Thus, the CoH/ductular unit, with somewhat variable anatomy (Fig. 4A) begins in the periportal parenchymal region as the first twig of the biliary tree, crosses the limiting plate, becoming a somewhat larger interlobular bile duct. The numbers, lengths, and shapes of the CoH/ductule units depend on the source and hence normalcy of the specimens and on the application of immunohistological markers, e.g., keratin 7 (K7), K19, or epithelial cell adhesion molecule (EpCAM).1, 5,6,7 Without

immunostaining, there is an average of 0.4 ductules per portal tract (range 0-4) in normal human liver,8 whereas median values of 2.5-5 ductules per portal tract were observed after application of the K7 immunostain.9,10 Historically, human DRs have been grouped on the basis of morphology buy BGJ398 Bortezomib clinical trial into “typical” and “atypical”, terms originally applied in and based on rodent studies.11 This terminology is discouraged, because a classification of DRs based on a quite limited set of experimental

conditions in rodents cannot readily accommodate the range of patterns seen clinically; DRs are diverse, covering a spectrum of features rather than clear subphenotypes, which will now be described (Fig. 1). DR morphologies may range from well-formed ductules with recognizable lumina to irregular counterparts without obvious lumina, sometimes merely consisting of check details a string of cells. Variable phenotypes between both ends of this spectrum can be present concomitantly in a single specimen, depending on the etiology and evolution of the disease. Even greater complexity emerges when there are concomitant disease processes such as primary sclerosing

cholangitis (PSC) with both obstructive and regenerative DRs.12 Classification schemes suggested by Desmet12 and Turanyi et al.13 have attempted to integrate the histologic features, inciting disease, and/or immunophenotyping of DR, but these have not been subjected to a consensus-building process of review and are not (yet) recommended for DR subclassification. Biliary obstruction produces the most well-known example of DR, featuring a multiplication of small ductules at the periphery of edematous portal stroma. The ductules show variable nuclear size and contain no bile. Obstructive-type DRs may be extraordinarily prominent, seemingly replacing parenchyma with markedly expanded portal tracts, but these can rapidly resolve. When bile concretions are present in dilated ductular lumina (“cholangitis lenta” or ductular cholestasis) a superimposed septicemia should be considered, either from cholangitis or a distant source.

Of 44 cryptogenic Selleckchem Navitoclax cirrhosis patients who underwent liver biopsy, 17 (39%) had NCIPH and 8 had “true cryptogenic cirrhosis.” NCIPH and true cryptogenic cirrhosis patients were 27 (range, 14-59) and 42 (range, 25-67) years old, respectively; 10 and 4 patients, respectively, were males. Hepatic venous pressure gradient measured in 15 NCIPH and 4 true cryptogenic cirrhosis patients was 7 (range, 1-21) and

18 (range, 10-27) mmHg, respectively (P = 0.012). Liver biopsies were performed percutaneously in 4 NCIPH patients and transjugularly in 13. Number of cores in percutaneous biopsies was 3 per patient and 3 (range, 1-6) in transjugular biopsies; length of the largest core was 13 (range,12-15) in percutaneous and 12 mm (range, 6-16) in transjugular biopsies. The number of portal tracts in liver biopsies was 10 (range, 5-20). Liver biopsies showed no significant fibrosis (6 patients), mild portal/periportal fibrosis (10), moderate fibrosis (1), mild perisinusoidal fibrosis (1), abnormal portal venous ectasia (6), and mild diffuse sinusoidal dilatation (8); no patient had cirrhosis or severe fibrosis. In summary, in 2009-2010 and 2005-2007,4

39%-48% of patients with clinical diagnosis of cryptogenic cirrhosis who underwent liver biopsy at our center had NCIPH. Ashish Goel*, Banumathi Ramakrishna†, Kadiyala Madhu*, Uday Zachariah*, Jeyamani Ramachandran*, Shyamkumar N. Keshava‡, Elwyn Elias§, Chundamannil E. Eapen*, * Departments of Hepatology, Christian Medical College, Vellore, India, † Pathology, Christian selleck screening library Medical JQ1 College, Vellore,

India, ‡ Radiology, Christian Medical College, Vellore, India, § Liver Unit, University Hospital Birmingham , Birmingham, United Kingdom. “
“Background and Aim:  The major transporter responsible for bile acid uptake from the intestinal lumen is the apical sodium-dependent bile acid transporter (ASBT, SLC10A2). Analysis of the SLC10A2 gene has identified a variety of sequence variants including coding region single nucleotide polymorphisms (SNPs) that may influence bile acid homeostasis/intestinal function. In this study, we systematically characterized the effect of coding SNPs on SLC10A2 protein expression and bile acid transport activity. Methods:  Single nucleotide polymorphisms in SLC10A2 from genomic DNA of ethnically-defined healthy individuals were identified using a polymerase chain reaction (PCR)-based temperature gradient capillary electrophoresis (TGCE) system. A heterologous gene expression system was used to assess transport activity of SLC10A2 nonsynonymous variants and missense mutations. Total and cell surface protein expression of wild-type and variant ASBT was assessed by Western blot analysis and immunofluorescence confocal microscopy. Expression of ASBT mRNA and protein was also measured in human intestinal samples.

At present, several click here other therapeutic agents are expected to be approved for daily use and we plan to revise these guidelines at appropriate intervals, as new evidence comes to hand. Inhibitors of hepatitis C virus (HCV) NS3-4A protease are classified into 2 groups on the basis of their molecular structures, linear inhibitors with no branches and macrocyclic inhibitors containing macrocycles. Macrocyclic small molecule compounds show superior affinity and selectivity for therapeutic target proteins.[2] Whereas TVR is a first-generation protease inhibitor with linear

structure, SMV is a second-generation protease inhibitor with macrocyclic structure discovered during the optimization process for early protease inhibitors.[3] In vitro resistance testing has yielded different drug resistance profiles, due to their different structures, with cross resistance to SMV seen in TVR resistant mutations at amino acids 155 and 156, whereas mutations at amino acids 36, 54 and 170 were sensitive to SMV, and mutations

at amino acids 80 and 168 resistant to SMV alone.[4] Pharmacokinetic studies have shown that once daily administration of SMV provides effective plasma levels 24 h post-dose.[5] SMV shows inhibitory activity against HCV genotypes 1, 2, 4, 5 and http://www.selleckchem.com/products/azd-1208.html 6, with particularly strong anti-proliferative action against genotypes 1a and 1b. In September 2013, the use of SMV in clinical setting was approved in combination with Peg-IFN + RBV in patients with chronic hepatitis C with genotype 1 and a high viral load (≥5.0 log IU/mL). Phase II trials of SMV + Peg-IFN + RBV combination therapy for genotype 1 chronic hepatitis C include the Japanese DRAGON study (treatment-naïve patients),[6] and the overseas PILLAR study (treatment-naïve patients)[7] and

the ASPIRE trial (relapsers following previous treatment and non-responders to previous treatment).[8] Based on the results of these studies, the SMV dosage was set at 100 mg once daily for clinical phase III studies in Japan, and 150 mg selleck products once daily for overseas studies. Published Japanese clinical phase III studies comprise the CONCERTO-1 (treatment-naïve patients),[9] CONCERTO-2 (non-responders to previous treatment),[10] CONCERTO-3 (relapsers following previous treatment),[10] and CONCERTO-4 (treatment-naïve patients, non-responders, and relapsers) trials.[11] Published overseas clinical phase III studies comprise the QUEST-1 (treatment-naïve patients),[12] QUEST-2 (treatment-naïve patients),[13] and PROMISE (relapsers) studies.[14] The subjects for the Japanese clinical trials were patients with chronic hepatitis C (excluding cirrhosis) with genotype 1 and a high viral load (≥5.0 log IU/mL), aged 20–70 years (Table 1).

Instances of near vertical lunges gave us the unique opportunity to use the signal from the accelerometer to

obtain a fine scale record of the body accelerations involved in lunging. We found that lunges contain extreme accelerations reaching 2.5 m/s2 in certain instances, which are then followed by decelerations. When animals are intensively feeding the inter-lunge interval is similar for both deep and shallow lunges suggesting a biomechanical constraint on lunges. However, the number of lunges per dive varies from one for shallow feeding (<25 m) to a median of six for deeper dives. Different feeding GDC-0449 order patterns were evident in the kinematic record, for deep and shallow feeding bouts with the much greater mean turn rates occurring in shallow feeding. “
“Reduced reproductive success has contributed to lack of recovery of the endangered western North Atlantic right whale (Eubalaena glacialis). Here we examined the specific life history period from just before birth through the first year to estimate calf and perinatal losses between 1989 and 2003. The lower Selleck Belnacasan bound estimate (17 mortalities from 208 calving events) included documented calf mortalities and presumed deaths from serious injury

or disappearance from the sighting record. The upper bound estimated potential calf losses from females with delayed first parturition (>10 yr) and shortened (2 yr) or lengthened (≥4 yr) calving intervals, if the female migrated to the calving ground during these intervals. Because cows were sighted in the calving ground predominantly in years when they

were available to calve, adult females sighted there in a possible calving year without a calf were assumed to have experienced a perinatal loss. Twenty-eight potential perinatal losses were detected, bringing the upper bound of calf and perinatal mortality to 45 (3.0 calves/yr). The high frequency of lengthened calving intervals in E. glacialis suggests that abortion and neonatal losses are contributing to lower reproductive success compared to Southern Hemisphere right whales (Eubalaena australis). “
“We investigated selleck screening library the characteristics and composition of 4,506 humpback whale pods observed in Hervey Bay between 1992 and 2005. We use these data to analyze and model the variability of pod size and composition, and to assess the importance of Hervey Bay for particular classes of humpback whales. Pods ranged in size from one to nine individuals. Pairs were the most frequent pod type (1,344, 29.8%), followed by mother-calf alone (1,249, 27.7%), trios (759, 16.8%), singletons (717, 15.9%), and 4+ whales (437, 9.7%). Of the 4,506 pods, calves were present in 40%, and 10.8% of all pods had one or more escorts present. Of the 1,804 pods observed with calves present, 1,251 (69.4%) were mothers alone with their calves. The size and composition of pods in the study area varied significantly as the season progressed.

TFA intake is positively associated with markers (IL-6 and C-reactive protein [CRP]) of systemic inflammation in women with higher body mass index.[32] Lopez-Garcia et al. reported that a high-TFA diet induces

production of proinflammatory cytokines and a marker for inflammation (IL-6 and CRP) without overt inflammation, even in healthy subjects.[33] In a randomized, controlled trial in 50 healthy men, consumption of 8%E TFAs for increased plasma levels of IL-6 and CRP compared with consumption of equivalent amounts of oleic acid (cis-form).[34] It has been presumed that TFAs influence the function of multiple cell types, including immune cells acting as cause of inflammation.[3] Han et al. showed that the production of IL-6 and tumor necrosis factor (TNF)-α was higher in lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells isolated from human subjects who consumed check details a stick margarine diet containing 6.7% TFA (% energy) compared with those isolated from

subjects who consumed a soya bean oil diet containing 0.7% TFA.[35] Our preliminary examination showed that LPS-induced this website increase in IL-1β, IL-6, IL-23p19, and TNF-α in a macrophage cell line 1-(RAW264.7 cells) was significantly enhanced by TFAs (elaidic acid) exposure compared with oleic acid (cis-form of eladic acid) exposure in vitro (presented at DDW, May 2010, New Orleans). These findings suggest that TFAs may

promote inflammation mainly by an action on immune cells such as macrophages, leading to increased production of inflammatory cytokines. On the other hand, Zapolska-Downar et al. reported that TFAs can induce apoptosis of human umbilical vein endothelial cells in vitro.[36] Their findings suggest that TFAs may elicit inflammation not only by the action on immune cells but also may play a role in damaging and death of vascular endothelial cells because of apoptosis, leading to a microcirculatory disturbances in the tissue. Further determination of possible precipitating effect of TFAs on intestinal inflammation in terms of find more different responses among in various cell types in the intestinal tissue is necessary. These findings raise the possibility that TFA intake is a risk factor to exacerbate the symptoms of gut inflammation in addition to a risk factor for CHD, diabetes mellitus, and increasing of LDL in healthy subject. Thus, patients with gut inflammation, such as IBD, should avoid the biased lipid dairy diet as possible as they can and note the proportion of TFAs in their daily meal. “
“Aim:  To assess the regression of liver fibrosis after interferon (IFN) treatment in patients with chronic hepatitis C, liver stiffness (LS) was measured repeatedly and the factors associated with reduction of LS were assessed.

TFA intake is positively associated with markers (IL-6 and C-reactive protein [CRP]) of systemic inflammation in women with higher body mass index.[32] Lopez-Garcia et al. reported that a high-TFA diet induces

production of proinflammatory cytokines and a marker for inflammation (IL-6 and CRP) without overt inflammation, even in healthy subjects.[33] In a randomized, controlled trial in 50 healthy men, consumption of 8%E TFAs for increased plasma levels of IL-6 and CRP compared with consumption of equivalent amounts of oleic acid (cis-form).[34] It has been presumed that TFAs influence the function of multiple cell types, including immune cells acting as cause of inflammation.[3] Han et al. showed that the production of IL-6 and tumor necrosis factor (TNF)-α was higher in lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells isolated from human subjects who consumed AZD1208 a stick margarine diet containing 6.7% TFA (% energy) compared with those isolated from

subjects who consumed a soya bean oil diet containing 0.7% TFA.[35] Our preliminary examination showed that LPS-induced BMN 673 in vitro increase in IL-1β, IL-6, IL-23p19, and TNF-α in a macrophage cell line 1-(RAW264.7 cells) was significantly enhanced by TFAs (elaidic acid) exposure compared with oleic acid (cis-form of eladic acid) exposure in vitro (presented at DDW, May 2010, New Orleans). These findings suggest that TFAs may

promote inflammation mainly by an action on immune cells such as macrophages, leading to increased production of inflammatory cytokines. On the other hand, Zapolska-Downar et al. reported that TFAs can induce apoptosis of human umbilical vein endothelial cells in vitro.[36] Their findings suggest that TFAs may elicit inflammation not only by the action on immune cells but also may play a role in damaging and death of vascular endothelial cells because of apoptosis, leading to a microcirculatory disturbances in the tissue. Further determination of possible precipitating effect of TFAs on intestinal inflammation in terms of click here different responses among in various cell types in the intestinal tissue is necessary. These findings raise the possibility that TFA intake is a risk factor to exacerbate the symptoms of gut inflammation in addition to a risk factor for CHD, diabetes mellitus, and increasing of LDL in healthy subject. Thus, patients with gut inflammation, such as IBD, should avoid the biased lipid dairy diet as possible as they can and note the proportion of TFAs in their daily meal. “
“Aim:  To assess the regression of liver fibrosis after interferon (IFN) treatment in patients with chronic hepatitis C, liver stiffness (LS) was measured repeatedly and the factors associated with reduction of LS were assessed.

This new

subdomain structure was used for IRT-based scoring. Unlike traditional CLDQ scores, IRT-based scores closely approximated a normal distribution. With traditional CLDQ scoring, LD severity significantly influenced both general QOL scores and subdomain scores (ANOVA p<0.05). While LD severity significantly influenced IRT-based general QOL scores it did not significantly influence IRT-based subdo-mains www.selleckchem.com/products/dabrafenib-gsk2118436.html scores. Traditional subdomain scores correlated highly with general QOL scores (r>0.7), while IRT-based subdomain scores did not. When the effect of general QOL on traditional subdomain scores was accounted for, the influence of non-LD-related factors on traditional subdomain scores was greatly reduced. Interestingly, when the effect of general QOL was accounted for, the influence of LD severity on traditional subdo-main scores was no longer significant. CONCLUSIONS: The strong influence of general QOL on “LD-specific” subdomain scores from the CLDQ renders them susceptible to the influence of non-liver disease-related factors and causes their clinical significance to be overestimated. This study questions the clinical utility of CLDQ subdomain

scores. Disclosures: this website Robert Gibbons – Stock Shareholder: Psychiatric Assessments Inc. The following people have nothing to disclose: Sujit V. Janardhan, Andrew Aron-sohn, Jason Morris, David G. Beiser Background: Of the 3 million Americans chronically infected with Hepatitis C virus (HCV), it is estimated that only 25-50% are aware of their diagnosis. In August 2012, the CDC released recommendations for one-time HCV testing in persons born between 1945-1965 to improve screening in individuals at highest risk for chronic HCV infection. Aims: This study aims to assess the rate of HCV screening, follow-up testing, and linkage to care in an academic

primary care practice, selleckchem before and after the CDC birth cohort guidelines. Methods: All patients born 1945-1965 and seen in the primary care clinic at the University of Chicago from July 1st, 2010 to May 15th, 2013 were included in the study. Key demographics, results of HCV-related laboratory testing, and completion of hepatology follow-up were obtained from the electronic medical record database. All patients seen from July 2012 to May 2013 were identified as the post-guideline group. MedCalc software (medcalc.org) was used for statistical analysis as appropriate. Results: A total of 24,947 patients in the eligible birth cohort were identified; 16,811 and 8,066 fell in the pre- and post-guideline groups, respectively. Only one third of patients in the birth-cohort had screening by HCV antibody testing and this rate continued to be low in the post-guideline group (Table 1). For patients screening positive, rates of confirmatory testing with viral load, genotype analysis and referral to hepatology were high in both the pre- and post-guideline group (Table 1).

7-10 Genome-wide

find more association studies have demonstrated that genetic variations in the region near the interleukin-28B (IL28B) gene, which encodes interferon-λ3 (IFN-λ3), are associated with chronic HCV treatment response.11-14 In one candidate gene study15 and one genome-wide association study,14 it was demonstrated that genetic variations in the IL28B gene region are also associated with absence of HCV RNA in anti-HCV antibody–positive individuals (presumed spontaneous HCV clearance). However, studies performed to date are limited to chronic infection, lack longitudinal data to enable an examination of the effects of genetic variations in the IL28B gene region on the time to spontaneous HCV clearance, and are cross-sectional Midostaurin mouse in nature. We investigated the effect of genetic variations in the IL28B gene region on time to spontaneous HCV clearance and treatment-response following recent HCV infection in the Australian Trial in Acute Hepatitis C (ATAHC), a prospective trial of the natural history and

treatment of recently acquired HCV infection. AHR, adjusted hazards ratio; ALT, alanine aminotransferase; ATAHC, Australian Trial in Acute Hepatitis C; CI, confidence interval; HCV, hepatitis C virus; HIV, human immunodeficiency virus; IFN-λ3, interferon-λ3; IL-28B interleukin-28B; PEG-IFN, pegylated interferon-α2a; RVR, rapid virological response; SNP, single-nucleotide polymorphism; SVR, sustained virological response. The ATAHC study was a multicenter, prospective cohort click here study of the natural history and treatment of recent HCV infection, as previously described.3 Recruitment of HIV-infected and HIV-uninfected participants was from June 2004 through November 2007. Recent infection with either acute or early chronic HCV infection with the following eligibility

criteria: First positive anti-HCV antibody within 6 months of enrollment; and either: 1 Acute clinical hepatitis C infection, defined as symptomatic seroconversion illness or alanine aminotransferase (ALT) level greater than 10 times the upper limit of normal (>400 IU/mL) with exclusion of other causes of acute hepatitis, at most 12 months before the initial positive anti-HCV antibody; or All participants with detectable HCV RNA during the screening period (maximum 12 weeks) were assessed for HCV treatment eligibility. Participants unwilling to undergo treatment assessment and those with undetectable HCV RNA at screening continued to be followed. From screening, participants were followed for up to 12 weeks to allow for spontaneous HCV clearance and if HCV RNA remained detectable were offered treatment. Participants were then seen at baseline and 12 weekly intervals for up to 144 weeks (individuals receiving HCV treatment were also seen at 4-weekly intervals up to week 12). All study participants provided written informed consent.

5 day, 1.5%); (B) selleck chemicals the late postmoult (1.5 days, 4.5%); (C) the intermoult (13 days, 44%); (D) the premoult (15 days, 50%), which is subdivided in four periods based on the genesis of the dactylian

claw and the setae of the propodite; and finally (E) the exuviation. The relative durations of stages match those observed for crustaceans with short moulting cycles. The main features of the different stages are described below (Fig. 2). The early postmoult period (A) is 12 h long. The cuticle is thin, soft and sticky (Fig. 2a) because the exuvial fluid persists at the cuticular surface. The epidermis is tight to the new cuticle. The animal has little colour. In the late postmoult period (B; Fig. 2b), the new exoskeleton

is forming and the cuticle begins to harden, essentially by calcification. The intermoult stage is almost half the moulting cycle (Fig. 2c). The integument thickens (lower arrows Fig. 2a–d) and acquires definitive characteristics (colour, thickness, rigidity). In gammarids (and other crustacean species with weak skeleton calcification), no specific criterion defines the boundary between B and C. This boundary depends on the valuation of the progressive thickening of cuticle. Here, we arbitrarily subdivided the stage C in early and late intermoult to account for the thickness www.selleckchem.com/products/PLX-4720.html and the hardening (concomitant processes) of the tegument. The premoult is characterized by the apolysis, that is, the progressive

separation of the epidermis from the old cuticle, simultaneously with the beginning of the secretion of the new skeleton. Premoult can be subdivided in four phases. In the first stage in early premoult D0, the claw epidermis begins to separate from the cuticle, gradually from the distal end of the dactylian claw (upper arrows, Fig. 2d) to the more proximal regions of the propodite. Simultaneously, the setae epidermis withdraws from the old skeleton. Tissue retraction continues in the D1 stage (intermediate premoult) and is now visible in the propodite region. This stage is mainly characterized by the genesis of selleck screening library new setae. Invaginations appear around the matrix of the claw (left arrows, Fig. 2e) and setae. The secretion of the cuticle of the new claw continues; its cuticle becomes thicker and begins to refract, this refractiveness being accentuated at the end of the D1 stage (Fig. 2f). At the end of D1 and during the D2 stage (late premoult), the retraction of the new cuticle is maximal (Fig. 2g) and the thickness of the newly synthesized cuticle increases. This is particularly well visible at the level of the dactylopodite; here, the cuticle is around 1/5 thickness of the old one at the end of the stage. The setae are clearly formed (arrows, Fig. 2g). At the latter premoult stage (D3), which is about 2 days, the main part of the new skeleton is synthesized (Fig. 2h) and the animal prepares to exuviate.

Importantly, presence of PVT is a strong predictor for developing acute liver decompensation following radioembolization. Unlike previous studies, prior systemic chemotherapy did not predispose to the development of liver decompensation. Disclosures: Coleman Smith – Advisory Committees or Review Panels: Vertex, Gilead, Janssen; Grant/Research Support: Gilead, Abbvie, Janssen, Salix, BMS, Merck, Intercept Pharma, Lumena Pharma;

Speaking and Teaching: Merck, Vetex, Gilead, Bayer/ Onyx, BMS, Abbvie, Janssen The following people have nothing to disclose: Michael Min, Totianna Prudhomme, Eduardo Ehrenwald, Jill May, Kai Hanson, Andrew J. Henn, Joseph Leach Objectives: Human hepatocyte (HC) transplantation has promise as a bridge to organ transplantation or spontaneous recovery in acute liver failure (ALF).

The survival and function of transplanted hepatocytes is limited however. Mesenchymal stromal cells 3-MA solubility dmso (MSC) have been shown to enhance the survival and function of co-cultured HC in addition to having additional anti-inflammatory/anti-apoptotic properties. The mechanism of this is unknown. The aim of this study was to investigate this mechanism by examining cytokine and growth factor production in vitro using human cells and serum to mimic in vivo conditions. Methods: Human HCs were isolated from donor organs and MSC from umbilical cord. Cells were plated in monoculture U0126 ic50 or co-culture at a ratio of 6:1 (HC:MSC). After 24 hr, serum from patients with ALF, normal control or fetal calf serum (FCS) was added and then removed 24 hours later, cells were washed and standard culture medium added. Cytotoxicity (MTT/SRB), specific

hepatocyte death and albumin production were measured 24 and 48 hours following medium change. Thirteen cytokines/growth factors were measured in medium using a multiplex array (Biochip Array, Randox, UK). Results: At both time points, MSC monoculture had higher cytotoxicity following exposure click here to ALF serum versus control (>50% reduction in MTT activity/cell attachment, p<0.001). HC monoculture maintained MTT activity and cell survival and also increased albumin production in ALF serum versus FCS medium (482 v 54 ng/24hr/well). Co-cultured HC and MSC demonstrated improved MTT activity in ALF serum compared to HC or MSC monoculture (p<0.05). IL6, IL8 and Monocyte Chemoattractant Protein 1 (MCP1) were secreted by MSC but not HC monoculture and there was a significant increase in production in co-culture following culture in ALF serum (p<0.05): MCP1 production in co-culture was increased 8x (mean 234 v 25ng/l) and IL8 production 14x (219 v 14ng/l) following culture with ALF serum versus control. Hepatocyte Growth Factor (HGF) secretion was detected in MSC and HC monoculture in all 3 conditions but was highest following co-culture in ALF serum. IL1Receptor antagonist (IL1Ra) was also increased in all 3 co-culture conditions versus HC monoculture (p<0.05).