The principle of the technology is based on detecting hydrogen ions released in the reaction-induced changes of the pH

of the solution by an ion sensor when the nucleotide base is incorporated by DNA polymerase. Its read length of approximately selleck inhibitor 100 bp is comparable to that of other NGS systems, but the throughput is still lower, although increasing the size of the semiconductor chips could improve the throughput.[19, 20] Pacific Biosciences (PacBio, Menlo Park, CA, USA) developed a single molecule real-time sequencer based on single molecule real-time sequencing by the synthesis method with monitoring of the deoxyribonucleotide triphosphate (dNTP) uptake of DNA sequencing by DNA polymerase. The fluorescently labeled dNTP is incorporated and the fluorescent dye is separated from the DNA. The sequencing reaction is conducted on zero-mode wave guides (ZMW) that are small well-containers with detectors located at the bottom of the well. The detectors can capture the fluorescent dye. The DNA polymerase is immobilized

by only one molecule at the bottom. After the single template DNA is bound to the polymerase with incorporation of the fluorescently labeled dNTP, the DNA synthesis is performed. The DNA sequencing is conducted by detecting the separated fluorescent dye.[21] In January 2011, a paper from PacBio was published in the New England Journal of Medicine selleck products demonstrating the origin of the 2010 cholera outbreak in Haiti.[22] The PacBio RS was commercially released in early 2011 and had the advantage of a short time from equipping the library to sequencing, obtaining long reads and fewer errors or bias with PCR amplification. However, there is the disadvantage of low yield at high accuracy and low throughput. Nanopore sequencing technology has been developing since 1995 for determining

the sequence without nucleotide labeling and detection.[23] In brief, DNA sequencing with nanopore technology relies on the conversion of the electrical signals of nucleotides by passing through a nanopore, which is a specific protein pore covalently attached to the molecules. This approach is the most advanced and was demonstrated by Oxford Nanopore Technologies (Oxford Science Park, Oxford, UK).[24] Two nanopore sequencer models, the GridION sequencer which can perform large-scale sequencing, and the MinION sequencer, which is a portable and 上海皓元医药股份有限公司 disposable sequencer, are planned for release. The MinION sequencer is a breakthrough device that overturns the concept of previous sequencers. The size of this sequencer is almost the same as a Universal Serial Bus (USB) memory stick and, after plugging this sequencer into the USB port of a personal computer, sequencing can be performed just by loading the sample. So far, this nanopore sequencer has tremendously surpassed other NGS systems. But there is a problem in that the error rate is still high compared with the Illumina or SOLiD sequencers.

Endoscopically, ulcerating pattern was Staurosporine more common than hypertrophic and ulcerohypertrophic. The typical histologic findings of chronic granulomatous colitis with Langhan’s giant cells was noted in only 1/3 of cases. The presence of tissue positive TB-PCR complimented the diagnosis. Key Word(s): 1. Tuberculosis; 2. GI tract; 3. TB PCR; Presenting Author: JIN TAO Additional Authors: QI YANG, BIN WU Corresponding Author: JIN TAO Affiliations: The Third Affiliated Hospital of Sun Yat-Sen University Objective: To determine 1) whether inhibition of TNF-α ameliorated I/R-induced intestinal mucosal injury by suppressing cell apoptosis, 2) whether

TNF-α involves in caspase-dependent apoptotic signaling in intestinal I/R injury, 3) whether JNK signaling pathways activated by TNF-α response to cell apoptosis in intestinal I/R injury. Methods: In this study, the intestinal I/R was induced by 60-min occlusion of the superior mesenteric artery followed by 60-min reperfusion, and the rats were pretreated with PF-562271 chemical structure a TNF-α inhibitor pentoxifylline or a TNF-α antibody infliximab. After the animal surgery,

part of the intestine was collected for histological analysis. The mucosal layer was harvested for RNA and protein extraction, which were used for further real-time PCR, ELISA and Western blot analysis. The TNF-α expression, intestinal mucosal injury, cell apoptosis, the activation of apoptotic protein and JNK signaling pathway were analyzed. Results: I/R significantly enhanced expression of mucosal TNF-α in both mRNA and protein levels, induced severe mucosal injury and cell apoptosis, activated caspase-9/caspase-3, and initiated JNK signaling pathway. Pretreated with pentoxifylline markedly downregulated TNF-α in both mRNA and protein levels, whereas infliximab pretreatment did not affected the

expression of TNF-α induced by I/R. However, pretreatment with pentoxifylline medchemexpress or infliximab dramatically suppressed I/R-induced mucosal injury and cell apoptosis, and significantly inhibited the activation of caspase-9/3 and JNK signaling (P < 0.05). Conclusion: Our data suggested that TNF-α played a pivotal role in intestinal I/R injury; and pretreatment of both pentoxifylline and infliximab remarkably attenuated I/R-induced injury partly by inhibiting the TNF-α mediated apoptosis. Further, the results indicated that TNF-α mediated JNK activation response to intestinal I/R injury. Key Word(s): 1. TNF-α; 2. small intestine; 3. mucosa; 4. JNK; Presenting Author: GAIUS LONGCROFT-WHEATON Additional Authors: PRADEEP BHANDARI Corresponding Author: GAIUS LONGCROFT-WHEATON Affiliations: University of Portsmouth Objective: Endoscopic management of early colonic neoplasia or polyp cancer remains unclear. There are no national guidelines or good quality data to guide clinicians with these difficult lesions.

Analysis of these studies pinpoints that the anticancer effect of statins may be more intensive when given pre- and post-implantation of cancer.[45] Such an effect is dose-dependent and

more evident in metastases,[46] occurs Selleck Pictilisib via increased apoptosis, arrest of the cell cycle,[47] endoplasmic reticulum (ER) stress response, leading to autophagy,[50] and is partly due to the pleiotropic action of statins[55] being mediated by inhibition of synthesis of ubiquinone.[49] Of potential clinical interest, anticancer activity of statins may be potentiated by either enzastaurin,[48] an inhibitor of PKC (deemed to be the receptor protein of tumor-promoting phorbol esters) or celecoxib, a cyclooxygenase-2 (COX-2)-specific inhibitor that blocks the synthesis of prostaglandins from arachidonic acid.[51] Of major importance, further to hepatocytic cells, endothelial cells are an elective target of the action of statins as well.[53] Such an additional cell target accounts for the combined activity against both cancer and portal hypertension shown by statins, which will be discussed in detail

in paragraph on gastrointestinal hemorrhage. This study was conducted in various cell lines including human HCC cell lines Hep3B, HepG2, and Huh7; HCT116 wt and p53−/− cells. Murine embryonic fibroblast (MEF) cells. MEF autophagy-related gene 5−/− (Atg5−/−) cells. Rosuvastatin reduced the vessel anomalies and tumor growth and Smad inhibitor prolonged survival in HCC concurrent with activation of hepatic AMPK,

decreased steatosis, free fatty acids, and aminotransferases levels, and the expression of TNF-α and interleukin-6 mRNAs in the liver; increased serum adiponectin levels suggesting attenuation of the chronic inflammation induced by steatosis. This study conducted on human hepatocarcinoma cell line (Hep G2) determined the action of geraniol, in combination with simvastatin, 上海皓元医药股份有限公司 and the effect of simvastatin, geraniol and the combination of both on the biosynthesis of lipids from [14C]-acetate. Owing to the declining prevalence of competing etiologies, HCC is increasingly discovered against a background of metabolic disorders.[5, 56] NAFLD is a major player and provides an essential milieu in the development of HCC in those with metabolic syndrome.[3, 57] Owing to their potential therapeutic indication in NAFLD,[58] statins could hinder the development of HCC in this specific setting in as much as these two conditions are pathogenically linked to one another. Moreover, in theory, statins could exert a beneficial role in the chemoprevention/cure of HCC in those cases of HCC occurring in a viral chronic liver disease as well. Table 2 details the available evidence for the benefits of statins based on studies conducted in humans.

An important point already emphasized by Takayama et al. is the administration of PDGF-BB and VEGF in treating FHF. This is logical when these factors are low in the serum. Should FHF not be reversible, the potential of using these factors as a bridge to liver transplantation

is an area worthy of further investigation. This might buy time to wait for a deceased-donor liver graft or working up a suitable living liver donor. “
“Although injection drug use (IDU) and blood transfusions prior to 1992 are well-accepted risk factors for hepatitis C virus (HCV) infection, many studies that evaluated tattooing as a risk factor for HCV infection did not control for a history of Selleck Torin 1 IDU or transfusion prior to 1992. In this large, multicenter, case-control study, we analyzed demographic and HCV risk factor exposure history data from 3,871 patients, including 1,930 with chronic HCV infection (HCV RNA–positive) and 1,941 HCV-negative (HCV antibody–negative) controls. Crude and fully adjusted odds ratios (ORs) of tattoo exposure by multivariate logistic regression in HCV-infected versus controls were determined. As expected, IDU (65.9% versus 17.8%; P < 0.001), blood transfusion prior to 1992 (22.3% versus 11.1%; P < 0.001), and history of having one or more tattoos (OR, 3.81; 95% CI, 3.23-4.49; P < 0.001) were more common in HCV-infected patients than

in control subjects. Barasertib research buy After excluding all patients with a history of ever injecting drugs and those who had a blood transfusion prior to 1992, a total of 1,886 subjects remained for analysis (465 HCV-positive 上海皓元 patients and 1,421 controls). Among these individuals without traditional risk factors, HCV-positive patients remained significantly more likely to have a history of one or more tattoos after adjustment for age, sex, and race/ethnicity (OR, 5.17; 95% CI, 3.75-7.11; P < 0.001). Conclusion: Tattooing is associated with HCV infection, even among those without traditional HCV risk

factors such as IDU and blood transfusion prior to 1992. (HEPATOLOGY 2013;57:2117–2123) Hepatitis C virus (HCV) infection is the most common blood-borne infection in the United States, affecting over 3 million people1-4 of all ages, races, and sexes.5, 6 By 2007, HCV had superseded human immunodeficiency virus as a cause of death in the United States,4 yet approximately 50% to 75% of infected adults are unaware of their infection status.7, 8 Injection drug use (IDU) is currently the leading cause of transmission, accounting for 60% of new cases each year2, 3 through both the sharing of needles9, 10 and through drug preparation equipment11; however, approximately 20% of incident cases have no history of IDU or other parenteral exposure.12 As new and better medications for the treatment of HCV become available,13-15 measures to increase detection rates and engagement in care are paramount.

In conclusion, based on the performance demonstrated in this study, the Procleix HEV assay on the fully automated Panther System may be useful for both blood screening and diagnosis of HEV infection. Disclosures: Alanna Janssen – Employment: Hologic Lisa Danzig – Employment: Grifols Jeffrey M. Linnen – Employment: Hologic, Inc.; Stock Shareholder: Hologic, Inc. The following people have nothing to disclose: Edgar Ong, Robin Cory, Maria Babizki, Tim Shin, Andre Lindquist,

Ngoc-Anh Hoang, Lee P. Vang INTRODUCTION: There is limited data about the safety and effectiveness of sofosbuvir (SOF)-based therapies in “real-life” patients with HCV recurrence after liver transplantation (LT). AIM: To evaluate the safety and effectiveness of

SOF-based therapies in patients with HCV recurrence after LT. METHODS: This is a retrospective, multi-center study of patients with post-transplant HCV recurrence who received pegylated interferon (IFN) + ribavirin find more (RBV) + SOF (group 1) ; simeprevir (SMV) + SOF (group 2); SMV + SOF + RBV (group 3); or SOF + RBV (group 4). Treatment response by HCV RNA, cell counts, and adverse events (AE) were compared between groups. selleck inhibitor RESULTS: 59 patients (88% genotype 1a /1b, 51% F3/F4 fibrosis, 71% previously treated) were included in the analysis. Median time from transplant was 1297d (56-6209). There were no statistical differences in demographics, genotype, weight, fibrosis or laboratory parameters between the groups. Analysis of undetectable HCV RNA (UD) is shown in Table 1. Overall, 76% had generalized AE including fatigue, musculoskeletal complaints, headache and nausea, but the frequency of AE was similar between groups (p = 0.74). Serious AE including 1 death were reported in 14 patients (6 anemia/ 上海皓元医药股份有限公司 cytopenia, 2 infection, 6 unrelated to therapy). Hgb decrease by >2 g and development of significant anemia (Hgb <10 g/ dL) was more frequent in patients receiving

RBV [85.7%(1), 10.5%(2), 80%(3), 73.1%(4) p=<0.0001] and [71.4%(1), 10.5%(2), 20%(3), 57.7%(4) p=0.003], respectively. Leukopenia and thrombocytopenia were more common in patients who received IFN. (p=<0.0001 and 0.002, respectively). The need for growth factors was higher in the IFN and RBV containing groups (p=0.005) and blood transfusions were more common in RBV containing groups (p=0.028). No changes in immuno-suppression doses were needed during treatment for any of the groups. SVR data will be presented. CONCLUSIONS: On treatment response using SOF based regimens in the treatment of HCV post-transplant appears promising. Treatment is well tolerated overall, but side effects are increased with RBV or IFN use. No immunosupression changes are needed when using SOF or SIM. Longer term data will help confirm safety and effectiveness in “real-life” patients. No significant difference between groups at week 2 and 4. Disclosures: Joseph Ahn – Advisory Committees or Review Panels: gilead; Grant/Research Support: bms Helen S.

[109-111] An example of the potential advantage of LDLT over LRLT would be in recipients with genetic hepatopathies (e.g., Alagille

STAT inhibitor syndrome) when the donor may be an asymptomatic relative and not a good candidate if they share common alleles. To consider LDLT, LT must 1) be the only therapeutic option, or 2) deceased donor LT is not an option, or 3) a deceased donor organ has not become available. Furthermore, for the LDLT to be ethically appropriate, the likelihood the recipient will survive following LDLT should be high, the mortality risk to the donor low, and the donor is well informed of the risks to his/her short- and long-term health.[108] Considerable pressure is placed on the potential donor from both internal and external sources to save the life of a child or relative. These pressures should be addressed throughout the donor evaluation process to ensure the donor’s “free will” to proceed with liver donation

and have the ability to confidentially remove him or herself from consideration at any time. Consideration of LDLT for a child with acute liver failure has raised concerns XL765 mouse that the emergent clinical environment might be coercive to a potential donor and impede honest informed consent. While coercion is difficult to assess, postoperative evaluation of donors have found positive emotional and psychological outcomes regardless of the outcome for the patient.[112] Pediatric patients with acute liver failure who received LDLT had decreased wait times to LT, decreased cold ischemia time, and improved survival compared to a group who received a cadaveric donation.[113] In addition medchemexpress to the standard evaluation requirements to assess general health status, surgical risks, volume of the segments to be removed, and evidence of a transmissible virus, the

potential donor will require additional assessments that include psychological assessment and social support systems. If the potential recipient has an inherited metabolic disease, the feasibility of a parent wishing to serve as an LRLT donor should be determined in the context of the child’s genetic condition.[114] LRLT has been successfully performed using heterozygote donors for conditions such as Crigler-Najjar syndrome type 1,[115] Wilson’s disease,[116] carbamoyl-phosphate synthase 1 deficiency,[117] propionic acidemia,[118] arginosuccinic aciduria,[119] progressive familial intrahepatic cholestasis,[120] alpha-1 antitrypsin deficiency,[121] tyrosinemia,[121] Alagille syndrome,[122] and others. In patients with Alagille syndrome receiving LRLT, poor recipient outcomes or technical failure due to bile ducts being too small to utilize are reported if the donor has bile duct hypoplasia.[122] Children receiving an LRLT for arginosuccinic aciduria may still require arginine supplementation during periods of physiological stress or fasting due to persistent deficiency in extrahepatic tissues.[119] 30.

5D). Based on numerous studies, TGF-β has been recognized as a proapoptotic and profibrotic master cytokine in hepatocytes3, 9-11; therefore, we hypothesized that sorafenib may potentially exert both antiapoptotic and antifibrotic effects by disrupting TGF-β signaling. To test this hypothesis we first confirmed the protective effect selleck chemicals of sorafenib in blocking apoptosis in primary hepatocytes. As shown in Fig. 6A, caspase-3 activity was attenuated when cells were treated with sorafenib. Further experiments demonstrated

that exposure of primary hepatocytes to sorafenib eventually led to a significant decrease in the expression of proapoptotic genes, such as Bad, Bax, and Caspase 3 (Fig. 6B), indicating that this drug prevents hepatocytes from undergoing apoptosis. Because primary hepatocytes may also contribute to the production of ECM,8 we subsequently assessed the GSK126 manufacturer effects of sorafenib on collagen production in vitro. In response to external TGF-β1 stimulation, primary hepatocytes up-regulate the production of fibrotic matrix components, including procollagen type I (col I), procollagen type III (col III), and collagen IV α1. Interestingly, these changes were substantially attenuated after treatment with sorafenib (Fig. 6C), suggesting an antifibrotic role of

sorafenib in counteracting ECM accumulation. This effect was further supported by real-time qPCR analysis assessing gene expression profiles of sorafenib-treated hepatocytes, which revealed a profound decrease in the expression of Timp-3, a tissue inhibitor of metalloproteinases that is expressed only in hepatocytes.33 Likewise, the expression of the 上海皓元医药股份有限公司 potent profibrotic factors TGF-β1 and CCN2 (connective tissue growth factor) were reduced by ≈44% to 58% after sorafenib treatment (Fig.

6C). Taken together, these results clearly provide in vitro evidence that sorafenib exerts both antiapoptotic and antifibrotic effects against TGF-β signaling in mouse hepatocytes. In 2005, sorafenib became the first oral agent approved for the treatment of patients with advanced RCC. Previous reports have largely focused on the role of sorafenib in tumor progression and apoptosis through blocking multiple receptor tyrosine kinases.13-15, 34 In this study we uncovered a novel capacity of sorafenib to antagonize TGF-β signaling and, consequently, to counteract TGF-β1-induced concomitant EMT and apoptosis in mouse hepatocytes. We observed that sorafenib treatment significantly decreased Smad2/3 phosphorylation (Fig. 1C and Supporting Fig. S2) and the expression of TGF-β target genes, such as CCN2, ColIa1, and Smad7 (Figs. 1D, 5D, 6C), raising the possibility that sorafenib may directly or indirectly modify key proteins in the TGF-β signaling pathway.

Conclusion:  The epidemiology of gastric cancer in the experience of Hospital “José Carrasco Arteaga” corresponds to result of international data published in several studies. It should make new guidelines for asymptomatic patients older than 40 years taking into account genetic factors, educational, food, refrigeration of food, drinking water, and increase the detection rate of early gastric cancer of 7.1% to 50% as it is in Japan. Conducting Paclitaxel purchase annual checkups funded by the state and private enterprise in this way private employees and provide certificates updated every one or two years. Determination by histopathology, tumor type, and marker KI67 ploidies

of pre-neoplastic lesions such as polyps, villous tubules, low-grade dysplasia, metaplasia intestinal secretory type II B sulphomucins

to determine the degree of histological damage, and the presence of infection by H. pylori, since in our setting this is present in more than 50% in children under 10 years of age, especially the differentiated histological type. Key Word(s): 1. gastric cancer; 2. histopatology; 3. early cancer; 4. advanced cancer; Presenting Author: SHANJIN ZHANG Corresponding Author: SHANJIN ZHANG Affiliations: people’s hospital of yichun city Objective: To explore the causes of the common complications and its treatment and prevention measures through the retrospective analysis of 203 cases of ERCP examination. http://www.selleckchem.com/products/Cisplatin.html Methods: Through reviewing and summarizing 203 cases of clinical data from the diagnostic and therapeutic ERCP examinations from April 2007 to April 2007, analyzing the cause of the complications and treatment methods, effective preventive measures were explored. Results: 9 cases of complications were in 203 cases of ERCP examination (4.43%), and the incidence of diagnostic ERCP was 3.84% (5/130), complicating with acute pancreatitis in 4 cases, hemorrhage

in 1 case; the incidence of therapeutic ERCP was 5.47% (4/73), complicated with hemorrhage MCE in 2 cases, acute pancreatitis in 1 case, debris basket in 1 case. In 9 cases of complications, 5 cases with the medical therapy (55.56%), 4 cases with the surgical treatment (44.44%). Conclusion: Therapeutic ERCP complications were significantly higher than diagnostic ERCP, may due to a long time of operation and many equipments. The most common complications of diagnostic ERCP was acute pancreatitis, which related with reiterative development, difficult intubation, excessive contrast agents and high pressure. The most common complication of therapeutic ERCP was bleeding, relating with technical operation, accompanying with jaundice, and diabetes. Most of complications after the medical therapy were alleviated, and only a few severe complications required surgical treatment. Key Word(s): 1. ERCP complications; 2. treatment; 3.

The most common primary tumors are lung in men and breast in women; oral metastases from colorectal primary are exceedingly rare. In fact, gingival metastasis is a very rare and late presentation Raf inhibitor of colorectal carcinoma, and the consequent survival is just a few weeks or months. The gross appearance of gingival metastasis may be indistinguishable from other benign buccal lesions, such as pyogenic granuloma and giant cell granuloma. Histological examination with immunohistochemical

techniques is thus essential to confirm the diagnosis. Gingival metastasis can cause progressive discomfort, such as pain or bleeding, as illustrated in our case. Therefore, even in cases with advanced or disseminated disease, palliative treatment such as radiotherapy is necessary to improve the quality of life of patients. In selected cases with solitary oral metastasis, surgical resection can be considered. Contributed by “
“We read with interest the letter by Kershenobich et al. in Hepatology regarding the meta-analysis of randomized trials comparing Enzalutamide datasheet pegylated interferon (PEG-IFN) alpha-2a and alpha-2b in the treatment of chronic hepatitis C (CHC) by Awad et al.1, 2 We agree regarding the importance of a uniform study population

in treatment-naïve patients with CHC. This is especially true for the study by Laguno et al., which included patients coinfected with human immunodeficiency virus (HIV).3 We performed a meta-analysis of four available studies comparing PEG-IFN alpha-2a and peginterferon alpha-2b in the treatment of patients with

CHC who have concomitant HIV coinfection: one randomized,3 one prospective–retrospective,4 and two prospective studies5, 6 with one of them reported 上海皓元 as an abstract.6 A total of 1009 patients (581 treated with PEG-IFN alpha-2a; sample size, 63-557; mean age, 41 years; 69%-75% males) were treated in the four studies.3-6 Pooled analysis of the data showed that the odds of achieving rapid virologic response (RVR), early virologic response (EVR), and sustained virologic response (SVR) were similar with PEG-IFN alpha-2a and PEG-IFN alpha-2b (Table 1). Similarly, the odds of treatment discontinuation due to serious adverse effects were similar with PEG-IFN alpha-2a and PEG-IFN alpha-2b (Table 1). The data were homogeneous for all the analyses. There was no evidence to indicate any publication bias. After excluding the study reported as an abstract, the results with the two PEG-IFN compounds were still similar. The SVR rates were 36% and 35% with PEG-IFN alpha-2a and PEG-IFN alpha-2b, respectively. Subgroup analyses of the SVR based on the genotype status (genotype 1 or 4 and genotype 2 or 3) and viral load showed similar efficacy and safety data for the two types of PEG-IFN. The data were homogeneous without any suggestion of publication bias in all the analyses.

The most common primary tumors are lung in men and breast in women; oral metastases from colorectal primary are exceedingly rare. In fact, gingival metastasis is a very rare and late presentation EMD 1214063 cost of colorectal carcinoma, and the consequent survival is just a few weeks or months. The gross appearance of gingival metastasis may be indistinguishable from other benign buccal lesions, such as pyogenic granuloma and giant cell granuloma. Histological examination with immunohistochemical

techniques is thus essential to confirm the diagnosis. Gingival metastasis can cause progressive discomfort, such as pain or bleeding, as illustrated in our case. Therefore, even in cases with advanced or disseminated disease, palliative treatment such as radiotherapy is necessary to improve the quality of life of patients. In selected cases with solitary oral metastasis, surgical resection can be considered. Contributed by “
“We read with interest the letter by Kershenobich et al. in Hepatology regarding the meta-analysis of randomized trials comparing Selleckchem GPCR Compound Library pegylated interferon (PEG-IFN) alpha-2a and alpha-2b in the treatment of chronic hepatitis C (CHC) by Awad et al.1, 2 We agree regarding the importance of a uniform study population

in treatment-naïve patients with CHC. This is especially true for the study by Laguno et al., which included patients coinfected with human immunodeficiency virus (HIV).3 We performed a meta-analysis of four available studies comparing PEG-IFN alpha-2a and peginterferon alpha-2b in the treatment of patients with

CHC who have concomitant HIV coinfection: one randomized,3 one prospective–retrospective,4 and two prospective studies5, 6 with one of them reported MCE公司 as an abstract.6 A total of 1009 patients (581 treated with PEG-IFN alpha-2a; sample size, 63-557; mean age, 41 years; 69%-75% males) were treated in the four studies.3-6 Pooled analysis of the data showed that the odds of achieving rapid virologic response (RVR), early virologic response (EVR), and sustained virologic response (SVR) were similar with PEG-IFN alpha-2a and PEG-IFN alpha-2b (Table 1). Similarly, the odds of treatment discontinuation due to serious adverse effects were similar with PEG-IFN alpha-2a and PEG-IFN alpha-2b (Table 1). The data were homogeneous for all the analyses. There was no evidence to indicate any publication bias. After excluding the study reported as an abstract, the results with the two PEG-IFN compounds were still similar. The SVR rates were 36% and 35% with PEG-IFN alpha-2a and PEG-IFN alpha-2b, respectively. Subgroup analyses of the SVR based on the genotype status (genotype 1 or 4 and genotype 2 or 3) and viral load showed similar efficacy and safety data for the two types of PEG-IFN. The data were homogeneous without any suggestion of publication bias in all the analyses.