This prospective study investigated inhibitor development after c

This prospective study investigated inhibitor development after continuous infusion of factor concentrate for surgical procedures in subjects with VWD or a severe form of haemophilia (factor activity <1%). Observations were made on the occurrence of inhibitor formation, adverse events and virus seroconversions. Main inclusion criteria comprised a negative history of inhibitors to replacement factor concentrate, ≥50 exposure days to factor concentrate and anticipated surgery

requiring replacement factor coverage for ≥3 days. Therapy began ABT199 with a bolus dose of 30–50 IU kg−1 body weight of factor concentrate followed by continuous infusion with 3–4 IU kg−1 h−1. Continuous infusion dose of factor concentrate was adjusted based on factor levels measured at least once daily. In 46 subjects included in the study to date, no inhibitors have been identified at Selleckchem Nutlin-3a discharge or follow-up (3–4 weeks after surgery), and no thrombotic events or postoperative wound infections occurred. All subjects underwent surgery without major blood loss, and hemostatic efficacy was generally

rated ‘excellent’. The results of the current study are promising, although the number of subjects is too small to make a definitive statement about the incidence of inhibitor development during continuous infusion of factor concentrate. Therefore, this study will be continued. “
“Clinical problems associated with inhibitors in mild/moderate hemophilia are often considerable, since in the majority of cases adult patients are confronted with a change in phenotype from mild/moderate to severe. Although some

of the risk factors for inhibitor development are similar to those in severe hemophilia, others are specific for mild/moderate hemophilia. The study of the immune response in mild/moderate hemophilia A can help to elucidate some of the mechanisms underlying inhibitor formation and disruption of tolerance. Treatment MCE公司 of bleeding episodes and eradication of inhibitors in mild/moderate hemophilia require specific management and special attention should be paid to the prevention of this complication. “
“There are no evidence-based guidelines for antithrombotic management in people with haemophilia (PWH) presenting with acute coronary syndrome (ACS). The aim of the study was to review the current European Society of Cardiology guidelines, and to consider how best they should be adapted for PWH. Structured communication techniques based on a Delphi-like methodology were used to achieve expert consensus on key aspects of clinical management.

On the other hand, H pylori prevalence among HIV-infected childr

On the other hand, H. pylori prevalence among HIV-infected children from Uganda was surprisingly low, only 22.5% compared to the prevalence in healthy African children which is much higher [10]. The explanation for significantly lower prevalence in HIV-infected children is accidental eradication with frequent antibiotic therapy used for the treatment of infectious comorbidity. Muhsen et al.[11] studied the prevalence of H. pylori infection in different ethnic groups within the same geographic area and found

22.9% seropositivity among Jewish children and significantly higher 45.6% in Arab children in Israel. selleck screening library This difference was explained by different socioeconomic status, cultural habits and family size [11]. In an another study, risk factors for the acquisition and maintenance of the H. pylori infection were more than three siblings in the family, the use of well water for drinking, and male gender [12]. Conditions and clinical presentations anti-PD-1 antibody indicating or precluding search for H. pylori infection have been extensively reviewed in the recently published guidelines [13] and are summarized in the Table 1. Testing for H. pylori in children should be performed in properly

selected patients (Table 1) and with an adequate diagnostic procedure. Current recommendations do not approve a “test and treat” approach, but to select a patient in whom organic disease is expected based on detailed medical history and physical examination [13]. Therefore, diagnostic procedures should aim to determine underlying disease and not to detect H. pylori [13]. Although noninvasive tests yield high sensitivity and specificity, endoscopy with histopathology remains the only method that can detect

lesions associated with the infection, but also other possible causes of the patient’s symptoms [14]. As no single test is accurate enough for detection of H. pylori, current guidelines recommend 上海皓元 endoscopy with gastric biopsies and confirmation of infection with two different tests: either histopathology and rapid urease test or a culture [13]. Regarding noninvasive tests, recently published meta-analysis on the performance of the 13C-urea breath test (13C-UBT) showed relatively good accuracy especially in children older than 6 years of age (sensitivity 96.6%, specificity 97.7%) [15]. However, stool antigen-detection test do not depend on the age and has similar accuracy; meta-analysis on stool antigen-detection tests revealed that enzyme-linked immunosorbent assay (ELISA) monoclonal antibodies have the best performance, with sensitivity and specificity of 97% compared to ELISA polyclonal antibodies (sensitivity of 92%, specificity of 93%), and to one-step monoclonal antibody tests (sensitivity of 88%, specificity of 93%) [16]. Therefore, both of noninvasive tests, 13C-UBT and the accurate stool antigen-detection test, are recommended as reliable methods for evaluation of eradication rate in children [13].

3D, three-dimensional; BDL, bile duct ligation;

CCl4, car

3D, three-dimensional; BDL, bile duct ligation;

CCl4, carbon tetrachloride; cDNA, complementary DNA; CO2, carbon dioxide; DAPI, 4′,6-diamidino-2-phenylindole; DN, dominant-negative; FGF, fibroblast growth factor; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; H&E, hematoxylin and eosin; Hb, hemoglobin; HUVEC, human umbilical vein endothelial cell; LEC, liver endothelial cell; LPS, lipopolysaccharide; Pim inhibitor MLEC, murine liver endothelial cell; MMP, matrix metalloproteinase; mRNA, messenger RNA; MT, mutant; MTS, 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium; MyD88, myeloid differentiation protein 88; PCR, polymerase chain reaction; RT-PCR, real-time polymerase chain reaction; SEM, standard error of the mean; siRNA, short interfering RNA; TLR, toll-like receptor; TRAM, toll-like receptor adaptor Cell Cycle inhibitor molecule; VEGF, vascular endothelial growth factor; vWF, von Willebrand factor; WT, wild-type; YFP, yellow fluorescent protein. C3H/HeOuJ [TLR4–wild-type (WT)] mice and C3H/HeJ [TLR4-mutant (MT)] mice, which carry a spontaneous mutation that confers a loss of TLR4 function, were purchased from Jackson Laboratories (Bar Harbor, ME). These animals have similar levels of tumor necrosis

factor-α under basal conditions but impaired production in response to LPS.13 Bile duct ligation (BDL) and sham surgeries were performed as previously described.14 For carbon tetrachloride (CCl4)–induced fibrosis studies, CCl4 (1 MCE公司 mg/kg of body weight) or vehicle (olive oil) was injected intraperitoneally for a period of 6 weeks as previously described.15 LECs were isolated from mice as previously described,16, 17 and the purity was assessed (supplementary Fig- 1). All procedures were approved by the Mayo Clinic Institutional Animal Care and Use Committee. Human LECs (ScienCell, San Diego, CA) were grown under standard tissue

culture conditions [a humidified 5% carbon dioxide (CO2) incubator at 37°C] in media containing 5% fetal bovine serum, 2% endothelial cell growth supplement, and 1% penicillin/streptomycin (ScienCell). Retroviral transduction and short interfering RNA (siRNA) transfection were performed as we previously described.18 Two distinct siRNAs for TLR4 within the coding regions starting at 105 and 174 bp and MyD88 were gifts from Steven P. O’Hara, whereas TRAM siRNA was commercially obtained (Thermo Scientific). Human MyD88 full-length and dominant-negative N-terminal truncation MT constructs were polymerase chain reaction (PCR)–amplified from pUNO-hMyD88 and pDeNy-hMyD88 (InvivoGen), respectively, and the amplified fragments were subcloned into the pMMP retroviral vector.

We prospectively enrolled 28 consecutive anti-HCV–negative patien

We prospectively enrolled 28 consecutive anti-HCV–negative patients with an oncohematological

disease who first underwent chemotherapy from April 2006 to November 2007. All patients were screened for hepatitis B surface antigen (HBsAg), anti-HBs (antibody to hepatitis B surface antigen), anti-HBc (antibody to hepatitis B core antigen), and anti-HCV. The diagnosis and treatment of the oncohematological diseases were based on commonly accepted criteria. For each patient, samples of plasma and PBMCs were obtained at enrollment, at months 1 and 3 during chemotherapy, and then every 3 months after treatment discontinuation. The 28 patients were treated with chemotherapy for 4-12 months Ferrostatin-1 mw and observed after its discontinuation for 6-24 months. PBMCs were isolated from 5 mL whole blood by means of Histopaque (Sigma-Aldrich, St. Louis, MO) according to a standard technique and collected in aliquots of 2 × 106 cells. The presence of HCV RNA in plasma and PBMCs of all samples collected during the study was determined as previously reported.5 The detection limit in the plasma samples was around 40 IU/mL. The sensitivity of our method to detect HCV RNA in PBMC samples was assessed using HCV-positive PBMCs diluted in PBMCs obtained from an HCV RNA–negative

patient, as described by Halfon et al.6 Briefly, 2 × 106 PBMCs from an HCV RNA–positive Lumacaftor chemical structure patient quantified at 1.8 × 104 IU/2 × 106 PBMCs was sequentially diluted (1:10) in 2 × 106 HCV RNA–negative PBMCs; in these PBMC mixtures, HCV RNA was then quantified by real-time polymerase

chain reaction. The lowest detection limit by this method was 18 IU/2 × 106 cells. As a positive control for extraction of RNA from PBMCs, glucose-6-phosphate dehydrogenase medchemexpress (G6PDH) messenger RNA was sought in all PBMC samples collected (LightCycler h-G6PDH Housekeeping Gene Set; Roche Diagnostics, Branchburg, NJ). Table 1 shows the demographic, clinical, biochemical, and serological characteristics observed at the baseline in the 28 patients enrolled (Table 1). The three HBsAg-/HBV DNA–positive patients at the baseline were treated with telbivudine or entecavir. They became HBV DNA–negative within 6 months while still under treatment and remained so throughout the observation; the 16 HBsAg-negative/anti-HBc–positive patients received lamivudine prophylaxis and never showed circulating HBsAg or HBV DNA. No plasma or PBMC sample collected during the study was HCV RNA–positive. All PBMC samples collected were positive for G6PDH messenger RNA. No patient in the present study became positive for HCV RNA in plasma or PBMCs while under chemotherapy for an oncohematological disease.

We prospectively enrolled 28 consecutive anti-HCV–negative patien

We prospectively enrolled 28 consecutive anti-HCV–negative patients with an oncohematological

disease who first underwent chemotherapy from April 2006 to November 2007. All patients were screened for hepatitis B surface antigen (HBsAg), anti-HBs (antibody to hepatitis B surface antigen), anti-HBc (antibody to hepatitis B core antigen), and anti-HCV. The diagnosis and treatment of the oncohematological diseases were based on commonly accepted criteria. For each patient, samples of plasma and PBMCs were obtained at enrollment, at months 1 and 3 during chemotherapy, and then every 3 months after treatment discontinuation. The 28 patients were treated with chemotherapy for 4-12 months GSK-3 inhibitor and observed after its discontinuation for 6-24 months. PBMCs were isolated from 5 mL whole blood by means of Histopaque (Sigma-Aldrich, St. Louis, MO) according to a standard technique and collected in aliquots of 2 × 106 cells. The presence of HCV RNA in plasma and PBMCs of all samples collected during the study was determined as previously reported.5 The detection limit in the plasma samples was around 40 IU/mL. The sensitivity of our method to detect HCV RNA in PBMC samples was assessed using HCV-positive PBMCs diluted in PBMCs obtained from an HCV RNA–negative

patient, as described by Halfon et al.6 Briefly, 2 × 106 PBMCs from an HCV RNA–positive Temozolomide patient quantified at 1.8 × 104 IU/2 × 106 PBMCs was sequentially diluted (1:10) in 2 × 106 HCV RNA–negative PBMCs; in these PBMC mixtures, HCV RNA was then quantified by real-time polymerase

chain reaction. The lowest detection limit by this method was 18 IU/2 × 106 cells. As a positive control for extraction of RNA from PBMCs, glucose-6-phosphate dehydrogenase 上海皓元 (G6PDH) messenger RNA was sought in all PBMC samples collected (LightCycler h-G6PDH Housekeeping Gene Set; Roche Diagnostics, Branchburg, NJ). Table 1 shows the demographic, clinical, biochemical, and serological characteristics observed at the baseline in the 28 patients enrolled (Table 1). The three HBsAg-/HBV DNA–positive patients at the baseline were treated with telbivudine or entecavir. They became HBV DNA–negative within 6 months while still under treatment and remained so throughout the observation; the 16 HBsAg-negative/anti-HBc–positive patients received lamivudine prophylaxis and never showed circulating HBsAg or HBV DNA. No plasma or PBMC sample collected during the study was HCV RNA–positive. All PBMC samples collected were positive for G6PDH messenger RNA. No patient in the present study became positive for HCV RNA in plasma or PBMCs while under chemotherapy for an oncohematological disease.

It remains unknown whether or not this discrepancy was due to typ

It remains unknown whether or not this discrepancy was due to typographic errors. In a recent histological study in Japan, Nakanishi et al.28 investigated the entire EGJ macroscopically and microscopically in surgically-resected specimens for upper and middle esophageal squamous cell carcinomas. They reported the existence of CG in the proximal stomach in all cases, and superficial esophageal check details CG in 95% of cases, with mean lengths of 13 mm and 4 mm, and ranges of 2–64 mm and 1–26 mm, respectively. The results clearly indicate the presence of both gastric and superficial esophageal CG and CM in almost all Japanese patients. The superficial esophageal CG are believed

to protect the squamous mucosa from acidic injury.7 Indeed, the Japanese Research Society of Gastric selleck products Cancer defines the gastric cardia as the region where the CG and the CM are located.33 However, the EGJ landmark used in that study was the angle of His. With this EGJ landmark, the authors could not confidently differentiate the mucosal EGJ from the columnar-lined esophagus that is not uncommon in the Japanese population.3 Recent endoscopic and

histological study results in Chinese patients are similar to those reported in Japanese patients. For example, Law et al. performed endoscopic biopsies at or immediately below the SCJ, which showed a normal appearance in 94% of cases, and none with the SCJ shifted proximally towards the esophagus.34 The authors reported the presence of CG in 73% of cases in the proximal stomach below the SCJ/EGJ line, but did not describe the status of oxyntocardiac glands.34 In another

histological study of the EGJ in 44 resected specimens for gastric cardiac cancer in Chinese patients, with 31 cases having the entire EGJ examined microscopically, Fan et al.5 used the most distal end of squamous mucosa, along with deep esophageal glands and ducts, as the landmarks of the EGJ to investigate the distribution of the CG.5,25 They found that the CG were distributed not only distally in the proximal stomach, with a mean length of 7 mm (range: 3–20 mm), but also proximally underneath the squamous mucosa into the distal superficial esophagus, with a mean length of 7 mm (range: 3–18 mm). In their report, chronic inflammation medchemexpress was present in 95% of cases, and 64% with Helicobacter pylori infection.5 The major limitations of their study included a small sample size and the potentially-confounding factor of cancer involvement in the tissues they studied. In summary, the results from recent studies in Japanese and Chinese populations show a universal presence of CG and the CM in the proximal stomach, and also in the distal superficial esophagus, with approximate lengths of 13 mm distally and 7 mm proximally from the EGJ, which differs substantially from the data reported in Europeans and Americans.

On cranial MR imaging and MR angiography, an aneurysm was suspect

On cranial MR imaging and MR angiography, an aneurysm was suspected in the V4 segment of the right vertebral artery. Angiography showed a fusiform dissecting aneurysm in the V4 segment of right vertebral artery. The final diagnosis was ruptured V4 segment aneurysm with subsequent symptomatic migration of hemorrhage into the spinal subarachnoidal-subdural space. The patient was treated endovascularly by coil occlusion of both the aneurysm and vertebral artery. This rare cause and possible mechanisms for spinal migration of intracranial hemorrhage after aneurysmal rupture is discussed. “
“Leukoencephalopathy with subcortical cysts has been described

in a variety of conditions. However, few reports have highlighted congenital CMV as a cause of this imaging finding. We report a 1-year-old girl with developmental JQ1 solubility dmso delay and sensorineural hearing loss whose MRI brain showed abnormal white matter and temporal cysts.

Congenital CMV infection was diagnosed retrospectively by examination of dried blood spot from the newborn screening card. “
“Recent reports have indicated that mechanical thrombectomy may have the potential to treat acute ischemic stroke. This study this website aims to describe the safety and effectiveness of Trevo Retriever, using Stentriever technology, in revascularization of patients with acute ischemic stroke. Prospective study evaluating the clinical, radiological, and functional outcome of 13 patients with an angiographically verified occlusion of the anterior cerebral circulation. All patients underwent thrombectomy with TR as monotherapy or in combination with intra-arterial thrombolysis, within the first 8 hours from the onset

of symptoms. Successful revascularization was defined as thrombolysis in cerebral ischemia grade 2a to 3. Good outcome was defined as modified Rankin Scale score ≤ 2. Median baseline National Institutes of Health Stroke Scale score was 19(16-22). The occlusion site was middle cerebral 上海皓元医药股份有限公司 artery in 8 patients and internal carotid artery in 5 patients. Revascularization was achieved in 10 of 13 patients (77%). The mean time from groin puncture to recanalization was 95 ± 31 minutes. No significant intra-procedural complications occurred. Four patients (30%) died during the 90-day follow-up period and 4 patients (30%) achieved functional independence. Early clinical experience suggests that the TR can allow safe and effective revascularization in certain subjects with acute ischemic stroke. The only approved treatment in patients with ischemic stroke presenting in the first 4.5 hours from symptom onset is intravenous tissue-type plasminogen activator (IV tPA).1, 2 Nonetheless, thrombolytic therapy in acute ischemic stroke is often ineffective or can be difficult to administer within the mentioned brief treatment window. The average time from stroke onset to arrival in an emergency department is between 3 and 6 hours.

Although heterogeneity was addressed statistically by applying a

Although heterogeneity was addressed statistically by applying a random effect model, we aimed to further investigate its potential sources where possible. Thus, the full dataset was utilized for investigation of heterogeneity by sensitivity analysis. In some studies, NAFLD patients were mostly recruited because of elevated

ALT levels; thus, there was a marked enrichment of patients with NASH and few of them showed simple steatosis. Moreover, potential selection bias when selecting patients for liver biopsy may also explain the heterogeneity. The current meta-analysis is useful to clearly

understand CP-673451 price the magnitude of the effect of rs738409 on the histological severity of NAFLD, which is far beyond the small magnitude observed for common variants on complex traits,29 and may be explained by the nonsynonymous nature of the polymorphism that induces an amino acid change of I for M (missense Ileu (ATC) Met (ATG)) with possible functional consequences.30 A potential limitation of this study is its reliance on two studies,3, 4 which included cases from the Nonalcoholic Steatohepatitis Clinical Research Network learn more (NASH CRN). This fact may limit the research results to liver disease severity. Hence, to circumvent this potential caveat, we performed the whole analysis about all the NAFLD-related phenotypes excluding the smaller study in terms of sample size3 (details in Supporting MCE公司 Table 3). We observed a very similar magnitude in the variant effect on the analyzed phenotypes. Data about a GWAS on NAFLD performed in female adults also from the NASH CRN was not included in this meta-analysis because rs738409 was not captured by the chip.9 Although 15 SNPs in the PNPLA3 were captured by the GWAS and none of them showed

significant association with NAFLD, it is important to note that among five variants, only rs2076211 was in moderate linkage disequilibrium (r2: 0.65) with rs738409 precluding any imputation even assuming access to the complete dataset. An interesting observation about the analysis of the significant association between rs738409 and liver enzymes is the 28% increase in serum levels observed in GG homozygous individuals, a relevant aspect that might be regarded when selecting patients for clinical trials, decision-making on indication of liver biopsy, and evaluation of the magnitude of any treatment response based on serum ALT levels.

[10, 11] In a previous study, we demonstrated that CCR5, but not

[10, 11] In a previous study, we demonstrated that CCR5, but not CCR1, regulates the trafficking of immune cells into the liver under normal conditions.[12] In addition, we also reported that in multidrug resistance 2 gene (Mdr2)-knockout (Mdr2-KO) mice, a strain that spontaneously develops chronic cholestatic hepatitis and fibrosis that is eventually followed by HCC,[13-15] the RANTES chemokine is highly expressed.[16] RANTES is a ligand for both CCR1 and CCR5. Based on these observations, we propose, in this study, that the trafficking

of immune cells to the liver mediated by CCR5 is critical for the development of inflammation-induced HCC.[12, 17] To test this hypothesis,

we studied the role of CCR1 and CCR5 Selleckchem HDAC inhibitor in Mdr2-KO mice. Therefore, we generated two new strains Stem Cell Compound Library screening from the Mdr2-KO mouse, the Mdr2:CCR5 and the Mdr2:CCR1 double knockouts (DKOs), and set out to compare inflammation and tumorigenesis among these strains. Animal experiments were performed according to a protocol approved by the animal care committee of Hebrew University (Jerusalem, Israel). All animals were kept on a 12-hour light/dark cycle in a pathogen-free animal facility with free access to food and water. Wild-type (WT) C57Bl/6J and CCR5-deficient mice were purchased from The Jackson Laboratory (Bar Harbor, ME). CCR1-deficient mice were acquired from Taconic Farms (Germantown, NY). FVB.129P2-Abcb4tm1Bor (Mdr2-KO; The Jackson Laboratory) mice were kindly given to us by Dr. Daniel Goldenberg MCE公司 from the Goldyne Savad Institute of Gene Therapy Hadassah University Hospital (Jerusalem, Israel) and crossed into the C57Bl/6 genetic background for at least nine generations. Double-mutant Mdr2:CCR5 and Mdr2:CCR1 DKO mice were generated by crossing Mdr2-KO with either CCR5- or CCR1-deficient mice and their

progeny were identified by polymerase chain reaction (PCR) analysis (for primer sequences, see the Supporting Materials). At ages of 1, 3, and 16 months, mice were sacrificed by a lethal dose of isoflurane anesthesia and livers were excised and weighed. All mice were injected intraperioneally (IP) with bromodeoxyuridine (BrdU; Sigma-Aldrich, Rehovot, Israel) at 1 mg/mouse in 10 µL per 1 g of body weight 3 and 24 hours before sacrifice. Liver specimens were either fixed in 4% buffered formalin or snap-frozen in liquid nitrogen for further analysis. Blood samples were collected monthly from the age of 1 month until 6 months by tail vein bleeding. Levels of liver enzymes in sera, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase, were measured with Reflotron (Roche, Mannheim, Germany). Magnetic resonance imaging (MRI) was performed on a horizontal 4.

Pain scores were assessed using visual analogue scale while QoL w

Pain scores were assessed using visual analogue scale while QoL was assessed using the EORTC-QLQ-30 instrument, Global health status/Quality of life score. Adverse events Paclitaxel were graded according to the ASGE lexicon’s severity grading system. Results: A total of 45 patients (age 63 ± 17 yr, female 35%, pancreatic cancer 78% underwent EUS-BD [REN 12, AG 7, TL 26 (Choledochoduodenostomy 18, Hepatogastrostomy 5, Hepatoduodenostomy 3)]. Reason for EUS-BD was obscured ampulla by invasive cancer or enteral stent

(65%), altered anatomy (11%), failed deep biliary cannulation (22%), and gastric outlet obstruction (2%). Electrocautery was used during 32% of procedures. EUS-guided cholangiography was successful in all patients (100%). Mean intra- or extra- hepatic bile duct diameter was 13.1 mm (range 1–25 mm). Stent placement Bioactive Compound Library in desired location (technical success) was achieved in 44 (97.8%) patients (metallic stent 40, plastic stent 5). Mean procedure time was 42.8 ± 33 mins. Clinical success was attained in 41/45 (91%) patients of who achieved technical success. There

was significant decrease in bilirubin at 4 weeks (246.2 ± 164.2 vs. 37.6 ± 27.3 μmol/L, p < 0.001). Mean length of hospital stay was 2.9 days. A total of 5 (11.1%) adverse events occurred (2 moderate: bile leak, sheared wire and 3 mild: 1 pancreatitis, 2 pain managed conservatively). During long-term follow-up of 113.4 ± 109.3 days, 10 patients died because of disease progression with patent stents in place at a mean of 80.4 ± 77.8 days after EUS-BD. One patient had stent occlusion (metal stent) treated with endoscopic cleansing

and placement of plastic stent. Three patients had stent migration (metal stents). QoL score improved 4 weeks after medchemexpress EGBD (39.3 ± 20.0 vs. 50.0 ± 22.2, P = 0.33). Conclusions: Excellent efficacy and safety of EUS-BD in the management of distal malignant biliary obstruction after failed ERCP is demonstrated in a rigorous ongoing prospective international study. P SAXENA,1 V KUMBHARI,1 M EL ZEIN,1 A ABDELGELIL,1 S BESHARATI,1 A MESALLAM,1 T STEVENS,2 EJ SHIN,1 VK SINGH,1 AM LENNON,1 MI CANTO,1 MA KHASHAB1 1Division of Medicine, Department of Gastroenterology and Hepatology, Johns Hopkins Hospital, Baltimore, MD, USA, 2Division of Medicine, Department of Gastroenterology and Hepatology, Cleveland Clinic, Cleveland, OH, USA Background: Emerging data suggests that needle aspiration techniques have direct effect on yield of EUS-FNA. Standard FNA procedures involve use of “no-suction” or “suction” aspiration techniques. However, recent data suggests that using minimal negative pressure provided by pulling the needle stylet slowly and continuously (capillary suction technique) is associated with improved diagnostic yield.