All patients were risk stratified using the Glasgow-Blatchford bleeding score (GBS). Continuous data was assessed using the Mann-Whitney test and categorical data using Fisher’s exact test. Results: Of 373 patients with a primary diagnosis of UGIB, 56 (15%) presented with CGV. The mean age was 63 years (range 15–93) and 40 (71.4%) were male. 30 (54%) presented with isolated CGV while 26 (46%) presented with CGV plus melaena (22) and/or haematemesis (8, 5-Fluoracil research buy defined as haematemesis documented prior to ED presentation). No statistically significant differences in age or co-morbidity

burden were detected between the two groups. At endoscopy, patients presenting with isolated CGV were more likely to have a Mallory Weiss tear (4 vs 1, p = NS) or inflammatory or erosive disease of the oesophagus, stomach or duodenum (18 vs 14, p = NS). Patients presenting with

CGV plus haematemesis or melaena (CGV+HM) were more likely to have ulceration or malignancy (10 vs 2, p = 0.007). The two ulcers in isolated CGV patients were Forrest 3 and check details did not require endoscopic therapy. CGV+HM patients were more likely to be anticoagulated (19 vs. 10, p = 0.0038), require blood transfusion (15 vs. 7, p = 0.013), have a lower haemoglobin on presentation (110 vs. 128, p = 0.016) and have a higher GBS (7.8 vs. 4.7, p = 0.009). No differences were recorded in the number of patients on a Proton Pump Inhibitor (PPI) or treated with intravenous PPI during admission. One patient died nine days after gastroscopy from an unrelated condition. Conclusion: Patients presenting with coffee ground vomiting as the sole presenting symptom of an upper gastrointestinal bleed have a low risk of serious pathology being found at endoscopy. This implies that these patients do not require urgent medchemexpress endoscopy. M ROBERTSON,1 A MAJUMDAR,1

R BOYAPATI,1 W CHUNG,1 R TURBAH,1 J WEI,1 R VAUGHAN,1 S LONTOS1 1Department of Gastroenterology and Liver Transplant Unit, Austin Hospital, Heidelberg, Australia Introduction: Multiple algorithms predicting outcomes in upper gastrointestinal bleeding (UGIB) have been developed, the most widely used of which are the Glasgow-Blatchford (GBS) and Rockall scores. AIMS65 is a novel risk stratification score designed to predict inpatient mortality. The AIMS65 score assigns 1 point for each of the following: albumin level <30 g/L, INR > 1.5, altered mental status, systolic blood pressure <90 mmHg and age older than 65 years. Compared with existing scores, AIMS65 has the advantages of not being weighted and can be easily calculated with pathology values routinely obtainable in the emergency department. Objective: To assess the AIMS65 score as predictor of inpatient mortality in patients presenting with acute UGIB.

The double strandedness of the RNA duplex configuration is believed to be essential for the efficient loading of the miR guide strand into the RISC complex.

In order to increase stability and improve cellular uptake of the miR duplex, it is formulated with lipid nanoparticles (LNPs).18 To date, the LNP-mediated delivery of an RNA duplex limits its tissue distribution primarily to the liver (including hepatic stellate cells). The characteristics of an LNP-enclosed miR-29 mimic render liver fibrosis an attractive disease indication for the initial clinical proof of experiments. It is believed that similar underlying mechanisms are involved in the development of fibrosis in different organs. Further advances in oligonucleotide delivery technology will enable the evaluation of whether an miR-29 mimic could be an effective

therapy for fibrotic conditions of other organs. ECM, extracellular matrix; LNP. selleck lipid nanoparticle; miR, microRNA; miRNA, microRNA; mRNA, messenger; RNA, pre-miR; precursor microRNA; pri-miR, primary microRNA transcript; RISC, RNA interference-induced silencing complex; TGF-β, transforming growth factor β “
“We read with great interest the meta-analysis by Wang et al.,1 who evaluated the diagnostic accuracy of magnetic resonance elastography (MRE) and diffusion-weighted imaging (DWI) for the staging of hepatic fibrosis. The authors concluded that MRE is more reliable for staging hepatic fibrosis. This is a significant contribution to our knowledge, as recent NVP-BGJ398 supplier advances in MRI techniques have made the use of these methods common in clinical practice. In our opinion, attention must also be focused on several technical parameters of MRI methods before physicians can safely interpret the results. The standard MRI scanners currently use a 1.5-Tesla magnetic field. This is also the type of scanner that was used in all the studies included in the meta-analysis by Wang et al. Theoretically, new-generation 3-Tesla scanners could enhance the ability for hepatic fibrosis staging. Especially for DWI, another vital parameter is the apparent diffusion coefficient (ADC) and its b value. ADC reflects diffusion in a MCE公司 quantitative

way and b value illustrates the sensitivity of a DWI sequence. The higher the b value, the more sensitive the sequence is to diffusion effects.2 Conflicting results have been published on the optimal b value for hepatic fibrosis staging.3 This was also remarkably reflected in the great variation of b values used in the studies of the meta-analysis. We recently presented our preliminary results on hepatic fibrosis staging in a small cohort of patients with nonalcoholic fatty liver disease (NAFLD) using a 3-Tesla MRI scanner.4 DWI was performed in the axial plane with tridirectional diffusion gradients using three b values: 0, 500, and 1000 s/mm2. Fibrosis stage was poorly associated with ADC at a b value of 500 s/mm2 (r = −0.30, P = 0.27).

EMSA was performed to measure the activation of CAR and c-myc. Pooled nuclear samples (n = 3) from ILK/ liver−/− and WT mice were used for performing EMSA using a commercial kit from Signosis (Sunnyvale, CA). Biotinylated DNA binding consensus sequence were also purchased from Signosis. Paraffin-embedded liver sections (4 μm thick) were used for immunohistochemical staining. Antigen retrieval was achieved by heating the slides in the microwave at high power in 1× citrate buffer for 10 minutes. The tissue sections were blocked in blue blocker for 20 minutes followed by incubation with mouse PCNA antibody overnight at 4°C. The primary antibody

was then linked to biotinylated secondary antibody click here followed by routine avidin-biotin complex method. Diaminobenzidine was used as the chromogen, which resulted in a brown reaction product. PCNA-positive cells were counted in low-power fields (200×) in four sections from four different knockout or control livers. RNA was extracted from frozen liver tissues with Trizol (Invitrogen) according to the manufacturer’s instructions. RNA,

5 μg, was reverse transcribed to complementary DNA (cDNA) with Superscript III reverse transcriptase (Invitrogen). Standard PCR was performed with Taq polymerase (Qiagen, CA). The primers for hepatocyte growth factor (HGF) were bought from SA Bioscience (Frederick, MD). PCR products were resolved on 2% agarose gels and visualized with ethidium bromide. Expression levels of UGT1A1 MCE were determined by quantitative RT-PCR (qRT-PCR) using SYBR SB203580 datasheet green and levels were normalized relative to expression of cyclophillin in each sample. Fold change in gene expression was calculated by using the 2(-ΔΔCt) method. Reverse-transcribed samples were amplified in parallel on an ABI prism 7000 SDS instrument (Applied Biosystems,

Foster City, CA). qRT-PCR for each sample was performed in triplicate in a 20-μL reaction with 50 ng of cDNA, 5 picomoles of each primer, and 1× SYBR green PCR mix (Applied Biosystems). The standard conditions for real-time PCR were as follows: 2 minutes at 50°C, 10 minutes at 95°C, followed by 40 cycles of 15 seconds denaturation at 95°C, and elongation at 60°C for 45 seconds. A dissociation curve analysis was performed at the end of every run. A no-RT and a no-template control was also included in every run. The liver-to-body weight ratios were measured in WT and ILK/liver−/− mice at days 1, 2, 3, 5, and 7 after TCPOBOP administration. The WT showed a maximum of 2.5-fold increase (day 5) in liver-to-body weight ratio as compared to 0 day (Fig. 1B). On the other hand, the ILK/liver−/− mice showed a maximum of 3.5-fold increase (day 7) in liver-to-body weight ratio as compared to 0 day. By day 7 the WT mice showed a 2.5-fold increase in liver weight, whereas the ILK/liver−/− mice showed a 3.7-fold increase (Fig. 1A).

55 Eradication of the overgrowth by open label antibiotic treatment resolved symptoms to the extent of Rome I criteria turning negative in 48% of patients.55 Such a high frequency of SIBO, however, has not been reproduced in subsequent studies, including those from Asia.14,46,54 The unusually high frequency of SIBO in the

initial studies might be related to the criteria used to diagnose SIBO.55 In the earlier studies, rise in breath hydrogen 20 parts per million (PPM) above basal levels within 90 min after ingestion of lactulose was considered diagnostic of SIBO.55 This criterion has not been validated. Moreover, it presumes that mouth-to-cecum transit CP-673451 nmr time is always greater than 90 min, so that a peak in breath hydrogen within 90 min after lactulose ingestion must be due to bacterial fermentation in the small bowel. However, such a presumption may not be correct. Mouth-to-cecum transit time in Asian populations is often shorter than 90 min. For example, median mouth-to-cecum transit time in 12 healthy Indian subjects was 65 min (range 40–110 min).44 In a study of 45 healthy Taiwanese, mean mouth-to-cecum transit time was 85 min (SD 37).56 Therefore, a large proportion of these healthy subjects would Ibrutinib nmr have been diagnosed having SIBO if the lactulose HBT criterion had been used. Conventionally, diagnosis of SIBO by lactulose HBT is based

on the occurrence of two peaks in lactulose HBT.57 However, using such criteria, sensitivity

of lactulose HBT for diagnosis of SIBO is 31%, while specificity is 86%.57 It is concluded that lactulose HBT may not be appropriate for the diagnosis of SIBO, at least in Asia. In some studies, glucose hydrogen breath test (GHBT) has been used for diagnosis of SIBO. In one study, sensitivity and specificity were 44% and 80%, respectively.57 However, in that study, methane was not estimated, resulting in low sensitivity medchemexpress of the test. Since 14–35% of the population harbor methanogenic flora in their gut,58 estimation of methane is expected to increase the sensitivity of the test to detect SIBO. In a study from India, nine of 69 (13%) patients had SIBO using GHBT without estimation of methane.46 In another study, 25 of 225 (11%) patients with IBS had SIBO using GHBT as compared with 1/100 controls.14 Considering the fact that GHBT has a sensitivity of 44% only, both these studies could have underestimated the frequency of SIBO. In a study from Korea on 39 patients with IBS and 49 healthy controls, frequency of SIBO using lactulose HBT (SIBO diagnosed by an early peak within 90-min or a double peak) 49% versus 26%, respectively; the frequency using GHBT among IBS and controls was comparable.54 Table 2 summarizes the studies on SIBO in patients with IBS from Asia. Most used GHBT and found a frequency of SIBO among patients with IBS to be consistently around 10%; in contrast, SIBO was absent in most controls.

55 Eradication of the overgrowth by open label antibiotic treatment resolved symptoms to the extent of Rome I criteria turning negative in 48% of patients.55 Such a high frequency of SIBO, however, has not been reproduced in subsequent studies, including those from Asia.14,46,54 The unusually high frequency of SIBO in the

initial studies might be related to the criteria used to diagnose SIBO.55 In the earlier studies, rise in breath hydrogen 20 parts per million (PPM) above basal levels within 90 min after ingestion of lactulose was considered diagnostic of SIBO.55 This criterion has not been validated. Moreover, it presumes that mouth-to-cecum transit selleck products time is always greater than 90 min, so that a peak in breath hydrogen within 90 min after lactulose ingestion must be due to bacterial fermentation in the small bowel. However, such a presumption may not be correct. Mouth-to-cecum transit time in Asian populations is often shorter than 90 min. For example, median mouth-to-cecum transit time in 12 healthy Indian subjects was 65 min (range 40–110 min).44 In a study of 45 healthy Taiwanese, mean mouth-to-cecum transit time was 85 min (SD 37).56 Therefore, a large proportion of these healthy subjects would selleck compound have been diagnosed having SIBO if the lactulose HBT criterion had been used. Conventionally, diagnosis of SIBO by lactulose HBT is based

on the occurrence of two peaks in lactulose HBT.57 However, using such criteria, sensitivity

of lactulose HBT for diagnosis of SIBO is 31%, while specificity is 86%.57 It is concluded that lactulose HBT may not be appropriate for the diagnosis of SIBO, at least in Asia. In some studies, glucose hydrogen breath test (GHBT) has been used for diagnosis of SIBO. In one study, sensitivity and specificity were 44% and 80%, respectively.57 However, in that study, methane was not estimated, resulting in low sensitivity 上海皓元医药股份有限公司 of the test. Since 14–35% of the population harbor methanogenic flora in their gut,58 estimation of methane is expected to increase the sensitivity of the test to detect SIBO. In a study from India, nine of 69 (13%) patients had SIBO using GHBT without estimation of methane.46 In another study, 25 of 225 (11%) patients with IBS had SIBO using GHBT as compared with 1/100 controls.14 Considering the fact that GHBT has a sensitivity of 44% only, both these studies could have underestimated the frequency of SIBO. In a study from Korea on 39 patients with IBS and 49 healthy controls, frequency of SIBO using lactulose HBT (SIBO diagnosed by an early peak within 90-min or a double peak) 49% versus 26%, respectively; the frequency using GHBT among IBS and controls was comparable.54 Table 2 summarizes the studies on SIBO in patients with IBS from Asia. Most used GHBT and found a frequency of SIBO among patients with IBS to be consistently around 10%; in contrast, SIBO was absent in most controls.

58,59 In an open-label study, 23 ECH and 31 CCH patients were admitted to the hospital for treatment with repetitive intravenous DHE.60 All patients became headache free while being treated with IV DHE: 10 patients MLN0128 manufacturer (16%) after the first dose, an additional 12 (19%) during the first day of hospitalization,

and 22 (34%) more became headache free by the second day of hospitalization. By day 3, greater than 90% of patients were headache free and by day 5 all were headache free. At 3 months after discharge, >90% of ECH patients and 44% of CCH patients remained headache free. Approximately 83% of patients reported no AEs from IV DHE. Reported AEs included nausea, non-cardiac chest tightness, and a metallic taste. Ergotamine tartrate, 3-4 mg per day in divided doses, may be administered for 2 to 3 weeks for transitional prophylaxis.58,61 Administration just before bedtime may help to prevent nighttime attacks. With an individually

tailored pharmacologic treatment plan, the majority of CH patients will achieve satisfactory results. For those who remain refractory to medical treatment, a number of invasive procedures are available. These include peripheral nerve blocks, peripheral or central neurostimulation and, as a last resort, ablative selleck inhibitor surgery. Peripheral nerve block, mostly targeting the greater occipital nerve (GON), may also be used in less refractory patients, as an adjunct to pharmacologic therapy. Efficacy

of GON block in CH treatment was suggested by Anthony in the 1980s.62 More recently, the procedure was investigated as CH treatment in a number of studies, with the majority showing positive results.63-66 Peres et al evaluated the effect of GON block in 14 patients with CH.63 Patients received GON block ipsilateral to the head pain using lidocaine 1% and triamcinolone 40 mg. Patients were evaluated before and 1 week after the block. Nine (64%) patients had good or moderate response. The procedure was well tolerated. Ambrosini et al evaluated the effect of suboccipital injection of lidocaine 2% with betamethasone, compared with lidocaine and saline, in 23 CH patients in a randomized, controlled study.64 The CH attacks disappeared within 72 hours in 85% of medchemexpress the lidocaine + betamethasone group (with 61% remaining attack free for 4 weeks) compared with none in the lidocaine + saline group. Injections were well tolerated. Afridi et al examined the efficacy of GON block, using lidocaine 2% and methylprednisolone, in patients with refractory chronic daily headache.65 Their sample included 19 patients with CH who received 22 injections. Thirteen of the injections (59%) resulted in a complete or partial response, with a median duration of 12 and 21 days, for complete and partial response, respectively.

In the overall cohort, 9.3% of patients showed clinical signs of liver cirrhosis at 35 years after infection. Liver disease progression largely depended on HCV infection status. The highest proportion of patients with clinical signs of end-stage liver disease was observed in the non-SVR group (15.3%), whereas decreased cirrhosis rates were detected IWR-1 in the SVR group (6%) and in patients with self-limited HCV infection (1.1%; P = 6.2 × 10−6). Overall survival was significantly enhanced after SVR, compared to treatment-naïve patients or non-SVR (P = 0.027). Conclusion: The present study provides further evidence for a mild, but significant, disease progression at 35 years

after infection in the German HCV (1b)-contaminated

anti-D cohort. Patients with self-limited HCV infection or SVR after antiviral treatment Galunisertib mouse were protected from progressive liver disease and showed the best clinical long-term outcome. (Hepatology 2014;58:49–57) Hepatitis C virus (HCV) infection is the leading cause of end-stage liver disease (ESLD) in the world and represents a major burden for national health systems.[1] The World Health Organisation (WHO) and international consensus conferences refer to the high chronification rate of HCV infection, the risk of subsequent HCV-related complications, including end-stage liver cirrhosis and hepatocellular carcinoma (HCC) and the high costs for antiviral therapy, respectively, liver transplantation (LT).[2, 3] It is estimated that HCV-related morbidity and mortality

will increase in the next decade.[4-6] The predicted cumulative probability of cirrhosis approximates 20% at 20 years after HCV infection and increases to 45% at 30 years after infection.[7] However, recent estimates on the natural fibrosis progression rates of hepatitis C largely depend on study design, study setting, and the selected study population. In theory, prospective multicenter, community-based long-term follow-up studies in large representative patient cohorts with a defined onset of HCV infection from a single identified source constitute the optimal setting for the evaluation of the natural course of chronic HCV infection.[8] Therefore the well-documented iatrogenic medchemexpress single-source HCV outbreaks in recipients of HCV-contaminated anti-D immunoglobulin (Ig) in Ireland (1977-1978) and Germany (1978-1979) provided valuable insight into the acute and chronic course of HCV infection in the past.[9-12] We have previously reported on the outcome of the German HCV (1b)-contaminated anti-D cohort at 20 and 25 years after infection and demonstrated a very low cirrhosis rate of only 0.5% in the overall cohort at 25 years after infection.[11, 12] The aim of the present 35-year follow-up study was to reevaluate the liver disease progression in this unique cohort after another decade of data accrual in our prospective, community-based, multicenter study.

[12] During this decade, simple (all oral regimens), tolerable, short-duration Neratinib (6–12 weeks) therapy with extremely high efficacy (cure rates above 90%) should become the norm for the HCV-infected population.[13, 14] The broad implementation of such therapeutic regimens has the potential to produce one of the major turnarounds in disease burden seen globally in public health and clinical medicine. However, the high cost of DAA regimens and competing public health priorities may limit

the potential impact of new HCV therapies. In this context, it is crucial to examine various treatment strategies for their capacity to limit the projected advanced liver disease burden and associated costs. This analysis explores three scenarios that incorporate different levels of treatment efficacy, eligibility, and uptake. As previously described,[15-17] country-specific inputs were used to construct a disease progression model in Microsoft Excel (Microsoft Corporation, Redmond, WA, USA) to quantify the HCV-infected population and associated costs from 2013 to 2030. Uncertainty and sensitivity analyses were completed using Crystal Ball, an Excel add-in by Oracle (Redwood Shores, CA, USA). Beta-PERT distributions were used to model uncertainty associated with

all inputs. Sensitivity http://www.selleckchem.com/products/LY294002.html analysis was used to identify the uncertainties that had the largest impact on peak prevalence in 2025. Monte-Carlo simulation was used to determine the 95% uncertainty interval for cost and prevalence. Population data were organized by sex, 5-year age groups, and year (1950–2100) and obtained from the United Nations population database.[18] In Australia, the number of people with chronic HCV (viremic population) in 2012 was estimated at 230 000[3] (Table 1). For the age and gender distribution of the infected population, notification data for hepatitis C infection (newly acquired MCE公司 and unspecified) from 1995 to 2013 were utilized to calculate age-

and gender-specific HCV detection rates by 5-year age group. The notified population was aged to the year 2013, accounting for mortality and HCV treatment–induced viral clearance. When constructing the age and gender distribution (Fig. 1), it was assumed that all people diagnosed after 2010 were alive in 2013. For other data years, it was assumed that diagnosed individuals aged ≥ 70 (1994), ≥ 75 (1996–2000), ≥ 80 (2001–2005), ≥ 85 years (2006–2010) were lost to mortality.[19] The genotype distribution of the prevalent population was estimated using data from an Australian study[20] as follows: genotype 1 (G1) = 54.5%, G2 = 5.2%, G3 = 36.8%, G4 = 1.9%, G6 = 1.6%. Age- and gender-specific transition probabilities were used to progress people annually through each disease state, as described in by earlier work.[16] Model outcomes were validated using published estimates for prevalent populations by disease state in Australia.

Another obstacle to AAV-mediated gene transfer for HA gene therapy is the size of the FVIII coding sequence, which at 7.0 kb far exceeds the normal packaging capacity of AAV vectors. Packaging of large expression cassettes into AAV vectors has been reported but this is a highly inconsistent process resulting in low yields of vector particles with reduced infectivity [49, 50]. AAV vectors encoding the BDD-FVIII variant that is around 4.4 kb in size show promising results using canine FVIII but further evaluation of this approach using human BDD-FVIII is required. Other approaches include the co-administration

of two AAV vectors separately encoding the FVIII heavy- and light chains whose intracellular association in vivo leads to the formation of a functional molecule. The alternative two AAV vector approach exploits the tendency of these vectors GS-1101 cell line to

form head to tail concatamers. Therefore, by splitting the expression cassette such that one AAV vector contains a promoter and part of the coding sequence, as well as a splice donor site, whereas the other AAV vector contains the splice acceptor site and the remaining coding sequence. Following in vivo head to tail concatemerization a functional transcript is created that is capable of expressing full-length FVIII protein [51-53]. We have developed an AAV-based gene transfer approach that addresses both the size constraints and inefficient FVIII expression. Expression of human FVIII was improved 10-fold by re-organization of the wild-type medchemexpress cDNA of human http://www.selleckchem.com/products/LDE225(NVP-LDE225).html FVIII according to the codon usage of highly expressed

human genes [54-56]. Expression from B-domain-deleted codon optimized FVIII molecule was further enhanced by the inclusion of a 17 amino-acid peptide that contains the six N-linked glycosylation signals from the B domain required for efficient cellular processing. These changes have resulted in a novel 5.2 kb AAV expression cassette (AAV-HLP-codop-hFVIII-V3), which is efficiently packaged into recombinant AAV vectors and capable of mediating supraphysiological level of FVIII expression in animal models over the same dose range of AAV8 that proved to be efficacious in subjects with haemophilia B. Our novel AAV-HLP-codop-hFVIII-V3 cassette substantially improves the prospects of safe and effective gene transfer for haemophilia A. We are currently in the process of developing clinical grade AAV-HLP-codop-hFVIII-V3 for use in human subjects in the context of a clinical trial, which we hope will open in early 2015. The design of this clinical trial will be discussed in greater detail during the meeting. Recombinant retroviruses used in clinical gene therapy applications have been extensively engineered for efficient transfer of nucleic acid sequences into human cells. The most significant modification is the creation of replication incompetent viruses.

In conclusion, patient survival of HCV-positive recipients after LDLT was feasible. In addition to the consideration for known risk factors such as older donor, episodes of ACR and absence SVR, right liver graft could be preferable for HCV positive recipients in an LDLT setting. Disclosures: The following people have nothing to disclose: Tomohiro Tanaka, Nobuhisa Akamatsu, Yasuhiko Sugawara, Junichi Kaneko, Sumihito Tamura, Taku Aoki, Yoshihiro Daporinad Sakamoto, Kiyoshi Hasegawa, Norihiro Kokudo Background:

The Procleix HEV assay is a qualitative in vitro nucleic acid test for the detection of hepatitis E virus (HEV) RNA. The assay is currently under development and runs on the Procleix Panther system, a fully automated instrument that allows random access of samples and continuous loading of reagents during processing.

Aims: Studies were performed to characterize the sensitivity, specificity, and reproducibility of the selleck Procleix HEV assay on the Panther system. Methods: Studies were conducted to assess the analytical sensitivity using the HEV WHO International Standard (PEI code 6329/10) and RNA transcripts of all 4 clinically relevant HEV genotypes (1, 2, 3a, 3b, 3f and 4c), and clinical specificity of the assay using multiple lots of reagents. Clinical sensitivity was assessed by testing 40 HEV positive blood donor specimens with viral load titers ranging from 10 to 1,000,000 IU/mL. Assay reproducibility,

performance in plasma and serum samples MCE from cadaveric specimens, and the effect of potentially cross-contaminating infectious agents, interfering substances, and donor and donation factors were determined. Results: The Procleix HEV assay showed a 95% limit of detection (LOD) of 7.9 IU/ mL (95% CI: 6.63-9.83 IU/mL) using the WHO Standard and detected all the HEV genotype transcripts with 95% LOD values ranging from 7.9 to 17.7 copies/mL. A total of 4,494 plasma samples obtained from volunteer whole blood donations were screened for HEV RNA with a resulting clinical specificity of 99.98% (95% CI: 99.87-100%). The 40 HEV positive blood donor specimens were detected at a rate of 98.75% when tested undiluted. When tested over three days with multiple instruments, reagent lots, and operators, the assay showed reproducible results with the intra-run factor contributing the largest source of variability. The assay showed 100% specificity and sensitivity in the presence of potentially cross-contaminating infectious agents, interfering substances, donor and donation factors, and for cadaveric samples. Summary/Conclusions: Preliminary results indicated that the assay was sensitive (95% LOD: 7.9 IU/mL) and specific (99.98% specificity). The assay was also shown to detect the 4 clinically relevant HEV genotypes and was highly reproducible.