The disorder is far more common than was believed only one or two decades ago. The overwhelming majority of spontaneous CSF leaks occur at the level of the spine, particularly the thoracic spine. Spontaneous leaks at the skull base do occur but only rarely. Spontaneous CSF leaks can no longer be equated with postpuncture headaches. There is considerable variability in clinical presentations, imaging findings, and CSF findings including CSF pressures that can be within normal limits. CSF volume depletion (CSF hypovolemia) rather than decreased CSF pressure

appears to be the pathogenetic core as the independent variable. CSF pressures, clinical manifestation, and MRI abnormalities are variables dependent on the CSF volume. The term “SIH” no longer appears broad Selleck LY2835219 enough to embrace all of these variables. Terms such as CSF volume depletion

or CSF hypovolemia have appeared in the literature and have been used interchangeably with spontaneous CSF leak. The anatomy of spontaneous CSF leaks is often complex and different see more from a simple hole or a rent. It is typically not the same as what is encountered in CSF leaks resulting from LP, epidural catheterization, or craniospinal surgeries. Clinical stigmata of disorders of connective tissue matrix can be seen in a significant minority of the patients with spontaneous CSF leaks. This very likely plays a role in the weakness of the dural sac, formation of meningeal diverticula, and pathogenesis of the disorder. Not all headaches in spontaneous CSF leaks are orthostatic and not all orthostatic

headaches result from CSF leaks. Sometimes after treatment of CSF leak, whether by EBP or surgery, a rebound increased intracranial pressure may occur, which is often self-limiting but sometimes may require treatment. The rate of CSF leakage in spontaneous Dimethyl sulfoxide CSF leaks may vary considerably. Fast-flow and slow-flow leaks each present special diagnostic challenges. Novel diagnostic techniques have been quite helpful in locating the site of the leak in fast-flow leaks. Locating the site of slow-flow leaks remains challenging. EBP has emerged as treatment of choice when initial conservative measures including time have failed. These may be targeted or blind (presumed distant from an undetermined leak site) or single level or bilevel. Epidural injection of fibrin glue also has utility in selected cases. Combined EBP and fibrin glue injections have also been tried but it needs special considerations. Surgery aimed at stopping the leakage is often undertaken when less invasive measures (such as EBP) have failed. It is essential to determine the site of the leak by appropriate imaging before surgery is undertaken. The author thanks Mrs. Lori Lynn Reinstrom, Research Administrative Assistant, Mayo Clinic-Rochester, for her excellent editorial assistance and Mr. John V.

Familial linkage analysis on several affected and unaffected individuals of several generations made it possible to map gene locus on chromosome 7q35 and to demonstrate its association with HP.25,26 Subsequent studies reported a mutation (365G > A) that results in arginine to histidine substitution at 122 position (R122H) in cationic trypsinogen gene [protease, serine, 1 (trypsin 1) (PRSS1), OMIM 276000] to be associated

with hereditary pancreatitis.27 Other PRSS1 alterations including A16V, N29T, R116C, R122C and several other genetic alterations have been reported in families with suspected HP or in patients without a family history.28 The current model of PRSS1 Abiraterone mutations suggests that the identified mutations cause enhanced auto-activation of trypsinogen to trypsin, or prevent prematurely activated trypsin from being inactivated by autolysis. Familial aggregations,

find more seen in about 8% of TCP patients, suggest a genetic etiology for TCP.29 However, subsequent studies on PRSS1 have reported its association with HP and CP in western populations but not with TCP.30,31 Triplication (copy number variation) of a 605 kilobase segment containing the PRSS1 and PRSS2 genes has been reported in HP.32 A study by Masson et al.33 revealed the molecular basis of 6% of young ICP patients. However copy number variations with regard PRSS1 and PRSS2 genes were not associated with TCP patients. Although it has been hypothesized that mutations in anionic trypsinogen [protease, serine, 2 (trypsin 2) (PRSS2), OMIM 601564] contribute to the disease by a mechanism similar to that of PRSS1, studies by various groups in ICP and TCP patients did not find associated polymorphisms

in PRSS2.34,35 A glycine to arginine change at codon 191 in PRSS2 analyzed in a European population has been demonstrated to play a protective role against CP.36 Further functional studies on purified recombinant G191R protein revealed that generation of a novel tryptic cleavage site within the mutated gene product makes the enzyme hypersensitive CYTH4 to autocatalytic proteolysis, thus playing a protective role in CP. A recent European multicentre study reported the protective role of p.G191R mutation, indicating subjects carrying a heterozygous p.G191R mutation have an approximately 3-fold decreased risk of developing CP compared with carriers of the wild-type allele.37 Cystic fibrosis transmembrane regulator (CFTR, OMIM 602421) gene is associated with alcoholic pancreatitis and ICP, where about 13.4%38 and 25.9%39 of patients in two studies were shown to carry at least one mutation in the gene. An earlier study on western populations revealed an association of CFTR mutations with ICP and the possibility of its interaction with PRSS1 and SPINK1 mutations.40 However, the frequency of CFTR mutations was found to be very low in TCP patients.

The patients were divided into four groups on the basis of the location of their cortical lesion: occipito-temporal, occipito-parietal, rostro-dorsal parietal, or frontal-prefrontal. The six tasks were: direction discrimination, speed discrimination, motion Selleck PF-6463922 coherence, motion discontinuity, two-dimensional form-from-motion, and motion coherence – radial. We found both qualitative and quantitative differences among the motion impairments in the four groups: patients with frontal lesions or occipito-temporal lesions were not impaired on any task. The other two groups had substantial

impairments, most severe in the group with occipito-parietal damage. We also tested eight healthy control subjects on the same tasks while they were scanned by functional magnetic resonance imaging. The BOLD signal provoked by the different tasks correlated well with the locus

of the lesions that led to impairments among the different tasks. The results highlight the advantage of using psychophysical techniques and a variety of visual tasks with neurological patients to tease apart the contribution of different cortical areas to motion processing. “
“Converging evidence suggests that autobiographical memory and episodic future thinking share a common neurocognitive basis. Although previous research has shown that traumatic brain injury (TBI) can impair the ability to remember the personal past, Cell Cycle inhibitor episodic future thinking has not previously been systematically find more examined within this population. In this study, we examined the ability to remember events in the personal past and the ability to imagine possible events in the personal future in a sample of moderate-to-severe TBI patients.

We present data on nine patients and nine healthy controls, who were asked to report a series of events that had happened to them in the past and a series of events that might happen to them in the future. Transcriptions were scored according to a reliable system for categorizing internal (episodic) and external (semantic) information. For each event described, participants also completed two modified Autobiographical Memory Questionnaire items to assess self-reported phenomenal qualities associated with remembering and imagining. In addition, TBI patients underwent neuropsychological assessment. Results revealed that TBI patients recalled/imagined proportionally fewer episodic event-specific details for both past and future events compared to healthy controls (η2p = 0.78). In contrast, there were no group differences in ratings of phenomenal characteristics. These results are discussed in relation to theories suggesting that remembering and imagining the future are the expression of the same underlying neurocognitive system.

It is not known whether coagulation factor concentrate infusion affects primary haemostasis or induces an acute inflammatory response. In this study, the influence of a factor VIII (FVIII) concentrate bolus infusion on platelet activation and responsiveness, endothelial activation, and inflammation in adult patients with severe haemophilia

A was assessed. VWF showed a mild, but significant decrease 15 min after FVIII infusion (85.02 IU dL−1) vs. before infusion (92.04 IU dL−1; P = 0.017), while ADAMTS-13 levels also show a mild but significant decrease from 66.1 ng mL−1 before infusion, to 53.9 ng mL−1 (P = 0.012) 15 min after and 50.8 ng mL−1 (P = 0.050) 60 min after infusion. Platelet P-selectin expression decreased 15 min (33.3 AU) and 60 min (38.7 AU)

after infusion compared to before infusion (41.3 AU; P = 0.018 and 0.036). In conclusion, a single infusion of a high dose AZD6244 ic50 FVIII concentrate in haemophilia A patients may influence primary haemostasis by decreasing VWF, ADAMTS-13 and the number of circulating activated platelets. These effects possibly occur as a consequence of binding of the infused FVIII to VWF, influencing its processing. PI3K inhibitor When treating severe haemophilia A patients with coagulation concentrate infusion, one should realize this does not merely correct FVIII levels but also may influence primary haemostasis. “
“Summary.  Women with factor X deficiency (FXD) who want to become pregnant face uncertain risks to themselves STK38 and to an unborn infant from haemorrhagic complications during pregnancy and at parturition. Women with FXD may also experience difficulty achieving pregnancy secondary to haemorrhagic symptoms of the reproductive organs. Case reports describe differences in bleeding phenotypes and pregnancy outcomes that are not easily correlated

with prepregnancy bleeding symptoms or factor X levels. The aim of this article is to identify factors for consideration and information to assist the physician in counselling women with FXD who want to become pregnant, and to offer guidelines for management where appropriate. We identified cases of pregnancy among women with FXD and their outcomes from the literature; 15 women with 24 pregnancies were identified and 18 were successful. The women in this small cohort did not have an increased rate of spontaneous abortion, (8.3% vs. 13.5% in the general US population) but did have a 2.5-fold increased risk of preterm labour (37.5% vs. 12.2% in the general US population). The role of prophylaxis to control reproductive haemorrhagic symptoms, including haemorrhagic complications of pregnancy has not yet been defined, but use of prophylaxis may allow more women to be able to attempt pregnancy.

9 y.o. Rates of en bloc resection and en bloc plus R0 resection were 94.4% (473/501) and 96.2% (482/501), respectively. 22 patients underwent additional colectomy due to histopathologocal assessment of ESD specimen according to The Japanese Society for Cancer of the Colon and Rectum (JSCCR) guidelines. Local recurrence was detected in 1 lesion (0.31%). In this case, the resection had been piecemeal. The disease-specific survival was 100% because no patients died of colorectal neoplasms. 26 patients died of other coexisting disease. The 3-year and 5-year overall survivals were 96.5% and 90.9% during median follow-up of 61.9

and 73.3 months, respectively. Conclusion: Colorectal ESD showed good long-term outcomes and acceptable ABT-263 rate of en bloc resection and en bloc R0 resection. Key Word(s): 1. endoscopic submucosal dissection (ESD); 2. long-term outcome; 3. overall survival Presenting Author: HAJIME TAKISAWA Additional Authors: TETSUJI TERAZAWA, TAKU

SAKAMOTO, YASUO KAKUGAWA, YUTAKA SAITO Corresponding Author: HAJIME TAKISAWA Affiliations: National Cancer Center Hospital, National Cancer Center Hospital, National Cancer Center Hospital, National Cancer Center Hpspital Objective: In Japan, disease rate and mortality rate for colorectal cancer (CRC) is increasing and disease rate of inflammatory bowel disease (IBD) is increasing as well. In diagnosing CRC and IBD, colonoscopy is an effective method. The low screening rate when a colonoscopy is recommended as a follow-up test to a positive fecal occult-blood testing (FOBT) is problematic, however. One possible explanation for this low screening rate among women patients

might be their selleck anxiety and hesitance to undergo a colonoscopy with male physicians. Although several studies have indicated that women prefer Baricitinib female physicians for breast or genital examinations, there are only few reports on whether women prefer female endoscopists since colon disease is not specific to women. The aim was to investigate whether women patients preferred to undergo colonoscopies for the first time conducted by female doctors. Methods: Subjects are women who received colonoscopies as a follow-up test to a positive FOBT or an asymptomatic screening examination for the first time aged 40 years or older. Researchers chronicled patients‘ colonoscopist sex preference before and after the colonoscopies, along with patient characteristics, by utilizing a self-administered questionnaire (period: April 2012 to March 2013). Results: There were 275 subjects. The survey prior to the exam showed that 98 women (35.6%) (A) preferred female colonoscopists, 173 women (62.9%) had (B) no preference, and 4 women (1.5%) (C) preferred male colonoscopists. The post exam survey showed (A) 30.2%, (B) 66.2% and (C) 3.6%. In women younger than 45 years, while the proportion who preferred female colonoscopist is 60%, which was only 28% at 45 years of age or older. Significant difference (p < 0.

The prediction workflow has been performed by considering only those miRNAs found significantly deregulated (i.e. by a fold-change of at least two). For each miRNA, we obtained three lists that we matched to consider all the possible intersections. We finally retained only those genes predicted by all three algorithms. We assumed that the predictions obtained following this criteria, should have a minor degree of uncertainty since they originate from algorithms with different underlying principles. To reduce complexity, mTOR inhibitor we also filtered out every gene found in both upregulated and downregulated miRNAs lists, considering only those genes with

unambiguous behavior. This improvement would have certainly helped Jin et al. to avoid misleading overlap of functional categories in their lists. Finally,

to take into account the cooperative effect of different miRNAs on the same target gene, we ranked a list of genes targeted by two or more miRNAs. buy GW-572016 The list of target genes that we obtained following this bioinformatics workflow was finally subjected to functional classification using DAVID.16 In summary, both the paper by Jin et al.12 and our own work (Alisi et al.7)) provide clear examples of how many data are contained in “simple” miRNA expression profile experiments, and the difficulty in developing an understanding of the pathogenic mechanism leading to the transition from steatosis to NASH. In conclusion, we believe that an integrated approach of differentbioinformatics analyses for microRNA expression and regulation studies, although remaining predictive without appropriate experimental validations of predicted target genes, could lead to a deeper understanding of gene expression patterns and their regulation

in the pathogenesis of important liver diseases like NAFLD. “
“Host factors play an important role in all facets of the hepatitis these C virus (HCV) life cycle and one such host factor is signal transducer and activator of transcription 3 (STAT3). The HCV core protein has been shown to directly interact with and activate STAT3, while oxidative stress generated during HCV replication in a replicon-based model also induced STAT3 activation. However, despite these findings the precise role of STAT3 in the HCV life cycle remains unknown. We have established that STAT3 is actively phosphorylated in the presence of replicating HCV. Furthermore, expression of a constitutively active form of STAT3 leads to marked increases in HCV replication, whereas, conversely, chemical inhibition and small interfering RNA (siRNA) knockdown of STAT3 leads to significant decreases in HCV RNA levels. This strongly implicates STAT3 as a proviral host factor.

2 ± 7.1, 27.7 ± 5.9, and 23.4 ± 5.5, respectively, as shown in Fig. 1B. There were statistical differences in the degree of net cytotoxicity induced by TLR3-L+TLR4-L activation of LMC in cells from PBC when compared to similarly activated LMCs from other control liver diseases (PBC versus HBV-related cirrhosis: P = 0.03, PBC versus HCV-related cirrhosis: P = 0.02, PBC versus alcohol-related cirrhosis: P = 0.02). Subsequently, in efforts to confirm that the activation by TLR4-L (LPS) and TLR3-L (poly I:C)

was Compound Library chemical structure indeed induced by way of the respective TLR pathways, use was made of pretreatment of the activation agents with previously defined optimum concentrations of polymyxin B for LPS and chloroquine for poly I:C. As shown in Fig. 1C, polymyxin B inhibited CTL activity in a dose-dependent manner and chloroquine inhibited CTL activity even at the lowest concentration used. The ability of cells to induce cytotoxic activity against autologous BEC following the ligation of TLR3-L+TLR4-L was next examined. Cultures of LMC, stimulated with TLR3-L+TLR4-L, were used to either isolate enriched populations of Mo, T cells, NK cells, or isolate cultures depleted of each of these cell lineages. These enriched and this website depleted cell cultures were assessed for their cytotoxicity against autologous BEC. Unfractionated

TLR3-L+TLR-4-activated LMC were used for purposes of a positive control. As shown in Fig. 2, whereas Mo did not demonstrate Bumetanide any significant cytotoxicity against autologous BEC (CTL activity; 0.6 ± 5.4%), LMC depleted of Mo demonstrated significant cytotoxicity against autologous BEC (CTL activity; 33.2 ± 6.8%). Similarly, whereas T cells did not demonstrate significant cytotoxicity against autologous BEC (CTL activity; 0.8 ± 4.5%), LMC depleted of T cells had significant cytotoxicity against autologous BEC (CTL activity; 24.0 ± 10.0%). On the other hand, whereas NK cells demonstrated

significant cytotoxicity against BEC (CTL activity; 28.0 ± 11.0%), LMC depleted of NK cells did not show significant cytotoxicity against autologous BEC (CTL activity; 2.0 ± 1.1%). These data indicate that it is the NK cell lineage following TLR3-L and TLR4-L stimulation that is responsible for significant cytotoxic activity against autologous BEC. Representative data from one PBC patient is shown in Fig. 2. In efforts to identify the potential mechanisms by which activation of TLR3-L+TLR4-L in cultures of LMC generate cytotoxic activity of NK cells against autologous BEC, data obtained in preliminary studies showed that the activation of enriched population of NK cells with TLR3-L+TLR4-L did not lead to significant cytotoxicity against autologous BEC (Fig. 3A). These data indicate that the generation of cytotoxic activity against autologous BEC was likely due to the presence of a second population of cells.

The cause of PGCH is unknown and probably multifactorial; possibilities include a virus,8,

9 drugs and herbal remedies,10 and autoimmune changes.11, 12 In addition, reports have been published about patients who have undergone liver transplantation.13, 14 Our patient received Pil-Food. Severe changes in liver function tests occurred, she was positive for antinuclear antibody autoreactivity, and a histological examination found abundant AZD8055 nmr areas of multinucleate giant cells with marked periportal and parenchymal hepatocellular necrosis and inflammation. Because all the aforementioned alterations appeared during the long-term ingestion of Pil-Food [a composition developed by Synthelabo that contains D,L-methionine, see more L-(+)-cysteine hydrochloride, L-cysteine, enzymes and animal protein hydrolysates, millet extract, calcium pantothenate, vitamin B2 phosphate, vitamin B6, biotin (vitamin H), and vitamin E] and a successful corticosteroid response was attained, we speculate that this hepatic autoreactivity could be related to the Pil-Food treatment.15, 16 Moreover, just like patients with drug-induced AIH,1 our patient did not require long-term immunosuppressive therapy. We believe that this case highlights (1) that the breakdown of immune tolerance by drugs is able to trigger liver autoreactivity and (2) that some cases of PGCH may present a rapid and effective response

to corticosteroid therapy instead of a fulminant or progressive course. Ricardo Moreno-Otero M.D.* ‡, Maria Trapero Marugán M.D.* ‡, Luisa García-Buey M.D.* ‡, Asunción García-Sancchez mafosfamide M.D.†, * Digestive Diseases Service, Hospital Universitario de La Princesa, Universidad Autónoma de Madrid, Madrid, Spain, † Pathology Service, Hospital Universitario de La Princesa, Universidad Autónoma de Madrid,

Madrid, Spain, ‡ Centro de Investigación Biomédica en Red, Instituto de Salud Carlos III, Madrid, Spain. “
“A 53 year-old man presented with a 5-month history of severe diarrhoea and abdominal cramping immediately occurring after tube feeding. The Percutaneous Endoscopic Gastrostomy (PEG) tube was inserted 2 years previously, for enteral feeding, following diagnosis of an oropharyngeal carcinoma. The patient had no signs or symptoms of peritonitis. The skin surrounding the tube was inflamed with brown odorous fluid exuding. Upon checking the tube position using upper endoscopy no inner bumper was seen within the stomach. A fistulogram through the feeding tube revealed typical haustration of the colon rather than expected gastric appearances (Figure 1A). CT confirmed misplacement, localizing the position of the bumper in the transverse colon (Figure 1B, arrow). A gastrocolic fistula could not be visualized. Colonoscopy showed the inner bumper located near the splenic flexure (Figure 2A).

Luxon, MD, PhD 2:20 – 2:40 PM Academic Advancement Adrian M. Di Bisceglie, MD 2:40 -

3:00 PM Understanding Clinical Epidemiology and Biostatistics W. Ray Kim, MD 3:00 – 3:20 PM Making the Most of the Mentee-Mentor Relationship Anna Mae Diehl, MD 3:20 – 3:30 PM Panel Discussion Competency Training Workshop Friday, November 1 12:30 – 3:00 PM Room Syk inhibitor 152B Competency Training Workshop COURSE DIRECTORS: Oren K. Fix, MD, MSc K. Gautham Reddy, MD This workshop is designed to assist Transplant Hepatology Program Directors, Program Coordinators, clinical faculty, and trainees in Transplant Hepatology, Gastroenterology and Internal Medicine in understanding the changes occurring in Transplant Hepatology training and assessment. Attendees will develop a better understanding of competency-based medical education specifically learned from the experience of the GI/Transplant Hepatology pilot training program. They will be able to better see more understand the new Transplant Hepatology milestones and their use in assessing and evaluating trainees and reporting to ACGME. Attendees will be updated on the progress of the Next Accreditation System (NAS) and gain

a better understanding of its impact on Transplant Hepatology training and assessment beginning in July 2014, including a focus on the responsibilities of the Clinical Competency Committee and the need for faculty development in these areas. Learning Objectives: Describe the experience, progress and future developments of the GI/Transplant Hepatology pilot training program Identify the knowledge of the Transplant Hepatology milestones and how to apply them in the assessment and evaluation of trainees Describe the composition and role of the Clinical Competency Committee Prepare for the Next Accreditation System 12:30 – 12:40 PM Introduction Bruce A. Luxon, MD, PhD 12:40 – 1:00 PM The

Methane monooxygenase Next Accreditation System: Compliance for Transplant Hepatology Fellowships K. Gautham Reddy, MD 1:00 -1:20 PM Update on the GI/Transplant Hepatology Pilot Training Pathway Oren K. Fix, MD, MSc 1:20 – 1:40 PM Results of the Pilot Perceptions Survey and Perspectives from a Gastroenterology Fellow Dina Halegoua-De Marzio, MD 1:40 – 1:50 PM Discussion 1:50 – 2:05 PM Break 2:05 – 2:25 PM The Transplant Hepatology Training Landscape of the Future John R. Lake, MD 2:25 – 3:00 PM Panel Discussion and Q & A Steven K. Herrine, MD, K. Gautham Reddy, MD, Oren K. Fix, MD, MSc and Andrew Keaveny, MD 3:00 – 3:00 PM Panel Discussion and Q & A Andrew Keaveny, MD AASLD Postgraduate Course Friday, November 1 3:30 – 7:30 PM Hall E/General Session New Treatments in Liver Disease A New Era of Diagnostics, Therapeutics and Intervention in Hepatology COURSE DIRECTORS: Adrian M.

Luxon, MD, PhD 2:20 – 2:40 PM Academic Advancement Adrian M. Di Bisceglie, MD 2:40 -

3:00 PM Understanding Clinical Epidemiology and Biostatistics W. Ray Kim, MD 3:00 – 3:20 PM Making the Most of the Mentee-Mentor Relationship Anna Mae Diehl, MD 3:20 – 3:30 PM Panel Discussion Competency Training Workshop Friday, November 1 12:30 – 3:00 PM Room selleck inhibitor 152B Competency Training Workshop COURSE DIRECTORS: Oren K. Fix, MD, MSc K. Gautham Reddy, MD This workshop is designed to assist Transplant Hepatology Program Directors, Program Coordinators, clinical faculty, and trainees in Transplant Hepatology, Gastroenterology and Internal Medicine in understanding the changes occurring in Transplant Hepatology training and assessment. Attendees will develop a better understanding of competency-based medical education specifically learned from the experience of the GI/Transplant Hepatology pilot training program. They will be able to better Tyrosine Kinase Inhibitor Library ic50 understand the new Transplant Hepatology milestones and their use in assessing and evaluating trainees and reporting to ACGME. Attendees will be updated on the progress of the Next Accreditation System (NAS) and gain

a better understanding of its impact on Transplant Hepatology training and assessment beginning in July 2014, including a focus on the responsibilities of the Clinical Competency Committee and the need for faculty development in these areas. Learning Objectives: Describe the experience, progress and future developments of the GI/Transplant Hepatology pilot training program Identify the knowledge of the Transplant Hepatology milestones and how to apply them in the assessment and evaluation of trainees Describe the composition and role of the Clinical Competency Committee Prepare for the Next Accreditation System 12:30 – 12:40 PM Introduction Bruce A. Luxon, MD, PhD 12:40 – 1:00 PM The

Metformin manufacturer Next Accreditation System: Compliance for Transplant Hepatology Fellowships K. Gautham Reddy, MD 1:00 -1:20 PM Update on the GI/Transplant Hepatology Pilot Training Pathway Oren K. Fix, MD, MSc 1:20 – 1:40 PM Results of the Pilot Perceptions Survey and Perspectives from a Gastroenterology Fellow Dina Halegoua-De Marzio, MD 1:40 – 1:50 PM Discussion 1:50 – 2:05 PM Break 2:05 – 2:25 PM The Transplant Hepatology Training Landscape of the Future John R. Lake, MD 2:25 – 3:00 PM Panel Discussion and Q & A Steven K. Herrine, MD, K. Gautham Reddy, MD, Oren K. Fix, MD, MSc and Andrew Keaveny, MD 3:00 – 3:00 PM Panel Discussion and Q & A Andrew Keaveny, MD AASLD Postgraduate Course Friday, November 1 3:30 – 7:30 PM Hall E/General Session New Treatments in Liver Disease A New Era of Diagnostics, Therapeutics and Intervention in Hepatology COURSE DIRECTORS: Adrian M.