The following people have nothing to disclose: Claire Meyer, Sandeep K. Trip-athy Background. It is well known that liver and lung

injury can occur simultaneously during severe inflammation (e.g. multiple organ failure). However, whether these are parallel or interdependent (i.e. liver:lung axis) mechanisms is unclear. Previous studies have shown that chronic alcohol consumption greatly increases the risk of mortality caused by acute respiratory distress syndrome (ARDS). The potential contribution of subclini-cal liver disease driving this effect of ethanol on the lung has not been determined. Therefore, the purpose of this study was to develop a model of concomitant liver and lung injury in the setting of chronic alcohol exposure, followed by an acute inflammatory stimulus. Methods. Male mice were exposed to ethanol-containing Lieber-DeCarli diet or pair-fed control diet for 6w. At the end of the feeding period, some animals were administered LPS to induce selleck ARDS-like lung damage and sacrificed either 4 or 24 h after LPS exposure. The expression of cytokine mRNA in lung and liver tissue were determined by real-time PCR. Cytokine levels in the BAL and plasma were determined by Luminex assay. Changes in the ECM proteome of the liver and lung were determined by LC-MS. Results. As expected, the combination of EtOH and LPS caused liver injury, as indicated

by significantly increased levels of ALT/AST in the plasma. EtOH preexposure also increased the number and learn more size of inflammatory foci in the liver tissue caused by LPS. In the lung, EtOH preexposure

enhanced pulmonary inflammation and alveolar hemorrhage caused by LPS exposure. The combination of EtOH and LPS resulted in a unique pro-inflammatory mRNA expression profile in the two organs. As expected, eth-anol preexposure significantly increased hepatic TNFα mRNA expression and increased TNFα levels in the systemic circulation. In contrast, EtOH preexposure significantly increased pulmonary mRNA expression of the TNFα responsive genes MIP-2 and KC in the lung in the absence of a significant increase in TNFα mRNA or protein in lung tissue or BAL fluid, respectively. Additionally, EtOH exposure caused dynamic, transitional changes in the expression of ECM components (e.g. fibrin and fibronectin) in both the liver 上海皓元 and lung. Conclusions. EtOH pre-exposure enhanced both liver and lung injury caused by LPS. Enhanced organ injury corresponded with unique changes in the expression of pro-inflammatory cytokines in the liver (i.e. TNFα) and the lung (i.e. MIP-2, KC). EtOH preexposure also contributed to transitional changes in the ECM profile and increased expression of extracellular matrices which may play direct role in enhanced inflammation and injury in the two organs. Jesse Roman – Advisory Committees or Review Panels: Cellgene; Grant/Research Support: Actelion, Intermune, Novartis The following people have nothing to disclose: Veronica L.

However, in clinical trials, treatment-experienced patients, particularly those with cirrhosis, had suboptimal SVR rates. We assessed the efficacy and safety of sofosbuvir plus peginterferon find more and ribavirin (SOF+Peg-IFN+RBV) administered for 12 weeks to treatment-experienced patients with HCV genotypes 2 and 3, with and without cirrhosis. We enrolled 47 patients in this open-label, non-randomized, uncontrolled phase 2 study. The primary endpoint was the proportion of patients with sustained virologic response at 12 weeks after cessation of study treatment (SVR12). The overall rate of SVR12 was 89% (95% CI: 77–97). Rates of SVR12 were

higher in patients with genotype 2 than in those with genotype 3, 96% (95% CI: 78–100) and 83% (95% CI: 62–95), respectively. Rates of SVR12 were similar in patients with and without cirrhosis: for genotype 2, 93% of patients with cirrhosis and 100% of patients

without cirrhosis achieved SVR12, and for genotype 3, the SVR12 rate was 83% in patients both with and without cirrhosis. One patient discontinued study treatment because of an adverse event and four patients experienced serious adverse events. The most common adverse events were influenza-like illness, fatigue, anemia, and neutropenia. Conclusion: selleckchem In treatment-experienced patients with HCV genotypes 2 and 3, 12-week administration of SOF+Peg-IFN+RBV provided high SVR rates, irrespective of cirrhosis status. No safety concerns were identified. (Hepatology 2014;) “
“A 64-year-old woman presented to the Emergency Department with abdominal pain and vomiting. Her past medical record included rectal 上海皓元医药股份有限公司 cancer seventeen years ago managed with abdmino-perineal resection (Miles procedure). She also had hypertension, chronic obstructive pulmonary disease requiring home oxygen, hypercoagulable state due to prothrombin gene mutation and deep vein thrombosis on acenocumarol. On abdominal palpation a large parastomal hernia in left lower quadrant was present and the abdomen was diffusely tender. Investigations

showed: platelet count: 500000/microliter, INR: 4.14, D-dimer: 269.9 mg/L (normal range: 0-0.49), LDH: 486 U/l, AST: 57 U/l, GGT: 37 U/l and potassium: 5.8 mmol/l. The remaining parameters were normal. Abdominal CT showed severe gastric dilatation associated with a parastomal hernia that contained the gastric antrum (Figures 1 and 2). There was also thrombosis of celiac trunk, splenic infarctation and collateral circulation had developed in the gastrohepatic ligament. Gastric decompression was performed using a nasogastric tube and 2600 cc of a blood-stained gastric juice was drained. The parastomal hernia was manually reduced. Gastroscopy showed ischemic changes in the fundus and mid-third of the stomach was seen. No pyloric stenosis was present. Gastric mucosa biopsy showed edema, congestion and mild chronic inflammation. After 5 days, patient fully recovered with a normal oral intake. The patient refused surgical treatment and follow-up.

Sensorimotor input, in particular, depends upon getting information from healthy-uninjured joints, ligaments, muscles and skin [91]. Bleeding into joints and muscles with subsequent sequellae contributes to the relationship between injuries or degenerative joint disease and decreased

balance [93]. Taking an individualized approach to each patient is very important, because PWH may have balance impairments that are not only related to their bleeding disorder, but also as a function of normal ageing with decline in vision, proprioception [93], vestibular function, and the use of medication such as anti-depressants. Prescribing appropriate treatment for balance impairment Protease Inhibitor Library screening requires identifying the causes of the impairment itself. Thorough assessment is the fundamental element of a successful balance improvement programme. Several clinical tests have been developed and are commonly used in clinical practice such as the Timed Get Up and Go Test, Berg Balance Test and Functional Reach Test, while computerized balance testing systems are increasingly used for clinical evaluation

in countries that can afford them. A variety of exercises can be used to treat balance impairment, but the basic rule is to start with simple exercises and progress to more complex ones. The recommendation is to begin with stable surfaces such as lying on the hard floor, sitting on a rigid chair, kneeling and standing. Then, progressive exercises such as shifting weight from this website one leg to another, trunk rotations, arm/leg movements and blindfolding are added. In the later phase movable surfaces such as steppers, rehabilitation balls or balance boards are introduced. Patients should be educated

to exercise at home and those with significant balance impairment encouraged to utilize assistive devices such as walkers, crutches or canes. Limited joint function and muscle flexibility changes can alter posture and movement strategies. Muscle strength is necessary for maintenance and performance of proper movement, and good proprioception is needed to provide input about accurate joint or body position. If any of these important elements is impaired, all of them can contribute to balance impairment. In this case it is necessary to modulate exercise programmes to eliminate the basic problem, and then to treat the balance impairment, as balance is essential MCE公司 for performing daily activities and leading an independent life. Function represents all physical activities performed by a person, and exists between the level of body and participation, according to the International Classification of Functioning [94]. Basically, a person’s bodily condition will determine his physical achievements and strongly affects the way he will function in society. In dealing with PWH, we have to be aware of the difference between acute and chronic situations, and how these differences affect regular physiotherapy sessions.

Bleeding learn more lesions included Dieulafoy’s ulcer, Mallory- Weiss tear, duodenal ulcer, post surgical anastomosis bled and gastric ulcer after polypectomy. After basic life support was provided, all patients underwent emergent and elective endoscopy. Results: These comprised 49 (66.2%) males and 25 (33.8%) females. The mean age was 48.2 ± 6.4years for males and 40.6 ± 2.2years for females. Mallory-Weiss tear and Dieulafoy’s lesion constituted the majority of bleeding lesions 26 and 17 respectively requiring EBL. Other causes were: pre-pyloric ulcer 11; duodenal ulcer 9;

ulcers in antrum 5; post polypectomy bled 3; Anastomosis bleed 1; malignant lesions 2. Bleeding stopped after endoscopic therapy in 96.5% of patients. The single failure was in bleeding from a pre pylori lesion which was treated by using injection

sclerotherapy with 1:10000 adrenaline solution where EBL was not successful. GSK2118436 price Conclusion: EBL provides safe and effective modality for hemostasis in NVUGIB. EBL could be considered as a primary or alternative method of choice for treatment of endoscopic hemostasis in patients with NVGIB. Key Word(s): 1. haemostasis; ; 2. EBL; 3. NVUGIB; Presenting Author: ILZE KIKUSTE Additional Authors: ANITA LAOINA, KONRADS FUNKA, ALDIS RUTKIS, HERBERTS KURS, VIKTORS SAULE, PAVELS JANOVICS, MARCIS LEJA Corresponding Author: ILZE KIKUSTE Affiliations: University of Latvia; Riga East University Hospital; Riga East University medchemexpress Hospital; Riga East University Hospital Objective: The aim of the study was TO assess conventional white light gastroscopy findings in patients with changed serum pepsinogen

tests (high risk group) and calculate the sensitivity and specificity of endoscopy for the diagnosis of atrophy based on histological diagnosis of atrophy. Methods: The study was a subanalysis of a larger randomly selected cross-sectional sample of the general population in Latvia recruited from November 2008 to July 2009 with the primary objective of exploring cardiovascular risk factors. The selected individuals underwent a structured interview and blood sample collection. From the total number of 6000 invitees, in 3807 cases pepsinogen I (PgI) and pepsinogen II (PgII) was measured in plasma by Eiken (Eiken Chemical Co., Tokyo, Japan) pepsinogen test systems and PgI/PgII ratio was calculated. Patients with a PgI level <70 ng/ml and PgI/PgII ratio <3 (indicating any degree gastric mucosal atrophy) were invited for upper gastrointestinal cconventional white light endoscopy from January 2012 to July 2012. For adequate staging and grading of gastric mucosa atrophy, at least four non-targeted biopsies of two topographic sites (at the lesser and greater curvature, from both the antrum and the corpus) were taken and clearly labelled in separate vials; additional target biopsies of lesions were also taken.

5 months with serial measurements of HBV DNA, the authors found that HBV below 2000 IU/mL is a powerful (and unique) protective factor for both long-term Temsirolimus manufacturer low recurrence and overall survival. This study adds more data to answer three closely related questions on recurrence of HCC after surgical resection in hepatitis B patients: How important is the HBV viral load as the predictor of recurrence? What is the most desirable HBV DNA level?

Could anti-HBV treatment, either with interferon or nucleos(t)ide analogs, prevent the development of new HCC? First, this study revisits the critical question of whether ‘less HBV DNA (equals) less HCC recurrence’. Up to now, many factors (host, tumor and virus) have BAY 57-1293 in vitro been identified to predict HCC recurrence. Recognized host factors include older age, male gender, excessive alcohol drinking and presence of cirrhosis.6–9 Tumor factors include large tumor size,

multiple lesions, poor differentiation (higher alpha fetoprotein [AFP]), vascular invasion, microsatellite lesions and intrahepatic metastases. In addition, several studies have reported that viral factors, including HBV DNA virus load, genotype C, HBeAg and pre-core mutation, served as independent factors of cancer recurrence in HBV-related HCC patients.6–9 Among all of these factors HBV DNA level has consistently been identified as the most important factor, with the highest hazard ratio or risk ratio by multivariate regression analysis, not 上海皓元医药股份有限公司 only before HCC or at the time

of surgical resection,6,7 but more importantly after resection.5,8,9 In An’s and other cohort studies, HBV DNA was detected at 3-month intervals after surgery, and patients with persistently low serum HBV DNA (<2000 or <20 000 IU/mL) had a lower recurrence rate compared with patients with fluctuating or sustained high HBV DNA. Recently, several studies have reported on the relation of HBV DNA and the time of HCC recurrence after surgery.10,11 They found that high HBV DNA virus load was associated with late recurrence, especially 1 or 2 years after curative resection, while tumor factors were associated with early HCC recurrence always during the first year. Late recurrence of HCC is more likely induced by new tumor genesis other than dissemination of the primary HCC. Thus, an accurate description of HBV DNA after HCC resection would be: ‘lower sustained HBV DNA, lower HCC late recurrence’. Second, knowing that continuous lower HBV DNA favors clinical outcomes, what would be the desirable HBV DNA level to prevent long-term HCC recurrence? In An's study, it was shown that HBV DNA <2000 IU/mL was the cut-off value. This fits the REVEAL study with long-term follow-up of a total of 3653 individuals showing serum HBV DNA level >2000 IU/mL being a strong risk predictor of HCC independent of HBeAg, serum alanine aminotransferase level, and liver cirrhosis.

Only five SNPs showed a consistent significant association (P < 0.05). In another case-control population (507 cases and 215 controls), these SNPs were tested for association with HCC. However, only one SNP (rs17401966) was confirmed in this replication sample (P =

selleck inhibitor 3.9 × 10−5). Again, this finding could be replicated in another independent case-control population (751 cases and 509 controls) as well as by evaluation of the rs17401966 transmission status in 159 family trios (cases and their unaffected parents) with HBV-related HCC, which allows a family-based association test robust against population stratification (transmission disequilibrium test) for the presence of genetic linkage between a marker locus and a disease susceptibility locus. The combined analysis of the three independent case-control populations (1962 cases and 1430 controls) from different Chinese regions as well as the combination of these and the genome-wide association data (2310 cases and 1789 controls) provided evidence for a highly significant association of rs17401966 at a genome-wide level (P = 5.1 × 10−15 and P = 3.4 × 10−19, respectively). HCC risk was significantly reduced in the presence of the mutant [G] allele of the

rs17401966 SNP (odds ratio = 0.61; confidence interval = 0.55-0.67). Risk-allele frequencies were 19.3% in patients with HCC (n = 2310), 27.7% in non-HCC controls (n = 1,789), NVP-LDE225 and 31.4% in non-HBV carriers (n = 185). Pairwise linkage disequilibrium analysis (measured by r2) revealed a linkage disequilibrium block of about 244 kilobases mapping to chromosome 1p36.22,

flanking rs17401966, and spanning the genes KIF1B (encodes a kinesin superfamily member involved in the transport of organelles and vesicles), PDG (protein involved in the pentose phosphate metabolism), and the 3′-end of UBE4B (encodes ubiquitin MCE公司 conjugation factor E4 involved in multiubiquitin chain assembly). Multiple logistic regression analysis and haplotype analysis suggested that there might be a single susceptibility locus in this region, which was only attributable to rs17401966 (NM_015074.3: c.2537+518A>G), which is located in intron 24 of KIF1B. Regardless of the fact that the only common nonsynonymous SNP at this region (rs2297881) showed no disease association, it remains unclear whether rs17401966 is in linkage disequilibrium with a disease-causing mutation or whether the SNP itself has a direct influence on HCC development. The identified susceptibility locus on chromosome 1p36.22 lies in a region that has been identified to be commonly affected by chromosomal losses or gains in several malignancies such as colorectal cancer, breast cancer, neuroblastoma, and also in HCC.

Calcineurin inhibitors, including both tacrolimus and cyclosporine, have been associated with a dose-dependent increase in the posttransplant risk of HCC recurrence.6 Conversely, sirolimus has shown anticancer properties in in vitro and animal models, both alone or in combination with doxorubicin or sorafenib.7–12 Sirolimus PF-02341066 mouse can

prevent angiogenesis by interfering with vascular endothelium growth factor (VEGF)-mediated pathways in endothelial cells, thus limiting the growth of tumors,7 and also impacts established tumors, by inducing extensive microthrombi and so inhibiting tumor growth.9, 13 Although these animal data are clear, clinical studies are less convincing. We have demonstrated good outcomes with the use of sirolimus in a noncontrolled trial, and more recently the groups at the University of Colorado in Denver and Fudan University in Shanghai demonstrated better survivals in patients on sirolimus compared to control liver recipients.4, 14–16 Although all show similar trends, these retrospective studies included limited numbers of patients, and possible confounding variables could not be taken into account Doxorubicin in vivo due to the limited sample size. The present study is based on a large registry transplant population and evaluates the impact of immunosuppression on survival in an attempt to define the best posttransplant

treatment combination for HCC patients. AFP, alpha fetoprotein, HCC, hepatocellular carcinoma; HBV, hepatitis B virus;

HCV, hepatitis C virus; HR, hazard ratio; 上海皓元医药股份有限公司 HRSA, Health Resources and Services Administration; MELD, Model for End-Stage Liver Disease; OPTN, Organ Procurement and Transplantation Network; SRTR, Scientific Registry of Transplant Recipients; TTV, total tumor volume; UNOS, United Network for Organ Sharing. This study analyzed data from the Scientific Registry of Transplant Recipients (SRTR). The SRTR data system includes data on all donors, wait-listed candidates, and transplant recipients in the United States, submitted by the members of the Organ Procurement and Transplantation Network (OPTN), and has been described elsewhere.17 The Health Resources and Services Administration (HRSA), US Department of Health and Human Services, provides oversight to the activities of the OPTN and SRTR contractors. The study was reviewed and approved by the Health Research Ethics Board at the University of Alberta. The study population included all adult (≥16 years) patients who received an isolated liver transplantation from March 2002 to March 2009. In order to ensure that all subjects had a significant exposure to the drugs, only individuals kept on the same maintenance immunosuppression protocol for at least 6 months posttransplant (or until death) were further selected. Overall, 25,201 out of 39,859 patients receiving a liver transplant during the study period were excluded.

Methods Bile duct ligation (BDL) was performed on wildtype rats, which received

atorvas-tatin (15mg/kg*d) for click here one week starting at one, two, three, four and five weeks after BDL (T1-T5), while controls remained untreated. Hepatic fibrosis was analyzed by immunohisto-chemistry and hepatic hydroxyproline content. TGFβ levels were measured by RT-PCR. Proteolytic activity of MMP-2 was examined by zymography. Levels of type I, III, IV and VI collagen degradation by MMP activity (C1M, C3M, C4M and C6M) and formation of type III and IV collagen (PRO-C3 and P4NP7S) markers were assessed by specific ELISAs in serum probes. Results Serum markers of ECM neo-epitopes reflected significantly the remodelling of the ECM in the liver and were able to distinguish between early (T1-T3) and severe fibrosis (T4-T5). Statin treatment was associated with significantly lower levels of neo-epitopes, especially when therapy was initiated in the stage of severe fibrosis (T4-T5). Furthermore, the neo-epi-tope markers were correlated to hepatic expression of profi-brotic cytokines TGFb1 and TGFb2. The formation markers PRO-C3 and P4NP7S as well as degradation markers C4M and C6M correlated significantly with

MMP-2 activity in rats with severe fibrosis. Discussion Determination of ECM neo-epitopes in serum allowed us to distinguish between mild and severe fibrosis and to assess ECM remodeling. With respect to the results during Fulvestrant concentration statin therapy, neo-epitopes might serve as read-out for efficacy of anti-fibrotic treatment. Disclosures: Diana J. Leeming – Employment: Nordic Bioscience Mette J. Nielsen -Grant/Research Support: Nordic Bioscience A/S Morten A. Karsdal – Stock 上海皓元医药股份有限公司 Shareholder: Nordic Bioscience The following people have nothing to disclose: Robert Schierwagen, Sabine Klein, Tilman Sauerbruch, Aleksander Krag, Jonel Trebicka BACKGROUND/AIMS:

LOXL2 is a key enzyme that promote-scross-linking of collagen type I and is expected to be a novel therapeutic target for liver fibrosis. The efficacy of LOXL2 inhibitor on panlobular fibrosis has been previously demonstrated in hepatotoxin-induced models, however the efficacy in biliary-type fibrosis is not known. We studied the therapeutic efficacy of a novel anti-LOXL2 monoclonal antibody in two mouse models of primary sclerosis cholangitis (PSC)-like biliary fibrosis. METHODS: We developed an improved mouse model resembling human PSC with rapidly progressive fibrosis and early-onset portal hypertension by backcrossing the Mdr2 mutation on a fibrosis susceptible background (BALB/c). Anti-LOXL2 therapeutic antibody (AB0023mAB, 30mg/kg) or control antibody (M64, 30mg/kg) were administered i.p. twice a week in Mdr2-/-.BALB/c mice (n = 10 per group) from age 4 weeks to 8 weeks, and in C57BL/6 mice fed 3,5- diethoxycarbonyl- 1,4-dihydrocollidine (DDC)- diet for 4 weeks (n=9-11 per group).

J. Lenting and K. Mertens, unpublished observations). Given the observation that VWF prevents binding of the FVIII procofactor to many of the FVIII receptors, it is possible that increased FVIII expression levels in the presence of VWF could partially be explained by VWF preventing re-uptake of FVIII by the producing cell. Provided that FVIII

escapes re-uptake by the cell, it is quickly captured into a complex with its carrier VWF [80]. VWF is crucial in maintaining FVIII plasma levels, which is illustrated by the severely reduced FVIII levels in patients that lack circulating VWF (e.g. von Willebrand disease type 3). The notion that FVIII levels are also reduced in cases of impaired complex formation (e.g. von Willebrand disease BMN 673 chemical structure type 2N) demonstrates that VWF protection is only valid when VWF and FVIII are circulating in the complex. Within this complex, VWF may prolong survival of FVIII in the circulation by preventing the interaction of FVIII with its clearance receptors. It is of importance to realize that this protection is not absolute! First, complex formation between FVIII and VWF follows the laws of thermodynamics in that the amount of FVIII that is in the complex is determined by the affinity constant for complex formation and the

concentrations of the individual proteins. Indeed, it has been reported that while the majority PDGFR inhibitor of FVIII (92–95%) is in complex with VWF, a small but significant portion (2–5%) circulates as free FVIII protein [81,82]. This portion is therefore susceptible to clearance by the various receptors. Second, the possibility exists that conditions at the cellular surface influence the stability of the FVIII/VWF complex, favouring its dissociation. For instance, Sarafanov et al. [70] proposed that the VWF/FVIII complex is 上海皓元医药股份有限公司 bound to HSPG at the cellular surface, resulting

in dissociation of the complex. Subsequently, FVIII is transferred to LRP1, whereas VWF is released back into the circulation. Meijer et al. [83] have recently presented a similar concept, based on studies using fluorescent FVIII-fusion proteins. Their observations differed from those by Sarafanov et al. [70] in that the complex only dissociated at the cellular surface following conformational changes within the VWF molecule. Taken together, the influence of VWF on FVIII clearance is apparently more complex and less straightforward than previously anticipated. What adds to this complexity is that FVIII may also be subject to clearance as part of the VWF complex. The multimeric VWF protein is subject to clearance as well, and it seems conceivable that a substantial part of FVIII is cleared while being bound to VWF. In support of this possibility is our observation that VWF and FVIII co-localized into similar cells, when injected as a complex into VWF-deficient mice [84]. This may seem in contradiction with some observations that VWF interferes with FVIII internalization by a number of cell types [32,33,83].

Although many of them are benign, a significant percentage are premalignant. Currently, endosonography (EUS) and fine needle aspiration (FNA) makes morphology and cytopathology analysis of cyst fluid for pancreatic

selleck compound cystic lesion possible. By these techniques pre- operative differentiation of benign from malignant or potentially malignant pancreatic cystic lesions can be done with 80% accuracy. Methods: In 68 patients with pancreatic cysts, we studied demographic information and the results of EUS imaging, the cystic cytopathology and analysis of cystic fluid amylase and CEA levels. Results: Sixty eight patients were included in the study with an average age of 51 years. Forty six patients were female (68%). Analysis of the lesions were performed based on the cytology findings as well as the other results (CEA, Amylase, cyst morphology, and history of pancreatitis). Patients with pseudo cysts with an average age of 41.4 years, were the youngest of the study population, and those with cystic adenocarcinoma were the oldest with an average age of 61.7 years. the most common types of lesions were 26.5% pseudo cysts (n = 9), 16.2%MCN (n = 11), 14.7% SCA (n = 10), 13.2% IPMN (n = 9)

and 13.2% cystic adenocarcinoma (n = 9). The most common locations of cysts were 35.2% in Enzalutamide molecular weight the head (n = 25). With the exception of the neuroendocrine tumors, all other types of lesions were more MCE common in females than males. The most septations in the cysts were observed in

the cystic adenocarcinomas, SCA, and IPMN. Lesions smaller than 2 cm occurred most frequently in IPMN, while pseudo cysts were all greater than 2 cm. Conclusion: Forty seven percent of patients in this study had malignant or premalignant lesions, who despite being asymptomatic, need routine follow-ups or surgery. Endosonography plays an important role in the diagnosis and treatment of the cystic tumors of the pancreas. Diagnosing premalignant lesions and providing the appropriate treatment increases patient’s survival and the diagnosis of benign cysts, leads to fewer unnecessary surgeries. Key Word(s): 1. serous cystadenoma; Presenting Author: MARC GIOVANNINI Additional Authors: FABRICE CAILLOL, ANNE-ISABELLE LEMAISTRE, BERTRAND PUJOL, BERTRAND NAPOLÉON Corresponding Author: MARC GIOVANNINI Affiliations: Institut Paoli Calmettes; Hôpital privé Jean Mermoz Objective: Needle-based Confocal Laser Endomicroscopy (nCLE) is an imaging technique, which enables microscopic observation of solid organs, in vivo and in real-time, during an EUSFNA procedure.