Patients received UDCA at a dose of 28 to 30 mg/kg/day (Axcan Pharma, Mont-St. Hiliare, Canada) in divided doses given with meals or an identical placebo. Serum samples were obtained at entry into the study and at the end of treatment. All available paired samples were retrieved and used for analysis of the bile acid composition. Disease progression to cirrhosis, development of varices, cholangiocarcinoma, liver transplantation, and death during the trial were considered clinical endpoints. Serum bile acids were analyzed qualitatively by conventional gas chromatography-mass

spectrometry (GCMS) and quantitatively by isotope-dilution GCMS, as described previously, with the following modification: alkaline hydrolysis with 2 M sodium hydroxide in 90% (vol/vol) ethanol selleck chemicals (1 hour at

67°C) was performed instead of enzymatic hydrolysis with cholylglycine hydrolase.14 Deuterium-labeled LCA, deoxycholic acid (DCA), chenodeoxycholic acid (CDCA), cholic acid (CA), and UDCA as internal standards were obtained from CDN Isotopes (Pointe-Claire, Canada). Baseline characteristics were calculated as medians and ranges for continuous variables. The number and percent in each group were tabulated for categorical variables. Bile acid concentrations were calculated as means and standard deviations. The chi-square test of independence was used to determine selleck compound statistical significance for categorical data. For the continuous variables, the Wilcoxon rank sum test was used. Baseline characteristics with

a significance of P ≤ 0.2 were entered into a multivariate model of multiple linear regression analysis to explore possible correlations per bile acid. From 2001 to 2005, 150 patients with PSC were entered into the study. Serum for bile acid analysis was available at the baseline and at the end of the study (mean treatment duration DOK2 = 2.38 ± 0.56 years) for 56 of these patients. The baseline characteristics of this subset of patients versus the remaining patients (n = 94) are shown in Table 1. Patients analyzed for their bile acid composition were younger (41.8 versus 49.3 years), were more likely to have concomitant inflammatory bowel disease (93% versus 68%), and had a lower Mayo risk score (0.015 versus 0.58). The baseline characteristics of this cohort of patients by treatment were comparable as well (Table 2). At the baseline, the bile acid pool consisted of CA (32%), LCA (13%), DCA (21%), UDCA (11%), and CDCA (23%). GCMS spectra indicating the prevalence of significant amounts (>0.05 μmol/L) of uncommon bile acids were not observed. Only traces of hydroxylation products of UDCA were occasionally seen.15 The GCMS systems that were used did not separate UDCA from isoUDCA. Patients who had undergone colectomy (n = 12) had significantly lower levels of DCA (P < 0.

Patients received UDCA at a dose of 28 to 30 mg/kg/day (Axcan Pharma, Mont-St. Hiliare, Canada) in divided doses given with meals or an identical placebo. Serum samples were obtained at entry into the study and at the end of treatment. All available paired samples were retrieved and used for analysis of the bile acid composition. Disease progression to cirrhosis, development of varices, cholangiocarcinoma, liver transplantation, and death during the trial were considered clinical endpoints. Serum bile acids were analyzed qualitatively by conventional gas chromatography-mass

spectrometry (GCMS) and quantitatively by isotope-dilution GCMS, as described previously, with the following modification: alkaline hydrolysis with 2 M sodium hydroxide in 90% (vol/vol) ethanol LY2835219 (1 hour at

67°C) was performed instead of enzymatic hydrolysis with cholylglycine hydrolase.14 Deuterium-labeled LCA, deoxycholic acid (DCA), chenodeoxycholic acid (CDCA), cholic acid (CA), and UDCA as internal standards were obtained from CDN Isotopes (Pointe-Claire, Canada). Baseline characteristics were calculated as medians and ranges for continuous variables. The number and percent in each group were tabulated for categorical variables. Bile acid concentrations were calculated as means and standard deviations. The chi-square test of independence was used to determine Pifithrin-�� statistical significance for categorical data. For the continuous variables, the Wilcoxon rank sum test was used. Baseline characteristics with

a significance of P ≤ 0.2 were entered into a multivariate model of multiple linear regression analysis to explore possible correlations per bile acid. From 2001 to 2005, 150 patients with PSC were entered into the study. Serum for bile acid analysis was available at the baseline and at the end of the study (mean treatment duration Dimethyl sulfoxide = 2.38 ± 0.56 years) for 56 of these patients. The baseline characteristics of this subset of patients versus the remaining patients (n = 94) are shown in Table 1. Patients analyzed for their bile acid composition were younger (41.8 versus 49.3 years), were more likely to have concomitant inflammatory bowel disease (93% versus 68%), and had a lower Mayo risk score (0.015 versus 0.58). The baseline characteristics of this cohort of patients by treatment were comparable as well (Table 2). At the baseline, the bile acid pool consisted of CA (32%), LCA (13%), DCA (21%), UDCA (11%), and CDCA (23%). GCMS spectra indicating the prevalence of significant amounts (>0.05 μmol/L) of uncommon bile acids were not observed. Only traces of hydroxylation products of UDCA were occasionally seen.15 The GCMS systems that were used did not separate UDCA from isoUDCA. Patients who had undergone colectomy (n = 12) had significantly lower levels of DCA (P < 0.

13 In this open-label, randomized, controlled trial of 125 patients, randomly assigned to either lactulose or non-lactulose treatment, 20% (12/61) and 47% (30/64) developed overt hepatic encephalopathy, respectively (P = 0.001).13 In this study, non-response to lactulose was reported in

patients with hyponatremia and very high venous ammonia levels.13 The study by Sharma et al. in this issue of the Journal of Gastroenterology and Mitomycin C solubility dmso Hepatology14 examined the effectiveness of lactulose in the prevention of hepatic encephalopathy following an acute variceal bleed. The study involved the randomization of 70 patients to either 30 mL lactulose three to four times per day (ultimately to ensure 2–3 semiformed stools per day) or non-lactulose. Inclusion criteria included admission within 24 h of gastrointestinal bleed, no history of lactulose intake in the preceding 6 weeks, and no significant distracting comorbidity.14 The inclusion of patients with a prior history of encephalopathy rendered it

as neither a primary nor secondary prophylaxis study. Bleeding was assessed and managed in accordance with Baveno IV guidelines, and hepatic encephalopathy was assessed as per West Haven criteria by two independent assessors. Approximately one-sixth of patients in each group received terlipressin instead of somatostatin as a vasoactive drug. Nineteen patients developed clinically-overt hepatic encephalopathy; 14% (5/35) in the lactulose group and 40% (14/35) in the non-lactulose group (P = 0.03), giving selleckchem a relative risk reduction of

66%.14 The resultant increase in length of hospital stay of those who developed encephalopathy was also significant (11 ± 2.2 vs 7 ± 1.8 days, P = 0.001).14 Those in the control group were treated with lactulose therapy once hepatic encephalopathy did develop. Confounding precipitants of hepatic encephalopathy are difficult to separate, although there were no significant SPTLC1 biochemical differences between the two groups. Alternative therapies for hepatic encephalopathy include antibiotics, such as neomycin, that reduce ammonia-producing bacteria. These have been used in the long-term treatment of hepatic encephalopathy.4 However, more recently, they have lost favor secondary to their side-effect profiles. Rifaximin is a semisynthetic rifamycin-based antibiotic with gut-specific action as a result of its poor solubility and absorption.15 The negligible plasma levels of rifaximin bode well for avoiding potential drug resistance.15 Solid evidence for the use of rifaximin in the treatment of hepatic encephalopathy is largely a consequence of the randomized, controlled trial conducted by Bass et al.16 In that study, rifaximin was compared to placebo in patients in remission from recurrent hepatic encephalopathy, with breakthrough episodes reported in 22% (31/140) of patients in the rifaximin group and 46% (73/159) in the placebo group (P < 0.001).

13 In this open-label, randomized, controlled trial of 125 patients, randomly assigned to either lactulose or non-lactulose treatment, 20% (12/61) and 47% (30/64) developed overt hepatic encephalopathy, respectively (P = 0.001).13 In this study, non-response to lactulose was reported in

patients with hyponatremia and very high venous ammonia levels.13 The study by Sharma et al. in this issue of the Journal of Gastroenterology and find more Hepatology14 examined the effectiveness of lactulose in the prevention of hepatic encephalopathy following an acute variceal bleed. The study involved the randomization of 70 patients to either 30 mL lactulose three to four times per day (ultimately to ensure 2–3 semiformed stools per day) or non-lactulose. Inclusion criteria included admission within 24 h of gastrointestinal bleed, no history of lactulose intake in the preceding 6 weeks, and no significant distracting comorbidity.14 The inclusion of patients with a prior history of encephalopathy rendered it

as neither a primary nor secondary prophylaxis study. Bleeding was assessed and managed in accordance with Baveno IV guidelines, and hepatic encephalopathy was assessed as per West Haven criteria by two independent assessors. Approximately one-sixth of patients in each group received terlipressin instead of somatostatin as a vasoactive drug. Nineteen patients developed clinically-overt hepatic encephalopathy; 14% (5/35) in the lactulose group and 40% (14/35) in the non-lactulose group (P = 0.03), giving Selleck Ulixertinib a relative risk reduction of

66%.14 The resultant increase in length of hospital stay of those who developed encephalopathy was also significant (11 ± 2.2 vs 7 ± 1.8 days, P = 0.001).14 Those in the control group were treated with lactulose therapy once hepatic encephalopathy did develop. Confounding precipitants of hepatic encephalopathy are difficult to separate, although there were no significant Meloxicam biochemical differences between the two groups. Alternative therapies for hepatic encephalopathy include antibiotics, such as neomycin, that reduce ammonia-producing bacteria. These have been used in the long-term treatment of hepatic encephalopathy.4 However, more recently, they have lost favor secondary to their side-effect profiles. Rifaximin is a semisynthetic rifamycin-based antibiotic with gut-specific action as a result of its poor solubility and absorption.15 The negligible plasma levels of rifaximin bode well for avoiding potential drug resistance.15 Solid evidence for the use of rifaximin in the treatment of hepatic encephalopathy is largely a consequence of the randomized, controlled trial conducted by Bass et al.16 In that study, rifaximin was compared to placebo in patients in remission from recurrent hepatic encephalopathy, with breakthrough episodes reported in 22% (31/140) of patients in the rifaximin group and 46% (73/159) in the placebo group (P < 0.001).

However, the potential benefits of erythropoietin must be weighed against its potential side effects, the fact that its use in HCV therapy is

not approved by the FDA, and its considerable cost. If a PI treatment–limiting adverse event occurs, PegIFN and RBV can be continued provided SCH727965 chemical structure that an on-treatment response had occurred. There are no data to help guide substitution of one for the other HCV PI. If a patient has a serious adverse reaction related to PegIFN and/or RBV, the PegIFN and/or RBV dose should be reduced or discontinued. If either PegIFN and/or RBV are discontinued, the HCV PI should be stopped. Additional information on management of other adverse events can be found in the package insert. Because patients with CHC frequently receive medications in addition to those used to treat HCV infection, and because the PIs can inhibit hepatic drug-metabolizing enzymes such as cytochrome P450 2C (CYP2C), CYP3A4, or CYP1A, both BOC and TVR were studied for potential interactions with a number of drugs likely to be coadministered. These included statins, immune suppressants, drugs used to treat HIV coinfection, opportunistic infections, mood disorders, click here and drug addiction support medications. Both BOC and TVR, were noted to cause interactions with several of the drugs examined, either increasing

or decreasing pharmacokinetic parameters. It is particularly important, therefore, that the medical provider review this information as listed in the package insert for each of the drugs before starting treatment for CHC. This information Cepharanthine can be obtained at the FDA Web site: www.accessdata.fda. gov/scripts/cder/drugsatfda/index.cfm. Other helpful sites are: http//:222.drug-interactions.com and www. hep-druginteractions.org Emergence of antiviral-resistant variants during PI-based therapy has been observed during all trials and is associated with virological failure and relapse (Tables 2 and 3). Mutations that confer either high or low level resistance to BOC and TVR cluster around the catalytic site of the NS3/4A serine protease. Similar

variants were detected in both BOC and TVR-treated subjects, suggesting that some degree of cross-resistance exists between the two PIs. In both phase 3 studies, sequence analysis of the NS3/4A region was performed in all subjects at baseline and for all subjects who failed to achieve an SVR. Antiviral resistant variants were detected in a small proportion of patients at baseline, 7% in the BOC studies and 5% in the TVR trials, but did not appear to impact response to either PI.25, 26 Therefore, there is currently no clinical indication for baseline resistance testing. Among treatment-naïve patients receiving a BOC regimen, antiviral resistant variants developing during treatment were observed overall in 16% of patients (Table 2).

In fact, serum BA levels in 8-week CBDL mice were 20-fold higher in WT mice (2,851 ± 1,097 μmol/L), compared to 8-week CBDL FXR−/− mice (110 ± 21 μmol/L), and kidney fibrosis in long-term

CBDL FXR−/− mice was indeed ameliorated, as demonstrated by Sirius Red staining and significantly lower renal hydroxyproline levels (Fig. 8B). To additionally rule out a general resistance of FXR−/− mice to renal fibrosis, we compared the degree of renal fibrosis in response to unilateral ureter ligation (UUL; as a noncholestatic condition). Selleckchem Epigenetics Compound Library Notably, we found no differences in fibrotic response after UUL in FXR−/− mice, compared to WT mice (Fig. 8C). Collectively, these findings indicate that FXR−/− mice are protected from long-term, but not early, CBDL-induced tubular epithelial injury, which can be explained by declining and less hydrophobic serum BA levels in FXR−/− mice (but not WT) over time. Next, we hypothesized AZD1208 chemical structure that prefeeding hydrophilic norUDCA 7 days before CBDL could protect against tubular epithelial injury,

because norUDCA represents the main BA in serum and urine after feeding and undergoes substantial renal elimination.[29] Indeed, norUDCA prefeeding was able to prevent tubular epithelial injury in 3-day CBDL mice, as demonstrated by PAS- and AQP2-stained kidney sections (Supporting Fig. 5). To substantiate our

concept with human pathological findings, we screened our pathological archives for patients with cholestatic liver disease and cholemic nephropathy in whom both tissues were available Quinapyramine for examination. Kidney histology frequently showed tubular casts, interstitial nephritis, and renal fibrosis as well as characteristic collecting duct lesions (Supporting Fig. 6). Renal tubular injury is a major, perhaps underestimated, and still poorly understood cause of renal dysfunction in advanced liver diseases.[3, 4, 30] We hypothesized that cholestatic liver dysfunction with systemic accumulation of potentially toxic BAs, together with their exaggerated compensatory urinary elimination, may contribute to AKI in such patients. Therefore, we established and characterized a mouse model of progressive cholestatic liver disease associated with tubulointerstitial nephritis and renal fibrosis and impaired renal function, which offers novel perspectives to study the mechanisms and novel treatment strategies for cholemic nephropathy.[9] Experimental studies from the 1940s and 1950s frequently used dogs and indeed showed structural renal alterations including interstitial nephritis and renal fibrosis in cholestasis.

In fact, serum BA levels in 8-week CBDL mice were 20-fold higher in WT mice (2,851 ± 1,097 μmol/L), compared to 8-week CBDL FXR−/− mice (110 ± 21 μmol/L), and kidney fibrosis in long-term

CBDL FXR−/− mice was indeed ameliorated, as demonstrated by Sirius Red staining and significantly lower renal hydroxyproline levels (Fig. 8B). To additionally rule out a general resistance of FXR−/− mice to renal fibrosis, we compared the degree of renal fibrosis in response to unilateral ureter ligation (UUL; as a noncholestatic condition). click here Notably, we found no differences in fibrotic response after UUL in FXR−/− mice, compared to WT mice (Fig. 8C). Collectively, these findings indicate that FXR−/− mice are protected from long-term, but not early, CBDL-induced tubular epithelial injury, which can be explained by declining and less hydrophobic serum BA levels in FXR−/− mice (but not WT) over time. Next, we hypothesized Selleck GDC941 that prefeeding hydrophilic norUDCA 7 days before CBDL could protect against tubular epithelial injury,

because norUDCA represents the main BA in serum and urine after feeding and undergoes substantial renal elimination.[29] Indeed, norUDCA prefeeding was able to prevent tubular epithelial injury in 3-day CBDL mice, as demonstrated by PAS- and AQP2-stained kidney sections (Supporting Fig. 5). To substantiate our

concept with human pathological findings, we screened our pathological archives for patients with cholestatic liver disease and cholemic nephropathy in whom both tissues were available Cobimetinib in vivo for examination. Kidney histology frequently showed tubular casts, interstitial nephritis, and renal fibrosis as well as characteristic collecting duct lesions (Supporting Fig. 6). Renal tubular injury is a major, perhaps underestimated, and still poorly understood cause of renal dysfunction in advanced liver diseases.[3, 4, 30] We hypothesized that cholestatic liver dysfunction with systemic accumulation of potentially toxic BAs, together with their exaggerated compensatory urinary elimination, may contribute to AKI in such patients. Therefore, we established and characterized a mouse model of progressive cholestatic liver disease associated with tubulointerstitial nephritis and renal fibrosis and impaired renal function, which offers novel perspectives to study the mechanisms and novel treatment strategies for cholemic nephropathy.[9] Experimental studies from the 1940s and 1950s frequently used dogs and indeed showed structural renal alterations including interstitial nephritis and renal fibrosis in cholestasis.

2b). The transiently transfected cells indeed responded to treatment with 15 μM PEITC involving a disintegration of the microtubular filaments over a 25–35-min period followed by the formation Ixazomib ic50 of apoptotic blebs surrounding the cells (Fig. 2b,c). Cells treated with vehicle control were observed for up to 1 h without any apparent changes in the microtubular network or formation of apoptotic blebs (Fig. 2d), which suggests that treatment of Kato-III cells with PEITC leads to deformation of microtubular filaments to presumably contribute to a shift in the cell cycle distribution and ultimately induction of apoptosis. As MKN74 cells responded differently to PEITC treatments compared

with Kato-III cells

when assayed for the effects on proliferation, cell cycle distribution, and appeared to form less apoptotic blebs, these cells were further investigated in order to elucidate if these cells in fact became significantly apoptotic by PEITC treatments. Subjecting MKN74 cells treated with PEITC for 48 h to a flow cytometry-based apoptosis assay kit resulted in an increase in the relative number of apoptotic cells from 10% in the vehicle control treated culture to 13% and 16% in the cultures treated with 5 and 15 μM, respectively (Fig. 3a). Y-27632 in vitro The weak response in apoptotic cells coincided with the findings when PEITC-treated MKN74 cells were analyzed for caspase-3 activity (Fig. 3b). Cells were treated with 5–15 μM PEITC for 48 h before harvested and analyzed for caspase-3 activity which revealed a weak dose-dependent effect of PEITC on caspase-3 activity in MKN74 cells. Further, we investigated the effect of PEITC on the GSH pool of MKN74 cells as ITCs readily bind to the sulfhydryl group of GSH which may disturb the intracellular redox balance in cells. The reduction selleck chemical of total intracellular GSH in MKN74 cells treated with 1–5 μM PEITC for 5 h was approximately 20% and, surprisingly, did not respond dose-dependently (Fig. 3c). This reduction was presumably insufficient

to disturb the intracellular redox homeostasis and further induce secondary effects such as increased reactive oxygen species (ROS) level. Flow cytometric analysis of MKN74 cells treated with 1–5 μM PEITC for 5 h showed no significant differences in ROS levels (data not shown). The dietary plant phytochemical PEITC is thought to contribute to chemoprevention against several types of human cancer diseases alongside with other plant phytochemicals enriched in a diet with cruciferous vegetables. Moreover, PEITC has also been suggested for clinical treatment of cancer as it may cure resistance to cancer drugs and thus sensitize cancer cells to these drugs.[22] It is therefore important to understand the underlying mechanisms upon the PEITC entry to a cancer cell.

2C). Their lean mass was also similar (Fig. Navitoclax mouse 2D). There was also no difference in the adiposity

index in HSD-fed or HFD-fed Pnpla3+/+ and Pnpla3−/− mice (data not shown). In addition, we detected no difference in the weights of gonadal, subcutaneous, or brown adipose depots in Pnpla3+/+ and Pnpla3−/− mice (data not shown). Experiments on the in vitro differentiation of stromal vascular cells isolated from Pnpla3+/+ and Pnpla3−/− mice revealed no difference in the efficiency of adipocyte differentiation or TG accumulation between the two genotypes (Supporting Fig. 1A,B), which agrees with the fact that the adipose depot mass was similar in these mice. Furthermore, the basal and β-adrenergic agonist–stimulated lipolysis in fully differentiated stromal vascular cells in vitro (Supporting Fig. 1C,D) as well as in mice in vivo (Supporting Fig. 1E,F) was similar between wild-type and Pnpla3−/− cells or mice, indicating that, unlike

ATGL and hormone-sensitive Ivacaftor order lipase, Pnpla3 does not contribute significantly to basal or β-adrenergic agonist–stimulated lipolysis. The nonsynonymous rs738409 SNP in PNPLA3 was predicted to cause the loss of PNPLA3 enzymatic activity, a consequence functionally similar to the targeted inactivation of Pnpla3 in our mouse model.3-6 Microscopic examination of Pnpla3−/− mouse liver sections revealed normal histology (data not shown). We analyzed liver TG content in wild-type and Pnpla3−/− mice fed regular chow, and after they had been placed on three different fatty liver–inducing diets. As shown in Table 1, mice in C57BL/6 background

fed the different fatty liver–inducing diets (including HSD, HFD, and MCD diets) displayed varying degrees of increased liver TG content compared with mice fed CHD. However, there was no significant difference in the degree of hepatic TG accumulation between wild-type and Pnpla3−/− mice under each type of diet, indicating that loss of Pnpla3 had no direct impact on liver TG accumulation. Genetic variations at PNPLA3 have been reported to be associated with increased serum levels of liver enzymes in human populations.3, 5 We found that serum ALT and AST levels varied with the diet conditions (Table 1), being highest in mice fed an MCD diet, which Glycogen branching enzyme may be related to the significant liver damage and inflammation induced by this diet. However, no difference in ALT or AST level was observed between the two genotypes, suggesting that lack of Pnpla3 in mice does not cause an elevated aminotransferase response in liver either under CHD or after the mice were fed the different fatty liver–inducing diets. To further analyze whether loss of Pnpla3 affects fatty liver development associated with a genetic form of obesity, we intercrossed the Lepob/+ mice with Pnpla3−/− mice to produce Lepob/ob/Pnpla3+/+ and Lepob/ob/Pnpla3−/− mice. The obesity phenotype was unchanged in these mice.

Suchy, Yumirle P. Turmelle, Peter F. Whitington, Jeffrey Moore, VX-765 ic50 Averell H. Sherker, Patricia R. Robuck, Ronald J. Sokol 11:45 AM 112: Beta-blockers do not impact negatively on survival rates in cirrhotic patients with diuretic resistant ascites. A Danish nationwide population based study Ulrich C. Bang, Thomas Benfield, Lars Hyldstrup, Jens-Erik B. Jensen, Flemming Bendtsen 12:00 PM 113: The Rising Burden of Herbal and Dietary Supplement Induced Hepatotoxicity in the U. S. A Victor

J. Navarro, Huiman X. Barnhart, Herbert L. Bonkovsky, Timothy J. Davern, Robert J. Fontana, Lafaine Grant, Jay H. Hoofnagle, K. Rajender Reddy, Leonard B. Seeff, Jose Serrano, Averell H. Sherker, Andrew Stolz, Jayant A. Talwalkar, Maricruz Vega, Raj Vuppalanchi 12:15 PM 114: Serum keratin fragment 18 (CK18) levels significantly predict changes in liver histology in children and adolescents with nonalcoholic fatty liver disease (NAFLD): Results from the TONIC trial Ajay K. Jain, Ross B. Deppe, Katherine P. Yates, Megan Comerford, Howard C. Masuoka, Jean P. Molleston, Inhibitor Library chemical structure Jeffrey B. Schwimmer, Joel E. Lavine, Elizabeth M. Brunt, James Tonascia, David E. Kleiner, Naga P. Chalasani Professional Development Workshop Monday, November

4 11:45 AM -1:15 PM Renaissance Hotel, Congressional Hall B Professional Development Workshop MODERATORS: Gyongyi Szabo, MD PhD Claudia O. Zein, MD Simona Rossi, MD What does “success” mean to you now and how has that Calpain been changing? In what ways would you like to increase your influence? Gaining clarity in these areas greatly assists you to make wise decisions

about your priorities and to achieve the results you want in your work and life. This session offers a number of lenses and strategies that will help you manage tensions between your career development and organizational needs and to achieve resiliency in the face of constant change. Learning Objectives: Clarify what “power,” “success” and “influence” means to you Make more strategic choices regarding their commitments Mangage tensions between career development and organizational needs Speak effectively about their goals and accomplishments Apply insights into gender-related differences in these skill areas 11:45 AM -1:15 PM How is Your Vision of Success and Influence Changing? Developing Strategies that Work for You Janet Bickel, MA American College of Physicians (ACP) Lecture Monday, November 4 12:30 -1:30 PM 152A ACP Lecture This lecture is intended to introduce the concept of high value care to the membership of AASLD. The high value care initiative was started by the American College of Physicians (ACP) in 2010 to increase awareness of unsustainable national health care costs and to help practicing physicians simultaneously reduce waste and improve the quality of care they provide to patients. The lecture will introduce a novel case based curriculum to encourage open discussion of these important issues. The content will be a mixture of clinical and basic knowledge.