Publications by authors named "Yukiko Saitou"

We herein report a clinical pitfall regarding the treatment of a case of pulmonary tuberculoma in a patient with chronic hepatitis C. The patient presented with both chronic hepatitis C and pulmonary tuberculoma, and we initiated treatment of the chronic hepatitis C first due to the potential for liver injury; however, the patient's condition worsened in terms of the pulmonary tuberculosis. This case highlights the need to select the initial treatment for pulmonary tuberculoma, not chronic hepatitis C.

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Aim: To investigate the reduction of cell viability in human hepatocellular carcinoma (HCC) cell lines induced by inhibition of nuclear factor kappa B (NF kappa B).

Methods: HLE, SKHep1, and HepG2 were incubated and E3330 was used to compare the stimulation of some chemotherapeutic drugs with that of TNF family, Fas ligand, TNF alpha and TNF-related apoptosis-inducing ligand (TRAIL) at the point of the reduction of cell viability by inhibiting NF kappa B.

Results: E3330 decreased NF kappa B levels in HLE cells stimulated by TNF and TRAIL.

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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in tumor cells, but not in most normal cells. The role of TRAIL in hepatic cell death and hepatic diseases is not well understood. The present study investigated the expression of TRAIL and TRAIL receptors (TRAIL-Rs) in patients with hepatitis C virus infection using immunohistochemistry and examined physiological roles under viral infection in the HepG2 cell line.

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The inhibitors of apoptosis (IAPs) family regulate apoptosis by preventing the action of the central execution phase, and function as mediators and regulators of the anti-apoptotic activity of the v-Rel and NF-kappaB transcription factor families. The targeting of IAPs may be a promising strategy, but it is not well elucidated in human hepatocellular carcinomas (HCCs). We have therefore investigated the effects of the down-regulation of IAPs (XIAP or survivin) on the TNF-related apoptosis-inducing ligand (TRAIL) and chemotherapeutic agents that induced apoptosis in human HCC cells.

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A systemic vitamin K analog, compound 5 (Cpd 5), possesses the ability to inhibit cell growth of tumor cells. Therefore, we investigated the effect of Cpd 5 in human hepatocellular carcinoma (HCC) cell lines and evaluated its role in apoptosis. Human HCC cell lines were cultured and treated with Cpd 5.

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Aim: To detect the expression of a proliferation-related ligand on human hepatocellular carcinoma (HCC) cell lines (SK-Hep1, HLE and HepG2) and in culture medium.

Methods: APRIL expression was analyzed by Western blotting in HCC cell lines. Effects of APRIL to cell count and angiogenesis were analyzed, too.

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Unlabelled: The efficacy of continuous arterial infusion chemotherapy through a subcutaneously implanted port has been reported with less adverse effects than systemic chemotherapy in hepatobilliary malignancies. However, macrocytic anemia is sometimes seen during this therapy. In 25 patients (22 with hepatocellular carcinoma, 3 with cholangiocellular carcinoma) treated with cisplatinum (10mg/day) and 5-Fluorouracil (5-FU) (250 mg/day), the frequency of anemia and its etiologies were evaluated.

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Aim: To analyze the risk factors of hepatocellular carcinoma (HCC) recurrence after radiofrequency ablation (RFA) treatment with HCV-associated hepatitis.

Methods: Twenty-six patients with HCV-associated HCC who were followed-up for more than 12 mo were selected for this study. Risk factors for distant intrahepatic recurrences of HCC were evaluated for patients in whom complete coagulation was achieved without recurrence in the same subsegment as the primary nodule.

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Aim: To evaluate the clinical utility of serum fibrosis markers, including YKL-40, in patients with HCV-associated liver disease.

Methods: A total of 109 patients with HCV-associated liver disease were enrolled. We measured serum type IV collagen, amino-terminal peptide of type III procollagen (PIIIP), hyaluronic acid (HA), YKL-40 levels and biochemical.

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The TNF-like weak inducer of apoptosis (TWEAK) can induce diverse cellular responses, including cell death, inflammation, migration, and proliferation in various transformed cell lines. We investigated TWEAK sensitivity, TWEAK effects on nuclear factor-kappaB activation, and expression of TWEAK in the HT-29, LS180, SK-CO-1 and SW480 human colonic adenocarcinoma cell lines, all of which express the TWEAK receptor (Fn14). TWEAK alone induced cell death in SW480 cells and induced cell death of HT-29 cells after addition of IFN-gamma, actinomycin D or cycloheximide.

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p53 is a tumor suppressor protein with numerous biological functions including transformation, regulation of cell growth, differentiation and apoptosis. The TNF-related apoptosis-inducing ligand (TRAIL) can induce apoptosis in various transformed cell lines. We investigated the effects of combining wild-type p53 gene transduction by adenoviral infection (Ad-p53) with addition of TRAIL on cell death, expression levels of TRAIL receptors (TRAIL-R1, TRAIL-R2), FLICE inhibitory protein (FLIP) and X-linked inhibitor of apoptosis protein (XIAP) on human hepatocellular carcinoma (HCC) cell lines.

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The aim of this study was to clarify the perioperative hemodynamics of liver grafts without vascular complications during and early after liver transplantation from living donors. This study was carried out in 4 child recipients (lateral segment left lobe grafts) and 6 adult recipients (right lobe grafts) of liver transplantation from living donors. The hemodynamics of the hepatic artery, portal vein, and hepatic vein of the grafts during and until 7 days after surgery were studied by Doppler ultrasonography.

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It has been demonstrated that CD34-positive cells isolated from human peripheral blood differentiate into endothelial cells and contribute to neoangiogenesis in adults. We investigated the role of CD34-positive endothelial cells in liver samples from patients with hepatitis B virus (HBV)-associated chronic liver diseases. Tissue sections were obtained by liver biopsy from 25 patients with HBV-associated chronic liver diseases and were examined by immunohistochemistry using anti-CD34, anti-von Willebrand factor (vWF), and anti-vascular endothelial growth factor (VEGF) antibodies.

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TNF-like weak inducer of apoptosis (TWEAK) is a member of the TNF family whose transcripts are expressed in various human tissues. Since TWEAK has a variety of biological activities, we investigated TWEAK sensitivity, expression, and physiological role in human hepatocellular carcinomas (HCCs). Tweak receptor was detected in four kinds of HCC cells.

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The peroxisome proliferator-activated receptor-gamma (PPARgamma) high-affinity ligand, 15-deoxy-Delta-12,14-PGJ(2) (15d-PGJ(2)), is toxic to malignant cells through cell cycle arrest and apoptosis induction. In this study, we investigated the effects of 15d-PGJ(2) on apoptosis induction and expression of apoptosis-related proteins in hepatocellular carcinoma (HCC) cells. 15d-PGJ(2) induced apoptosis in SK-Hep1 and HepG2 cells at a 50 micro M concentration.

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The X-linked inhibitor of apoptosis (XIAP) is a member of a novel family of inhibitors of apoptosis. Since suppression of apoptosis is fundamentally important for carcinogenesis and tumor growth, we investigated the expression and function of XIAP in human hepatocellular carcinomas (HCCs). XIAP was expressed constitutively in HCC cell lines.

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A staging system for hepatocellular carcinoma was reported from Italy (CLIP). In this study, we evaluate the CLIP scoring system and establish a new scoring system for predicting the prognosis of patients with hepatocellular carcinoma. Patients (n=141) who were diagnosed and who underwent initial treatment at our single institution were recruited retrospectively into this study.

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The TNF-receptor family has a dual signaling pathway, including induction of apoptosis and NF-kappaB activation associated with cell survival. Hepatocellular carcinoma (HCC) cells express TNF-receptor family members and the signaling from these receptors induces NF-kappaB activation. However, the role of Fas in induction of NF-kappaB activation in HCC cells is not well understood.

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