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S W Chung

Publications and source records attributed to S W Chung.

At least 19 recordsLinked to original sources
PubMed2006

Promoter methylation of helicase-like transcription factor is associated with the early stages of gastric cancer with family history.

BACKGROUND: To investigate the clinicopathological significance of promoter methylation of the helicase-like transcription factor (HLTF) in primary gastric cancer. PATIENTS AND METHODS: Two-hundred fifty six patients participated in this study. Methylation status of HLTF gene was evaluated in fresh-frozen tissues by the methylation-specific polymerase chain reaction. All statistical analyses were two-sided, with a 5% type I error rate. RESULTS: Aberrant methylation of HLTF was found in 98 (38%) of 256 gastric cancer patients. HLTF methylation was significantly associated with a family history in the early stages of gastric cancer, regardless of histologic types. In intestinal-type cases, HLTF methylation occurred in 15 (56%) of 27 patients with family histories, and in 26 (31%) of 85 patients without family histories (P = 0.02). In diffuse-type cases, patients with family histories were also found to exhibit a higher prevalence of HLTF methylation than those without family histories (61% vs. 34%; P = 0.009). HLTF methylation in both of the histologic types occurred in about 70-90% of the early stage cases in which the patient had a family history and in 15-30% of cases in which the patient did not have a family history. In our multivariate logistic regression analysis, the stage 1-2 cases with family histories were determined to carry a higher risk of HLTF methylation than did the stage 3-4 cases without family histories in both the intestinal-type (OR = 6.01, 95% CI = 1.20-30.01, P = 0.02) and the diffuse-type cancers (OR = 8.25, 95% CI = 1.67-40.86, P = 0.009). CONCLUSIONS: These results suggest that HLTF methylation may play a crucial role in the early stages of gastric carcinogenesis in patients with family histories and may be a valuable susceptible marker for the risk of gastric cancer in individuals with family histories.

Aged↗
PubMed2005

Recurrent hepatocellular carcinoma after liver transplantation mimicking post-transplantation lymphoproliferative disorder.

Approximately 5% of patients with end-stage cirrhosis undergoing orthotopic liver transplantation have occult hepatocellular carcinoma. Careful follow up is required to detect recurrent tumour, and knowledge of the patterns of recurrence may avoid diagnostic confusion with other malignancies, such as post-transplantation lymphoproliferative disorder. This case report illustrates an unusual presentation of recurrent hepatocellular carcinoma in a 56-year-old man presenting with a para-aortic soft tissue mass, thought clinically and radiologically to represent lymphoma or post-transplantation lymphoproliferative disorder. This case demonstrates that recurrent hepatocellular carcinoma can present late after transplantation as retroperitoneal lymphadenopathy, and should alert physicians and radiologists to be aware of the radiological appearances of recurrence and of the need for early biopsy to avoid diagnostic confusion with other malignancies.

Carcinoma, Hepatocellular↗
PubMed2005

Development of water quality models for supporting NH3-N control in a dam regulated river.

A seasonal occurrence of high ammonia nitrogen (NH3-N) concentrations has hampered chemical treatment processes of a water plant in Geum river of Korea. Monthly flow allocation from upstream dam is important for downstream NH3-N control. In this study, water quality models based on multiple regression (MR) and artificial neural network (ANN) methods were developed to support dam operations through providing forecasted NH3-N concentrations. The models were calibrated with 7 years of monthly data, and verified with another 3 years of independent data. In the models, the NH3-N concentration for next time step is dependent on dam outflow, river water quality such as alkalinity, temperature, and NH3-N of previous time step. During the calibration phase, the ANN models compared to MR models showed a better agreement with observed data as indicated with small RMSE and high R2 values. However, in the verification phase, the performance of ANN models was decreased and showed a little difference to MR models. From the model comparisons, it is recommended for both ANN and MR models to include the autocorrelation of NH3-N concentrations up to 3-lag months to avoid overestimation during low flow season.

Ammonia↗
PubMed2004

Hepatic abscesses after liver transplantation secondary to traumatic intrahepatic bile duct injuries in a cadaveric allograft donor.

We report the case of an ultimately successful liver transplant recipient whose post-transplant course was complicated by the early development of multiple abscesses in the graft. Post-transplant cholangiography identified multiple shear injuries to the second and third order intrahepatic bile ducts, originating from blunt trauma to the donor liver. Treatment was non-operative following recent reports of the successful management of intrahepatic bile duct injury in the stable trauma patient. This discussion adds to the limited literature available on the transplantation of injured donor livers, despite this being a relatively common practice. Further experience is needed in determining the appropriate criteria for the use of traumatized donor livers. Cholangiography carried out on the back table may help to determine if such injured livers are suitable for transplantation.

Aged↗
PubMed2002

Enhancement of 1 alpha,25-dihydroxyvitamin D(3)-induced differentiation of human leukaemia HL-60 cells into monocytes by parthenolide via inhibition of NF-kappa B activity.

1. Transcription factors such as NF-kappa B provide powerful targets for drugs to use in the treatment of cancer. In this report parthenolide (PT), a sesquiterpene lactone of herbal remedies such as feverfew (Tanacetum parthenium) with NF-kappa B inhibitory activity, markedly increased the degree of human leukaemia HL-60 cell differentiation when simultaneously combined with 5 nM 1 alpha,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)). PT by itself did not induce HL-60 cell differentiation. 2. Cytofluorometric analysis indicated that PT stimulated 1,25-(OH)(2)D(3)-induced differentiation of HL-60 cells predominantly into monocytes. 3. Pretreatment of HL-60 cells with PT before the 1,25-(OH)(2)D(3) addition also potentiated the 1,25-(OH)(2)D(3)-induced HL-60 cell differentiation in both a dose- and a time-dependent manner, in which the enhanced levels of cell differentiation closely correlated with the inhibitory levels of NF-kappa B binding activity by PT. 4. In contrast, santonin, a sesquiterpene lactone without an inhibitory activity of NF-kappa B binding to the kappa B sites, did not enhance the 1,25-(OH)(2)D(3)-induced HL-60 cell differentiation. 5. In transfection experiments, PT enhanced 1,25-(OH)(2)D(3)-induced VDRE-dependent promoter activity. Furthermore, PT restored 1,25-(OH)(2)D(3)-induced VDRE-dependent promoter activity inhibited by TNF-alpha, an activator of NF-kappa B signalling pathway. 6. These results indicate that PT strongly potentiates the 1,25-(OH)(2)D(3)-induced HL-60 cell differentiation into monocytes via the inhibition of NF-kappa B activity and provide evidence that inhibition of NF-kappa B activation can be a pre-requisite to the efficient entry of promyelocytic leukaemia cells into a differentiation pathway.

Cell Differentiation↗
PubMed2002

Hydroquinone, a reactive metabolite of benzene, enhances interleukin-4 production in CD4+ T cells and increases immunoglobulin E levels in antigen-primed mice.

Exposure to cigarette smoke is known to increase the risk of the development of allergic disease. The mechanism is not well understood. In this study, we determined the effect of hydroquinone (HQ), a major metabolite of benzene present in large quantities in cigarette tar, on interleukin-4 (IL-4) production by CD4+ T cells. HQ significantly enhanced IL-4 production by keyhole limpet haemocyanin (KLH)-primed CD4+ T cells in a dose-dependent manner. The enhancing effect of HQ on IL-4 production was maximal at a concentration of 50 micro m. It increased the level of IL-4 production approximately 10-fold. HQ enhanced IL-4 mRNA expression and also IL-4 gene promoter activity, suggesting that the enhancing effect of HQ on IL-4 production may occur at the transcriptional level. Furthermore, the injection of KLH-primed mice with HQ resulted in a significant increase in the levels of IL-4 and immunoglobulin E. These findings provide evidence that HQ, a major component of cigarette tar, may enhance allergic immune responses by inducing the production of IL-4 in CD4+ T cells.

Animals↗
PubMed2001

Inhibition of interleukin-12 production in lipopolysaccharide-activated mouse macrophages by parthenolide, a predominant sesquiterpene lactone in Tanacetum parthenium: involvement of nuclear factor-kappaB.

Pharmacological control of interleukin-12 (IL-12) production may be a key therapeutic strategy for modulating immunological diseases dominated by type-1 cytokine responses. In this study, we investigated the effects of parthenolide, an anti-inflammatory sesquiterpene, on the production of IL-12 from mouse macrophages stimulated with lipopolysaccharide (LPS). Parthenolide potently inhibited the LPS-induced IL-12 production in a dose-dependent manner. The effect of parthenolide on IL-12 p40 promoter activation was analyzed by transfecting RAW264.7 monocytic cells with p40 promoter/luciferase constructs. The repressive effect mapped to a region in the p40 promoter containing a binding site for nuclear factor-kappaB (p40-kappaB). Furthermore, activation of macrophages by LPS resulted in markedly enhanced binding activity to the kappaB site, which significantly decreased upon addition of parthenolide. These results suggest that parthenolide-induced inhibition of IL-12 production in macrophages may explain some of the biological effects of parthenolide including its anti-inflammatory activity.

Animals↗
PubMed2001

A single point mutation at the 3'-untranslated region of Ran mRNA leads to profound changes in lipopolysaccharide endotoxin-mediated responses.

By functional cDNA expression cloning, we have previously established that Ran is important in lipopolysaccharide (LPS) signaling. This was achieved by functional comparison between two cDNAs, differing by a single base substitution within the 3'-untranslated region of the cDNA. This point mutation results in a striking RNA conformational change. No dramatic difference in total RNA at steady state could be found between the two molecules. However, at the protein level, RanC/d (from 870C mRNA) was 5-10-fold higher than RanT/n (from 870T mRNA) and this difference was not observed in non-hematopoietic cells transduced with the same vectors. This tissue-specific difference correlated with a difference in LPS endotoxin responses in corresponding hematopoietic cells. Importantly, the amounts of Ran- C/d and RanT/n proteins were similar initially but the difference became obvious with time. Both Ran proteins migrated from the cytoplasm to the nucleus, but Ran from RanC/d migrated faster than that of RanT/n. RanT/n protein preferentially remained in the cytoplasm and its overall amount was reduced at steady state, consistent with its degradation by intracellular proteases known to be involved in LPS-mediated signal transduction. As the two proteins are identical, the faster RanC/d nuclear localization and a preferred initial cytoplasmic RanT/n distribution suggest a difference in mRNA intracellular localization between the two molecules, as dictated by their RNA structural difference. By pulse-chase experiments, RanC/d proteins are more resistant to degradation than RanT/n protein; there also appear to have two populations of RanT/n proteins, one may reside in the cytoplasm and the other, in the nucleus. More RanC/d GTPase accumulated in the nuclei would conceivably alter the potency of signal transduction and therefore down-modulate LPS-mediated biological responses.

3' Untranslated Regions↗
PubMed2001

Capsaicin potentiates 1,25-dihydoxyvitamin D3- and all-trans retinoic acid-induced differentiation of human promyelocytic leukemia HL-60 cells.

Human promyelocytic leukemia HL-60 cells are differentiated into monocytic or granulocytic lineage when treated with 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] or all-trans retinoic acid, respectively. In this study, the effect of capsaicin, an active component of the red pepper of the genus Capsocum, on cell differentiation was investigated in a HL-60 cell culture system. Treatment of HL-60 cells with 5-30 microg/ml capsaicin for 72 h inhibited cell proliferation and induced a small increase in cell differentiation. Interestingly, synergistic induction of HL-60 cell differentiation was observed when capsaicin was combined with either 5 nM 1,25-(OH)2D3 or 50 nM all-trans retinoic acid. Flow cytometric analysis indicated that combinations of 1,25-(OH)2D3 and capsaicin stimulated differentiation predominantly to monocytes whereas combinations of all-trans retinoic acid and capsaicin stimulated differentiation predominantly to granulocytes. Capsaicin enhanced protein kinase C activity in 1,25-(OH)2D3- and all-trans retinoic acid-treated HL-60 cells. In addition, inhibitors for protein kinase C [bisindolylmaleimide (GF-109203X), chelerythrine, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7)] and an inhibitor for extracellular signal-regulated kinase [2-(2'-amino-3'-methoxyphenyl)-oxanaphthalen-4-one (PD-098059)] significantly inhibited HL-60 cell differentiation induced by capsaicin in combination with either 1,25-(OH)2D3 or all-trans retinoic acid. These results indicate that capsaicin potentiates 1,25-(OH)2D3- or all-trans retinoic acid-induced HL-60 cell differentiation and that both protein kinase C and extracellular signal-regulated kinase are involved in the cell differentiation synergistically enhanced by capsaicin.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2001

Specific association of Type I c-Abl with Ran GTPase in lipopolysaccharide-mediated differentiation.

Each of several isoforms of c-Abl may be involved in different biological functions. Type I c-Abl has been shown to be involved in LPS-induced differentiation and Type IV c-Abl, apoptosis. Ran has recently been shown to be involved in LPS endotoxin signal transduction. Here we show that Type I c-Abl associates with Ran. Formation of this complex is specific, as Ran did not associate with the highly homologous Type IV c-Abl isoform. In non-stimulated lymphoid B cells, Type I c-Abl tyrosine kinase is inactive, whereas Type IV kinase is active. Formation of Type I c-Abl/Ran complex and activation of Type I c-Abl kinase activity are LPS dose-dependent. This complex is detectable in B cells of endotoxin-sensitive inbred mice but absent in B cells of endotoxin-resistant mice. These findings therefore suggest that Type I c-Abl and Ran are important targets in lipopolysaccharide-induced biological responses of hematopoietic cells.

Animals↗
PubMed2001

Establishment of Porphyromonas gingivalis-specific T-cell lines from atherosclerosis patients.

Porphyromonas gingivalis-specific T-cell lines were established from atherosclerotic lesions from two patients. T-cell lines were found to be a mixture of CD4+ and CD8+ T-cells producing variable amount of interferon-gamma, interleukin-4 and interleukin-10. The two patients have had a periodontal disease whose anti-P. gingivalis immunoglobulin G titers were significantly elevated, and P. gingivalis was the one of the predominantly cultivable microorganisms. This is the first report of the successful establishment of P. gingivalis-specific T-cell lines from atherosclerotic patients.

Antibodies, Bacterial↗
PubMed2001

Inhibition of interleukin-12 production in lipopolysaccharide-activated mouse macrophages by hpyericin, an active component of Hypericum perforatum.

Hypericin, an active component of Hypericum perforatum, was evaluated for the regulation of interleukin-12 (IL-12) production in mouse macrophages. Hypericin significantly inhibited IL-12 production in lipopolysaccharide-activated macrophages in a dose-dependent manner (IC50 = 1.45 micrograms/ml). Furthermore, hypericin potently inhibited the activation of IL-12 gene promoter, suggesting that hypericin negatively regulated IL-12 production at the transcription level. These results may explain some known biological activities of hypericin including its anti-rheumatic effect.

Animals↗
PubMed2001

Induction of immune hyporesponsiveness after portal vein immunization with ovalbumin.

BACKGROUND: Previous work has demonstrated prolonged allograft survival after donor-specific portal vein immunization before the transplantation. The purpose of this study was to examine the potential mechanism of portal vein-induced hyporesponsiveness after portal vein immunization with the soluble protein ovalbumin. METHODS: Balb/c mice were immunized with a portal vein injection of ovalbumin. After the immunization, in vivo delayed-type hypersensitivity response and in vitro proliferative response of ovalbumin-specific T cells were assessed to determine host immune response. Type 1 (IL-2, IL-12, IFN-gamma) and type 2 (IL-4, TGF-beta) regulatory cytokines were assessed by semiquantitative reverse transcriptase polymerase chain reaction. Sera anti-ovalbumin IgG, IgG1, and IgG2a were measured by enzyme-linked immunosorbent assay, and the antigen-presenting ability of liver nonparenchymal cells (NPCs) was assessed by T-cell proliferation to ovalbumin in vitro. RESULTS: There was significant inhibition of ovalbumin-specific delayed-type hypersensitivity and T-cell proliferation in portal vein-immunized mice compared with intraperitoneal-immunized or control mice. Reverse transcriptase polymerase chain reaction analysis results showed that lymphocytes from portal vein-immunized mice exhibited decreased type 1 and increased type 2 cytokine messenger RNA expression compared with intraperitoneal-immunized or control animals. The type 2 cytokine response of lymphocytes from ovalbumin portal vein-immunized mice correlated with increased sera ovalbumin-IgG1 and decreased IgG2a. The results of an antigen-presenting assay revealed that liver NPCs were deficient antigen-presenting cells compared with adherent cells from heart or spleen. CONCLUSIONS: Processing of ovalbumin by hepatic NPCs results in hyporesponsiveness to ovalbumin by an impaired type 1 cytokine response and a preferential shift toward a type 2 cytokine response, possibly because of defective antigen presentation by hepatic NPCs. Intrahepatic processing of antigen may play an important role in the development of strategies to reduce host immunoreactivity against transplanted allografts.

Animals↗
PubMed2001

The involvement of Ran GTPase in lipopolysaccharide endotoxin-induced responses.

By functional cloning, we have established that Ran GTPase is involved in LPS-induced signal transduction. This has been accomplished by several functional comparisons of the two cDNAs, Lps(n)/Ran (or RanT/n) and Lps(d)/Ran (or RanC/d), which were isolated from cDNA libraries of LPS responder and hyporesponder mice, respectively. The letter n refers to the "normal" phenotype and the letter d refers to the "deficient" phenotype. Consistent with our previous results, more animal studies indicated that adenoviral transduction of RanC/d cDNA, but not RanT/n cDNA, into sensitive mice conferred significant resistance against endotoxin challenge. Thus the incorporation of RanC/d cDNA into gene therapy protocols as a therapeutic sequence remains very attractive. At steady state, hematopoietic cells transduced with RanC/d cDNA led to about a 10-fold increase in exogenous Ran protein compared with RanT/n cDNA. Furthermore, our cumulative data suggest that a slight elevation of Ran protein in B cells enhances LPS responsiveness, but the same elevation of Ran in macrophages does not. On the other hand, a high level of overexpression of Ran in both macrophages and B cells down-regulates LPS signal transduction. Thus LPS-induced signal transduction in macrophages and B cells is likely to occur via different signaling pathways.

Animals↗
PubMed2000

Oxidized low density lipoprotein inhibits interleukin-12 production in lipopolysaccharide-activated mouse macrophages via direct interactions between peroxisome proliferator-activated receptor-gamma and nuclear factor-kappa B.

Lipopolysaccharide (LPS) increases the production of interleukin-12 (IL-12) from mouse macrophages via a kappaB site within the IL-12 p40 promoter. In this study, we found that oxidized low density lipoprotein (oxLDL) inhibited this LPS-stimulated production of IL-12 in a dose-dependent manner while native LDL did not. OxLDL inhibited p40 promoter activation in monocytic RAW264.7 cells transiently transfected with p40 promoter/reporter constructs, and the repressive effect mapped to a region in the p40 promoter containing a binding site for nuclear factor-kappaB (NF-kappaB) (p40-kappaB). Activation of macrophages by LPS in the presence of oxLDL resulted in markedly reduced binding to the kappaB site, as demonstrated by the electrophoretic mobility shift assays. In contrast, native LDL did not inhibit the IL-12 p40 promoter activation and NF-kappaB binding to the kappaB sites, suggesting that oxidative modification of LDL was crucial for the inhibition of NF-kappaB-mediated IL-12 production. 9-Hydroxyoctadecadienoic acid, a major oxidized lipid component of oxLDL, significantly inhibited IL-12 production in LPS-stimulated mouse macrophages and also suppressed NF-kappaB-mediated activation in IL-12 p40 promoter. The NF-kappaB components p50 and p65 directly bound peroxisome proliferator-activated receptor-gamma (PPAR-gamma) in vitro. In cotransfections of CV-1 and HeLa cells, PPAR-gamma inhibited the NF-kappaB transactivation in an oxLDL-dependent manner. From these results, we propose that oxLDL-mediated suppression of the IL-12 production from LPS-activated mouse macrophages may, at least in part, involve both inhibition of the NF-kappaB-DNA interactions and physical interactions between NF-kappaB and PPAR-gamma.

Animals↗
PubMed2000

Therapeutic anti-tumor response induced with epitope-pulsed fibroblasts genetically engineered for B7.1 expression and IFN-gamma secretion.

Mouse fibroblasts (H-2(b)) were genetically engineered to express a co-stimulatory B7.1 and an IFN-gamma (Fb/IFN-gamma/B7.1). The Fb/IFN-gamma/B7.1 cells were then pulsed with an ovalbumin epitope (amino acids 257-264, SIINFEKL, H-2K(b)-restricted) as a model antigen (Fb/IFN-gamma/B7.1/OVA) and tested for the induction of OVA-specific cytotoxic T lymphocytes (CTLs) in C57BL/6 mice (H-2(b)). Genetically engineered fibroblasts lacking either IFN-gamma or B7.1 were constructed and used as controls. Immunization with the Fb/IFN-gamma/B7.1/OVA cells induced strong cytotoxic activity against OVA-expressing EL4 (EG7) tumor cells but not against other H-2(b) tumor cells, such as EL4, C1498, and B16F1. The magnitude of the cytotoxic response in mice with the Fb/IFN-gamma/B7.1/OVA cells was significantly higher than that in mice immunized with any other cell construct. CD8(+) T cells with OVA-specific cytotoxic activity were predominant in mice immunized with Fb/IFN-gamma/B7.1/OVA cells. Furthermore, treatment with Fb/IFN-gamma/B7.1/OVA cells significantly prolonged the survival period of EG7 tumor-bearing mice. Anti-tumor CTL immunity by the Fb/IFN-gamma/B7.1/OVA cells could be induced without the help of host antigen-presenting cells, CD4(+) T cells, or NK1.1(+) cells. Our results suggest that fibroblasts can be genetically modified into efficient antigen-presenting cells for the induction of antigen-specific CTL response in cancer immunotherapy.

Animals↗