Until further data are available, i.v. infusion of high-dose PPI after endoscopic treatment of bleeding peptic ulcers remains the most studied and best proven strategy. “
“Hirschfield GM, Liu X, Han Y, Gorlov IP, Lu Y, Xu C, et al. Variants at IRF5-TNPO3, 17q12-21

and MMEL1 are associated with primary biliary cirrhosis. Nat Genet 2010;42:655-657. (Reprinted with permission.) We genotyped individuals with primary MAPK Inhibitor Library cell line biliary cirrhosis and unaffected controls for suggestive risk loci (genome-wide association P < 1 × 10−4) identified in a previous genome-wide association study. Combined analysis of the genome-wide association and replication datasets identified IRF5-TNPO3 (combined P = 8.66 × 10−13), 17q12-21 (combined P = 3.50 × 10−13) and MMEL1 (combined P = 3.15 × 10−8) as new

primary biliary cirrhosis susceptibility loci. Fine-mapping studies showed that a single variant accounts for the IRF5-TNPO3 association. As these loci are implicated in other autoimmune conditions, these findings confirm genetic overlap among such diseases. Liu X, Invernizzi P, Lu Y, Kosoy R, Lu Y, Bianchi I, et al. Genome-wide meta-analyses identify three loci associated with primary biliary cirrhosis. Nat Genet 2010;42:658-660. (Reprinted with permission.) A genome-wide association screen for primary Selleck Cabozantinib biliary cirrhosis risk alleles was performed in an Italian cohort. The results from the Italian cohort replicated IL12A and IL12RB associations, and a combined meta-analysis using a Canadian dataset identified newly associated loci at SPIB (P = 7.9 × 10−11, odds ratio (OR) = 1.46), IRF5-TNPO3 (P = 2.8 × 10−10, OR = 1.63) and GPX6 17q12-21 (P = 1.7 × 10−10, OR = 1.38). The 2009 publication of the first genome-wide association study (GWAS) of primary biliary cirrhosis (PBC)

represented a key point in the evolution of our understanding of the genetic basis and thus pathogenesis of this disease.1 This landmark study identified, in a reproducible fashion, genetic associations between PBC and human leukocyte antigen as well as polymorphisms in the genes encoding the interleukin-12 (IL-12) α-chain and the IL-12 receptor β-chain. Two recent publications from Canadian, American, and Italian groups add an important further dimension to our knowledge base with respect to the genetic basis of PBC and build on the original study.2, 3 Taken together, these two new studies replicate the original genetic associations with the IL-12 pathway, and importantly, through individual and combined analyses, they identify further associated loci. Critically, the newly identified loci are again associated with the biology of the interaction between antigen-presenting cells (APCs) and CD4+ T cells, which is thought to be critical to the development of the autoreactive immune responses underpinning PBC.4 The advent of these new data make now a good time to reflect on what we now know and to identify potential future directions for research.

“
“We present results from a field study of inorganic carbon (C) acquisition by Ross Sea phytoplankton during Phaeocystis-dominated early season blooms. Isotope disequilibrium experiments revealed that HCO3− was the primary inorganic C source for photosynthesis in all phytoplankton assemblages. From these experiments, we also Ceritinib manufacturer derived relative enhancement factors for HCO3−/CO2 interconversion as a measure of extracellular carbonic anhydrase activity (eCA). The enhancement factors ranged

from 1.0 (no apparent eCA activity) to 6.4, with an overall mean of 2.9. Additional eCA measurements, made using membrane inlet mass spectrometry (MIMS), yielded activities ranging from 2.4 to 6.9 U · [μg chl a]−1 (mean 4.1). Measurements of short-term C-fixation parameters revealed saturation kinetics with respect to external

inorganic carbon, with a mean half-saturation constant for inorganic carbon uptake (K1/2) of ∼380 μM. Comparison of our early springtime results with published data from late-season Ross Sea assemblages showed that neither HCO3− utilization nor eCA activity was significantly correlated to ambient CO2 levels or phytoplankton taxonomic composition. We did, however, observe a strong negative relationship between surface water pCO2 and short-term 14C-fixation rates for the early season survey. STA-9090 supplier Direct incubation experiments showed no statistically significant effects of pCO2 (10 to 80 Pa) on relative HCO3− utilization or eCA activity. Our results provide insight into the seasonal regulation of C uptake by Ross Sea phytoplankton across a range of pCO2 and phytoplankton taxonomic composition. “
“Stratospheric

Tyrosine-protein kinase BLK ozone depletion increases the amount of ultraviolet-B radiation (UVBR) (280–320 nm) reaching the surface of the earth, potentially affecting phytoplankton. In this work, Anabaena sp. PCC 7120, a typically nitrogen (N)-fixing filamentous bloom-forming cyanobacterium in freshwater, was individually cultured in N-deficient and N-enriched media for long-term acclimation before being subjected to ultraviolet-B (UVB) exposure experiments. Results suggested that the extent of breakage in the filaments induced by UVBR increases with increasing intensity of UVB stress. In general, except for the 0.1 W · m−2 treatment, which showed a mild increase, UVB exposure inhibits photosynthesis as evidenced by the decrease in the chl fluorescence parameters maximum photochemical efficiency of PSII (Fv/Fm) and maximum relative electron transport rate. Complementary chromatic acclimation was also observed in Anabaena under different intensities of UVB stress. Increased total carbohydrate and soluble protein may provide some protection for the culture against damaging UVB exposure. In addition, N-deficient cultures with higher recovery capacity showed overcompensatory growth under low UVB (0.1 W · m−2) exposure during the recovery period.

5). We also determined the effects of EGCG analogues, including EC, ECG, and EGC, on DNR-mediated growth inhibition (Fig. 3C). ECG, which like EGCG also inhibits CBR1 LDE225 in vitro, showed significant enhancement of DNR-mediated cell growth inhibition in both HepG2 (P < 0.01) and SMMC7721 (P < 0.05), whereas EGC and EC, which weakly inhibited CBR1 in vitro, did not show an obvious synergic effect with DNR. Thus, there is a

correlation between the inhibition of CBR1 and the enhancement of DNR-mediated tumor cell growth by EGCG and its analogues. We next examined the effect of EGCG on DNR-induced G2/M cell cycle arrest by fluorescence-activated cell sorting analysis. As shown in Fig. 3D and Supporting Information Fig. 6A, DNR treatment of cells induced a reduction of the cell number in the G1 phase and a corresponding increase in the G2/M phase population. In contrast, 10 μM EGCG alone had no effect on the cell cycle progression. However, a combination of 10 μM EGCG and 0.04 μM DNR resulted in an increase in the percentage of G2/M cells from 52.8% (DNR alone) to 62.4% (EGCG and DNR) in HepG2 NVP-BKM120 in vitro cells. For SMMC7721 cells, EGCG and 0.03 μM DNR induced a 10.4% increase in cells in the G2/M

phase versus DNR alone. EGCG was thus capable of enhancing the DNR-induced G2/M cell cycle arrest, and this reflected the ability of EGCG to enhance the inhibition of cell proliferation by DNR. We also examined the effect of EGCG on DNR-induced apoptosis with flow cytometry (Fig. 3E and Supporting

Information Fig. 6B). EGCG alone at 20 μM did not induce apoptosis. However, EGCG at the same concentration increased DNR-induced apoptosis from 36.4% to 45.2% in HepG2 cells. For SMMC7721 cells, the percentage of apoptosis increased from 12.8% (DNR alone) to 17.2% (DNR and EGCG). These results strongly suggest that EGCG is capable of enhancing the antitumor activity of DNR. To further verify that the synergic effect of EGCG with DNR is mediated by CBR1, we generated Hep3B-CBR1 cells stably expressing CBR1 and control Edoxaban Hep3B cells stably transfected with empty pcDNA3.1(-)/myc-HIS vector (pcDNA). The ectopic expression of CBR1 was confirmed by western blotting in Hep3B-CBR1 cells (Fig. 4A). Hep3B-pcDNA cells and Hep3B-CBR1 cells were treated with DNR, EGCG, or EGCG and DNR. As shown in Fig. 4B, the treatment of Hep3B-pcDNA cells with 0.4 μM DNR led to 34.4% cell viability in comparison with the untreated cells, whereas the cell viability of Hep3B-CBR1 was 52.9%. Hep3B-CBR1 cells were more resistant to DNR than Hep3B-pcDNA, whereas no differences were observed for these two lines in their resistance to 5-fluorouracil (5-FU; P > 0.05; Fig. 4C). The treatment of Hep3B-CBR1 cells with EGCG and 0.4 μM DNR decreased the cell viability from 52.9% to 39.0% (P < 0.01; Fig. 4B).

Similarly, information collated check details about the secondary ITT schedule (pdVWF/FVIII) comprised: inhibitor titres at rescue, bleeding frequency, concomitant therapy, and complications relating to access. Importantly, 5 of 11 patients were from our institution and therefore had the same threshold for switching from rFVIII to pdVWF/FVIII. Data for these five patients are presented in Table 6. Within the study timeframe, one boy (patient number 4) was tolerized and had normal recovery with a consistently negative inhibitor titre; the patient had no bleeds and did not require bypassing agents. Among the other four patients, inhibitor

titres were low after approximately 2 years of follow-up; two of

these four patients (numbers 2 and 5) had reasonable recovery, such that bleeds could be treated with FVIII rather than bypassing agents. No patients required bypassing agents during the study period. Interestingly, one boy (patient number 1) had a Haemophilia Joint Health Score of 0, even though he had click here had inhibitor present for approximately 6 years. All five patients required some form of immunosuppressive therapy, and the most rapid, positive results manifested in the two boys who switched from rFVIII to pdVWF/FVIII at the same time as they received a course of rituximab. Currently, four of the five patients treated with pdVWF/FVIII ITT at our institution remain on pdVWF/FVIII with normal or near-normal recovery: FVIII levels are detectable at 48 h post-dose. Three of the five patients do not require bypassing agents, and three of the five have also had no spontaneous bleeds. One boy has an inhibitor level of

approximately 2 BU, but has measurable FVIII at 48–72 h postdose. One boy has switched to treatment with FVIII inhibitor bypassing activity (FEIBA) and is experiencing DOK2 more frequent bleeding than during high-dose ITT. None of the five boys was tolerized, according to the definition employed in the International Immune Tolerance Study [30]. Thus, overall, the important conclusion can be drawn that high-dose ITT with pdVWF/FVIII is markedly effective in preventing bleeds, but tolerization with such therapy on its own did not seem to work in this small cohort of boys with very resistant inhibitors. The authors received an honorarium from Grifols S.A. for their participation in the symposium and production of the article. The authors thank Content Ed Net for providing valuable editorial assistance in the preparation of the article; funding for this assistance was provided by Grifols S.A. “
“Summary.  Gene therapy of haemophilia has been initiated through a number of approaches including expression in muscle, liver and omental implanted fibroblasts, or i.v. injection of an expression construct under the control of a ubiquitous promoter.

Oral triptans may not be the optimal therapy in the presence of migraine-associated gastroparesis because these agents rely on gastric motility and gastrointestinal absorption and may be ineffective or slowly or inconsistently effective in the presence of gastroparesis. Similarly, nasal spray preparations are not wholly absorbed in the nasal passages. Sprays

often enter the LEE011 nasal pharynx and are swallowed, so they, too, depend in part on gastrointestinal absorption. Most of the therapeutic challenges presented by gastrointestinal signs and symptoms of migraine relate to the impact of these signs and symptoms on drug delivery. Nausea delays drug delivery by causing patients to delay taking oral medications. Gastroparesis delays drug delivery via an impact on drug absorption. Vomiting prevents drug delivery through expulsion of medication. Nonoral drug delivery routes that negate or minimize the impact of gastrointestinal signs and symptoms selleck screening library should be useful in overcoming these challenges. The choice of nonoral drug delivery routes should be customized to the individual patient and migraine attack. Strengths and limitations of triptan delivery systems are listed in the Table.[12] Sumatriptan injection is rapidly effective but appears to have a greater side effect burden than other triptan formulations[12] – probably because the injection produces higher maximal concentrations

than the other forms. Moreover, many patients dislike using injections. Triptan nasal sprays, besides relying in part on gastrointestinal absorption, have a bitter taste, which can be particularly adverse for patients experiencing nausea and/or vomiting.[12] The bitter or bad taste can lead the patient to delay or avoid treatment. Health care providers need to work with their patients to address the still-all-too-frequent problem of treatment failure in migraine. First, health care providers need to have greater appreciation of the importance of nausea, vomiting, and gastroparesis as Montelukast Sodium factors affecting

migraine prognosis and treatment success. Second, health care providers need to systematically assess migraine patients for gastrointestinal signs and symptoms. Finally, patients and health care providers need to be willing to practice customized migraine care, in which patients tailor the treatment and formulation to the characteristics and context of the individual migraine episode. Support for the viability of formulation-based, customized care comes from studies conducted in clinical practice, where patients given the flexibility to choose among triptan formulations to manage their migraines did not restrict themselves to one formulation but instead chose a formulation best suited to the characteristics of the individual migraine episode.[26, 27] The author acknowledges Jane Saiers, PhD (The WriteMedicine, Inc.), for assistance with writing the manuscript. Dr. Saiers’ work was funded by NuPathe Inc. “
“Objective.

” All the data are needed, including safety and conflicts of interest, and clinically relevant measures of efficacy, both while on and following withdrawal from therapy. Results must be clinically meaningful, reproducible, and understandable. Only then can organizations such

as the Cochrane Collaboration reliably estimate the benefit of new therapies. Approval of new drugs is a huge commitment for government agencies. Because many are for the same disease, “cost-effectiveness analysis” has become a “business of its own” used not only by treating physicians, but also health-insurance agencies and stockbrokers. In Britain, where selleck kinase inhibitor government promises “universal” access to treatment, the National Institute for Health and Clinical Excellence was established partly to assess cost-effectiveness of new treatments and technologies and unify access across all health districts.8 The downside of limiting access to agents not shown to be cost-effective is their unavailability to specific individuals anxious for a reprieve from fatal illness (e.g., sorafenib), if only for a few months.9 Thereby, a conflict arises between what is cost-effective for a population and that which is not cost-effective, but still has seemingly tangible benefits for an individual. Though some

of these expensive Pexidartinib medications may make only minor differences in life expectancy, with time, these small, incremental advances may eventually lead to dramatic improvements in outcome (e.g., treatments for breast cancer). This review focuses Staurosporine cell line first on some mistakes and/or misinterpretations of clinical trials since the 1970s that may have interfered with the production of reliable data (for the most part, from my own experiences). An RTC is the most rigorous assessment of a new agent’s

therapeutic effect. Randomization is now done in blocks of 4, 6, 10, and so on, depending on expected recruit numbers. When possible, both patient and investigator should be blinded to the randomization. In terms of clinical-trial expertise, I was very naïve in 1968, when part of my job was to monitor patients in follow-up in the 5-year trial of azathioprine for primary biliary cirrhosis (PBC). Neither single nor double blinding had been considered in the trial design, and no formal patient-evaluation process had been outlined! Fortunately, there were only 45 recruits—we had not calculated the sample size needed to show a difference in outcome (i.e., death) at 5 years! All documentation was with pen and paper. Every result had to be accurately transferred from many different sheets of paper, thereby limiting the reliability of the reporting—desktop computers did not exist back then.

Although guidelines suggested some regimens for the third therapy,2 the optimal third therapy has not been established. To determine the optimal third therapy we have to know the resistance/susceptibility of the

bacteria to antibiotics. However, it has not been proposed for the patients having multiple-antibiotic-resistant Selleckchem Neratinib H. pylori infection. In addition, CYP2C19 genotype is important in designing optimal regimen for each patient in PPI-based combination therapy.3 We experienced a suggestive case with multiple-antibiotic-resistant H. pylori infection that was successfully treated with susceptible drugs with optimal dose of PPI according to the profiles of antibiotics resistance/susceptibility test and CYP2C19 genotype, by designing a tailor-made regimen modified from the classical quadruple therapy.1,4 A 44-year-old

woman who sometimes felt mild epigastralgia and was suspected of having a gastric ulcer scar on mass screening for gastric cancer with barium X-ray examination in 2006, underwent upper gastrointestinal endoscopy at Inoue Clinic, Moriyama, Shiga, Japan. The diagnosis was chronic gastritis without peptic ulcer or scar. She had a this website history of operation for acute peritonitis because of acute appendicitis at age 12 years, and chronic rhinitis for recent 10 years approximately. In 2008, she had a urea breath test and was found to be H. pylori-positive, for which she was given the standard first eradication therapy in Japan (lansoprazole [LPZ], AMPC and CAM for 7 days) (Table 1).2 However, the treatment failed to eradicate the infection and the recommended second therapy of rabeprazole (RPZ), AMPC, and MNZ for 7 days was prescribed (Table 1).2 It also failed, so she underwent endoscopy to obtain biopsy specimens from the stomach for bacterial culture and drug susceptibility test Methocarbamol using the agar dilution method. Breakpoints of AMPC and CAM were applied according to the criteria of the Japanese Society

of Chemotherapy5 and the breakpoint of MNZ was obtained from the literature.6 The minimum inhibitory concentrations (MICs) showed the bacteria were both CAM- and MNZ-resistant and non-sensitive to AMPC (Table 2), so the patient was referred to the Department of Medicine/Gastoenterology, Social Insurance Shiga Hospital, Otsu, Shiga, Japan. At that time, she refused a test for CYP2C19 genotype or another endoscopic examination to obtain tissue samples for bacterial culture to search other antibiotics to which the bacterial strains would be susceptible. So we had to decide the next regimen empirically. Because the strains of the cultured bacteria were not sensitive to the antibiotics that are used in the standard eradication therapies, other antibiotics had to be used, but that can create new antibiotic-resistant strains, namely, multiple-antibiotic-resistant bacteria.

For this purpose, mice received 30 μg total plasmid DNA (8 μg pT/KRas-G12V, 8 μg pT3/EF1α-myrAkt1,

pT3/EF1α-shRp53, and 6 μg pPGK-SB13) in 0.9% saline at a final volume of 10% of the animal’s this website body weight by tail vein injection within 5 seconds. At the time of tumor development (palpable tumors occurred at 6-10 weeks postinjection), mice were sacrificed and tumors were harvested for subsequent isolation of immortalized cell lines. Isolated tumors were dissected and incubated for 30 minutes at 37°C in RPMI1640+Glutamax (Life Technologies) supplemented with 200 μg/mL of collagenase IA, collagenase IV, and hyaluronidase IV, 300 μg/mL dispase, and 50 μg/mL DNase I (Sigma). Separated cells were purified using a 40-μm strainer, washed once, and were then cultured in DMEM+Glutamax with 10% FCS (Life Technologies) and penicillin/streptomycin (Seromed) at 37°C in 5% CO2. Cells were cultivated for at least 4 weeks (eight passages) to reduce the content

of fibroblasts and subsequently subcloned by limiting dilution. After 2-3 weeks of cultivation, several single-cell clones showing epithelial morphology were selected and expanded for subsequent classification and functional experimentation. Deletions of MAVS, IRF3, and IFNAR genes were confirmed by polymerase chain reaction (PCR). For detailed information on plasmids, see the Supporting Materials and Methods. All mouse experimental HSP activation work was performed at TWINCORE in compliance with animal welfare regulations. Methods for in vitro transcription and electroporation of HCV RNA are described elsewhere[2] and were employed with the minor Baf-A1 manufacturer modification that 4 × 106 cells were transfected

and 4 × 105 cells were seeded onto 6-well culture plates. To inhibit HCV replication or to analyze dependence on cyclophilin A, medium was supplemented with 500 U/mL mouse IFNα-1 (PBL Interferon Source, Piscataway, NJ), 5 μg/mL of the HCV polymerase inhibitor 2′-C-methyladenosine (2′CMA) or increasing doses of the cyclophilin inhibitor cyclosporine A (CsA, Sigma) 4 hours posttransfection. Cells and supernatants were harvested at 4, 24, 48, and 72 hours postelectroporation. In order to determine particle release, supernatants were used to infect naive Huh-7.5 cells. Luciferase activity of reporter viruses was analyzed as described elsewhere.[2] Infectivity of WT HCV particles was titrated by a limiting dilution assay (TCID50) as described previously.[2] Additional methods are posted as online Supporting Information. In human liver cells, HCV replication is sensed by host-derived pattern recognition receptors. These include retinoic acid inducible gene I-like (RIG-I), which signals by way of MAVS to induce translocation of IRF-3 into the nucleus and activation of the IFN-beta promoter. In turn, secreted IFN-beta binds to the type I interferon receptor (IFNAR) and downstream signaling induces gene expression of numerous interferon stimulated genes (ISGs) which establish an antiviral state.

UPR is activated during pancreatitis to restore ER homeostasis. Although www.selleckchem.com/products/AZD1152-HQPA.html protein kinase RNA-like ER kinase (PERK) is associated with the UPR through phosphorylation of eukaryotic initiation factor 2-alfa (eIF2-a), the role of PERK signaling pathway in pancreatitis is not fully clarified. We investigated the significance of PERK signaling pathway in severe acute pancreatitis in mice using an elF2-a dephosphorylation inhibitor, salubrinal. Methods: Severe acute pancreatitis was induced by intraperitoneal injection of cerulein (CER) at a dose of 50 mg/kg six times at 1 hour

intervals. Moreover, LPS was administered at a dose of 10 mg/kg as the septic challenge immediately after the completion of CER injections. Salubrinal was administered intraperitoneally immediately after LPS injection and six hours later. Mice were sacrificed at 24 hours after the first injection of CER and the severity of pancreatitis was histologically graded with a scoring system.

Serum amylase and proinflammatory cytokine levels were measured. Expression of ER stress-related proteins was examined by western blotting. Results: The severity of pancreatitis in mice treated with salubrinal was significantly attenuated compared with control Venetoclax manufacturer mice. Serum amylase and proinflammatory cytokine levels were lower in salubrinal-treated mice than those of control mice. Expression level of 78 kDa glucose regulated protein (GRP78), activating transcription factor 4 and phosphorylated eIF2-a protein were elevated in mice

treated with salubrinal compared with control groups. Conclusion: Inhibition of eIF2-a dephosphorylation decreased ER stress and reduced severe acute pancreatitis in mice. Augmentation of PERK signaling pathway could be a potential therapeutic option for the treatment of acute pancreatitis. Key Word(s): 1. ER stress salubrinal pancreatitis PERK signaling Presenting Author: RAVINDRA L SATARASINGHE Additional Authors: DILUMI ATIGALA, NARMATHEY THAMBIRAJAH, CHAMPIKA GAMAKARANAGE, SACHITH C WIJESIRIWARDENE Corresponding Author: RAVINDRA L SATHARASINGHE Affiliations: Sri Jayawardenepura General Hospital, Sri Jayawardenepura General Hospital, Sri Jayawardenepura General Hospital, Sri Jayawardenepura DNA ligase General Hospital Objective: To study the clinical profile of adult Sri Lankans admitted to a tertiary referral centre having acute pancreatitis Methods: Case notes of patients who were diagnosed as having acute pancreatitis admitted to Sri Jayawardenepura General Hospital, Sri Lanka from 1.1.2011 to 31.12.2013, were retrospectively analysed to obtain the required data. Results: There was a total of 55 patients with an age range of 17 to 84 years, with a mean of 39.5 ± 15.3 SD years. The sex ratio was male:female −10 : 3, with females having a mean age of 48.2 ± 16.3 SD years, and males having a mean age of 38.1 ± 14.

Six patients died of pancreatic cancer, and 9 patients died from other illness. The 5-year survival rate stratified with or without HS at the latest examination and with concomitant PDAC were 98.3%,

90.5% and 57.1%. The prognosis of the patients with developing PDAC was significantly poor. Conclusion: The malignant transformation of IPMN is not uncommon. We need to concern about developing concomitant PDAC for surveillance of IPMNs. Key Word(s): 1. IPMN; 2. EUS; 3. guideline Presenting Author: NAOKI OKANO Additional Authors: YOSHINORI IGARASHI, SEIICHI HARA, KENSUKE TAKUMA, ITARU KAMATA, YUI KISHIMOTO, TAKAHIKO MIMURA, KEN ITO Corresponding Author: AZD0530 NAOKI OKANO Affiliations: Toho University Omori Medical Center, Toho University Omori

Medical Center, Toho University Omori Medical Center, Toho University Omori Medical Center, Toho University Omori Medical Center, Toho University Omori Medical Center, Toho University Omori Medical Center Objective: Recently endoscopic ultrasonography-guided fine-needle aspiration (EUS-FNA) has been performed widely for pathological diagnosis of pancreatic carcinoma. This study aimed to evaluate the AP24534 chemical structure value of cytological diagnosis by ERCP and EUS-FNA for pancreatic carcinoma. Methods: Between June 2011 and March 2014, seventy patients who were Methisazone suspected to have a pancreatic mass by conventional ultrasonography, computed tomography and magnetic resonance imaging were enrolled. Pancreatic duct brushing cytology and/or pancreatic juice cytology sampling by ERCP (ERCP group) and EUS-FNA were performed for the cytological diagnosis of pancreatic

tumor (EUS-FNA group). Results: Final diagnosis were pancreatic carcinoma in 62, autoimmune pancreatitis in 5 and chronic pancreatitis in 3. Successful sampling rate of ERCP group was 97% and that of EUS-FNA group was 97% in case of pancreatic carcinoma. Overall result; the sensitivity, specificity and accuracy were 45%, 100% and 51% in the ERCP group. In contrast the sensitivity, specificity and accuracy were 81%, 100% and 83% in the EUS-FNA group. With regard to complications, pancreatitis occurred in eight patients, severe in one, in the ERCP group. Fever occurred in two patients in the EUS-FNA group. There were significant difference on the sensitivity, accuracy and complication rate in the both groups (P < 0.01). Conclusion: EUS-FNA is more sensitive and safer for the cytological diagnosis of pancreatic carcinoma. EUS-FNA should be considered as the initial examination when a patient is suspected for pancreatic carcinoma. Key Word(s): 1. EUS-FNA; 2.