99+/−14.24°, .62+/−.38 cm/second/mmHg, and .41+/−.13, respectively. Gain exhibited a difference by age (P = .03). PS, gain, and Mx values showed excellent interhemispheric correlation (r > .8; P < .001). PS and gain showed good reliability (R ICC = .632, L ICC = .576; P < .001). PS and Mx showed fair correlation (r = −.37; P < .001). CA EPZ015666 parameters obtained by time- and frequency-domain methods correlate well, and show good interhemispheric and test-retest reliability. Group means from healthy controls may provide adequate norms for determining abnormal CA in cerebrovascular patients. “
“Previous studies have found gray

matter alterations in the cerebellum and in the visual system in both adults and adolescents with schizophrenia. The present study was conducted to investigate whether white matter tracts associated with these regions are also affected in the early stages of the disorder. Using a 1.5 Tesla magnetic resonance imaging (MRI) scanner and fiber tracking, the optic radiations and the middle cerebellar peduncles were examined in 13 adolescents with first-admission schizophrenia and 13 healthy controls matched for age, gender, school type, and handedness. Patients with schizophrenia displayed significantly BGJ398 mw decreased fractional anisotropy in the optic radiations, but no differences in the middle cerebellar peduncles compared to healthy controls. Our findings of altered fiber integrity in the optic radiations in adolescents

with schizophrenia are in line with gray matter alterations in the visual cortices previously reported in the same sample and are in accordance with other studies that found decreased fractional anisotropy in these regions. These findings support the view that the visual system plays an important role in the pathogenesis of schizophrenia and may enhance our understanding of associations between

the visual cortex and symptoms of the disorder. “
“Carotid intraplaque hemorrhage leads to plaque progression and ischemic events. learn more Detection can be accomplished with 3T T1w sequences, but may be limited by false-positive lipid/necrosis. The purpose of this study was threefold: (1) to determine if magnetization-prepared rapid acquisition with gradient-echo (MPRAGE) detects intraplaque hemorrhage versus lipid/necrosis; (2) if 3T MPRAGE image quality is retained at 1.5T; and (3) to determine observer agreement. MPRAGE positive areas were compared to hemorrhage and lipid/necrosis areas from 100 carotid endarterectomy slides in 12 subjects using multivariable linear regression. Image quality was determined between 3T and 1.5T in 716 carotid arteries using t-tests and multivariable linear regression. Kappa analysis was used to determine agreement. Intraplaque hemorrhage, not lipid/necrosis, was a significant predictor of MPRAGE positive area before and after adjusting for confounders (slope = .52 vs. .51, P < .001). Image quality at 3T was slightly lower than 1.5T (mean 3.87 vs. 4.

Methods: Use of Metylene blue and direct puncture of Bilary tree. Results: We present a case of a 55 old man, who have been submitted to a Whipple procedure due to a pancreatic head tumor, with a CHILD reconstruction. One year later, he presents with cholestasis – alkaline phosphatase 1313 U/L, gama-glutamyltransferase 834 U/L, alanine aminotransferase 83 U/L, aspartate aminotransferase 80 U/L, Raf activation total bilirubin 6,5 mg/dl and direct bilirubin 5,5 mg/dl. Abdominal ultrasound and computed tomography revealed dilated intra and extrahepatic bile ducts, with a diameter of 20 millimetres. Patient was submitted to an ERCP, but hepatojejunal

anastomosis wasn’t found. An echoendoscope was introduced through afferent loop and a transjejunal EUS-guided puncture of

intrahepatic bile duct, with a 19-gauge needle, was performed. Cholangiography revealed dilation of biliary tree already described and an anastomotic stenosis. Blue methylene was injected into biliary tree to allow anastomosis identification. A duodenoscope was then inserted and anastomosis recognized by outflow of blue methylene. Deep cannulation with a sphincterotome was performed, without difficulty. We made an efficient selleck chemicals dilation of the anastomosis with a TTS balloon inflated up to 12 millimetres. Biopsies were taken. Patient was discharged 24 hours later, clinically well. Conclusion: This case illustrates the difficulty oftentimes found on biliary access in patients with an altered surgical anatomy. EUS was an essential complement to ERCP, allowing find more anastomostic identification

by dye outflow and leading to an effective therapeutic procedure. Key Word(s): 1. Blue Methylene; 2. Ultrasound; 3. ERCP; 4. Anastomotic; Presenting Author: HUI XU Additional Authors: JING YU Corresponding Author: HUI XU Affiliations: General Hospital of Chengdu Military Region Objective: Objective To probe the nasal obstruction tube placement technology, and to evaluate the efficacy and value its treatment of small bowel obstruction. Methods: 28 cases of small bowel obstruction in patients admitted in our hospital from January 2009 to February 2013 (treatment group), We insert the guidewire placed ileus vacuum tube into the stomach through the side of the nasal cavity, which is fixed by the assistant, then insert gastroscope into intestinal obstruction catheter descending part of duodenum sent gastroscopy auxiliary through the mouth. We chose another 32 cases of small bowel obstruction patients as controls (control group), implementation of fasting, gastric tube decompression, enema, for more traditional methods of treatment. Observe and compare the effects of the two groups. Results: All the catheters of the treatment group successfully arrived the desired position.

A number of agents in other classes are in human trials as well. Polymerase inhibitors have somewhat lower efficacy than protease inhibitors,

but appear to have a higher intrinsic barrier to emergence of drug resistance [28]. Cyclophilin inhibitors target host proteins that the virus utilizes and appear quite potent as well with a good resistance profile, but need better characterization in terms of side-effect profiles [29]. NS5a inhibitors this website have also shown promising results in early trials. The opportunity to cure more patients with chronic HCV infection is now a reality, as multiple new agents become available. The next decade will see a rapid evolution of treatment modalities that will provide greater efficacy, less toxicity and shorter treatment duration. This will usher in the beginning of the end for chronic HCV infection. Human parvovirus B19 (B19) circulates worldwide. In temperate climates, epidemic manifestations occur more commonly in late winter, spring or early summer. B19 infection is commonly associated with rash-like illness in children [30]. B19 seroprevalence increases with age so that by the time one reaches adulthood, 50% of individuals have circulating B19-specific IgG. B19 infects, Idasanutlin ic50 replicates in and destroys the precursor cells that are responsible for

producing mature red blood cells. In an infected individual, destroying the source of mature red blood click here cells will result in dramatically lower haematocrit levels and a temporary anaemic state [31,32]. For those individuals who have disorders that shorten their red cell half-life, B19 infection worsens the presentation producing a more severe transient aplastic crisis. Symptoms in a B19 infected individual will vary considerably from one person to the next. An individual

can be infected and yet be completely asymptomatic, or have a mild flu-like illness, or a life-threatening illness. Despite the infected individual’s presentation, the viral load present within their bloodstream can be extremely high, at ∼1012 genome equivalents mL−1 (geq mL−1). This poses the risk that virus can be transmitted by transfusion of blood components obtained from asymptomatic viremic donors [33,34]. The incidence of B19 in the blood of healthy donors ranges from 1 in 20 000 to 1 in 50 000 donors [34,35]. The risk of transmission is greater when the blood components are made from pooled units compared with those made from single units. This fact places those individuals requiring repeated doses of any of these blood products at risk of becoming infected with B19 over time, including individuals living with haemophilia, who require life-long administration of clotting factor concentrate [34,36]. B19 DNA has also been detected in numerous batches of albumin, factor VIII, factor IX, clotting factor concentrates and immunoglobulin [37,38].

100–102 Like Bcl2, BclXL, and Cox-2, Grp-78 affords a survival advantage to cells, as well as protection against cytotoxic insult. The regulation of the Myb gene is predominantly at the level

of transcription; more specifically, transcriptional elongation.103 Notably, an attenuation region within the first intron is the principal determinant of whether mRNA is generated; this region is subject to mutations in Wnt-activated and mismatch repair-deficient CRC cell lines and primary tumors.103 No mutations in Myb coding exons have been reported, although occasional examples of amplification in CRC cell lines exist.88 The role of Myb in stroma has not been specifically investigated in the GI tract, but such a role is clearly important in hemopoiesis.104 There is abundant evidence DZNeP cell line for an intimate link between inflammation-associated hyperactivation of NFκB and

pStat3, including the coincident presence of NFκB, Stat3, and of Myb binding sites in the regulatory elements of many pro-survival genes. NFκB selleck chemical and Stat3-mediated signaling also converge on the epithelial–mesenchymal transition (EMT) process. Thus, IL-6-mediated Stat3 activation promotes EMT through the transcriptional induction of the E-cadherin repressor snail, while activation of NFκB promotes post-translational stabilization of the Snail protein.105 However, Stat3 signaling prolongs nuclear retention of canonically-activated NFκB through RelA/p50 acetylation and associated interference with its nuclear export.106 Meanwhile, unphosphorylated Stat3 can compete with IKKβ for binding to, and activation

of, unphosphorylated NFκB, to trigger transcription of target genes independent of their binding sites for NFκB and/or Stat3. Both transcription factors can also act in a hierarchical fashion as part of a feed-forward loop, whereby NFκB induction of the RNA binding protein Lin28 blocks processing of the let-7 microRNA, and thereby derepresses the transcription of IL-6.86 Epistatic interaction also exists between aberrantly-activated Stat3 and Wnt/β-catenin pathways, for instance, based on the selleck compound observation that tumors in the CAC-challenged gp130Y757F mice harbor activating mutations in β-catenin, and that gp130Y757FApcMin mice show increased tumor multiplicity, while enterocyte-specific Stat3 ablation reduced tumor incidence in ApcMin mice. While these two pathways share a common transcriptional response of Myc and cyclinD1 and other proliferative target genes, IL-11 administration and excessive Stat3 activation also facilitate survival of epithelial cells, conferring them with the capacity to repopulate the intestine after radiation damage. Stat3 seems to increase the pool of “stem” cells susceptible to tumor-inducing mutation, including LOH in ApcMin mice akin to the role of IL-6–Stat3 signaling in maintaining a dynamic equilibrium between stem and non-stem cancer cells.

849), respectively.

The optimal cut-off HBsAg level and HBsAg reduction to predict HBsAg seroclearance were <200 IU/mL (sensitivity, 84.2%; specificity, 73.4%) and 0.5 log IU/mL/year (sensitivity, 62.8%; specificity, 88.7%), respectively. For patients with HBsAg levels ≥200 IU/mL, an annual 0.5-log reduction was highly predictive of subsequent HBsAg seroclearance (AUROC, 0.867; 95% CI: 0.778-0.956). Conclusion: To conclude, serum HBsAg <200 IU/mL and 0.5-log reduction in HBsAg were predictive of HBsAg seroclearance within 3 years of follow-up. These parameters may serve as good indicators for the consideration of treatment duration and cessation for chronic hepatitis B. (HEPATOLOGY 2012;56:812–819) Seroclearance of the hepatitis B surface antigen (HBsAg) during the natural history of chronic hepatitis www.selleckchem.com/products/Etopophos.html B (CHB) is associated with favorable long-term Idasanutlin datasheet outcomes,1, 2 although the development of hepatocellular carcinoma (HCC) remains possible.3-5 The incidence of HBsAg seroclearance ranges between 0.5% and 2.26% per year.3, 5, 6 HBsAg seroclearance is the ultimate treatment

endpoint for CHB, but occurs only infrequently after pegylated interferon (Peg-IFN)7 or nucleoside analog therapy.8-10 The recent development of serum HBsAg quantification has provided an additional tool in monitoring both treated and untreated CHB patients.11 Serum HBsAg titers were initially proposed as a surrogate marker for hepatitis B virus (HBV) covalently

closed circular DNA. But, a recent study found such a correlation to exist only in hepatitis B e antigen (HBeAg)-positive, and not in HBeAg-negative, disease.12 Several recent studies have highlighted the differences in HBsAg titers throughout the natural history of CHB, but are limited by their cross-sectional nature.13, 14 A recent longitudinal study demonstrated the variations in HBsAg levels in different disease phases of CHB. A serum HBsAg reduction of more than 1 log reflects improved immune control and increases the probability find more of HBsAg seroclearance.15 Two recent studies from Asia followed up 390 and 103 HBeAg-negative patients, respectively, and found a HBsAg level of <100 IU/mL predictive of eventual HBsAg seroclearance.16, 17 These longitudinal studies, however, were all limited by the very small number of patients with HBsAg seroclearance (n < 20). Another recent study consisting of 46 patients with HBsAg seroclearance suggested the optimal level to predict HBsAg seroclearance to be HBsAg <200 IU/mL.18 However, the relationship between HBsAg and HBV DNA preceding HBsAg seroclearance and the possible combined use of both markers in predicting HBsAg seroclearance have not been studied. The value of serum HBV DNA levels in predicting HBsAg seroclearance remains controversial.

Thus, our findings suggest that IFN-α may not play an important role in inducing NK cell activation in the HBV patients of our study. In addition to the aforementioned cytokines, NK cell receptor ligands expressed on target cells can also regulate NK cell activity through the binding of NK cell receptors.29 Several studies have reported that the NKG2D/NKG2D ligand pathway may contribute to NK cell–mediated hepatocyte injury.16, 36 Although we have not found the up-regulation of several NK cell activating ligands in the livers of IA patients, the PARP inhibitor up-regulated

NK cell activating receptors and down-regulated inhibitory receptors on hepatic NK cells from IA patients likely have increased sensitivity to activation by target cells and contribute to the increased NK cell functions in these patients. In addition, similarly to previous studies,14, 15 our data also indicated that TRAIL expression on NK cells was increased in IA patients, and the blockade of TRAIL could slightly reduce NK-mediated target apoptosis (data not shown). However, we failed to find FasL up-regulation on NK cells, which is also responsible for NK cell–mediated hepatocyte injury.16 It is plausible to speculate

that Osimertinib NK cells may use different ligands to mediate liver damage in various disease progression stages of HBV infection, and this may account for the discrepancy between these studies. Future studies should investigate whether this differential expression of hepatic cytokines can trigger various

effector pathways of NK cells to induce liver injury during HBV infection. Notably, the present study, in contrast to previous reports of NK cells in chronic HBV infection,13, 19 preferentially defines the role of hepatic NK cells in HBeAg-positive individuals. In comparison with CHB patients in these two reports,13, 19 IA patients enrolled in our study were younger see more and had more severe liver injury, which was indicated by high ALT levels (median = 196 U/L, range = 41-1298 U/L) and more active viral replication (>8 log IU/mL). These differences may account to some extent for the discrepancy in the NK cell frequency and phenotype even in IFN-γ production between the present study and the two recent reports.13, 19 In addition, different stimulation methods may lead to different results.23 Nevertheless, an important finding of the present study is that activated NK cells were skewed toward cytolytic activity in situ in the livers of IA patients but without a concomitant increase in IFN-γ production. These findings, in combination with recent reports of CHB patients13 and chronic HCV infection,15 support the concept that enhanced NK cytolytic activity may mediate liver injury, whereas insufficient and/or deficient IFN-γ production by NK cells may not be sufficient to achieve viral clearance.

In murine models of alcoholic liver disease the engagement of IFN-β pathways is known to protect against liver inflammation. Although patients with alcoholic cirrhosis have bacterial translocation VX-809 research buy and LPS release, their ability to activate IFN-β is unknown. We hypothesized that LPS induction of IFN-β and IFN-stimulated genes (ISGs) might be defective in immune cells from patients with alcoholic cirrhosis. Aims: To assess IFN-β pathways in immune cells from patients with alcoholic cirrhosis and healthy

subjects as well as the effects of other PAMPs and the influence of the etiology of cirrhosis. Methods: 75 patients with cirrhosis (64 alcoholic, 11 HCV) and 33 healthy subjects were included. Peripheral blood mononuclear cells (PBMCs) were obtained and cells were stimulated or not with PAMPs or increasing concentrations of “exogenous” IFN-β. PAMPs included LPS, polyIC alone (TLR3 agonist) or combined with lipofectamine (RIG-I-like receptors agonist). Cell production of IFN-β was measured in the supernatant by ELISA. RT-qPCR monitored expression of 47 bona fide ISGs. Results: LPS-induced

IFN-β production was found to be significantly lower (-64%) in cells from patients with alcoholic cirrhosis than in “healthy” cells. Even if the 47 ISGs were induced (>2-fold) in both groups, 68% of LPS-induced ISGs had a significantly lower expression in “alcoholic”

than “healthy” cells. Similar differences Alvelestat in IFN-β production and ISG induction were found in alcoholic and healthy cells check details when the 2 other PAMPs were used. Compared to healthy cells, alcoholic cells had a significant rightward shift in the concentration-response curve to IFN-β for each ISG induction, indicating that defective IFN-β signaling played a role in ISG under-expression in alcoholic cirrhosis. Finally, during LPS stimulation, while 32 ISGs were under-expressed in alcoholic cells, the expression of only 9 ISGs was significantly decreased in “HCV” cells indicating that defective ISG induction is a hallmark of alcoholic cirrhosis. Multivariate analysis showed that low basal ISG expression in alcoholic cells played a major role in decreased PAMP-induced ISG induction, which is another mechanism of inhibition. Conclusions: This study shows that inhibition of IFN-β production, signaling and ISGs induction is a multilevel process that is specific for PAMP-activated immune cells in patients with alcoholic cirrhosis. These results suggest that defective IFN-β pathways may be an important factor of susceptibility to liver inflammation in alcoholic cirrhosis.

WT and TGR5 KO mice had similar

body weights; however, KO mice had a significantly smaller liver/body-weight ratio (Fig. 1A,B). Hepatocyte size, analyzed on phalloidin-stained liver sections, was similar in WT and TGR5 KO mice (Supporting Fig. 1A). Hematoxylin and eosin (H&E) staining revealed normal liver histology in the majority Maraviroc molecular weight of WT and TGR5 KO mice, although approximately 20% of TGR5 KO mice exhibited mild portal inflammation and fibrosis (Supporting Fig. 1B). Basal biochemical blood parameters (alanine aminotransferase [ALT], alkaline phosphatase [ALP], bilirubin, total bile acids [TBA], glucose, and insulin concentrations) fell in the normal range in both genotypes (Supporting Table 2). After PH, TGR5

KO mice exhibited a significantly slower liver mass restoration (Fig. 1C and Supporting Fig. 2A,B) and a reduced mitotic activity, as compared to WT mice, especially at 2 and 3 days, whereas at later time points (days 5 and 9), there was a significant trend to compensate this deficit in TGR5 KO mice (Fig. 1D-F). A majority of TGR5 KO mice (60%-75%) exhibited jaundice as soon as 2-3 days after PH and recovered Adriamycin datasheet afterwards. H&E staining after PH showed, exclusively in TGR5 KO mice, periportal patchy hepatocyte necrosis (Fig. 2A), increasingly extensive up to 72 hours, closely mimicking clusters of injured hepatocytes (“bile infarcts”) observed after BDL in mice.[20] At 5, 9, and 15 days afterwards PH, hepatocyte necrosis and inflammatory infiltrates progressively declined (data not shown), whereas periductular fibrosis appeared in a majority of TGR5 KO mice (day 15), but was lacking at day 21 (Supporting Fig. 2E). In WT mice, TBA raised immediately after PH in plasma,[3]

but also in liver during the first hours (Fig. 2B,C). Although this rise was transient in WT mice, massive and prolonged TBA accumulation in both plasma and liver was observed in TGR5 KO mice. No increase in post-PH mortality was noticed in TGR5 KO, as compared to WT mice (data not shown). The TGR5 KO phenotype could not be explained by a deficient hepatic adaptive response to post-PH BA overload, because Na+ taurocholate cotransporting polypeptide (NTCP), cholesterol 7α-hydroxylase (CYP7a1), organic solute transporter beta (OST-β), and bile salt export pump (BSEP) selleck messenger RNAs (mRNAs) were adequately regulated. This regulation was even stronger in TGR5 KO mice at days 3 and 5, when necroticoinflammatory injury and cholestasis were peaking, suggesting that FXR-dependent pathways were functional in those mice (Supporting Fig. 3E). In line with the fact that post-PH injury observed in TGR5 KO livers was suggestive of bile-induced toxicity,[20] we first observed that liver necrosis occurred very early on (4 hours) after PH in TGR5 KO mice, at a time when BA—in particular, hydrophobic BA—had already accumulated in liver (Supporting Fig. 4A-D).

When the results of a single study were reported in more than one publication, only the most recent and complete data were included in the meta-analysis. Studies were included in the analysis if (1) they were RCTs comparing any therapy with placebo, no treatment, or supportive care; (2) they included HCC patients with or without metastatic disease; (3) 1-year or 2-year survival was assessed as an outcome measure of the effect of the treatment; and (4) they had been published or accepted for publication as full-length articles. Among the 485 studies reviewed (Fig. 1), 30 RCTs8–37 met the inclusion criteria. Studies were excluded if they

did not have an adequate control arm; if they were nonrandomized or if they enrolled randomized and nonrandomized patients; and if they were published

Palbociclib cell line only in abstract form. CT99021 purchase The rationale for excluding studies published as abstracts only was that the methodological quality could not be assessed. The RCTs were reviewed using a list of predefined, pertinent questions that concerned the characteristics of patients, treatments, outcomes, and study validity. Each trial was evaluated and classified by three independent investigators (C.C., A.C., and G.C.). Discrepancies among reviewers were infrequent (overall interobserver variation of <10%) and were resolved by discussion. The methodological quality of the studies was assessed by five principal criteria (Supporting Table 1), using those established by Jadad et al.38 and Bañares et al.,39 as suggested by the Panel of Experts in HCC-Design Clinical Trials.4 The quality of trials was evaluated according to each separate component. The maximum possible score was 10 points. Pooled estimates of 1-year and 2-year survival rates were calculated using random-effects logistic regression analysis after applying sample weights according to the sample size. Heterogeneity among studies was assessed with the Pearson chi-squared test. Three different methods were used to explore and explain the diversity

among studies: (1) stratum analysis of variables suspected of having caused inconsistency, (2) selleck meta-regression, and (3) subgroup analysis. Therefore, stratum-specific rates of the 1-year and 2-year survival rates for different patient-level and study-level covariates were calculated. We used 16 stratifying variables: publication year, study validity, study location, mean age, percentage of males, percentage of alcohol-related liver disease, percentage of hepatitis B virus (HBV)–related liver disease, percentage of hepatitis C virus (HCV)–related liver disease, percentage of performance status 0 subjects, mean serum albumin, mean total bilirubin, prothrombin activity, percentage of solitary tumors, percentage of portal thrombosis, percentage of Child-Pugh A patients, and percentage of Okuda stage I patients.

3, P = 0.0252) or with lower serum albumin level (<3.3 g/dL, P = 0.0004). In the univariate analysis, HOMA-IR (P = 0.0420) and albumin (P = 0.0036) were significantly associated with recurrence of HCC. Multivariate analysis revealed

albumin (odds ratio = 0.01, 95% confidence interval = 0.0002–0.015, P = 0.0001) and HOMA-IR (odds ratio = 3.85, 95% confidence interval = 1.57–14.2, P = 0.0015) to be independent predictors for recurrence of HCC. Conclusion:  Serum albumin level and HOMA-IR were independent risk factors for recurrence of stage I HCC after curative RFA in HCV-positive patients. Patients with these factors require closer surveillance. “
“To evaluate the dynamic computed selleck kinase inhibitor tomography (CT) appearance of tumor response after stereotactic body radiation therapy (SBRT) for hepatocellular carcinoma (HCC) and reconsider response evaluation criteria for SBRT that Imatinib ic50 determine treatment outcomes. Fifty-nine patients with 67 tumors were included in the study. Of these, 56 patients with 63 tumors underwent transarterial chemoembolization using lipiodol prior

to SBRT that was performed using a 3-D conformal method (median, 48 Gy/four fractions). Dynamic CT scans were performed in four phases, and tumor response was evaluated by comparing tumor appearance on CT prior SBRT and at least 6 months after SBRT. The median follow-up time was 12 months. The dynamic CT appearance of tumor response was classified into the following: type 1, continuous lipiodol accumulation without early arterial enhancement (26 lesions, 38.8%); type 2, residual early arterial enhancement within 3 months after SBRT (17 lesions, 25.3%); type 3, residual early arterial enhancement more than 3 months after SBRT (19 lesions, 28.4%); and type 4, shrinking low-density area without early

arterial enhancement (five lesions, 7.5%). Only two tumors with residual early arterial enhancement did not demonstrate remission more than 6 months after SBRT. The dynamic CT appearance after SBRT for HCC was classified into four types. Residual early arterial enhancement disappeared within 6 months in selleck chemical most type 3 cases; therefore, early assessment within 3 months may result in a misleading response evaluation. “
“Aim:  Hepatic steatosis is one of the factors limiting the virological response to interferon-based antiviral therapy for chronic hepatitis C (CH-C) patients infected with genotype 1, while contradictory results have been reported for genotype 2. We aimed to clarify the effect of hepatic steatosis on therapeutic outcome and cumulative positivity of serum HCV RNA in CH-C patients infected with genotype 2 treated by peginterferon (PEG-IFN)α2b and ribavirin (RBV) combination therapy.