Similarly, allelic variants of TIM-1 in humans have been associated with susceptibility to asthma and other atopic diseases as well as susceptibility to autoimmune

diseases, suggesting that Tim-1 may have a role in regulating both autoimmune and allergic diseases 10. In the immune system, Tim-1 is expressed on CD4+ Palbociclib T cells upon activation 11. Under polarizing conditions, its expression was sustained preferentially on Th2 cells but not on Th1 or Th17 cells 11–13. Recent studies suggest that a small portion of B cells express Tim-1 which may serve as a marker for germinal center B cells 14, 15. Initial studies suggested that Tim-1 on T cells is a positive regulator of T-cell activity. Crosslinking of Tim-1 with an agonistic anti-Tim-1 mAb (clone 3B3) or with its ligand, Tim-4, costimulated see more T-cell proliferation 11, 12. Furthermore, we have shown that this agonistic anti-Tim-1 mAb enhances both CD3 capping and T-cell activation 16, suggesting that Tim-1 might be intimately involved in regulating TCR-driven activation. Indeed, it has been reported that human TIM-1 physically associates with the TCR/CD3 complex and upregulates activation signals 17. This agonistic anti-Tim-1 mAb prevented the development of respiratory tolerance and increased pulmonary

inflammation by substantially increasing the production of IL-4 and IFN-γ 11. The same antibody enhanced both pathogenic Th1 and Th17 responses in vivo and worsened experimental Tolmetin autoimmune encephalomyelitis (EAE) in an autoimmune disease setting 16. Since this anti-Tim-1 mAb increased Th2 responses in vitro 11, but enhanced both Th1 and Th17 responses in vivo 11, 16, this raised the issue of whether Tim-1 might be expressed on other cells besides T cells,

which could explain these differences in T-cell responses. Here we report that Tim-1 is constitutively expressed on DCs. Using agonistic anti-Tim-1 mAb, we show that Tim-1 signaling promotes the activation of DCs, which subsequently enhance effector T-cell responses, but inhibit Foxp3+ Treg responses. In an autoimmune disease setting, when given with immunogen, agonistic anti-Tim-1 mAb not only worsens EAE in disease-susceptible mice but also abrogates resistance and induces EAE in genetically resistant mice. Collectively, our findings show that Tim-1 is constitutively expressed on DCs, and Tim-1 signaling in DCs serves to decrease immune regulation by Tregs and to promote effector T-cell responses. To test our hypothesis that Tim-1 may be expressed on and affect the function of other cell types than T cells, we examined different populations of immune cells for Tim-1 expression ex vivo. As shown in Fig. 1A, Tim-1 expression was low or undetectable on unactivated CD4+ or CD8+ T cells, B cells (CD19+), or macrophages (CD11b+CD11c–).

At confluence, the cells were trypsinized and the cellular expansion growth rate of both HC– and SSc–MSCs was evaluated by cell count in a Burker chamber at each passage and expressed in terms of population-doubling (PD) using the formula: log n/log 2, where n is the cell number of the confluent monolayer divided by the initial number of cells seeded. We further assessed Ki67 gene expression, which is associated strictly with cell proliferation [28]. Selleck KPT-330 A more detailed

description of this assay is discussed in the section regarding quantitative polymerase chain reaction (qPCR). To confirm the human MSC phenotype, plastic adherent cells were analysed for the expression of surface-specific antigens by flow cytometry, as established elsewhere [4]. The cells were stained with the Cobimetinib following conjugated monoclonal antibodies: fluorescein isothiocyanate (FITC)-conjugated or phycoerythrin (PE)-conjugated monoclonal antibodies, including CD14, CD34, CD45,

CD105, CD90 and CD73. FITC- and PE-conjugated isotypes were used as negative controls. Analysis was performed using Cytomics FC500 (Beckman-Coulter, Brea, CA, USA). The capacity of MSCs to differentiate along osteogenic and adipogenic lineages was assessed as described elsewhere [4]. Briefly, for osteogenic differentiation cells were plated at 104 cells/cm2 in MSC medium supplemented with 10% FBS, 10 nM dexamethasone, 100 μg/ml ascorbic acid and 10 mM β-glycerophosphate (all from Sigma, St Louis, MO, USA). After 21 days, the osteogenic differentiation was demonstrated by deposition of mineral nodules detected by alizarin red S staining. Adipogenic differentiation was induced by adding culture medium supplemented with 10% FBS, 0·5 mM isobutyl methylxanthine, 1 μM dexamethasone, 10 μg/ml insulin and 70 μM indomethacin (all from Sigma) to MSCs. After 21 days’ culture, adipogenesis was measured by the accumulation of lipid-containing vacuoles stained with Oil red

O. Cultured MSCs were collected by trypsinization, washed three times and resuspended 1 × 106/300 μl with phosphate-buffered saline (PBS; Euro Clone). Cells were fixed in 700 μl of ice-cold 100% ethanol at 4°C for a minimum of 30 min. The cell suspension was centrifuged at 1700 g for 5 min and washed twice with PBS+0·1% BSA (Kedrion, Lucca, Italy). Finally, the cell Tau-protein kinase pellets were incubated with propidium iodide (PI; Sigma) (50 μg/ml)/RNase (Sigma, St Louis, MO, USA) (250 ug/ml)/0·1% Triton X (Sigma) solution for 1 h and analysed with Cytomics FC500 (Beckman-Coulter). The senescence-associated β-Gal assay was performed as described previously using a commercial kit (senescence detection kit; Calbiochem, Merck KGaA, Darmstadt, Germany). Briefly, MSCs were detected, fixed for 10 min in the fixative solution, then washed and incubated overnight at 37°C with fresh β-Gal staining solution. Cells were washed with PBS and counted using a light microscope (Eclipse Ti-S, Nikon, Florence, Italy).

Search terms included renal dialysis or chronic renal failure or kidney failure chronic or renal insufficiency chronic or haemodialysis and vitamin B6 (explode) or vitamin B6deficiency or pyridoxine or pyridoxal phosphate/pyridoxal-5-phosphate. In addition, reference lists of articles were examined for additional studies to meet the inclusion criteria. Exact search strategies are available online (Appendix S1). Two reviewers independently evaluated articles for eligibility. All identified abstracts were reviewed and inclusion/exclusion criteria applied. Included were

studies in the haemodialysis population where there were evident biochemical measures of vitamin B6, see more or had vitamin B6 reported in the title. Studies were excluded when subjects were paediatric, animal/rat studies, case reports, peritoneal dialysis, kidney transplantation, if they were reviews or commentaries, or in languages other than English. For abstracts selected by either reviewer, the full-text article was retrieved and reviewed. Once full articles were obtained, studies with no biochemical vitamin B6 measures, or studies where subjects were on high supplementation doses for the duration of the study,

were further excluded. Of the remaining studies, the vitamin B6 measures were tabulated and then further inclusion/exclusion applied. Any disagreement was resolved by consensus. The final yield included studies that specified percentage of subjects with vitamin B6 deficiency, had measures of B6 status both before Talazoparib concentration and post dialysis, or discussed current technologies shown to affect vitamin B6 status. Reviewers independently extracted data and considered study quality from all selected studies. The data extraction Rebamipide form prepared included information around study design, baseline demographics, laboratory measures of vitamin B6 including timing (before vs post dialysis) and type of laboratory assay used, supplementation protocol where applicable, dialyser, and any influences on or conclusions about vitamin B6 status. The PEDro scale based on the Delphi list was used to rate methodological quality.17 The

following indictors of methodological rigor were scored independently as either present or absent: (i) specification of eligibility criteria, (ii) random allocation, (iii) concealed allocation, (iv) prognostic similarity at baseline, (v) subject blinding, (vi) therapist blinding, (vii) assessor blinding, (viii) >85% follow up for at least 1 key outcome, (ix) intention to treat analysis, (x) between-group statistical analysis of at least 1 key outcome, and (xi) point estimates of variability provided for at least 1 key outcome. Criteria 2–11 are used for scoring purposes, so that a score from 0 to 10 can be obtained.17 Interobserver agreement percentage was calculated. Any disagreements between the two reviewers were resolved by discussion until consensus was reached.

This suggests that siglec-E up-regulation on macrophages represents a negative feedback pathway that

limits the inflammatory response to LPS signalling. A potential limitation of receptor over-expression and the use of antibodies to cross-link siglecs is that they may trigger non-physiological signalling pathways. Siglecs are normally masked on the cell surface via cis interactions with cell-expressed sialic acids, which limits the ability of exogenous trans ligands to induce clustering at Lumacaftor chemical structure the cell surface. Furthermore, the natural siglec–sialic acid interactions are much weaker than the siglec–antibody interactions and typically in the affinity range of 100–1000 μm. Alternative in vitro approaches include the use of synthetic sialylated carbohydrates to cross-link siglecs, which might better approximate the natural interactions between siglecs and their ligands on other cells in terms of both affinity and avidity. Siglec-deficient mice are proving useful in determining the precise regulatory role of siglecs as discussed further

below. Siglec-G is predominantly expressed on B cells, including the B1a Adriamycin datasheet cell population that is important for making rapid T-independent IgM responses to bacterial carbohydrate antigens as well as natural antibodies.41 Hoffmann et al.41 showed that siglec-G-deficient mice had a large expansion of the B1a population which began early in development and this was independently confirmed by Ding et al.42 The expansion was specific to B1a B cells and not follicular B2 B cells, which also express siglec-G.41,42 Mixed radiation chimeras prepared with 1 : 1 ratios of wild-type and siglec-G-deficient bone marrow cells, demonstrated that

the effect of siglec-G in controlling cellular expansion is B-cell intrinsic.41 The B1a-cell expansion in siglec-G-deficient mice was not the result of increased cell cycling but rather reduced turnover rate as shown by lower bromodeoxyuridine incorporation.41 These data are suggestive of increased survival find more of B1a cells in siglec-G−/− mice, possibly through increased B-cell receptor signalling. Over-expression of siglec-G inhibited B-cell-receptor-mediated Ca2+ signalling and the siglec-G-deficient B1a cells exhibited exaggerated calcium signalling and increased IgM production.41 A similar phenotype has been observed in SHP-1-deficient mice, which exhibit expansion of the B1-cell population and higher B-cell receptor-induced calcium signalling in B cells. This suggests that SHP-1 plays a role downstream of siglec-G to give rise to its inhibitory function.43 This newly defined role of siglec-G may explain the naturally muted signalling response of B1a cells when compared with the B2 population in which siglec-G does not seem to play a functional role despite relatively high levels of expression.

After induction of chronic colitis the colons of both Bim–/–and wild-type mice appeared with an opaque, thickened, more granular mucosa and an altered vascular pattern. Bim–/– animals exhibited significantly higher MEICS score compared to wild-type mice (5·1 ± 1·7, R428 n = 7 versus 2·7 ± 1·8, n = 5 respectively; Fig. 2b). Spleens of healthy wild-type mice were significantly smaller than those of Bim–/– animals. Upon DSS, the spleen weight increased

significantly in wild-type animals (P < 0·05) and highly significantly in Bim–/– animals (P < 0·01, Fig. 3a). Induction of chronic colitis was followed by a typical reduction of colon length. Shortening of the colon was significant in DSS-receiving Bim–/– animals compared to the respective controls (8·1 ± 0·5 cm upon water, n = 5, versus 7·0 ± 0·8 cm upon DSS, n = 5 for wild-type animals. 8·8 ± 0·4 cm upon water, n = 7, versus 7·8 ± 0·5 cm upon DSS, n = 7, P < 0·05 for Bim–/– mice; Fig. 3b). Increase of spleen weight upon chronic DSS-induced colitis correlated with a decrease in colon length for both wild-type controls and Bim–/– mice Selumetinib (P < 0·05). Combining data from wild-type controls and Bim–/– mice upon both water and DSS, no significant relationship between spleen

weight and colon length could be determined because of the significant difference in the spleen weight between wild-type and Bim–/– in mice without inflammation. Also on a microscopic level, more severe P-type ATPase colitis was found for Bim–/– mice compared to wild-type mice. In female animals without chronic DSS-induced colitis, the Bim knock-out did not alter the total histological score compared to the wild-type (1·2 ± 0·6 versus 1·3 ± 0·6, respectively; Fig. 3c). The total histological score for Bim–/– mice with induced chronic colitis was increased significantly compared to the water-treated

mice. The score for epithelial damage considering crypt morphology and loss of goblet cells remained unchanged when comparing DSS-receiving Bim–/– and wild-type mice (Fig. 3c, white bars). In contrast, Bim–/– animals with chronic colitis exhibited a significantly increased inflammatory infiltrate of lymphocytes into the mucosa and submucosa compared to wild-type mice (4·4 ± 0·8 versus 3·1 ± 1·0, respectively; P < 0·05; Fig. 3c, light grey bars). This also led to a significantly higher total histological score for Bim–/– mice with chronic colitis compared to wild-type mice (6·7 ± 1·4 versus 4·9 ± 0·4 respectively; P < 0·05; Fig. 3c, dark grey bars). The results were confirmed in a second experiment of chronic DSS-induced colitis in female mice (n = 5 each group, not shown). In a third experiment in male Bim–/– mice, similar data were obtained (n = 5 each group, not shown). In these animals, more severe inflammation for Bim–/– animals compared to wild-type mice was determined upon chronic DSS-induced colitis.

There were major differences between the responses of these two groups and those of the general AAAAI respondents whose SCH 900776 purchase clinical practice was composed of < 10% of PID patients.

These differences included the routine use of intravenous immunoglobulin therapy (IVIg) for particular types of PIDs, initial levels of IVIg doses, dosing intervals, routine use of prophylactic antibiotics, perceptions of the usefulness of subcutaneous immunoglobulin therapy (SCIg) and of the risk to patients’ health of policies adopted by health-care funders. Differences in practice were identified and are discussed in terms of methods of health-care provision, which suggest future studies for ensuring continuation of appropriate levels of immunoglobulin replacement therapies. Primary immunodeficiency diseases (PIDs) comprise check details a group of more than 150 distinct diseases arising from 120 different genetic abnormalities that affect development and/or function of the immune system [1]. Despite the heterogeneity of PIDs, impairment of immunity results in the common hallmark of susceptibility to infection. While once thought to be exceedingly rare, symptomatic primary immunodeficiencies are now appreciated to range from 1:500–1:500 000

in the general population in the United States and Europe [2,3]. A random digit dialling telephone survey in 2007 estimated that one in 1200 people within the United States are diagnosed with an immunodeficiency [4], Dimethyl sulfoxide although this included selective immunoglobulin

A deficiency (IgAD), which is not usually clinically significant. These diseases have been considered rare, thus controlled studies investigating clinical interventions are scarce. In an effort to address these issues, several regions have created national registries for PIDs to enable epidemiological studies. In the absence of controlled studies of therapeutic interventions for patients with PIDs, efforts have been organized to describe expert practice in order to ascertain consistencies, differences and outstanding questions. In the United States a recent survey of expert practice has been performed of the members of the American Academy of Allergy, Asthma and Immunology (AAAAI) [5]. In the majority of centres in the United States, immunology is a subspeciality with combined training in allergy and certifying examinations covering both clinical disciplines. In Europe, clinical immunology is sometimes, although not always, a distinct and separate subspeciality; in many other countries, PID patients are managed by physicians or paediatricians working in related specialities. With this difference in mind, we sought to compare the expert practice of PID between members of the European Society for Immunodeficiencies (ESID) and the AAAAI.

Malaria remains one of the main global infectious diseases and cerebral malaria is a major complication, often fatal in Plasmodium falciparum-infected children and young adults [1]. Cerebral malaria pathophysiology is still poorly understood, combining cerebral vascular obstruction, and exacerbated immune responses. Indeed, investigations

in humans and mice documented Lapatinib in vitro the sequestration of erythrocytes, parasitized or not, platelets and leucocytes in cerebral blood vessels with an increased proinflammatory cytokine expression [1-3]. The specific role of T cells in cerebral malaria pathogenesis has been difficult to address in humans. In mice however, T-cell sequestration and activation in the brain are crucial steps for experimental cerebral malaria (ECM) development after Plasmodium berghei ANKA (PbA) infection [4-7]. In particular, αβ-CD8+

T cells sequestrated in the brain play a pathogenic, effector role for ECM development [6], and we showed recently a role for protein kinase C-θ (PKC-θ) in PbA-induced ECM pathogenesis [8]. Besides being a critical regulator of TCR signaling and T-cell activation, PKC-θ is involved in interferon type I/II signaling in human T cells [9]. Type II IFN-γ is essential NSC 683864 molecular weight for PbA-induced ECM development [10-12], promoting CD8+ T-cell accumulation in the brain [7, 12-14]. Type I IFNs are induced during viral infection but they also contribute Afatinib mouse to the antibacterial immune response. In Mycobacterium tuberculosis infection, types I and II IFNs play nonredundant protective roles [15], while type I IFNs inhibit IFN-γ hyper-responsiveness by repressing IFN-γ receptor expression in a Listeria monocytogenes infectious model [16]. Moreover, type I IFNs role in central nervous system (CNS) chronic inflammation is ambiguous [17].

IFN-β has proinflammatory properties and contributes to some auto-immune CNS diseases, while IFN-β administration is routinely used in relapsing-remitting multiple sclerosis treatment, characterized by inflammatory cell infiltration to the CNS, including Th1 and Th17 [17]. Crossregulations between type I and type II IFNs have been documented [18-21], they can have similar or antagonistic effects, and type I IFN-α/β precise role in ECM development after sporozoite or merozoite infection remains unclear. Here, we addressed the role of IFN-α/β pathway in ECM development in response to hepatic or blood-stage PbA infection, using mice deficient for types I or II IFN receptors. Unlike IFN-γR1−/− mice that were fully resistant to ECM, we show that IFNAR1−/− mice are partially protected after sporozoite or merozoite infection. Magnetic resonance imaging (MRI) and angiography (MRA) confirmed the reduced microvascular pathology and brain morphologic changes in the absence of type I IFNs signaling.

50/1.82–188.39, P = 0.014). Host IL-28B genetic variants played a role in Asian relapsers but not nonresponders retreated with peginterferon/ribavirin. Direct antiviral

agents might be possibly avoidable in Asian relapsers with favorable IL-28B genotype. “
“Aim:  A genetic polymorphism of inosine triphosphate pyrophosphatase (ITPA) has been associated with pegylated-interferon/ribavirin (PEG-IFN/RBV)-induced anemia in chronic hepatitis C patients. However, correlation of the genetic variant with anemia following liver transplantation has not been determined. Methods:  Sixty-three hepatitis CH5424802 C virus (HCV)-positive patients who underwent liver transplantation and PEG-IFN/RBV therapy were enrolled. The rs1127354 was determined for each individual. Results:  There was no relationship with anemia or RBV dosage in patients carrying the CC allele (CC group, n = 43) and those carrying the CA allele (CA group, n = 20). The incidence of hemoglobin Adriamycin datasheet (Hb) decline >3 g/dL (CC: 4.7%, CA: 0%) was relatively low, whereas the incidence of Hb levels <10 g/dL (CC: 18.6%, CA: 30.0%) was high. Univariate analysis revealed that splenectomy inversely correlated with Hb levels <10 g/dL at 4 weeks (P = 0.04). Among the 22 patients who did not undergo splenectomy, the incidence of Hb levels <10 g/dL tended to be lower in the seven patients carrying the CA allele (28.6%)

than in the 15 patients with the CC allele (60.0%). Conclusion:  The ITPA genetic polymorphism does not correlate with post-transplant PEG-IFN/RBV-induced anemia. Splenectomy is useful in preventing anemia regardless of the ITPA genotype. “
“Background and Aim:  Previous Suplatast tosilate studies investigating the association between the glutathione S-transferase Tl (GSTT1) null genotype and colorectal cancer (CRC) risk in the Asian population have reported controversial results.

Thus, a meta-analysis was performed to clarify the effect of the GSTT1 null genotype on CRC risk in the Asian population. Methods:  A comprehensive study was conducted, and 12 case-control studies were finally included, involving a total of 4517 CRC cases and 6607 controls. Subgroup analyses were performed by the sample size. Results:  A meta-analysis of all 12 studies showed that the GSTT1 null genotype was significantly associated with an increased CRC risk in the Asian population (odds ratio [OR] = 1.10, 95% confidence interval [CI] = 1.02–1.19, the P-value of the OR [POR] = 0.02, the value of the heterogeneity analysis [I2] = 42%). A more obvious association was observed after the heterogeneity was eliminated by excluding one study (OR = 1.15, 95% CI: 1.06–1.25, POR = 0.001, I2 = 0%). This association was further identified by both subgroup analyses and a sensitivity analysis. Conclusions:  This meta-analysis suggests that the GSTT1 null genotype contributes to an increased colorectal cancer risk in the Asian population.

Wall volume increased more when the largest lipid cluster was located close to the lumen. The volume of lipid increased when fewer lipid clusters were present at baseline. The volume of calcium increased with greater volume of lipid at baseline. A similar multivariate analysis was used to evaluate the impact of various vascular risk factors (statin use, smoking, hypertension, and diabetes) on carotid imaging features. The volume of calcium increased more in patients on statins (coefficient 4.79, 1.73

to 7.86, P = .002) (Supp Fig 6). The volume of lipid increased more in older patients (coefficient 0.36, 0.21 to 0.50, P < .001) and in patients who smoked (coefficient 8.89, 6.82 to 10.95, P < .001) selleck inhibitor (Supp Fig 7). This study of patients undergoing emergent CT evaluation for symptoms of acute ischemic stroke shows that there are a number of imaging markers that significantly predict the evolution of CT imaging features of carotid artery atherosclerotic disease over a 1-year period. Wall volume increased more when the largest lipid cluster

was located close to the lumen. The volume of lipid increased more when fewer lipid clusters were present at baseline. The volume of learn more calcium increased with greater volume of lipid at baseline. Moreover, our results indicate that in our study population, certain risk factors—age, smoking, hyperlipidemia/statin use—have a significant impact on the evolution of CT patterns of carotid disease. Older patients and patients who smoked had a greater increase in the volume of lipid over 1 year. Patients who were on statins had a greater increase in the volume of calcium. Smoking and hyperlipidemia are well-known risk factors for the progression of atherosclerotic disease and clinical events related to that disease.[11, 12, 14-17, 22-27] However, the exact mechanisms behind their influence on the progression of this disease are not entirely clear. Our results provide some possible additional insight into

these mechanisms. The patients who smoked had a greater increase in the number of lipid clusters over 1 year. High PAK6 lipid content is one aspect of plaque morphology that is characteristic of the “vulnerable plaque.”[2-5] So, smoking may increase the lipid content of plaques, increasing plaque vulnerability and the risk for future clinical events of stroke or TIA. Statin use rather than hyperlipidemia per se was looked at in this study. The volume of calcium increased more in patients using statins. So, the protective value in statins may partly lie in their propensity to increase calcification of atherosclerotic plaques, thus increasing plaque stability and decreasing clinical events.

Results: There is no significant differences in the frequencies of genotypes and alleles between cases and controls (CD group vs. control group, P = 0.121; UC group vs. control group, P = 0.852). Glu216Lys polymorphism has no relationship with the clinical types of UC and CD (P > 0.05). Conclusion: SNP Glu216Lys in BPI is not associated with IBD in Chinese population. The contribution of genetic determinants differ significantly

between ethnicities. Key Word(s): 1. IBD; 2. phenotypes; 3. SN; 4. BPI; Presenting Author: METIN BASARANOGLU Corresponding Author: METIN BASARANOGLU Affiliations: Ankara YIH Objective: We investigated health care seeking behaviour in patients with IBD. Methods: We performed a retrospective Apoptosis Compound Library screening cohort study among patients with IBD. Delayed diagnosis term was analyzed for each patient. Results: Of the Selleckchem SB431542 282 patients with IBD, 181 were male (64%). Mean age was 40.1 ± 14.7 years (median: 38, range: 14–79 years). In pts with IBD: The delayed diagnosis term (seeking

health care behaviour) was 3.1 ± 2.7 months (median: 2 and range: 0–18 months); 3.0 ± 2.3 in males (median: 2 and range: 0–12 months) vs. 3.2 ± 3.2 months (median: 2 and range: 0–18 months) in females (p > 0.05). Delayed diagnosis term was 3.2 ± 2.6 months (median: 2.0 months; 0–15 months) in patients with ulcerative colitis. There was no difference for delayed diagnosis between males 3.1 ± 2.2 months (median: 3.0; 0–12 months) vs females 3.4 ± 3.4 months (median: 2; 0–15 months) (p > 0.05). Delayed diagnosis term was 3 ± 2.8 months (median: 2.0 months; 0–18 months) in patients with crohn’s disease. There was no difference for delayed diagnosis between males 3.0 ± 2.7 months (median: 2.0; 0–10 months) vs females 3.0 ± 3.0 months (median: 2.0; 0- 18 months) (p > 0.05). Conclusion: There Verteporfin was a delay for the health care seeking in patients with IBD. In further analysisi, there was no difference among the patients with IBD, UC, and CD and no difference between male and female gender. Key Word(s): 1. bowel disease; 2. health care; 3. seeking; 4. delay; Presenting Author: WANG YING Additional Authors:

LIBI MIN, YI JING, CHEN JIANG Corresponding Author: LIBI MIN Affiliations: First affiliated hospital of nanchang university Objective: To evaluate the therapeutic effect and mechanism of glutamine in treatment of experimental colitis in mouse. Methods: Fifty BALB/C mouse were randomly divided into 5 groups (n = 10 per group): normal control group, model group, 5-aminosalicylic acid (5-ASA) group, glutamine group, and combination of 5-ASA and glutamine group Inflammatory scores and mucosal morphological changes were evaluated under light microscope. The leves of TNF-α, IL-1β, IL-10 and NF-κB were determined by immunohistochemistry. Results: Compared with model group, Inflammation score (5.93 ± 1.01a, 4.46 ± 0.82 vs 8.34 ± 1.12a, both P < 0.01), lesions of colonic mucosa (1.88 ± 0.34, 1.