S31) Moreover, the decline

in annual survival rate afte

S3.1). Moreover, the decline

in annual survival rate after 2004 in the year model was not statistically significant, though in the age model, decline after age 17 was. In males, however, the year model produced a better fit to data than the age model (Fig. S3.2). Nevertheless, the survival-year model added information, because it revealed fluctuations in young Cell Cycle inhibitor animals not evident in the age model (Appendix S3). Survival was high in 1986, low in 1987, then increased until 1989 before settling on a long plateau (Fig. S3.3). The 1986–1986 variation was a cohort effect: first-year survival was high for the 1985 cohort relative to the 1986 and 1987 cohorts in both males and females. The cohort difference, however, did not persist in older

animals (Fig. S3.1, Fig. S3.2). The age model produced an intermediate estimate for first-year survival, averaging the three cohorts. Annual survival of adult females was high from age BGB324 5 to 16, averaging 86%/yr, but then declined abruptly. This is a higher rate and a longer duration of prime survival than we expected and the first evidence for senescence in survival rates of northern elephant seals. Our earlier work did not detect the decline in female survival because there were no data on females older than 15 yr (Le Boeuf and Reiter 1988, Reiter and Le Boeuf 1991). Schwarz et al. (2012) found limited power in estimating survival beyond age 15 due to the small number of animals retaining tags. Average male survival was <72%/yr at all ages and lower than female survival after age 3, as reported in earlier studies (Clinton and Le Boeuf 1993). Neither our MCE current analysis nor the earlier work detected senescence in male survival, but high mortality throughout life meant few males were still living at age 12 when senescence would be most likely. On the other hand, our earlier study did detect declining competitive ability in males past age 12 (Clinton and Le Boeuf 1993). Juvenile survivorship in the current study was 31% from weaning to

age 3 and similar in the two sexes, a rate close to the average reported across several previous cohorts (Le Boeuf and Reiter 1988, Le Boeuf et al. 1994). This average masked variation, however, and low survival in 1986–1987 may have been due to poor foraging conditions associated with an El Niño event (Trenberth and Stepaniak 2001, Crocker et al. 2006). Our earlier study of juvenile survival also described substantial year-to-year fluctuations (Le Boeuf et al. 1994). These rates of survivorship, though, began at weaning and omit pup mortality, and 10% of pups in the Año Nuevo mainland colony died before weaning in 1985–1987 (Le Boeuf et al. 2011). In population modeling, the relevant rate of juvenile survivorship (from birth) was thus 28%, not 31%. Dispersal of branded animals to nearby colonies—“prospecting” for alternative breeding sites—also confirms earlier observations (Le Boeuf et al. 1974, 2011).

7C,F) As noted in the whole livers, the mRNA expression levels o

7C,F). As noted in the whole livers, the mRNA expression levels of collagen 1α1, collagen 1α2, and α smooth muscle actin (αSMA) were significantly increased in HSCs from the MCD and HF diet-fed groups compared with the corresponding control diet-fed groups. These increases were significantly enhanced by the increased intake of cholesterol (Fig. 1A,D). The mRNA expression levels of PPARγ1 in HSCs were significantly lower in the MCD and HF diet-fed groups than in the corresponding control diet-fed groups. In addition,

these decreases were significantly enhanced by the increased intake of cholesterol (Fig. 1A,D). Contrarily, the mRNA expression levels of SREBP2 were significantly higher in HSCs learn more from the MCD and HF diet-fed groups than in those from the corresponding control diet-fed groups, and these increases were significantly enhanced by the increased intake of cholesterol (Fig. 1A,D).

The total and nuclear protein levels of PPARγ were lower in HSCs from the MCD and HF diet-fed groups than in those from the corresponding control diet-fed groups and these decreases were significantly enhanced by the increased intake of cholesterol (Fig. 1B,E). Meanwhile, the levels of the nuclear form of SREBP2 were significantly higher in HSCs from the MCD and HF diet-fed groups than in those from the corresponding control diet-fed groups. Furthermore, these increases were significantly enhanced by the increased intake of cholesterol (Fig. 1B,E). Similar to SREBP2 expression, the expression levels of LDLR and miR-33a in HSCs were significantly higher buy RXDX-106 in the MCD and HF diet-fed groups than in the corresponding control diet-fed groups. These increases were significantly enhanced by the increased intake of cholesterol (Fig. 1C,F). The total and nuclear forms of PPARγ were abundant in day 1 (quiescent) HSCs but declined in day 3 and 5 (activating) and day 7 (activated) HSCs (Fig. 2A). Meanwhile,

the nuclear form of SREBP2 was scarce in day 1 HSCs, and its expression increased 上海皓元 at days 3 and 5, and day 7 HSCs (Fig. 2A). Correspondingly, the PPARγ1 and SREBP2 mRNA expression levels were similar to the protein expression levels (Fig. 2A). Furthermore, the expression levels of LDLR and miR-33a in HSCs increased along with their activation (Fig. 2B). PPARγ-siRNA treatment significantly increased the expression levels of SREBP2, LDLR, and miR-33a in quiescent HSCs (Fig. 2C). Similarly, treatment with the PPARγ antagonist significantly increased the expression levels of SREBP2, LDLR, and miR-33a in quiescent HSCs in a dose-dependent manner (Fig. 2D). On the other hand, overexpression (O/E) of PPARγ1 significantly decreased the levels of SREBP2, LDLR, and miR-33a expression in activated HSCs (Fig. 2E). SREBP2-siRNA treatment significantly decreased the mRNA expression level of LDLR (Fig. 2F).

These recent discoveries will not only drive functional studies b

These recent discoveries will not only drive functional studies but will also hold the promise of developing novel this website disease-specific treatments. (HEPATOLOGY 2011;) Primary biliary cirrhosis (PBC) is a chronic cholestatic liver disease characterized by progressive destruction of small and medium size intrahepatic bile ducts, leading to cirrhosis and ultimately liver transplantation or death.1 PBC has an

estimated prevalence of 1 in 1000 in women over the age of 40, and ursodeoxycholic acid is the only approved therapy.2 The pathogenesis of PBC is clearly autoimmune,3 as indicated by specific serum- and cell-mediated responses against defined epitopes of self antigens, and by a striking female predominance (female-to-male ratio of approximately 10 to 1). In addition, epidemiological data indicate that family members of patients have an increased risk of developing PBC or another

autoimmune disorder. On the basis of these considerations, the current hypothesis on the etiopathogenesis of PBC implies that this disease is the result of a genetic predisposition that is PS-341 cost permissive for a still unknown environmental agent, possibly xenobiotic or infection.1 For decades, PBC has been considered to have a unique genetic background when compared to other autoimmune diseases because of the strong familial clustering but weak associations with genetic polymorphisms.4 Indeed, despite numerous candidate-gene association studies that were performed, no conclusive data on specific genes have been obtained. In addition,

it is worth noting that linkage analysis was poorly feasible in PBC based on the advanced age at diagnosis and the rarity of the disease. In contrast, recent evidences have strengthened the importance of genetic susceptibility in determining disease onset and severity, including a role for sex chromosome abnormalities in affected women5, MCE公司 6 and high concordance for disease in monozygotic twins.7 The human leukocyte antigen (HLA) loci, located in the major histocompatibility complex (MHC), are the most genetically diverse loci in the human genome8 (Fig. 1). HLA genes encode cell-surface molecules that by means of peptide presentation mediate key immunological events, such as definition of self-tolerance or cellular immune responses to tumors and pathogens.9, 10 Similar to other genetically complex diseases,11 HLA has been extensively studied in PBC, but for decades data have cumulatively suggested only a weak association with the class II HLA DRB1*08 allele.4 This was likely because early studies had several potential limitations: (1) insufficient statistical power due to inadequate sample sizes, (2) lack of careful matching between cases and controls, (3) earlier studies did not rely on molecular analysis, and (4) multiple replications have rarely been carried out.

It is warranted to elucidate the mechanism of protective effect i

It is warranted to elucidate the mechanism of protective effect in patients with NAFLD. Figure 1. Time-to-BCR according to the presence of NAFLD. Disclosures: The

following people have nothing to disclose: Won-Mook Choi, Jeong-Hoon Lee, Young Ju Lee, Young Youn Cho, Yuri Cho, Dong Hyeon Lee, Su Jong Yu, Yoon Jun Kim, Jung-Hwan Yoon, Cheol Kwak, Hyo-Suk Lee (Introduction) Useful biomarkers for diagnosing nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) are anticipated. In order to discover novel biomarkers, especially for activity and steatosis in NAFLD, we performed metabolomic screening. (Patients) This study included 105 NAFLD patients and 48 healthy controls. Using capillary electrophoresis and liquid chromatography with mass spectrometry, we analyzed low molecular-weight metabolites. Both activityrelated and steatosis-related metabolites were detected. Predictive calculation systems of activity Deforolimus mw and steatosis were established, and area under the curve (AUC), sensitivity and specificity Talazoparib chemical structure for diagnosis were investigated. (Results) 1. Twelve significant metabolites for activity were

detected. Five were amino acids or amino acid-related molecules, 1 bile acid, and 1 nitric oxide-related molecule, as well as others. Pro is the best metabolite for activity detection (5.84 in mild activity vs 6.85 in moderate-severe activity, p=0.006). Predictive calculation system for moderate-severe activity was established with 7 metabolites. AUC was 0.66, sensitivity 70% and specificity 64%.2. Sixteen significant metabolites for steatosis 上海皓元医药股份有限公司 were detected. Ten were amino acids or amino acid-related molecules, 2 bile acids, and 1 fatty acid-related molecule, as well as others. Gly is the best metabolite for steatosis detection (2.66 in mild steatosis vs 2.23 in moderate-severe activity, p=0.0016). Predictive calculation system of moderate-severe steatosis was established with 15 metabolites. AUC was 0.81, sensitivity 79% and specificity 77%. (Conclusion) Several metabolic products were found as biomarkers of activity and steatosis in NAFLD, and they could also be useful

for diagnosis of these conditions. The diagnostic ability of these metabolites and the predictive calculation system will be confirmed by validation study. Disclosures: The following people have nothing to disclose: Katsutoshi Tokushige, Etsuko Hashimoto, Kazuhisa Kodama, Maki Tobari, Noriko Matsushita, Tomomi Kogiso, Makiko Taniai, Nobuyuki Torii, Keiko Shiratori BACKGROUND: Hepatitis C virus (HCV) has been strongly associated with fibromyalgia, but fibromyalgia in patients with non-alcoholic steatohepatitis (NASH) has not been previously assessed. METHODS: We prospectively recruited patients in an outpatient hepatology clinic with cirrhosis due NASH, alcohol, and HCV. Patients with known inflammatory conditions and cancers were excluded.

Taken together, these results show

that overexpression of

Taken together, these results show

that overexpression of miR-17-5p is able to enhance the migration of HCC cells by activating the p38-HSP27 pathway. When miR-17-5p was inactivated, the migration of HCC cells was significantly reduced. These data substantially support the idea that miR-17-5p has a vital function in the migration of HCC cells. miR-17-5p expression was analyzed in 13 metastatic HCCs (group 1), 12 nonmetastatic HCCs (group 2), and five normal liver tissue samples (group 3) by way of quantitative real-time polymerase chain reaction. Notably, miR-17-5p was up-regulated in the majority of examined metastatic HCCs (Fig. 8A), with nine of 13 (69.2%) metastatic HCC tissue samples displaying more than 50% up-regulation. Next, we analyzed the profiles of HSP27 and p38 MAPK in primary human

HCC tissue by way of immunoblot analysis (groups 1-3). Among the 30 human Rucaparib in vivo samples analyzed, total HSP27 and phosphorylated HSP27 levels increased in 10 out of 13 metastatic HCC (group 1), but this was observed in only two out of 12 nonmetastatic HCCs (Fig. 8B,C). Phosphorylated p38 was also up-regulated in group 1 HCC tissues (Supporting Fig. 2). Collectively, these data suggest that deregulation of miR-17-5p and the profile of HSP27 may contribute to the progression of HCC. Previous studies on the influence of miR-17-5p on protein expression were limited to single protein analyses, primarily using western blotting and reporter assays.15, 16, 25 It is unknown how much translational control is exerted by miR-17-5p at a genome-wide scale. We used DIGE to measure changes in the synthesis Pexidartinib in vivo of several thousand proteins in response to miR-17-5p overexpression.

Those changes may include direct and indirect effects of miR-17-5p. Two recent studies18, 19 analyzed changes in the proteomes of cells in response to individual miRNAs using quantitative mass spectrometry. The authors stated that this approach was a powerful means by which to identify miRNA targets. However, biosignal transduction is a cascade reaction, so the downstream medchemexpress effects are remarkably easy to detect. Therefore, in addition to information regarding specific targets, identification of proteins indirectly regulated by miRNAs may yield more information. In this study, the identified cellular proteins were indirectly regulated by miR-17-5p and were involved in the stress response, signal transduction, and metabolism (Supporting Table 3). HSP27, a member of the small HSP family, is induced by stress and protects against heat shock, hypertonic stress, oxidative stress, and other forms of cellular injury in numerous cell types.26, 27 Overexpression of HSP27 has been reported in many kinds of tumor tissues and is found to be associated with poor prognoses for astrocytic brain tumor,28 breast cancer,29 ovarian carcinoma,30 and HCC.

Cher-venak, Lorrie A Hartel, Bashar

Aqel, Vijayan Balan,

Cher-venak, Lorrie A. Hartel, Bashar

Aqel, Vijayan Balan, Thomas J. Byrne, Elizabeth J. Carey, Jorge Rakela AIM: Although the epidemiologic link between type 2 diabetes selleck screening library Mellitus (DM) and chronic hepatitis C (CHC) is well established, the impact of diabetes control on outcomes of antiviral therapy is not clear. We aimed to assess the sustained virolog-ical response (SVR) in diabetic CHC patients according to the use of metformin and insulin. METHODS: One hundred and fifty-one genotype 1 CHC patients underwent treatment for 48 weeks with peginterferon and ribavirin, PI3K inhibitor were retrospectively divided into two groups as having type 2 DM (n=37) and not (n=114). Within the diabetic group 10 patients were receiving insulin, while the remaining 27 patients were treated with met-formin. HCV-RNA and ALT levels were measured at baseline; at weeks 4, 12, 24, and 48 during the treatment period; and the follow-up weeks 24. Groups were compared in terms of SVR. We also identified independent factors of treatment failure. RESULTS: Diabetic patients had a lower SVR compared with nondiabetic patients

(41% vs. 60%, respectively, P=0.043). While SVR was higher in diabetic patients receiving metformin compared to those receiving insulin [SVR rate of 13/27 (48%) compared to 2/10 (20%), P=0.127], the difference was not statistically significant. The multiple logistic regression analysis revealed that DM (odds ratio [OR] =2.17, 95% confidence interval [CI]= 1.02-4.62, P=0.042), compensated cirrhosis (OR=3.83, 95% CI=0.97-15.20, P=0.044), and insulin therapy (OR=5.40, 95% CI=1.11-26.35, P=0.021) were identified 上海皓元医药股份有限公司 as independent

significant negative predictive factors for SVR. CONCLUSION: In conclusion, DM was associated with impaired virologic response to peginterferon-ribavirin treatment in genotype-1 CHC patients even though diabetes was controlled. Also, insulin therapy seems another important negative predictive factor for SVR. Disclosures: The following people have nothing to disclose: Umit B. Dogan, Mustafa S. Akin, Gunay Camuz BACKGROUND: The clinical usefulness of detecting NS3/4A protease inhibitor (PI) -resistant variants is unclear. METHODS: 270 Japanese patients infected with hepatitis C virus (HCV) genotype 1b, received triple therapy of peginterferon (PEG-IFN) plus ribavirin with telaprevir (TVR; 252 patients) or simeprevir (SMV; 18 patients).

,[1] showed that administration of antiplatelet treatment (aspiri

,[1] showed that administration of antiplatelet treatment (aspirin or clopidogrel) to rodents with chronic necroinflammatory liver disease related to HBV reduced the severity of liver fibrosis and the development of HCC, along with a reduction of HBV-specific CD8+ T cells and of HBV-nonspecific inflammatory cells. The second article, from Sahasrabuddhe et al.,[2] is an epidemiological study based on a very large cohort from the National Institutes of Health (NIH)

American Association of Retired Persons (AARP) Diet and Health Study database, analyzing the survival in self-reported use of aspirin or nonaspirin nonsteroidal RG-7388 manufacturer antiinflammatory drug (NSAID) in patients with HCC and chronic liver disease. The study enrolled 300,504 patients who completed a survey at baseline from 1995-1996, and then a follow-up “risk-factor” survey 6 months later, which included information on the use of NSAIDs. Primary HCC incidence was identified through linkage with state cancer registries and the National Death Index, until 2006. Patients who died from chronic

liver disease were also identified until 2008. Hazard ratios were calculated using a Cox regression model after adjusting Deforolimus chemical structure for age, sex, race, cigarette smoking, alcohol consumption, diabetes, and body mass index (BMI). The authors found that of the 250 patients with HCC and 428 deaths from CLD, aspirin use was associated with reduced risk of developing HCC and death due to CLD, whereas use of nonaspirin NSAID was associated with only reduced death from CLD. The use of aspirin alone was MCE公司 associated with a 41% reduced risk of developing HCC and a 51% reduced risk of death from CLD not related to HCC. The users of only nonaspirin NSAID were also at reduced risk of death for CLD by 34%, but the risk of developing HCC remained unchanged. There is biological plausibility to these associations; in fact, the role of the inflammatory field in liver cirrhosis and cancer has been suggested by a number of studies, stemming from the knowledge that liver cancer occurs in the setting of a chronic inflammatory

state. The effects of aspirin and nonaspirin NSAID rely on several possible mechanisms, only partly related to the inhibition of Cox enzymes and prostaglandins, such as a decrease in angiogenesis and in cancer cell proliferation, increase in apoptosis, and reduction in proinflammatory cytokine production. Sitia et al.[1] found that the effects of aspirin were present in HBV-related carcinogenesis, but not in chemical liver carcinogenesis. Most of the cases of HCC in patients affected with HBV occur after years of immune-mediated necroinflammation characterized by functionally ineffective virus-specific CD8+ T-cell response that fails to eliminate the virus from the liver. In this situation, the virus-specific CD8+ T-cell response maintains a cycle of low-level liver injury/inflammation through the recruiting of virus-nonspecific inflammatory cells that exacerbate the inflammatory reaction.

S population

S. population CP-868596 mw may be limited. In addition, some of these studies were based on small patient numbers and/or limited duration of follow-up, which may have affected their power. The pathogenesis of NAFLD and the factors promoting the progression to NASH and end-stage

liver disease among patients with metabolic syndrome are complex. Recent research has generated stimulating hypotheses on the roles of oxidative stress and lipotoxicity, cytokine action, and molecular and genetic factors that may promote development and progression of NAFLD.36-39 The frequent co-occurrence of metabolic conditions and their interplay complicates the examination of each individual metabolic factor’s contribution to liver disease and hepatocarcinogenesis. For example, it has been acknowledged that the hyperinsulinemia and insulin resistance that

frequently co-occur with (central) obesity plays a main role in the development of hepatic steatosis through deposition of free fatty acids and their metabolites in liver tissue.6, 37 However, chronic liver disease may also cause hepatic insulin resistance, favoring de novo lipogenesis and progression of hepatic steatosis, as well as the development of metabolic risk factors such as diabetes mellitus, dyslipoproteinemia, and hypertension.6, 37 In addition, factors that cause necroinflammation (e.g., cytokines, oxidative stress) may also promote hepatic steatosis, which further complicates the delineation of cause Erlotinib concentration and effect.6 Over MCE公司 the last couple of years, several cohort, case-control and population-based studies have reported the association of diabetes mellitus, obesity, and risk for both types of liver cancer (HCC, ICC).40, 41 These findings support an individual contribution of metabolic

conditions to the development of NAFLD. Few of these studies, however, investigated the combined effects of all metabolic risk factors as defined by the metabolic syndrome on HCC and ICC risk. Among other HCC and ICC risk factors, HCV infection can cause hepatic steatosis and insulin resistance that is mediated by a genotype-dependent interference of the viral core protein with intracellular insulin signaling.42 Some studies also suggest a synergistic effect of HCV infection, metabolic risk factors, and liver cancer risk.43, 44 In this study, however, no statistically significant interaction was observed between HCV infection and metabolic syndrome (data not shown). Although the size of the current study (3649 HCC cases, 743 ICC cases) is quite large, the study had several limitations, including the reliance on medical claims data. It should be noted, however, that Medicare files capture 100% of the coverage claims for tests, outpatients visits, and hospitalizations for patients age 65 years and older with continuous enrollment in Medicare part A and part B.

S population

S. population AZD3965 clinical trial may be limited. In addition, some of these studies were based on small patient numbers and/or limited duration of follow-up, which may have affected their power. The pathogenesis of NAFLD and the factors promoting the progression to NASH and end-stage

liver disease among patients with metabolic syndrome are complex. Recent research has generated stimulating hypotheses on the roles of oxidative stress and lipotoxicity, cytokine action, and molecular and genetic factors that may promote development and progression of NAFLD.36-39 The frequent co-occurrence of metabolic conditions and their interplay complicates the examination of each individual metabolic factor’s contribution to liver disease and hepatocarcinogenesis. For example, it has been acknowledged that the hyperinsulinemia and insulin resistance that

frequently co-occur with (central) obesity plays a main role in the development of hepatic steatosis through deposition of free fatty acids and their metabolites in liver tissue.6, 37 However, chronic liver disease may also cause hepatic insulin resistance, favoring de novo lipogenesis and progression of hepatic steatosis, as well as the development of metabolic risk factors such as diabetes mellitus, dyslipoproteinemia, and hypertension.6, 37 In addition, factors that cause necroinflammation (e.g., cytokines, oxidative stress) may also promote hepatic steatosis, which further complicates the delineation of cause mTOR inhibitor and effect.6 Over 上海皓元 the last couple of years, several cohort, case-control and population-based studies have reported the association of diabetes mellitus, obesity, and risk for both types of liver cancer (HCC, ICC).40, 41 These findings support an individual contribution of metabolic

conditions to the development of NAFLD. Few of these studies, however, investigated the combined effects of all metabolic risk factors as defined by the metabolic syndrome on HCC and ICC risk. Among other HCC and ICC risk factors, HCV infection can cause hepatic steatosis and insulin resistance that is mediated by a genotype-dependent interference of the viral core protein with intracellular insulin signaling.42 Some studies also suggest a synergistic effect of HCV infection, metabolic risk factors, and liver cancer risk.43, 44 In this study, however, no statistically significant interaction was observed between HCV infection and metabolic syndrome (data not shown). Although the size of the current study (3649 HCC cases, 743 ICC cases) is quite large, the study had several limitations, including the reliance on medical claims data. It should be noted, however, that Medicare files capture 100% of the coverage claims for tests, outpatients visits, and hospitalizations for patients age 65 years and older with continuous enrollment in Medicare part A and part B.

Key Word(s): 1 Ursodeoxycholic acid; 2 colorectal adenomas; 3

Key Word(s): 1. Ursodeoxycholic acid; 2. colorectal adenomas; 3. colorectal cancer; 4. systematical review; Presenting Author: CHAN SEO PARK Additional Authors: BYUNG IKBYUNG IK, KYEONG OKKYEONG OK, SI HYUNGSI HYUNG, SUNG BUMSUNG BUM Corresponding Author: BYUNG IKBYUNG IK Affiliations: Yeungnam Trametinib purchase University College of Medicine Objective: Rectal carcinoid tumors ≤1 cm in size can be treated by endoscopic resection. The aim of this study was to investigate the clinical feature and to clarify the treatment outcome

of a technique named endoscopic submucosal resection with a ligation device (ESMR-L) in a large number of rectal carcinoid tumors. Methods: Between March 2007 and February 2013, 66 cases of carcinoid tumors in colorecum were detected and 55 cases of carcinoids estimated at 10 mm or less in diameter. 59 cases were treated endoscopically. 7 cases were removed by endoscopic biopsy, 13 cases were removed by conventional endoscopic mucosal resection (EMR) and 39 cases were removed by endoscopic submucosal resection with a ligation device (ESMR-L). The clinical feature, selection of treatment, complete resection rate, local recurrence, distant metastases and complications associated with the procedure were analyzed. Results: Of

66 cases were 37 males and 29 females with a mean age of 50.70 ± 12.53 years. Tumor size ranged from 0.3 to 2 cm in diameter, with an average

size of 0.83 ± 0.41 cm. Carcinoids were located in rectum (62 cases), sigmoid 上海皓元 colon (3 cases) and cecum (1 case). Distribution of rectal carcinoids were located in the 6.63 ± 2.98 cm Daporinad in vivo from anal verge. 52 cases of rectal carcinoids were treated by EMR or ESMR-L. The mean lengths of hospital stay were 2.7 days. Complete resection of the lesions was obtained in 88.5% (46/52). The complete resection rates were 61.5% (8/13) by conventional EMR and 97.4% (38/39) by endoscopic submucosal resection with a ligation device. ESMR-L was superior to conventional EMR in terms of complete resection (p = 0.003). Minor bleeding associated with the ESMR-L occurred in two lesions (5.1%), but all cases were successfully managed with hemoclips. Histopathologically, all tumors were confined to submucosal layer. 2 cases were with lymphovascular invasion, 1 case was with perineural invasion and 7 cases were with remnant tumor cells at resection margin. But, neither local recurrence nor distant metastasis of all rectal carcinoids was detected during a median follow-up period of 49.6 ± 14.6 months. Conclusion: In our studies, ESMR-L proved to be a safe and effective procedure to resect rectal carcinoid tumors measuring less than 1 cm in a diameter. And ESMR-L is decidedly superior to conventional endoscopic polypectomy. Key Word(s): 1. Carcinoid tumor; 2. Rectum; 3.