• Journal of Gastric Cancer
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• v.15 no.2
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• pp.121-126
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• 2015

Purpose: We evaluated the socio-personal and clinical factors that can affect preoperative quality of life to determine how to improve preoperative quality of life in patients with gastric cancer. Materials and Methods: The preoperative quality of life data of 200 patients (68 females and 132 males; mean age $58.9{\pm}12.6years$) with gastric cancer were analyzed according to socio-personal and clinical factors. The Korean versions of the European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire Core (QLQ) 30 and the EORTC QLQ-STO22, a gastric cancer-specific module, were used to assess quality of life. Patients were asked to complete the questionnaire preoperatively by themselves. Results: Patients with a higher academic background and stage I disease tended to have higher global health status scores. Highly educated younger men had better physical functioning scores. Highly educated and well-nourished patients with stage I cancer had higher role functioning scores. Married patients had better emotional scores. The symptom scales were affected by sex, age, education level, nutrition, and cancer stage. Conclusions: Preoperative quality of life in patients with gastric cancer can be improved by nutritional support and treatment of symptoms caused by disease progression. Psychological support may be helpful for patients with a poor quality of life.

• Molecules and Cells
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• v.19 no.1
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• pp.131-136
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• 2005

The ETV6-NTRK3 gene fusion, first identified in the chromosomal translocation in congenital fibrosarcoma, encodes a chimeric protein tyrosine kinase with potent transforming activity. ETV6-NTRK3-dependent transformation involves the joint action of NTRK3 signaling pathways, and aberrant cell cycle progression resulting from activation of Mek1 and Akt. The level of glutathione (GSH) was found to be markedly increased in ETV6-NTRK3-transformed NIH3T3 cells. The activities of the two GSH biosynthetic enzymes as well as of glutathione peroxidase, together with their mRNAs, were also higher in the transformed cells. The transformed cells were able to grow in the presence of GSH-depleting agents, whereas the control cells were not. L-Buthionine-(S,R)-sulfoximine (BSO) inhibited activation of Mek1 and Akt in the transformed NIH3T3 cells. These observations imply that up-regulation of GSH biosynthesis plays a central role in ETV6-NTRK3-induced transformation.

• YAKHAK HOEJI
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• v.52 no.5
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• pp.384-393
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• 2008

We examined the effect of green tea extract (GTE) and L-theanine combination on the $A{\beta}_{1-42}$-induced memory dysfunction. GTE and combination were administrated into mice for 3 weeks followed by injection of $A{\beta}_{1-42}$ to induce memory impairment. GTE and L-theanine administration significantly improved cognitive ability and reduced $A{\beta}_{1-42}$ level accompanied with the inhibition of neuronal cell death and activities of secretase. These results suggest that GTE and L-theanine combination may be a useful for preventing for the development or progression of Alzheimer's disease.

• Journal of Korean Academy of Fundamentals of Nursing
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• v.11 no.1
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• pp.49-58
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• 2004

Purpose: This study was done to identify the relationship of expressions of hostility, trait anger, and anger in patients with Coronary Artery Disease (CAD). Method: Ninety patients between 30 and 80 who were admitted to A hospital participated in the study. Data were collected through a questionnaire survey using convenience sampling. The research tool consisted of 24 questions by Costa et al (1986) and 10 questions specifically on anger from the Korean version (Chon, Hahn, & Lee, 1998) of the State-Trait Anger Inventory by Spielberger (1988). All of the questions were answered using a 4-point Likert scale. The data were analyzed with SPSS Win version 10.0. Result: Mean scores for hostility, trait anger, anger-out, anger-in, and anger-control were 2.51, 2.19, 1.93, 1.85, and 2.56, respectively. Hostility and trait anger showed a significantly positive correlation to anger-out and anger-in. Conclusion: This study presented baseline data that indicate that psychosocial factors are associated with the occurrence and progression of CAD. Accordingly, various programs that include psychological interventions are required to diminish the level of hostility and anger. Also, further studies should be conducted with larger patient populations.

• Korean Journal of Bronchoesophagology
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• v.11 no.1
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• pp.37-41
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• 2005

Deep neck infections mean infection in the potential spaces and facial planes of the neck, either abscess formation or cellulitis. Deep neck infections are caused by dental, salivary gland, pharyngeal and tonsillar infections. Sometimes, deep neck infection may be caused by tuberculosis in case of immunodefiecient patients. Acquired immunodeficiency syndrome(AIDS) is a disease associated with defective cell-mediated immunity after infected with human immunodeficiency virus(HIV). The chance of opportunistic infection in patients of AIDS increases as the level of immunodeficienty progresses. Human immunodeficiency virus infection is the most single significant risk factor for progression of pulmonary tuberculosis to extrapulmonary sites. In patients infected with HIV, the rate of extrapulomonary tuberculosis rises upto $60\%$. We report a case of a 47 year old male patient with AIDS associated with deep neck infection by tuberculosis.

• Journal of Dental Anesthesia and Pain Medicine
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• v.18 no.2
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• pp.89-95
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• 2018

Background: Incorrect administration of an anesthetic during local anesthesia is one of the most important causes of pain symptoms in patients scheduled for dental procedures. The current study assessed the severity of damage to periodontal tissue following different rates of anesthetic administration. Methods: The research was conducted on 50 outbred male rats with a body mass of 180-240 g. The anesthetic used was 1% articaine. Results: The results showed that administration of the anesthetic at a rapid pace caused structural damage to the periodontal tissue. Further, signs of impaired microcirculation were noted at all rates of administration. Biochemical studies demonstrated changes in the level of glucose and enzymes with the rapid introduction of the anesthetic, indicating severe systemic stress response of the body. Conclusions: Injection of local anesthetic at any rate of introduction induces vascular congestion in the microcirculatory bloodstream and exudative reactions. Rapid introduction of an anesthetic causes progression of structural changes in the gingival tissue.

• Journal of Microbiology and Biotechnology
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• v.17 no.5
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• pp.840-846
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• 2007

Human prostate-specific antigen(PSA), a 33 kDa serine protease with comprehensive homology to glandular kallikrein, is secreted from prostatic tissue into the seminal fluid and enters into the circulation. The level of PSA increases in the serum of patients with prostatic cancer and hence is widely employed as a marker of the disease status. In particular, an enzymatically active PSA that is a form cleaved at the N-terminal seven-amino-acids prosequence, APLILSR, of proPSA may play an important roll in the progression of prostate cancer. Thus, the presence of the active form would selectively discriminate the cancer from benign prostatic hyperplasia. In this study, we developed a convenient purification method for the acquisition of active PSA and proPSA. Recombinant proPSA and active PSA were expressed directly in Escherichia coli, easily and efficiently isolated from inclusion bodies, refolded, and purified. Moreover, the enzymatic activity of the recombinant active PSA was confirmed as serine protease using chromogenic chymotrypsin substrate. This purified active PSA could be further applied to scrutinize the biological or conformational characteristics of the protein and to develop specific diagnostic and/or therapeutic agents against prostate cancer.

• Molecules and Cells
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• v.26 no.4
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• pp.329-337
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• 2008

Src-family kinases are critically involved in the control of cytoskeleton organization and in the generation of integrin-dependent signaling responses, inducing tyrosine phosphorylation of many signaling and cytoskeletal proteins. Activity of the Src family of tyrosine kinases is tightly controlled by inhibitory phosphorylation of a carboxy-terminal tyrosine residue, inducing an inactive conformation through binding with its SH2 domain. Dephosphorylation of C-ter tyrosine, as well as its deletion of substitution with phenylalanine in oncogenic Src kinases, leads to autophosphorylation at a tyrosine in the activation loop, thereby leading to enhanced Src activity. Beside this phophorylation/dephosphorylation circuitry, cysteine oxidation has been recently reported as a further mechanism of enzyme activation. Mounting evidence describes Src activation via its redox regulation as a key outcome in several circumstances, including growth factor and cytokines signaling, integrin-mediated cell adhesion and motility, membrane receptor cross-talk as well in cell transformation and tumor progression. Among the plethora of data involving Src kinase in physiological and pathophysiological processes, this review will give emphasis to the redox component of the regulation of this master kinase.

• Molecules and Cells
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• v.43 no.2
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• pp.198-202
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• 2020

Comprehensive inhibition of RUNX1, RUNX2, and RUNX3 led to marked cell suppression compared with inhibition of RUNX1 alone, clarifying that the RUNX family members are important for proliferation and maintenance of diverse cancers, and "cluster regulation of RUNX (CROX)" is a very effective strategy to suppress cancer cells. Recent studies reported by us and other groups suggested that wild-type RUNX1 is needed for survival and proliferation of certain types of leukemia, lung cancer, gastric cancer, etc. and for their one of metastatic target sites such as born marrow endothelial niche, suggesting that RUNX1 often functions oncogenic manners in cancer cells. In this review, we describe the significance and paradoxical requirement of RUNX1 tumor suppressor in leukemia and even solid cancers based on recent our findings such as "genetic compensation of RUNX family transcription factors (the compensation mechanism for the total level of RUNX family protein expression)", "RUNX1 inhibition-induced inhibitory effects on leukemia cells and on solid cancers through p53 activation", and "autonomous feedback loop of RUNX1-p53-CBFB in acute myeloid leukemia cells". Taken together, these findings identify a crucial role for the RUNX cluster in the maintenance and progression of cancers and suggest that modulation of the RUNX cluster using the pyrrole-imidazole polyamide gene-switch technology is a potential novel therapeutic approach to control cancers.

• Molecules and Cells
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• v.42 no.7
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• pp.546-556
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• 2019

Protein phosphatase 4 (PP4) is a crucial protein complex that plays an important role in DNA damage response (DDR), including DNA repair, cell cycle arrest and apoptosis. Despite the significance of PP4, the mechanism by which PP4 is regulated remains to be elucidated. Here, we identified a novel PP4 inhibitor, protein phosphatase 4 inhibitory protein (PP4IP) and elucidated its cellular functions. PP4IP-knockout cells were generated using the CRISPR/Cas9 system, and the phosphorylation status of PP4 substrates (H2AX, KAP1, and RPA2) was analyzed. Then we investigated that how PP4IP affects the cellular functions of PP4 by immunoprecipitation, immunofluorescence, and DNA double-strand break (DSB) repair assays. PP4IP interacts with PP4 complex, which is affected by DNA damage and cell cycle progression and decreases the dephosphorylational activity of PP4. Both overexpression and depletion of PP4IP impairs DSB repairs and sensitizes cells to genotoxic stress, suggesting timely inhibition of PP4 to be indispensable for cells in responding to DNA damage. Our results identify a novel inhibitor of PP4 that inhibits PP4-mediated cellular functions and establish the physiological importance of this regulation. In addition, PP4IP might be developed as potential therapeutic reagents for targeting tumors particularly with high level of PP4C expression.