The aim of this study is to evaluate the feasibility of pCLE for

The aim of this study is to evaluate the feasibility of pCLE for the duodenum neoplasms. Methods: After training the diagnosis of several typical CLE images of normal mucosas, adenomas and carcinomas of duodenum, 15 case images (5 normal mucosas, 5 adenomas, 5 carcinomas) were selected. 12 different endoscopists (2 ∼ 16 years) diagnosed the images and were compared with the histopathological diagnoses (biopsy, ESD specimen) by the pathologist. Results: The accuracy of the 15 case images diagnosed by the endoscopists was 66.7 ∼ 93.3% ALK inhibitor and the rate did not relate to the years of experience of the endoscopy.

The accuracy of the normal mucosa, adenoma, and carcinoma were 73.3%, 68.3%, 100%, respectively. The accuracy, sensitivity and specificity for carcinomas were 100%. Conclusion: The results of CLE and histopathological diagnoses were relatively high in this study, regardless of the years of experience of the endoscopy. This study suggeste

d that the model image of CLE will make possible to differentiate carcinoma or non-carcinoma. Further studies based on a large number of cases are necessary to clarify this suggestion. Key Word(s): 1. Probe-based confocal laser endomicroscopy (PCLE) Presenting Author: SHINTARO MINOWA Additional Authors: MARI HAYASHIDA, DAISUKE SAITO, AKIHITO SAKURABA, YUJI YAMADA, YASUHARU YAMAGUCHI, GENICHI KOYAMA, HIROSHI YAMAZAKI, SHIN’ICHI TAKAHASHI Corresponding Author: SHINTARO MINOWA Affiliations: Kyorin University School of Medicine, Kyorin Kinase Inhibitor Library solubility dmso University School of Medicine, Kyorin University School of Medicine, Kyorin University School of Medicine, Kyorin University School of Medicine, Kyorin University School of Medicine, National Institute of Infectious Diseases, Kyorin University School of Medicine Objective: A 20 year-old Japanese female had visited southeast and west Asian countries for several times on business during 2 years. She admitted a hospital due to sudden onset of convulsion. A brain magnetic resonance imaging (MRI) detected numerous small cystic lesions in the brain cortex and basal ganglia. The patient was referred to the Neurology Department

of Kyorin University Hospital for a suspected brain selleck chemical infection such as toxoplasmosis. Methods: The brain MRI showed numerous cystic lesions in exhibiting a typical ‘hole-with-a-dot’ sign that is highly characteristic of NCC. Since the serum antibody and cerebrospinal fluid antibody was positive for NCC she was diagnosed as NCC. Although the eggs and proglottids of Taenia solium were not detected in feaces,capsule endoscopy was performed prior to anthelmintic treatment to determine whether the Taenia solium had exists on the digestive tract. If Taenia solium exist on the digestive tract, the antiparasitic agent may be induce NCC by destroying proglottids. Because the parasite eggs and the hexacanth larvae may moving in systemic.

43 As shown in Fig 4, hepatic expression of activated pSTAT1 was

43 As shown in Fig. 4, hepatic expression of activated pSTAT1 was markedly higher in HFD-fed IL-10−/−IL-6−/− and IL-10−/−STAT3Hep−/− dKO mice compared with IL-10−/− mice, indicating that IL-6/STAT3 activation is responsible for inhibiting STAT1 activation. In conclusion, IL-10−/− mice displayed Everolimus datasheet greater liver inflammatory response but less steatosis after ETOH or HFD feeding compared with WT mice, and inflammation-associated IL-6/STAT3 activation contributes to the reduced steatosis in these mice. Interestingly, hepatic IL-6/STAT3 is also activated

in WT mice after ETOH or HFD feeding, but to a lesser extent compared with IL-10−/− mice (Figs. 1-3). This finding suggests that endogenous IL-10 plays an important role in inhibiting hepatic IL-6/STAT3 activation, which may account for the weak activation of this signaling pathway in the liver in WT mice during ETOH or HFD feeding. buy GSK1120212 It has been reported that hepatic levels of IL-10 were elevated in mice after an 8 weeks of HFD feeding;28

however, we did not observe hepatic IL-10 up-regulation in WT mice after 12 weeks of HFD or 4 weeks of ETOH feeding. In contrast, we observed marked up-regulation of hepatic IL-10 mRNA in mice fed with HFD for 1 year (unpublished data). Furthermore, it has been reported that hepatic expression of IL-10 mRNA is not up-regulated in obese individuals without fatty liver but markedly up-regulated in those with fatty liver, which is further increased in individuals with NASH.44 This suggests that hepatic IL-10 is elevated after long-term HFD consumption in patients and

in mice, which may play a compensatory role in preventing inflammation in fatty liver disease. The fact that IL-10−/− mice had greater liver inflammatory response but less steatosis suggests that inflammation, as reported previously, may not only promote the development of fatty liver by producing TNF-α and IL-1 but may also ameliorate the fatty liver by producing cytokines (such as IL-6) that activate STAT3. Therefore, the overall effect of inflammation on hepatic steatosis is determined by the balance between detrimental cytokines that promote steatosis and hepatoprotective cytokines that prevent steatosis. It is of keen interest to explore the effect of inflammation on steatosis in patients with ASH and NASH. Recently, this website Bertola et al.44 reported that the liver of obese patients without obvious steatosis (S0) was associated with elevation IL-6 but not TNF-α and IL-1β. It is plausible that such elevation of inflammation-associated IL-6 plays a compensatory role in preventing the development of steatosis in the early stage of nonalcoholic fatty liver in obese patients. The liver of obese patients with severe steatosis (S3) and NASH was associated with highest fold induction of IL-6, followed by TNF-α and IL-1β. It is probable that the steatosis in these patients is modulated negatively by IL-6 but positively by TNF-α and IL-1β.

pylori strain Of particular interest are the results regarding r

pylori strain. Of particular interest are the results regarding runx3 promoter methylation, which were described by Park et al. [46] in intestinal metaplasia and confirmed by Katayama et al. [47] who showed runx3 promoter

methylation occurs in gastric epithelial cells co-cultured with macrophages exposed to live H. pylori. Among the epigenetic alterations following H. pylori infection, deregulation of microRNAs (miRs) expression might also be relevant for pathogenesis. miRs are non coding small RNAs which control mRNA translation and they frequently are deregulated in human cancers. Ando et al. [48] studied the methylation status of a series of miRs in a series of gastric cancer cell lines, GDC-0449 datasheet in primary gastric cancers, and in gastric mucosa Fulvestrant from patients with or without H. pylori infection,

and provided evidence that H. pylori infection is associated with higher methylation of miR-124. Gao et al. [49] demonstrated a reduction of miR-218 in gastric cancer tissue, but also a putative amplification of this reduction by H. pylori infection. In vitro experiments with overexpression or silencing of miR-218 allowed the authors to demonstrate that miR-218 induces apoptosis and decreases cell proliferation by promoting ECOP (epidermal growth factor receptor coamplified and overexpressed protein) degradation, which decreases NF-kB activation. Interference with these miR methylations might provide novel options for fighting gastric cancer development in H. pylori-infected patients. The inflammatory response induced by H. pylori is a key event linked to pathogenesis. Significant insights, summarized in Fig. 1, have been made in the last year on the interactions between H. pylori, mucosal dendritic cells and IL17. The readers are referred to the article on the host response of this issue for more data regarding H. pylori and inflammation. In conclusion, in the last year

an impressive number of papers have been published on H. pylori genetic variation of genes encoding OMPs, on microbe mimicry with host antigens, on factors that alter host-cell signaling and modulate the host’s immune response. These new insights allow us to improve our knowledge on the pathogenetic mechanism and the true nature of this click here pathogen, paving the way to better understanding its role in the human disease. In addition, this knowledge may lead to develop a more personalized diagnosis and tailored treatment of H. pylori-related gastrointestinal diseases. The authors declare no conflict of interest. “
“Background: Helicobacter pylori is mainly acquired in childhood. Although adult studies reported a high prevalence of H. pylori infection in Portugal, the actual rate in children remains unknown. This study aimed to determine the prevalence and the incidence of H.

e, against HIV, HSV, influenza virus

e., against HIV, HSV, influenza virus Trichostatin A and HCV) by targeting virus entry, reverse transcription or gene expression. Aims. To investigate the potential antiviral effect of Flavocoxid (containing the natural flavonoids, baicalin and catechin) against HBV and

to verify whether the antiviral control exerted by Entecavir (ETV) in HBV-replicating cells may be enhanced by its use in combination with FLAV. Methods. HepG2 cells were transfected with linear wild-type HBV genomes. HBV replicating cells were treated with different dosages of Flavocoxid to determine the drug inhibitory concentrations (IC50). Treatment with Flavocoxid or ETV or with drugs combination started 3 hours after transfection and was renewed every other day for 7 days. Total HBV replicative intermediates, viral transcripts and cccDNA levels were evaluated in untreated and treated HepG2 cells by quantitative real-time PCR, Southern and Northern blots experiments. To

analyse AZD3965 supplier the epigenetic modulation of HBV cccDNA the cccDNA-ChIP assay was applied to untreated and treated cells Results. The analysis of HBV transcription/replication in the presence or absence of Flavocoxid enabled to determine that IC50 for the drug was 75 μg/mL. HBV replicative intermediates in cell treated with ETV, FLAV, or FLAV + ETV were decreased by 47%, 68%, and 83%, respectively,

compared with untreated HBV-replicating HepG2 cells. After exposure to ETV, FLAV or FLAV + ETV, Northern blot analysis showed that HBV pregenomic RNA levels were decreased this website by 31%, 87%, and 85% respectively, compared with untreated HBV-replicating cells. Levels of HBV cccDNA in the nuclei of cells treated with FLAV or FLAV + ETV were reduced by 34% and 23%, respectively, whereas treatment with ETV, failed to decrease cccDNA. HBsAg amount was reduced by 20%, 75%, and 60% in the supernatant of cells treated with ETV, FLAV, and FLAV + ETV, respectively, compared with untreated cells. Epigenetic analysis showed that cccDNA-bound H4 histones were hypoacetylated in cells treated with ETV, FLAV, or FLAV + ETV and that the recruitment of HDAC1 histone deacetylase was increased at higher levels both in FLAV and FLAV + ETV treated cells. The binding to the cccDNA of NFkB transcriptional regulator was strongly reduced in all treated cells Conclusions. The results of our study demonstrate that Flavocoxid: (a) is capable to inhibit HBV replication, (b) exerts its antiviral activity against HBV at multiple levels and (c) acts synergistically with ETV in a cell-based HBV replication system.

It is well known that alcohol abstinence is related to maintenanc

It is well known that alcohol abstinence is related to maintenance or even reductions of Buparlisib molecular weight HVPG values in patients receiving or not receiving drug therapy,9, 20 whereas alcohol consumption clearly worsens portal hypertension both in the short21 and long term.9 Lastly, it is worth remarking that, in contrast to the study by Villanueva et al.,9 the loss of long-term response in our responders could not be attributed to a reduction of drug doses during follow-up due to intolerance or noncompliance. Only five patients (12.5%) in our cohort had their doses reduced, three of whom maintained the initial response. The present study was designed to evaluate the hemodynamic

evolution and outcomes of responders. Consequently, the comparison between the outcomes of initial responders and nonresponders is not suitable, because there are relevant differences between those groups in terms of baseline

risks, treatments received, and follow-up times. Nonetheless, two secondary observations derived from the analysis of the whole study cohort deserve consideration. First, the prognosis of those patients who rebled before the second HVPG was dismal (seven deaths and five transplants of 13 patients), which confirms data from previous studies. Second, the protection from rebleeding of nonresponders, which were kept from FK228 mouse the beginning with endoscopic ligation combined with drug therapy, was excellent. The low rebleeding rate of initial nonresponders (12%) could be related at least in part to a shorter follow-up (26 months) or a higher incidence of competing events in this subcohort, although the competing risk analysis suggested otherwise. However, from our results and from that of recent observations,22 we clearly feel that adding ligation to drug therapy in nonresponders (instead of switching them to ligation alone, as in the majority of previous studies) could be an effective approach, which should be nevertheless evaluated in a randomized controlled trial. The potential practical implications of the present study are straightforward. Our results suggest that, in an HVPG-guided

prophylactic regimen, responders could be safely treated with drug therapy alone during the learn more first 1-2 years, but whether this strategy remains effective in the long term is unknown. Consequently, it would be reasonable to reassess HVPG regularly in patients with viral cirrhosis and/or active alcohol consumption and to protect patients who have lost their response. Early rebleeders (those who rebleed before the second HVPG) may be regarded as candidates for more aggressive therapies (such as early TIPS)23 or liver transplantation, and initial or long-term nonresponders may be considered to have ligation added to drugs. All these potential implications should be ideally tested in randomized controlled trials. Before these results could be transferred to patient care, several limitations related to the design of our study should be taken into account.

Results:  There was a sustained virological response (SVR) rate o

Results:  There was a sustained virological response (SVR) rate of this treatment in 90% of the patients, and sex, age and HD duration

had no affect. Slight adverse this website effects such as fever, malaise and itching were observed during the treatment periods but none serious in any of the patients. Also, no significant difference in adverse effect was observed between 3 MIU and higher dose (6 MIU) groups. Conclusion:  Because IFN-β can be administrated easily into the circuit of HD, adverse effects can be monitored earlier and taken measures against quickly. Taken together, IFN-β-based therapy has a potential for HCV treatment in HD patients but further studies for the patients who have higher viral loads will be required to confirm this. “
“The survival of patients with hepatocellular carcinoma GPCR Compound Library concentration (HCC) is often individually different even after surgery for

early-stage tumors. Gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid (Gd-EOB-DTPA)-enhanced magnetic resonance imaging (MRI) has been introduced recently to evaluate hepatic lesions with regard to vascularity and the activity of the organic anion transporter OATP1B3. Here we report that Gd-EOB-DTPA-enhanced MRI (EOB-MRI) in combination with serum alpha-fetoprotein (AFP) status reflects the stem/maturational status of HCC with distinct biology and prognostic information. Gd-EOB-DTPA uptake in the hepatobiliary phase was observed in ∼15% of HCCs. This uptake correlated with low serum AFP levels, maintenance of hepatocyte function with the up-regulation of OATP1B3 and HNF4A expression, and good prognosis. By contrast, HCC showing reduced Gd-EOB-DTPA uptake with high serum AFP levels was associated with poor prognosis and the activation of the oncogene FOXM1. Knockdown of HNF4A in HCC cells showing Gd-EOB-DTPA uptake resulted in the increased expression of AFP and FOXM1 and the loss

of OATP1B3 expression accompanied by morphological changes, enhanced tumorigenesis, and loss of Gd-EOB-DTPA uptake in vivo. HCC classification selleckchem based on EOB-MRI and serum AFP levels predicted overall survival in a single-institution cohort (n = 70), and its prognostic utility was validated independently in a multi-institution cohort of early-stage HCCs (n = 109). Conclusion: This noninvasive classification system is molecularly based on the stem/maturation status of HCCs and can be incorporated into current staging practices to improve management algorithms, especially in the early stage of disease. (Hepatology 2014;60:1674–1685) “
“Liver fibrosis occurs as a result of several chronic liver diseases and leads to portal hypertension, cirrhosis and liver failure, often requiring liver transplantation.


of their accumulation suppressed metastatic gr


of their accumulation suppressed metastatic growth,13 thus reinforcing the idea that myeloid cells are important for metastatic development in the liver. Here we report a different prometastatic CD11b/Gr1mid myeloid subset associated with CRC liver metastases. Recruitment of these cells was dependent on CCL2/CCR2 and its inhibition markedly reduced tumor burden. Moreover, depletion of the CD11b/Gr1mid subset significantly decreased tumor cell selleck products proliferation. Cells analogous to the CD11b/Gr1mid subset were identified in patients with CRC liver metastases, underscoring their potential for therapeutic manipulation. ANOVA, analysis of variance; cDNA, complementary DNA; CRC, colorectal cancer; DT, diphtheria toxin; DTR, diphtheria toxin receptor; FACS, fluorescence-activated cell sorting; GFP, green fluorescent protein; IL, interleukin; KO, knockout; LLC, lung Lewis carcinoma; PBS, phosphate-buffered saline; SCID, severe combined immunodeficiency; TIMP-1, tissue inhibitor of metalloproteinase 1; VEGFR1, vascular endothelial growth factor receptor 1. The sources of mice,

cell lines, and patient samples are detailed in the Supporting Information. Animal procedures were performed in accordance with the UK Animal (Scientific Procedures) Act 1986 and followed local ethics review. Tumor cells (5 × 105/100 μL phosphate-buffered saline [PBS]) were injected into the spleens of C57BL/6, CCR2 knockout (KO), severe combined immunodeficiency (SCID), or CD11b-diphtheria toxin receptor (DTR) mice. The spleens were removed,

and the mice were sacrificed on day 14. To inhibit CCL2, C57BL/6 mice received daily intraperitoneal injections of CCL2 antibody (15 μg/mouse; R&D Systems) or rat immunoglobulin G2b control (R&D Systems) following tumor cell inoculation. CD11b-DTR or C57BL/6 mice received diphtheria toxin (7.5 ng DT/g body weight; List Biological Laboratories) or PBS see more via intraperitoneal injection on day 7 and 9, and sacrificed on day 11. Bone marrow cells were isolated from female C57BL/6-Tg(UBC-GFP)30Scha/J mice (provided by Prof. Richard Cornall, University of Oxford, UK), and 2 × 106 cells were transferred intravenously into C57BL/6 mice on day 11. Mice were sacrificed on day 12. Single cell suspensions were prepared from livers, bone marrow, and blood as described in the Supporting Information and were adjusted to 107 cells/mL for fluorescence-activated cell sorting (FACS) analysis. Antibodies used are detailed in the Supporting Information. FACS analysis was performed using a FACSCalibur flow cytometer (BD Biosciences) and analyzed with FlowJo software version 7.2.5 (Tree Star, Ashland, OR). RNA was isolated with Trizol (Invitrogen) and complementary DNA (cDNA) (0.5 μg) synthesized using the SuperScript VILO cDNA kit (Invitrogen).

These “mixed” families were assigned a “family diagnosis” using t

These “mixed” families were assigned a “family diagnosis” using the following criteria: “MO” when the proband suffered from MO and less than 20% of affected members suffered from a different type of migraine and “MA” when at least 20% of the affected family members suffered from headaches preceded by an aura. According to these criteria, 30 (49%) families were “MO,” 27(44%) were “MA,” and 4 (7%) were FHM. Known migraine loci already had see more been excluded in this sample by SSCP screening and linkage (specifically, CACNA1A, chromosome 19 and 1, and “Finnish Locus” on chromosome 4). Two hundred and seventeen of all included persons were affected;

126 had MO, 70 had MA, and 15 had migraine with selleck products hemiparetic aura. One was

diagnosed with “acephalgic” migraine, and 5 with probable migraine. We assigned the status “unknown” to all patients with insufficient information available and also to all not meeting all criteria for migraine but also not meeting criteria for any other type of headache; 42 patients were recorded in this manner. We had 163 blood samples from unaffected relatives. On 32 family members we had full information but no blood samples. Details of family structure are shown in the Table. Genotyping.— Venous blood samples were collected from 380 subjects, and genomic DNA was extracted by standard procedure.30 In a first round, we screened 18 fluorescent-labeled markers spaced on an average of 10 cM apart and spanning the entire X-chromosome (Linkage Mapping Panel 28, Applied Biosystems, Foster City, CA, USA). A positive logarithm of the odds (LOD) score at Xp22 and allele sharing at Xq24-q28 then prompted further evaluation of additional markers in both regions (Xp22: DXS7100, DXS996, DXS1223, DXS1053; Xq24-q28: DXS8028, DXS1200,

DXS1193, DXS1123, DXS8069, DXS8011). The order and distances between the markers were determined on the basis of their physical and genetic location, respectively, and according to the combined published data (; The amplification reactions were run in microtiter 96-well selleck chemicals plates with standard conditions on a MJ Research thermocycler. Depending on marker performance, there was some minor variation of annealing temperature and MgCl concentration. The PCR products subsequently were pooled for electrophoresis and supplemented with an internal size standard. A high through-put capillary electrophoresis system was used (ABI DNA Analyzer 3700, Applied Biosystems), and GENESCAN® and GENOTYPER® software was used for allele scoring (Applied Biosystems). All genotypes were verified by human inspection. Pedcheck 1.1 was used to detect genotyping errors.31 If the mistyping could not be resolved by review of the data, the suspected genotypes were set to unknown. Linkage Analysis.

001), as were the numbers of B cells expressing the CD80+ recepto

001), as were the numbers of B cells expressing the CD80+ receptor and monocytes expressing the activation marker NKR-P1A (Table 2). Of note, we also observed the marked expansion of dendritic cells (by 2.3-fold [P < 0.05]) in the MLNs of rats with cirrhosis. Thereafter, we explored the contribution of enteric bacteria to the activation of MLNs and circulating immune system cells. Although no episodes of bacterial translocation were detected in rats with cirrhosis or control rats (culture-negative MLNs), bacterial DNA was demonstrated in the MLNs of 15 of the 28 rats with cirrhosis (53.6%) (Table 3) and in no

control animals (P < 0.01). As illustrated in Fig. 1, there is a close association between the immune system alteration observed in the MLNs of rats with cirrhosis and the presence of bacterial beta-catenin pathway DNA fragments. Indeed, the numbers of activated Th cells, B cells, and monocytes in the MLNs of rats with cirrhosis without bacterial CpG motifs were similar to those observed in control rats. Accordingly, RAD001 levels of the proinflammatory cytokines TNFα and IL-6 were only elevated in the MLNs of rats with cirrhosis and bacterial DNA (Fig. 2). We went on to examine the relative contributions of liver/HLN and/or enteric bacterial driven-mesenteric inflammation to the activated immune system cells observed in the circulation of rats with cirrhosis. To this end, we

analyzed the activation status of immune cells in peripheral blood according to the presence of bacterial DNA in MLNs and in response to bowel decontamination with nonabsorbable antibiotics, as well as correlations among activated immune cells in the compartments studied. As shown in Fig. 1, the numbers of total and activated Th cells and monocytes in the peripheral blood of rats with cirrhosis without bacterial DNA in MLNs were significantly greater than in control animals, but similar to those observed in rats with cirrhosis with bacterial selleck chemical DNA. Bowel decontamination normalized the number and activation state of immune cells in the MLN, but did not affect immune cell subpopulations in peripheral

blood or HLN (Table 4). We did not detect fragments of bacterial DNA in the MLNs of any of the antibiotic-treated rats with cirrhosis. Indeed, the broad-spectrum nonabsorbable antibiotics abrogated the expansion of recently activated CD134+ and CD62L− Th cells, inflammatory monocytes, and dendritic cells in the MLNs of rats with cirrhosis, whose values were no longer significantly different from those found in control animals. In contrast, antibiotics lacked any significant effects on the distribution and activation status of immune cells in the HLNs and peripheral blood of rats with cirrhosis (Table 4). Notably, we observed direct correlation between the percentage of recently activated Th cells (r = 0.59, P < 0.01) and inflammatory monocytes (r = 0.64, P < 0.01) found in the blood and HLNs of individual rats with cirrhosis (Fig.

This study is performed to investigate the effect of CPAP on post

This study is performed to investigate the effect of CPAP on post-prandial LOS pressure, TLOSRs and gastro-oesophageal reflux in healthy individuals. Methods: Two 2-h postprandial manometric and pH recordings were performed at least 2 weeks apart, in 13 awake, healthy, semi-recumbent individuals. CPAP was applied with a standard mask pressure of 10 mmHg. Sham CPAP was performed using a modified CPAP unit in which a nasal mask with multiple 10 quarter-inch drilled

holes to allow for adequate exchange with the environment. The recordings were analysed for the numbers of TLOSRs the proportion of TLOSRs associated with acid reflux, basal LOS pressure and duration of oesophageal pH < 4. Results: The mean numbers of TLOSR were almost identical between the two groups; 8.2 ± 2.7 and 8.2 ± 6.7. The mean numbers of acid reflux with the Tamoxifen purchase actual CPAP nasal mask and sham CPAP nasal mask and machine were 4.6 ± 3.6 and 3.3 ± 2.9 respectively (p = 0.38), and the percentage of TLOSRs which were associated with acid reflux between the two groups were 54.3 ± 36.0 and 44.3 ± 35.0 respectively (p = 0.32). The basal LOS pressure did not show any significant difference between the

two groups as well. Conclusion: CPAP did not increase post-prandial LOS pressure, or reduce the incidence of TLOSRs and reflux episodes in normal healthy subjects. Further studies in patients with reflux disease, particularly those with hiatus hernia, should be explored. Key Word(s): 1. CPAP; 2. LOS Pressure; 3. GORD; 4. Healthy Volunteers; Presenting Author: REDENTORPANGAN ALQUIROZ Additional Authors: IAN HOMERY CUA Corresponding Author: REDENTORPANGAN ALQUIROZ Affiliations: St. Luke’s Medical Center Objective: Chronic constipation is a very common functional gastrointestinal disorder which can be associated with significant impairments in quality of

life for some people with the condition. Its management has, traditionally, been based on dietary and lifestyle changes and the use of a variety of laxative agents. Prucalopride, appears to be highly selective for the serotonin selleck compound 5-HT4 receptor and is, therefore, a potent stimulator of gut motility. The main objective of this meta-analysis is to test the clinical efficacy and safety of the selective and high affinity serotonin-4 (5-HT4) receptor agonist prucalopride in the management of chronic constipation. Methods: Articles were identified through MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials and internet electronic databases. We searched abstracts, lists of review articles and retrieved studies by manual and internet search strategies. Two reviewers independently assessed trial quality and extracted data. Analyses were performed using the Mantel-Haenszel test. Random effects models were used when heterogeneity was noted. Results: A total of six (6) studies with total sample size of 3616 patients were included.