“The taxonomic assignment of Prorocentrum species is based

“The taxonomic assignment of Prorocentrum species is based on morphological characteristics; however, morphological variability has been found for several taxa isolated from different geographical regions. In this study, we evaluated species boundaries of Prorocentrum hoffmannianum and Prorocentrum belizeanum based on morphological and molecular data. A detailed morphological analysis was done, concentrating on the periflagellar

beta-catenin inhibitor architecture. Molecular analyses were performed on partial Small Sub-Unit (SSU) rDNA, partial Large Sub-Unit (LSU) rDNA, complete Internal Transcribed Spacer Regions (ITS1-5.8S-ITS2), and partial cytochrome b (cob) sequences. We concatenated the SSU-ITS-LSU fragments and constructed a phylogenetic tree using Bayesian Inference (BI) and Maximum Likelihood (ML) methods. Morphological analyses indicated that the main characters, such as cell size and number of depressions per valve, normally used to distinguish P. hoffmannianum from P. belizeanum, overlapped. No clear differences were found in the periflagellar area architecture. P. hoffmannianum and P. belizeanum were a highly supported monophyletic clade separated into three

sub-clades, which broadly corresponded to the sample collection regions. Subtle morphological overlaps found in cell shape, size, and ornamentation lead us to conclude that P. hoffmanianum and P. belizeanum might be considered conspecific. The molecular data analyzes did not separate P. hoffmannianum MCE and P. belizeanum into two morphospecies, and thus, we considered them FK506 research buy to be the Prorocentrum hoffmannianum species complex because their clades are separated by their geographic origin. These geographic and genetically distinct clades could be referred to as ribotypes: (A) Belize, (B) Florida-Cuba, (C1) India, and (C2) Australia. This article is protected by copyright. All rights reserved. “
“A new photosynthetic planktonic marine dinoflagellate, Azadinium dexteroporum sp. nov., is described from the Gulf of Naples (South Tyrrhenian Sea, Mediterranean Sea). The plate formula of the species, Po, cp, X, 4′, 3a, 6″, 6C,

5?S, 6‴ and 2″″, is typical for this recently described genus. Azadinium dexteroporum is the smallest rep-resentative of the genus (8.5 μm average length, 6.2 μm average width) and shares the presence of a small antapical spine with the type species A. spinosum and with A. polongum. However, it differs from all other Azadinium species for the markedly asymmetrical Po plate and the position of the ventral pore, which is located at the right posterior end of the Po plate. Another peculiarity of A. dexteroporum is the pronounced concavity of the second intercalary plate (2a), which appears collapsed with respect to the other plates. Phylogenetic analyses based on the large subunit 28S rDNA (D1/D2) and the internal transcribed spacer (ITS rDNA) support the attribution of A.

In the March 6 issue of the Annals of Internal Medicine, there is

In the March 6 issue of the Annals of Internal Medicine, there is an article entitled “Screening for Liver Acalabrutinib mw Cancer: A Rush to Judgment”.1 In it, the investigators criticize the AASLD recommendations on screening for HCC.2, 3 The basis for their criticism is that the only randomized, controlled trial (RCT) that showed a benefit4 to screening was statistically invalid. They imply that there is no reliable information on HCC screening, and that therefore AASLD should not be recommending screening to patients at risk for HCC. However, in addition to the AASLD, other organizations, such as the U.S. Veterans

Administration,5 the World Gastroenterology Association,6 European Association for Study of the Liver,7 Aloxistatin supplier and the liver disease societies of several Asian countries8, 9 consider the Chinese study to be valid and recommend screening for HCC. The National Comprehensive Cancer Network in the United Sstates also recommends HCC screening.10 All these recommendations recognize the presence of a well-defined at-risk population and the availability of effective treatment for early-stage disease. There have been two RCTs of HCC screening in China.4, 11 The first found no difference between the screened and unscreened group.11 However, the conduct of this trial made it impossible to show a difference.

Resection was to be used as the treatment of early-stage HCC, but a large proportion of those with screen-detected HCC did not undergo resection. Therefore, this trial failed for methodological reasons and not because screening was ineffective. The second trial, also in China,4 used a cluster randomization method, but then analyzed the results on an individual patient

basis. This is not statistically correct. The argument by the investigators of the Annals of Internal Medicine article is that if the study had been correctly analyzed, there would be no statistical difference between the screened and unscreened groups; and furthermore, even 上海皓元医药股份有限公司 if the study had shown a difference in mortality, the results would not be applicable in North America, because in North America, the dominant cause of HCC is hepatitis C, not hepatitis B. Therefore, they argue, HCC screening was not worthy of a high level of recommendation. There are two issues here: The first is the level of evidence, and the second is the recommendation and the strength of the recommendation. At the time of the initial guidelines, the AASLD was using a grading system that had broader categories with some overlap. A grade 1 level of evidence was defined as that based on RCTs and, to some extent, was to encompass the general consensus of experts in the field who treat these types of patients on a day-to-day basis.

Symptoms vary depending on location and degree of inflammation, a

Symptoms vary depending on location and degree of inflammation, and diagnosis most often entails mucosal biopsy. Treatment varies from dietary intervention to pharmacologic therapy with immunosuppressive agents. The incidence of these disorders appears to be on the rise and future treatment options will require controlled trials. “
“Background:  Interstitial cells of Cajal (ICCs), which express c-Kit receptor tyrosine kinase (KIT), play an important role in gastrointestinal motility. Loss of ICCs likely contributes to diabetic gastrointestinal motility disorder, however, the mechanism of attrition remains

unknown. Here, we test the hypothesis that the bone marrow-derived progenitors are an important source of intestinal ICCs and that decreased homing of these progenitors in diabetes contributes to ICC diminution. Methods:  Wild type mice were X-ray irradiated, transplanted with bone marrow (BMT) from green fluorescence BMS-907351 cell line protein (GFP)-transgenic (TG)-mice and subsequently made diabetic

by streptozotocin (STZ) injection. Intestinal homing of GFP-positive bone marrow-derived cells was examined 2 or 5 months after STZ treatment. Results:  In the BMT-mice, we found many GFP-positive bone marrow-derived cells (BMDCs) in most parts of the intestinal area, the number Navitoclax in vivo of BMDCs was significantly decreased in diabetic mice compared with nondiabetic controls. As a representative area, we further examined the myenteric plexus of the proximal small intestine, and found that the cell numbers of ICCs marked by c-Kit-positive immunoreactivity were decreased by more than 40% in diabetic versus nondiabetic mice. Furthermore, numbers of c-Kit+/GFP+ and c-Kit+/GFP- cells were similar in nondiabetic mice, and decreased by 45.8% and 42.0%, respectively,

in diabetic mice. Conclusion:  These results suggest that the decreased homing from the bone marrow is a major cause of ICC loss in the intestine in diabetes mellitus. “
“V-set and Ig domain-containing 4 (VSIG4, CRIg, or Z39Ig), a newly identified B7-related cosignaling molecule, is a complement receptor and a coinhibitory ligand that negatively regulates T-cell immunity. 上海皓元 Despite its exclusive expression on liver Kupffer cells (KCs) that play key roles in liver tolerance, the physiological role of VSIG4 in liver tolerance remains undefined. Mice lacking VSIG4 had poor survival rates and severe liver pathology in a concanavalin A (ConA)-induced hepatitis (CIH) model, which could be prevented by adoptive transfer of VSIG4+ KCs. The absence of VSIG4 rendered endogenous liver T- and natural killer T (NKT)-cells more responsive to antigen-specific stimulation and impaired tolerance induction in those cells against their cognate antigens. T-cell costimulation with VSIG4.Ig suppressed Th1-, Th2-, and Th17-type cytokine production and arrested the cell cycle at the G0/G1 phase but did not induce apoptosis in vitro.

Thirty patients with chronic hepatitis C virus (HCV) genotype 1 i

Thirty patients with chronic hepatitis C virus (HCV) genotype 1 infection were randomized to receive a 14-day course of BMS-790052 (1, 10, 30, 60, or 100 mg once daily or 30 mg twice daily) or placebo in a ratio of 4:1. The mean maximum decline from GS-1101 baseline in HCV RNA ranged from 2.8 to 4.1 log10 IU/mL; the placebo group showed no evidence of antiviral activity. Most patients experienced viral rebound on or before day 7 of treatment with BMS-790052 monotherapy; viral rebound was associated with viral variants that had been previously implicated in resistance development in the in vitro replicon system. The PK profile was supportive of once-daily dosing with

median peak plasma concentrations at 1-2 hours postdose and mean terminal half-life of 12-15 hours. Steady state was achieved following 3-4 days of daily dosing.

BMS-790052 was well tolerated in all dose groups, with adverse events occurring with a similar frequency in BMS-790052- and placebo-treated groups. There were no clinically relevant changes in vital signs, laboratory, or electrocardiogram parameters. Conclusion: BMS-7590052 is the first NS5A replication complex inhibitor with multiple dose proof-of-concept in clinic. At doses of 1-100 mg daily, BMS-790052 was well tolerated, had a PK profile supportive of once-daily dosing, and produced a rapid and substantial decrease in HCV-RNA levels in patients chronically infected with HCV genotype 1. (HEPATOLOGY 2011 The current treatment selleck kinase inhibitor of chronic hepatitis C virus (HCV) infection, a regimen of

pegylated interferon alpha (PEG-IFN)-2a or -2b, and ribavirin 上海皓元医药股份有限公司 (RBV) remains unsatisfactory, particularly in the large number of patients with HCV genotype 1 infection, whose sustained viral response rates are currently ≈40%.1 However, treatment for HCV infection is rapidly evolving with the introduction of direct-acting antiviral (DAA) agents.2, 3 The combination of telaprevir, an HCV NS3 protease inhibitor, with PEG-IFN alpha-2a and RBV has been associated with sustained viral response rates of 61%-67% in patients with genotype 1 infection.2 Telaprevir is administered three times a day and has been associated with adverse events (AEs) such as rash and anemia.4 There continues to be an unmet medical need for additional DAA agents with different mechanisms of action and resistance patterns that are easy to administer, more effective, and well tolerated. Focusing on the critical importance of nonstructural protein 5A (NS5A) for HCV replication, BMS-790052 was identified as a potent and highly selective inhibitor of HCV based on inhibitor binding and mapping, inhibitor-induced resistant substitutions, and crystal structure modeling. In vitro data have shown that BMS-790052 inhibits HCV genotype 1 replicons with a median 50% effective concentration of ≤50 pM, whereas BMS-790052-resistant variants remain fully sensitive to interferon alpha and small-molecule inhibitors of HCV protease and polymerase.

HCV recurrence after LT is almost universal and severity depends

HCV recurrence after LT is almost universal and severity depends on several host, viral, donor, and transplant factors. Graft and patient survival are significantly reduced after LT in HCV-positive recipients.[1-4]

A subset of patients (2%) may develop see more post-LT cholestatic hepatitis C, which is characterized by persistent cholestasis of at least 4 weeks in duration, high HCV RNA levels, hepatocyte ballooning, rapid progression to graft failure, and, in the absence of biliary and hepatic artery complications, sepsis and drug-related cholestasis.[5] The overall outcome of antiviral therapy in this group of patients is suboptimal, although it can be successfully pursued in select patients. The unique challenges of HCV treatment in this population include management of AEs, adjusting immunosuppressive regimens because of

DDIs in those on direct-acting antivirals (DAAs), and monitoring for graft rejection. Although selection criteria for treatment of chronic HCV in LT patients is variable, antiviral therapy is generally considered in those who develop significant or progressive recurrent HCV disease, as defined by moderate-to-severe necroinflammatory activity (grade 3-4) and/or significant fibrosis (stage 2-4) on histologic evaluation.[6] Treatment of recurrent HCV in LT recipients, particularly with successful viral eradication, is associated with increased graft and patient survival.[7] In various experiences published, the majority of patients included Selleck Crizotinib were genotype 1, had a reduced dose of RBV (400-800 mg/day) and/or PEG-IFN, and had use of ESAs. The pooled estimate of sustained viral response (SVR) from prospective

studies was 24%-40%, and virologic relapse was 21%-43%. Biochemical and histological responses were observed in approximately 50% of treated patients.[8, 9] Two thirds of 上海皓元 patients required dose reductions of either PEG-IFN or RBV and one fourth discontinued treatment early.[2] The approval of two protease inhibitors, telaprevir and boceprevir, has ushered in a new era of HCV treatment. In those with chronic HCV, one of these have been used in combination with PEG-IFN and RBV, and the regimens have enhanced response rates and shortened duration of therapy, whereas they have added to the side-effect profile.[10] Cost of treatment for boceprevir triple therapy is variable, and in instances of treatment duration similar to this case, the expense of therapy is approximately $71,000.[11] However, there are other expenses of close monitoring and frequently following immunosuppression drug levels, which then increase the cost relative to a patient who has not had LT. An incremental rate and degree of anemia has been observed with both TT regimens, which does present a challenge in the transplant recipients who are prone to anemia.

PTN and PTPRZ1 are known to control the egress of stem cells from

PTN and PTPRZ1 are known to control the egress of stem cells from bone marrow. Methods: Livers were harvested from PTN-GFP (PTN reporter) mice, PTN-PTN-knockout (KO) mice, PTPRZ1-KO mice, and wild type (WT) controls (n=6-9 mice/group) 2 weeks after bile duct ligation (BDL). Effects Sirolimus on expression of PTN and PTPRZ1, and the DR were evaluated by qRT PCR, quantitative immunohistochemistry (IHC), and hepatic hydroxyproline assay. LPCs and HSC

from WT, PTN-KO, and PTPRZ1-KO mice were also treated directly with PTN to characterize tyrosine-phosphorylated proteins and assess effects on gene expression, migration, and growth. Results: Although freshly-isolated HSC and LPC lines expressed PTN and PTPRZ1 mRNAs, neither PTN nor PTPRZ1 protein was find more demonstrated in healthy liver. BDL induced strong expression of PTN mRNA and protein in MF-HSC and dramatically increased PTPRZ1 expression in MF-HSC and ductular-appearing LPCs. In WT mice, BDL triggered a DR characterized by periportal accumulation of collagen, Krt19(+) ductular cells, and aSMA(+) MF derived from desmin (+) HSC. All aspects

of this DR were significantly increased in PTN-KO mice and significantly suppressed in PTPRZ1-KO mice. PTN had no effect on the viability or growth of cultured LPCs or MF-HSC but directly inhibited migration of both cell types. The anti-migratory actions of PTN required PTPRZ1 because PTN inhibited migration in HSC that expressed PTPRZ1, but not PTPRZ1-KO HSC. PTN treatment of PTPRZ1(+) liver cells caused accumulation of several phosphoproteins, including an obligatory component of adherens junctions and a protein that regulates podosome function and integrins. Conclusions: The “stemness” factor, pleiotrophin, and its receptor, PTPRZ1, regulate the ductular reaction to liver injury by controlling the migration of resident cells in putative adult liver progenitor niches. Disclosures: John P. Chute – Board Membership: C2Regenerate Anna Mae Diehl – Consulting: 上海皓元医药股份有限公司 Roche; Grant/Research Support: Gilead, Genfit The following people have nothing to disclose: Gregory A. Michelotti,

Anikia Tucker, Mariana V. Machado, Marzena Swiderska-Syn, Steve S. Choi, Leandi Kruger, Katherine S. Garman, Cynthia A. Moylan, Cynthia D. Guy, Heather Himburg MicroRNAs (miRNAs) are small non-coding RNAs that regulate the course of cholestatic liver diseases. miR-125 is a highly conserved family of miRNAs that regulate cellular proliferation during cholestatic liver injury. These miRNAs also regulate the expression of VEGF that potentiates fibrosis during liver injury. miR-125 targets several growth factors (e.g., VEGF) and matrix metalloproteases (MMPs), a dysregulation of which leads to aberrant proliferation, metastasis and cell invasion. Biliary hyperplasia in bile duct ligated (BDL) rats is accompanied by enhanced angiogenesis and fibrosis.

7 Several studies, including those by Jiao et al, using a rabbit

7 Several studies, including those by Jiao et al., using a rabbit fibrosis model,19 and by Cardoso et al., using isolated perfused cirrhotic rat and human livers,20 have demonstrated that an increase in portal venous blood flow produced by mechanically pumping not only increases portal inflow pressure, but also decreases intrahepatic portal resistance (IHPR)

and dilates sinusoidal spaces in cirrhotic liver, changes that resulted in improving liver function. In liver cirrhosis, portal hypertension is characterized by increased intrahepatic vascular resistance Osimertinib supplier and elevated splanchnic blood flow. Hepatic stellate cells play a crucial role in regulating sinusoidal vascular tone by their contraction. In turn, such contractility is regulated by a counterbalance between vasoactive agents, such as endothelin-1, and vasorelaxing agents, such as nitric oxide (NO). Recent studies have shown that NO production in hepatic sinusoidal endothelial cells is decreased in the cirrhotic

liver, leading to increased intrahepatic resistance.21,22 Generally, the increased shear stress induced by blood flow augments NO production in the vascular endothelium and mediates vasodilatation.23 This decreased IHPR Pifithrin-�� price might result from sinusoidal dilatation by NO overproduction following the augmented portal medchemexpress blood flow.19 One clinical study in 14 cirrhotic patients who underwent B-RTO showed that hepatic blood flow significantly increased 4 weeks after the procedure and was associated with reduced IHPR.18 B-RTO is likely to enhance portal blood flow, and subsequently to reduce IHPR through shear stress-induced vasodilatation, finally leading to improve liver function. Mechanical portal pumping might be a useful therapeutic modality in cirrhotic portal hypertension, but it would be a difficult procedure to apply in the clinical setting. Therefore, we suggest that B-RTO could be a

procedure potentially to enhance portal blood flow with benefits in intrahepatic hemodynamics that are similar to those elicited by mechanical portal pumping. In the present study, the authors demonstrated that patients with an increase in HVPG ≥ 20% showed a significant improvement of liver function 6 months after B-RTO, whereas those with an increase in HVPG < 20% showed no significant change. Shear stress is determined mainly by three factors: vessel radius, flow rate, and viscosity.23 It is calculated from the flow rate, pressure change, and vessel length. If viscosity and vessel length are considered constant in the intrahepatic portal venous system, shear stress in the portal venous system can be estimated as an index calculated from the changes in portal pressure and portal blood flow.

Conclusions— The available

Conclusions.— The available BIBW2992 evidence suggests that naproxen sodium is more effective but may cause more adverse events than placebo in the acute treatment of moderate to severe migraine. It is effective in reducing headache intensity, rendering pain-free at 2 hours

and improving migraine-associated symptoms. However, its effectiveness relative to other active comparators needs to be better defined by appropriate head-to-head clinical trials. “
“To evaluate the geographic location of the United Council for Neurologic Subspecialties (UCNS)-certified headache subspecialists as compared with ratios of expected migraine and chronic migraine populations in the United States. The UCNS is a professional medical organization that accredits fellowship programs and certifies physicians who demonstrate U0126 nmr competence in various neurologic

subspecialties, including headache medicine. There are a limited number of UCNS-certified headache subspecialists currently practicing in the United States. All of the UCNS-certified headache subspecialists were geographically located and compared with demographic data about state populations obtained from the U.S. Census. The expected migraine and chronic migraine populations were calculated for each state based on recently published epidemiologic data. Ratios of UCNS-certified headache subspecialists to expected migraine and chronic migraine populations were compared for each state. These data were then organized by U.S. Census region and division. As

of the 2012 examination cycle, 416 UCNS-certified headache subspecialists are currently practicing in the United States. The states with MCE the highest number of headache subspecialists include New York, California, Ohio, Texas, Florida, and Pennsylvania. Six states have zero headache subspecialists, eight states have one headache subspecialist, and five states have two headache subspecialists. As per the U.S. Census, the total U.S. population for ages 12 years and older is 259,908,563. The total expected migraine population (11.79% of the general population) for ages 12 years and older is 30,594,362. The total expected chronic migraine population (0.91% of the general population) for ages 12 years and older is 2,361,397. The states with the best ratios of headache subspecialists to expected migraine and chronic migraine populations include the District of Columbia, New Hampshire, New York, and Nebraska. Besides states with zero headache subspecialists, the states with the worst ratios of headache subspecialists to expected migraine and chronic migraine populations include Oregon, Mississippi, Arkansas, and Kansas. When organized by U.S. Census regions, the Northeast has the best ratios of headache subspecialists to expected migraine and chronic migraine populations, while the West has the worst ratios of headache subspecialists to expected migraine and chronic migraine populations. In terms of U.S.

Ascaris lumbricoides seropositivity correlated with elevated IgE

Ascaris lumbricoides seropositivity correlated with elevated IgE and anti-inflammatory Th2-IgG1 responses to H. pylori, while Toxoplasma gondii seropositivity was linked to elevated IgE, pro-inflammatory Th1-IgG2, IgG3, and IgG4 responses to H. pylori. These infections may have an impact on inflammatory responses to H. pylori and may partially explain differences in gastric cancer risk in Colombia [19]. Hirsch et al. [20] were able to detect H. pylori DNA by PCR in several plaque and root canal samples, and cultured H. pylori from two root canals, suggesting that root canals of endodontic-infected deciduous teeth may be a reservoir for H. pylori

and serve as a potential source of transmission. Mother-to-child transmission AG-014699 solubility dmso was suspected in 2 of 3 families, and father–child transmission in one family in the study by Osaki et al. [21] using multilocus sequence typing (MLST) of total DNA extracted from fecal specimens. Helicobacter pylori infection is recognized as a cause of gastritis and peptic ulcer disease (PUD) in children. Symptoms, except those related to PUD, are nonspecific. Only a small proportion of children develop symptoms and clinically relevant gastrointestinal disease [22]. Dore et al. [9], in a cross-sectional sero-epidemiologic study,

found that nausea or vomiting and diarrhea were significantly associated with H. pylori infection (OR 2.2 and 2.1, respectively), but not with abdominal pain or heartburn. Perforated ulcer is rare, but several cases Lapatinib of peritonitis secondary to duodenal perforation have been described [23, 24]. Helicobacter pylori infection not only causes damage to the gastric epithelium, it also plays a potential pathogenic role in several extraintestinal diseases. Bradbeer et al. [25] described the resolution of recurrent headaches in a child 上海皓元 after eradication of H. pylori infection and postulated this possible association. Controversy exists concerning the relationship of H. pylori infection and

somatic growth retardation in children. Dehghani et al. [26] evaluated the relationship between H. pylori infection and growth parameters in Indian children and concluded that symptomatic infection does not appear to influence linear growth. The gastrointestinal hormone ghrelin is a gut–brain peptide that regulates food intake in humans and has strong growth hormone-releasing activity. Decreased appetite in H. pylori-infected children has been related to low plasma ghrelin levels which returned to normal after H. pylori eradication. Deng et al. [27] evaluated plasma and gastric ghrelin production as well as body mass index (BMI), before and after treating H. pylori infection in 50 Chinese children, divided into two groups based on the success of H. pylori treatment. They found that plasma and tissue ghrelin levels increased substantially after treatment in the group with therapeutic success, but only minor changes were observed in the group with treatment failure.

3% Likewise

the AUROC of vascular diverging angle for di

3%. Likewise

the AUROC of vascular diverging angle for discriminating advanced liver fibrosis from mild to moderate liver fibrosis was 0.873 with sensitivity of 94.1% and specificity of 75.0%. Conclusions: The present results indicated that Superb Micro-vascular Imaging potentially predicts hepatic fibrosis by detecting fine vessels present in the vicinity of liver surface, even though further investigation is needed in a large number of patients. Disclosures: Takeshi Sato – Employment: Toshiba Medical Systems Corporation The following people have nothing to disclose: Nobuko Koyama, Jiro Hata, Noriaki Manabe, Hiroshi Imamura, Ken Haruma, Keisuke Hino Background: Liver biopsy is the gold standard used to diagnose hepatic fibrosis/steatosis. Transient elastography which is used in some centers is a non-invasive test BMS-777607 price preferred by patients. We investigated the use of a novel technique called shear wave elastography (SWE). Aims:To determine the optimal location for obtaining SWE measurements, compare it with liver biopsy and to investigate the accuracy of grayscale sonography hepatorenal index (HRI) in screening for hepatic steatosis. Methods:100 consecutive patients undergoing percutaneous liver biopsy between Feb 2014 and May 2014 were recruited from the outpatient clinics of Ochsner Medical Center. SWE measurements were obtained in hepatic segments V/VI and VII/

VIII. HRI http://www.selleckchem.com/products/poziotinib-hm781-36b.html was calculated at the midportion of the right kidney. A single liver pathologist determined liver fibrosis (METAVIR) and steatosis. Analysis of Variance (ANOVA) was employed to analyze the degree of fibrosis and SWE measurements and Student’s t-test was used to analyze HRI and degree of steatosis. Results: Patient characteristics: We investigated 57 males and 43 females- (40 OLT recipients). 54 patients had HCV infection, 14 had hepatomegaly alone and 32 had a variety of autoimmune liver diseases. SWE measurements: There was no correlation found between SWE measurements and age, gender, AST/ALT, bilirubin and the presence of steatosis. There was however, a statistically significant difference in the mean SWE seen in patients with a BMI<40 vs BMI>40 (p<0.0001).

OLT patients had similar SWE values to non-OLT patients. There was no statistically significant MCE公司 inter-observer variation (3 technologists). SWE measurements and fibrosis: Segment VII/VIII SWE was able to distinguish normal liver (p< 0.01) and stage 1 fibrosis (0.008) from stage 4 fibrosis. Similar results were seen with segment V/VI SWE. When SWE measurements for both areas were combined, there was a significant difference between stage 1 vs stage 3 (p<0.011), stage 1 vs stage 4 (p< 0.005) and stage 0 vs stage 4 (p< 0.033). HRI measurements: HRI measurements for patients with <5% steatosis vs those with >5% steatosis were different (P<0.0002). Summary: a) SWE can distinguish normal liver/mild fibrosis from cirrhosis in both non-OLT and OLT patents. b) BMI>40 may affect SWE measurements.