1.A Study on the Relation between Glaucoma and Quality of Life.
Gil Joong YOON ; Doek Bae KIM ; Phl Joong YANG ; Ki Soon KIM
Journal of the Korean Ophthalmological Society 2003;44(2):472-484
PURPOSE: This study was performed to find the relation between glaucoma and the quality of life (QOL). METHODS: The questionnaire survey and ophthalmologic examination was made in 105 glaucoma patients under treatment at ophthalmology clinic of a university hospital and 120 normal persons who had undergone an routine health check-up from June 1st, 2000 and June 30th, 2001. The questionnaire was composed of general characteristics, health-related behavior and the short form-36 health survey for QOL. Using the t-test, analysis of variance (ANOVA), Pearson's correlation analysis and analysis of co-variance (ANCOVA), we examined the relationship between glaucoma and QOL. RESULTS: 1. By t-test or ANOVA various domains of QOL showed statistically significant difference by sex, age, coverage of medical insurance, family history of glaucoma, past history of systemic diseases, educational level, marital status, smoking and drinking status. Visual acuity showed significant positive correlation with QOL and horizontal and vertical cup-to-disk (C/D) ratio showed significant negative correlation with QOL. 2. By ANCOVA to find the association of glaucoma with QOL controlling other related characteristics of subjects, QOL of the glaucoma group showed lower than that of the normal group, but the differences were not statistically significant. CONCLUSIONS: QOL of glaucoma patients was lower than that of normal persons without glaucoma considering sex, age, health insurance system, family history of glaucoma, past history of systemic disease, educational level, marital status, smoking status, drinking status and visual acuity, so further study will be necessary to observe the change of QOL according to progression of glaucoma and treatment status.
Drinking
;
Glaucoma*
;
Health Surveys
;
Humans
;
Insurance
;
Insurance, Health
;
Marital Status
;
Ophthalmology
;
Quality of Life*
;
Surveys and Questionnaires
;
Smoke
;
Smoking
;
Visual Acuity
2.Astrocyte elevated gene-1 overexpression in hepatocellular carcinoma: an independent prognostic factor.
Hae Il JUNG ; Taesung AHN ; Sang Ho BAE ; Jun Chul CHUNG ; Hyungjoo KIM ; Susie CHIN ; Dongjun JEONG ; Hyon Doek CHO ; Moon Soo LEE ; Hyung Chul KIM ; Chang Ho KIM ; Moo Jun BAEK
Annals of Surgical Treatment and Research 2015;88(2):77-85
PURPOSE: Astrocyte elevated gene-1 (AEG-1) plays important roles in tumorigenesis such as proliferation, invasion, metastasis, angiogenesis, and chemoresistance. We examined the expression of AEG-1 in patients with hepatocellular carcinoma (HCC). METHODS: Eighty-five samples were collected from patients with HCC who underwent surgery and were histopathologically confirmed to have HCC. Two independent pathologists, experienced in evaluating immunohistochemistry and blinded to the clinical outcomes of the patients, reviewed all samples. They determined AEG-1 expression semiquantitatively by assessing the percentage of positively stained immunoreactive cells and staining intensity. Clinicopathological data were analyzed in association with prognosis. RESULTS: The association was estimated by univariate and multivariate analyses with Cox regression. Tumor size (hazard ratio [HR], 2.285; 95% confidence interval [CI], 1.175-4.447; P = 0.015), microvascular invasion (HR, 6.754; 95% CI, 1.631-27.965; P = 0.008), and AEG-1 expression (HR, 4.756; 95% CI, 1.697-13.329; P = 0.003) were independent prognostic factors for overall survival. Those for disease-free survival rate were tumor size (HR, 2.245; 95% CI, 1.282-3.933; P = 0.005) and AEG-1 expression (HR, 1.916; 95% CI, 1.035-3.545; P = 0.038). The cumulative 5-year survival and recurrence rates were 89.2% and 50.0% in the low-expressing group and 24.5% and 82.4% in the high-expressing group, respectively. CONCLUSION: The results suggest that AEG-1 overexpression could serve as a valuable prognostic marker in patients with HCC.
Astrocytes*
;
Carcinogenesis
;
Carcinoma, Hepatocellular*
;
Disease-Free Survival
;
Humans
;
Immunohistochemistry
;
Multivariate Analysis
;
Neoplasm Metastasis
;
Prognosis
;
Recurrence
3.The Effect of Metformin Treatment on CRBP-I Level and Cancer Development in the Liver of HBx Transgenic Mice.
Jo Heon KIM ; Md Morshedul ALAM ; Doek Bae PARK ; Moonjae CHO ; Seung Hong LEE ; You Jin JEON ; Dae Yeul YU ; Tae Du KIM ; Ha Young KIM ; Chung Gu CHO ; Dae Ho LEE
The Korean Journal of Physiology and Pharmacology 2013;17(5):455-461
Retinoids regulate not only various cell functions including proliferation and differentiation but also glucose and lipid metabolism. After we observed a marked up-regulation of cellular retinol-binding protein-I (CRBP-I) in the liver of hepatitis B virus x antigen (HBx)-transgenic (HBx Tg) mice which are prone to hepatocellular carcinoma (HCC) and fatty liver, we aimed to evaluate retinoid pathway, including genes for the retinoid physiology, CRBP-I protein expression, and retinoid levels, in the liver of HBx Tg mice. We also assessed the effect of chronic metformin treatment on HCC development in the mice. Many genes involved in hepatic retinoid physiology, including CRBP-I, were altered and the tissue levels of retinol and all-trans retinoic acid (ATRA) were elevated in the liver of HBx Tg mice compared to those of wild type (WT) control mice. CRBP-I protein expression in liver, but not in white adipose tissue, of HBx Tg mice was significantly elevated compared to WT control mice while CRBP-I protein expressions in the liver and WAT of high-fat fed obese and db/db mice were comparable to WT control mice. Chronic treatment of HBx Tg mice with metformin did not affect the incidence of HCC, but slightly increased hepatic CRBP-I level. In conclusion, hepatic CRBP-I level was markedly up-regulated in HCC-prone HBx Tg mice and neither hepatic CRBP-I nor the development of HCC was suppressed by metformin treatment.
Adipose Tissue, White
;
Animals
;
Carcinoma, Hepatocellular*
;
Fatty Liver
;
Hepatitis B virus
;
Incidence
;
Lipid Metabolism
;
Liver*
;
Metformin*
;
Mice
;
Mice, Transgenic*
;
Retinoids
;
Retinol-Binding Proteins, Cellular*
;
Trans-Activators
;
Tretinoin
;
Up-Regulation
;
Vitamin A