These drug combinations were analyzed using the combination index (CI) as well as Prichard and Shipman’s method.34 Each drug was combined with FQ at different fractions of their IC50 value. Combination of FQ with boceprevir and IFN-α resulted in an additive effect, as reflected by a CI of 0.97 (± 0.03) and 1.08 (± 0.18), respectively. Furthermore, synergy was also observed for some higher concentrations, as measured by Prichard and Shipman’s method34 (Fig. 7). HCV entry represents an attractive target for antiviral intervention, with opportunities to prevent multiple virus-receptor interactions and interfere with virus-cell membrane fusion.35 In this study,

we showed that FQ exhibits a genotype-independent antiviral activity against HCV by inhibiting a postbinding and postinternalization step of HCV entry into target cells and by blocking cell-to-cell spread between neighboring cells. Although FQ is an analog of CQ, its mechanism of action is potentially Seliciclib ic50 different.12 The mechanism of inhibition by CQ involves impaired endosomal-mediated virus entry, CDK activation most likely through the prevention

of endocytosis and/or endosomal acidification. In contrast, FQ has weaker base properties, compared to CQ.36 This difference could potentially explain the lack of antiviral activity of FQ against viruses such as vesicular stomatitis virus, influenza virus, or Sindbis virus,14 whereas CQ blocks cell entry of these viruses as well as other pH-dependent viruses.37-39 Other interesting features of FQ are its higher lipophilicity (at pH 7.4) and the peculiar conformation provided by an intramolecular hydrogen bond present in nonpolar conditions, which result in a better potency for FQ to cross membranes.40 In addition, FQ has also been AMP deaminase shown to specifically generate reactive oxygen species and induce lipid peroxidation.40, 41 Recently, it has been shown that HCV envelope proteins form large molecular complexes stabilized by intermolecular disulfide bonds.42 This observation strongly suggests that the entry process necessitates a rearrangement of these disulfide

bonds for the fusion process to take place. Therefore, it is possible that the oxidative properties of FQ in acidic conditions could inhibit the fusion process by affecting reorganization of the disulfide bonds within endosomes. FQ inhibits a postbinding and postinternalization step of HCV entry into target cells. Indeed, FQ does not affect binding of HCVcc to Huh-7 cells or the expression of specific cellular entry factors. Furthermore, the effect of FQ on HCVpp strongly suggests that FQ affects the entry function of HCV envelope proteins and not the lipoprotein moiety associated with the virion. Our data also show that FQ blocks HCV entry by inhibiting the fusion process. Finally, the S327A-resistant mutation identified in this work suggests that E1 could be the target of FQ. In addition to its effect on HCV entry, FQ can also affect HCV RNA replication, albeit at higher concentrations.

[28, 29] It is likely that complex, ethnically based differences in immune response to HCV underlie the benefit of matching grafts from AA donors to AA liver recipients. Most famously, IL28-B CC (versus non-CC) genotype has a well-described linkage to viral clearance pretransplant; and the disparity of CC prevalence in AAs versus non-AAs partially explains poorer response to interferon-based treatments.[23, 30] Charlton and colleagues[31] have recently confirmed that IL28B CC recipient status and CC donor status are positively associated with postliver transplant sustained viral response.

Kinase Inhibitor Library cell assay Interestingly, however, genotype CC donors were associated with greater posttransplant fibrosis, graft failure, and liver-related death.

Biggins et al.[32] recently confirmed these latter findings with more severe HCV disease seen with IL28B CC grafts, especially when transplanted into non-CC recipients. It may be that the lower likelihood of IL28B-CC genotype among AA donors underlies the superior outcomes in HCV-positive AA recipients receiving AA Fulvestrant supplier donor grafts. Our study has limitations inherent to the retrospective collection of donor characteristics and recipient outcomes in a large database. However, the size of the database and the relatively standardized, prospective collection of pretransplant recipient and donor data add statistical power and generalizability to our results. It represents the largest possible cohort of HCV-positive AAs recipients and is consistent with prior results from multicenter and center-specific studies of HCV disease outcomes in AA recipients.[5, 14] In summary, we identified the key donor factors associated with graft survival Methane monooxygenase among AA LT recipients with HCV: donor age, donor

race, and CIT. The AADRI-C will be helpful to clinicians making decisions about specific donor offers for HCV-positive AAs, in guiding the intensity of post-LT monitoring and timing of post-LT antiviral therapy, and in framing discussions with AA recipients regarding graft selection. Ultimately, with the use of AADRI-C, as well as improved therapeutic interventions, it is anticipated that AA LT recipients with HCV will enjoy the same post-LT outcomes as other non-AA liver recipients. Additional Supporting Information may be found in the online version of this article. “
“Platelets have a very close relationship with the liver, the source of thrombopoietin. Thrombocytopenia is common in patients with acute liver injuries such as acute liver failure, acute exacerbation of chronic hepatitis B, and acute-on-chronic liver failure.[1-3] And patients’ platelet count often improves once the acute liver injury is resolved. The degree of thrombocytopenia also parallels the extent of chronic hepatic injury.

26 In addition, covered stents in the gastrointestinal tract may be more susceptible to food impaction while, in the bile duct, biofilms may develop in a similar way to those in plastic stents. Stents inserted into the bile duct to overcome biliary obstruction can be composed of either plastic or metal. Plastic stents become obstructed by biofilms after 2–6 months but can be readily exchanged. SEMS facilitate bile flow for a longer period but cause pressure necrosis

and pseudo-epithelialization over time and become buried within the bile duct wall.28 Because of this, the stent is very difficult to extract once it has been inserted.29 With covered stents, there have also HDAC activation been concerns about the frequency of migration and the frequency of complications such

as cholecystitis and pancreatitis. Risks for migration are minimized by the use of stents with uncovered ends. Cholecystitis and pancreatitis can be caused by obstruction of the cystic duct and main pancreatic duct, respectively, but clinical studies indicate similar frequencies of these complications with covered stents as with uncovered stents.30 The physical properties and characteristics of biliary metal stents, colonic metal stents and gastroduodenal stents are outlined in Tables 1–3. Various esophageal stents are shown Nutlin-3 research buy in Fig. 1. The Wallstent for the esophagus is made from cross-hatched stainless steel wire and exerts a strong radial force. Two models are currently available, Wallstent II and Flamingo Wallstent. The Wallstent II is covered with silicon polymer except for 2 cm on both ends while the Flamingo Wallstent is designed for use in the lower esophagus and is partially covered with polyurethane.22 The enteral Wallstent TTS (through-the-scope) has been developed for use in patients

with malignant strictures of the stomach and duodenum. Stents Methocarbamol have a length of 60–90 mm with an internal diameter of 20–22 mm. These stents have sharp metal ends and are uncovered without flares. More recently, a WallFlex enteral duodenal stent, composed of nitinol, has become available for the management of malignant strictures of the pylorus, duodenum and large intestine. The stent has blunt ends, a mid-body diameter of 25 mm and can be inserted through endoscopes with a working channel of larger than 3.7 mm. Wallstents used in the biliary system include a stainless steel uncovered stent and a nitinol stent covered with silicon. With the uncovered stent, there is substantial shortening at the time of insertion and exposed wires have the potential to damage the duodenal wall. Although tightly woven wires may limit tumor ingrowth, stents become obstructed after 4–5 months in 20–40% of patients.31,32 Whether tumor ingrowth can be further impeded by nitinol stents covered with silicon has not been determined. The Ultraflex stent used in the esophagus (Fig.

We hypothesized that IL-1 7A may also play a direct role by enhancing activation of HSC. Aim: The aim of this study was to characterise the effect of IL-1 7A exposure on activation of HSC and induction of fibrogenic signaling in these cells Methods: The human HSC line LX2 and primary human HSCs were stimulated with increasing doses of IL-17A and compared to TGF-β and PBS-treated cells as positive and negative controls, respectively. Activation of HSCs was evaluated by qRT-PCR for alpha-smooth muscle actin (α-SMA), Neratinib order collagen type I (COL1A1) and

tissue inhibitor of matrix metalloproteinase I (TIMP-I). Results were correlated with protein expression by western blots and picro-Sir-ius red staining for collagen deposition. Cell surface expression of the cytokine receptors TGF-β-RII and IL-17RA was evaluated by flow cytometry. Signaling through the TGF-β receptor was evaluated

by examining phosphorylation of SMAD2/3 by Western following cytokine stimulation. Results: IL-1 7A alone did not induce activation of HSC. However, IL-1 7A sensitized HSCs to the action of suboptimal doses of TGF-β as confirmed by strong induction of α-SMA, collagen type I and TIMP-I gene expression and protein production. IL-1 7A specifically up-regulated and stabilized the cell surface expression of TGF-β-RII following stimulation. Pretreatment of HSCs with IL-1 7A enhanced signaling through the TGF-β-RII Crizotinib cell line as observed by increased phosphorylation of SMAD2/3 in response to stimulation with sub-optimal doses of TGF-β. Conclusion: Our results suggest a novel pro-fibrotic function for IL-1 7A through sensitization of HSCs to the action of TGF-β. IL-1 7A acts through up-regulation and stabilization of the TGF-β-RII leading to increased SMAD2/3 signaling. These findings represent a novel example of cooperative signaling between an immune cytokine and a fibrogenic receptor. Disclosures: Scott L. Friedman – Advisory Committees or Review Panels: Pfizer Pharmaceutical, Sanofi-Aventis; Consulting: Abbott Laboratories, Conatus Pharm, Exalenz, Genenetch, Glaxo Smith Kline, Hoffman-La Roche, Intercept Pharma, Isis Pharmaceuticals, Melior

Discovery, Nitto Denko Corp., Debio Pharm, Synageva, Gilead Pharm., Ironwood Pharma, Alnylam Pharm, Tokai Pharmaceuticals, Bristol Myers Squibb, Takeda Pharmaceuticals, Nimbus Discovery, Isis Pharmaceuticals; Methocarbamol Grant/Research Support: Galectin Therapeutics, Tobira Pharm, Vaccinex Therapeutics; Stock Shareholder: Angion Biomedica The following people have nothing to disclose: Thomas Fabre, Hassen Kared, Naglaa H. Shoukry Background Progression of liver fibrosis is characterized by synthesis and degradation of extracellular matrix (ECM). Matrix-metalloproteinases (MMP) cleave collagen fibres at a specific site generating soluble fragments of ECM (neo-epitopes). The levels of these neo-epitopes may reflect the stage of liver fibrosis and could allow the monitoring of anti-fibrotic therapies.

6%) considered themselves to have knowledge about MOH to some (n = 149; 66.5%) or a greater extent (n = 54; 24.1%; Table 2). Ten percent reported that they had no knowledge about MOH at all (n = 21). There was no difference in knowledge between professional categories or between groups with different working experience. Of 189 respondents, almost half (n = 88; 46.6%) had learned about MOH through their

university/vocational education. The other respondents (n = 101) had learned about it through, eg, colleagues or internal training at the pharmacy. Of those who learned through university/vocational education, more than one third (n = 31; 35.2%) perceived BGJ398 concentration their knowledge to be extensive. This was significantly higher compared with those who learned about MOH in other ways (n = 21; 20.8%; P = .027). The actual knowledge on MOH varied Belnacasan mouse between different questions asked. The results on the question concerning characteristics of individuals with a higher risk of developing MOH are shown in Table 3. Among those who perceived themselves as having some or extensive knowledge about MOH, more than half marked the correct category for the factor age (n = 114; 60.3%) as well as gender (n = 137; 71%), but only one third were correct concerning educational level (n = 63;

32.8%). Those who reported no knowledge at all did not respond to these questions, nor to the question on medications causing MOH. Of 189 respondents, fewer than 10% (n = 16; 8.6%) knew that all 5 medications listed can cause development of MOH. The type of medication most frequently missed was ergotamine (n = 48). Among those who included only 1 medication in their response (n = 32), the 2 most frequent answers were NSAIDs (n = 24; 75%) and paracetamol (n = 5; 16%). Among those who learned about MOH during their university/vocational education, 5.6% indicated that all 5 medications can cause

MOH, compared with 11.6% among those who learned about MOH in other ways (P = .190). Regarding the question about treatment advice on MOH (n = 218), 40% responded correctly, ie, that treatment should be in the form of abrupt withdrawal from or a tapering down of medications. A somewhat higher proportion (41.7%) gave Bumetanide other answers, eg, referral to a doctor, relaxation exercises, or regular life habits. Almost one fifth of the respondents (n = 39; 17.8%) reported that they did not know. Among those who had learned about MOH during their university/vocational education, 47.1% knew the correct advice, compared with 35.7% among those who had learned about MOH in other ways (P = .120). The relationship between self-perceived and actual knowledge is presented in Table 4. Actual knowledge on treatment advice differed significantly between groups of self-perceived knowledge. The Pearson correlation analyses showed no significant correlations between self-perceived and actual knowledge for any group in relation to source of knowledge about MOH.

Rat stellate cells, a gift from Dr. Hsuan-Shu Lee at NTUH, were characterized as described.20 Mouse portal fibroblasts were freshly isolated from C57BL6 mice according to a published protocol.21 Cells were used at low-passage AZD5363 numbers (less than 10 and 5 for stellate cells and portal fibroblasts, respectively). Student’s t test was used to evaluate the differences between two different parameters. A two-sided P-value of

less than 0.05 was considered statistically significant. To establish whether HAI-1 and HAI-2 expression is changed in BA, we performed Q-PCR to analyze their messenger RNA (mRNA) levels in the livers of BA patients, including two groups of patients who received the Kasai operation: patients without disease progression (BA1 group, average age at biopsy: 59.0 days), patients with disease progression in need of LT (BA2 group, average age at biopsy: 52.2 days), and a third group of patients receiving LT (LT group, average age at surgery: 330.7 days) due to endstage BA. Liver samples with NH (NH group, average age at biopsy: 51.6 days, no significant difference in the age of biopsy between NH, BA1, and Poziotinib BA2 groups) and from the nontumor (near-normal) part of patients with metastasized liver tumors were also included as controls. The results showed that HAI-1 expression was significantly increased in the livers of BA patients compared with that in the NH group

(Fig. 1A) (BA2 versus NH, P < 0.05; BA1 and BA2 versus NH, P < 0.01). Moreover, the extent of HAI-1 up-regulation was increased in endstage BA (LT versus BA1, P < 0.05; LT versus BA2, P < 0.01; LT versus BA1 and BA2, P < 0.01). Similarly, HAI-2 expression was significantly increased in the livers of the LT group compared with NH and BA1 groups (Fig. 1A; LT versus NH, P < 0.01; LT versus BA1, P < 0.05). In addition, immunofluorescence (IF) microscopy showed that in normal liver both HAIs were selectively expressed in the bile duct (Fig. 1B), whereas in BA livers HAI-1- or HAI-2-positive cells were found in the ductular reactions

of portal areas, including bile duct- and ductule-like structures, cell clusters, Clomifene and even in single cells (Fig. 1B). To further determine whether the up-regulation of both HAIs in human BA livers was caused by obstructive jaundice, we employed two widely used murine models of obstructive cholestasis, in which the pathology is induced by bile-duct ligation18 or rotavirus infection.22 In the first model we surgically ligated the mouse bile duct for 2 weeks to induce obstructive cholestasis and portal fibrosis; control mice received sham operations. Silver staining, used to highlight collagen (Fig. 1C), showed that the bile-duct ligation successfully induced portal fibrosis and ductal proliferation. In the second model we infected newborn mice with rotaviruses and euthanized them after 2 weeks.

Results are expressed as median and range and mean ± standard deviation. For statistical analyses, the Student t test was used. Significance was defined as P < 0.05. We

initially characterized the “purinergic phenotype” of wild-type and quiescent NK cells with regard to the expression of ectonucleotidases and P2 receptors (Fig. 1A,C) using the procedures described previously for NKT cells.14 CD39/E-NTPDase1 expression is dominant among all NK cell ectonucleotidases, including ecto-nucleotide pyrophosphatase/phosphodiesterases (Enpp) and alkaline phosphatases. CD73/5′ ectonucleotidase (Nt5e) is expressed at very low levels by NK cells (Fig. 1A). Hence, sorted hepatic NK cells efficiently hydrolyze adenosine diphosphate (ADP) with respective generation

of adenosine monophosphate (AMP); but these cells largely do not generate adenosine (Fig. 1B). Deletion of CD39 can be shown to substantially delay generation of AMP from ADP. These data clearly demonstrate that extracellular nucleotides can be efficiently hydrolyzed to AMP by NK cells from wild-type mice, whereas cells from CD39-null mice show markedly attenuated phosphohydrolysis resulting in decreases in levels of derived AMP and adenosine. In contrast, wild-type NKT cells express both CD39 and CD73 ecto-enzymes at high levels and will generate adenosine as an end-product.14 No compensatory up-regulation of NTPDase activity is observed in NK cells

where CD39 has been deleted, as is also the case of NKT cells and other immune cells null for CD39 (BGJ398 mw Supporting Fig. 1A).8, 13–15 We note that expression of P2 receptors in NK cells is restricted to P2Y1, P2Y2, P2Y14, P2X3, and P2X6 (Fig. 1C). NK cells also express P1 receptors with the A2A subtype expressed at the highest level, followed by A3 and A2B at lower levels; NK cells do not express the A1 receptor subtype. Deletion of CD39 does not impact messenger RNA levels of P2-receptors in either quiescent or activated cells (Supporting Fig. 1B). In order to exclude differences in baseline activation of CD39-null versus wild-type NK cells, we compared expression of various surface markers Endonuclease of the two NK cell subtypes isolated from spleens (Fig. 2). The major recognized activation markers did not differ between wild-type and mutant NK cells purified from nonmanipulated wild-type and mutant mice null for CD39. However, CD39-null NK cells did exhibit decreased levels of CD27 with altered patterns of killer cell lectin-like receptor subfamily G, member 1 (KLRG1) expression. The comparable levels in purinergic receptors and the altered levels of CD27 and KLRG1 persisted after activation of NK cells with IL-12 and IL-18 in vitro (data not shown). In a standard mouse model of partial, warm hepatic IRI, the left liver lobe was clamped for 75 minutes. Reperfusion was allowed in different groups for 3 hours, 24 hours, and 4 days.

Obesity is associated with severer forms of liver pathology and fibrotic progression in NASH.37 While some controversy remains over the causes of the current obesity pandemic, there is strong evidence of increased caloric consumption in the last 20–30 years which correlates well with increasing weight and waist circumference.38 What drives over-nutrition is a complex interaction of biology (genes) and environment (behavior),

but the following are all likely contributors: central appetite regulation, food/energy intake, energy expenditure and metabolic regulation (Fig. 1). Mammals are physiologically attuned to regulate food intake according to bodily energy needs. Such regulation is exerted by several hormones that either act rapidly to influence day-to-day food intake (reviewed in 39,40), or act more slowly to regulate adipose TSA HDAC cell line storage lipid. Long-term appetite regulators include insulin and leptin, which exert their effects on appetite centers in the hypothalamus and brainstem.40 Obesity resulting from over-eating (hyperphagia) involves defects in this control system. While insulin and adiponectin play some role in modulating appetite, discussion

here will focus on the PLX4032 in vitro role of leptin, which several studies have shown has a more important role in the central nervous system (CNS) control of food intake and energy expenditure. Originally identified as a major anorexigenic peptide,41 leptin arises from white adipose tissue

(WAT), and serum levels increase in proportion to total body fat content to alert the brain to the state of body adiposity.42,43 Leptin crosses the blood-brain barrier via a saturable process and interacts, via liganding to the long form of the leptin receptor (LEPRb), with two distinct neuronal populations. The first synthesize and release orexigenic peptides, neuropeptide Y (NPY)44 and Agouti-related protein (AgRP).45 The second express the anorexigenic molecule, melanocyte stimulating hormone (α-MSH), derived from pro-opiomelanocortin (POMC),46 learn more and cocaine and amphetamine-regulated transcript (CART).47 Thus, as shown in Fig. 2, leptin binds LEPRb on NPY/AgRP neurons to suppress these appetite-stimulating pathways, while simultaneously activating the appetite-suppressing POMC/α-MSH pathway (Fig. 2). In over-weight patients with NAFLD, leptin circulates in abundance and clearly fails to suppress appetite.48 Such CNS resistance to leptin action is now understood in terms of defective LEPRb signaling, involving several possible molecular mechanisms (Fig. 3). Leptin deficiency is the basis of obesity and NAFLD in ob/ob mice as well as rare cases of severe, monogenic childhood obesity (that can be corrected by exogenous leptin therapy).49–51 Mutations of the LEPRb occur in db/db mice and fa/fa (Zucker) rats, and are also rarely found in humans (Table 2).

There was a statistically significant difference between the Ni-Cr control subgroup and the other two bleached subgroups, while there was no difference between the two bleached subgroups. Results also showed that increasing the concentration of bleaching agents increased the surface roughness of all the tested alloys. There was a statistical difference between the Ni-Cr alloy and the other two alloys in all tested subgroups except the in-office SB203580 clinical trial bleached subgroup, for which no difference between the surface roughness of the Ni-Cr alloy and the Co-Cr-Ti alloy was found. Scanning electron

microscopic examination revealed surface deteriorations in the two bleached subgroups for all tested ceramometallic alloys. Conclusion: Surface topographic alterations occurred as a result of the application of bleaching agents. These alterations increased with the increase of the carbamide peroxide concentration. “
“Purpose: This study evaluated the effects of different bar materials on stress distribution in an overdenture-retaining bar system with a vertical misfit between implant and bar framework. Materials and Methods: A three-dimentional finite element model was created including two titanium implants and a bar framework placed in the anterior part of a severely reabsorbed jaw. The model set was exported to mechanical simulation software, where displacement was applied to simulate the screw torque limited by 100-μm vertical misfit. Four bar materials

(gold alloy, silver-palladium PS-341 clinical trial alloy, commercially pure titanium, cobalt-chromium alloy) were simulated in the analysis. Data were qualitatively evaluated using Von Mises stress given by the software. Results: The models showed stress concentration in cortical bone corresponding to the cervical part of the implant, and in cancellous bone corresponding to the apical part of the implant; however, in these regions few changes were observed in the levels of stress on the different bar materials analyzed. In the bar framework, screw, and implant, considerable increase in stress was observed when the elastic modulus of the bar material was increased. Conclusions: The different materials

of the overdenture-retaining bar did not present considerable influence on the stress levels in the periimplant bone tissue, while the mechanical components of the system were more sensitive to the material see more stiffness. “
“Purpose: This study assessed masticatory efficiency and duration of the masticatory cycle in 14 asymptomatic patients with severe bone resorption. All patients had worn complete dentures for over 10 years. Recall visits were scheduled at 5 months and 1 year after receiving new dentures. Materials and Methods: Fourteen patients were evaluated in this study. The Research Diagnostic Criteria questionnaire and tests of the efficiency and duration of the masticatory cycle were performed with artificial food before, 5 months after, and 1 year after new dentures were delivered.

Conclusions: The spliceosome factor SART1 is not IFN-inducible but is an IFN effector gene. SART1 exerts its anti-HCV action through direct transcriptional downregulation for some ISGs (e. g., IFIH1) and alternative splicing for others, including EIF4G3, G〇RASP2, and ZFAND6. SART1 does not have effects on IFN receptor or components. Taken together,

these data imp ulates ISGs in a non-classical manner. Disclosures: Raymond ī. Chung – Advisory Committees or Review Panels: Idenix; Consulting: Enanta; Grant/Research Support: Gilead, Merck, Mass Biologic, Gilead see more The following people have nothing to disclose: Wenyu Lin, Chuanlong Zhu, Jian Hong, Lei Zhao, Qikai Xu, Pattranuch Chusri, Nikolaus Jilg, Dahlene N. Fusco, Esperance A. Schaefer, Cynthia Brisac, Lee F. Peng “
“Aim:  To evaluate changes Hydroxychloroquine in liver function parameters and risk factors 1 year after percutaneous radiofrequency ablation (RFA) therapy in patients with hepatocellular carcinoma (HCC). Methods:  Subjects in this retrospective study comprised 45 patients with HCC who underwent RFA therapy (RFA alone, n = 25; transcatheter arterial embolization therapy before RFA, n = 20) and showed no recurrence of HCC 1 year after RFA.

Serial changes in serum total bilirubin, albumin, prothrombin time and Child–Pugh score (CPs) were evaluated before and after RFA. In addition, Cox proportional hazards regression analysis was used to clarify risk factors for aggravation of liver function after RFA therapy. Results:  Serum albumin levels showed a significant decrease from before (3.6 ± 0.4 g/dL) to 12 months

after RFA therapy (3.2 ± 0.4 g/dL; P ≤ 0.05). CPs was significantly increased from before (6.4 ± 1.4) to both 6 months (6.8 ± 1.9; P ≤ 0.05) and 12 months after RFA (6.9 ± 2.0; P ≤ 0.05). Based on stepwise multivariate analysis, CPs of 9 or more before RFA was selected as a check details significant risk factor for long-term aggravation of liver function after RFA. Conclusion:  Liver function parameters, particularly serum albumin level, gradually and dominantly decreased in HCC patients with grade B and C according to the CPs classification over the course of 1 year after RFA therapy. A CPs of 9 or more represents a major risk factor for the aggravation of liver function after RFA therapy. “
“Aim:  Non-alcoholic steatohepatitis (NASH) patients frequently have hypertension, which is considered to be an important predictive factor for the subsequent development of hepatic fibrosis. The renin-angiotensin system is also known to contribute to the progression of NASH. Various types of functional single-nucleotide polymorphisms (SNPs) involved in the development of NASH have been proposed. Angiotensinogen (AGT) gene SNPs related to cardiovascular diseases have been reported. We aimed to evaluate the involvement of the AGT gene haplotype in Japanese NASH patients.