[4, 6] In this study, we report our experience of using MRA in the detection of Az and associated aneurysms in our institute. To our knowledge, this is one of the largest MRA investigations to date relating to the Az and associated aneurysms.

Between January 2008 and March 2011, MRA was performed in a total of 3,572 consecutive hospitalized patients (1,897 male, 1,675 female) aged 8-100 years (mean age, 61.99 ± 15.26 years) in our hospital (the Sixth Affiliated https://www.selleckchem.com/products/Lapatinib-Ditosylate.html People’s Hospital, Shanghai Jiao Tong University). The study protocol was reviewed and approved by the Institutional Review Board. Informed consent for study participation was provided by patients or their immediate family members (if the patient’s clinical status precluded him or her from granting consent). We established a database where all MRA data focusing on intracranial vessels and the main clinical information of the patients were recorded and stored. Through the database, we could easily screen and categorize the MRA data using different search key words. All MRA examinations were performed on a 3.0 T system (Achieva X-Series, Philips Medical Systems, Amsterdam, The Netherlands) with a Sense-Head-8

receiver head coil. The 3-D-T1-fast field sequences were used to obtain time-of-flight (TOF)-MRA images; the detailed parameters of the sequences have been described in our previous paper.[7] The acquired image datasets were then transferred to a workstation (EWS 2.5.3.0, Philips Medical Systems), where 3-dimensional (3-D) image Selleckchem Venetoclax reconstruction was rendered with VR by use of a 3-D specialist software package (Volume Inspection, Philips Medical Systems). During VR postprocessing, the posterior circulation system was removed by using the single artery highlighting method to reduce artery overlay and highlight the anterior circulation. With an arbitrary rotation, the VR MRA images were allowed to render a comprehensive vision of the anterior circulation system. The merits afforded by VR MRA make it a useful tool for identifying an Az from other ACA anomalies, especially bihemispheric www.selleck.co.jp/products/atezolizumab.html ACA. Two experienced observers (M.H.L and H.Q.T), both blind to all clinical

information and independent of each other, interpreted all 3-D-TOF-MRA datasets on an offline workstation, where all MRA images, including source images, maximum intensity projection and VR images, were displayed on screen. The observers were allowed to adjust the appropriate threshold of window width and level and rotate the VR images arbitrarily for comprehensive visualization. Interobserver disagreements were resolved by consensus in a joint session. The presence of an Az was identified according to the same criteria described in previously published literatures.[1-4] If associated aneurysms were present, their size, location, shape, and clinical information were recorded in detail. The descriptive statistics analysis was performed by use of SPSS (version 13.0, SPSS Inc., Chicago, IL, USA).

4A). The increase of HSPC-related markers is more prominent at 4 weeks of age than at 1 year. Histologically, A6-positive cells appear as early as 3-4 weeks of age in parenchyma and the hyperplastic ductal region of albNScko livers, whereas no A6+ signals are detected in NSflx/flx livers (Fig. 4B). The majority of A6+ cells also coexpress the CK19 antigen on serial sections of 4 um in thickness (Fig. 4C). To determine the role of NS in liver regeneration, Cabozantinib datasheet we analyzed responses of albNScko and NSflx/flx livers to CCl4 treatment at 2 weeks of age when Cre expression and DNA damage were

maximal and histological changes and serum measurement of hepatocellular injury were mild in albNScko livers. Liver samples were collected in pairs from CCl4- and oil-treated mice at the first, second, or fourth day of the injection. NSflx/flx livers show acute pericentral necrosis with infiltrating leukocytes during the first 2 days after injection

(Fig. 5A1, white arrows). Without CCl4 exposure, albNScko livers contained regenerative nodules and nonregenerative regions (Fig. 5A2, perinodule). In response to CCl4 treatment, albNScko livers began to show not only the same acute pericentral necrosis and leukocyte infiltration as observed in NSflx/flx livers, but also severe hydropic degeneration (black arrows) in the perinodular areas (Fig. 5A3). Notably, the regenerative nodules were relatively resistant AZD6738 to the acute necrotic effect of CCl4 treatment (Fig. 5A4), which is consistent with their lower expression of the key enzyme, CYP2E1, that metabolizes CCl4 and forms free radicals (Supporting Fig. 4A). Mice recovered from CCl4-triggered pericentral necrosis after 4 days (Supporting Fig. 4B). Unlike NSflx/flx livers, which show no increase of CK19+ cells after CCl4-induced damage, albNScko

livers displayed a significant increase of CK19+ bile ductules and small CK19+ progenitor-like cells located in the periportal region in response to CCl4 treatment (Fig. 5B and Supporting Fig. 4C). Immunostaining on serial sections showed that the numbers of A6- and CK19 double-positive progenitor cells were increased by CCl4 treatment in albNScko ifoxetine livers (Fig. 5C). Consistently, the number of Sox9 and CK19 double-positive cells was also increased in CCl4-treated albNScko livers (Supporting Fig. 4D). Supporting the idea that HSPCs may be expanded in CCl4-treated albNScko livers, qRT-PCR assays demonstrated that the messenger RNA levels of two HSPC-related markers, EpCAM and AFP, were both up-regulated in albNScko livers after CCl4 treatment (Fig. 5D). The increase of EpCAM occurred within 1 day, peaked on the second day, and dropped after 4 days, whereas the increase of AFP was found primarily on the second day of the injection.

2%, 3.5%, and 1.8 %of the binding affinity of the wild-type, respectively. Both K- and S-mutant-immunized mice had moderate cross CTL response to wild-type epitope, but not to each other. SK-mutant-immunized

mice had weak CTL response to S mutant and the wild-type epitopes, but not to K mutant epitope. The wild-type-immunized mice had much weeker CTL response to K and S mutant epitope compared to the wild-type epitope. ELISOPT assay showed that wild-type-immunized mouse had strong response to wild-type epitopic peptide stimulation, but spot number reduced 89%, 90%, and 93 %to K, S, and SK mutant epitopic peptide stimulation respectively. The killing effect was significantly lower to the mutant target cells than the wild-type ones. Conclusion: HBV CTL-epitopic ABT-737 cell line mutation might be a factor influencing disease progression of HBV infection. env183-191 mutations may decrease the binding

affinity of the epitope to CTL and weaken the specific CTL response. Disclosures: The following people have nothing to disclose: Zhihui Xu, Yihui Rong, Yan Liu, Xiaodong Li, Shaoli You, Dongping Xu, ShaoJie Xin Background: HBx regulatory protein is required for HBV cccDNA transcription/viral replication and contributes to HBV oncogenicity. HBx affects the epigenetic control of both HBV viral chromatin and cellular genes. ChIPSeq experiments in HBV replicating cells have shown that HBx specifically binds to a large number of genomic sites and potentially regulates the expression of several genes and non coding RNAs. Lcn-RNAs are endogenous cellular RNAs Carfilzomib molecules Progesterone longer than 200 nt capable to regulate gene expression at various levels, including chromatin modification, transcription and post-tran-scriptional processing. Objectives: Aim of this study was to identify and characterize lncRNAs targeted by HBx. Methods: High-throughput sequencing of anti-HBx ChIP-enriched DNA (ChIPSeq) was performed in HBV replicating HepG2 cells. Hits were validated in independent ChIP experiments by TaqMan real-time PCR

using lncRNA specific primers. HBx targeted lncRNAs expression was assessed both by PCR (isoforms evaluation) and real-time RT-PCR (quantification). Results: ChIPSeq analysis identified 39 lncRNAs targeted by HBx. We focus here on HBx regulation of DLEU2 and the intragenic/overlap-ping TRIM13 gene, hsa-mir-15 and hsa-mir-16. Up-regulation of specific DLEU2 splicing variants correlates with HCC development whereas hsa-mir-15 and hsa-mir-16 are down-regulated in HCCs. We show that HBx binds to and induces increased histone acetylation at the DLEU2 promoter. HBx binding results in: a) a different DLEU2 splicing profile leading to over-expression of a shorter isoform; b) down-regulation of the hsa-mir-15 and hsa-mir-16; c) up-regulation of the antisense autophagic gene TRIM13.

Studies were performed in mouse cholangiocytes isolated from normal mice (BALB/c) and immortalized by transfection with the simian virus 40 large-T antigen gene.4 These cells demonstrate identical properties to freshly isolated small and large mouse cholangiocytes.3 Cells were maintained in culture as described.3, 4 Additional studies

of P2 receptor https://www.selleckchem.com/products/sorafenib.html expression were performed in primary cholangiocytes isolated from C57BL/6 mice (Charles River, Wilmington, MA) as previously described.16, 17 All animal experiments were performed in accordance with a protocol approved by the Scott & White Institutional Animal Care and Use Committee and in accordance with the Guide for the Care and Use of Laboratory Animals published by the U.S. National Institutes of Health (NIH Publication No. 85-23, revised 1996). Total RNA was extracted using TRIZOL Reagent (Invitrogen, Carlsbad, CA) and 1 μg RNA was reverse transcribed in the presence of 100 pmol oligo-deoxythymidine primer. For reverse transcription polymerase chain reaction (RT-PCR), aliquots of 5% of the

total complementary this website DNA were amplified with TaqDNA polymerase in a reaction mixture containing 20 pmol of 5′ and 3′ primers specifically designed for various P2X and P2Y receptors (Supporting Information Methods and Supporting Information Table 1). MLCs and MSCs were grown to confluence on coverglass (Fig. 2), loaded

with 2.5 μg/mL of fura-2-acetoxymethyl ester (fura-2-AM; TEF Laboratories, Austin, TX), placed in a perfusion chamber (RC-25F/PHA; Warner Instruments) on Tau-protein kinase the stage of an inverted fluorescence microscope (Nikon TE2000), and the inflow and outflow ports were connected to a syringe pump. Changes of [Ca2+]i (the intracellular calcium concentration) were measured at excitation wavelength of 340 nm (calcium-bound fura-2-AM) and 380 nm (calcium-free fura-2-AM), and emission wavelength of 510 nm and [Ca2+]i was calculated. Confluent MSCs and MLCs were incubated with acetylated α-tubulin antibody (Sigma), as a marker for the primary cilium, and rhodamine phalloidin (Invitrogen) to label actin. Imaging was performed using a PerkinElmer UltraVIEW ERS spinning disk confocal microscope (PerkinElmer, Boston, MA). Imaris 5.0 (Bitplane, Inc., Saint Paul, MN) was used for three-dimensional volume rendering of z-stacks. Exocytosis was assessed by real time imaging using the fluorescent dye FM1-43 (Molecular Probes, Inc., Eugene, OR) as previously described.

There are two

previously published proteomics studies using serum25 or liver tissue26 from patients across the spectrum of NAFLD. In the first and BGB324 only other proteomics study using serum samples, Younossi et al.25 identified 12 protein peaks with significant differential expression when patient groups and controls were compared. In a recent proteomics study utilizing liver tissue from patients with NAFLD and controls, Charlton et al.26 identified nine proteins with differential expression between study groups, and all proteins exhibited functions previously implicated in the pathogenesis of NAFLD and NASH, including biological response to increased hepatic lipid content, inflammation, mediation of fibrosis, and fatty acid transport. Our study utilized an ion-intensity based, label-free quantitative proteomics approach (LFQP) that has gained popularity in recent years as the performance of mass spectrometers has improved.27–30 Using this LFQP approach, we detected 1,738 proteins in serum samples obtained from control subjects and NAFLD patients. Of these proteins, expression of 605 proteins differed significantly (q < 0.05) between any two patient groups. Further analysis revealed that expression of 229 proteins differed significantly when control subjects were compared with any

of the three NAFLD patient groups. There were no significant differences observed between the simple steatosis and NASH groups, Galeterone Selleck MK0683 suggesting that systemic markers of fatty liver and NASH may not be present in serum from patients with mild disease. However, there were 55 proteins that were different between the simple steatosis and NASH F3/F4 group and 15 proteins that differed between the NASH and NASH F3/F4 patients. These proteins may be particularly helpful in identifying biomarkers to diagnose and stage NAFLD and NASH. We further analyzed the biological significance of all priority 1 proteins with a significant change (q < 0.05) of at least 14% (1.14-fold change) based on the maximum observed change of the internal standard, chicken lysozyme. As described

below, several of these biological processes have been previously implicated in the pathogenesis of NAFLD and NASH and many of these identified proteins are only synthesized by the liver. Fifteen of the proteins that changed significantly are involved in immune system regulation and inflammation. One example is retinol binding protein 4 (RBP4), a protein we identified as having significantly decreased expression with increasing NAFLD severity. RBP4 is a cytokine synthesized by both the liver and adipose tissue that carries vitamin A in the blood and is involved in the development of insulin resistance.31, 32 Although some studies have shown an increase in serum RBP4 levels in patients with NAFLD,33, 34 a recent study by Nobili et al.

Disruption of the epithelial barrier Trametinib clinical trial is often associated with the increase of cell shedding. This study aims to investigate the mechanisms how mucosal protectants maintain the integrity of intestinal epithelial barrier in

indomethacin-induced enteropathy by observing real-timely the gap density using confocal laser endomicroscopy (CLE). Methods: A method to evaluate real-timely the intestinal epithelial barrier damage after administration of indomethacin in rats were established using a new technique CLE by investigating the gap density in small intestine. Then the mucosal protectant teprenone and proton pump inhibitor rabeprazole were given by gavage before and after the administration of indomethacin. Then, the mechanisms of how these medicines affect the intestinal epithelial barrier were investigated by investigating gap density and TNF- α pathway. Results: Gaps could be clearly observed by CLE, Gap density increased after indomethacin administration. During this process, the expressions of TNF- α, NF-kB and Caspase-3 were up-regulated while the expressions of tight junction were down-regulated. Teprenone and rabeprazole could interfere in the damage process and protect the integrity of the epithelial

barrier. Conclusion: CLE can be more objective, accurate and real-time to selleckchem investigate gap density. Teprenone and rabeprazole could prevent indomethacin-induced intestinal demage and improve the integrity of the epithelial barrier mediated by the intervention of TNF-α pathway. Key Word(s): 1. Epithelial barrier; 2. endomicroscopy; 3. Gap density; 4. TNF- α; Presenting Author: YING KIT LEUNG Corresponding Author: YING KIT LEUNG Affiliations: Precious Blood Hospital Objective: We have previously demonstrated that the vasculature in villi are of the reverse fountain pattern, one-uo, one down pattern or the reticular pattern. Whether these pertain to a arteriole-venule pattern

or mainly comprise of capillaries is not yet confirmed Verteporfin scientifically. The aim of this study is to visualize how blood elements flow in the vasculature of the villi in a living human under sedation, hence infer the basic characteristic of such blood vessels. Methods: Ten subjects underwent colonoscopy and probe-based confocal laser endomicroscopy (pCLE) were included into the study. The indications of the procedure being: inflammatory bowel disease, familial adenomatous polyposis, colonic polyps and abdominal pain. Fluorescein was injected after the small intestine was entered, and the villi examined with pCLE which took video images at 12/sec. The velocities of cellular movement in the vessels were determined during playback of the videos, and compared with similar measurement of flow around colonic crypts. Results: Blood elements of diameter around 7–10 microns, move in the vessels in an episodic manner.

Buffering intracellular Ca2+ nearly completely abolished ATP-induced Ca2+ signals (Fig. 9A, B). Moreover, when formation of InsP3 or its target channels were blocked, there was also a significant reduction in ATP-induced Ca2+ release (Fig. 9C, D). These results provide evidence that intracellular Ca2+ signals are required PLX4032 supplier for insertion of Mrp2 into the plasma membrane, and in particular suggest that Ca2+ released by an InsP3R-dependent mechanism is responsible for targeting of Mrp2. The current work shows that InsP3R2 KO hepatocytes have defective Ca2+ signaling and organic anion secretion, and that insertion of Mrp2

into the plasma membrane is Ca2+ dependent. InsP3R2 KO mice develop normally, and no gross phenotypical alteration

has been described. However, double-knockout mice lacking both InsP3R2 and InsP3R3 have deficient secretion of saliva and pancreatic zymogens, which results in an inability to fully digest and absorb nutrients. Pancreatic acinar cells isolated from these double-knockout animals have decreased Ca2+ release and accumulate zymogen granules, presumably reflecting impaired exocytosis.43 In the current work, Ca2+ signals in hepatocytes selleckchem isolated from InsP3R2 KO mice showed reduced amplitude, and there was an increase in rise time of the Ca2+ signals. Together these kinetic

parameters of Ca2+ signaling indicate a significant impairment in Ca2+ release in the InsP3R2 KO cells. This effect is consistent with the observation that pericanalicular InsP3R2 are essential to create a trigger zone to initiate and propagate Tolmetin Ca2+ waves in rat hepatocytes,12, 14 much like what is observed in pancreatic acinar cells16, 44 and in cholangiocytes.32, 45 The results presented here also demonstrate decreased Mrp2 activity in sandwich cultures of InsP3R2 KO hepatocytes. This effect is likely attributable to the action of InsP3R2 as an intracellular Ca2+ release channel, because the effect was duplicated by chelation of cytosolic Ca2+. This apparent effect of Ca2+ could be attributable to regulation of transporter activity, trafficking, or expression. The absence of InsP3R2 did not affect either expression levels or localization of Mrp2, however. Instead, TIRF measurements suggested that release of intracellular Ca2+ promotes insertion of rat Mrp2 into the plasma membrane. This is consistent with previous observations that Ca2+ and PKC act as regulators of exocytosis in the liver46 and also with reports showing that tauroursodeoxycholic acid induces Ca2+ release24 and Ca2+-dependent exocytosis25 and activates conventional PKCs, leading to Mrp2 insertion into the canalicular membrane.

Several minutes later, the same cell assembled additional hot spots at different locations

along the cell base that also generated many vesicles and then disappeared (images not shown). Many of these dynamin-associated vesicles were seen translocating in a linear path, as if along find more cytoskeletal filaments. This observation suggests that dynamin may remain on the motile vesicle, rather than immediately dissociating as predicted.13 We counted the number of vesicles generated during a typical hot spot lifetime (10-15 minutes) and observed an average steady state release of 4-6 vesicles/min (4 cells counted). Most remarkable is that each hot spot undergoes a 2 to 3-minute burst that generates 15-20 vesicles per minute during which the structure physically “dissolves.” This is exceptionally rapid

when compared with the release of multiple vesicles from conventional clathrin pits (1-2 vesicles/min).20 The rapid vesicle formation from Dyn2/clathrin/AP2 hot spots suggests that these are endocytic structures that are either continuous with the PM or reside as an internal endocytic sorting compartment. Because the HRP marker used to label hot spots by EM (Fig. 1C) was internalized by cells over a 45-minute time period, it is possible that the endocytic hot spots, while in intimate proximity with the PM, represent internal endocytic sorting compartments. To test if these endocytic structures are distinct from or continuous with the PM, we utilized Ruthenium red (RR), an electron-dense dye, to label the cell surface and

any invaginations Lenvatinib cost continuous with the external environment. Because the dye is included in the primary fixative, thereby preventing its internalization, membrane compartments stained with the dye represent extensions of the PM. As expected, cells stained with RR, processed for EM, and sectioned transverse to the substrate showed very dark apical and basal PMs, whereas internal membrane Inositol monophosphatase 1 systems were only lightly stained (Fig. 4A,B). In control cells (Fig. 4A), small patches of dark, tubular invaginations were observed extending from the basal, but not the apical, PM. These structures were nearly identical in dimensions to those observed in the HRP-labeled cells that were sectioned en face (Fig. 1) and appear as a “side view” of the endocytic hot spots shown in the previous figures. Most important, these endocytic structures were darkly stained with the RR dye, indicating that they are continuous invaginations of the PM. Because GFP-tagged Dyn2 associates with the endocytic hot spots (Figs. 1-3), we predicted that disruption of Dyn2 function would alter the number and complexity of the RR-positive PM invaginations. To test this hypothesis, cultured cells were microinjected with one of two purified polyclonal antibodies that we have used in previous studies to inhibit dynamin function.

This study was approved by the institutional review board of Yamaguchi University Hospital (H25-8). Venous blood samples were obtained in the morning after overnight fasting. Complete blood cell counts; prothrombin time (PT); and serum levels of total bilirubin,

aspartate aminotransferase (AST), alanine aminotransferase (ALT), γ-glutamyltransferase, total protein, albumin, total cholesterol, triglycerides, fasting glucose and immunoreactive insulin were measured in all patients by standard laboratory techniques. Hemoglobin A1c levels were measured in 60 patients. In addition, we calculated FIB-4, a simple and non-invasive index of fibrosis.[18] KU-57788 clinical trial The index was calculated automatically using the following formula: age (years) × AST (IU/L) / platelet count (109/L) × ALT (IU/L)1/2. For cut-off values, we used previously designated values: FIB-4 index of less than 1.45 and more than 3.25.[18, 19] The ratio of BCAA to tyrosine level and serum levels of BCAA and tyrosine were assayed using a commercially available kit (Daiyacolor-BTR, Toyobo, Osaka, Japan), in which the normal ranges of BTR, BCAA and tyrosine in healthy subjects were 4.41–10.05, 344–713 and 51–98 μmol/L, respectively. Insulin resistance was evaluated on the basis of fasting levels of plasma glucose and insulin, according

to HOMA-IR.[20] HOMA-IR was calculated using the following formula: glucose (mg/dL) × insulin (μU/mL) / 405. The presence of IR was defined as a HOMA-IR of 2.5 or more; this HOMA-IR selleckchem value has previously been used as a cut-off

indicating a high Racecadotril probability of IR.[18] Histological examination was performed in 31 patients (echo-guided liver biopsy in 27 patients and surgical resection in four patients); 40 patients did not undergo histological examination. Echo-guided liver biopsy was performed using a 16-G biopsy needle. Fibrosis was staged according to the METAVIR score as follows: F0, no fibrosis; F1, portal fibrosis without septa; F2, portal fibrosis with few septa; F3, numerous septa without cirrhosis; and F4, cirrhosis.[21] The data are expressed as mean ± standard deviation. The correlation between HOMA-IR and each variable was evaluated by Spearman’s rank correlation coefficient. A receiver–operator curve (ROC) was generated by plotting the sensitivity against 1-specificity. The area under the curve (AUC) was calculated to compare the predictive validity of variables and to determine optimal cut-off values to predict a high HOMA-IR (≥2.5), as follows: AUC of more than 0.9, high accuracy; 0.7–0.9, moderate accuracy; 0.5–0.7, low accuracy; and 0.5, a chance result.[22, 23] An AUC of 0.7 or more reflected the discriminative power to predict HOMA-IR outcome within the observed range of each variable. Univariate and multivariate analyses were performed using logistic regression.

When tumor recurrence was evaluated in 31 patients who underwent TBF-based partial hepatectomy, only three cases (9.7%) developed recurrences in the same segment, indicating that most recurrences due to systemic IM or MC could not be prevented if anatomical segmentectomy was performed (Fig. 7). In addition, no local, cutting-edge (<1 cm) recurrences were observed in these patients. A recent study revealed that the impact of TBF-based hepatectomy on survival is comparable to that of anatomical hepatectomy.[15] These findings are very convincing because the high-risk area of local IM was completely resected by this type of surgery. Therefore, compared Obeticholic Acid cost with anatomical hepatectomy, TBF-based hepatectomy

for HCC is less invasive and enables us to preserve more liver function with comparable curability. Because locoregional treatment click here cannot prevent hepatic recurrences by systemic IM or MC, these need to be treated with systemic chemotherapy. The occurrence of MC after surgery may also be suppressed by treating the underlying chronic hepatitis. TUMOR BLOOD FLOW-BASED hepatectomy

for HCC is basically identical to anatomical hepatectomy in terms of the concept that tumor spreads through the portal blood flow where tumor blood flows in. The difference is whether or not the confirmation of TBF area as safety margin is done before surgery. TBF-based hepatectomy is minimally invasive but as sufficiently curative as anatomical hepatectomy because the high-risk

area of local IM is identified and completely resected. “
“Background And Aims:  The aims of the present study were to evaluate the role of moderate-to-severe endoscopic gastric atrophy (EGA) on predicting Operative Link on Gastritis Assessment (OLGA) gastritis stage, and to assess the association of high-stage OLGA gastritis with gastric neoplasia in patients with non-ulcer dyspepsia. Methods:  A cross-sectional study was carried out on 280 dyspeptic outpatients. EGA was assessed according to the Kimura–Takemoto classification. Gastritis stage was established according to Phosphatidylinositol diacylglycerol-lyase the OLGA staging system and gastric neoplasia was assessed according to the Vienna classification. The pathologists who read the specimens were kept blind to the endoscopic results. Results:  The mean age of patients was 46.1 years (range 20–78 years) with a male-to-female ratio of 1:1. High-stage gastritis (e.g. stage III or IV) was confirmed in 13 (4.6%) patients. All of these patients were more than 40 years-of-age (P = 0.01), had Helicobacter pylori infection (P = 0.0006) and moderate-to-severe EGA (P < 0.001). Low-grade dysplasia was found in seven patients: 4/13 (30.7%) with high-stage gastritis versus 3/267 (1.1%) with low-stage gastritis (P < 0.001). Six of these patients had moderate-to-severe EGA (P = 0.048). The sensitivity, specificity, positive predictive value and negative predictive value of this endoscopic finding in high-stage gastritis diagnosis were 100%, 57.