Agardh D. muelleri M.E. Ramírez et A.F. Peters D. gayana Montagne subsp. patagonica (Asensi) comb. nov. A.F. Peters, E.C. Yang, F.C. Küpper & Prud’Homme van Reine subsp. tabacoides (Okamura) comb. nov. A.F. Peters, E.C. Yang, F.C. Küpper & Prud’Homme van Reine subsp. foliacea (V.A. Pease) comb. nov. A.F. Peters, E.C. Yang, F.C. Küpper & Prud’Homme van Reine subsp. sivertsenii (Baardseth) comb. nov. A.F. Peters, E.C. Yang, F.C. Küpper & Prud’Homme van Reine D. patagonica Asensi D. tabacoides Okamura D. foliacea V.A. Pease D. sivertsenii Baardseth subsp. firma (C. Agardh) comb. nov. A.F. Peters, E.C. Yang,

F.C. Küpper & Prud’Homme van Reine subsp. peruviana (Montagne) comb. nov. A.F. Peters, E.C. Yang, F.C. Küpper & Prud’Homme van Reine synonyms in subsp. herbacea: D. latissima Setchell & Gardner D. munda Setchell et N.L. Gardner D. mexicana E.Y. Dawson D. firma (C. Agardh) Skottsberg D. peruviana Alpelisib price Montagne Our isolates of D. ligulata from Brittany (France) and from Galicia (Spain) clustered together showing that European samples of this species are slightly genetically different from individuals from Argentina, Chile, New Zealand, and western Canada. Nevertheless, all together they form a highly supported clade, which represents

D. ligulata sensu stricto. However, samples belonging to three other taxa fell within the same clade: D. distans (C. Agardh) J. Agardh, D. muelleri M.E. Ramírez et A.F. Peters and D. gayana Montagne. The latter was not formally MG-132 ic50 included in our analysis because of

incomplete data; rbcL sequences place it close to D. muelleri, as did the previous analysis of ITS data (Peters et al. 1997). To accommodate these three taxa we propose to regard D. distans, which showed no genetic difference from a D. ligulata sample from Argentina, as a narrow growth form of D. ligulata. This classification would agree with the original treatment of this form (Sporochnus ligulatus var. distans; Agardh 1824). For D. muelleri and D. gayana, which show more significant morphological differences from D. ligulata (and from each other), we propose reduction to subspecific rank (see Table 4 and New Combinations section). Desmarestia ligulata [subsp. ligulata] f. distans (C. Agardh) comb. nov. A.F. Peters, E.C. Yang, F.C. Küpper, & Prud’Homme van Reine Basionym and early description: Sporochnus ligulatus medchemexpress var. distans C. Agardh (1824) in Systema Algarum p. 261. Desmarestia ligulata subsp. muelleri (M.E. Ramírez et A.F. Peters) comb. nov. A.F. Peters, E.C. Yang, F.C. Küpper, & Prud’Homme van Reine Basionym and early description: Desmarestia muelleri M.E. Ramírez et A.F. Peters (1993) in Canadian Journal of Botany 70: p. 2442, figs. 12, 15, 34, 42, 43. Desmarestia ligulata subsp. gayana (Montagne) comb. nov. A.F. Peters, E.C. Yang, F.C. Küpper, & Prud’Homme van Reine Basionym and early description: Desmarestia gayana Montagne (1852) in Flora Chileana, Plantas cellulares 2, Algas in Gay, C. (ed.) Historia fisica y politica de Chile 8: p. 243, pl. 14, fig.

51 In a study in esophagogastric cancer, 100 patients were randomized to treatment with a covered Wallstent, Ultraflex stent or Gianturco-Z stent. Again, all groups had good palliation from dysphagia but major complications were more frequent in the Gianturco-Z stent group.23 In another randomized study, covered Wallstents were compared with covered Ultraflex stents in 53 patients with lower esophageal

cancer. The stents were equally effective for palliation with similar rates for complications.52 Larger diameter stents reduce the risk of recurrent dysphagia caused by stent migration, tumor ingrowth or food obstruction but are associated with higher rates for complications.53 With uncovered stents, tumor ingrowth causing recurrent dysphagia occurs in check details 20–30% of patients.22 Tumor ingrowth can find more be minimized by the use of covered stents but the frequency of migration of the stent increases, sometimes up to 28%.22,54–56 Reflux after stent insertion appears to be minimized by the use of stents with antireflux valves.57 After stent insertion in the upper esophagus, patients may have the sensation of a foreign body for at least 1 week but the symptom settles with time.58 Foreign body sensations can also be minimized by the use of a specifically designed Wallstent or by the use of stents with

restricted expansion of the proximal flange.59,60 Covered stents should always be used for malignant fistulae

in the esophagus and for esophageal perforation. Most of the published experiences are in case reports or small comparative studies.45,61–69 After the insertion of stents, symptoms improve in approximately 90% of patients, a similar response rate to bypass surgery (gastroenterostomy). Furthermore, stents have been associated with lower procedure-related morbidity, mortality and cost.45,63 Stents also provide a better quality of life than gastrostomy tubes64,65 but reintervention rates medchemexpress (15–40%) are higher for stents than for gastrojejunostomy.66 In addition, symptoms fail to improve in some patients despite the apparent successful deployment of stents. This may be related to a functional gastric outlet obstruction caused by diffuse carcinomatosis or malignant infiltration of the celiac axis.62 In a systematic review that included 606 patients, stents were successfully deployed in 97% and symptoms improved in 89%. Most patients were able to eat at least soft foods and mean survival was 12 weeks.67 In a multicenter study, stents were inserted in 176 patients with obstructing cancers of the pancreas, stomach or gallbladder. The majority of patients (70%) had duodenal strictures and stents were successfully deployed in 98% of patients. On follow-up, 84% of patients were able to maintain an oral diet and median survival was 21 weeks.

Blood pressure was measured to the nearest 1 mmHg by an automatic sphygmomanometry (BP-203

RV III B; Nippon COLIN, Komaki, Japan). Elevated blood pressure or hypertension was diagnosed if resting blood pressures were 130/85 mmHg or more or if the participants had either a history of hypertension or use of antihypertensive ICG-001 cell line medication, respectively. Abdominal ultrasonographic examination was performed using convex-type real-time electronic scanners (SSA 250 and 300; Toshiba Medical, Tokyo, Japan) by 10 technicians without any information about any present illness. All images were printed on the sonographic papers and reviewed by other technicians and physicians. Fatty liver was assessed according to the modified criteria reported previously.30–33 Liver brightness (diagnosed by difference of more than 10 from the average of liver and renal cortical echo amplitudes), attenuation of echo penetration and decreased visualization of veins were included as criteria. Logistic regression analyses were, find more respectively, performed to determine the risk of IFG or T2DM in both men and women separately. We evaluated two models in both sexes; an age-adjusted and a multivariate model with adjustment for age (< 40, 40–49, 50–59 and ≥ 60 years),

BMI (< 25 kg/m2, 25–29.9 kg/m2 and ≥ 30 kg/m2), alcohol drinking (none, occasional, daily or unknown), smoking (never, ever or unknown), family history of DM (yes, no or unknown) and fatty liver (yes or MCE no) which were assessed in 2000. We also determined the interaction between fatty liver and BMI in a separate study. BMI was incorporated into the models as a continuous variable. In order to simplify interpretation, BMI was transformed by subtracting 22 (centerization). Statistical differences among groups were identified using one-way anova, followed by multiple comparisons using Bonferroni’s method. The χ2-test and Fisher’s test were employed for comparison of prevalence of fatty liver, IFG, and T2DM. Logistic regression analyses were performed

using computer software (SPSS ver. 13.0 for Windows; SPSS, Chicago, IL, USA). P-values less than 0.05 were considered significant. Incidences of newly diagnosed IFG and T2DM between 2000 and 2005 were, respectively, 5.9% and 0.8% overall (7.6% and 1.0% in men and 3.8% and 0.5% in women). They were 10.6% and 2.9% in men with fatty liver, and 5.2% and 0.6% in men without fatty liver. For women, the respective figures were 9.4% and 2.0% with fatty liver, and 2.6% and 0.4% without fatty liver. In both sexes, the differences were significant. The 78.0% of male and 71.3% of female participants with fatty liver in 2000 were assessed as fatty liver in 2005. Table 1 shows the characteristics of the subjects by fatty liver status in men and women.

We describe the clinical, biochemical profile of ACLF and the effect of acute insult and associated complications on the natural course of patients. Methods: Patients diagnosed to have ACLF as per APASL guidelines were prospectively enrolled. Patients were evaluated for the clinical presentation, etiology of acute decompensation and underlying chronic liver disease Opaganib nmr and in hospital mortality. Patients were further classified as ACLF-1 when no organ failure except liver, ACLF-2 when had one organ failure along with liver, ACLF-3 when two organ failure along with liver and ACLF-4 with ≥3 organ

failure along with liver. Results: One thirty four patients with ACLF (mean age 44.2 ± 10.3 years; M/F 128 : 8) were included. Median serum bilirubin 14.5 (5–45.9 mg%), mean CTP score (10.4 ± 1.9), mean MELD score (25.6 ± 7.7) and median hospital stay was (7,1–35 days). Alcoholic hepatitis (n = 79, 59%) followed by hepatitis B virus reactivation (n = 23, 17 %) were the commonest acute events. Underlying chronic liver disease was due to

alcohol (n = 92, 69%), HBV (n = 17, 13%) and cryptogenic in 20 (15%). Ascites was present in 118 (88%), hepatic encephalopathy (50, 37%), sepsis (11, 8.2%), chest infection (22, 16%), spontaneous bacterial peritonitis (17, 13%), acute kidney injury in see more 52 (39%). Overall mortality during hospitalization was (n = 60, 45%). Mortality was 19% in ACLF-1, 45% in ACLF-2, 78% in ACLF-3 and 100% in ACLF-4. Patients who died had significantly lower age but higher CTP score, MELD score, sepsis, lower respiratory infections, acute kidney injury, HE and number of organ failure compared to survivors. On multivariate analysis only loss of >2 organ failure either at presentation or development during hospital stay was predictor of mortality. Conclusion: Alcoholic hepatitis and hepatitis B virus were common acute insults in ACLF patients

and loss of more than two organ function either at presentation or during hospital stay is an independent predictor of mortality in these patients. Measures to control medchemexpress sepsis and organ failure should be initiated early in the course of ACLF patients. Key Word(s): 1. ACLF, APASL; Presenting Author: BINGYONG ZHANG Additional Authors: YUXIU YANG Corresponding Author: BINGYONG ZHANG Affiliations: Henan Provincial Hospital Objective: To observe the long-term effect of autologous bone marrow mononuclear cell transplantation for decompensated cirrhosis Methods: 32 decompensated liver cirrhosis patientsn were selected department in gastroenterology department of henan province people’s hospital. Self-Bone marrow mononuclear cells were separated from each patient, and infused into the patient’s body under aseptic conditions via hepatic artery. The patient’s indexes of liver function and symptom were detected and recorded before cell infusion, and at 7 d, 1 m, 3 m, 6 m, 12 m and 24 m after infusion.

Therefore, miRNAs are implicated in many important cellular processes, such as cell-cycle progression, cell differentiation, apoptosis, and cytoskeletal reorganization. Increasing evidences demonstrated the interplay between miRNAs BYL719 ic50 and epigenetic alterations in human cancers. For example, the oncogenic, enhancer of zeste homolog 2 (EZH2), has been found to be overexpressed in various cancer tissues, and EZH2 is targeted by miR-101, miR-124, and miR-214.29-31 Frequent down-regulation of these miRNAs in human cancers thereby accounted for the up-regulation of EZH2. Similar examples have also been reported

between the niR-29 family and DNMT3A/B,32 miR-449 and histone deacetylase 1,33 and miR-200c and Bmi-1.34 All these evidences suggested that miRNAs may play a crucial role in modulating epigenetic events. In this study, we explored the possibility of miRNA deregulation as a contributing factor in SUV39H1 expression in human HCC. Interestingly, in silico analysis of SUV39H1 3′ UTR suggested the potential regulation of SUV39H1 mRNA by miR-125b. We have previously identified miR-125b as the tumor-suppressor miRNA that is frequently down-regulated in HCC.22 In this study, we experimentally validated the complementary binding between miR-125b and SUV39H1 3′ UTR by luciferase reporter assay. Ectopic expression of

miR-125b apparently reduced endogenous selleck chemicals llc MCE SUV39H1 mRNA and protein levels in HCC cell lines. In concordance with our findings, a recent study indicated that miR-125b up-regulation may contribute to the increased expression of inflammatory genes in vascular smooth muscle cell (VSMC) of type 2 diabetic db/db mice by targeting SUV39H1.22 Opposite to the VSMCs of db/db mice, miR-125b is frequently down-regulated in human HCC. Interestingly, an inverse correlation was observed between SUV39H1 and

miR-125b expression in clinical human HCC samples. Therefore, we speculated that targeting of SUV39H1 by miR-125b may be a conserved event throughout the mammalian cell system, and up-regulation of SUV39H1 in HCC was contributed by the loss of miR-125b. In conclusion, we provide the first evidence that SUV39H1 is an important oncogene that contributes to HCC tumor growth and metastasis. Besides this, up-regulation of SUV39H1 was, in part, the consequence of tumor-suppressive miRNA-125b underexpression in HCC. This observation further suggested the possible interplay between miRNA and histone methylation during the course of liver carcinogenesis. Our findings have enriched the knowledge of the molecular mechanisms underlying hepatocarcinogenesis and provide potential targets for future therapeutic invention. The authors thank Ms. Tracy CM Lau from the Faculty Core Facility and Mr.

[17]

Clinical trial investigators often do not see the full analysis of the whole dataset, and the draft reports are usually written by a professional writer, leading to a further degree of separation of the investigators from the data. These are a few examples of where misconduct can exist beyond the direct reach of the researcher. There is a key question I sometimes ask myself: is there a gap in our perception between initiatives to promote RCR and the apparent increase in proven cases of research misconduct? Is it enough to publish click here and promote guidance on good/best practice, or should there be additional measures to encourage researchers to apply the guidance in their everyday conduct? While heads of universities and research institutes may have confidence in their guidance documents on the RCR and have codes of conduct for the investigation of allegations of research misconduct, they may find it difficult to totally assure

themselves and their governing bodies that all of the research conducted in their institution is compliant with this guidance. Many will trust and hope it is, but the monitoring of research practices and the audit of research processes and outcomes, I would suggest, are not currently sufficient to allow this to be stated with confidence. JQ1 in vivo So what additional measures would be required to 上海皓元医药股份有限公司 allow research leaders to be able to give that assurance to others about their research outputs? I believe we need to do more to discourage and detect research misconduct. While the majority of research-intensive universities and research institutes have good guidance documents, they are not always widely read or assimilated. An increasing number of institutions are requiring researchers to confirm in writing that they have read these documents prior to taking up an appointment and that they will

comply with their contents. There will always be a need to embed the principles of good practice not just in individuals but also in research groups to ensure a high-quality, honest and supportive culture. In addition, I would suggest that there will also be a need for the introduction of measures to monitor research practice to enable institutions to be able to give assurance to their funders and governing bodies that the research is not only of high-quality but also of impeccable integrity. This will inevitably mean the promotion of even higher quality supervision and monitoring by the leaders of research groups and research disciplines, and a requirement that evidence should be provided that it has actually taken place. This monitoring process might be enhanced further by random spot audits of research projects and programs.

Palpitations have previously been identified as uncommon for tacrolimus and as common for boceprevir (when taken together with PEG-IFNα and ribavirin).6, 16 The PK of coadministered boceprevir and the calcineurin inhibitors have not been studied in liver transplant patients, which is a limitation for

interpretation of these data. The data in the present study were derived from healthy subjects, and the magnitude of the potential interaction between cyclosporine or tacrolimus and boceprevir in liver transplant patients is not known. Blood concentrations of the calcineurin inhibitors in liver transplant patients with recurrence of HCV are subject to a wider range of influences than those in healthy subjects, which in turn could result in greater interpatient

variability. HCV infection itself appears to reduce the dose of cyclosporine or tacrolimus Opaganib mw required to achieve a given blood level, probably because of down-regulation of hepatic CYP3A4, impaired function of hepatic P-gp, or both.17 The effect is reversed when the HCV-associated inflammatory response is eliminated by antiviral therapy.18 In addition, liver function can change with time after transplantation.19 Based on the results from the present study, dose reductions of cyclosporine should be anticipated when administered with boceprevir and should be guided by close monitoring of cyclosporine blood levels and frequent assessments selleckchem of renal function and cyclosporine-related side effects. For tacrolimus, significant dose reduction and prolongation of the dosing interval will be required, along with close monitoring of tacrolimus concentrations and frequent assessments of renal function and tacrolimus-related side effects. Plasma concentrations of other commonly used immunosuppressants such as sirolimus and everolimus may also be increased during coadministration with boceprevir. Thus, close monitoring of immunosuppressant 上海皓元医药股份有限公司 blood levels is recommended here as well. This

situation is comparable to that of HIV-coinfected patients after liver transplantation who require treatment with ritonavir-boosted HIV protease inhibitors concomitantly with cyclosporine or tacrolimus. HIV protease inhibitors (eg, lopinavir, darunavir, atazanavir, and ritonavir) are all potent CYP3A4 inhibitors, and several reports describe dose reductions of up to 99% of the calcineurin inhibitors when coadministered with HIV protease inhibitors, with dosing schedules of less than once weekly to maintain adequate cyclosporine and tacrolimus concentrations, or both.20-22 Similarly, a preliminary report of the use of telaprevir in a small number of recipients after liver transplantation suggests that tacrolimus dose reduction and prolongation of the dosing interval have been generally well tolerated.

There was no proven correlation between Helicobacter spp. and colorectal cancer. However, in another review, Risch summarized and analyzed seven published studies (three case–control studies and four cohort studies) with regard to pancreatic cancer odds ratio (OR) for H. pylori positivity Selleckchem Pirfenidone [58]. The author found that H. pylori colonization significantly increased the risk for pancreatic cancer, with a pooled OR for this combined analysis of 1.65 (95% CI: 1.30–2.09). In light of a published case–control study that showed increased risk of pancreatic cancer with non-O blood groups (A, B, and AB) compared to O [59]. Risch postulated that N-nitroso compounds

have blood-borne trophic effects on pancreatic ductular epithelium that act combined with H. pylori infection, embedded in the background of host genetic variations and ABO that may affect other aspects of inflammatory response, could lead to development of pancreatic cancer. Koshiol et al. [60] conducted the study of 350 lung adenocarcinoma cases, 350 squamous cell carcinoma cases, and 700 nested controls within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC) cohort of male Finnish smokers. To test the associations between H. pylori seropositivity (ELISA) and lung cancer risk using conditional logistic Proteasome inhibitor regression,

controls were one-to-one matched by age and date of baseline serum draw. The results of medchemexpress this study did not found an association between H. pylori seropositivity and either adenocarcinoma (OR 1.1, 95% CI: 0.75–1.6) or squamous cell carcinoma (OR 1.1, 95% CI: 0.77–1.7), and the results were similar

for CagA- and CagA+ H. pylori seropositivity. Nevertheless, these results should be considered in regard to the relatively high H. pylori seropositivity in 79.7% of cases and in 78.5% of controls. Still, a possible association between H. pylori infection and lung cancer remains intriguing because lungs develop embryologically from the same endodermal cells that line the GI tract and contain cells that produce peptide hormones like gastrin, leaving open the possibility that trophic effects in conjunction with systemic effects of local inflammation (H. pylori lipopolysaccharide) may promote cellular proliferation in the lungs, as well. In conclusion, in the last year, several diseases have been investigated for a possible association with H. pylori infection. Considering the high number of papers published so far, we may easily state that this topic is still one of the most fascinating inside the H. pylori research area. Competing interests: the authors have no competing interests;][#,63]?> “
“Evidence has shown benefits of single-strain probiotics for Helicobacter pylori eradication. We investigated the effects of adding a multistrain probiotic compound on bismuth-containing quadruple therapy for H. pylori infection. Adult patients with peptic ulcer disease and confirmed H.

There was no proven correlation between Helicobacter spp. and colorectal cancer. However, in another review, Risch summarized and analyzed seven published studies (three case–control studies and four cohort studies) with regard to pancreatic cancer odds ratio (OR) for H. pylori positivity Selleckchem BGJ398 [58]. The author found that H. pylori colonization significantly increased the risk for pancreatic cancer, with a pooled OR for this combined analysis of 1.65 (95% CI: 1.30–2.09). In light of a published case–control study that showed increased risk of pancreatic cancer with non-O blood groups (A, B, and AB) compared to O [59]. Risch postulated that N-nitroso compounds

have blood-borne trophic effects on pancreatic ductular epithelium that act combined with H. pylori infection, embedded in the background of host genetic variations and ABO that may affect other aspects of inflammatory response, could lead to development of pancreatic cancer. Koshiol et al. [60] conducted the study of 350 lung adenocarcinoma cases, 350 squamous cell carcinoma cases, and 700 nested controls within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study (ATBC) cohort of male Finnish smokers. To test the associations between H. pylori seropositivity (ELISA) and lung cancer risk using conditional logistic Selleck Anti-infection Compound Library regression,

controls were one-to-one matched by age and date of baseline serum draw. The results of MCE this study did not found an association between H. pylori seropositivity and either adenocarcinoma (OR 1.1, 95% CI: 0.75–1.6) or squamous cell carcinoma (OR 1.1, 95% CI: 0.77–1.7), and the results were similar

for CagA- and CagA+ H. pylori seropositivity. Nevertheless, these results should be considered in regard to the relatively high H. pylori seropositivity in 79.7% of cases and in 78.5% of controls. Still, a possible association between H. pylori infection and lung cancer remains intriguing because lungs develop embryologically from the same endodermal cells that line the GI tract and contain cells that produce peptide hormones like gastrin, leaving open the possibility that trophic effects in conjunction with systemic effects of local inflammation (H. pylori lipopolysaccharide) may promote cellular proliferation in the lungs, as well. In conclusion, in the last year, several diseases have been investigated for a possible association with H. pylori infection. Considering the high number of papers published so far, we may easily state that this topic is still one of the most fascinating inside the H. pylori research area. Competing interests: the authors have no competing interests;][#,63]?> “
“Evidence has shown benefits of single-strain probiotics for Helicobacter pylori eradication. We investigated the effects of adding a multistrain probiotic compound on bismuth-containing quadruple therapy for H. pylori infection. Adult patients with peptic ulcer disease and confirmed H.

01), and in groups of Tim-3 antibody pretreatment were significantly lower than those in untreated groups(P < 0.01). The expression of Foxp3 in colonic mucosa were significantly lower in all model groups click here than those in the corresponding control groups(P < 0.05), and in groups of Tim-3 antibody pretreatment were significantly higher than those in untreated groups(P < 0.01). The expression of SIGIRR in colonic mucosa were significantly lower in all model group than

those in control group(P < 0.05) in untreated groups, and in groups of Tim-3 antibody pretreatment were significantly higher than those in untreated groups(P < 0.05). The expression of TLR4, MyD88 and NF-κBp65 in colonic mucosa Rapamycin were significantly higher in all model groups than those in the corresponding control groups(P < 0.05, 0.01), and in groups

of Tim-3 antibody pretreatment were significantly lower than those in untreated groups(P < 0.05, 0.01). Conclusion: Tim-3 antibody treatment can alleviate mice colitis, increase expression of Foxp3 and SIGIRR, and decrease the expression of MyD88 and NF-κB p65, which suggest that Tim-3 antibody may alleviate the inflammation of IBD by up-regulating Foxp3 + Treg reaction and inactivating of TLRs/NF-κB signaling pathway. Key Word(s): 1. IBD; 2. Tim-3; 3. Treg cell; 4. Toll-like receptor; Presenting Author: YONG XIE Additional Authors: NANJIN ZHOU, PING WANG, MEIJUN ZHONG, ZHIRONG MAO, JINGXUAN PEI, YANG YANG, ZHIFA LV Corresponding Author: YONG XIE Affiliations: Digestive Disease Institute, the First Affiliated Hospital of Nanchang University, Nanchang, China.; Institute of Medical Sciences of Jiangxi province Objective: To observe the effect of intervention of Tim-1 signal pathway on different types of experimental colitis in mice, to provide the basis for using Tim-1 as the target for the treatment of IBD. Methods: 54 BALB/c mice were randomly allocated into six groups: MCE ① Mice + IgG1(control); ② DSS model + IgG1; ③ TNBS model + IgG1; ④ Mice + Tim-1-Ab(control); ⑤ DSS model

+Tim-1-Ab; ⑥ TNBS model + Tim-1-Ab. To observe the disease activity index (DAI), change of pathohistology, expression of Foxp3, MyD88, TLR4 and SIGIRR in colonic mucosa. Results: 1. The DAI score and pathohistological severity score of colon(The degrees of colon inflammation, pathological depth and crypt destruction) were significantly higher in all model groups than those in the corresponding control groups(P < 0.01), and in groups of Tim-1 antibody pretreatment were significantly higher than those in untreated groups(P < 0.05).2. The expression of Foxp3 in colonic mucosa were significantly lower in all model groups than those in the corresponding control groups(P < 0.01), and in groups of Tim-1 antibody pretreatment were significantly lower than those in untreated groups(P < 0.05).3.