inflammatory effects. However, the mechanisms of action underlying the compound's anticancer activity have not been fully elucidated. In this study, the apoptotic effects of DADS were investigated in DU145 human prostate carcinoma cells. Our results showed that DADS markedly inhibited the growth of the DU145 cells by induction of apoptosis. Apoptosis was accompanied by modulation of Bcl-2 and inhibitor of apoptosis protein (IAP) family proteins, depolarization of the mitochondrial membrane potential (MMP, ΔΨm) and proteolytic activation of caspases. We also found that the expression of death-receptor 4 (DR4) and Fas ligand (FasL) proteins was increased and that the level of intact Bid proteins was down-regulated by DADS. Moreover, treatment with DADS induced phosphorylation of mitogen-activated protein kinases (MAPKs), including extracellular-signal regulating kinase (ERK), p38 MAPK and c-Jun N-terminal kinase (JNK). A specific JNK inhibitor, SP600125, significantly blocked DADS-induced-apoptosis, whereas inhibitors of the ERK (PD98059) and p38 MAPK (SB203580) had no effect. The induction of apoptosis was also accompanied by inactivation of phosphatidylinositol 3-kinase (PI3K)/Akt and the PI3K inhibitor LY29004 significantly increased DADS-induced cell death. These findings provide evidence demonstrating that the proapoptotic effect of DADS is mediated through the activation of JNK and the inhibition of the PI3K/Akt signaling pathway in DU145 cells. © 2012 by the authors; licensee MDPI, Basel, Switzerland. Source


Rhyu D.-W.,Kosin University | Kang Y.-J.,Kosin University | Ock M.-S.,Kosin University | Eo J.-W.,Pusan National University | And 6 more authors.
International Journal of Molecular Sciences | Year: 2014

Human endogenous retroviruses (HERV) env proteins have been recently reported to be significantly up-regulated in certain cancers. Specifically, mRNA and protein levels of HERV-K (HML-2) are up-regulated in the blood plasma or serum of breast cancer patients. Here, we collected blood samples of 49 breast cancer patients and analyzed mRNA expressions of various HERVs env genes including HERV-R, HERV-H, HERV-K, and HERV-P by real-time PCR. The expression of env genes were significantly increased in the blood of primary breast cancer patients but were decreased in patients undergoing chemotherapy to a similar level with benign patients. When we compared the group currently undergoing chemotherapy and those patients undergoing chemotherapy simultaneously with radiotherapy, HERVs env genes were reduced more in the chemotherapy only group, suggesting that chemotherapy is more effective in reducing HERV env gene expression than is radiotherapy. Among chemotherapy groups, HERV env gene expression was the lowest in the taxotere- or taxol-treated group, suggesting that taxotere and taxol can reduce HERVs env expression. These data suggest the potential to use HERVs env genes as a diagnosis marker for primary breast cancer, and further studies are needed to identify the mechanism and physiological significance of the reduction of HERV env gene expression during chemotherapy. © 2014 by the authors; licensee MDPI, Basel, Switzerland. Source

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