The media was subsequently collected after 1 or 2 hours AML12 mo

The media was subsequently collected after 1 or 2 hours. AML12 mouse hepatocytes (ATCC) were grown in DMEM/F12 media supplemented with 10% FBS and ITS (Invitrogen). Cells were pretreated with 200 ng/mL of actinomycin D (ActD) for 30 minutes. Media was then changed to 150 μL of conditioned Kupffer cell media plus 200 ng/mL ActD. After 18 hours, media was removed and cells were fixed. Cells were quantitated by crystal violet assays and hepatocyte number was calculated based on a standard curve.19

TNF-α antibody (AB-410-NA) was from R&D Systems. Primary hepatocytes were pretreated with 200 ng/mL of ActD in Williams E media + 5% FBS for 30 minutes. Media was then changed to include increasing amounts of recombinant mouse TNF-α (Peprotech, Rocky Hill, NJ) plus ActD. After 18 hours, media was removed and cells were fixed and quantitated by crystal violet assays. Metformin order Cells were collected and homogenized in 2× Laemmli Buffer. For HGFL determination, cells were cultured in serum-free media and the media was collected after 36 hours. Media was concentrated with Amicon Ultra-4

centrifugal selleck chemicals llc filters (Millipore, Billerica, MA). Protein concentrations were determined using the Micro BCA Kit (Pierce Biotechnology, Rockford, IL). Primary antibodies used were anti-NF-κB p65, anti-pNF-κB p65 Ser536, anti-pIKKα/β, anti-IKKβ anti-Caspase-3 (Cell Signaling, Boston, MA), anti-HGFL (T-19, Santa Cruz Biotechnology, Santa Cruz, CA). Mice were injected with 0.8 μg LPS and 30 mg GalN in saline and normalized to 30 g body weight Resminostat (500 μL total volume) or GalN alone. This low dose of LPS does not alter mortality in the Ron TK-deficient mice, but when combined with GalN induces significant liver injury.7, 16 Blood was collected and plasma alanine aminotransferase

(ALT) levels were determined at Shriners Hospital. Paraffin-embedded sections of liver tissue were analyzed by TUNEL staining.16 For each liver tissue section per mouse, the number of TUNEL-positive cells in three random high-powered fields was counted by an investigator blinded to treatment group. Statistical significance for all analyses was determined by Student’s t test, Logrank, or one-way analysis of variance (ANOVA) using GraphPad Prism 3.03 software (La Jolla, CA). Error bars represent standard error of the mean (SEM). Quantitative data directly comparing Ron expression in liver macrophages (Kupffer cells) and in liver parenchymal cells in the mouse are lacking. To examine Ron expression in mouse Kupffer cells and hepatocytes, populations of murine Kupffer cells and hepatocytes were collected. The isolated Kupffer cells ranged in purity from 90%-95% following centrifugal elutriation based on F4/80 immunostaining (Fig. 1A) and the ability of the cells to ingest fluorescent beads (data not shown). Hepatocyte identity was confirmed with albumin immunostaining and purity was over 99% (Fig. 1A).

2% exploding, 398% ocular, 168% imploding + ocular, 46% implod

2% exploding, 39.8% ocular, 16.8% imploding + ocular, 4.6% imploding + exploding, 10.2% exploding + ocular, and 5.6% had all 3 types (imploding + exploding + ocular).

Two patients did not choose a pictorial representation of headache. According to patients’ responses to the question “Is your headache pain pushing in or pushing out of your head or is it located within your Daporinad cost eye socket (ocular)? (check all that apply),” 20.5% of patients had imploding headaches, 10.8% exploding, 23.6% ocular, 20.5% imploding + ocular, 3.6% imploding + exploding, 16.4% exploding + ocular, and 4.6% had all 3 types (imploding + exploding + ocular). Three patients did not choose a written descriptor of headache. Reasons for nonresponse were not elucidated. According to physicians’ diagnoses according to scripted questionnaire, 18.7% of patients had imploding headaches, 22.7% exploding, and 7.1% ocular headaches, while 16.2% had imploding + ocular, 9.1% imploding + exploding, 22.2% exploding + ocular, and 4% had all 3 types MK-2206 research buy (imploding + exploding + ocular). Ten subjects (5%) had pain directionality that varied within an individual migraine attack (ie, intra-attack variability), and 11 (6%) subjects had different pain directionalities from 1 migraine attack to another (ie, inter-attack variability). A total of 77 patients used prophylactic medications, and among them, 14 (18.2%) had imploding, 18 (23.4%) had exploding, 6

(7.7%) had ocular only, 7 (9.1%) had imploding + ocular, 9 (11.7%) had imploding + exploding, 19 (24.7%) had exploding + ocular, and 4 (5.2%) had all 3 types. One hundred twenty-one patients did not use prophylactic meds: 23 (19.0%) had imploding, 27 (22.3%) had exploding, 8 (6.6%) had ocular NADPH-cytochrome-c2 reductase only, 25 (20.7%) had imploding + ocular, 9 (7.4%) had imploding + exploding, 25 (20.7%) had exploding + ocular, and 4 (3.3%) had all 3 types. There was no difference in the distribution of headache directionality between subjects using

prophylactic medication and subjects not using such medications (P = .4549). There was weak agreement, Kappa coefficient 0.33 (P < .0001) between physician diagnosis of pain directionality and patient self-assignment via answering the written question about pain directionality. There was weak agreement, Kappa coefficient 0.35 (P < .0001), between physician diagnosis of pain directionality and patient self-assignment via selection of representative pictures. There was weak agreement, Kappa coefficient 0.35 (P = .0005), between subject self-assignment of pain directionality via answering the written question about pain directionality and choosing from representative pictures. Concordance between methods of assigning pain directionality was also determined for each pain direction separately. For imploding headaches, there was moderate agreement between physician diagnosis according to scripted questionnaire and patient self-assignment via selection of representative pictures (Kappa coefficient 0.50, P < .

These may include both fertility and pregnancy issues Maintainin

These may include both fertility and pregnancy issues. Maintaining contact with the medical team can benefit women approaching the menopause by preparing them psychologically for the

change and its associated symptoms. “
“Haemophilic arthropathy causes pain and a severely restricted range of motion, and results in a significant reduction in quality of life. When conservative treatments have failed, orthopaedic surgery is recommended for these patients with severe haemophilic arthropathy. However, surgery for haemophilia patients is challenging due to high complication rate such as infection, delayed wound healing and mortality. The aim of this study was to evaluate the incidence of early complications and identify preoperative risk factors of surgery for haemophilia patients. We report STI571 a series of haemophilia patients undergoing elective orthopaedic surgery between 2006 and 2012. During CH5424802 this period, 119 surgeries in 81 patients were

prepared and 118 surgeries in 80 patients were actually performed. Four deep bacterial infections and four delayed wound healings occurred within 6 months postoperatively. One patient died preoperatively and four patients died postoperatively. Only the presence of inhibitor was a significant risk factor for infection. We found no risk factor related to delayed wound healing. Our data revealed alkaline phosphatase, albumin, platelet, alpha-fetoprotein, presence of ascites and child classification C as predictors of perioperative mortality following elective orthopaedic surgery. Our role is to identify potential patients who present with risk factors for complications and attempt to seek the best determination of treatment strategy for these people. “
“The use of pulsed ultrasound (PUS) and low level laser therapy (LLLT) in patients with haemophilia

has been recommended for supportive treatment of acute and chronic phases of haemarthrosis but its role has not been supported by experimental evidence. The purpose of the present study was to evaluate the effect of these modalities on joint swelling, friction and biomechanical parameters of articular CHIR-99021 order cartilage. An experimental rabbit knee haemarthrosis model was used to test the hypothesis that LLLT and PUS favourably impacted on the biotribological and biomechanical properties of cartilage after joint bleeding. To test this, 35 male albino rabbits weighing 1.5–2 kg were used. The left knee of 30 rabbits was injected with 1 mL of fresh autologous blood two times per week for four consecutive weeks to simulate recurrent haemarthrosis; five rabbits served as non-bleeding controls. Ten rabbits were treated with PUS and 10 with LLLT and the remaining 10 were not treated. The treatments were started after 2 days and the treatment duration was planned for 5 days (sessions) in ultrasound and laser groups.

A 64-gene profile reproducibly differentiated severe NAFLD from m

A 64-gene profile reproducibly differentiated severe NAFLD from mild NAFLD, and a 20-gene subset within this profile correlated with NAFLD severity, independent of other factors known to influence NAFLD progression. Multiple genes involved with tissue repair/regeneration and certain metabolism-related genes

were induced in severe NAFLD. Ingenuity Pathway Analysis and IHC confirmed deregulation of metabolic and regenerative pathways in severe NAFLD and revealed overlap among the gene expression patterns of severe NAFLD, cardiovascular disease, and cancer. Conclusion: By demonstrating specific metabolic and repair pathways that are differentially activated in livers with severe NAFLD, gene profiling identified novel targets that can be exploited to improve diagnosis and treatment of patients who are at greatest risk for NAFLD-related find more morbidity and mortality. (Hepatology 2014;59:471–482) “
“Obstructive cholestasis induces liver injury, postoperative complications, and mortality after surgery. Adaptive control of cholestasis, including bile salt homeostasis, is necessary for recovery and survival. Peripheral serotonin is a cytoprotective neurotransmitter also associated with liver regeneration. The effect of serotonin on cholestatic liver

injury is not known. Therefore, we tested whether serotonin affects the severity of cholestatic liver injury. We induced cholestasis by ligation of the bile duct (BDL) in either wild-type (WT) mice or mice lacking peripheral Quinapyramine serotonin (Tph1−/− and immune thrombocytopenic [ITP] mice). Liver injury was assessed by the levels of plasma aspartate aminotransferase (AST), alanine aminotransferase DAPT purchase (ALT) and tissue necrosis. Bile salt–regulating genes were measured by quantitative polymerase chain reaction and confirmed by western blotting and immunohistochemistry. Tph1−/− mice displayed higher levels of plasma AST, ALT, bile salts, and hepatic necrosis after 3 days of BDL than WT mice. Likewise, liver injury

was disproportional in ITP mice. Moreover, severe cholestatic complications and mortality after prolonged BDL were increased in Tph1−/− mice. Despite the elevation in toxic bile salts, expression of genes involved in bile salt homeostasis and detoxification were not affected in Tph1−/− livers. In contrast, the bile salt reabsorption transporters Ostα and Ostβ were up-regulated in the kidneys of Tph1−/− mice, along with a decrease in urinary bile salt excretion. Serotonin reloading of Tph1−/− mice reversed this phenotype, resulting in a reduction of circulating bile salts and liver injury. Conclusion: We propose a physiological function of serotonin is to ameliorate liver injury and stabilize the bile salt pool through adaptation of renal transporters in cholestasis. (HEPATOLOGY 2012;56:209–218) Bile salts are biological detergents produced primarily by hepatocytes for digestion and absorption of fatty nutrients in the intestines.

The authors considered a number of interesting hypotheses[10] Am

The authors considered a number of interesting hypotheses.[10] Among them the most plausible includes the fact that some of the patients may have had a subclinical partial portal vein thrombosis at the study entry, which was undetected because Doppler ultrasonography of the abdomen was not performed at enrollment. Perhaps the sustained platelet increase following treatment with eltrombopag, risk factors such as an imbalance of coagulation,[16] portal hypertension selleck and reduced blood flow, local inflammation or endothelial injury could have acted in combination to exacerbate subclinical portal vein thrombosis in these patients. Another interesting hypothesis

could be that platelets in cirrhosis are overactivated, as shown by the increased urinary excretion of markers of in vivo platelet activation observed in these patients. It is possible that the relatively rapid increase p38 MAPK inhibitors clinical trials of the number of overactivated platelets may have acted as a trigger for thrombosis.[17] In conclusion, the study of Afdhal et al.[10] shows that the strategy of using eltrombopag in patients with cirrhosis undergoing elective invasive procedures is effective in increasing the platelet count and thus avoiding platelet transfusion, but carries

the risk of increasing the rate of thrombotic events. On the other hand, the benefit of increasing platelet counts in this population in order to prevent hemorrhagic events has not yet been established. Hence, the benefit of improving hemostasis at the expenses of increasing thrombotic risk should be carefully evaluated in individual patients. Armando Tripodi, Ph.D. “
“Background and Aim:  Studies on normal values of liver stiffness (LS) in subjects at “low risk” for liver disease are scant. The aim of the present study was to assess liver stiffness values in the subjects without overt liver disease with normal alanine aminotransferases (ALT)

and to determine potential factors, which may influence these Farnesyltransferase values with special reference to newly suggested updated upper limits of normal for ALT. Methods:  Liver stiffness measurements were performed in 445 subjects without overt liver disease (mean age, 41.1 ± 13.6; male, 73.5%) and normal liver enzymes. Results:  Mean LS value was 5.10 ± 1.19 kPa. LS values were higher in men than in women (5.18 ± 1.67 vs 4.86 ± 1.24 kPa, respectively, P = 0.008); in subjects with higher body mass index (BMI) category (Normal, overweight and obese subjects; 4.10 ± 0.75, 5.08 ± 0.66, and 6.05 ± 1.28 kPa, respectively; P < 0.001); in subjects with metabolic syndrome than in those without (5.63 ± 1.37 vs 5.01 ± 1.14 kPa, P = 0.001); and in subjects with ALT levels more than updated limits of normal compared to subjects with ALT levels less than updated limits of normal (5.68 ± 1.21 vs 4.77 ± 1.05 kPa, P < 0.001). On multiple linear regression, BMI and ALT was found to be significant predictor of LS.

F W G Leebeek has served on advisory boards and received resea

F. W. G. Leebeek has served on advisory boards and received research funding Inhibitor Library supplier from Baxter and CSL Behring. M. Makris has served as a consultant and received honoraria for lecturing from CSL Behring. P. M. Mannucci receives speaker fees from Grifols and serves on the scientific board of Baxter. R. Winikoff has received reimbursement from CSL Behring for attending symposiums. E. Berntorp has received research grants from CSL Behring. E. Berntorp designed research, performed research, interpreted data, wrote the manuscript,

gave final approval of the version to be published; T. Abshire designed research, performed research, interpreted data, wrote the manuscript, gave final approval of the version to be published; A. Federici Ganetespib supplier designed research, performed research, interpreted data, wrote the manuscript, gave final approval of the version to be published; M. Alvárez performed research; J. Bowen collected data, analysed data, wrote the manuscript; M. Carcao designed research, performed research, gave critical review of the content; J. Gill designed research, performed research;

N. Key performed research, gave critical review of the content; P. Kouides designed research, performed research; K. Kurnik designed research, gave critical review of the content; A. Lail analysed the data, wrote the manuscript; F. Leebeek designed research, performed research, gave critical review of the content; M. Makris designed research, performed research, gave Histone demethylase critical review of the content; P. Mannucci designed research, performed research, gave critical review of the content; R. Winikoff designed research, performed research. “
“Summary.  Congenital defects of platelets or plasma proteins involved in blood coagulation generally lead to bleeding disorders. In some of these disorders, patients with a severe phenotype are prone to spontaneous bleeds with critical consequences. This situation occurs more commonly in haemophilia A and haemophilia B and to a certain extent in severe forms (type 3) of von Willebrand disease. Defects in other plasma coagulation

proteins and platelet factors are relatively rare, with an incidence of ≤1: 1–2 million. Molecular genetic studies of the human coagulation factors, especially factors VIII and IX, have contributed to a better understanding of the biology of these genetic disorders, the accurate detection of carriers and genetic counselling, and have also fostered new therapeutic strategies. This article reviews the evolution of genetics over the last five decades as a tool for bleeding disorder investigations, the recent advances in molecular techniques that have contributed to improved genetic diagnosis of this condition, and the development and utility of proficiency testing programmes and reference materials for genetic diagnosis of bleeding disorders.

Our comprehensive multivariate regression model, which included m

Our comprehensive multivariate regression model, which included mean maximum longevities of 40 families as the dependent variable JAK inhibitor and family-level means for the eight independent variables, explained 80.3% of the variance in maximum life spans (Table 2). Details of the results are presented in Appendix 3. Among the independent variables, mean mass, diet and sociality were highly significant predictors, and breeding insularity was marginally significant

(P=0.053). The multivariate regression model of the Passeriformes dataset, which included mean maximum longevities of 17 families as the dependent variable and family-level means for the eight independent variables, explained 69.6% of the variance in maximum life spans (Appendix 3, F=2.2898, d.f.=8, 16, r2=69.6%, P=0.13). However, none of the independent variables significantly predicted mean maximum longevities of passeriform families, probably due to large inter-family variability and small sample sizes (i.e. ≤10 species for nine of the 17 passerine families).

Maximum longevities of several species in our data base (Appendix 2) were anomalously Selleckchem Crizotinib low relative to congeners, for example, Puffinus auricularis, Puffinus gravis, Anas diazi, Anas fulvigula and Anas laysanensis. Longevity records for these species at least likely are artifacts of inadequate sampling. We therefore removed them and re-ran the model. The significance of the overall results was unchanged and, as before, mass, diet and sociality were significant predictors and breeding insularity was marginally significant. Apparently

longevities of these ‘questionable’ species did not have a Phosphoglycerate kinase major influence on the results, especially since we analyzed family-level mean values. Of course data deficiencies and biases may have existed for other species as well, but we were unable to identify them a priori. Our ‘total evidence’ approach (Sherman, Holland & Shellman Sherman, 2008) assumes that any unknown data shortcomings were more likely to obfuscate associations with extrinsic variables that actually exist than to falsely create relationships that do not occur. To explore the details of the relationships revealed by the multivariate model we conducted a posteriori analyses of each significant variable individually, using species-level data. Maximum longevities were significantly related to body masses in the comprehensive dataset (Fig. 2a) and in the family Passeriformes (Fig. 2b). Regarding diets, in the comprehensive dataset (Fig. 3a) mean maximum longevities of herbivorous species (c.

Under either type of nutrient limitation, the cellular C:N ratio

Under either type of nutrient limitation, the cellular C:N ratio increased through the light period and decreased through the dark period over all growth rates, indicating a higher diel variation of C metabolism than that of N. Daily average cellular C:N ratios were higher at lower dilution rates under both types of nutrient limitation but cell enlargement was only observed at lower dilution rates under P-limitation. Carbon specific growth rates during the dark period positively correlated with cellular daily growth rates (dilution rates), with net loss of C during night at the lowest growth rates under N-limitation. Under P-limitation, dark C specific growth rates were close to zero at low dilution

rates but also exhibited an increasing trend at high dilution rates. In general, diel variations of cellular Trichostatin A C:N were low when dark C specific growth rates were high. This result indicated that the fast growing cells performed dark C assimilation at high rates, hence diminished the uncoupling of C and N metabolism at night. “
“Since the 1970s, Puget Sound,

Washington State, USA, has experienced an increase in detections of paralytic shellfish toxins (PSTs) in shellfish due to blooms of the harmful dinoflagellate Alexandrium. Natural patterns of climate variability, such as the Pacific Decadal Oscillation (PDO), and changes in local environmental factors, such as sea surface temperature (SST) and air temperature, have been linked to the observed increase in PSTs. However, the lack of observations of PSTs in shellfish prior to the 1950s has inhibited statistical assessments of longer-term trends Mannose-binding protein-associated serine protease in climate LY294002 price and environmental conditions on Alexandrium blooms. After a bloom, Alexandrium cells can enter a dormant cyst stage, which settles on the seafloor and then becomes entrained into the sedimentary record. In this study, we created a record of Alexandrium spp. cysts from a sediment core obtained from Sequim Bay, Puget Sound.

Cyst abundances ranged from 0 to 400 cysts · cm−3 and were detected down-core to a depth of 100 cm, indicating that Alexandrium has been present in Sequim Bay since at least the late 1800s. The cyst record allowed us to statistically examine relationships with available environmental parameters over the past century. Local air temperature and sea surface temperature were positively and significantly correlated with cyst abundances from the late 1800s to 2005; no significant relationship was found between PDO and cyst abundances. This finding suggests that local environmental variations more strongly influence Alexandrium population dynamics in Puget Sound when compared to large-scale changes. “
“Heterosigma akashiwo (Hada) Hada ex Y. Hara et Chihara is a bloom-forming alga that has been associated with fish kills in coastal regions worldwide. Dense blooms of this species occur annually in Delaware’s inland bays, USA.

[email protected] copy number was observed to be similar in HBV-positive Chine

[email protected] copy number was observed to be similar in HBV-positive Chinese individuals and our Korean controls (t test P = 0.477), but differed significantly between the HBV-positive Chinese individuals and our HBV-positive Korean cases (P = 6.572 × 10−13) (Supporting Table S5). Hence, we conclude that hepatitis virus find more infection status, per se, does not account for observed CNV differences between our cases and controls. In our investigation of the association of genomic variation with disease, we also examined individual SNPs in HCC patients and healthy Korean controls. The set of SNPs most strongly correlated with HCC by a trend test

was enriched for polymorphisms in genes involved in antigen presentation. Three of the eight variants with the highest association to liver cancer (rs9267673, rs2647073, and rs3997872) lie in the MHC class II locus (Table 3). None of the three variants is in LD with either of the others. The variant rs9267673 is located adjacent to the gene C2. rs2647073 is in LD with SNPs in a set of genes that includes HLA-DRB1, HLA-DRB6, HLA-DRB5, and HLA-DRA. The SNP rs3997872, on the other hand, is in LD

with SNPs in the HLA-DQA1, HLA-DQB1, HLA-DQA2, and HLA-DQB2 loci. All three SNPS are independently associated with HCC, showing neither an additive nor multiplicative effect. Interestingly, in addition to their association with HCC, two of the three SNPs (rs9267673 and rs2647073) show association to LC (P 0.0052 and 0.0007, respectively). In contrast, rs3997872 is only weakly associated with LC (P is 0.0408) (Supporting Table S3). Comparison selleck inhibitor of SNP allele frequencies in HCC and LC patients, identified two variants that distinguish liver cancer from

cirrhosis (Table 4). An SNP, rs2880301, is located within the TPTE2 gene; the second, rs2551677, lies in a gene-poor region of 2q14.1. Both polymorphisms are distinct from those identified in the comparison of HCC patients and Korean controls. We also examined HCC individuals to determine whether risk alleles at SNPs associated with cancer (Table 3) correlate with hepatitis virus infection status. All eight variants show an adjusted P > PJ34 HCl 0.11 for association with HBV and an adjusted P > 0.48 for association with HCV (Supporting Table S6). Thus, viral infection status does not account for the observed association between SNPs in LD to immune response genes and liver cancer. Finally, we observe no significant association between SNPs in HLA-DP, which has been implicated in HBV susceptibility in Asian populations18 and HCC. We next evaluated whether multiple SNPs in a common biological network, each with a modest individual effect, were associated with HCC. In order to reduce complexity and statistical noise, we first selected the 1,000 most significant SNPs from Stage 1 and Stage 2 and assigned them to biological pathways based on their linkage disequilibrium to genes in the NCI Protein Interaction Database.

Results: Of 200 patients examined with EUS, upper gastrointestina

Results: Of 200 patients examined with EUS, upper gastrointestinal submucosal leision was diagnosed in 102 cases (51%), upper gastr ointestinal benign mucosal lesion in 16 cases (8%), gastroesophogeal malignant tumor

in 20 cases (10%), metastastic lymph node of tumor in 10 cases (5%), bile and pancreatic diseases in 52 cases (26%), Biopsyspecimens enough for patholog ical diagnosis were acquired in 32 of 40 EUS-FNA (80%) patients. Conclusion: Echogastroscopy check details has important clinical value in the diagnosis and therapy of upper gastrointestinal and its adjacent lesions. Key Word(s): 1. Echogastroscopy; 2. Fine needle; 3. puncture; 4. tumor; Presenting Author: XUN HUAN Additional Authors: CAICHANG CHUN Corresponding Author: CAICHANG CHUN Affiliations: university of jiujiang Objective: Survey the role for simethicone to reduce air bubbles gastric mucus which are frequent sources of artifacts in endoscopic ultrsonography (EUS). Methods: 107 patients who referred for EUS examination in our hospital, they were randomized into two groups: the simethicone group and sterile group. To compare gastric mucus, MI-503 in vitro air bubbles and artifacts in the two groups. Results: The air bubbles in simethicone group is obviously less than sterile group, the difference was statistically significantly

(P < 0.05), the gastric mucus in simethicone group is less than sterile group, there was no significant difference. The ZD1839 in vitro artifacts in simethicone group is obviously less than sterile group, the difference was statistically significantly (P < 0.05). Conclusion: Simethicone improved endoscopic visualization and reduced artifacts during EUS. Key Word(s): 1. Application; 2. simethicone; 3. endoscopic; 4. ultrsonography; Presenting Author: LEI WANG Additional Authors: ZHENDONG JIN, ZHAOSHEN LI Corresponding Author: LEI WANG Affiliations: Changhai Hospital Objective: Though surgical resection is the primary choice for the treatment of pancreatic neuroendocrine tumors (pNETs), it still lacks effective

palliative treatment for cases with recurrence or loss of surgical indications. Radiofrequency has been widely used in clinical for tumor therapy and has showed benefits in the treatment of liver cancer and early esophageal cancers. Here we report a case of postoperative recurrence of pNET treated with EUS-guided radiofrequency. Methods: The patient is a 30-year-old woman presented with abdominal pain and haematemesis ten years ago. She underwent subtotal gastrectomy because of duodenal bulb stricture along with incomplete abstruction five years ago. Similar symptoms recurred after surgery. EUS revealed pancreatic neuroendocrine tumor. One year ago, the patient underwent the distal pancreatectomy and spleen-cholecystectomy. The pNET was confirmed pathologically (Figure 1).