Multiple

treatment options are available for replacing missing central incisors. The management demands a multidisciplinary approach involving the orthodontist, prosthodontist, and periodontist. Treatment planning requires consideration of a variety of clinical and nonclinical factors. This clinical report attempts to demonstrate different strategies for the management of unilaterally and bilaterally missing central incisors. “
“Purpose: The aim of this study was to evaluate RXDX-106 molecular weight the effectiveness of adhesive primers (APs) applied to Co-Cr and Ni-Cr metal alloys on the bond strength of resin cements to alloys. Materials and Methods: Eight cementing systems were evaluated, consisting of four resin cements (Bistite II DC, LinkMax, Panavia F 2.0, RelyX Unicem) with or without their respective APs (Metaltite, Metal Primer II, Alloy Primer, Ceramic Primer). The two types of

dental alloys (Co-Cr, Ni-Cr) were cast in plate specimens (10 × 5 × 1 mm3) from resin patterns. After casting, the plates were sandblasted with aluminum oxide (100 μm) and randomly STI571 cost divided into eight groups (n = 6). Each surface to be bonded was treated with one of eight cementing systems. Three resin cement cylinders (0.5 mm high, 0.75 mm diameter) were built on each bonded metal alloy surface, using a Tygon tubing mold. After water storage for 24 hours, specimens were subjected to micro-shear testing. Data were statistically analyzed by two-way ANOVA and Tukey’s studentized range test. Results: The application of Metal Primer II resulted in a significantly higher bond strength for LinkMax resin cement when applied in both metal alloys. In general, the cementing systems had higher bond strengths in Co-Cr alloy than in Ni-Cr. Conclusions: The use of AP between alloy metal surfaces and resin cements did not increase the bond strength for most cementing systems evaluated. “
“Langerhans cell

histiocytosis (LCH) is a disease of unknown etiology with a frustrating and unpredictable course. Surviving adult patients suffering Florfenicol from the multisystem type of the disease present with problems in most organs. This article presents the oral rehabilitation of a 28-year-old patient, with multisystem sequelae that included the oral cavity, classifying him as a Class IV American College of Prosthodontists Prosthodontic Diagnostic Index patient. A 5-year course of treatment is analyzed, starting from merely replacing missing teeth with a removable partial denture. The second stage of prosthetic rehabilitation included replacement of the removable prosthesis with fixed partial dentures. The final and most important aspect of treatment was the 2-year follow-up, when the patient presented with no problems or adverse effects.

Multiple

treatment options are available for replacing missing central incisors. The management demands a multidisciplinary approach involving the orthodontist, prosthodontist, and periodontist. Treatment planning requires consideration of a variety of clinical and nonclinical factors. This clinical report attempts to demonstrate different strategies for the management of unilaterally and bilaterally missing central incisors. “
“Purpose: The aim of this study was to evaluate click here the effectiveness of adhesive primers (APs) applied to Co-Cr and Ni-Cr metal alloys on the bond strength of resin cements to alloys. Materials and Methods: Eight cementing systems were evaluated, consisting of four resin cements (Bistite II DC, LinkMax, Panavia F 2.0, RelyX Unicem) with or without their respective APs (Metaltite, Metal Primer II, Alloy Primer, Ceramic Primer). The two types of

dental alloys (Co-Cr, Ni-Cr) were cast in plate specimens (10 × 5 × 1 mm3) from resin patterns. After casting, the plates were sandblasted with aluminum oxide (100 μm) and randomly Doxorubicin cell line divided into eight groups (n = 6). Each surface to be bonded was treated with one of eight cementing systems. Three resin cement cylinders (0.5 mm high, 0.75 mm diameter) were built on each bonded metal alloy surface, using a Tygon tubing mold. After water storage for 24 hours, specimens were subjected to micro-shear testing. Data were statistically analyzed by two-way ANOVA and Tukey’s studentized range test. Results: The application of Metal Primer II resulted in a significantly higher bond strength for LinkMax resin cement when applied in both metal alloys. In general, the cementing systems had higher bond strengths in Co-Cr alloy than in Ni-Cr. Conclusions: The use of AP between alloy metal surfaces and resin cements did not increase the bond strength for most cementing systems evaluated. “
“Langerhans cell

histiocytosis (LCH) is a disease of unknown etiology with a frustrating and unpredictable course. Surviving adult patients suffering either from the multisystem type of the disease present with problems in most organs. This article presents the oral rehabilitation of a 28-year-old patient, with multisystem sequelae that included the oral cavity, classifying him as a Class IV American College of Prosthodontists Prosthodontic Diagnostic Index patient. A 5-year course of treatment is analyzed, starting from merely replacing missing teeth with a removable partial denture. The second stage of prosthetic rehabilitation included replacement of the removable prosthesis with fixed partial dentures. The final and most important aspect of treatment was the 2-year follow-up, when the patient presented with no problems or adverse effects.

or later. Patients were classified into 2 groups: group I = urgent DBE (n = 74), group II = non-urgent DBE (n = 46). Results: Baseline characteristics of patients were similar between two groups. The diagnostic yield in urgent DBE was significantly higher than non-urgent DBE (73% vs. 30%; p < 0.001). Endoscopic interventions were performed in 43% of patients in urgent DBE group whereas 13% of patients in non-urgent DBE group underwent interventions (p = 0.001). The endoscopic findings and interventions

are shown in Table 1. At 30-day after DBE, recurrent bleeding rates were not different in both groups (13% in urgent DBE vs. Proteasome inhibitor 11% in non-urgent DBE). Conclusion: Urgent DBE in overt OGIB provided significant R788 research buy higher diagnostic and therapeutic yield than non-urgent DBE. However, it did not impact on the recurrent bleeding rate. Key Word(s): 1. small bowel bleeding; 2. balloon endoscopy; 3. urgent endoscopy; Table 1 The baseline characteristics of patients and the results of DBE between two groups Baseline characteristics Urgent DBE Non-urgent DBE p-value (n = 74) (n = 46) NS: non-significant Presenting Author: THANTHAN AYE Additional Authors: AYE AYE THAN, MIN ZAW HTUN, KHIN SAN AYE Corresponding Author: THANTHAN AYE Affiliations: University of Medicine (2), Yangon Objective: Gastrointestinal stromal tumor (GISTS) is the commonest gastrointestinal mesenchymal tumor. The small intestinal GISTS

account for 30–40%. Gastrointestinal(GI) bleeding is produced by pressure necrosis and ulceration of the overlying mucosa with resultant hemorrhage from disrupted vessels, commonly present with obscure GI bleeding. Massive lower gastrointestinal bleeding is a rare and unusual symptom of GISTs, especially in young patients. GISTs mimic with tuberculosis but association is rare. Methods: A 35-year-old apparently healthy man complaining of massive bleeding per rectum had been referred to us for endoscopic evaluation. Both Upper and lower GI endoscopy did not reveal active bleeding source except blood

coming from terminal ileum. Since no cause for the GI bleed was found and due to ongoing bleeding per rectum, patient was subjected to laparotomy. A tumor about 1.5 x 2 cm at the anterior border of small intestine near jejuno-ileal junction Urocanase was found. Multiple seedlings were also noted in serosa of small intestine and peritoneum with moderate ascites. Resection of the tumor bearing portion of small bowel was done. Histology showed tumor was composed of sheets of interlacing bundles of neoplastic spindled and stroma cells. Mitosis was infrequent (<5/50HPF). The adjacent bowel wall contained scattered caseating epitheloid granulomas replete with multinucleated Langhan’s giant cells. CD 117 was positive. Histology of parietal peritoneum revealed caseating epitheloid tubercles. Chest radiography did not show pulmonary tuberculosis. Patient was treated with anti-tuberculous treatment.

This makes it unlikely that BMP ligand-trap proteins, modification or degradation of BMP-Rs,

or Everolimus R-Smad deactivation play an important role in the modulation of the BMP effect by HGF or EGF. Further, total nuclear Smad1/5/8 is not decreased by HGF treatment (Fig. 5A). Additional modulation at the ligand-receptor level is provided by BMP pathway inhibitors including BAMBI,21 Smad 6,22, 23 and Smad7, the latter already known to play a role in hepcidin regulation.7, 24 The concentrations of BAMBI and inhibitory Smads determine their effect on signaling.23 We used whole-cell lysates of primary mouse hepatocyte cultures treated with BMP and HGF or EGF to examine the protein levels of the three inhibitors. After overnight incubation, neither Smads 6 or 7 (Supporting Fig. S6A,B) nor BAMBI (data not shown) were induced by growth factor treatments. Growth factors have been reported to decrease the total Smad1 pool by proteasomal degradation.25 GSK1120212 molecular weight Treatment with HGF had no effect on total Smad1 or Smad5 (Supporting Fig. S6C,D) in the 2 hours following HGF treatment or overnight

(data not shown). Treatment with EGF also did not cause a change in total Smad 1/5/8 in whole cell lysates (Fig. 5B). The common mediator Smad4 is also a target for regulatory input and its ubiquitination leads to its degradation in the proteasome.26 Decreased Smad4 in the context of hepcidin reporter suppression by hypoxia was recently described.27 From hepatocytes treated with BMP6 with and without HGF, we blotted nuclear lysates for Smad4. Smad4 levels in

the nucleus were unaffected by HGF, indicating that the BMP signal had adequate access to co-Smad for formation of transcription complexes (Supporting Fig. S6E). Thus, the mechanism for growth factor suppression of hepcidin does not include overall degradation of the receptor-activated Smad pool or Smad4. The linker region between the two globular domains of Smad1 can be phosphorylated by several kinases, including the mitogen-activated protein kinase (MAPK) ERK2, cyclin-dependent kinases (CDK), and glycogen Tolmetin synthase kinase-3β (GSK3β)25 and the modification inhibits nuclear translocation of Smads. Growth factors including HGF and EGF induce linker phosphorylation28 acting to limit BMP signaling during development. After growth factor treatment of BMP6-stimulated hepatocytes, immunoblots for phospho-Smad1/5/8 showed moderately decreased nuclear localization of phospho-Smad/1/5/8 (Fig. 6). The difference between the growth-factor treated nuclear lysates and the control lysates was statistically significant for both growth factors by pairwise t test when four repeated experiments were analyzed together for each growth factor. We next considered modes of BMP pathway suppression that target the Smad transcriptional complex. The Smad transcriptional complex is nucleated by R-Smad/Smad4, but the binding affinity is regulated by DNA-binding coactivators or corepressors such as TGIF.

Occult hepatitis B (OBI) can

be associated Selleck Pifithrin �� with a chronic hepatitis C virus (HCV) infection. Even in the absence of serological markers of hepatitis B, some patients in the study had OBI, which may have affected their treatment response. Cacciola et al.11 studied 200 patients with a chronic HCV infection. In their study, they found that an OBI virus infection was more common (33%) in HCV patients versus controls, and this association might have affected the treatment response with interferon therapy. We wonder if they have additional data about the serological status of the patients with respect to their OBI status. In conclusion, the study performed by Harrison et al.1 will certainly broaden our horizons with respect to the treatment of chronic HCV. However, we would like to share our concerns about the study, and we hope to have a scientific discussion with the authors. Tugrul Purnak M.D.*, Cumali Efe Regorafenib in vitro M.D.†, Yavuz Beyazit M.D.‡, Ersan Ozaslan M.D.*,

* Department of Gastroenterology, Ankara Numune Education and Research Hospital, Ankara, Turkey, † Department of Internal Medicine, Bitlis Government Hospital, Bitlis, Turkey, ‡ Department of Gastroenterology, Yuksek Ihtisas Training and Research Hospital, Ankara, Turkey. “
“Primary liver cancer encompasses both hepatocellular carcinoma (HCC) and cholangiocarcinoma (CC). The Notch signaling pathway, known to be important for the proper development of liver architecture, is also a potential driver of primary liver cancer. However, with four known Notch receptors and several Notch ligands, it is not clear which Notch pathway members play the predominant role in

liver cancer. To address this question we utilized antibodies to specifically target Notch1, Notch2, Notch3 or Jag1 in a mouse model of primary liver cancer driven by AKT and NRas. We show that inhibition of Notch2 reduces tumor burden by eliminating highly malignant hepatocellular carcinoma- and cholangiocarcinoma-like tumors. Inhibition of the Notch ligand Jag 1 had a similar effect, triclocarban consistent with Jag1 acting in cooperation with Notch2. This effect was specific to Notch2, as Notch3 inhibition did not decrease tumor burden. Unexpectedly, Notch1 inhibition altered the relative proportion of tumor types, reducing HCC-like tumors but dramatically increasing CC-like tumors. Finally, we show that Notch2 and Jag1 are expressed in, and Notch2 signaling is activated in, a subset of human HCC samples. Conclusions: These findings underscore the distinct roles of different Notch receptors in the liver and suggest that inhibition of Notch2 signaling represents a novel therapeutic option in the treatment of liver cancer. (Hepatology 2014;) “
“In the February 2013 issue of Hepatology, in the Clinical Observations article entitled “Flipping the switch” (volume 57, pages 851-852; doi: 10.1002/hep.26193), by Rishi Agarwal, Joseph Buell, and Nathan J.

The median time to loss of resistant Galunisertib molecular weight variants was 13 months overall (Table 2) (13, 15, and 9 months for prior null and partial responders, and relapsers, respectively). The median time to loss of the common genotype 1b variants (position 54 and 156; 3-4 months) was generally less than that of the common genotype 1a variants (position 36, 155, and 36+155; 13-15 months). This subanalysis of peginterferon/ribavirin treatment-experienced patients treated with the HCV protease inhibitor telaprevir in the REALIZE trial explored the effect of peginterferon/ribavirin lead-in, prior peginterferon/ribavirin treatment response,

genotype subtype, and baseline variants on treatment outcome, and further characterized the emergence of resistance in patients who did not achieve an SVR. No new telaprevir-resistant variants were detected and the pattern of resistance pathways selleck compound was consistent with

that seen in treatment-naïve patients.19 Importantly, this analysis also showed that resistant variants could no longer be detected by population sequencing in the majority of patients after a median follow-up time of 11 months. Prior to treatment in the REALIZE trial, predominant variants resistant to protease inhibitors were generally detectable by population sequencing in only a very small percentage (typically <3%) of patients, which is in agreement with other studies including those in the treatment-naïve setting.19-21 Also in line with other studies,20, 22, 23 the presence of resistant variants at baseline does not necessarily preclude successful treatment (i.e., SVR) in all patient groups,

especially in prior relapsers. However, there might have been an effect in prior null responders. Regarding the use of a 4-week peginterferon/ribavirin lead-in phase before the initiation of telaprevir, no differences in the rates of on-treatment virologic failure or relapse were observed between the concurrent and delayed initiation of telaprevir. Further, the use (or not) of a peginterferon/ribavirin Farnesyltransferase lead-in had no significant effect on the number of patients who had emergent telaprevir-resistant variants, or on the type of variants observed following virologic failure. The data from this virologic analysis are in agreement with results from the primary analysis of the REALIZE trial,4 in which SVR rates were similar between the telaprevir-based treatment arms with and without a lead-in. Therefore, our findings confirm that a peginterferon/ribavirin lead-in is not required with telaprevir. In contrast, a Phase 2 study of boceprevir previously suggested that lowering HCV RNA levels with a 4-week peginterferon/ribavirin pretreatment may reduce the emergence of protease-resistant variants, decrease viral breakthrough rates during treatment, and increase SVR rates.

Results: the results of these studies are indicated as follows: Standard triple therapy with the probiotic Bifidus infantis co-administered for 10 days led to an eradication rate of 90.4%. A lead-in period using the probiotic alone for 14 days followed by the standard triple therapy with the probiotic Bifidus Infantis co-administered for another 10 days, led to an eradication rate of 91.6%. Sequential therapy with the probiotic Bifidus Infantis co-administered for 10 days led to an eradication rate of 92.1%. Lactobacillus Rhamnosus GG yielded a lesser rate of success when used as replacement for Bifidus infantis in the triple therapy

group (79.6% learn more vs 88.4% respectively). Multiple strains probiotic formulas as a single agent (Multilac and Afterbiotic): still ongoing study but interim results of available data indicate a lesser rate of success than Bifidus infantis or Lactobacillus rhamnosus alone (74.3% vs 88.4% respectively). Conclusion: Adding the probiotic Bifidus infantis as an adjuvant to the standard or modified triple, and the sequential or modified sequential therapy led to better

results than the cure rates obtained by the conventional medical therapy (p = 0.001). RAD001 in vitro Bifidus infantis used alone appeared to have a higher potency than Lactobacillus Rhamnosus GG or a multistrain tablet of probiotics in this respect. It is also noteworthy that the probiotics Bifidus infantis, lactobacillus Rhamnosus GG, Multilac, and afterbiotic not only improved the success of eradication but also had led to a significant improvement in the clinical symptoms response after treatment and to a considerable reduction in the incidence of antibiotic associated diarrhea. Key Word(s): 1. Probiotics; 2. Triple therapy; 3. Sequential treatment; 4. H. pylori;

Presenting Author: ADNANM ABU HAMMOUR Additional Authors: ASADIZZIDDIN DAJANI, MOHAMMEDALI EL NOUNOU, MOHAMMEDABDULLAH ZAKARIA Corresponding Author: ADNANM ABU HAMMOUR, ASADIZZIDDIN DAJANI Affiliations: AMC; ADSC; mnc Objective: Over the past decade a worldwide trend of decline in the cure rates of H. pylori is observed. Current eradication rates achieved by the standard triple therapy alone are below 70%. A retrospective survey C-X-C chemokine receptor type 7 (CXCR-7) done 2009 in the UAE revealed a similar experience with reported eradication rates of 69.8%, while earlier eradication rates reported by our group was (95%).This decline in H.Pylori eradication was confirmed by a prospective study that was done in 2011. This decline is believed to be due to the rising clarithromycin and metronidazole resistance caused by the injudicious use of these antibiotics leading to increased activity of the efflux pump of H. pylori, and/or to the emergence of the 23S r-RNA point mutations of the microbe. This led to reduced cure rates by 20–30%.

“
“Netherlands Cancer Institute, Division of Gene Regulation, Plesmanlaan 121, 1066CX, Amsterdam, The Netherlands Chronic hepatitis B virus (HBV) infection is a major buy Sotrastaurin risk factor for liver cancer development. HBV encodes the hepatitis B virus X (HBx) protein that promotes transcription of the viral episomal DNA genome by the host cell RNA polymerase II. Here we provide evidence that HBx accomplishes this task by a conserved and unusual mechanism. Thus, HBx strongly stimulates expression of transiently transfected reporter constructs, regardless of the enhancer and promoter sequences. This activity invariably requires HBx

binding to the cellular UV-damaged DDB1 E3 ubiquitin ligase, suggesting a common mechanism. Unexpectedly, none of the reporters tested is stimulated by HBx when integrated into the chromosome, despite remaining responsive to their cognate activators. Likewise, HBx promotes gene expression from the natural HBV episomal template but not from selleck products a chromosomally integrated HBV construct. The same was observed with the HBx protein of woodchuck HBV. HBx

does not affect nuclear plasmid copy number and functions independently of CpG dinucleotide methylation. Conclusion: We propose that HBx supports HBV gene expression by a conserved mechanism that acts specifically on episomal DNA templates independently of the nature of the cis-regulatory sequences. Because of its uncommon property and key role in viral transcription, HBx represents an attractive target for new antiviral therapies. (HEPATOLOGY 2012;56:2116–2124) Chronic infection by hepatitis B virus (HBV) affects close to 400 million people worldwide and is a leading cause of hepatocellular carcinoma, one of the most common human cancers.1 HBV belongs to the hepadnavirus family of DNA viruses that also includes woodchuck hepatitis virus and ground

squirrel hepatitis virus.2 HBV replicates its genome in a manner very analogous to retroviruses, by reverse transcription (RT) of an RNA intermediate into double-stranded DNA that serves as template for transcription by the host cell RNA Polymerase II (Pol II) (reviewed3). A distinctive feature of HBV, those however, is that the viral DNA genome does not integrate into the chromosome of the newly infected cell but instead is maintained as a covalently closed circular DNA (cccDNA) molecule. The cccDNA is transcribed into four major RNA species encoding the viral proteins, including a more than full-length transcript termed the pregenomic RNA. The pregenomic RNA is then reverse-transcribed in the cytoplasm within newly formed viral particles. As the cccDNA does not replicate, a pool of 10-100 copies of the cccDNA is maintained by recycling of a small proportion of the newly synthesized viral DNA genomes into the nucleus. HBV encodes the nonstructural hepatitis B virus X (HBx) protein that is conserved among mammalian hepadnaviruses, suggesting an important function.

Based on our data that c-Met–negative HCC cells do not respond to c-Met inhibition, we propose that c-Met inhibition may show a blunted survival benefit within all HCC patients. We propose that c-Met inhibitor trials

would perhaps show an improved benefit for c-Met–positive HCC, a personalized approach that requires patients to be stratified based on c-Met expression prior to treatment. This type of personalized treatment has been used in the field of breast cancer for over a decade in the treatment of HER-2–positive disease with HER-2 inhibitors.37, 38 One potential factor driving poor prognosis is that c-Met activation JAK inhibitor is linked to invasion and metastasis.39 Although the exact mechanisms that initiate invasion and metastasis in HCC are unknown and likely multifactorial, a transition to a mesenchymal phenotype has been proposed by Thiery31 and Bernards and Weinberg32 to be a critical step. Using a murine

liver cancer model, we demonstrated recently that an activated HGF/c-Met pathway drives a mesenchymal phenotype, with aggressive and invasive growth.24 Establishing a Caspase inhibitor metastatic lesion is a complex, multistep process. One central finding in metastatic carcinoma is loss of E-cadherin.23, 40 E-cadherin is an important cell–cell adhesion molecule, and inhibition of E-cadherin transcription is a critical part of maintaining a mesenchymal phenotype with the capability of invasion. E-cadherin transcriptional repression is associated

with poor prognosis and metastatic disease in a variety of carcinomas, including advanced HCC.33 Other factors that likely contribute to metastatic HCC include activation of broader EMT programs by the E-box repressors Zeb1/Zeb2, Twist, and Snail and increased matrix metalloproteinase expression. Understanding the specific mechanisms by which EMT initiators and downstream pathways signal through E-cadherin transcriptional repressors will be important in terms of designing targeted therapy for metastatic disease. At present, the specific role of c-Met inhibition in targeting metastatic disease has not been established. Upon ligand binding, c-Met undergoes autophosphorylation of specific tyrosine residues within the intracellular domain. Tyrosine phosphorylation Montelukast Sodium is critical for the activation of the intrinsic kinase of c-Met, which propagates multiple downstream signaling pathways such as PI3K/Akt and MAPK/Erk.8, 13-15 c-Met phosphorylation-induced activation of the PI3K/Akt and MAPK/Erk pathways controls cell proliferation, resistance to apoptosis, and cytoskeletal rearrangement. c-Met inhibition is able to suppress both PI3K/Akt and MAPK/Erk pathways in c-Met–positive HCC cells in vitro, and c-Met inhibition appears to be more effective at reducing cancer cell proliferation compared with combination treatment with PI3K and MEK1 inhibitors.

Considering these two different pathogenetical ways is adalimumab just as suitable in UC as in CD? Aim: assessment of intracellular changes of colonic mucosa in UC, before and after adalimumab treatment; Methods: Eight patients (21–62 years, 7 women) with moderate/severe UC (Disease Activity Index-UCDAI > 6, Endoscopic

Index-EI > 4) were included. All patients received adalimumab (Humira) subcutaneous: 160 mg at week 0, 80 mg at week 2 and afterwards 40 mg at a 2 week interval. Colonoscopy was performed before and 6 months after the initial administration of adalimumab. Biopsies obtained during colonoscopy were processed specifically, stained with uranyl acetate and check details lead citrate and examined with a JEM-1010 transmission electron microscope. Results: Before treatment we noticed severe alterations of the epithelium- depletion of microvilli, shattering of epithelial junctions, cytoplasmic vacuolization,

dilatation of the endoplasmic reticulum, pycnotic nuclei, destruction of mitochondria and Golgi complexes which conducted to drastic reduction of cell metabolism. Rarefaction of the goblet cells, together with abnormal mucus formation and secretion was observed. The corresponding chorion showed degeneration of collagen fibres and smooth muscle cells, obstructed capillaries, neutrophilic and mononuclear infiltration. After adalimumab therapy, we noticed improvement in morphology www.selleckchem.com/products/fg-4592.html and function of epithelial organelles, rich Tyrosine-protein kinase BLK mucus secretion and recovery of the chorionic components. The clinical response observed in all our patients was supported by a descent in UCDAI. Endoscopic severity diminished as well- with 7 out of 8 cases entering remission (EI≤4). Conclusion: At the end of treatment the ultrastructural assessment clearly showed signs of epithelial barrier recovery -one of the goals of UC treatment. These features may contribute to a better understanding of UC pathogenicity and mechanism of action of the anti-TNF-alpha therapies. Key Word(s): 1. ulcerative colitis; 2. adalimumab; 3. ultrastructure;

Presenting Author: CONG LIANG Additional Authors: LIN ZHOU, JIE LIANG, YONGZHAN NIE, KAICHUN WU, DAIMING FAN Corresponding Author: KAICHUN WU Affiliations: Xijing Hospital of Digestive Disease; Xijing Hospital of Digestive Disease Objective: Infliximab has been an important agent for inflammatory bowel disease (IBD) in the past decade. 40–50% of the patients lose response initially or after a period of time, which critically restricts the efficacy. Quite a few studies suggest loss of response may be contributed by the formation of antibodies-to-infliximab (ATIs). However, the relationship between ATIs and clinical response to Infliximab remains controversial. Thus, the aim of this study was to identify whether ATIs could be a predictor of loss of response to infliximab. Methods: We searched PubMed, EMBASE and the Cochrane Library for controlled trials to April 2013.