Although opacification grade in the intrahepatic left portal vein

was not statistically significant between CO2-based and ICM-based images (P = 0.1515), check details weak opacification was significantly frequent on CO2-based images (weak 10, sufficient 10) compared to ICM-based images (weak 0, sufficient 20; P = 0.0003) in the intrahepatic right portal vein. Inter-reviewer agreement was excellent between the two reviewers for CO2-based images (kappa = 0.913) and ICM-based images (kappa = 0.924). Conclusions:  Carbon dioxide may be a first-line contrast material for evaluating portal vein images by PTP. “
“Serum testosterone is reduced in up to 90% of men with cirrhosis, with levels falling as liver disease advances. Testosterone is an important anabolic hormone, with effects on muscle, bone, and haematopoiesis. Many of the features of advanced liver disease are similar to those seen in hypogonadal

men, including sarcopenia, osteoporosis, gynecomastia and low libido. However the relative contribution of testosterone deficiency to the symptomatology of advanced liver disease has not been well established. More recently it has been demonstrated that low testosterone in men with cirrhosis is associated with increased mortality, independent of the classically recognised prognostic factors such as MELD score. Only several small clinical trials have examined the role of testosterone therapy in men with cirrhosis, PS-341 none of which have resolved the issue of whether or not testosterone is beneficial. However, in men with organic hypogonadism due to structural

hypothalamic-pituitary-testicular axis disease, testosterone therapy has been shown to improve muscle mass, bone mineral density, increase haemoglobin and reduce insulin resistance. Despite initial concerns linking testosterone with hepatocellular carcinoma, more recent data suggests that this risk has been overstated. MCE公司 There is therefore now a strong rationale to assess the efficacy and safety of testosterone therapy in cirrhosis in well-designed randomised controlled trials. “
“miR-17-5p is overexpressed in hepatocellular carcinoma (HCC), but the specific regulatory mechanisms of miR-17-5p in HCC remain unknown. We investigated the molecular basis of miR-17-5p as an oncogene in human HCC cell lines. Our in vivo and in vitro data indicate that miR-17-5p up-regulates the migration and proliferation of HCC cells. Interestingly, proteomic and western blotting assays revealed that miR-17-5p significantly activates the p38 mitogen-activated protein kinase MAPK pathway and increases the phosphorylation of heat shock protein 27 (HSP27). Our results also suggest that E2F1-dependent down-regulation of Wip1 regulates miR-17-5p-p38-HSP27 signaling.

Mutations in the CD40 gene have also http://www.selleckchem.com/products/KU-60019.html been reported in select patients with hyper-IgM syndrome. However, there is no defect in the CD40 gene, suggesting that the hyper-IgM observed in PBC has a different origin. In conclusion, these findings suggest an important role

of CD40L modulation in PBC and emphasize the importance of mechanisms that disrupt the epigenetic regulation of CD40L. “
“Aim:  Apelin (APLN), the endogenous ligand of angiotensin-like receptor 1 (APJ), is a peptide necessary for embryonic and tumor angiogenesis. Little is known about the localization and changes of APLN expression including the sinusoids in human cirrhotic liver, which might contribute to portal hypertension. This study was designed to elucidate the localization and change of APLN expression in human liver during the progression of cirrhosis. Methods:  Twelve normal liver specimens, eight specimens of Child–Pugh grade A cirrhosis, and 10 specimens of Child–Pugh grade C cirrhosis were studied. APLN protein and gene expression was examined by immunohistochemistry, western blotting, immunoelectronic microscopy, and laser captured microdissection (LCM) followed by polymerase chain reaction (PCR) in sinusoid. Results:  In control liver tissue, APLN was localized mainly on arterial endothelial cells and hepatic arterioles in the portal tract. In cirrhotic liver tissue, aberrant APLN expression was observed

in periportal capillary endothelial cells corresponding to capillarized sinusoids, and in proliferated arterial capillaries selleck chemicals in the fibrotic septa. Significant overexpression of APLN at protein level in cirrhotic liver was demonstrated by western blotting MCE (P < 0.01 Child–Pugh A and C versus control, P < 0.01 Child–Pugh A versus C). APLN mRNA expression in the sinusoid was confirmed by LCM-PCR. Conclusion:  In humans, APLN protein and gene were overexpressed in cirrhotic liver compared with normal liver, and the magnitude increased as cirrhosis progressed. Especially in end-stage cirrhosis, APLN was strongly expressed in proliferated arterial capillaries directly connected with the sinusoids, suggesting a role of APLN in the proliferation of arterial

capillaries in cirrhosis. “
“In the mouse embryo, hematopoietic progenitor cells migrate to the fetal liver (FL) between gestational days (E) 9.5 and 10.5, where they rapidly expand to form the main fetal reservoir of hematopoietic cells. The embryonic megakaryocyte progenitors (MKPs) in the E11.5 FL were identified as CD49fHCD41H (and c-KitDKDR+CD42+CD9++CD31+) cells, expressing several hepato-specific proteins. Unlike adult bone marrow megakaryocytes (MKs), embryonic MKPs were CD45− and represent an abundant population in the FL. The CD49fHCD41H MKPs purified by cytometry differentiated in vitro to produce proplatelets, independent of thrombopoietin stimulation, and they responded to stimulation with adenosine diphosphate, thrombin, and the PAR4 thrombin receptor-activating peptide.

18 Approximately half of the FHBL subjects are carriers of mutations in the ApoB gene, whereas the causes for other FHBL patients are not known.19 Intriguingly, PLA2GXIIB−/− mice display compromised ApoB-VLDL secretion and develop severe fatty liver partially resembling those displayed by FHBL patients. It is therefore reasonable to speculate that some of those FHBL patients without mutations in the ApoB gene may have aberrant expression or activity levels of HNF-4α, MTP, and PLA2GXIIB. We thank Ms. Xuehua Zheng,

Ibrutinib mw Mr. Yichu Liu, Dr. Hui Zhi, Dr. Zhaoyu Lin, and the staff at the Animal Center of GIBH for assistance throughout the project. This study was supported by the Knowledge Innovation Program of the Chinese Academy of Sciences (No. KSCX1-YW-10), National Key Science and Technology Specific Projects of China (2008ZX10001-001), and National Science Fund for Distinguished Young Scholars of China (No.30688004). Ribociclib mouse Additional Supporting Information may be found in the online version of this article. “
“Impaired T-cell responses in chronic hepatitis C virus (HCV) patients have been reported to be associated with the establishment of HCV persistent infection. However, the mechanism for HCV-mediated T-cell dysfunction is yet to be defined.

Myeloid-derived suppressor cells (MDSCs) play a pivotal role in suppressing T-cell responses. In this study we examined the accumulation of MDSCs in human peripheral blood mononuclear cells (PBMCs) following HCV infection. We found that CD33+ mononuclear cells cocultured with HCV-infected hepatocytes, or with HCV core protein, suppress autologous T-cell responses. HCV core-treated CD33+ cells exhibit a CD14+CD11b+/lowHLADR−/low phenotype with up-regulated expression of p47phox, a component of the NOX2 complex critical for reactive oxygen species (ROS) production. In contrast,

immunosuppressive factors, arginase-1 and inducible nitric 上海皓元 oxide synthase (iNOS), were not up-regulated. Importantly, treatment with an inactivator of ROS reversed the T-cell suppressive function of HCV-induced MDSCs. Lastly, PBMCs of chronic HCV patients mirror CD33+ cells following treatment with HCV core where CD33+ cells are CD14+CD11b+HLADR−/low, and up-regulate the expression of p47phox. Conclusion: These results suggest that HCV promotes the accumulation of CD33+ MDSC, resulting in ROS-mediated suppression of T-cell responsiveness. Thus, the accumulation of MDSCs during HCV infection may facilitate and maintain HCV persistent infection. (HEPATOLOGY 2012) Hepatitis C virus (HCV) infection in humans is almost invariably associated with viral persistence leading to chronic hepatitis, which in turn predisposes the infected individual to hepatocellular carcinoma and the necessity of a liver transplant.

pylori interactions within a cellular biology context will undoubtedly be rewarding. Infection with H. pylori is known to lead to the release of many chemo- and cytokines; however, more comprehensive characterization of their individual roles is still required. Wong et al. [22] recent characterization of macrophage migration inhibitory factor (MIF) expression in mice infected

with H. pylori revealed that a negligible inflammatory response in H. pylori-infected MIF-deficient mice correlated with a substantially reduced inflammatory T-cell response, characterized by lower IFN-γ and TNF-α production. Inflammation in response to H. pylori infection may not only be induced by recruitment of leukocytes, selleck inhibitor but, alternatively, the induction of IL-1β by H. pylori neutrophil-activating protein (HP-NAP) may increase survival of inflammatory monocytes, and in turn neutrophils extending the local life time of these cells, as shown by Cappon

et al. [23]. Several studies have shed more light to the many facets of IL-1β in this infection, such as the loosening of tight junctions by disrupting claudin-4 [24], and the involvement of sonic hedge hog signaling in IL-1-dependent reduction in gastric acid output [25]. Thus, step-by-step, we are gaining an increased understanding of why the genetic background of IL-1/IL-1R impacts the course of H. pylori-triggered disease [26]. In recent years, the study of a novel selleckchem class of regulators, small RNAs, has gained momentum [27]. Small or micro RNAs (miR) are noncoding RNAs mostly transcribed by RNA polymerase II. They are processed by ribonucleases in the nucleus and further in the cytoplasm by the machinery that also generates small interfering RNAs and by other enzymes. The mature miRs (classified using a nomenclature of the kind medchemexpress miR followed by a number, e.g. miR-155) preferentially bind to complementary sequences in the 3′ UTRs of target mRNAs leading

to degradation or inhibition of translation. Depending on the target gene, this can affect multiple host cell processes, including cell development, differentiation, and even malignant transformation, possibly also gastric cancer [28]. Over 700 miR species are predicted from the human genome, and for a number of them a role in regulating expression of genes in cells of the immune system has been demonstrated (for recent review see [27]). Specific microarrays have been produced to detect miR sequences in samples of small RNAs to allow parallel assessment of miR expression. Matsushima et al. [29] used this technology to investigate signatures of 470 miRs in biopsies from Japanese H. pylori infected patients in comparison with non-infected controls. From a total of 242 miRs detected, 55 miRs showed differential abundance in these samples. Validation with another patient cohort revealed that the levels of 30 miRs were consistently decreased in infected patients.

The results with cholesterol homeostasis genes correlated with changes in nuclear localization of key regulators of cholesterol and bile acid homeostasis (e.g., sterol regulatory element binding protein-2 and liver receptor homolog-1); however, the pattern of these changes was less clear. For example, although expression of CYP7A1 in foz/foz mice fed HFD was less than half that of WT mice fed chow, nuclear localization of liver receptor homolog-1 was not different between these groups.

The authors then showed that insulin in vitro at similar levels found in foz/foz mice (up to 20 ng/mL)13 changed the expression of some of the cholesterol synthesis genes in a pattern similar to what was observed in vivo (e.g., sterol regulatory element binding protein-1, low-density lipoprotein receptor, and bile acid Ipilimumab mouse export protein). These in vitro results, although supportive of the concept that the authors promote, have some limitations. First, the authors did Metformin price not study the effect of these insulin concentrations directly on cholesterol flux in these cells. Second, these results ignore the fact that plasma insulin levels are equally elevated in foz/foz mice fed chow,13 which would imply that they would expect similar expression changes with

foz/foz mice on chow diet, which was not observed in their animal models (see Figs. 1-3 in van Rooyen DM et al.10). The last series of experiments are to test the effect of titrating cholesterol into the standard HFD on liver damage in the foz/foz mice. The results demonstrate that foz/foz mice accumulate CE and FC and develop inflammatory liver damage even on HFD without cholesterol and that these variables increase as the percentage of dietary cholesterol rises. Interestingly, HFD-fed WT mice do not develop significant liver

injury until dietary cholesterol 上海皓元 levels are high enough to accumulate in the liver. However, it should be noted that there are key differences between WT and foz/foz mice that cannot be explained simply by differential abilities to accumulate cholesterol. For example, at even the highest concentration of cholesterol (2%), the authors observed few fibrotic changes in WT mice, which is in contrast to foz/foz mice that were fibrotic even in the absence of added dietary cholesterol (see Fig. 6 in van Rooyen DM et al.10). Issues that remain after this study include whether the results observed here are specific to Alström syndrome, or are more generally applicable to fatty liver disease. First, it is unclear if the magnitude of increase in cholesterol observed in this study is relevant to human fatty liver disease. For example, hepatic CE levels do not differ between control, NAFLD and NASH in humans, but were >50-fold higher in foz/foz mice.11 Furthermore, hepatic FC levels are only 20% elevated in NASH versus NAFL, versus a much stronger increase in foz/foz mice.

26 IU/ml and 1592.46s/co, respectively (P>0.05). 39 infants did not appear congenital malformations with normal Apgar score and developmental indicators at birth. At 7 months after birth, no infants developed HBV infection, a 100 %success rate of blocking mother-to-infant transmission of HBV was achieved. Conclusion: Telbivudine treatment effectively and safely prevents mother-to-infant transmission of HBV from chronically infected mothers with a high degree of infectivity late in pregnancy. Disclosures:

The following people have nothing to disclose: Qiuju Sheng, GSK126 in vivo Yang Ding, Han Bai, Jingyan Wang, Chong Zhang, Lianrong Zhao, Xiaoguang Dou Background: Sequential therapy particularly with drugs with low barrier to resistance posed a high risk of emergence of multi-drug resistance (MDR) and presented a management issue and unmet need in chronic hepatitis B (CHB) treatment. We evaluated the antiviral efficacy and BYL719 safety of entecavir (ETV) plus tenofovir (TDF) combination therapy in patients with MDR CHB. Methods: In this prospective, multicenter study, patients with MDR CHB, defined as measurable serum HBV DNA (≥ 60 IU/mL) while on any rescue treatment regimen for at least 24 weeks and the presence of documented genotypic resistance

to both nucleoside analogue(s) and nucleotide analogue at any previous time, were treated with ETV 1.0mg and TDF 300mg combination therapy for 48 weeks. Results: Of the 73 consecutive patients screened in this study, a total of 64 eligible patients, who had previously failed to a median three lines of antiviral therapy (range 2-6), were included. At baseline, median age was 47.0 years, 80.8% were male,

89.1% were HBeAg(+), median HBV DNA was MCE 4.24 (range 2.11-6.73) log10 IU/ml, and mean ALT was 39.7 IU/ml. By week 4, 12, 24 and 48, 15/64 (23.4%), 36/64 (56.3%), 43/64 (67.2%) and 56/63 (85.9%) patients achieved a HBV DNA < 60 IU/ml, respectively. The median reduction of HBV DNA from baseline to 4 weeks and 48 weeks was 1.23 log10 IU/ml and 2.39 log10 IU/ml, respectively. Although 5 patients experienced virological breakthrough, all were transient and no additional/novel mutation was detected in any patients. Two patients lost HBeAg, but no HBeAg seroconversion was observed for 48 weeks. ETV plus TDF combination therapy was well tolerated, and no clinical significant adverse events were noticed during the study period. Conclusions: Our results show that, in difficult-to-treat MDR CHB patients with a high exposure to multiple antiviral drugs, ETV plus TDF combination therapy can provide a very high rate of viral suppression through 48 weeks of treatment.

We also examined IgM and CXCL13 staining with liver tissue samples of PBC, whereas IgM positive cells were observed in only one case (10%). However, in this case, CXCL13 was also positively stained in the bile duct cells. We speculate that aberrant

expression of CXCL13 in the bile duct invites IgM positive cells into the liver of PBC. It could still be possible that the IgM positive cells enter the liver and affect bile duct damage in PBC, because previous studies demonstrated that IgM positive cells are distributed to PBC-specific hepatic lesions such as altered bile duct[17] and granuloma.[18] Also, B-cell depletion using anti-CD20 antibody improves cholangitis in PBC model mice[19] and reduces blood CH5424802 mouse alkaline phosphatase level in humans,[20] supporting this idea. In conclusion, IgM positive cells were detected in lymph follicles, and excess IgM could be produced in the spleen of PBC. Furthermore, CXCL13 could contribute to this process. Future studies should address how the spleen including the IgM memory B cells and FDC affect PBC pathology and formation of hepatic lesions. THIS WORK WAS supported by a Grant from the Ministry of Health,

Labor and Welfare of Japan and JSPS KAKENHI Grant-in-Aid for Scientific Research (C) no. 24590952 and (B) no. 24390181. “
“Background and Aim:  The rapid Tanespimycin price increase in inflammatory bowel disease (IBD) incidence confirms the importance of environment in its etiology. We aimed to assess the role of childhood and other environmental risk factors medchemexpress in IBD. Methods:  A population-based case-control study was carried out in Canterbury, New Zealand. Participants comprised 638 prevalent Crohn’s disease (CD) cases, 653 prevalent ulcerative colitis (UC) cases and 600 randomly-selected sex and age matched controls. Exposure rates to environmental risk factors were compared. Unadjusted and adjusted odds ratios (OR) with 95% confidence intervals (CI) are presented. Results:  A family history of IBD (CD OR 3.06 [2.18–4.30], UC OR 2.52 [1.90–3.54]), cigarette smoking

at diagnosis (CD OR 1.99 [1.48–2.68], UC OR 0.67 [0.48–0.94]), high social class at birth (CD and UC trend, P < 0.001) and Caucasian ethnicity (CD OR 2.04 [1.05–4.38], UC OR 1.47 [1.01–2.14]) were significantly associated with IBD. City living was associated with CD (P < 0.01). Being a migrant was associated with UC (UC OR 1.40 [1.14–2.01]). Having a childhood vegetable garden was protective against IBD (CD OR 0.52 [0.36–0.76], UC OR 0.65 [0.45–0.94]) as was having been breast-fed (CD OR 0.55 [0.41–0.74], UC OR 0.71 [0.52–0.96]) with a duration-response effect. Appendicectomy, tonsillectomy, infectious monomucleosis and asthma were more common in CD patients than controls (P < 0.01). Conclusions:  The importance of childhood factors in the development of IBD is confirmed.

2B). Whereas hepatocytes in cirrhosis had a wider rate of proliferation than those in normal liver, the difference did not reach statistical significance in

this study. p21 and PCNA labeling indices showed no significant difference between EpCAM(+) hepatocytes and EpCAM(−) hepatocytes (Fig. 3). The telomere lengths were measured by studying from 50 to 214 telomere dots www.selleckchem.com/products/apo866-fk866.html (telomere length signal detected by quantitative fluorescence in situ hybridization) according to cell type in nine cases of normal liver (Fig. 4G; Supporting Table 3). In normal liver, there was no significant difference in telomere lengths among normal hepatocytes, canal of Hering cells and bile duct cells (Fig. 5A), nor did they differ according to age or sex. In selleck cirrhotic livers, the telomere lengths were measured by studying from 33 to 189 telomere dots according to cell type in six cases (Fig. 4G; Supporting Table 4). When comparing

the telomere lengths between EpCAM(+) hepatocytes and EpCAM(−) hepatocytes in cirrhosis, the telomere lengths of EpCAM(−) hepatocytes were significantly shorter than those of EpCAM(+) hepatocytes (P = 0.046). In addition, EpCAM(+) hepatocytes showed relatively shorter telomere length than ductular reactions (P = 0.057), whereas EpCAM(−) hepatocytes showed significantly shorter telomere length than ductular reactions (P = 0.016) (Figs. 4 and 5A). There was no significant difference in telomere length according to patient age in both cirrhotic and normal livers. When the telomere lengths of ductular reactions, EpCAM(+) hepatocytes, and EpCAM(−) hepatocytes were traced in each patient, there was gradual telomere shortening from ductular reaction to EpCAM(+) hepatocytes and to EpCAM(−) hepatocytes (Fig. 5B). A growing body of work in the last few decades has identified cells of the ductular reactions in human livers in diverse but usually severe

acute and chronic liver diseases as being the equivalent of the oval cells seen in rodent models of injury.1, 2, 5, 11-16, 18 As such, the ductular reactions are thought to be the transit amplifying cells deriving from activation of the stem cell compartments of the liver.1, 7 Like oval cells, the 上海皓元医药股份有限公司 cells are thus thought to have at least two possible differentiation pathways, toward hepatocytes and toward cholangiocytes, the dominant direction being determined by the presence of injury and the nature and severity of that injury. In diseases with a predominance of hepatocyte injury, the ductular reaction is triggered by acute destruction of large amounts of parenchyma11 or by senescence of hepatocytes by chronic low level injury, and presumably results in hepatocyte replenishment from the stem/progenitor cell compartments.

Various factors affecting the achievement of the optimal trough level were compared between the achievement and non-achievement groups. A univariate analysis was done first, followed by a multivariate analysis for items with P < 0.25. The remission rate after 4 weeks

was compared between the Exp and Non-Exp groups. In our hospital, subjective and objective findings needed for the disease activity index (DAI, also known as the “Sutherland index”)[16] or other activity VX-770 solubility dmso indices are entered in electronic medical records daily for hospitalized UC patients, and blood tests are performed at least once a week. For severe colitis, blood tests are usually checked twice per week. Thus, the DAI score can be calculated accurately even retrospectively. In this study, the DAI entered in patients’ medical records was used to evaluate selleck inhibitor activity. However, because all patients did not undergo endoscopy 4 weeks after the start of therapy,

a partial DAI (pDAI) score excluding the endoscopic subscore was used to define remission. Patients with pDAI ≤ 1 were defined as in remission, and patients with other scores and patients who underwent surgery within 4 weeks after the start of therapy were defined as being in non-remission. The frequency and types of adverse effects were investigated. When Tac is used in patients aged 60 years or older in our hospital, cotrimoxazole is administered at the usual dosage with the aim of preventing Pneumocystis pneumonia (PCP). An unpaired t-test was used to test for differences in mean values, and the chi-square test or Fisher’s exact test was used to compare frequencies. Multivariate analysis was used to analyze factors involved in achieving the optimal trough levels. All statistical analyses were done using SPSS ver. 16.0 (SPSS Inc., Chicago, IL, USA). Written, informed consent was obtained from all subjects. This study was approved by the ethical review board of Fukuoka University. The subjects in this study MCE were 25 men and 21 women with a mean age of 40.9 ± 13.8 years and

a mean duration of disease of 4.9 ± 5.2 years. The DAI score on day 0 of Tac was 10.9 ± 1.2, and the pDAI score was 7.8 ± 1.2. Pretreatments involved steroid therapy in 35 patients, accounting for 78% of all cases. Of these 35 patients, 25 received intravenous steroids, and the remaining 10 took oral steroids. Other treatments were cytapheresis in six patients, cyclosporine A (CyA) and infliximab in one patient each, and 5-aminosalicylic acid with an immunomodulator in two patients. Fasting management with total parenteral nutrition was selected in 22 patients, which corresponded to about half of the 45 patients in this study. Hydrocortisone was administered intravenously in 20 of these 22 patients, the large majority.

Conclusion: There is only poor to moderate correlation between 2D and 3D manometry findings. Even in patients with normal pressure values for RP and SP, there is a high possibility of detecting abnormalities in the 3DPP. Key Word(s): 1. 3 Dimensional; Sorafenib 2. Anorectal manomtry; Presenting Author: DAKSHITHA WICKRAMASINGHE Additional Authors: SUPUN SENARATNE, CHAMILA PERERA, NANDADEVA SAMARASEKERA Corresponding Author: DAKSHITHA WICKRAMASINGHE Affiliations: none Objective: Stoma care is a specialized area in nursing but in Sri Lanka, there

were only a handful of trained stoma care nurses. In June 2012, the Ministry of Health conducted a 4 week full time course in Stoma Therapy for nurses. Methods: Participants completed a questionnaire derived from a validated questionnaire used in a previous publication, which evaluated basic demographic see more details and some aspects of patient care. The questionnaire was administered on the 1st day of the program and at the completion. Data were analyzed using Wilcoxon signed-rank test. Results: There were 24 males and 37 females. The mean age was 31.5 (± 5.5) years. All participants completed the questionnaire. The

mean years in nursing was 9.5 (± 5.5) years. All 15 domains of patient care had improved at the end of the program (Biggest increase was seen in staff confidence category (average increase in score 63.5%)). The 3 domains that had the biggest improvement in descending order are; the confidence to select different appliances to suit different conditions (Z = −6.638, P < 0.0001), having material for proper patient

teaching (Z = −6.323, P < 0.001) and confidence in educating patients (Z = −6.544, P < 0.001). Our results suggest that a 4 week course provides adequate knowledge and confidence to function as stoma care nurses. The responses also indicates that the program was successful in making them confident in managing stoma patients and functioning independently and the program was successful in providing a comprehensive training and a holistic approach. Conclusion: A 4 week stoma care training program for trained nurses provides the participants 上海皓元 with the necessary knowledge and confidence to function independently. Programs of this nature can be conducted in developing countries with limited resources, using local resource personnel with minimal cost to the state. Key Word(s): 1. Stoma care nurse; 2. Training; 3. Developing country; 4. Effectiveness; Presenting Author: JIE HONG Additional Authors: YURONG WENG, YANAN YU, LINLIN REN, JING-YUAN FANG Corresponding Author: JIE HONG Affiliations: Gastroenterology Objective: c9orf140 is a novel gene that has been recently isolated and indentified by the mRNA differential display (mRNAD), which is associated with cell proliferation and tumorigenesis in Gastric caner. Moreover, it was reported that the expression of c9orf140 is significantly elevated in colorectal caner (CRC) tissues when compared with normal tissues.