With comparison to other methods, capsule endoscopy is simple, affordable, and has been proved to be the best test for early diagnosis of small bowel Crohn’s disease in this study. Key Word(s): 1. Capsule Endoscopy; 2. Crohn’s Disease; 3. Diagnosis; Presenting Author: ZHANGXIANG LIAN Additional Authors: JIANGHAI XING Corresponding Author: JIANGHAI XING Affiliations: guangxi medical university Objective: To assess the diagonostic value of EUS

forGI tract neuroendocrine tumors. Methods: 16 cases of neuroendocrine tumors diagnosed at the First Affiliated Hospital of Guangxi Medical University from December 2002 to December 2012 were retrospectively analyzed. The feature of the EUS imaging was compared with PD98059 supplier traditional diagnostic method and evaluated the diagnostic value. Results: Of the 16 Neuroendocrine tumors, 7 (43.8%) were in the pancreas: 6 islet-cell tumors (one in the pancreatic head, two in the pancreatic body, two in the pancreatic tail, one in the junction of head and body); 1 vasoactive intestinal

peptide tumors was in the pancreatic head. On EUS, pancreatic neuroendocrine tumors presented as hypoechoic masses with clear margins and maybe halo-like changes (discontinuous hyperechoic edge). Of the 16 Neuroendocrine tumors, 6 (37.5%) were rectal carcinoid in the rectum (from the anus 3∼8 cm, mean 5.5 cm). On EUS, rectal carcinoid presented selleck chemical as hypoechoic masses with clear margins in mucosal or submucosal lesions. Of the 16 Neuroendocrine

tumors, 2 (12.5%) were in the stomach : 1 stomach carcinoid was in greater gastric curvature and it presented as hypoechoic masses in mucosal; 1 stomach neuroendocrine tumor was in greater gastric curvature and it presented as hypoechoic masses in submucosal lesions. 1 (6.2%) was adrenal gland chromaffinoma in the left adrenal gland and it presented as hypoechoic masses in the pancreas, anechoic shadow with median strip and thick wall in the left adrenal. 15 neuroendocrine tumors all were definitely diagnosed by pathology. 7 underwent surger; 3 underwent ESD; 2 underwent EUS-FNA; 2 underwent EMR. The accuracy rate of EUS for preoperative localization Carbachol was 93.7%. Conclusion: EUS can provide accurate preoperative localization and pathologic evidence for pancreatic neuroendocrine tumors. EUS has the the value in diagnosis and guiding EMR for enteron carcinoid. Key Word(s): 1. EUS; 2. neuroendocrine tumor; 3. diagnosis; 4. FNA; Presenting Author: YADONG FENG Additional Authors: HONG ZHU, SHUPING YANG, LIANZHEN YU, XUELIANG LI, RUIHUA SHI Corresponding Author: RUIHUA SHI Affiliations: First Affiliated Hospital of Nanjing Medical University; shupyang@yahoo.

Accordingly, NK cells from patients that spontaneously cleared the virus displayed a stronger IFN-γ secretion than those developing chronic infection. Finally, we observed high expression of NKG2D and NKp46, respectively, to be associated with self-limiting course of aHCV. Accordingly, we found that blocking of these NK cell receptors significantly

impaired antiviral NK cell activity. Conclusion: Our data suggest DMXAA manufacturer a strong IFN-γ-mediated antiviral NK cell response to be associated with a self-limited course of AHC in HIV+ patients. (Hepatology 2014;59:814–827) “
“Hepatic iron accumulation is considered to be a cofactor that influences liver injury and hepatocarcinogenesis. Aim of this study is to determine whether serum ferritin (SF) levels relate to overall survival (OS) and time to recurrence (TTR) in hepatocellular carcinoma (HCC) patients

see more treated with percutaneous radiofrequency ablation (RFA). We measured SF levels in 103 HCC patients (median age 70, M/F = 82.5%/17.5%) who underwent RFA between 2005 and 2010. Correlation between SF and other prognostic factors at baseline was analyzed. SF levels were entered into a Cox model and their influence on OS and TTR was evaluated in univariate and multivariate analyses. SF did not correlate with α-fetoprotein (rho: −0.12, P = 0.22), neutrophil/lymphocyte ratio (rho: −0.1020, P = 0.30), Model for End-Stage Liver Disease (rho: 0.18, P = 0.06), Child-Pugh score (P = 0.5), or Barcelona Cancer of the Liver Clinic stage (P = 0.16). A log-rank test found the value of 244 ng/mL as the optimal prognostic cut-off point for SF. Median OS was 62 months (54–78) and survival rate was 97%, 65%, and 52% at 1, 4, and 5 years, respectively. Performance buy Tenofovir status and SF were the only predictors of OS at multivariate analysis. Median TTR was 38 months (34–49) with a recurrence-free survival

rate of 82.5%, 26.2%, and 23.3% at 1, 4, and 5 years, respectively, while SF and age were the only predictors of TTR. SF level, possibly reflecting the degree of hepatic inflammation and fibrosis, is a negative risk factor for survival and recurrence after percutaneous RFA in HCC patients. “
“Service des Maladies de l’Appareil Digestif, Hôpital Huriez, CHRU de Lille, Lille, France Activation of Kupffer cells plays a central role in the pathogenesis of alcoholic liver disease. Because cannabinoid CB2 receptors (CB2) display potent anti-inflammatory properties, we investigated their role in the pathogenesis of alcoholic liver disease, focusing on the impact of CB2 on Kupffer cell polarization and the consequences on liver steatosis. Wild-type (WT) mice fed an alcohol diet showed an induction of hepatic classical (M1) and alternative (M2) markers. Cotreatment of alcohol-fed mice with the CB2 agonist, JWH-133, decreased hepatic M1 gene expression without affecting the M2 profile.

The grant numbers covering the experiments are 06/1137 and 11/0342. All animal experiments were performed under S2-conditions in the central animal facility of Hannover Medical School. NOD/Ltj (NOD) and NOD.CB17-Prkdcscid/J (NOD scid) mice were bred in specific pathogen-free facilities at Hannover Medical School. For hydrodynamic gene transfer experiments 15-20 μg of the plasmid were diluted in a total volume of 2 mL phosphate-buffered saline (PBS) and injected rapidly intravenously into NOD mice. The unpaired Student 2-tailed t test or one-way analysis of variance (ANOVA) with Tukey’s posttest was performed using the GraphPad Prism program: *difference significant with P  ≤  0.05;

**very significant, P  ≤  0.01; ***extremely significant, P  ≤  0.001; P  >  0.05 was considered to be not significant (ns). Additional methods are described in the Supporting Material. Selleckchem CHIR 99021 The new induced emAIH model described here is based on an immunological danger signal combined with expression of a hepatic autoantigen. We used self-limited, hepatotropic adenovirus as a danger signal to trigger the immune response and the human and murine FTCD as common autoantigen in AIH. To this end, FTCD (Supporting Fig. 1A) and eGFP as control were cloned in a replication-deficient adenoviral vector.

Cell lines were eGFP-positive under the fluorescence microscope after transducing with Ad-eGFP (data not shown). Western blots were stained with human anti-LC1-positive serum that recognized SCH727965 in vitro human FTCD. The human anti-LC-1 serum bound to hFTCD-transduced cells, but not to control infected cells (Supporting Fig. 1B). Therefore, FTCD was expressed in hepatocytes after Ad-FTCD infection in a tertiary structure which could recognize by human autoimmune sera. As described by others,[11] adenoviral infection per

se can be used to induce a transient hepatic inflammation in animal models. Therefore, NOD mice were infected with 1 × 10[10] particles of Ad-hFTCD and Ad-eGFP. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were elevated at week 1 and week 2 in both groups. Values reached up to 900 and 1200 U/L of serum for AST and ALT, respectively, but returned to serum levels around the upper normal limit at later timepoints Reverse transcriptase (Fig. 1A). This ALT and AST elevation was transient and not significantly different between mice infected with Ad-hFTCD or Ad-eGFP, which was in line with all hepatitis-like animal models up to date.[12-14] Ad-eGFP transduced hepatic cells, therefore eGFP-expressing cells were detectable in the liver transiently at days 1 and 5, but not at day 20 (Fig. 1B). Likewise, adenoviral DNA could not be identified by polymerase chain reaction (PCR) from liver tissue at week 12 after infection, demonstrating the self-limiting course of acute adenoviral infection (Supporting Fig. 2).

Threats allow individuals to modify the behaviour of potential competitors without incurring the costs and risks associated with escalated fights (Maynard Smith, 1974) but are only likely to be effective where threatening individuals have the capacity to inflict costs on others sufficiently large to inhibit their behaviour (Parker, 1974; Andersson, 1980; Cant & Johnstone, 2009). In many societies, dominant individuals also punish subordinates that infringe their interests, inflicting fitness www.selleckchem.com/products/bmn-673.html costs that

offset the benefits of repeating the same behaviour. Where there are large asymmetries in power or dominance rank between individuals, the costs of punishing are often very low while costs inflicted on victims can be extremely high so that punishment is likely to be an evolutionary stable strategy (Clutton-Brock & Parker, 1995a). Punishing tactics may be used to reduce the incidence of feeding competition by subordinates, to constrain their access to social partners or to coerce them into cooperative behaviour (Hauser, 1992; Reeve, 1992). Subordinates PF2341066 that repeatedly infringe the interests of the same dominant individual may receive progressively larger punishments and may, eventually, be evicted from the group or even killed (Clutton-Brock & Parker, 1995a). However, while anecdotal examples of punishment are common,

experimental evidence of the benefits of punishing tactics to the punisher are rare in wild animals. One of the few examples of the consequences of punishment yet available is provided by experiments with cleaner wrasse, which involved presenting a dominant Inositol oxygenase and a subordinate with a choice of two foods, one preferred and one less preferred, which were immediately reversed if the subordinate

began feeding on the preferred food (Raihani, Grutter & Bshary, 2010). After repeated trials, dominants learned to attack subordinates if they began to eat the preferred food and subordinates learned to avoid this choice. The fact that fish are capable of learning to avoid choices that incur punishment by dominants suggests most mammals are likely to be capable of similar learning processes and that punishing tactics are often likely to increase the fitness of dominants. Conflicts of interest between group members also lead to regular harassment. For example, where two females are competing for divisible resources, repeated attempts to gain access by subordinate competitors may eventually raise the costs of continued defence to dominants until they reach a point where the net benefits of maintaining exclusive access are lower than the costs of defence. Situations of this kind resemble a ‘war of attrition’ where the winner is the individual that can afford to persist for the longest time (Clutton-Brock & Parker, 1995b). Persistent harassment can occur in a variety of circumstances.

We also investigated whether pharmacological interventions that modulated

hepatic CSAD mRNA abundance also mediated changes in renal CSAD mRNA abundance. We found that FXR agonist treatment did not alter CSAD abundance in kidney. Furthermore, renal CSAD abundance was not altered in Shp−/− mice. These data suggest that there are liver-specific regulatory components controlling hepatic CSAD response to bile acids, and that these are possibly missing or differentially regulated in kidney. It will be PARP inhibitor interesting to examine candidate liver-specific components for CSAD transcriptional regulation because both FXR and SHP (though at low levels) are expressed in kidney.[40, 41] The possibility

of extrahepatic CSAD regulation by FXR agonists should be kept in mind as human clinical trials are underway using pharmacological FXR agonists. Bile acid CoA:amino-acid N-acyltransferase and BACS, two enzymes involved in bile acid conjugation to taurine and glycine, have been demonstrated to undergo FXR-dependent regulation via a promoter inverted repeat (IR-1)[16] In the present study, we observed that this website pharmacological FXR agonist activation reduced hepatic BAT but not BACS mRNA expression. In addition, BAT and BACS mRNA abundance were similar in WT and Shp−/− mice. Taken together, these data suggest that BAT and BACS are not potently regulated by nuclear receptors SHP and FXR and neither gene appears to be regulated in tandem with CSAD. We were surprised to find that, despite a more than eightfold elevation CSAD in Shp−/− mice, hepatic hypotaurine was only 2–3-fold elevated, and hepatic taurine content did not differ from WT controls. Furthermore, PtdIns(3,4)P2 we could not detect a genotype-dependent difference in serum taurine or hypotaurine levels. One explanation could be that the excess taurine generated in the liver is partially utilized to conjugate the excess bile acids produced in Shp−/− mice.[7, 8] Because murine bile

acids are primarily taurine conjugated,[42] we would not expect a substantial alteration in the ratio of taurine:glycine-conjugation of bile acids in Shp−/− mice. In other words, while the fraction of tauro-conjugated bile acids did not differ between WT and Shp−/− mice, the overall concentration of serum tauro-conjugated bile acids was elevated in Shp−/− mice because of the increased total bile acid re-circulating pool in these mice (Fig. 4f). It is also possible that additional homeostatic mechanism such as CSAD substrate availability and altered urinary excretion act to modulate any changes in taurine concentrations that could occur in Shp−/− mice. These data suggest the need for further studies of amino acid homeostasis under conditions where bile acid metabolism is perturbed.

pylori gastritis were dependent on the extent, topography and severity of the infection; e.g. the gastric cancer risk increased exponentially with the progression of gastritis towards an achlorhydric or hypochlorhydric stomach with Staurosporine chemical structure severe mucosal atrophy and intestinal metaplasia. The earlier studies of Strickland and McKay proposed the topographic classification of atrophic gastritis into types A and B which constituted the core issue of the System. The A type indicating a corpus limited atrophic gastritis of autoimmune origin in patients with achlorhydria and with serological signs of the autoimmunity.8

Type B indicated atrophic gastritis without an autoimmune background and with atrophy limited to the antrum. This B subtype was considered “idiopathic” but was, after the discovery of H. pylori, realized to be typically related to H. pylori infection. It corresponds with the type of atrophic gastritis considered multifocal (MAG; multifocal atrophic gastritis) by Pelayo Correa in his reports from the 80s,14 or atrophic gastritis of the AB type by Glass and Pitchumoni from the 70s.15 In 1988, gastritis of “C type” was proposed by Wyatt and Dixon indicating reactive gastric lesions that were neither H. pylori associated nor autoimmune, and believed to be “chemical”

(reactive) or drug induced in nature.16 see more An important morphological parameter incorporated into the Sydney System from the literature was the “activity” of the gastritis. The activity of gastritis was first proposed and emphasized by Whitehead, Truelove and Gear in 1972.17 In their classification Dipeptidyl peptidase of gastritis, the Schindler—Glass-Pitchumoni—type topographical pattern of chronic gastritis was accepted but was complemented with the

concept of the “activity”. The “activity” indicated the co-existence of polymorphonuclear inflammation alongside the mononuclear one. This phenomenon we now consider to reflect the reaction of the host against the infection and to be strongly associated with the risk of the progression of gastritis to an atrophic pattern which is also related to the acquisitions of cytotoxic H. pylori strains. It is noteworthy that the guidelines presented in the Sydney System are still valid and applicable some 20 years later. In our view this is because the Sydney System was an appropriate synthesis at the time of the old knowledge on chronic gastritis mentioned above with the new data and knowledges about H. pylori acquisition and its consequences. It must be said the Sydney System was not a classification in strict terms but more a practical guideline that provided what we hoped might become a flexible universal gastritis reporting grid. It allowed for a standard rapid documentation of the extent and severity of the gastritis at the time of examination of the patient. H.

Elucidating the relationship between amino acid substitutions and metabolic alteration is an important step in understanding the mechanism of HCV interferon resistance. “
“Steatosis is a common histological feature of chronic liver disease, especially alcoholic and non-alcoholic fatty liver disease, as well as chronic hepatitis C. A recent study showed that evaluating the controlled attenuation parameter (CAP) with transient elastography was an efficient way of non-invasively determining the severity of hepatic steatosis. The objective of this study was to prospectively evaluate the utility of CAP for diagnosing steatosis in patients with chronic liver disease. One hundred and fifty-five consecutive patients

with suspected chronic liver disease underwent steatosis diagnosis using CAP, blood sample analyses, computed tomography for assessing the liver/spleen Doxorubicin ratio and liver biopsy. Steatosis was graded according to the percentage of fat-containing hepatocytes: S0, less than 5%; S1, 5–33%; S2, 34–66%; and S3: more than 66%. The CAP was significantly correlated with steatosis grade, and there were significant Smoothened inhibitor differences between the CAP value of the S0 patients and those of the patients with other grades of steatosis. S0 and S1–3 hepatic steatosis were considered to represent mild and significant steatosis, respectively.

The CAP values of the patients with mild and significant steatosis were significantly different (P < 0.0001). The area under the receiver–operator curve (AUROC) value of the CAP for diagnosing significant steatosis was 0.878 (95% confidence interval, 0.818–0.939), and the optimal CAP cut-off value for detecting significant steatosis was 232.5 db/m. Nintedanib (BIBF 1120) In multivariate analysis, the CAP (P = 0.0002) and the liver to spleen ratio (P = 0.004) were found to be significantly associated with significant steatosis. The CAP is a promising tool for rapidly and non-invasively diagnosing steatosis. “
“The consensus meeting for the diagnosis, management and treatment for hepatitis C was held in 45th annual meeting for the Japan Society of Hepatology

(JSH) in June 2009 where the recommendations and informative statements were discussed including organizers and presenters. The Several important informative statements and recommendations have been shown. This was the fourth JSH consensus meeting of hepatitis C, however, the recommendations have not been published in English previously. Thus, this is the first report of JSH consensus of hepatitis C. The rate of development of hepatocellular carcinoma (HCC) in HCV-infected patients in Japan is higher than in the USA, because the average age of the HCV-infected patients is greater and there are more patients with severe fibrosis of the liver than in the USA. In Japan, more than 60% of HCV-infected patients are genotype 1b infection, and they show lower response to perinterferon and ribavirin combination treatment.

Results: Crown material had no significant effect on microleakage (p= 0.67);

however, cement type had a significant effect (p < 0.0001), with Panavia F 2.0 resulting in lower microleakage scores than RelyX Unicem. Conclusions: Compared to the self-adhesive cement, the resin cement with separate primer/bonding agent resulted in significantly lower microleakage scores, irrespective of crown material. "
“This article describes a new, precise, and simple method for making an impression with an individual tray for a patient with microstomia. In this method, a Pindex system on the handle of the tray was used for attaching two parts of the sectional tray. “
“Purpose: This study evaluated the degree of conversion (DC) of four indirect resin composites (IRCs) with various compositions processed in different polymerization units and investigated the effect of thermal aging on the flexural MG-132 research buy strength and Vicker’s microhardness. Materials and Methods: Specimens were prepared from four IRC materials, namely Gr 1: Resilab (Wilcos); Gr2: Sinfony (3M ESPE); Gr3: VITA VMLC (VITA Zahnfabrik);

Gr4: VITA Zeta (VITA Zahnfabrik) using special molds for flexural strength test (N = 80, n = 10 per group) (25 × 2 × 2 mm3, ISO 4049), for Vicker’s microhardness test (N = 80, n = 10 per group) (5 × 4 mm2) and for DC (N = 10) using FT-Raman Spectroscopy. For both flexural strength and microhardness tests, half of the specimens were randomly stored in distilled water at 37°C for 24 hours (Groups 1 to 4), and the other half (Groups 5 to were subjected to thermocycling (5000 cycles, 5 to 55 ± 1°C, dwell time: 30 seconds). Flexural strength was measured in a universal testing machine (crosshead speed: 0.8 mm/min). Microhardness test was performed at 50 g. The data were analyzed using one-way and two-way ANOVA and Tukey’s test (α= 0.05). The correlation between flexural strength and STK38 microhardness was evaluated with Pearson’s correlation test (α= 0.05). Results: A significant effect for the type of IRC and thermocycling was found (p=

0.001, p= 0.001) on the flexural strength results, but thermocycling did not significantly affect the microhardness results (p= 0.078). The interaction factors were significant for both flexural strength and microhardness parameters (p= 0.001 and 0.002, respectively). Thermocycling decreased the flexural strength of the three IRCs tested significantly (p < 0.05), except for VITA Zeta (106.3 ± 9.1 to 97.2 ± 14 MPa) (p > 0.05) when compared with nonthermocycled groups. Microhardness results of only Sinfony were significantly affected by thermocycling (25.1 ± 2.1 to 31 ± 3.3 Kg/mm2). DC values ranged between 63% and 81%, and were not significantly different between the IRCs (p > 0.05). While a positive correlation was found between flexural strength and microhardness without (r = 0.309) and with thermocycling (r = 0.100) for VITA VMLC, negative correlations were found for Resilab under the same conditions (r =−0.

To find their expression profile, we tested whether hepatic insulin resistance elicited by HFD feeding affects the miRNA levels. In particular, the levels of miR-122 were significantly decreased in mice fed an HFD, implying that miR-122 dysregulation may be associated with the induction of PTP1B (Fig. 1B,

lower). The buy FK506 levels of other miRNAs were not changed (Fig. 1B, lower). miR-1 (a muscle-specific miRNA) was not detected in the liver. Next, a cell model was used to assess the expression profile of the miRNAs. Treatment of HepG2 cells with tumor necrosis factor-α (TNF-α) weakly, but significantly, increased PTP1B mRNA levels (Fig. 1C). TNF-α treatment induced PTP1B to a much greater extent (Fig. 1C), and decreased levels of the miRNAs predicted to bind the 3′UTR of the mRNA (Fig. 1D). Our in vivo and in vitro findings in conjunction with the database analyses suggested that miR-122 dysregulation might contribute to the posttranscriptional regulation of PTP1B. Next, we explored the functional role of miR-122 in the repression of PTP1B. First, in vitro assays were performed using miR-122 inhibitor or its mimic. Transfection of HepG2 cells with miR-122 inhibitor induced PTP1B (Fig. 2A), whereas miR-122 mimic transfection diminished its expression (Fig. 2B). Consistently,

transfection with miR-122 inhibitor increased the level Selleckchem CP-673451 of PTP1B mRNA, whereas miR-122 mimic transfection decreased selleck chemicals llc it (Fig. 2C,D), indicating that miR-122 may facilitate the degradation of PTP1B mRNA. To further prove a direct interaction between miR-122 and its binding site within the mRNA, luciferase activities from the PTP1B 3′UTR reporter construct were measured. As expected, miR-122 inhibitor transfection significantly increased luciferase expression from pEZX-PTP1B luciferase construct, whereas its mimic transfection decreased it (Fig. 2E,F), which verifies PTP1B as a direct target of miR-122. JNK1 dampens the normal insulin response by inhibiting IR signaling through serine phosphorylation of IRS1/2, playing a role in the development of obesity and insulin resistance.13 Because JNK1 is closely linked to IR in mice fed an HFD or cell models

exposed to TNF-α,12 we measured the levels of miR-122 and PTP1B in HepG2 cells transfected with the construct encoding for HA-tagged JNK1 (HA-JNK1) or a dominant-negative form of JNK1 (DN-JNK1). Overexpression of JNK1 decreased miR-122 levels, as verified by an increase in the miR-122 3′UTR luciferase activity, whereas that of DN-JNK1 had the opposite effect (Fig. 3A,B). In addition, enforced expression of JNK1 increased the pEZX-PTP1B luciferase activity and induced PTP1B protein levels (Fig. 3C). DN-JNK1 transfection exerted the opposite effect (Fig. 3D). JNK2 overexpression had no effect on miR-122 or PTP1B levels (Fig. 3E). These results showed that JNK1, but not JNK2, represses miR-122 levels, which may lead to the induction of PTP1B.

The remaining 461 patients (264 men, 197 women; age range 38–93 years; mean age 68.2 ± 8.7 years) were enrolled in this study. They consisted of 107 (23.2%) elderly subjects, aged Enzalutamide cell line 75 years or over, and 354 non-elderly subjects. According to the estimate released by the National Cancer Center, Japan, the number of liver cancer mortalities in Japanese persons aged over 75 years increased, whereas that of subjects under 75 years decreased between 2004 and 2008.16 Additionally, the incidence of liver cancer continually increased in Japanese persons over 75 years

until 2005, whereas the incidence in persons under 75 years reached its peak in 2003.17 Therefore, we divided subjects into two groups (those <75 years and those ≥75 years) to analyze and discuss the strategy of treatment for elderly HCC patients. The indication for RFA treatment was that HCC consisted of five or fewer nodules, with each nodule having a maximum diameter of 30 mm, or that HCC consisted of a single tumor, regardless of size, and that hepatic function was not Child–Pugh grade C. MK-8669 manufacturer Radiofrequency ablation treatment was applied to cases (n = 226) that were not considered

to be suitable for resection for the following reasons: (i) impairment of liver function, and (ii) an excessive number of tumors or cardiopulmonary dysfunction. In addition, we applied RFA in cases (n = 235) where patients chose ablation therapy

even though surgery was also feasible. Exclusion criteria for RFA were: (i) click here total bilirubin concentration over 3 mg/dL; (ii) platelet count under 30 000/mm3; (iii) prothrombin activity under 50%; (iv) ascites that could not be controlled by nutritional therapy and diuretics; and (v) patients with portal vein tumor thrombosis or extrahepatic metastasis. When four or more nodules were detected or the largest nodule was over 3 cm, RFA was preceded by transcatheter arterial chemoembolization (TACE) using epirubicin and gelatin sponge particles. Using combined examinations from ultrasonography and dynamic computed tomography (CT) scans or dynamic magnetic resonance imaging (MRI) or CT during angiography, diagnosis of HCC was confirmed in cases where the contrast pattern of the nodule in CT or MRI was hypervascular in the arterial phase and hypovascular in the portal phase. If the nodules were not consistent with typical contrast patterns for HCC, a needle biopsy of the tumor was taken for pathological diagnosis. The American Joint Committee on Cancer (AJCC)/International Union Against Cancer (UICC) 6th edition staging system for HCC was used for Tumor–Node–Metastasis (TNM) classification.18 The following three RF systems were used. From January 2000 to March 2000, 25 patients underwent RFA treatment using an RF 2000 generator system (Radio Therapeutics, Mountain View, CA, USA).