4 This association with VLDL allows the virus to bind to target cells through lipoprotein receptors.5 The low-density lipoprotein (LDL) receptor (LDLR) has, therefore, been proposed as another entry factor for HCV.6 Furthermore, by utilizing HCV particles isolated from patients, a correlation has been shown between the accumulation of HCV RNA into primary hepatocytes, expression of LDLR messenger RNA, and LDL entry.7 Finally, the potential involvement of the LDLR in HCV entry has also been recently reported in the hepatitis C virus produced in cell culture DAPT in vitro (HCVcc) system.8, 9 Nascent VLDL particles released into plasma are not ligands for the LDLR. However,

upon processing by lipoprotein lipase (LPL), which hydrolyzes the triglycerides in the core of lipoprotein particles, a large proportion (70%) of the resulting intermediate density lipoproteins (IDLs) is efficiently removed from plasma by hepatocytes.

This process is believed to depend on the interaction between LDLR and apolipoprotein E (ApoE), located on Alpelisib manufacturer IDL. The remaining IDL in the circulation is converted to LDL by a reaction catalyzed by hepatic lipase, which further reduces the amount of triglycerides in lipoprotein particles and enables interaction between LDLR and apolipoprotein B (ApoB) exposed on LDL particles.10 Although data from several studies support the involvement of the LDLR in HCV entry, some discrepancies remain. Here, we reinvestigated the role of the LDLR in the HCV life cycle by comparing selleck chemicals llc virus entry to the mechanism of lipoprotein uptake. We show that HCV particles can interact with the LDLR. However, this interaction does not necessarily lead to a productive infection. Furthermore, our data indicate a role for the LDLR as a lipid-providing receptor, which modulates viral RNA replication. ApoB, apolipoprotein B; ApoE, apolipoprotein

E; CD, cluster of differentiation; CEs, cholesterol esters; CHO, Chinese hamster ovary; DiI, 1,1′-dioctadecyl 3,3,3′-tetramethylindocarbocyanine; DMEM, Dulbecco’s modified Eagle’s medium; ER, endoplasmic reticulum; FBS, fetal bovine serum; HCV, hepatitis C virus; HCVcc, hepatitis C virus produced in cell culture; HCVpp, hepatitis C virus pseudoparticle; hLDLR, human low-density lipoprotein receptor; HSPG, heparan sulfate proteoglycan; IDL, intermediate-density lipoprotein; LDL, low-density lipoprotein; LDLR, low-density lipoprotein receptor; LPL, lipoprotein lipase; mAb, monoclonal antibody; PBS, phosphate-buffered saline; PC, phosphatidylcholine; PE, phosphatidylethanolamine; RT-qPCR, quantitative real-time reverse-transcriptase polymerase chain reaction; SINV, Sindbis virus; sLDLR, soluble form of human low-density lipoprotein receptor; SRBI, scavenger receptor BI; siRNA, small interfering RNA; THL, tetrahydrolipstatin; VLDL, very-low-density lipoprotein; ????VSV, vesicular stomatitis virus.

Upper portion of metalic stent was grasped by a grasping forceps

and removed from HKI-272 cost esophagus by pulling out with the gastroscope. Minimal hemorrhage was noted. Fistula was closed in the follow-ups. Results: When SEMSs were found to be embedded, a fully covered SEPS or fully covered SEMS was placed inside the partially uncovered SEMS. Subsequent removal of both stents was possible after a period of 2 weeks. Conclusion: In cases with scoliosis, a combination of stent-in-stent technique and ablation of the tissue at the distal end by APC is safe and effective for the removal of partially covered SEMSs that are embedded in the esophageal wall. Key Word(s): 1. esopagus; 2. metalic stent; 3. plastic stent; Presenting Author: MUHAMMETCEMIL SAVAS Additional Authors: NIMET YıLMAZ, IRFAN KORUK, ABDURRAHMAN KADAYIFCI Corresponding Author: MUHAMMETCEMIL SAVAS Affiliations: Prof. Dr. Objective: Laparoscopic adjustable gastric banding (LAGB) is considered to be a safe and effective method of weight loss and reduction of comorbidities associated with obesity. Pouch enlargement, band slip, band erosion, port-site infections and port breakage represent the complications most commonly associated with LAGB. Band erosion and penetration into stomach is an uncommon complication of LAGB. The recommended Crenolanib manufacturer treatment is complete removal of the eroded gastric band laparoscopically or via laparotomy. Removing a band

that has eroded into the stomach can be fraught with difficulty owing to the extensive inflammatory response around the proximal stomach and left lobe of the liver. In addition, one must deal with the closure of a gastrotomy that results from opening the capsule around the eroded band. This report describes a case of successful endoscopic management of intragastric penetrated adjustable gastric band in a patient with

morbid obesity. Methods: 26-year old male patient who had Laparoscopic Adjustable Gastric Banding 5 years ago, applied to gastroenterology Anacetrapib clinic with upper abdominal dyscomfort. His weight is 150 kg and height 190 cm. He had a history of port site infection and port revision operation 2 years ago. Gastroscopy revealed an eroded and partially penetrated gastric band in the fundus of stomach. Half of the band was seen in stomach. A guidewire passed through the band and and pulled up from the mouth. Two ends of guidewire which was looping the eroded gastric band were put into mechanical lithotriptor and cut the band. Later on, two pieces of cutted gastric band removed from stomach by snare. Minimal hemorhage encountered at entry sites of the band into stomach and port site on the abdomen. Results: Patient discarged from hospital at the same day without any complication. He was well in 3 and 6 months controls. Conclusion: A high index of suspicion is required for diagnosis of band erosion as most patients are asymptomatic.

225 In contrast, the mean mitochondrial diameter was higher in NASH compared selleck with fatty liver.225 Actually, some ultrastructural abnormalities of liver mitochondria could appear well before NASH.225,226 At the moment, there is no definite explanation for the progressive decline of MRC activity during NASH, although some hypotheses can be put forward (Fig. 4). Several MRC complexes including COX are sensitive to ROS and RNS.227,228 In addition, COX can be inhibited by low levels of NO229

and inactivated by 4-hydroxynonenal (4-HNE), a reactive aldehyde generated during lipid peroxidation.230 ROS overproduction within mitochondria could be favored by higher CYP2E1 expression and lower levels of mitochondrial GSH (mtGSH) (Fig. 4). TNF-α is able to impair MRC activity, possibly by inducing hypoxia inducible factor-1α (HIF-1α) and mtDNA damage.5,57,231,232 In addition, Kupffer cell-derived interferons could also impair MRC activity.20 Some lipid derivatives

such as FAs can directly inhibit several enzymes involved in MRC and OXPHOS.12,233,234 Moreover, saturated FAs are able to activate c-Jun N-terminal kinase and trigger Selleckchem Ferrostatin-1 the mitochondrial membrane permeability transition, thus inducing mitochondrial release of cytochrome c and apoptosis.40,235 Reduced adiponectin action in liver could be involved, since this adipokine seems to control MRC activity.236 Plasma adiponectin levels are indeed decreased in NAFLD, and especially in NASH.184,202,237 Moreover, lower hepatic expression of AdipoR1 and AdipoR2 is found in NASH,52,238-240 although other studies reported increased expression.237,241 Another mechanism could be higher activity of forkhead box O1 transcription factor (FoxO1), linked to IR.27 Indeed, FoxO1 activation is able to reduce the content of different MRC polypeptides, possibly by decreasing heme synthesis and impairing PGC1α activity.172 Reduced PGC1α activity could also be secondary to oxidative stress and inflammation, as previously mentioned (Fig. 4).197,198

Numerous drugs are currently tested in order ID-8 to alleviate fatty liver and NASH. These treatments can have different pharmacological effects including improvement of insulin sensitivity, stimulation of lipid oxidation, as well as reduction of DNL, oxidative stress, and inflammation.63,242,243 Regarding mtFAO, some investigations showed that fatty liver could be alleviated by further stimulating the already enhanced capacity for lipid oxidation.75,77 Drug-induced stimulation of mtFAO could have, however, deleterious consequence over the long term if this is not associated with concomitant improvement of MRC. Indeed, an imbalance between mtFAO and MRC activity induces ROS overproduction,5,7,17,63,171 as previously mentioned. Hence, it will be important in the future to find therapeutic strategies able to restore both mtFAO and MRC activity in a coordinated manner.

Initial clinical outcomes occurred more frequently among subjects with cirrhosis (7.5% per year) than subjects with fibrosis (3.3% per year) (P < 0.0001). Child-Turcotte-Pugh (CTP) score ≥7 was the

most common first outcome, followed by hepatocellular carcinoma. Following occurrence of a CTP score ≥7, the rate of subsequent events increased to 12.9% per year, including a death rate of 10% per year. Age and sex did not influence outcome rates. Baseline platelet selleck count was a strong predictor of all clinical outcomes. During the 8 years of follow-up, death or liver transplantation occurred among 12.2% of patients with advanced fibrosis and 31.5% of those with cirrhosis. Conclusion: Among patients with advanced hepatitis C who failed peginterferon and ribavirin therapy, the rate of liver-related outcomes, including death and liver transplantation, is high, especially once the CTP score reaches at least 7. (HEPATOLOGY 2011) Most published data on the rate of progression of chronic hepatitis C, except after transfusion-associated non-A, non-B hepatitis,1 have been derived from single-center studies, which were often small and lacked protocol-driven

systematic data collection.1-10 Based on such reports, the annual incidence of progression to hepatic decompensation in compensated cirrhosis has been estimated to be ≈6% (range, 4%-8%). In the Hepatitis C Antiviral Long-term Treatment against Cirrhosis (HALT-C) Trial,11, 12 we enrolled 1,050 patients with histologically advanced chronic hepatitis C who had failed to AZD2014 manufacturer achieve a sustained virologic response with peginterferon-ribavirin therapy; subjects were assigned randomly to receive low-dose

peginterferon alfa-2a (90 μg/week) or no further treatment for 3.5 years.11 Because the treated and untreated control groups experienced similar rates of clinical progression,12 the combined HALT-C Trial cohort provided a unique opportunity to determine rates BCKDHA of clinical progression in a large, prospectively followed population with histologically advanced, compensated chronic hepatitis C. Extension of the study beyond the 3.5-year randomized treatment phase for up to 8 years provided the opportunity to characterize prospectively the course of advanced chronic hepatitis C more comprehensively than has been possible heretofore. In this article, we describe the frequency and temporal development of the major clinical outcomes of hepatic decompensation. We also describe the sequential emergence of laboratory changes associated with hepatic dysfunction and their relationship to clinical outcomes. ALT, alanine aminotransferase; CTP, Child-Turcotte-Pugh; HALT-C, Hepatitis C Antiviral Long-term Treatment against Cirrhosis; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; MELD, model of end-stage liver disease. The design of the HALT-C Trial (ClinicalTrials.gov #NCT00006164) and results of this randomized trial of peginterferon maintenance therapy were described.

Group size estimates were updated throughout the encounter and the largest estimate was used as the provisional group size. Photo-identification was used after the encounter to confirm identified individuals or reveal individuals not identified during the encounters. The final group size for an encounter was a product of in-water

identification and photo-identification afterwards. The end of an encounter occurred when the dolphins moved away or were unable to be observed reliably (e.g., if they were traveling or swimming against a strong current). The researchers moved on to search for another group. Sometimes dolphins from a previous encounter would be sighted again shortly afterwards with other individuals. If the majority of the animals were the same, the researchers resumed the previous encounter. Only if the composition of the group changed by 50% or more, were they ABT 199 considered a different group and a new encounter began. Only groups where more than 50% of individuals were identified were included in analyses. If an individual was resighted twice or more in the same day, they were included in analysis only if there was at least a 50% difference in group composition. Calves were not included in analyses as their associations are dependent on their mothers’ associations. Coefficients of association see more (CoAs) were calculated using the half-weight

index (Cairns and Schwager

1987) with the software program SOCPROG 2.3 (Whitehead 2009). CoAs were calculated for pooled years 1991–1993, 1994–1996, 1997–1999, and 2000–2002. These pooled years permit O-methylated flavonoid enough individuals to be included, while giving representative results. The last year, 2002, was chosen as a cut-off point in the long-term data set because the area was impacted by hurricanes in 2004, after which about 30% of the population was lost (Elliser and Herzing, in press). In the same study area, significant changes in community/social structure were documented in the sympatric bottlenose dolphin population following similar losses of individuals and influx of new immigrants (Elliser and Herzing 2011). CoAs were calculated for pairs of noncalf individuals of known sex using two sighting criteria: (1) those sighted at least six times per pooled period or (2) at least 10 times per pooled period. Similar results were found for both sighting criteria (Elliser and Herzing 2012). The results did not differ using the higher sighting criterion, so we used the six sightings criterion because it allowed for the inclusion of more individuals. In a concurrent study (Elliser and Herzing 2012), SOCPROG was used to conduct permutations to test the null hypothesis of random associations and no preferred/avoided companions (Christal and Whitehead 2001, Whitehead 2009).

This systematic review used the GBD Study operations guidelines, which divide the world into 21 regions based on geography and epidemiological profiles.10 The purpose PI3K inhibitor of this study was to estimate the age-specific anti-HCV seroprevalence in each of

the 21 world regions in 1990 and in 2005 through a systematic review and meta-analysis of primary national data sources and articles published for peer review between 1980 and 2007. The seroprevalence was modeled using the age-averaging random effects generalized negative binomial spline model from DisMod III,11 the latest iteration of the generic disease modeling system for model-based meta-analysis for descriptive epidemiology, developed by the Institute of Health Metrics and Evaluation (IHME) at the University of Washington.

The results of this meta-analysis and the estimates produced by the models identify regions and age groups with high prevalence, and predict prevalence in areas where data are sparse or not available. The anti-HCV seroprevalence estimated in this systematic review is the first step towards https://www.selleckchem.com/products/Belinostat.html modeling the global burden of disease for HCV infection. EIA, enzyme immunoassay; GBD, Global Burden of Disease Study; HBV, hepatitis B virus; HCV, hepatitis C virus; HDV, hepatitis D virus; IHME, Institute of Health Metrics and Evaluation; MESH, Medical Subject Headings; NHANES, National Health and Nutrition Examination Survey;

PWID, persons who use injecting drugs; UI, uncertainty interval; WHO, World Health Organization. Three Ovid databases, Medline, Embase, and Cinahl, were used to allow for a thorough systematic literature search. An attempt was made to include gray literature and other databases, but was abandoned when the ability to search systematically varied widely. As part of a larger body of work to estimate global prevalence for hepatitis B, C, and D, these databases were simultaneously searched for articles published over a 27-year period (1980-2007) that reported the prevalence of hepatitis B, C, and D PD184352 (CI-1040) virus infections. Medical Subject Headings (MESH) were used to search articles and freetext to search article abstracts that contained (1) a term related to hepatitis B (HBV), C, or D (HDV) or their markers of infection, and (2) a term related to prevalence, incidence, or disease burden. Due to limited resources, the results were restricted to articles in English only, which exclude 14.8% of the articles found in this search prior to deduplication, and application of selection criteria (Fig. 1). Abstracts were screened and were required to report prevalence or incidence of hepatitis B or C. Articles were excluded if they reported prevalence from a high-risk population or if the data reported were incomplete.

2B). The sensitizing effect was further evidenced by an increase of cell apoptosis in response to treatment with sorafenib and lapatinib (Fig. 2C). We thus conclude that targeting Pirfenidone price NPM sensitizes HCC cells to oncogenic kinase inhibitors, such as sorafenib and lapatinib. NPM exerts its death evasion

activity via a mechanism independent of p53 function. NPM was up-regulated in Huh7, Hep3B, and Mahlavu cells following treatment with UV, cisplatin, and doxorubicin (Fig. 3A). Meanwhile, we also observed the induction of BAX expression, a key effector initiating mitochondria-mediated cell death, in all three cell lines (Fig. 3A). Simultaneous induction of NPM (antiapoptosis) and BAX (proapoptosis) represents hormetic mechanisms regulating cell survival versus death in response to stress.7, 26 To understand how NPM helps HCC cells evade death, we first inspected subcellular distribution of NPM and BAX in response to cell stress. Before UV irradiation, NPM was mainly located in the nucleoli and partially in the nucleoplasm (Fig. 3B, left), whereas BAX was primarily located in nucleoplasm and some in the cytoplasm (Fig. 3C, upper left).

Following UV irradiation, NPM was translocated from nucleoli to nucleoplasm, and a set of NPM was further translocated to the cytoplasm (Fig. 3B, right). On the other hand, BAX was translocated to the cytosol and accumulated in the mitochondria (Fig. 3C), particularly in cells undergoing apoptosis (Fig. 3C, right). Notably, as being transfected with siRNA to down-regulate the expression of NPM, cells with relatively Doxorubicin order low NPM expression usually presented with aggregation of BAX in the mitochondria and undergoing apoptosis (Fig. 4A), whereas cells with relatively high NPM level presented with less degree of mitochondrial accumulation of BAX and more resistance Bay 11-7085 to apoptosis induction (Fig. 4A). Interestingly, colocalization of NPM and BAX in the cytoplasm was

noted in some cells presenting with cytoplasmic NPM (Fig. 4B). These findings suggest that the antiapoptosis activity of NPM is involved in blockade of mitochondrial translocation of BAX. The observation that colocalization of a set of NPM with BAX in cytoplasm in HCC cells with relative resistance to death stimuli intrigued us to examine the role of NPM in mitochondrial translocation of BAX in HCC cells. As shown in Fig. 5A, the NPM level in the cytosol of Mahlavu cells was increased after UV irradiation, while NPM was not detected in the mitochondria either before or after UV irradiation. On the other hand, the amount of BAX was increased in both the cytosol and the mitochondria after UV irradiation. Silencing of NPM expression decreased the cytosolic BAX, but increased the mitochondrial BAX, suggestive of blockade of BAX mitochondrial translocation by NPM in response to UV treatment. Prohibitin and glyceraldehyde 3-phosphate dehydrogenase were used as the markers for mitochondrial and cytosolic components, respectively.

Three hundred and thirty-three patients were enrolled in the study from the Nanjing Stroke Registry. They underwent both cerebral DSA and MRI. Age, sex, and vascular risk factors were collected. Atherosclerosis was scored from grade 0 to 4. Leukoaraiosis was scored from grade 0 to 3. Cerebral artery stenosis was not correlated with the presence of leukoaraiosis. There were no correlations between the number of cerebral moderately or more severely stenotic arteries and the severity of leukoaraiosis in periventricular, deep, or whole white matter (P = .747, .268, and .608, respectively). Old

age (odds ratio = 1.103, P = .027) and hypertension (odds ratio = 2.748, P = .003) were correlated with leukoaraiosis in the periventricular white matter. Old age (odds ratio = 1.073, P = .031) and prior stroke (odds ratio = 2.678, P = .002) were BMN 673 clinical trial correlated with leukoaraiosis in

the deep white matter. No apparent correlation exists between cerebral artery stenosis and the presence and severity of leukoaraiosis. “
“Intravascular ultrasound (IVUS) has provided invaluable real-time information during carotid artery stenting (CAS). We present a case of IVUS-guided thrombus extraction during CAS. A 46-year-old man underwent an urgent right CAS under proximal flow reversal for embolic protection for a hemodynamically significant symptomatic near-occlusion of the internal carotid artery. IVUS was used to evaluate immediate poststenting results and identify potential thromboembolic material extruding through the tines of the stent. An intraluminal this website thrombus was identified with IVUS after the stent was deployed. This led to the use of a second stent in an attempt Exoribonuclease to trap the thrombus. Ultimately, the thrombus was removed with the use of a multipurpose-angled catheter under IVUS guidance. The artery reconstituted almost completely after stent placement, and the patient’s condition improved significantly. IVUS identification of intraluminal thrombus allowed additional maneuvers to be performed to prevent distal embolization and postprocedure

stroke. “
“Arterial spin labeling (ASL) is a relatively new MR perfusion technique that requires validation. One hundred patients with an acute hemispheric ischemic stroke were imaged within 6 hours of symptom onset with perfusion CT (CTP), and at 24 hours with MRI perfusion imaging, including ASL and bolus dynamic susceptibility contrast (DSC) imaging. Baseline CTP was used to define tissue at risk. This was used to determine persistent hypoperfusion, or hyperperfusion, on 24-hour ASL maps. Using 24 hour ASL, 48 of 100 patients showed hyperperfusion, and 41 showed persistent hypoperfusion. None of the PWI maps identified hyperperfusion. Compared to patients with persistent hypoperfusion on ASL, patients with hyperperfusion had less progression of acute CTP mismatch tissue to infarction at 24 hours (P= .05).

001)).Of the patients who had lower urine-NGAL on day1(n=14), none had persistent AKI and 3 had transient AKI. Day1 urine-NGAL had a high probability to predict persistent AKI as well as mortality. At a cut off of 221ng/ml, urine-NGAL had a sensitivity and specificity of 65% in predicting severe pancreatitis (AUC=0.755,p=0.013). NGAL levels were significantly more than the controls

both in serum and urine on both days. Conclusion: NGAL(both serum and urinary) predicts AKI in acute pancreatitis. Day1 urine-NGAL can be used to predict AKI, both its occurrence and persistence and can be used to monitor renal failure in patients with SAP. Key Word(s): 1. pancreatitis; 2. NGAL; 3. AKI; 4. severity; Presenting Author: RAGESHBABU THANDASSERY Additional Authors: USHA DUTTA, SREEKANTH APPASANI, RAGHAVENDRA Small Molecule Compound Library PRASADA, THAKURDEEN YADAV, KARTAR SINGH, NIKHIL CHAUDHARY, AJAY BAHL, RAKESH KOCHHAR Corresponding Author: RAGESHBABU THANDASSERY Affiliations: EX 527 in vivo Department of Gastroenterology, PGIMER; Department of Cardiology, PGIMER Objective: Cardiovascular failure occurs in

one third of patients with severe acute pancreatitis (SAP). There is paucity of information on underlying mechanisms contributing to cardiovascular failure, the spectrum of cardiovascular dysfunction and its impact on outcome. AimTo study the occurrence of electrocardiography from changes (ECG), cardiac dysfunction (CD) in SAP, characterize the type of CD (systolic, diastolic or combined) and describe its impact on final outcome.

Methods: 72 patients with SAP and hypotension were prospectively studied for the occurrence of CD, nature of CD and its influence on hospital course and mortality. All patients had 12 lead ECG recorded on day 1, day 3 and day 7 in addition to the continuous ECG monitoring during ICU stay. Cardiac enzymes (Troponin I and Creatine phospho kinase MB) were measured at day 1 and day 3. All the patients underwent trans-thoracic echocardiography examination on day1 of hospitalization. Results: Of 72 patients (mean age of 39.1±12.9, 44 males); 58 (80.6%) had transient and 14 (19.4%) persistent hypotension. 47 (65.3%) patients had CD and of them 28 (59.6%) had diastolic dysfunction (DD), 8 (17%) had systolic dysfunction and 11(23.4%) had combined CD. Abnormal ECG findings were noted in 58 (80.6%) patients and were mostly ST segment and T wave changes. 10 (13.9%) patients had percutaneous drain placement, 12 (16.7%) underwent surgery and 14 (19.4%) succumbed to illness. Univariate analysis showed that patients with diastolic dysfunction had significantly higher mortality (hazard ratio- 3.6, 1.0, 12.5 and p value 0.032). Multivariate analysis showed APACHE II (odds ratio 20.60, CI=3.31-128.26, p=0.001) (odds ratio 7.2, CI=6.1-8.1, p<0.001) as independent predictors of mortality.

Anders, MD, PhD Hepatology Associates Course Hepatology Associates Course Sunday, November 3 8:00 AM -1:30 PM Room 147 COURSE DIRECTORS: Linda M. Stadheim, RN Mary Panther, RN 5.5 CME Credits / 5 Contact Hours This one day course aims to provide basic and advanced up-to-date knowledge

for the management of patients with liver disease. Learning Objectives: Explain the current nonalcoholic steatohepatitis (NASH) practice guidelines and appropriate, patient specific strategies to treat NASH & nonalcoholic fatty liver disease (NAFLD) www.selleckchem.com/products/ABT-263.html Identify patient selection indication for liver biopsy or a non-invasive alternative to stage fibrosis Describe controversial decisions with transplant patient selections and orgean allocations including split vs full liver transplant Discuss benefits and risks of Coffee, CAM and Cannabis in the liver patient Examine complex Hepatitis C (HCV) treatment populations and identify appropriate strategies to LEE011 molecular weight manage difficult HCV treatment side effects 8:00 – 8:05 AM Opening Remarks

Session I MODERATORS: Donald Gardenier, DNP Linda M. Stadheim, RN 8:05 – 8:45 AM NASH & NAFLD: Cutting Through the Fat Andrea A. Gossard, NP 8:45 – 8:55 AM Awarded Poster Presentation Geri Hirsch, MSN, RN-NP and Gail Butt, MD 8:55 – 9:30 AM Biopsy versus Non-invasive Approaches to Assessing Fibrosis R. Todd Stravitz, MD 9:30 – 9:40 AM Awarded Poster Presentation Amy Nelson, BSN, RN, ACRN 9:40 – 10:20 PDK4 AM Liver Transplantation Controversies Jacqueline Laurin, MD 10:20 – 10:30 AM Discussion 10:30 – 11:00 AM Break and Brunch Session II MODERATORS: Mary Panther, RN Dustin C. Latimer, PA-C 11:00 – 11:45 AM HCV Triple Therapy Lessons Learned Antonio J. Sanchez, MD 11:45 AM – 12:30 PM Point-Counterpoint: Hepatitis C Treatment Douglas R. LaBrecque, MD and Paul Y. Kwo, MD 12:30 – 1:00 PM Coffee, CAM and Cannabis: Stirring the Pot Kiran Bambha, MD 1:00 – 1:30 PM Discussion and Closing Thomas E. Starzl Transplant Surgery State-of-the-Art Lecture Sunday, November 3 9:30 – 10:00 AM Hall

E/General Session Regenerative Medicine: New Approaches to Healthcare SPEAKER: Anthony Atala, MD MODERATOR: Kenneth D. Chavin, MD, PhD Patients with diseased or injured organs may be treated with transplanted organs. There is a severe shortage of donor organs which is worsening yearly due to the aging population. Regenerative medicine and tissue engineering apply the principles of cell transplantation, material sciences, and bioengineering to construct biological substitutes that may restore and maintain normal function in diseased and injured tissues. Stem cells may offer a potentially limitless source of cells for tissue engineering applications and are opening new options for therapy. Recent advances that have occurred in regenerative medicine will be reviewed and applications of these new technologies that may offer novel therapies for patients with end-stage tissue and organ failure will be described.