OBJECTIVES: The aims of this paper were to develop the composite deprivation index (CDI) for the sub-district (Eup-Myen-Dong) levels based on the theory of social exclusion and to explore the relationship between the CDI and the standardized mortality ratio (SMR). METHODS: The paper calculated the age adjusted SMR and we included five dimensions of social exclusion for CDI; unemployment, poverty, housing, labor and social network. The proxy variables of the five dimensions were the proportion of unemployed males, the percent of recipients receiving National Basic Livelihood Security Act benefits, the proportion of households under the minimum housing standard, the proportion of people with a low social class and the proportion of single-parent household. All the variables were standardized using geometric transformation and then we summed up them for a single index. The paper utilized the 2004-2006 National Death Registry data, the 2003-2006 national residents' registration data, the 2005 Population Census data and the 2005-2006 means-tested benefit recipients' data. RESULTS: The figures were 115.6, 105.8 and 105.1 for the CDI of metropolitan areas (big cities), middle size cities and rural areas, respectively. The distributional variation of the CDI was the highest in metropolitan areas (8.9 - 353.7) and the lowest was in the rural areas (26.8 - 209.7). The extent and relative differences of deprivation increased with urbanization. Compared to the Townsend and Carstairs index, the CDI better represented the characteristics of rural deprivation. The correlation with the SMR was statistically significant and the direction of the CDI effects on the SMR was in accordance with that of the previous studies. CONCLUSIONS: The study findings indicated mortality inequalities due to the difference in the CDI. Despite the attempt to improve deprivation measures, further research is warranted for the consensus development of a deprivation index.
Humans ; Logistic Models ; Male ; *Mortality ; *Prejudice ; *Psychosocial Deprivation ; Republic of Korea ; Social Class ; Social Justice ; Socioeconomic Factors ; Statistics as Topic

OBJECTIVES: This study estimated the annual socioeconomic costs of food-borne disease in 2008 from a societal perspective and using a cost-of-illness method. METHODS: Our model employed a comprehensive set of diagnostic disease codes to define food-borne diseases with using the Korea National Health Insurance (KNHI) reimbursement data. This study classified the food borne illness as three types of symptoms according to the severity of the illness: mild, moderate, severe. In addition to the traditional method of assessing the cost-of-illness, the study included measures to account for the lost quality of life. We estimated the cost of the lost quality of life using quality-adjusted life years and a visual analog scale. The direct cost included medical and medication costs, and the non-medical costs included transportation costs, caregiver's cost and administration costs. The lost productivity costs included lost workdays due to illness and lost earnings due to premature death. RESULTS: The study found the estimated annual socioeconomic costs of food-borne disease in 2008 were 954.9 billion won (735.3 billion won-996.9 billion won). The medical cost was 73.4 - 76.8% of the cost, the lost productivity cost was 22.6% and the cost of the lost quality of life was 26.0%. CONCLUSIONS: Most of the cost-of-illness studies are known to have underestimated the actual socioeconomic costs of the subjects, and these studies excluded many important social costs, such as the value of pain, suffering and functional disability. The study addressed the uncertainty related to estimating the socioeconomic costs of food-borne disease as well as the updated cost estimates. Our estimates could contribute to develop and evaluate policies for food-borne disease.
*Cost of Illness ; Costs and Cost Analysis ; Efficiency ; Foodborne Diseases/*economics ; Health Services/economics/utilization ; Humans ; *Models, Economic ; *Quality-Adjusted Life Years ; Republic of Korea ; Severity of Illness Index ; Socioeconomic Factors

Cell replacement therapy using neural progenitor cells (NPCs) following ischemic stroke is a promising potential therapeutic strategy, but lacks efficacy for human central nervous system (CNS) therapeutics. In a previous in vitro study, we reported that the overexpression of human arginine decarboxylase (ADC) genes by a retroviral plasmid vector promoted the neuronal differentiation of mouse NPCs. In the present study, we focused on the cellular mechanism underlying cell proliferation and differentiation following ischemic injury, and the therapeutic feasibility of NPCs overexpressing ADC genes (ADC-NPCs) following ischemic stroke. To mimic cerebral ischemia in vitro , we subjected the NPCs to oxygen-glucose deprivation (OGD). The overexpressing ADC-NPCs were differentiated by neural lineage, which was related to excessive intracellular calcium-mediated cell cycle arrest and phosphorylation in the ERK1/2, CREB, and STAT1 signaling cascade following ischemic injury. Moreover, the ADC-NPCs were able to resist mitochondrial membrane potential collapse in the increasingly excessive intracellular calcium environment. Subsequently, transplanted ADC-NPCs suppressed infarct volume, and promoted neural differentiation, synapse formation, and motor behavior performance in an in vivo tMCAO rat model. The results suggest that ADC-NPCs are potentially useful for cell replacement therapy following ischemic stroke.
Animals ; Arginine ; Brain Ischemia ; Calcium ; Cell Cycle Checkpoints ; Cell Proliferation ; Central Nervous System ; Humans ; In Vitro Techniques ; Membrane Potential, Mitochondrial ; Mice ; Models, Animal ; Neurons ; Phosphorylation ; Plasmids ; Stem Cells ; Stroke ; Synapses ; Zidovudine

Cerebral toxoplasmosis is often life-threatening in an immunocompromised patient due to delayed diagnosis and treatment. Several differential diagnoses could be possible only with preoperative brain images of cerebral toxoplasmosis which show multiple rim-enhancing lesions. Due to the rarity of cerebral toxoplasmosis cases in Korea, the diagnosis and treatment are often delayed. This paper concerns a male patient whose cerebral toxoplasmosis was activated 21 years post kidney transplantation. Brain open biopsy was decided to make an exact diagnosis. Cerebral toxoplasmosis was confirmed by immunohistochemistry and PCR analyses of the tissue samples. Although cerebral toxoplasmosis was under control with medication, the patient did not recover clinically and died due to sepsis and recurrent gastrointestinal bleeding.

Background and Objectives: Air pollution, particularly particulate matter (PM), has a variety of adverse effects on human health. PM is known to induce cell death through various pathways, including pyroptosis. Despite its significance, research on PM-induced pyroptosis in nasal epithelial cells remains limited. This study aimed to explore PM-induced pyroptosis in cultured human nasal epithelial cells. Methods: For the in vitro experiments, human nasal epithelial cells were cultured. Cell viability was assessed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, while cell death was evaluated through propidium iodide (PI) staining and lactate dehydrogenase (LDH) release measurement. Protein expression levels related to pyroptosis were examined via western blot using antibodies against NOD-like receptor family, pyrin domain containing 3 (NLRP3), cleaved caspase-1 (CASP1 P20), gasdermin D (GSDMD)-N, and glyceraldehyde phosphate dehydrogenase. Immunofluorescent staining with a CASP1 P20 antibody was conducted to visualize cellular localization. Enzyme-linked immunosorbent assay was utilized to quantify interleukin (IL)-1β and IL-18 protein levels. Results: Treatment with PM resulted in decreased cell viability, elevated LDH release, and intensified PI staining, indicating cell death. Pyroptosis was confirmed by the elevated expression of NLRP3, CASP1 P20, and GSDMD-N, along with increased levels of IL-1β and IL-18. Inhibiting the NLRP3 inflammasome with MCC950 reduced the PM-induced effects on protein expression and cytokine release, highlighting the role of the NLRP3 inflammasome in PM-triggered pyroptosis in human nasal epithelial cells. Conclusion We showed that PM triggers pyroptosis in human nasal epithelial cells, driven by NLRP3 inflammasome-dependent signaling pathways.

Mycobacterium abscessus has been identified as an emerging pulmonary pathogen in humans. Previously, it was documented that a spontaneously formed rough variant of M. abscessus causes persistent and invasive infection in mice, while a smooth isogenic variant does not. However, little is known for immune responses elicited by M. abscessus variants artificially induced by culture conditions and their culture filtrate antigens. Thus, morphological variants of M. abscessus type strain (ATCC19977T) were generated by an acidic and low oxygen culture conditions. Overall comparison between the variant and its original smooth strain showed that the rough variant was less virulent than original smooth strain in murine bone-marrow derived macrophage. To understand the basis for the difference, the protein expression pattern in the culture filtrates of each strain was analyzed by 1-dimensional electrophoresis. Generally, the protein expressions were more influenced by pH conditions than oxygen pressures. Interestingly, several proteins, mainly lower than 30 kDa molecular weight, were uniquely expressed in normal culture conditions. In contrast, several high molecular weight proteins (>55 kDa) were induced by acidic and low oxygen culture conditions. These findings not only provide new insights of association between morphological change and the virulence, but may also be useful in the design of immunological diagnosis and vaccines for M. abscessus infection.
Animals ; Electrophoresis ; Humans ; Hydrogen-Ion Concentration ; Immunologic Tests ; Macrophages ; Mice ; Molecular Weight ; Mycobacterium ; Oxygen ; Proteins ; Sprains and Strains ; Vaccines

We report a case of a 61-year-old man who presented with a cough and abdominal discomfort. CT scan of the chest showed two lesions across both lungs, and an abdominal CT scan revealed multiple hypodense lesions in the spleen with cystic lesions on the splenic hilum. Upper gastrointestinal tract endoscopy found creamy yellowish discharge through a fistula between the stomach and splenic hilum. Under fluoroscopic guidance, forceps was inserted into the fistula tract, and forcep biopsy was done. The pathology was consistent with tuberculosis, and a nine-month anti-tuberculosis medication regimen was started. Imaging performed three months after finishing medication indicated improvement of splenic lesions, and the gastro-splenic tract was sealed off. This case is a very rare clinical example of secondary splenic tuberculosis with a gastro-splenic fistula formation in an immunocompetent patient.
Antitubercular Agents/therapeutic use ; Fluoroscopy ; Gastric Fistula/pathology ; Gastroscopy ; Humans ; Male ; Middle Aged ; Spleen/diagnostic imaging/pathology ; Splenic Diseases/*diagnosis/diagnostic imaging/pathology ; Tomography, X-Ray Computed ; Tuberculosis, Splenic/*diagnosis/drug therapy/microbiology ; Ultrasonography

BACKGROUND: In spite of the improvement in the quality of artificial heart valves and surgical techniques, the incidence of the complications following valve replacement is still high. We reviewed the clinical results of the valve replacements performed in Korean University Anam Hospital during the last 26 years. MATERIAL AND METHOD: The data of 571 patients who received valve replacement between December 1976 and December 2003 were reviewed. RESULT: There were 304 cases of MVR which was the most common procedure performed. There were 122 cases of AVR, and 111 cases of AVR with MVR. Among the 47 patients who received redo operation 38 cases were redo cases including 31 cases of MVR. 32.5% of the patients who had tissue valve replacement had second valve replacement with 10.2+/-3.9 years interval. 24.3% (139/571) of the patients developed valve related complications and cerebral infarction was the highest in frequency. Atrial fibrillation was related with increased complication rates and the mechanical valve replaced group had higher hemorrhagic complication rate than tissue valve replaced group. The operative mortality was 3.68% and the most common cause of the failure was low output syndrome. The operative mortality was higher in the patient group who had valve replacement before the year 1990. The patient group who had mechanical valve replacement had higher operative mortality rate than the tissue valve group. The 5-year survival rate was 92.2% and 10 year survival rate was 85.7%. CONCLUSION: The operative mortality of valve replacement has been improved. The mechnical valve replaced patients had higher hemorrhagic complication rate than the tissue valve replaced patients and more tissue valve replaced patients received redo valve replacement.
Atrial Fibrillation ; Cerebral Infarction ; Heart Valve Diseases ; Heart Valves* ; Heart* ; Heart, Artificial ; Humans ; Incidence ; Mortality ; Survival Rate

Far-infrared rays (FIR) are known to have various effects on atoms and molecular structures within cells owing to their radiation and vibration frequencies. The present study examined the effects of FIR on gene expression related to glucose transport through microarray analysis in rat skeletal muscle cells, as well as on mitochondrial biogenesis, at high and low glucose conditions. FIR were emitted from a bio-active material coated fabric (BMCF). L6 cells were treated with 30% BMCF for 24 h in medium containing 25 or 5.5 mM glucose, and changes in the expression of glucose transporter genes were determined. The expression of GLUT3 (Slc2a3) increased 2.0-fold (p < 0.05) under 5.5 mM glucose and 30% BMCF. In addition, mitochondrial oxygen consumption and membrane potential (ΔΨm) increased 1.5- and 3.4-fold (p < 0.05 and p < 0.001), respectively, but no significant change in expression of Pgc-1a, a regulator of mitochondrial biogenesis, was observed in 24 h. To analyze the relationship between GLUT3 expression and mitochondrial biogenesis under FIR, GLUT3 was down-modulated by siRNA for 72 h. As a result, the ΔΨm of the GLUT3 siRNA-treated cells increased 3.0-fold (p < 0.001), whereas that of the control group increased 4.6-fold (p < 0.001). Moreover, Pgc-1a expression increased upon 30% BMCF treatment for 72 h; an effect that was more pronounced in the presence of GLUT3. These results suggest that FIR may hold therapeutic potential for improving glucose metabolism and mitochondrial function in metabolic diseases associated with insufficient glucose supply, such as type 2 diabetes.

Far-infrared rays (FIR) are known to have various effects on atoms and molecular structures within cells owing to their radiation and vibration frequencies. The present study examined the effects of FIR on gene expression related to glucose transport through microarray analysis in rat skeletal muscle cells, as well as on mitochondrial biogenesis, at high and low glucose conditions. FIR were emitted from a bio-active material coated fabric (BMCF). L6 cells were treated with 30% BMCF for 24 h in medium containing 25 or 5.5 mM glucose, and changes in the expression of glucose transporter genes were determined. The expression of GLUT3 (Slc2a3) increased 2.0-fold (p < 0.05) under 5.5 mM glucose and 30% BMCF. In addition, mitochondrial oxygen consumption and membrane potential (ΔΨm) increased 1.5- and 3.4-fold (p < 0.05 and p < 0.001), respectively, but no significant change in expression of Pgc-1a, a regulator of mitochondrial biogenesis, was observed in 24 h. To analyze the relationship between GLUT3 expression and mitochondrial biogenesis under FIR, GLUT3 was down-modulated by siRNA for 72 h. As a result, the ΔΨm of the GLUT3 siRNA-treated cells increased 3.0-fold (p < 0.001), whereas that of the control group increased 4.6-fold (p < 0.001). Moreover, Pgc-1a expression increased upon 30% BMCF treatment for 72 h; an effect that was more pronounced in the presence of GLUT3. These results suggest that FIR may hold therapeutic potential for improving glucose metabolism and mitochondrial function in metabolic diseases associated with insufficient glucose supply, such as type 2 diabetes.