Biomedical subjects

Su Young Kim

Publications and source records attributed to Su Young Kim.

At least 19 recordsLinked to original sources

PubMed2007

Economic cost of dementia patients according to the limitation of the activities of daily living in Korea.

BACKGROUND: Dementia is expected to become a significant social burden in the future. However, there are few reports that have estimated the total economic cost of dementia, particularly according to the limitation in the activities of daily living (ADL) in Korea. OBJECTIVES: This study is to analyze the health care expenditures and cost per dementia patient, and estimated the total economic cost of dementia. METHODS: Caregivers of 609 dementia patients, who were randomly selected from a nationwide claim database of the Korean National Health Insurance Corporation, were interviewed using structured questionnaire in the period of September 2005. The total cost including the direct and indirect costs during a year was calculated. The patients were stratified into three limitation groups according to their ADL score. The cost according to the three limitation groups was analyzed. The national cost of dementia patients was then estimated. RESULTS: The total cost per dementia patient in Korea was $7,462. The direct and indirect costs were $6,626 and $836 per patient, respectively. The cost increased with increasing degree of limitation in the patient's ADL. Over a 1-year period, the total cost per patient in the low limitation group was lower ($3,698) than that of the moderate ($6,064) and high ($11,428) limitation group. CONCLUSIONS: This study demonstrates that the direct and indirect costs of dementia are considerately small for patients with lower limitation in their ADL. The total economic cost of dementia per year was estimated to be in the range of 1.3 to 3.3 billion dollars on assumptions in Korea.

Activities of Daily Living↗

PubMed2007

An ROC study of chest radiographs: 2K Versus 4K high-resolution soft-copy images.

Computed radiography of chest with a 4K image array was recently introduced. We performed a multiobserver study to compare the diagnostic accuracy of 2K (standard) and 4K (high quality) chest radiographs displayed on a 5-mega-pixel monitor (2K monitor). One hundred cases of posteroanterior chest radiographs (a total of 200 images) were selected by two chest radiologists. Those radiographs included pneumothorax (n = 14), nodules (n = 15), interstitial disease (n = 10), or neither abnormality (n = 61). These were interpreted by four radiologists in two separate sessions. They recorded their confidence scale for the presence or absence of abnormality. Diagnostic accuracy was determined by receiver operating characteristic (ROC) analysis for each observer. ROC analysis showed no statistically significant difference between the 2K and 4K modes for the detection of any of the different abnormalities by individual readers. Our preliminary study suggests that 2K mode would be sufficient for the detection of abnormality on chest radiograph and there is no considerable validity to incline toward the 4K mode in current picture archiving and communication system environment using 2K monitor. However, we think that additional investigation using more subtle parenchymal or rib lesion should be followed.

Humans↗

PubMed2006

Altered expression of the KLF4 in colorectal cancers.

KLF4 is an important regulator of cell proliferation and is maximally expressed in epithelial cells of the gastrointestinal tract. Inactivation of the KLF4 gene by genetic and epigenetic alterations has been reported in colorectal cancers, but the expression pattern of the KLF4 protein has not been studied. Here, to investigate the roles of KLF4 in colorectal carcinogenesis, we examined the expression pattern of the KLF4 protein in 123 colorectal cancers by immunohistochemistry using tissue microarray. Moderate to strong nuclear staining for KLF4 was found in normal colonic mucosa. Interestingly, loss of KLF4 expression was observed in 30 (24.4%) of 123 colorectal cancers. Statistically, loss of KLF4 protein expression was not associated with clinocopathologic parameters, including tumor stage (Bartholomew test, P>0.05), lymph node metastasis, differentiation, tumor location, and tumor size (chi2 test, P>0.05). These results indicate that loss of the KLF4 expression might play a role in tumor development as an early event for a subset of colorectal cancers.

Adenocarcinoma↗

PubMed2006

Genetic and expression analysis of the KCNRG gene in hepatocellular carcinomas.

The potassium channels are ubiquitous multisubunit membrane proteins, and potassium-dependent alterations in the membrane potential play an important role in the proliferation of many types of cells. This study analyzed the mutation, allelic loss and expression patterns of the KCNRG gene in 77 HCCs in order to determine if the KCNRG gene, which encodes the potassium channel regulating protein, is involved in the tumorigenesis of hepatocellular carcinoma (HCC). One KCNRG missense mutation, CGT CAT (Arg His) was found at codon 92 within the T1 domain. Hep3B hepatoma cells were transfected with the wild- or mutant-KCNRG to determine the effect of this mutation in KCNRG. Interestingly, the suppressive cell growth activity of the mutant-type KCNRG was significantly lower than that of the wild-type KCNRG. In addition, allelic loss was detected in 17 out of 64 (26.5%) informative HCC cases, and all were hepatitis B virus (HBV)-positive. Moreover, the allelic loss was closely related to an intrahepatic metastasis (P=0.0247), higher grade (P=0.0078) and clinical stage (P=0.0071). Expression analysis revealed 22 tumor tissues to have a loss of expression of the KCNRG transcript. These results suggest that genetic alterations and the expression of KCNRG might play an important role in the development and/or progression of a subset of HCCs.

Adult↗

PubMed2006

Identification of large-scale molecular changes of Autotaxin(ENPP2) knock-down by small interfering RNA in breast cancer cells.

To understand comprehensive molecular mechanisms by which Autotaxin (ENPP2) mediates, we identified large-scale molecular changes responsible for aberrant expression of Autotaxin (ATX) on breast cancer cells by using DNA microarrays. Transcriptional over-expression of ENPP2 gene was endogenously silenced by using RNA interference technique, and then recapitulated corresponding molecular changes in MDA435 breast cancer cells. Application of nonparametric Wilcoxon statistical analyses (P<0.05) and the selection criteria of 2-fold differential gene expression change resulted in the identification of 368 genes including 133 up-regulated and 235 genes under-expressed in ENPP2-silencing MDA435 cells. Most of the functional categories of identified genes are associated with cellular metabolism, cytoskeleton organization, transcription regulation, signal transduction as well as cellular organization and biogenesis. Our data suggest that the molecular signature identified by the ENPP2-silencing methods may represent potential candidates that can explain the complicated characteristics of ATX and may serve as biomarkers, for the development of molecular-targeting therapy, in human breast cancer.

Breast Neoplasms↗

PubMed2006

Somatic mutations of the ERBB4 kinase domain in human cancers.

The EGFR family consists of 4 receptor tyrosine kinases, EGFR (ERBB1), ERBB2 (HER2), ERBB3 (HER3) and ERBB4 (HER4). Recent reports revealed that the kinase domains of both EGFR (ERBB1) and ERBB2 gene were somatically mutated in human cancers, raising the possibility that the other ERBB members possess somatic mutations in human cancers. Here, we performed mutational analysis of the ERBB4 kinase domain by polymerase chain reaction-single-strand conformation polymorphism assay in 595 cancer tissues from stomach, lung, colon and breast. We detected the ERBB4 somatic mutations in 3 of 180 gastric carcinomas (1.7%), 3 of 104 colorectal carcinomas (2.9%), 5 of 217 nonsmall cell lung cancers (2.3%) and 1 of 94 breast carcinomas (1.1%). The 12 ERBB4 mutations consisted of 1 in-frame duplication mutation and 8 missense mutations in the exons, and 3 mutations in the introns. We simultaneously analyzed the somatic mutations of EGFR, ERBB2, K-RAS, PIK3CA and BRAF genes in the 12 samples with the ERBB4 mutations and found that 1 gastric carcinoma with ERBB4 mutation also harbored K-RAS gene mutation. Our study demonstrated that in addition to EGFR and ERBB2, somatic mutation of the kinase domain of ERBB4 occurs in the common human cancers, and suggested that alterations of ERBB4-mediated signaling pathway by ERBB4 mutations may contribute to the development of human cancers.

Adult↗

PubMed2006

Mutational analysis of the kinase domain of MYLK2 gene in common human cancers.

Genetic alterations of the genes encoding protein kinases have been implicated in the development of human cancers. Myosin light chain kinase 2, skeletal muscle (MYLK2) encodes a calcium/calmodulin-dependent serine/threonine kinase. In a recent study, MYLK2 gene was somatically mutated in colorectal carcinomas. The aim of this study was to explore the possibility that other common human carcinomas besides colorectal carcinomas harbored MYLK2 mutations in the kinase domain. We analyzed exons 6 and 7 eccoding the kinase domain of MYLK2 for somatic mutations in 60 gastric, 104 colorectal, 79 non-small cell lung, and 54 breast cancers using a polymerase chain reaction (PCR)-based single-strand conformation polymorphism (SSCP). We found one MYLK2 mutation in lung adenocarcinomas, but not in other cancers. The MYLK2 mutation detected was a missense mutation that would substitute an amino acid (E374D) However, there was no somatic mutation of the MYLK2 gene. These data suggest that the kinase domain of MYLK2 is rarely mutated in common human carcinomas and that it does not play a dominant role in cancer pathogenesis.

Adult↗

PubMed2006

Somatic mutations of ERBB2 kinase domain in gastric, colorectal, and breast carcinomas.

PURPOSE: Recent reports revealed that the kinase domain of the ERBB2 gene is somatically mutated in lung adenocarcinoma, suggesting the mutated ERBB2 gene as an oncogene in human cancers. However, because previous reports focused the mutational search of ERBB2 primarily on lung cancers, the data on ERBB2 mutations in other types of human cancers have been largely unknown. EXPERIMENTAL DESIGN: Here, we did a mutational analysis of the ERBB2 kinase domain by PCR single-strand conformational polymorphism assay in gastric, colorectal, and breast carcinoma tissues. RESULTS: We detected the ERBB2 kinase domain mutations in 9 of 180 gastric carcinomas (5.0%), in 3 of 104 colorectal carcinomas (2.9%), and in 4 of 94 breast carcinomas (4.3%). All of the detected ERBB2 mutations except for one in-frame deletion mutation were missense mutations. Of the 16 ERBB2 mutations detected, 4 affected Val777 in the exon 20 site, and 3 affected Leu755 in the exon 19 site. We simultaneously analyzed the somatic mutations of EGFR, K-RAS, PIK3CA, and BRAF genes in the 16 samples with ERBB2 mutations, and found that all of the 3 colorectal carcinoma samples with ERBB2 mutations harbored K-RAS mutations. CONCLUSION: This study showed that in addition to lung adenocarcinomas, ERBB2 kinase domain mutation occurs in other common human cancers such as gastric, breast, and colorectal cancers, and suggested that alterations of ERBB2-mediated signaling pathway by ERBB2 mutations alone or together with K-RAS mutations may contribute to the development of human cancers.

Aged↗

PubMed2006