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So-Young Kim

Publications and source records attributed to So-Young Kim.

At least 19 recordsLinked to original sources
PubMed2008

Extreme thrombocytosis associated with transient myeloproliferative disorder with Down Syndrome with t(11;17)(q13;q21).

A female patient with Down Syndrome (DS) had neonatal thrombocytosis with platelet counts exceeding 2,000 x 10(3)/microL and transient myeloproliferative disorder (TMD). Platelet counts remained elevated the first 2 months of life. A translocation located between chromosomes 17 and 11 was observed. We describe a patient with thrombocytosis and TMD showing an 11q13 translocation. The leukocytosis and thrombocytosis improved after an exchange transfusion.

Chromosomes, Human, Pair 11↗
PubMed2006

Application of far-infrared irradiation in the manufacturing process of green tea.

Seven kinds of green tea leaves were manufactured with far-infrared (FIR) irradiation, and the physicochemical characteristics of the green tea were determined. Appropriate FIR irradiation during the manufacturing process significantly increased the polyphenolic content of green tea. FIR irradiation at 90 degrees C for 10 min, replacing the roasting step, and of the fully processed green tea leaves (GTP3) increased the total phenol content of green tea from 475.6 to 811.1 mg/g and the total flavanol content from 175.7 to 208.7 mg/g, as compared to the control. Epigallocatechin and epigallocatechin gallate increased from 57.68 and 9.60 mg/g in a nonirradiated control to 89.88 and 16.33 mg/g in GTP3, respectively. Ascorbic acid, caffeine, and nitrite scavenging activities were also increased in GTP3. However, the overall color change of GTP3 was negligible. These results indicate that the chemical properties of green tea are significantly affected by FIR irradiation at specific stages of the manufacturing process of green tea leaves and that this FIR irradiation results in high-quality green tea.

Ascorbic Acid↗
PubMed2006

Dibutyryl cAMP stimulates the proliferation of SH-SY5Y human neuroblastoma cells by up-regulating Skp2 protein.

PURPOSE: We previously found that the proliferation of SH-SY5Y neuroblastoma cells is stimulated when cAMP is up-regulated by stable expression of stimulatory G protein. Therefore, this study was performed to investigate the mechanism whereby cAMP stimulates the proliferation of SH-SY5Y cells. METHODS: To investigate the effect of cAMP on cellular proliferation, SH-SY5Y neuroblastoma cells were treated with dibutyryl cAMP (dbcAMP), and then cell growth, thymidine incorporation and cell cycle phase distribution were analyzed. The expression and the activity of the molecules that regulate cell cycle progression were monitored by Western blot, RT-PCR, and kinase activity assay. RESULTS: Treatment with dbcAMP produced a biphasic effect on cellular proliferation; especially treatment with low concentration of dbcAMP (0.5 mM) showed a higher cellular proliferation rate and promoted G1/S transition in cell cycle. The dbcAMP (0.5 mM) treatment increased CDK2 activity, and it significantly decreased p27Kip1 expression with a decreased half-life of p27Kip1 protein. Moreover, dbcAMP (0.5 mM) increased the protein level and the stability of Skp2 with a concomitant decrease in its ubiquitination. CONCLUSIONS: cAMP up-regulates Skp2 protein by reducing its degradation probably through decreasing the ubiquitination of Skp2, which might result in accelerated degradation of p27Kip1, increase in CDK2 activity, and stimulation of SH-SY5Y cell proliferation in sequence.

Bucladesine↗
PubMed2006

Dexamethasone decreases xenograft response to Paclitaxel through inhibition of tumor cell apoptosis.

Glucocorticoid receptor (GR) activation has recently been implicated in the initiation of anti-apoptotic signaling pathways in epithelial cell lines grown in culture. However, the evidence that GR-mediated inhibition of tumor cell apoptosis is the mechanism that diminishes chemotherapy effectiveness in vivo is limited. We therefore initiated a breast cancer xenograft study to examine whether or not pretreatment with glucocorticoids (GCs) decreases tumor response to chemotherapy by inhibiting tumor cell apoptosis. Here we report a significant decrease in paclitaxel-induced apoptosis in xenografts from mice pretreated with dexamethasone (Dex). A significant difference in apoptosis in xenografts from Dex/paclitaxel versus paclitaxel treated animals was seen eight days following initiation of chemotherapy. Nine days later, mice treated with Dex/paclitaxel had significantly larger tumors compared with those that received paclitaxel alone (p = 0.032). Dex pretreatment did not significantly affect tumor cell proliferation rates. Taken together, these results demonstrate that systemic Dex administration results in significantly reduced breast cancer xenograft apoptosis in the context of chemotherapy treatment. We also found that systemic Dex treatment results in upregulation of the anti-apoptotic gene MKP-1 and downregulation of pro-apoptotic Bid and TRAIL genes in tumor cells six hours following Dex treatment. These in vivo gene expression changes correlated with significant inhibition of chemotherapy-induced apoptosis. Interestingly, the decreased chemotherapeutic response of Dex-pretreated tumors persisted for several weeks following treatment. These data suggest that GR-mediated transcriptional regulation of pro- and anti-apoptotic genes contributes to the mechanism through which GCs decrease paclitaxel-induced apoptosis.

Animals↗
PubMed2006

Membrane depolarization stimulates the proliferation of SH-SY5Y human neuroblastoma cells by increasing retinoblastoma protein (RB) phosphorylation through the activation of cyclin-dependent kinase 2 (Cdk2).

Membrane depolarization causes transmembrane ionic influxes that induce various gene expressions, and is involved in the processes of neuronal differentiation and apoptosis. However, the effect of membrane depolarization on neuronal proliferation has not been established. In this study, we aimed to investigate the effect of membrane depolarization on the proliferation of SH-SY5Y human neuroblastoma cells. Membrane depolarization induced by 50 mM KCl for 5 min significantly increased SH-SY5Y cell numbers and thymidine incorporation at 24 h after depolarization, and increased the phosphorylation and expression of retinoblastoma protein (RB), the activity of Cdk2 (without changing the activities of Cdk4 and Cdk6), and the expressions of cyclin A and cyclin E. Single and repeated depolarization (once a day for 6 days) had similar effects on RB, Cdks, and cyclins levels and activities. In summary, our results suggest that membrane depolarization may stimulate cellular proliferation by augmenting the expression of cyclin E leading to increases in Cdk2 activity and RB phosphorylation.

Cell Division↗
PubMed2006

Irisolidone, an isoflavone metabolite, represses JC virus gene expression via inhibition of Sp1 binding in human glial cells.

Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disease that results from an oligodendrocyte infection caused by the JC virus. Therefore, inhibiting the expression of JC virus is important for preventing and/or treating PML. This study found that irisolidone, an isoflavone metabolite, significantly inhibited the JC virus expression in primary cultured human astrocytes and glial cell lines. Studies examining the underlying mechanism revealed that a mutation of the Sp1 binding site downstream of the TATA box (Sp1-II) dramatically diminished the inhibitory activity of irisolidone. In addition, an irisolidone treatment repressed Sp1 binding to Sp1-II site, which is important for the basal JC virus promoter activity. The results suggest that the inhibitory effect of irisolidone against the JC virus may be attributed at least in part to the suppression of Sp1 binding to the JC virus promoter region. Therefore, the inhibition of the JC virus expression by irisolidone might provide therapeutic potential for PML caused by the JC virus.

Base Sequence↗
PubMed2006

Hydrogen peroxide is a mediator of indole-3-acetic acid/horseradish peroxidase-induced apoptosis.

Recently, we reported that a combination of indole-3-acetic acid (IAA) and horseradish peroxidase (HRP) induces apoptosis in G361 human melanoma cells. However, the apoptotic mechanism involved has been poorly studied. It is known that when IAA is oxidized by HRP, free radicals are produced, and since oxidative stress can induce apoptosis, we investigated whether reactive oxygen species (ROS) are involved in IAA/HRP-induced apoptosis. Our results show that IAA/HRP-induced free radical production is inhibited by catalase, but not by superoxide dismutase or sodium formate. Furthermore, catalase was found to prevent IAA/HRP-induced apoptotic cell death, indicating that IAA/HRP-produced hydrogen peroxide (H2O2) may be involved in the apoptotic process. Moreover, the antiapoptotic effect of catalase is potentiated by NADPH, which is known to protect catalase. On further investigating the IAA/HRP-mediated apoptotic pathway, we found that the IAA/HRP reaction leads to caspase-3 activation and poly(ADP-ribose) polymerase (PARP) cleavage, which was also blocked by catalase. Additionally, we found that IAA/HRP produces H2O2 and induces peroxiredoxin (Prx) sulfonylation. Consequently, our results suggest that H2O2 plays a major role in IAA/HRP-induced apoptosis.

Apoptosis↗
PubMed2006

Effect of far-infrared irradiation on catechins and nitrite scavenging activity of green tea.

The processed green tea leaves were irradiated by far-infrared (FIR) at eight temperatures (80, 90, 100, 110, 120, 130, 140, and 150 degrees C) for 10 min. After FIR irradiation, green teas were prepared by soaking the leaves in boiling water, and the physicochemical characteristics of the green tea were determined. FIR irradiation at 90 degrees C increased total phenol contents of green tea from 244.7 to 368.5 mg/g and total flavanol contents from 122.0 to 178.7 mg/g, compared with non-irradiated control. FIR irradiation also significantly affected the amounts of epigallocatechin and epigallocatechin gallate. Nitrite scavenging activity also increased with increasing FIR irradiation until the temperature reached 110 degrees C. However, the overall color changes of green tea irradiated with FIR at 90 and 100 degrees C were negligible. These results indicate that the chemical quality of green tea is significantly affected by FIR irradiation temperature of the green tea leaves.

Caffeine↗
PubMed2006

Ginseng saponin metabolite suppresses phorbol ester-induced matrix metalloproteinase-9 expression through inhibition of activator protein-1 and mitogen-activated protein kinase signaling pathways in human astroglioma cells.

Aberrant expression of matrix metalloproteinase-9 (MMP-9) is implicated in the process of invasion and angiogenesis of malignant tumors as well as in inflammatory diseases of the CNS. Therefore, the development of compounds that can inhibit or suppress MMP-9 is required to treat brain tumors. We investigated the effects of a ginseng saponin metabolite, compound K (20-O-(beta-D-glucopyranosyl)-20(S)-protopanaxadiol), on MMP-9 expression in human astroglioma cells. Compound K significantly inhibited the secretion and protein expression of MMP-9 induced by PMA. The inhibitory effect of compound K on MMP-9 expression correlated with decreased MMP-9 mRNA levels and suppression of MMP-9 promoter activity. The compound K-mediated inhibition of MMP-9 gene expression appears to occur via AP-1 because its DNA-binding and transcriptional activities were suppressed by the agent. Furthermore, compound K significantly repressed the PMA-mediated activation of p38 MAPK, ERK and JNK, which are upstream modulators of AP-1. Finally, compound K inhibited the in vitro invasiveness of glioma cells. Therefore, inhibition of MMP-9 expression by compound K might have therapeutic potential for controlling the growth and invasiveness of brain tumors.

Astrocytoma↗
PubMed2006

Synthesis and antiviral evaluation of novel open-chain analogues of neplanocin A.

Novel acyclic nucleoside analogues were designed and synthesized as open-chain analogues of neplanocin A. The coupling of the allylic bromide with purine bases using cesium carbonate afforded a series of novel acyclic nucleosides. The synthesized compounds Ia-II were evaluated for their antiviral activity against various viruses such as HIV HSV-1, HSV-2, and ECMV.

Adenosine↗
PubMed2006

Indole-3-acetic acid/horseradish peroxidase-induced apoptosis involves cell surface CD95 (Fas/APO-1) expression.

Recently, we showed that a combination of indole-3-acetic acid (IAA) and horseradish peroxidase (HRP) produces hydrogen peroxide (H2O2), and that this leads to the apoptosis of G361 human melanoma cells. In the present study, flow cytometric analysis confirmed that H2O2 is involved the IAA/HRP-induced apoptotic process. We also found that IAA/HRP increases cell surface CD95 (Fas/APO-1) expression, and that this is blocked by catalase treatment. Furthermore, blocking CD95 with a neutralizing antibody significantly restored IAA/HRP-induced apoptosis. In addition, the IAA/HRP-induced activations of CD95 downstream molecules, i.e., caspase-8, Bid, and caspase-3, were also inhibited by catalase. Moreover, a caspase-8 inhibitor significantly blocked IAA/HRP-induced apoptosis. These results indicate that IAA/HRP-induced apoptosis involves a CD95-initiated death receptor signaling pathway initiated by hydrogen peroxide.

Antibodies↗
PubMed2006

Light-activated indole-3-acetic acid induces apoptosis in g361 human melanoma cells.

Indole-3-acetic acid (IAA) activation by horseradish peroxidase (HRP) has been suggested as a new cancer therapy. Interestingly, we found that ultraviolet B UVB radiation also can activate IAA and produce free radicals in a dose-dependent manner. In this study, we attempted to identify the free radicals generated by UVB-irradiated IAA (IAAUVB), and to determine whether IAAUVB can induce the apoptosis of G361 human melanoma cells. Since IAA/HRP produces reactive oxygen species (ROS), we examined whether IAAUVB-generated radicals include ROS. Our results show that IAAUVB-induced free radical production is not inhibited by catalase, superoxide dismutase, or sodium formate, indicating that ROS are not generated by IAAUVB. On the other hand, IAAUVB caused lipid peroxidation, and this was blocked by Trolox, a water-soluble vitamin E derivative. Moreover, we found that IAAUVB caused apoptotic cell death and that this was inhibited by a low temperature. We further investigated IAAUVB-mediated apoptotic pathways, and found that IAAUVB causes caspase-8, Bid, caspase-3 activation, and poly (ADP-ribose) polymerase (PARP) cleavage. In addition, these apoptotic pathways were also blocked by low temperature. From these results, we propose that IAAUVB-induced free radicals cause human melanoma cell apoptosis via a death receptor-mediated apoptotic pathway.

Apoptosis↗
PubMed2006

Canine intestinal lactic acid bacteria agglutinated with concanavalin A.

Twenty-six out of 46 representative lactic acid bacteria (LAB) that we isolated from 36 dogs in a previous study were agglutinated by concanavalin A (ConA) at a concentration of 0.1563 mg/ml, while isolates did not agglutinate without the addition of ConA. Amongst the isolates, L. reuteri, L. mucosae, and E. canintestini agglutinated strongly, while L. gallinarum, L. kitasatonis, L. acidophilus, L. saerimneri, B. animalis ssp. animalis, P. acidilactici, and E. hirae did not agglutinate. ConA-agglutination of LAB was specifically inhibited by D-glucose, D-galactose, and D-mannose at a concentration of 1.563 mg/ml. Among the sugars, ConA-agglutination was strongly inhibited by D-mannose, while the inhibition level by D-glucose and D-galactose were lower than that of D-mannose. ConA- agglutination of all the LAB isolates was inhibited by D-mannose, except for L. reuteri (one species) and L. mucosae (two species). ConA-agglutination of Bifidobacterium spp. was inhibited by only D-mannose. Based on our results, ConA-agglutination of LAB seems to be strain-specific, but not species-specific.

Agglutination Tests↗
PubMed2006

[Factors affecting national health insurance mass screening participation in the disabled].

OBJECTIVES: As the disabled have higher prevalence rates and earlier onsets of chronic diseases than the non-disabled, their participation in mass screening is important for the early detection and intervention of chronic diseases. Nevertheless, in Korea, the disabled have lower participation rates in mass screening services than the non-disabled. The purpose of the study was to find determinants for the participation in the National Health Insurance (NHI) mass screening program among the disabled. METHODS: In this study, the NHI mass screening data of 423,076 disabled people, which were identified using the National Disability Registry (2003), were analyzed. Of the factors affecting the participation rates in mass screenings, the following variables were included for the analysis: socioeconomic stati, such as sex, age, category of health insurance program, region and income; disability characteristics, such as disability type, and severity. A multiple logistic regression analysis was used to evaluate the association between the participation rates, disability characteristics variables and demographic variables. RESULTS: The participation rate in mass screening of the disabled was 41.3%, but was lower in females, an age of more than 70 years, self-employed and for those with an average monthly insurance premium over 133,500 Won and in metropolitan regions. The participation rate was 1.31 times lower in females than males (95% CI=1.29-1.33); 3.50 times lower in the elderly (more than 70 years) than the younger (95% CI=3.33-3.67); 1.43 times lower in those who live in metropolitan areas (95% CI=1.40-1.46); 2.59 times lower for those in a health insurance program for the self-employed than for employees (95% CI=2.56-2.63); 1.19 times lower for the higher income (more than 133,500) than the lower income group (4,400-22,000) for the average monthly insurance premium (95% CI=1.15-1.23); 2.04 times lower for those with brain palsy and stroke disabilities than with auditory impairments (95% CI= 1.97-2.11) and 3.27 times for those with severe compared to mild disabilities (95% CI=3.15-3.40). CONCLUSIONS: The disabled with high severity, and locomotive and communication disabilities have lower participation rates in mass screening services in Korea.

Adolescent↗
PubMed2005

Mutation of the protein-O-mannosyltransferase enhances secretion of the human urokinase-type plasminogen activator in Hansenula polymorpha.

Human urokinase-type plasminogen activator (uPA) is poorly secreted and aggregates in the endoplasmic reticulum of yeast cells due to inefficient folding. A screen for Hansenula polymorpha mutants with improved uPA secretion revealed a gene encoding a homologue of the Saccharomyces cerevisiae protein-O-mannosyltransferase Pmt1p. Expression of the H. polymorpha PMT1 gene (HpPMT1) abolished temperature sensitivity of the S. cerevisiae pmt1 pmt2 double mutant. As in S. cerevisiae, inactivation of the HpPMT1 gene affected electrophoretic mobility of the O-glycosylated protein, extracellular chitinase. In contrast to S. cerevisiae, disruption of HpPMT1 alone caused temperature sensitivity. Inactivation of the HpPMT1 gene decreased intracellular aggregation of uPA, suggesting that enhanced secretion of uPA was due to improvement of its folding in the endoplasmic reticulum. Unlike most of the endoplasmic reticulum membrane proteins, HpPmt1p possesses the C-terminal KDEL retention signal.

Amino Acid Sequence↗
PubMed2005

Curcumin suppresses phorbol ester-induced matrix metalloproteinase-9 expression by inhibiting the PKC to MAPK signaling pathways in human astroglioma cells.

The aberrant expression of matrix metalloproteinase-9 (MMP-9) is implicated in the invasion and angiogenesis process of brain tumor. This study has investigated the effects of curcumin on MMP-9 expression in human astroglioma cell lines. Curcumin significantly inhibited the MMP-9 enzymatic activity and protein expression that was induced by PMA. The inhibitory effect of curcumin on MMP-9 expression correlates with the decreased MMP-9 mRNA level and the suppression of MMP-9 promoter activity. The curcumin-mediated inhibition of MMP-9 gene expression appears to occur via NF-kappaB and AP-1 because their DNA binding activities were suppressed by curcumin. Furthermore, curcumin strongly repressed the PMA-induced phosphorylation of ERK, JNK, and p38 MAP kinase, which were dependent on the PKC pathway. Therefore, the inhibition of MMP-9 expression by curcumin might have therapeutic potential for controlling the growth and invasiveness of brain tumor.

Antineoplastic Agents↗
PubMed2005

Curcumin is a potent broad spectrum inhibitor of matrix metalloproteinase gene expression in human astroglioma cells.

The abnormal expression of matrix metalloproteinases (MMPs) plays an important role in the invasion of malignant gliomas into the surrounding normal brain tissue. This study showed that curcumin has broad-spectrum inhibitory activity against MMP gene expression in human astroglioma cells. RNase protection assay showed that curcumin inhibited the PMA-induced mRNA expression of MMP-1, -3, -9, and -14. Curcumin repressed the DNA binding and transcriptional activities of AP-1, which is a common upstream modulator of MMP-1, -3, and -9 gene expression. In addition, curcumin suppressed the PMA-induced MAP kinase activities, which were differentially involved in modulating the MMPs. This suggests that the inhibition of MMP transcriptions by curcumin is mediated at least in part through the AP-1 and MAP kinase pathways. Curcumin was also found to significantly repress the in vitro invasion of glioma cells. Therefore, the broad-spectrum inhibition of MMP gene expression by curcumin might provide a novel therapeutic strategy for treating gliomas.

Antineoplastic Agents↗