• Radiation Oncology Journal
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• v.29 no.3
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• pp.191-198
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• 2011

Purpose: Although the role of squamous cell carcinoma antigen (SCC-Ag) as a predictive and prognostic factor for uterine cervical cancer has been identified in previous studies, 1) the effective patient group of screening for recurrence with SCC-Ag, 2) the relationship between SCC-Ag and recurrence site, and 3) the relationship between the change of SCC-Ag and treatment outcome or recurrence have not been described. Materials and Methods: The study included 506 patients with histologically proven uterine cervical cancer between January 1994 and December 2010. We determining the serum SCC-Ag level before treatment and after treatment, and conducted a retrospective review of the patients' records. We evaluated the sensitivity and specificity of SCC-Ag for the detection of tumor recurrence by comparing biochemical recurrence with clinical recurrence. Results: The pretreatment SCC-Ag level and the proportion of patients over 1.5 ng/mL were higher in poor prognostic patient group. In the univariate and multivariate analysis, pretreatment SCC-Ag showed a statistically significant correlation with tumor size, International Federation of Gynecology and Obstetrics (FIGO) stage, pathology. In patients with biochemical recurrence vs. those without, 5-year DFS and OS were 27.6 vs. 92.7% (p ${\leq}$ 0.001) and 53.7 vs. 92.5% (p ${\leq}$ 0.001), respectively. Conclusion: Our study reconfirmed the known function of pretreatment SCC-Ag, but could not confirm the function of biochemical response as a predictive factor for treatment and as a prognostic factor. There was no statistically significant relationship between SCC-Ag level and recurrence site. We confirmed the role of SCC-Ag as a follow-up tool for recurrence of disease and which patient groups SCC-Ag was more useful for.

• Journal of Korean Academy of Nursing
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• v.21 no.3
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• pp.365-382
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• 1991

This study was designed to measure the physical, mental-emotional and social health status of elderlies according to rural areas, medium - small cities, and large city environment. Data collection was done from July 18 to August 17 1990. The subjects were a convenience sample after their place of residence was stratified into large, medium- small cities and rural areas. Those who attended elderly centers in Seodaemun, Mapo, and Kangnam districts in Seoul were considered to be residents of a large city and interviewed by trained research assistants and student nurses. Elderlies living in Chungju, Jinju, Chuncheon, and Jeonju cities were coded as residents of medium-small cities and were interviewed by professors of nursing colleges. Rural residents were interviewed by the community health practioners working in community health clinics in North and South Kyongsang, North and South Jeolla, and Kyonggi provinces. The tool used in this study was the health assessment tool developed by Choi, Young Hee in 1990. This tool was organized into 20 physical health status, 17 mental - emotional health status, and 37 social health ststus items. Physical health status items consisted of six factors - personal hygiene activity ability, external activity utilizing traffic, mass media, and spare time ability, sexual ability, digestive system related ability, sexual ability, sensory ability, and elimination ability. Mental - emotional health status items consisted of two factors - mental health factor and emotional health factor. Social health status items consisted of seven factors -grandparental role ability, parental role ability, spoused role ability, friendship role ability, kinship role ability, group member role ability, and religious believer role ability. Data Analysis included frequencies, percentage, mean, standard deviation, ANOVA, and chi - square test. The results of the analysis are as follows : 1. The mean physical health status score for large city residents was 4.1132, for rural residents 4.0787, and for medium and small city residents 3.9565. There were significant differences according to residential area for personal hygiene activity ability, external activity ability, sexual ability, and digestive system related ability items 2. The mean mental -emotional health status score for rural residents was 3.8291, for medium and small city residents 3.7967, and for large city residents 3.7807. There was a significant difference according to residential area in the mental health ability item. 3. The mean social health status score for medium and small city residents was 3.0000, for rural residents 2.9362, and for large city residents 2.8960. There were significant differences according to residential area for kinship role ability and religious believer role ability items. The following conclusion was derived from the above results 1. The physical health status of elderlies residing in medium - small cities and in rural areas was lower than that of those residing in Seoul, a large urban area. Therefore, more medical facilities are needed in rural area so as to monitor their health, prevent disease, and promote their health. 2. The mental -emotional ststus and social health status of elderlies residing in the large city were lower than that of those residing in medium - small cities and rural areas. This may reflect weakening of the strong traditional family bond that may happen with urbanization. Continued support for elderly parents is essential and education should emphasize the traditional cultural norm and value of filial piety. 3. Facilities and programs for elderly are needed so that they may spend their time more valuably in their urban environment.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.11
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• pp.5767-5772
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• 2012

Introduction: Identification of simple and measurable prognostic factors is an important issue in treatment evaluation of breast cancer. The present study was conducted to evaluate the prognostic role of vascular invasion in lymph node negative breast cancer patients. Methods: in a retrospective design, we analyzed the recorded profiles of the 1,640 patients treated in the breast cancer department of Motahari clinic affiliated to Shiraz University of Medical Sciences, Shiraz, Iran, from January 1999 to December 2012. Overall and adjusted survivals were evaluated by the Cox proportional hazard model. All the hypotheses were considered two-sided and a p-value of 0.05 or less was considered as statistically significant. Results: Mean age in lymph node negative and positive patients was 50.0 and 49.8 respectively. In lymph node negative patients, the number of nodes, tumor size, lymphatic invasion, vascular invasion, progesterone receptor, and nuclear grade were significant predictors. In lymph node and lymphatic negative patients, vascular invasion also played a significant prognostic role in the survival which was not evident in lymph node negative patients with lymphatic invasion. Discussion: The results of our large cohort study, with long term follow up and using multivariate Cox proportional model and comparative design showed a significant prognostic role of vascular invasion in early breast cancer patients. Vascular invasion as an independent prognostic factor in lymph node negative invasive breast cancer.

• Tuberculosis and Respiratory Diseases
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• v.69 no.5
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• pp.337-347
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• 2010

Background: Transglutaminase-2 (TG-2) has been reported to play an important role in the process of fibrosis. However, TG-2 studies on fibroproliferation of acute lung injury (ALI) are absent. The purpose of this study was to investigate the role of TG-2 in the fibroproliferation of lipopolysaccharide (LPS)-induced ALI. Methods: The male C57BL/6 mice of 5 weeks age were divided into 3 groups; control group (n=30) in which $50{\mu}L$ of saline was given intratracheally (IT), LPS group (n=30) in which LPS 0.5 mg/kg/$50{\mu}L$ of saline was given IT, and LPS+Cyst group treated with intraperitoneal 200 mg/kg of cystamine, competitive inhibitor of TG-2, after induction of ALI by LPS. TG-2 activity and nuclear factor $(NF)-{\kappa}B$ were measured in lung tissue homogenate. Tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-$1{\beta}$, IL-6, myeloperoxidase (MPO), and transforming growth factor (TGF)-${\beta}1$ were measured using bronchoalveolar lavage fluids. Histopathologic ALI score and Mallory's phosphotunistic acid hematoxylin (PTAH) for collagen and fibronectin deposition were performed. Results: The TG-2 activities in the LPS group were significantly higher than the control and LPS+Cyst groups (p<0.05). The TNF-${\alpha}$ and IL-$1{\beta}$ concentrations and $NF-{\kappa}B$ activity were lower in the LPS+Cyst group than the LPS group (p<0.05). The LPS+Cyst group showed lower MPO, ALI score, TGF-${\beta}1$ concentration, and Mallory's PTAH stain than the LPS group, but the differences were not significant (p>0.05). Conclusion: Inhibition of TG-2 activity in the LPS-induced ALI prevented early inflammatory parameters, but had limited effects on late ALI and fibroproliferative parameters.

• BMB Reports
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• v.39 no.5
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• pp.469-478
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• 2006

Vascular endothelial growth factor (VEGF)-A, a major regulator for angiogenesis, binds and activates two tyrosine kinase receptors, VEGFR1 (Flt-1) and VEGFR2 (KDR/Flk-1). These receptors regulate physiological as well as pathological angiogenesis. VEGFR2 has strong tyrosine kinase activity, and transduces the major signals for angiogenesis. However, unlike other representative tyrosine kinase receptors which use the Ras pathway, VEGFR2 mostly uses the Phospholipase-$C{\gamma}$-Protein kinase-C pathway to activate MAP-kinase and DNA synthesis. VEGFR2 is a direct signal transducer for pathological angiogenesis including cancer and diabetic retinopathy, thus, VEGFR2 itself and the signaling appear to be critical targets for the suppression of these diseases. VEGFR1 plays dual role, a negative role in angiogenesis in the embryo most likely by trapping VEGF-A, and a positive role in adulthood in a tyrosine kinase-dependent manner. VEGFR1 is expressed not only in endothelial cells but also in macrophage-lineage cells, and promotes tumor growth, metastasis, and inflammation. Furthermore, a soluble form of VEGFR1 was found to be present at abnormally high levels in the serum of preeclampsia patients, and induces proteinurea and renal dysfunction. Therefore, VEGFR1 is also an important target in the treatment of human diseases. Recently, the VEGFR2-specific ligand VEGF-E (Orf-VEGF) was extensively characterized. Interestingly, the activation of VEGFR2 via VEGF-E in vivo results in a strong angiogenic response in mice with minor side effects such as inflammation compared with VEGF-A, suggesting VEGF-E to be a novel material for pro-angiogenic therapy.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.15 no.1
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• pp.44-51
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• 2012

Purpose: Tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) polymorphism has been suggested to play an important role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) in obese adults, and known to be a mediator of insulin resistance. In this study, we evaluated the role of TNF-${\alpha}$ promoter polymorphisms and insulin resistance in the development of NAFLD in obese children. Methods: A total of 111 obese children (M:F=74:37; mean age, $11.1{\pm}2.0$ yrs) were included. The children were divided into 3 groups: controls (group I, n=61), children with simple steatosis (group II, n=17), and children with non-alcoholic steatohepatitis (group III, n=33). Serum TNF-${\alpha}$ levels, homeostasis model assessment of insulin resistance (HOMA-IR), and TNF-${\alpha}$ -308 and -238 polymorphisms were evaluated. Results: There were no differences in TNF-${\alpha}$ polymorphism at the -308 or the -238 loci between group I and group II + III ($p$=0.134 and $p$=0.133). The medians of HOMA-IR were significantly different between group I and group II + III ($p$=0.001), with significant difference between group II and group III ($p$=0.007). No difference was observed in the HOMA-IR among the genotypes at the -308 locus ($p$=0.061) or the -238 locus ($p$=0.207) in obese children. Conclusion: TNF-${\alpha}$ promoter polymorphisms at the -308 and -238 loci were not significantly associated with the development of NAFLD in children; nevertheless, insulin resistance remains a likely essential factor in the pathogenesis of NAFLD in obese children, especially in the progression to NASH.

• Journal of the Korean Applied Science and Technology
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• v.35 no.2
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• pp.509-518
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• 2018

The purpose of this study was myokine product and role with physical activity and literature review. There is accumulating epidemiological evidence that a physically active life plays an independent role in the protection against type 2 diabetes, cardiovascular disease, colon cancer, dementia and even depression. And myokine has been regarded an important factor of exercise training and brain growth factor for the prevention of Alzheimier's disease. During exercise the release of anti-inflammatory myokine from contracting muscle controled the metabolic response, and IL-4, IL-6, IL-7, IL-10, and IL-15 controled muscle hypertrophy, myogenesis and angiogenenesis. IL-6 promoted the lipid metabolism through AMPK activation. IL-1Ra, IL-10 and sTNF-R inhibited $TNF-{\alpha}$ as the pro-inflammatory cytokine. IL-15 increased the releasing volume from contracting muscle, and promoted the anabolic factor of muscle growth. IL-7 and IL-8 activated the angiogenesis through the more activation of C-X-C receptor signal transmission.

• The Korean Journal of Physiology and Pharmacology
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• v.2 no.4
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• pp.479-491
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• 1998

In order to know the pathogenesis of adult respiratory distress syndrome (ARDS) in association with the oxidative stress by neutrophils, the role of platelet activating factor (1-0-alkyl-2-acetyl-snglycero-3-phosphocholine, PAF) was investigated during acute lung injury induced by interleukin- $1{\alpha}$ (IL-1) in rats. An insufflation of IL-1 into the rat's trachea increased the acetyltransferase activity in the lung and the increase of PAF content was followed. As evidences of acute lung injury by neutrophilic respiratory burst, lung leak index, myeloperoxidase activity, numbers of neutrophils in the bronchoalveolar lavage fluid, neutrophilic adhesions to endothelial cells and NBT positive neutrophils were increased after IL-1 treatment. In addition, a direct instillation of PAF into the trachea caused acute lung leak and the experimental results showed a similar pattern in comparison with IL-1 induced acute lung injury. For the confirmation of oxidative stress during acute lung leak by IL-1 and PAF, a histochemical electron microscopy was performed. In IL-1 and PAF treated lungs of rats, the deposits of cerrous perhydroxide were found. To elucidate the role of PAF, an intravenous injection of PAF receptor antagonist, WEB 2086 was given immediately after IL-1 or PAF treatment. WEB 2086 decreased the production of hydrogen peroxide and the acute lung leak. In ultrastructural study, WEB 2086 mitigated the pathological changes induced by IL-1 or PAF. The nuclear factor kappa B (NFkB) was activated by PAF and this activation was inhibited by WEB 2086 almost completely. Based on these experimental results, it is suggested that the PAF produced in response to IL-1 through the remodeling pathway has the major role for acute lung injury by neutrophilic respiratory burst. In an additional experiment, we can also come to conclude that the activation of the NFkB by PAF is thought to be the fundamental mechanism to initiate the oxidative stress by neutrophils causing release of proinflammatory cytokines and activation of phospholipase $A_2$.

• Molecules and Cells
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• v.20 no.2
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• pp.263-270
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• 2005

Transactivation of EGF-receptor (EGFR) by G-protein coupled receptors (GPCRs) is emerging as an important pathway in cell proliferation, which plays a crucial role in the development of atherosclerotic lesion. Angiotensin II (Ang II) has been identified to have a major role in the formation of atherosclerotic lesions, although the underlying mechanisms remain largely unclear. We hypothesize that Ang II promotes the proliferation and migration of smooth muscle cells through the release of heparin-binding epidermal growth factor like growth factor (HB-EGF), transactivation of EGFR and activation of Akt and Erk 1/2, with matrix metalloproteases (MMPs) playing a dispensable role. Primary rat aortic smooth muscle cells were used in this study. Smooth muscle cells rendered quiescent by serum deprivation for 12 h were treated with Ang II (100 nM) in the presence of either GM6001 ($20{\mu}M$), a specific inhibitor of MMPs or AG1478 ($10{\mu}M$), an inhibitor of EGFR. The levels of phosphorylation of EGFR, Akt and Erk 1/2 were assessed in the cell lysates. Inhibition of MMPs by GM6001 significantly attenuated Ang II-stimulated phosphorylation of EGFR, suggesting that MMPs may be involved in the transactivation of EGFR by Ang II receptor. Furthermore Ang II-stimulated proliferation and migration of smooth muscle cells were significantly blunted by inhibiting MMPs and EGFR and applying HB-EGF neutralization antibody, indicating that MMPs, HB-EGF and EGFR activation is necessary for Ang-II stimulated migration and proliferation of smooth muscle cells. Our results suggest that inhibition of MMPs may represent one of the strategies to counter the mitogenic and motogenic effects of Ang II on smooth muscle cells and thereby prevent the formation and development of atherosclerotic lesions.

• Biomolecules & Therapeutics
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• v.28 no.5
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• pp.405-413
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• 2020

Fibroblast-like synoviocytes (FLS) play a crucial role in initiating rheumatoid arthritis. B-cell activating factor (BAFF) plays a role in FLS survival as well as in B cell maturation and maintenance. Here, we investigated whether tumor necrosis factor (TNF)-α-induced BAFF expression controls FLS migration and whether BAFF expression in FLS could be regulated by KR33426 which is the inhibitor of BAFF binding to BAFF receptors (BAFF-R) by using MH7A synovial cells transfected with the SV40 T antigen. More TNF-α-treated cells migrated compared to the control. TNF-α increased BAFF expression in FLS, significantly. FLS migration was inhibited by the transfection with BAFF-siRNA. KR33426 also inhibited BAFF expression increased by TNF-α treatment in FLS as judged by western blotting, PCR, and transcriptional activity assay. Kinases including JNK, p38 and Erk were activated by TNF-α treatment. While JNK and p38 were inhibited by KR33426 treatment, no changes in Erk were observed. Transcription factors including p65, c-Fos, CREB and SP1 were enhanced by TNF-α treatment. Among them, c-Fos was inhibited by KR33426 treatment. Small interference(si)-RNA of c-fos decreased BAFF transcriptional activity. FLS migration induced by TNF-α was inhibited by the transfection with BAFF-siRNA. KR33426 increased Twist, Snail, Cadherin-11 and N-Cadherin. In contrast, KR33426 decreased E-cadherin and TNF-α-enhanced CCL2. Taken together, our results demonstrate that synovial cell migration via CCL2 expression could be regulated by BAFF expression which is decreased by KR33426 and c-Fos-siRNA. It suggests for the first time that the role of BAFF-siRNA on FLS migration might be matched in the effect of KR33426 on BAFF expression.