By contrast,

uptake of TBI by the liver was 40% lower in Dmt1liv/liv mice, compared with Dmt1flox/flox mice (Fig. 4B), revealing that hepatocyte DMT1 is partially required for hepatic uptake of iron from plasma transferrin. The effect was specific for the liver because TBI uptake was unaffected in kidneys, pancreas, or hearts of Dmt1liv/liv mice. To determine whether lower hepatic TBI uptake by Dmt1liv/liv mice represents a delay in clearance of plasma TBI, which may resolve at a later time, we measured the percentage of 59Fe in plasma 2 and 24 hours after injection. By 2 hours, the percentage of 59Fe in plasma did not differ between Dmt1flox/flox and Dmt1liv/liv mice (P = 0.11) (Fig. 4C), and by 24 hours, very little 59Fe was detectable in plasma. These data indicate Selleckchem Galunisertib that lower hepatic TBI uptake by Dmt1liv/liv mice does not represent a delay in clearance of plasma TBI. The percentage of 59Fe in the blood and spleen also did

not differ at either time point, suggesting that iron uptake into developing erythroid cells was unaffected in Dmt1liv/liv mice. Although lower hepatic TBI uptake in Dmt1liv/liv mice appears to directly result from inactivation of Dmt1, it is possible that it results from a secondary effect on other proteins implicated in TBI uptake. It is equally possible that the lack of an effect of hepatic Dmt1 inactivation on NTBI uptake is the result of compensatory responses in other proteins involved in NTBI uptake. MG-132 datasheet Therefore, we measured levels Demeclocycline of TfR1, TfR2, and ZIP14, which may also participate in TBI/NTBI uptake.[28, 29] Western blotting analysis revealed that levels of these proteins did not differ between Dmt1flox/flox and Dmt1liv/liv mice (Fig. 5A-C). To determine whether hepatocyte DMT1 is required to maintain iron status during iron deficiency, we compared iron status parameters of

Dmt1flox/flox and Dmt1liv/liv mice that were fed iron-deficient diets. After 3 weeks, mice became iron deficient, as compared to control (Dmt1flox/flox) mice fed a standard diet (Fig. 6A-D). However, no differences were observed between iron-deficient Dmt1flox/flox and Dmt1liv/liv mice. TBI uptake by livers of Dmt1flox/flox mice was higher in iron-deficient animals, compared to controls (36% versus 30%, respectively; P < 0.05) (Fig. 6E). By contrast, TBI uptake by livers of Dmt1liv/liv mice was not higher in iron-deficient animals, compared to controls, suggesting that DMT1 is required for enhanced TBI uptake into an iron-deficient liver. Confocal immunofluorescence (IF) microscopy was used to localize DMT1 in the liver. Human liver was used instead of mouse liver because IF staining of mouse tissue was too weak to allow for reliable localization. In hepatocytes, DMT1 displayed intracellular punctate staining with little, if any, staining of plasma membrane (Supporting Fig.

Dulbecco’s modified Eagle’s medium (DMEM), phosphate-buffered saline (PBS), glutaMAX-I, and goat, horse, MK-2206 solubility dmso and fetal calf sera were purchased from Invitrogen (Carlsbad, CA). 4′,6-Diamidino-2-phenylindole (DAPI) was from Molecular Probes (Invitrogen). EGCG was from Calbiochem (Merck Chemicals, Darmstadt, Germany), except when a set of green tea catechins, (+)-catechin, (−)-epicatechin (EC), (−)-epicatechin-3-gallate (ECG), (−)-epigallocatechin (EGC), and EGCG, was used, which was purchased from Extrasynthèse (Lyon, France).

Stocks were resuspended in dimethyl sulfoxide (DMSO) at 0.5 M. Other chemicals were from Sigma-Aldrich (St. Louis, MO). Mouse anti-E1 A4, 16 rat anti-E2 3/11, 17 mouse anti–yellow fever virus (YFV) envelope protein 2D12 (ATCC CRL-1689),

and mouse anti–bovine viral diarrhea virus (BVDV) NS3 Osc-23 18 monoclonal antibodies Selleck Acalabrutinib (mAbs) were produced in vitro. Cyanin 3 (Cy3)-conjugated goat antimouse immunoglobulin G (IgG) was from Jackson Immunoresearch (West Grove, PA). Huh-7, 19 HEK 293T (ATCC number CRL-11268), Vero (ATCC CCL-81), and Madin-Darby Bovine Kidney (MDBK; ATCC number CCL-22) cells were grown in DMEM, supplemented with glutaMAX-I and either 10% fetal calf serum (Huh-7, HEK

293T, and Vero) or 10% horse serum (MDBK). We used a modified Japanese fulminant hepatitis (JFH)1 virus containing titer-enhancing mutations, 20 in which the A4 epitope of HCV glycoprotein E1 of genotype 1a was reconstituted. 21 The JFH1-Luc plasmid, containing a Renilla Luciferase reporter gene, the JFH1-ΔE1/E2-Luc or JFH1-ΔE1/E2 clonidine plasmids, which contain an in-frame deletion in the E1/E2 region, and the JFH1/GND-Luc replication mutant, have been described previously. 21, 22 Infections were scored by measuring luciferase activity in cell lysates, using a Renilla luciferase assay system from Promega (Madison, WI), or by measuring infectivity by indirect immunofluorescence (IF) with anti-E1 mAb. For quantitative binding experiments, purified virus was obtained by the precipitation of HCV grown in cell culture (HCVcc)-infected Huh-7 cell supernatants with 8% polyethylene glycol 6000. Pelleted virus was then loaded onto a continuous 10%-40% iodixanol gradient.

Our results showed that rats only managed to prey on intact eggs when these were small (canary) and that they had great difficulty preying on medium-sized (hen) and even small (quail)-sized intact eggs, find more regardless of the rat’ body

mass, gender and habitat. Conversely, rats preyed extensively on previously damaged eggs of all sizes. Our findings suggest that preying on intact bird eggs without specific learning skills, such as rolling an egg to break it, may be challenging for the black rats. Moreover, our findings strongly indicate that bird susceptibility to egg predation by rats varies with island contexts and may depend on a combination of multiple additive and synergic factors. Experiments that allow for testing the multiple evolutionary and ecological factors explaining between-island or between-population variation in rodent impacts are needed to promote a better overview of the processes involved in bird population declines. “
“Many tropical ecosystems support exceptional levels of amphibian diversity, but in contrast to their temperate counterparts, BVD-523 purchase many aspects of their biology are little studied and poorly

understood. Demographic studies give valuable insights into the age structure and life histories of amphibian populations, thus they are of high importance in making accurate and precise conservation assessments in the light of current global Acyl CoA dehydrogenase amphibian declines. We analysed age structure and growth in a population

of the viviparous caecilian Geotrypetes seraphini, a caecilian amphibian from Mount Cameroon, Central Africa, by using skeletochronology. We detected lines of arrested growth (LAG) in mid-body vertebrae and interpreted them as indicators of a seasonal growth pattern. We expect that LAG are materialized at a rate of one per year. In our sample male reach sexual maturity at an early age (age class 0+), whereas females mature later (age class 1+). Maximum longevity in our sample was estimated at 4+ years. Body size (total length) was significantly smaller in males than in females. Our study shows that skeletochronology is a highly suitable method to determine caecilian growth and age. Caecilian amphibians show a high diversity of reproductive modes including unusual brood care and parental investment strategies. In order to deepen our understanding of their ecology and evolution, many more demographic studies on other species and lineages are needed. “
“Factors that affect group sizes in large ungulates are generally poorly understood for species from remote regions. Understanding grouping patterns is important for effective species management, but is lacking for the endangered Mongolian saiga (Saiga tatarica mongolica). We studied seasonal changes in the group size and social structure of saigas in relation to environmental and anthropogenic factors in western Mongolia during 2009–2012.

We used lentiviral constructs coupled either to green florescent protein or to thymidine kinase

and studied long-term, stable localization of cells using immunofluorescence (for evaluation at histological/tissue levels) or positron emission tomography (for whole body imaging). Further descriptions of the studies with long-term see more marking are provided in the online supplement. Figure 3 shows the total flux (photons per second) detected in animals within a consistent region of the area of the liver where cells were injected, either via the grafting method or direct injection of cells. In both healthy animals and those injured with CCl4, there was a noticeable difference at 12 and 48 hours in animals transplanted using grafting methods versus direct injection. The grafted animals had transplanted cells restricted

to the liver and yielded higher bioluminescent flux signals; this result is seen in the localization and distribution of bioluminescent signals (Figs. 4 and 5). By contrast, those transplanted via direct injection had transplanted cells in the liver and with significantly Metformin in vivo lower flux signals. The data are consistent with our hypothesis that transplantation of cells with hyaluronans enhances engraftment in the target organ. Direct injection without hyaluronans results in loss of cells either due to distribution to ectopic sites and/or due to loss of cell viability. Of importance is that grafting significantly reduced the extent of ectopic cell distribution.

Cells grafted to the liver using HA hydrogels were specifically localized to the injected liver tissue. Cells that were directly injected intrahepatically were observed to spread throughout the abdomen, giving a weaker signal, and were not localized Immune system to the initial transplanted area of the liver. At day 7, tissues in CCl4-treated mice were removed and fixed for histology (Fig. 6). In mice with HA grafts of hHSC transplants (left rows), cells formed large masses of transplanted cells in the areas of injection and transplantation, indicating a substantial area of humanized liver (50% or more positive staining in the field of view). Cells transplanted via direct injection of a cell suspension (middle row) resulted in small aggregates dispersed throughout the liver in the area of transplantation, and with the extent of humanization (∼10%-20% in the field of view) comparable to that reported by others as summarized in a recent review.35 Sham, positive, and isotype controls for albumin expression are also displayed (right row). Complementary studies with marked cells that were transplanted by a vascular route are described further in the Supplementary Information. These cells were transfected with a lentiviral construct derived from herpes simplex virus and expressing thymidine kinase (Supporting Figs. 1 and 2). They survived in culture in KM for more than 6 months (Supporting Fig. 3).

2C; inset in Ad/LacZ). The time-course of TG accumulation in MED1fl/fl and MED1ΔLiv mouse liver following Ad/PPARγ or Ad/LacZ tail vein injection is shown in Fig. 3A. Hepatic TG content remained nearly unchanged in MED1ΔLiv mice with

PPARγ overexpression (Fig. 3A). In contrast, PPARγ overexpression resulted in significant elevation of liver Raf inhibitor TG content in MED1fl/fl mice at days 4 and 6 (Fig. 3A). Plasma TG and cholesterol levels did not change with PPARγ overexpression in MED1fl/fl and MED1ΔLiv mice (Fig. 3B-D), indicating that neither the hepatic secretion of very-low-density lipoproteins nor the plasma clearance of these lipoproteins was affected by the treatment with Ad/PPARγ. Because PPARγ overexpression failed to induce hepatic steatosis in the absence of MED1, we investigated the role of MED1 in the adipogenic action of PPARγ in liver. Dramatic increases in the messenger RNA (mRNA) levels of classic fat

differentiation gene markers, such as aP2 were noted in mice expressing MED1 but not in MED1-null livers (Fig. 4A). Increases in the mRNA levels of stearoyl-CoA desaturase 1 (SCD-1), Foxo1, and glucose-6-phosphatase (G-6-P) were observed in MED1fl/fl mouse livers but not in MED1ΔLiv mouse liver following PPARγ expression (Fig. 4A). Expression levels of hepatic mRNA content PLX 4720 of peroxisomal β-oxidation enzymes, namely fatty acyl-CoA oxidase (Acox1),

enoyl-CoA hydratase/L-3-hydroxyacyl-CoA dehydrogenase (L-PBE), and 3-ketoacyl-CoA thiolase (PTL) in MED1ΔLiv mice increased to a lesser extent as compared to a modest level of induction observed in MED1fl/fl mice after PPARγ expression (Fig. 4A). These observations suggest that the peroxisomal β-oxidation pathway was activated as an attempt to burn the overload of fatty acid in steatotic liver.2, 6 PPARγ overexpression also increased fatty acid translocase (CD36) mRNA concentration in liver of both Carnitine palmitoyltransferase II MED1fl/fl and MED1ΔLiv mice (Fig. 4A). Moreover, the mRNA expression of lipid droplet protein genes CideA6, 23 and S3-126, 24 was barely detectable in MED1ΔLiv mice, but strongly induced in MED1fl/fl mice following PPARγ treatment (Fig. 4B). Interestingly, the mRNA levels of fat-specific gene 27 (FSP27),6 adipose differentiation-related protein (ADRP),24 and tail-interacting protein of 47 kDa (TIP47)24 showed no differences in MED1ΔLiv and MED1fl/fl mouse livers (Fig. 4B). ADRP protein content was higher in the livers of PPARγ-injected MED1fl/fl mice but not in MED1ΔLiv mice (Fig. 4C). This is likely due to ADRP being stabilized by intracellular lipid.24 Immunofluorescence and confocal microscopy revealed reductions in S3-12, ADRP, and CideA content in MED1ΔLiv mouse livers expressing PPARγ when compared to MED1fl/fl mouse (Fig. 4D).

8B,C). Moreover, Bcl-2, a known inhibitor of cell death, was almost absent in the TIMP-1−/− livers at 48 hours post-IRI (0.13 ± 0.08 versus 0.69 ± 0.19; P < 0.05) (Fig. 8A). Finally, phosphorylation of mTOR inhibitor Akt, a 57-kD protein-serine/threonine kinase with prosurvival-associated functions,22 was depressed in TIMP-1−/− livers (0.10 ± 0.07 versus 0.44 ± 0.30; P < 0.05) at 48 hours post-IRI (Fig. 8A). At 7

days post-IRI, Bcl-2 was still reduced (≈0.6-fold; P < 0.05) in TIMP-1−/− livers compared to controls. Hence, these results support a major protective role for TIMP-1 expression in hepatic IRI. The understanding of the functions of TIMPs in liver IRI has the potential to contribute to the development of novel therapeutic approaches to prevent hepatic IRI and, consequently, to improve the outcome of liver transplantation. In this study we investigated the functional significance of TIMP-1 expression in a well-established 90-minute mouse model of partial liver warm IRI.4 Interactions between ECM components and cell adhesion receptors regulate leukocyte functions; therefore, it is not unanticipated that enzymatic degradation of ECM can alter leukocyte behaviors.23 Indeed, cells employ proteolytic enzymes, particularly MMPs, to control the ECM turnover, to release growth factors, and to migrate across ECM.24 There is a growing body of evidence supporting key functions

for MMP expression Barasertib datasheet in the pathogenesis of liver diseases.3, 25, 26 In this regard, we have previously shown that MMP-9 regulates leukocyte recruitment and contributes to hepatic IRI.4 Although TIMP-1 can inhibit a broad range of MMPs, it is particularly potent for MMP-9.27 However, compared to MMP-9, the role of its natural inhibitor, TIMP-1, is virtually unknown in liver IRI. TIMP-1 expression is very low in naive livers and it is induced after liver IRI; however,

it is still insufficient to prevent an elevated MMP activity in liver IRI.11 In the present study we show that TIMP-1 deficiency resulted in further exaggerated up-regulation of MMP-9 activity Adenosine triphosphate and, more strikingly, it led to a poor survival rate after reperfusion. This is particularly interesting in that the model of partial liver IRI is nonlethal.14 Indeed, all TIMP-1+/+ mice survived hepatic IRI despite the significant damage detected in the livers after reperfusion; in contrast, only three out of eight TIMP-1−/− mice survived more than 4 days after liver IRI. In general, TIMP-1−/− mice showed additional impairment of liver function and more severe lesions, which likely led to their death between the second and fourth day postreperfusion. Although infiltrating leukocytes are recognized as mediators of hepatic IRI,3, 28 the mechanisms involved in their recruitment to sites of inflammatory stimulation in liver are still far from being understood. TIMP-1−/− livers showed massive leukocyte accumulation post-IRI.

In the whole population, the dose-adjusted strategy was more cost-effective than the full dose in terms of both LYG and QALY. Specifically, compared with BSC the full-dose strategy had an ICER of €63,197 for LYG and of €69,344 for QALY, while dose-adjusted strategy had an ICER of €25,874 for LYG and of €34,534 for QALY. As in the entire SOFIA cohort, in the BCLC B patients the dose-adjusted strategy was more cost-effective than the full dose in terms of both LYG and QALY. Specifically, compared with BSC the full-dose

strategy had an ICER of €44,794 for LYG and of €57,385 for QALY, while the dose-adjusted strategy had an learn more ICER of €41,782 for LYG and of €54,881 for QALY. Similarly, in BCLC C patients, considering both LYG and QALY, the dose-adjusted strategy was more cost-effective than the full dose. Specifically, compared with BSC the full-dose strategy had an ICER of €59,922 for LYG and of €65,551 for QALY, while the dose-adjusted strategy had an ICER of €20,896 for LYG and of €27,916 for QALY. Performing analysis in the subgroup of the SOFIA cohort obtained after excluding patients with early radiologic progression, ICER per QALY in dose-adjusted sorafenib strategies

marginally improved. Specifically in this subgroup of patients, dose-adjusted sorafenib strategy had an ICER per QALY of €25,569 for BCLC C and of €58,265 for BCLC B patients. One-way 17-DMAG (Alvespimycin) HCl sensitivity analysis was done FK228 molecular weight for two dominant strategies: dose-adjusted sorafenib therapy for both BCLC B and C HCC patients. Figure 3 summarizes the results of one-way sensitivity analyses, using tornado diagrams. Analyses showed that the results of the model were most sensitive to an assumption on survival rates of BSC patients, sorafenib treatment duration, and type of survival distribution. Changes in survival rates in patients managed with BSC had a great effect on cost-effectiveness. In fact, sensitivity

analysis with a hypothesized variation of survival of ±30% in BSC patients showed that ICER for QALY ranged significantly from €41,325 to €100,544 in BCLC B (Fig. 3A) and from €24,450 to €36,032 in BCLC C (Fig. 3B) patients treated with dose-adjusted sorafenib. The cost effectiveness of dose-adjusted sorafenib was sensitive to change (±30%) in the treatment duration. With a longer time of therapy, the ICER for QALY impairs both the BCLC B and BCLC C patients. Instead, for the sensitivity analysis on the disease costs, a variation of ±30% was assessed, and the model had low sensitivity. With an increase in the disease costs, the ICER for LYG and for QALY marginally increased in both BCLC B (Fig. 3A) and BCLC C (Fig. 3B) dose-adjusted strategies. Lower variations were found for both strategies by applying a discount rate ranging from 0% to 5%.

Methods: Among a total of 257 patients who received treatment for hepatolithiasis, 236 patients were eligible for analysis. 92 patients underwent liver resection (resection group) and 144 patients did not (non-resection group). The data was collected retrospectively and analyzed. Results: The incidence of cholangiocarcinoma was 6.8% (16/236) during follow-up period (mean 41 ± 41 months). Cholangiocarcinoma occurred 6.3% (6/95) and 7.1% learn more (10/141) in resection and non-resection group respectively (p = 0.263). When analyzed according to completeness of stone removal regardless of treatment modality, Cholangiocarcinoma incidence

was higher in patients with residual stone(10.4%) than patients with complete stone removal (3.3%), but there was no significant difference (p = 0.263). On univariate analysis, none of the factors (age, gender, CA19-9, stone location, bile duct stenosis, liver atrophy, stone recurrence and liver resection) showed relationship with the incidence of cholangiocarcinoma. Conclusion: Hepatic resection

for hepatolithiasis is considered to have a limited value in preventing of cholangiocarcinoma and the patients should be carefully followed even after hepatic resection. A combination of different treatment modalities is necessary to decrease the residual stone and improve the outcome of the patients with hepatolithiasis. Key Word(s): 1. cholangiocarcinoma; 2. hepatolithiasis; Adriamycin 3. hepatic

resection Presenting Author: TAE NYEUN KIM Additional Authors: SUNG BUM KIM, KOOK HYUN KIM, KYEONG OK KIM, SI HYUNG LEE, BYUNG IK JANG Corresponding Author: TAE NYEUN KIM Affiliations: Yeungnam University College of Medicine, Yeungnam University College of Medicine, Yeungnam University College of Medicine, Yeungnam University College of Medicine, Yeungnam University College of Medicine Objective: 50–55% of CBD stone patients without symptom at present may experience symptoms or complication related to CBD Etofibrate stone in the future. Studies about risk of performing ERCP in asymptomatic CBD stone patients has been scarce. The aim of our study was to compare ERCP complication rate between asymptomatic and symptomatic CBD stone patients. Methods: Patients diagnosed as CBD stone and underwent ERCP from Jan 2010 to Dec 2013 were included and their clinical data were collected and analyzed retrospectively. Patients without symptom associated with CBD stone were classified as asymptomatic group and with symptom as symptomatic group. Results: Among 323 patients with CBD stone, 306 patients had symptomatic CBD stone and 17 patients, asymptomatic CBD stone. Mean age of asymptomatic and symptomatic group was 68.2 ± 12.9 and 64.7 ± 17.0, respectively (p = 0.442) and male proportion was not significantly different between both groups (64.7% vs 50.3%, p = 0.248).

All patients were to receive the combination of full-dose peginterferon and ribavirin during the lead-in phase of the trial. Patients who remained viremic during the lead-in phase of treatment (lead-in patients), those who experienced virological breakthrough or this website relapse after initial response (breakthrough/relapser patients), and those who were nonresponders to peginterferon and ribavirin outside of the HALT-C trial (express patients) were randomized to maintenance therapy (peginterferon alpha-2a 90 μg weekly) or to remain as untreated controls for the next 3.5 years. Following completion

of the 3.5 years of the randomized trial, all patients were invited to continue follow-up without treatment until October 20, 2009. At entry, all patients were required to have an ultrasound, computed tomography (CT), or magnetic resonance imaging H 89 (MRI) demonstrating no evidence of hepatic mass lesions suspicious for HCC and to have an alpha fetoprotein (AFP) <200 ng/mL. All patients had a liver biopsy performed prior to enrollment. The Ishak scoring system was used to grade inflammation (0-18) and to stage fibrosis (0-6).13 The patients were seen every 3 months during the randomized phase of the trial and every 6 months thereafter. At each visit, patients were assessed clinically for outcomes and blood was drawn for complete blood count, hepatic panel (albumin, total bilirubin, aspartate aminotransferase [AST], alanine

aminotransferase [ALT], and alkaline phosphatase), creatinine, prothrombin time / international normalized ratio (INR), and AFP. Upper gastrointestinal endoscopy was performed at randomization to assess

for esophageal varices. Ultrasound was performed at randomization, 6 months after randomization, and then every 12 months during the randomized trial and every 6 months during the extended follow-up period. Patients with an elevated or rising AFP and those with new lesions on ultrasound were evaluated further with a CT or MRI. Diagnostic liver biopsy and HCC treatment were conducted at the discretion of investigators at each site. In this analysis, only patients randomized to no treatment were included because interferon even in low doses can have an effect on laboratory values. To assess changes in laboratory values Methocarbamol during follow-up, only patients who had been followed up to month 24 from enrollment (18 months after randomization to no treatment) with no outcomes up to that timepoint were included. Two clinical outcomes were analyzed: Outcome 1, Clinical decompensation, was defined as any of the following: variceal bleeding, ascites, spontaneous bacterial peritonitis, and hepatic encephalopathy; and Outcome 2, Liver-related deaths and liver transplantation. Diagnostic criteria were established for each clinical outcome and an Outcomes Review Panel adjudicated each outcome report. Only the first clinical outcome for each patient was included in this analysis.

Total RNA isolated from BE and paired NEM was subjected to real-time reverse-transcription–polymerase chain reaction analysis for DCAMKL-1, leucine-rich

repeat-containing G-protein-coupled receptor (LGR5), and Musashi-1 (Msi-1) mRNA expression. Results:  DCAMKL-1 was minimally expressed in squamous NEM, but increased in BE (with and without dysplasia) and EAC tissues. In EAC, we found increased stromal DCAMKL-1 staining compared to adjacent epithelia. Within the submucosa of dysplastic BE tissues, an increase in the endothelial cell expression of DCAMKL-1 was observed. Finally, an upregulation of DCAMKL-1, LGR5, and Msi-1 mRNA was seen in BE compared to squamous NEM. Conclusions:  In the present study, we report the progressive mTOR inhibitor increase of DCAMKL-1 expression in BE from dysplasia to EAC. Furthermore, there was an increase in putative stem cell markers DCAMKL-1, LGR5, and Msi-1 mRNA. Taken together, these data suggest that the regulation of resident stem cells might play an important role in the progression of BE

to EAC. “
“Aim:  The Clinical Research Committee of the Japan Society for Portal Hypertension has conducted a nationwide questionnaire survey to clarify the current status of ectopic varices in Japan. Methods:  A total of 173 cases of ectopic varices were collected. Results:  Duodenal varices were found Romidepsin purchase in 57 cases, and most of them were located in the descending to transverse parts. There were 11 cases of small intestinal varices and 6 cases of colonic varices, whereas 77 patients had rectal varices, accounting for the greatest proportion (44.5%). Other sites of varices were the biliary tract, anastomotic sites, the stoma, and the diaphragm. Liver cirrhosis was the most frequent diseases (80.3%) underlying

ectopic varices. It was noted that patients with rectal varices frequently had a history of esophageal varices (94.8%) and received endoscopic treatment (87.0%). The treatments for ectopic varices were as an emergency in 46.5%, elective in 35.4% and prophylactic in 18.2%. In emergency Nabilone cases, endoscopic therapy was most frequent (67.4%), followed by interventional radiology (IVR; 15.2%), and endoscopy-IVR combination (6.5%). Elective treatment was performed by endoscopy in 34.3%, IVR in 28.6%, combined endoscopy-IVR in 5.7%, and surgical operation in 25.7%. The prophylactic treatment was endoscopic in 50.0%, IVR in 33.3%, combined treatments in 11.1%, and prophylactic surgery in none. The change of ectopic varices after treatment was disappearance in 54.9%, remnant in 35.4% and recurrence in 9.7%. The rate of disappearance was significantly lower in rectal varices (40.8%) than in duodenal varices (73.4%). The patient outcome did not differ among the various sites of the lesion. Conslusions:  Current status of ectopic varices in Japan has been clarified by a nationwide questionnaire survey.