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ABSTRACT: Kaposi sarcoma (KS) is a vascular neoplasm, which is fairly prevalent in acquired immunodeficiency syndrome (AIDS) patients. Mucocutaneous and lymph node involvements are characteristic features of KS in AIDS patients. The involvement of gastrointestinal tract occurs in 40% of KS patients and leads to significant morbidity and mortality. In the highly active antiretroviral therapy (HAART) era, the rate of AIDS related KS has fallen with control of human immunodeficiency virus (HIV) viremia. However, it is still recognized as the primary AIDS-defining illness, and the proportion of AIDS diagnoses made due to KS ranged from 4.1% to 7.5%. In Korea, AIDS-related KS has been report in low rate incidence. Its gastrointestinal involvements are rarely reported. To date, five cases have been recorded in Korea. Herein, we present an additional case of gastrointestinal KS as the AIDS-defining illness and review of the Korean medical literature. (Korean J Gastroenterol 2012;60:166-171).
The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi 09/2012; 60(3):166-71.
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ABSTRACT: Transient receptor potential vanilloid type 1 (TRPV1) plays a crucial role in pain perception and its expression is up-regulated in patients with irritable bowel syndrome (IBS). The aim of this study was to investigate the potential association between Single nucleotide polymorphism (SNPs) of the TRPV-1 gene and patients with IBS.
We chose to focus on three SNPs in the human TRPV1 coding region (rs222749, rs9894618 and rs222747) in 80 healthy controls and 103 IBS patients. We developed the high resolution melting (HRM) method to determine the genotyping of rs222747 and rs9894618 and the genotyping of rs222749 was also determined by direct sequencing method.
The CG genotype of rs222747 was 58.8% in controls and 45.6% in the IBS group. The GG genotype of rs222747 was 15.0% in controls and 20.4% in the IBS group. The CT genotype of rs222749 was 313% in controls and 32.0% in the IBS group. The CC genotype of rs9894618 was 98.8% in controls and 100.0% in the IBS group. There was no significant difference in allele frequency of these three SNPs of the TRPV1 gene between controls and the IBS group. Also, no significant difference was observed between the IBS subtypes.
These results suggest that the SNPs of the TRPV1 gene may not be associated with IBS in Korean populations. Further studies with large cases are needed to validate the results of the present study.
Acta gastro-enterologica Belgica 06/2012; 75(2):222-7. · 0.64 Impact Factor
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So-Young Joo, Young-A Song,
Young-Lan Park,
Eun Myung,
Cho-Yun Chung,
Kang-Jin Park,
Sung-Bum Cho,
Wan-Sik Lee,
Hyun-Soo Kim,
Jong-Sun Rew,
Nack-Sung Kim,
Young-Eun Joo
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ABSTRACT: Epigallocatechin-3-gallate (EGCG), the primary catechin in green tea, has anti-inflammatory and anti-oxidative properties. The aim of the current study was to characterize the impact of EGCG on lipopolysaccharide (LPS)-induced innate signaling in bone marrow-derived macrophages (BMMs) isolated from ICR mice.
The effect of EGCG on LPS-induced pro-inflammatory gene expression and nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling was examined using reverse transcription-polymerase chain reaction, Western blotting, immunofluorescence, and the electrophoretic mobility shift assay.
EGCG inhibited accumulation of LPS-induced IL-12p40, IL-6, MCP-1, ICAM-1, and VCAM-1 mRNA in BMMs. EGCG blocked LPS-induced IκBα degradation and RelA nuclear translocation. EGCG blocked the DNA-binding activity of NF-κB. LPS-induced phosphorylation of ERK1/2, JNK, and p38 was inhibited by EGCG. U0126 (an inhibitor of MEK-1/2) suppressed the LPS-induced IL-12p40, IL-6, MCP-1, ICAM-1, and VCAM-1 mRNA accumulation in BMMs.
These results indicate that EGCG may prevent LPS-induced pro-inflammatory gene expression through blocking NF-κB and MAPK signaling pathways in BMMs.
Gut and liver 04/2012; 6(2):188-96. · 0.83 Impact Factor
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ABSTRACT: The recepteur d'origine nantais (RON) receptor tyrosine kinase is overexpressed in epithelial cancers, including gastric cancer. The aims of the present study were to evaluate whether RON affects tumor cell behaviors and oncogenic signaling pathways, and to document the relationship of its expression with various clinicopathological parameters in gastric cancer. The biological role of RON in tumor cell behaviors and oncogenic signaling pathways was investigated by using small interfering RNA in gastric cancer cell lines including AGS and MKN28. The expression of RON in gastric cancer tissues was investigated by using reverse transcription polymerase chain reaction and immunohistochemistry. Knockdown of RON suppressed tumor cell migration and invasion in AGS and MKN28, induced apoptosis through modulation of anti-apoptotic and pre-apoptotic genes and induced cell cycle arrest by decreasing cyclin D1, cyclin D3 and CDK4, and by inducing p21 and p27 expression. Signaling cascades, including Akt and mitogen-activated protein kinase (MAPK), were significantly blocked by knockdown of RON. Expression of RON was significantly associated with tumor size, depth of invasion, lymph node metastasis, tumor stage and poor survival. These results indicate that RON is associated with tumor progression via the inhibition of apoptosis and cell cycle arrest in human gastric cancer.
Pathology International 02/2012; 62(2):127-36. · 1.62 Impact Factor
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Cho-Yun Chung,
Young-Lan Park, Young-A Song,
Eun Myung,
Kyu-Yeol Kim,
Gi-Hoon Lee,
Ho-Seok Ki,
Kang-Jin Park,
Sung-Bum Cho,
Wan-Sik Lee,
Young-Do Jung,
Kyung-Keun Kim,
Young-Eun Joo
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ABSTRACT: Altered Recepteur d'Origine nantais (RON) expression transduces signals inducting invasive growth phenotype that includes cell proliferation, migration, matrix invasion, and protection of apoptosis in human cancer cells. The aims of the current study were to evaluate whether RON affects tumor cell behavior and cellular signaling pathways including activator protein-1 (AP-1) and Akt/forkhead box O (FoxO) in human colorectal cancer cells.
To study the biological role of RON on tumor cell behavior and cellular signaling pathways in human colorectal cancer, we used small interfering RNA (siRNA) to knockdown RON gene expression in human colorectal cancer cell line, DKO-1.
Knockdown of RON diminished migration, invasion, and proliferation of human colorectal cancer cells. Knockdown of RON decreased AP-1 transcriptional activity and expression of AP-1 target genes. Knockdown of RON activated cleaved caspase-3, -7, -9, and PARP, and down-regulated the expression of Mcl-1, survivin and XIAP, leading to induction of apoptosis. Knockdown of RON induced cell cycle arrest in the G2/M phase of cancer cells by an increase of p27 and a decrease of cyclin D3. Knockdown of RON inhibited the phosphorylation of Akt/FoxO signaling proteins such as Ser473 and Thr308 of Akt and FoxO1/3a.
These results indicate that knockdown of RON inhibits AP-1 activity and induces apoptosis and cell cycle arrest through the modulation of Akt/FoxO signaling in human colorectal cancer cells.
Digestive Diseases and Sciences 09/2011; 57(2):371-80. · 2.12 Impact Factor
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Nam-Chul Jin,
Hyun-Soo Kim,
Dae-Hyun Kim, Young-A Song,
Yeon-Ju Kim,
Tae-Jin Seo,
Sun-Young Park,
Chang-Hwan Park,
Young-Eun Joo,
Sung-Kyu Choi,
Jong-Sun Rew
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ABSTRACT: Ischemic colitis (IC) is usually a self-limiting disease. But, it can cause necrosis that requires urgent surgical treatment. We sought to evaluate clinical difference in IC patients between medical and surgical treatment groups, and to identify prognostic factors for adverse outcomes.
We conducted a retrospective analysis of clinical characteristics in patients with IC treated in Chonnam National University Hospital between May 2001 and April 2010. A total of 81 patients with IC were enrolled. We classified the patients into two groups-a medical treatment group and a surgical treatment group-and evaluated their clinical features, treatment outcomes and mortality.
Absence of hematochezia, vomiting, abdominal tenderness, abdominal rebound tenderness, heart rate over 90 beats/min, systolic blood pressure less than 100 mm Hg, hyponatremia and increased LDH or serum creatinine level were observed more frequently in surgically-treated patients (p<0.05). Most cases in the medically-treated group resolved without complications (98.3%). But, about half of the cases (52.4%) of the surgically-treated group resolved and the mortality rate was 47.6%.
In patients with ischemic colitis, several clinical factors are associated with surgical treatment. Although IC is often selflimited, our data suggests that special attention and aggressive therapy is warranted in treating these patients.
Clinical endoscopy. 09/2011; 44(1):38-43.
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Sung-Bum Cho,
Young-Lan Park, Young-A Song,
Kyu-Yeol Kim,
Gi-Hoon Lee,
Dae-Ho Cho,
Dae-Seong Myung,
Kang-Jin Park,
Wan-Sik Lee,
Ik-Joo Chung,
Sung-Kyu Choi,
Kyung-Keun Kim,
Young-Eun Joo
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ABSTRACT: The recepteur d'origine nantais (RON) receptor tyrosine kinase is highly expressed in various cancers including human hepatocellular carcinoma (HCC) and involved in tumor progression. The aims of the current study were to evaluate whether RON affects tumor cell behavior and oncogenic signaling cascades in HCC cells. We investigated the biologic role of RON on tumor cell behavior and oncogenic signaling cascades including Akt, c-Raf and extracellular signal-regulated kinase (ERK) by using the small interfering RNA (siRNA) in HCC cell lines, chang, HepG2 and Huh7. Knockdown of RON suppressed tumor cell migration and invasion in all tested HCC cell lines. The proportion of apoptotic cells induced by knockdown of RON was greater than that induced by transfection of the scramble siRNA in all tested HCC cell lines. Knockdown of RON resulted in cell cycle arrest in the G2/M phase of chang and Huh7 cells, and sub G1 phase of HepG2 cells. Knockdown of RON activated cleaved caspase-3 and PARP, and down-regulated the expression of Bcl-2, Bcl-xL and survivin, leading to induction of apoptosis in all tested cell lines. Knockdown of RON negatively regulates the progression of the cell cycle by decreasing cyclin D1 and D3, and increasing p21 and p27 in all tested cell lines. The phosphorylation of Akt, c-Raf and ERK1/2 signal proteins was significantly blocked by knockdown of RON in all tested cell lines. These results suggest that RON is associated with invasive and oncogenic phenotypes such as tumor cell migration, invasion, resistance to apoptosis and cell cycle arrest through the modulation of Akt, c-Raf and ERK signaling cascades in HCC cells.
Oncology Reports 08/2011; 26(6):1581-6. · 1.84 Impact Factor
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ABSTRACT: KAI1 COOH-terminal interacting tetraspanin (KITENIN) contributes to tumor invasion and metastasis in various cancers. The aim of current study was to evaluate whether KITENIN affects tumor cell invasion and prognosis in human colorectal cancers. We investigated the biologic role of KITENIN on tumor cell invasion by using small interfering RNA in Caco2, DLD1, and SW480. We evaluated the expression of KITENIN and activator protein-1 (AP-1) target genes in human colorectal cancer tissues. The tumor cell invasion was decreased by knockdown of KITENIN in three tested cell lines. The mRNA expression of cyclin D1 and COX-2 was decreased in KITENIN knockdown Caco2 and the mRNA expression of MMP-3 and COX-2 was decreased in KITENIN knockdown DLD1 and SW480. The extracellular-signal protein kinase 1/2 (ERK1/2) phosphorylation was decreased in KITENIN knockdown in three tested cell lines. Expression of KITENIN and AP-1 target genes was significantly increased in human colorectal cancer tissues. The ERK1/2, c-Jun N-terminal kinase (JNK) and p38 phosphorylations were increased in human colorectal cancer tissues. Expression of KITENIN was significantly associated with lymphovascular invasion, depth of invasion, lymph node metastasis, tumor stage and poor survival. These results indicate that KITENIN is associated with human colorectal cancer progression including invasion and metastasis.
Pathology International 04/2011; 61(4):210-20. · 1.62 Impact Factor
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Young-A Song,
Young-Lan Park,
Kyu-Yeol Kim,
Cho-Yun Chung,
Gi-Hoon Lee,
Dae-Ho Cho,
Ho-Seok Ki,
Kang-Jin Park,
Sung-Bum Cho,
Wan-Sik Lee,
Nacksung Kim,
Bong-Whan Ahn,
Young-Eun Joo
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ABSTRACT: Black tea has been shown to elicit anti-oxidant, anti-carcinogenic, anti-inflammatory and anti-mutagenic properties. In this study, we investigated the impact of black tea extract (BTE) on lipopolysaccharide (LPS)-induced NF-κB signaling in bone marrow derived-macrophages (BMM) and determined the therapeutic efficacy of this extract on colon inflammation.
The effect of BTE on LPS-induced NF-κB signaling and pro-inflammatory gene expression was evaluated by RT-PCR, Western blotting, immunofluorescence and electrophoretic mobility shift assay (EMSA). The in vivo efficacy of BTE was assessed in mice with 3% dextran sulfate sodium (DSS)-induced colitis. The severity of colitis was measured by weight loss, colon length and histologic scores.
LPS-induced IL-12p40, IL-23p19, IL-6 and IL-1β mRNA expressions were inhibited by BTE. LPS-induced IκBα phosphorylation/degradation and nuclear translocation of NF-κB/p65 were blocked by BTE. BTE treatment blocked LPS-induced DNA-binding activity of NF-κB. BTE-fed, DSS-exposed mice showed the less weight loss, longer colon length and lower histologic score compared to control diet-fed, DSS-exposed mice. DSS-induced IκBα phosphorylation/degradation and phosphorylation of NF-κB/p65 were blocked by BTE. An increase of cleaved caspase-3 and poly (ADP-ribose) polymerase (PARP) in DSS-exposed mice was blocked by BTE.
These results indicate that BTE attenuates colon inflammation through the blockage of NF-κB signaling and apoptosis in DSS-induced experimental colitis model.
BMC Complementary and Alternative Medicine 01/2011; 11:91. · 2.24 Impact Factor
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ABSTRACT: The aim of this study was to determine the impact of the black tea polyphenol, theaflavin, on the expression of adhesion molecules and activation of lipopolysaccharide (LPS)-induced innate signaling in rat intestinal epithelial (RIE) cells.
The effect of theaflavin on neutrophil adhesion, expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1, LPS-induced nuclear factor-kappa B (NF-κB), and mitogen-activated protein kinase (MAPK) signaling was examined by neutrophil adhesion assay, RT-PCR, Western blotting, immunofluorescence, and electrophoretic mobility shift assay (EMSA).
Theaflavin suppressed adhesion of neutrophils to LPS-stimulated RIE cells. LPS-induced ICAM-1 and VCAM-1 expressions were inhibited by theaflavin. LPS-induced IκBα phosphorylation/degradation and nuclear translocation of NF-κB/p65 were blocked by theaflavin. Also, theaflavin blocked NF-κB DNA-binding activity in EMSA. LPS-induced phosphorylation of JNK was inhibited by theaflavin. Bay11-7082 (a NF-κB inhibitor) and SP600125 (a JNK inhibitor) suppressed the LPS-induced ICAM-1 and VCAM-1 mRNA accumulations.
These results indicate that black tea polyphenol theaflavin suppresses LPS-induced ICAM-1 and VCAM-1 expressions through blockage of NF-κB and JNK activation in intestinal epithelial cells.
Agents and Actions 12/2010; 60(5):493-500. · 1.59 Impact Factor
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ABSTRACT: Shewanella algae infections are rare in humans. Previously reported cases of S. algae have mainly been associated with direct contact with seawater. We report a case of primary S. algae bacteremia occurring after the ingestion of raw seafood in a patient with liver cirrhosis that presented a fulminent course of necrotizing fasciitis.
Journal of Korean medical science 12/2009; 24(6):1192-4. · 0.84 Impact Factor
