1-4 These coated invaginations are believed to be liberated from the

PM by the combined efforts of lipid-modifying enzymes,5, 6 the actin-myosin cytoskeleton,7, 8 and the large guanosine triphosphate (GTP)ase dynamin.9-12 It is unclear how the location, interaction, and function of dynamin and other proteins are regulated. Further, whether these endocytic proteins assemble randomly along the PM or at discrete, predefined membrane areas similar to what occurs in the synapse is undefined. To better understand how the endocytic machinery in hepatocytes is spatially organized and temporally regulated, Akt inhibitor drugs we utilized confocal microscopy to observe these processes directly in living cultured epithelial cells expressing dynamin 2 (Dyn2) coupled to green fluorescent protein (GFP). Dynamin is a large GTPase that has been implicated in the final stages of clathrin-mediated endocytosis.9-12 In defined in vitro systems,

recombinant selleck dynamin alone can sever or deform lipid tubules, indicating that this enzyme has mechanochemical properties that could pinch forming vesicle buds from donor membrane compartments in cells. Because dynamin is considered a major component of the clathrin-coated pit-generating machinery, we predicted that recording the distribution of the labeled enzyme in cells over time would provide useful information about the function and distribution of the endocytic machinery in hepatocytes. The dynamins encompass a broad family of at least three distinct conventional gene products encoding multiple splice forms, which exhibit tissue-specific expression and reside at different cytoplasmic locations. In this study Acyl CoA dehydrogenase we tagged and expressed the Dyn2(aa) form, found predominantly in epithelial cells, in a nontransformed hepatocyte cell line derived from rat (Clone 9). Our findings were confirmed in primary rat hepatocytes isolated in culture. As for most epithelial cells, these cell

lines do not express Dyn1 or Dyn3, which are found in brain, lung, testis, and heart.13 We report here that hepatocytes expressing Dyn2(aa)-GFP display a distribution identical to untransfected cells stained with a Dyn2 antibody. Both tagged and endogenous Dyn2 localize to a punctate “lawn” of vesicular structures along the basal PM. Interestingly, interspersed among individual Dyn2 spots are large tubulovesicular structures that sequester the transferrin receptor 1 (TfR1) and stain positive for the endocytic coat proteins clathrin and AP2. Most remarkable is the highly dynamic nature of these Dyn2, clathrin, and AP2 structures. Time-lapse movies of transfected cells revealed that these endocytic regions generate large numbers of discrete endosomal vesicles. These findings suggest that the clathrin-based endocytic machinery maintains a dorsal/ventral distribution even in “nonpolarized” cells.

“
“Clinical Autophagy activator perspectives in hepatology aims to engage two experts with opinions supporting differing perspectives on the management of a case. Typically, the case represents an area of debate or evolving practice in clinical hepatology. The case described by Dr. Reddy provides an opportunity to discuss the benefits and risks of using a direct-acting antiviral as

part of a treatment regimen for aggressive post–liver transplant (LT) hepatitis C. A 54-year-old white man was diagnosed in 1995 with hepatitis C virus (HCV) infection genotype 1 (GT1), acquired from a blood transfusion in 1975. Between 1996 and 2002, the patient underwent three courses of treatment for HCV infection. He took traditional interferon (IFN) in 1996 for 6 months, IFN and ribavirin (RBV) for 7 months in 1998, and, last, pegylated interferon alfa-2b (PEG-IFN) and RBV in 2002. Unfortunately, he did not achieve viral clearance with any of these treatments. Over time, he had progressive liver disease and a liver biopsy revealed cirrhosis in 2003. His condition continued to decline with the development of complications of portal hypertension that included esophageal varices, mild hepatic encephalopathy, and ascites. In April 2007, the patient underwent a live donor

LT, receiving a right lobe from his son. His post-transplant course was complicated by recurrent HCV infection Selleckchem Palbociclib and the development of chronic active hepatitis and bridging fibrosis. In June 2009, he began treatment for recurrent infection with PEG-IFN and

RBV. The patient achieved a rapid virologic response, but relapsed after 48 weeks of treatment. A repeat biopsy performed in January 2011 demonstrated the development of cirrhosis. His IL28B genotype is C/T. Subsequently, when protease inhibitors became available, the decision was made to administer boceprevir as a part of a 48-week triple therapy (TT) regimen. A 4-week lead-in phase of PEG-IFN plus RBV (800 mg) was started, after which boceprevir Phloretin was added. TT was administered for 32 weeks, after which boceprevir was discontinued and PEG-IFN and RBV alone were administered for 12 weeks. Within the first 8 weeks of therapy, the patient’s HCV RNA was detectable, but not quantifiable. At week 12, HCV RNA was not detectable. The dose of tacrolimus was reduced because of the known drug-drug interactions (DDIs) between the calcineurin inhibitor (CNI) and boceprevir, and the level of tacrolimus was monitored closely with dosage alterations occurring when necessary. Adverse events (AEs) of therapy included fatigue, anemia, and syncope, requiring hospital admission. Anemia was managed with RBV dose reduction, erythropoietin-stimulating agent (ESA), and blood transfusion. Details of the course of his therapy, including management of his tacrolimus levels and dosage, are presented in Fig. 1.

The mean size of the lesions was 5.1 ± 4.5 mm (minimum, 2 mm; maximum, 24 mm). Repeated radiological evaluations were performed in 11 (47.8%) of the patients. No new white matter lesions

were detected in control MRI during follow up. Non-specific incidental white matter changes may be seen in children with headache. For normal clinical follow up, in the absence of evident benefits from repeated imaging studies, we suggest that repeated imaging studies are not warranted in every patient and should be tailored according to Selleck IDH inhibitor clinical course. “
“Objective.— To investigate the mechanism by which adenosine triphosphate (ATP) causes sensitization of trigeminal neurons and how dihydroergotamine (DHE) represses this modulatory effect. Background.— Dihydroergotamine is an effective treatment of migraine. CHIR-99021 cell line The cellular mechanisms of action of DHE in treating migraine attacks remain unclear. Methods.— In this study, neonatal rat trigeminal ganglia cultures were used to investigate effects of ATP, alpha, beta-methyl ATP (α,β-meATP), and DHE on intracellular calcium levels and calcitonin gene-related peptide (CGRP) secretion. Results.— Pretreatment with ATP or α,β-meATP caused sensitization of neurons, via P2X3 receptors, such that a subthreshold amount of potassium chloride (KCl) significantly increased intracellular calcium levels and CGRP

secretion. Pretreatment with DHE repressed increases in calcium and CGRP secretion in response to ATP-KCl or α,β-meATP-KCl treatment. Importantly, these inhibitory effects of DHE were blocked with an α2-adrenoceptor antagonist and unaffected by a 5HT1B/D receptor antagonist. DHE also decreased neuronal membrane expression of the P2X3 receptor. Conclusions.— Our findings provide evidence for a novel mechanism of action for DHE that involves blocking ATP-mediated sensitization of trigeminal neurons, repressing

stimulated CGRP release, and decreasing P2X3 membrane expression via activation of α2-adrenoceptors. “
“Objective.— To determine the predictability of future migraine attacks and to describe the effect of migraine on daily life during and between migraine attacks. Background.— Migraine is associated with substantial economic and humanistic burden. Selleckchem Vorinostat There is growing evidence that early intervention with triptans results in better treatment outcomes. However, this is dependent on a patient’s preparedness for an attack including having abortive medications readily accessible at headache onset. Methods.— Physician-diagnosed adult migraine sufferers, who treat with prescription or over-the-counter medications, completed 2 self-reported, Internet-based questionnaires, administered at baseline and following the resolution of the next migraine attack. The baseline questionnaire included the Migraine Disability Assessment questionnaire (MIDAS), questions about experiences on days between attacks, predictions of the date, time of day (5 time windows), and sufferer’s location (4 places) at the start of their next migraine.

We also incorporated inpatient and outpatient diagnosis files to ascertain the history of cardiovascular disease, peripheral vascular disease, cerebrovascular signaling pathway disease, retinopathy, nephropathy, neuropathy, depression, chronic kidney disease, chronic liver disease, and chronic lung disease based on ICD-9-CM codes. Patients were classified as having chronic liver disease if they had at least one hospital admission or outpatient

visit with a diagnostic code of hepatitis B virus infection (ICD-9-CM codes 070.2x, 070.3x, V02.61), hepatitis C virus infection (070.41, 070.44, 070.51, 070.54, V02.62), chronic hepatitis (571.4), liver cirrhosis (571.2, 571.5, 571.6),

or alcoholic liver disease (571.0x, 571.1x, 571.2, 571.3x). A previous validation study using hospital administrative database reported a positive predictive value of 90% with this definition. 23 Covariate information included age, gender, and socioeconomic status (i.e., using monthly income as a proxy). Conditional logistic regression was used to estimate the crude and adjusted odds ratio (OR) and 95% confidence interval (CI) for the association between rosiglitazone/pioglitazone and cancer occurrence with “nonuse” as the reference group. Potential covariates, including socioeconomic status (monthly income level), Opaganib supplier diabetes complications and comorbidities at cancer diagnosis, other antidiabetic agents, antihypertensive medications, statin, and aspirin were examined. In the multivariate analysis, we adjusted for the use of short-acting human insulin, sulfonylurea, metformin, as these science antidiabetic agents were reported to be associated with cancer risks and could potentially confound the association. Other variables were chosen by using stepwise selection with P values < 0.10 for model entry and > 0.05 for removal. The association

between rosiglitazone/pioglitazone and individual cancer incidence was separately estimated after adjustment for potential confounders specific to that cancer type. In the dose- and duration-response analyses, we calculated the ORs for higher (≥120 DDD) and lower cumulative dose (<120 DDD) use, and for cumulative treatment duration ≥3, 2-3, 1-2, and ≤1 years. A two-sided P value < 0.05 was considered statistically significant. Approximately 15% participants claimed at lease one prescription for pioglitazone. Assuming a correlation coefficient for pioglitazone use between case and control was 0.5 and an ORs was 0.8, a study of 2,500 cases and 4 controls for each case would have a power ≥80% at α = 0.05.

Filters were then centrifuged again for 2 min at 800g. The filtrates Staurosporine order were transferred to HPLC vials and stored at −20°C until measurement. Mass spectral experiments were performed on an ABI-SCIEX-4000 Q Trap (Applied Biosystems, Darmstadt, Germany), triple quadrupole mass spectrometer equipped with a TurboSpray® interface coupled

to an Agilent (Waldbronn, Germany) model 1100 LC. The LC equipment included a solvent reservoir, in-line degasser (G1379A), binary pump (G1311A), refrigerated autosampler (G1329A/G1330B), and temperature-controlled column oven (G1316A). After injection of 5 μL of sample, separation of lipophilic toxins was performed by reverse-phase chromatography on a C8 column (50 × 2 mm) packed with 3 μm Hypersil BDS 120 Å (Phenomenex, Aschaffenburg, Germany) and maintained at 25°C. The flow rate was 0.2 mL · min−1 and gradient elution was performed with two eluents, where eluent A was water and eluent B was methanol/water (95:5 v/v), both containing 2.0 mM ammonium formate and 50 mM formic acid. Initial conditions were elution with 5% B, followed by a linear gradient to 100% B within 10 min and isocratic elution until 10 min with 100% B. The program was then returned to initial conditions within 1 min followed by 9 min column equilibration (total run time: 30 min). Mass spectrometric parameters were as follows: curtain gas: 20 psi, CAD gas: medium, ion spray voltage: 5500 V, temperature: 650°C,

nebulizer gas: 40 psi, auxiliary gas: 70 selleck kinase inhibitor psi, interface heater: on, declustering potential: 121 V, entrance potential: 10 V, exit potential: 22 V, collision energy: 57 V. Selected reaction monitoring (SRM) experiments were carried out in positive ion mode by selecting the following transitions (precursor ion > fragment Dipeptidyl peptidase ion): m/z 534 > >150, 536 > >150, 540 > 164, 552 > 150, 628 > 150, 640 > 164, 644 > 164, 650 > 164, 658 > 164, 674 > 164, 678 > 150, 678 > 164, 692 > 150, 692 > 164, 694 > 150, 694 > 164, 698 > 164, 706 > 164, 708 > 164, 710 > 150, 720 > 164, 722 > 164, 766 > 164 and 784 > 164. Dwell times of 40 ms were used for each transition. BI and ML methods returned phylogenetic

trees with identical topologies. In the BI tree shown in Figure 1, the A. ostenfeldii/A. peruvianum complex appears to be genetically highly structured with the sequences analyzed falling into six distinct phylogenetic groups. The clustering did not conform to the morphospecies distribution. Strains assigned morphologically to A. peruvianum and strains identified as A. ostenfeldii intermingled in the tree. Lower nodes were generally poorly resolved. Analysis of larger D1-D2 LSU data sets focusing on unique sequences and intra-strain variability largely confirmed the initial analysis. In the D1-D2 phylogeny (Fig. 2), all the groups indicated in Figure 1 were present as separate highly supported (>0.95 branches except for the group 2 which had a branch support of only 0.

Co-precipitated proteins

were analyzed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS-PAGE) (12% gel) and subsequent immunoblot analysis. For co-immunoprecipitation, 4 μg of specific antibody and 500 μg of Huh 9-13 protein lysate were rotated for 2 hours at 4°C in a total volume of 500 μL PBS. Afterward, 2× washed protein A/G PLUS-Agarose (Santa Cruz Biotechnology, Santa Cruz, CA) was added and incubated overnight at 4°C. Thereafter, the samples were washed 3 times with Triton-wash-buffer, resuspended and denatured in 2× SDS-PAGE buffer for 5 minutes at 95°C, supplemented at 4°C for 1 minute at 13.000 rpm and subjected to SDS-PAGE (12% gel). It has been recently reported that the benzoquinoid mTOR inhibitor ansamycin antibiotic herbimycin A, which is known to inhibit the activity of viral Src and c-Src,13-16 affects HCV replication. However, due to the propinquity of herbimycin A to geldanamycin, which binds to Hsp90 and alters its function, this finding has been linked to a potential role of Hsp90 for HCV replication, but not to a possible role of c-Src for HCV replication.3 Indeed, as shown in Fig. 1, herbimycin A concentration-dependently almost completely abrogates HCV replication when analyzed in the subgenomic replicon cell lines

Huh 9-132 (Fig. 1), Huh 5-15, and Huh 11-7 (Supporting Information Fig. 1) with maximal inhibitory effects after an incubation period of 72 hours, depending on check details the concentration used. In line with these observations, treatment with 0.1 μM herbimycin A also strongly suppressed HCV replication in Huh7.5 cells persistently infected with the JC1 strain (Fig. 1D). In contrast to HCV, replication of vaccinia virus or vesicular stomatitis virus, both of which replicate as HCV at extranuclear sites

in the cytoplasm in Huh7 cells, was resistant to treatment with 0.1 μM herbimycin A. This finding suggests that the effect of herbimycin A on HCV replication is indeed specific rather than an unselective impairment of the host cell resulting in a curtailed efficiency of viral replication many (Supporting Information Fig. 2). To assess whether the inhibition of HCV replication by herbimycin A might be due to its inhibitory effect on c-Src, three different siRNAs directed against c-Src were established and used to suppress c-Src expression and compared with GFP siRNA as a control (Fig. 2A,B). In addition, as a second approach, a commercially available c-Src siRNA pool and respective nontarget control siRNA (Dharmacon) was used (Fig. 2C,D). As shown in Fig. 2, down-regulation of c-Src expression was achieved by all siRNAs used and resulted in an effective decrease of the abundance of HCV RNA (Fig. 2A) and protein (Fig. 2B,C). Thereby suppression of viral RNA and protein expression closely coincided with the degree c-Src expression was suppressed.

The results of this test may be used for decision-making

on eradication. In some articles, the results of 10 day sequential therapy and standard triple therapy were assessed [39-41]. Huang et al. [39] compared the results of H. pylori sequential therapy, and 7-day or 10-day standard triple therapy comprising omeprazole, amoxicillin, and clarithromycin. The authors demonstrated that the 10-day sequential therapy was significantly more effective than the standard 7-day or 10-day triple therapy in eradicating H. pylori infection. According to Giorgio et al. [42], the reason for triple therapy eradication failure was the resistance to clarithromycin. Xiong et al. [43] detected the clarithromycin-resistant H. pylori by performing PCR on stool samples from children. According to the authors, this method is reliable, rapid, noninvasive and should be recommended. Seo et al. [44] had selleck products studied antibiotic resistance to H. pylori in children for 20 years in Jinju, South Korea. The resistance rate to erythromycin increased significantly from 13.8% in 1990–1994 to 33.3% in 2005–2009 (p = .032). Clarithromycin resistance increased from 6.9 to 18.2% and metronidazole resistance decreased from 32.8 to 27.3%. A recent systematic review addressed the problem of H. pylori resistance to antibiotics and demonstrated high H. pylori resistance to first-line antibiotics

in Latin American countries; in comparison with adults, higher prevalences were observed in the three studies on children concerning resistance to clarithromycin (ranging from 19 to 27%) and dual resistance to clarithromycin and metronidazole (18%), whereas lower prevalences were reported for metronidazole (ranging from 13 to 78%), tetracycline (0%), and furazolidone (0%) [45]. Settin et al. investigated the effect of CYP2C19 genetic polymorphism on the cure rate of children who received proton-pump inhibitor-based triple therapy; 100 children with H. pylori-positive gastritis were included, and the

authors were able to show that the cure rate was higher among both the groups of heterozygote extensive and poor metabolizers compared with the homozygote extensive metabolizers (OR = 2.15, p > .05) concluding that there is a need for a therapy augmentation Protein kinase N1 or modification for the homozygote extensive metabolizers [46]. Wang and Huang [47] investigated Lactobacillus acidophilus and Bifidobacterium bifidum supplementation to triple therapy for H. pylori eradication and observed changes in intestinal flora. The probiotics supplementation was beneficial to H. pylori eradication compared with sole triple therapy, although without statistical significance. Lactobacillus acidophilus and E. coli showed no statistical difference before or after therapy in the treatment group with standard triple anti-H. pylori therapy and probiotics. Li et al. [48] carried out a meta-analysis of randomized controlled trials on the efficacy of probiotics in H.

RESULTS Anti-HDV-IgM correlated with histological inflammatory (p< 0.01) as well as with biochemical disease activity (ALT and AST p<0.01) and is associated

with the stage of liver disease (p< 0.01). Before therapy, anti-HDV-IgM levels did not differ between patients responding to therapy and nonresponder patients. However, anti-HDV-IgM levels significantly declined from baseline to week 96 of therapy in virological responder patients whereas anti-HDV-IgM OD values remains unchanged or even increased in most of the nonresponders. Antibody declines became evident already during week 24 of therapy in responding patients (responder vs. nonresponder GSK2126458 research buy W24 p=0.05; W48 p<0.01; W96 p=0.02). At week 24 ten out of 1 1 virological responders had an anti-HDV-IgM decline while this was only the case in five out of 1 1 nonresponders patients. CONCLUSIONS Anti-HDV-IgM testing is a cheap and reliable marker providing valuable additional information on disease activity in hepatitis delta. Moreover, anti-HDV-IgM testing could be used

as an on-treatment marker for response to individualize treatment and to avoid unnecessary exposure to PEG-IFNa. The value of this marker needs to be validated selleck in larger studies. Disclosures: Cihan Yurdaydin – Advisory Committees or Review Panels: Janssen, Roche, Merck, Gilead Selim Gurel – Speaking and Teaching: Glead, BMS, Roche, MSD, Glead, BMS, Roche, MSD Stefan Zeuzem – Consulting: Abbvie, Achillion Pharmaceuticals, Boehringer Ingel-heim GmbH, Bristol-Myers Squibb Co., Gilead, Novartis Pharmaceuticals, Merck & Co., Idenix, Janssen, Roche Pharma AG, Vertex Pharmaceuticals, Presidio, Santaris, Inc George V. Papatheodoridis – Advisory Committees or Review Panels: Janssen, Abbott, Boehringer, check details Novartis, BMS, Gilead, Roche; Consulting: Roche; Grant/Research Support: BMS, Gilead, Roche; Speaking and Teaching: Janssen,

Novartis, BMS, Gilead, Roche, MSD Kerstin Port – Speaking and Teaching: Roche Markus Cornberg – Advisory Committees or Review Panels: Merck (MSD Ger-mamny), Roche, Gilead, Novartis; Grant/Research Support: Merck (MSD Ger-mamny), Roche; Speaking and Teaching: Merck (MSD Germamny), Roche, Gilead, BMS, Novartis, Falk Michael P. Manns – Consulting: Roche, BMS, Gilead, Boehringer Ingelheim, Novartis, Idenix, Achillion, GSK, Merck/MSD, Janssen, Medgenics; Grant/Research Support: Merck/MSD, Roche, Gilead, Novartis, Boehringer Ingelheim, BMS; Speaking and Teaching: Merck/MSD, Roche, BMS, Gilead, Janssen, GSK, Novartis Heiner Wedemeyer – Advisory Committees or Review Panels: Transgene, MSD, Roche, Gilead, Abbott, BMS, Falk; Grant/Research Support: MSD, Novartis, Gilead, Roche, Abbott; Speaking and Teaching: BMS, MSD, Novartis, ITF The following people have nothing to disclose: Anika Wranke, Benjamin Heidrich, Stefanie Ernst, Armin Koch, Beatriz Calle Serrano, Florin A. Caruntu, Manuela G.

The virtual absence of the HFE C282Y mutation in Asia-Pacific populations makes

the HFE gene tests used in most Western nations superfluous. The sporadic nature of the mutations identified as causing iron overload in the Asia-Pacific means that a simple test is not possible for the genetic diagnosis of HH in this region. Using current technology, genetic diagnosis involves sequencing of the entire coding region of one or more of the known HH genes guided by clinical selleckchem and phenotypic data. This can be a costly process. Because such genetic testing is only performed by specialized research laboratories, the treating physician needs to go to far greater lengths to pursue a definitive diagnosis, which is required for family screening as well as to confirm individual diagnosis. Even then, for a variety of reasons, gene sequencing still often fails to identify the causative mutation leaving no genetic diagnosis to report. This combination of low awareness, high cost, and non-standardized methodology for definitive diagnosis is likely to lead to significant underrecognition of HH in non-European populations. With the development of next generation, sequencing has come the promise of high throughput

low-cost-per-base sequencing, providing a much greater chance of mutation identification in patients who are HFE gene test negative. While the information obtained from next generation PD-0332991 molecular weight sequencing is comprehensive, to date, the cost on a per-patient basis combined with the technical difficulty has rendered this an impractical method for diagnostic applications. However, recent developments in customizable platforms, improved automation, and improved downstream data analysis pipelining now allows rapid parallel deep sequencing of all known and potential causative genes to be achieved relatively economically. Using this

customized platform, selleck products the authors’ laboratory is now establishing an atypical iron disorder referral centre to fast track the genetic diagnosis of patients with atypical forms of HH. Our novel method involves the rapid amplification of the coding regions of 30 genes involved in iron metabolism, including all that have been implicated in primary iron overload disorders. In addition, the promoter sequences of 10 of these genes are also targeted. This amplification is achieved using an AmpliSeq custom panel (Life Technologies, Melbourne, Australia) to amplify the target genes in a massively multiplexed polymerase chain reaction. The amplified targets are then sequenced using the Ion Torrent Personal Genome Machine (Life Technologies) and resultant sequence analyzed through a bioinformatics pipeline to deliver a report detailing the sequence variants present.

We studied the predictive value of donor MBL genotyping for bacterial infections in our own center. The MBL genotypes of 290 donor livers used for orthotopic transplantation between 1987 and 2010 were determined. Notably, this cohort represents the largest single-center cohort of LT patients in which associations between the donor MBL2 genotype

and bacterial infections have been analyzed. In three different ways, we categorized donor livers as MBL-sufficient or MBL-insufficient selleck according to the stratification systems used in the cited studies, and we analyzed associations with clinically significant and laboratory-confirmed bacterial infections occurring during the first 3 months after LT by chi-square analysis with Fisher’s exact test (Table 1). Thirty-eight percent of LT recipients experienced one or more infectious episodes, and this is comparable to the numbers reported by the previous studies.1, 4, 5 Importantly, none of the three stratifications resulted in a statistically significant association between the donor MBL genotype and clinically significant infections. In addition, www.selleckchem.com/products/bmn-673.html when we analyzed associations with site-specific infections, independently of MBL genotype stratification, we observed no significant increases in the risk of intra-abdominal infections

or bacteremia in patients who underwent transplantation with MBL-insufficient livers. However, in two of the three types of MBL genotype stratification, significantly more pneumonia was diagnosed in patients who underwent transplantation with MBL-deficient livers. In conclusion, this retrospective study indicates that in selleck chemical our center, the donor MBL2 genotype is not helpful in predicting the risk of bacterial infection after LT. Lilian A. Curvelo M.D., Ph.D.*,

Emmeloes de Mare-Bredemeijer M.D.*, Ilse de Canck M.Sc.‡, Martine van Thielen M.Sc.‡, Geert Kazemier M.D., Ph.D.†, Herold Metselaar M.D., Ph.D.*, Jaap Kwekkeboom Ph.D.*, * Departments of Gastroenterology and Hepatology, Rotterdam, the Netherlands, † Surgery, Erasmus MC: University Medical Center Rotterdam, Rotterdam, the Netherlands, ‡ R&D Discovery, Innogenetics NV, Zwijnaarde, Belgium. “
“See article in J. Gastroenterol. Hepatol. 2010; 25: 259–263 Clearance of hepatitis B surface antigen (HBsAg) from serum, normalization of transaminase values, and appearance of antibodies against HBsAg (anti-HBs) are associated with disease resolution in acute or chronic hepatitis B virus (HBV) infections. However, transmission of HBV infection by blood containing antibodies against hepatitis B core antigen (anti-HBc) has been reported, indicating that serum from HBsAg-negative patients with markers of a past HBV infection may still contain infectious HBV particles.