Vitamin D deficiency or insufficiency is overwhelmingly

Vitamin D deficiency or insufficiency is overwhelmingly XAV-939 research buy associated with viral hepatitis, cirrhosis, and fatty liver diseases. Recent clinical trials have shown that vitamin D supplements

significantly enhance the efficacy of interferon plus ribavirin therapy through sustained virological response. A recent study showed that 25-dihydroxyvitamin D rather than 1,25-dihydroxyvitamin D could directly suppress hepatitis C virus assembly. Moreover, clinical evidence has shown that vitamin D deficiency is associated with alcoholic and non-alcoholic fatty liver diseases. In this review, we highlight some recent advances in vitamin D researches and clinical trails. Different from the classical definition of a vitamin, VD is neither

a co-enzyme factor nor an essential nutrient component. In addition to dietary sources from animals (VD3) or plants (VD2), VD can be synthesized in the skin from cholesterol under sunlight.[1] Driven by sunlight, 7-dehydrocholesterol in the skin cells is converted to pre-vitamin D3, which consequently undergoes an isomerization process to vitamin D3, also known as cholecalciferol. The first step in the synthesis of biologically active VD from vitamin D3 occurs in hepatocytes through 25-hydroxylation, catalyzed by Cyp2R1 or Cyp27A1.[1] Secreted from hepatocytes, 25(OH)D3 is conveyed by VD-binding protein (VDBP) to the kidneys, where it is additionally hydroxylated by 1-alpha-hydroxylase (Cyp27B1) to generate fully Selleckchem Lumacaftor activated form, 1,25-dihydroxyvitamin D, namely calcitriol. VD levels are also regulated by its degradation processes. Through a negative feedback loop, calcitriol can induce the catabolic enzyme 24-hydroxylase (Cyp24A1) in the kidneys as well as in other VD-targeting tissues, which inactivates VD and promotes it breakdown.[2] Furthermore, to ensure bioavailability, Cyp24A1 transcription is negatively regulated by parathyroid hormone (PTH) driven by low calcium levels. Serum 25(OH)D levels are usually a thousand times higher than 1,25(OH)2D levels, indicating that the limiting step for

synthesis of active VD is conducted mostly by 1-hydroxylation via the relative activities of between its synthesis by Cyp27B1 and degradation by Cyp24A1 in the Rebamipide same cells. In healthy individuals, serum levels are normally 25–40 ng/mL (62–99 nM) for 25(OH)VD3, and 20–45 pg/mL (48–108 pM) for 1,25(OH)2D3. In addition to the liver–kidney loop for the synthesis of 1,25(OH)2D3, the immune system can independently generate bioactive VD through a distinct regulatory mechanism. It was initially recognized that activated macrophages in sarcoidosis, a form of calcified lung fibrosis, could generate abundant calcitriol.[3] Later it was found that normal macrophages under lipopolysaccharide (LPS) and interferon-gamma stimulation could also produce calcitriol.

17 Due to limited numbers of study subjects in each category, gra

17 Due to limited numbers of study subjects in each category, grades (G) and stages (S) were combined for the analyses as follows: steatosis grade, G0-1, G2, and G3 or G0-1 and G2-3; lobular inflammation grade, G0-1 and G2 (no case had G3); hepatocyte ballooning grade, G0 and G1-2; portal inflammation, G0, G1, and G2 or G0-1 and G2; and fibrosis stage, S0, S1-2, and S3-4 or S0-2 and S3-4. An overall diagnosis was also recorded using

the following diagnostic categories: steatosis (NAFLD but see more not NASH), suspicious for steatohepatitis (SH) adult pattern, which is also referred to zone 3 or Type 1 pattern, suspicious for SH pediatric pattern, which is also referred to zone 1 or Type 2 pattern, definite SH adult pattern, and definite SH pediatric

pattern. Initially, 30 of the 56 slides were stained for SHh (n = 20), vimentin (Vim, n = 6), or alpha-smooth muscle actin (α-SMA, n = 4), and the remaining slides check details were costained for Gli2 and keratin 7 (Gli2/K7, n = 26). To buttress sample size, two of the Gli2/K7 costained slides were additionally stained for Vim, two of the Gli2/K7 costained slides were additionally stained for α-SMA, and five of the SHh-stained slides were additionally stained for K7. Thus, in total 20 slides were evaluated for SHh, 26 for Gli2, 31 for K7, 8 for Vim, and 6 for α-SMA. This approach was necessary because the number of available slides was limited. In order to determine which slides were used for which stain, cases were grouped

according to histologic severity and then slides were randomly selected from each group for 17-DMAG (Alvespimycin) HCl immunohistochemistry (Ihc) in order to have roughly equivalent numbers of cases within each category of histologic severity. Details of the Ihc methods and antibodies have been published.18, 19 Positive staining for SHh, Vim, and αSMA was semiquantified as a percentage of the total surface area in low-power fields (×100 magnification) and graded into five ranked categories: G1 (less than 20%), G2 (20-39%), G3 (40-59%), G4 (60-79%), and G5 (≥80%). Nuclear positivity for Gli2 and cellular positivity for K7 were counted in five randomly selected high-power fields (HPFs, ×200 magnification). The average counts of K7+, Gli2+, K7+/Gli2−, and K7+/Gli2+ cells per HPF were calculated and used for the analyses. Furthermore, the intensity and histologic location of SHh and Gli2/K7 staining was evaluated by a hepatopathologist (C.G.). After excluding fragmented samples, 16 SHh slides, 18 Gli2 slides, and 25 K7 slides were used in this subanalysis.

Methods: The expressions of FAF1 and FLIP proteins were detected

Methods: The expressions of FAF1 and FLIP proteins were detected by immunohistochemistry technique in gastric tissues of 53 patients with gastric cancer and 52 patients with gastric precancerous lesions of atrophic gastritis, and compared with those in 50 normal gastric mucosa tissues. Results: The expression rates of FAF1 protein were 84.0%,

53.85% and 28.30% in normal gastric tissue, gastric tissue of precancerous lesions and gastric cancer tissue, respectively, and there were significant differences among three groups. The expression rates of FLIP protein were 38.00% and 36.54% and 81.13% in these three groups, respectively. There were significant differences between the gastric cancer group and Compound Library mouse other two groups in expression rates of FLIP

protein (P < 0.01). FAF1 protein expression was related with histological differentiation of gastric carcinoma (P < 0.05). FLIP protein expression was related to the gastric cancer metastasis and TNM staging. Conclusion: 1) The expression rates of FAF1 protein in normal gastric Autophagy inhibitor molecular weight tissue, gastric precancerous lesions and gastric cancer reduced in turn. It indicated that the lack of FAF1 protein expression may play an important role in the differentiation, occurrence and development of gastric cancer. 2) The expression level of FLIP protein in gastric cancer tissues was obviously higher than those in the normal gastric tissue and gastric precancerous lesions. It indicated that the occurrence and transfer of gastric cancer might be related to

inhibition of FLIP on the apoptosis mediated by Fas/FasL. Key Word(s): 1. FAF1; 2. FLIP; 3. gastric cancer; 4. Qinghai area; Presenting Author: YANGBEI ZHU Additional Authors: JUN GAO, DUOWU ZOU Corresponding Author: DUOWU ZOU Affiliations: Changhai Hospital Objective: To determine the possible role of Vanilloid receptor 1 (TRPV1) and Bumetanide cannabinoid receptors (CB1 and CB2) in the dorsal root ganglion (DRG) of rats with chronic gastroesophageal reflux disease. Methods: Male Sprague-Dawley rats were randomly divided into reflux group (R group) and control group (S group), n = 6. To established the chronic reflux model, the fundus of the rat stomach was ligated and the pyloric sphincter was restricted. The expression of TRPV1 and CB1 in T1∼T3 DRGs were analyzed by immunofluorescence and Western blot. Results: The expression of TRPV1 in DRGs relative to GAPDH was up-regulated (0.98 ± 0.01 vs 0.64 ± 0.09, p = 0.001), and the integrated optical density (IOD) of TRPV1-positive neurons was also increased (905.24 ± 134.82 vs 648.43 ± 135.13, p = 0.000). While CB1 was negative-regulated (relative to GAPDH: 0.86 ± 0.05 vs 0.96 ± 0.06, p = 0.013; IOD: 677.06 ± 123.75 vs 836.89 ± 101.00, p = 0.013). At the same time, CB2 was decreased (relative to GAPDH: 0.75 ± 0.03 vs 0.81 ± 0.

A necrosis rate of 100% was assumed to indicate complete necrosis

A necrosis rate of 100% was assumed to indicate complete necrosis; a rate of 99% or less was considered to indicate incomplete necrosis. For the purpose of

evaluating the percentage of complete necrosis according to tumor size, the HCCs were grouped by size: ≤2, 2.1 to 3.0, and 3.1 to 5.0 cm. Continuous variables were reported as means and standard deviations, medians and ranges, or both; the differences between the subgroups were analyzed with the t test after the Levene correction, analysis of variance, or the Mann-Whitney test as appropriate. Categorical variables were reported as numbers and percentages, and the differences between the subgroups were analyzed with the chi-square test with a Yates correction. The amounts BAY 57-1293 in vivo of tumor necrosis were reported

both as continuous variables and as semiquantitative values, and the differences between subgroups were calculated. In order to identify the potential relationships between the covariates with respect to tumor necrosis, all variables significantly affecting tumor necrosis in the univariate analysis were entered into a multivariate logistic regression model to identify the independent predictors of complete tumor necrosis. A P value < 0.05 was considered statistically significant Erastin cell line in all cases. Statistical analysis was carried out with SPSS 13.0 (SPSS, Inc., Chicago, IL). The baseline clinical and tumor characteristics of the study group are reported in Table 1. Thirty-eight of the 67 patients underwent selective/superselective TACE exclusively (56.7%), 27 patients underwent lobar TACE exclusively (40.3%), and 2 patients were treated with a combination of the two techniques (3%). In the latter check details two cases, lobar TACE and selective TACE were each used in only one

lobe, and this allowed an assessment of the treatment outcome for each technique. In order to limit the risk of liver decompensation, we never performed whole lobe treatments of both lobes in the same session (or whole liver treatments). Thirty-eight patients had a single course of TACE (56.7%), and the remaining 29 had two or more courses (43.3%). The median time from the first TACE procedure to LT was 8.7 months (range = 1-32 months), and the median time on the waiting list was 6.2 months (range = 1-29 months). For patients who underwent more than one TACE session, the median time from the last imaging procedure to LT was 2.6 months (range = 1-92 days). No patient of the present series experienced major complications related to the procedure, and none underwent LT within 30 days of the procedure (this could be interpreted as an expression of rapid deterioration of liver function). The median hospital stays were 4.5 days after lobar procedures (range = 2-65 days) and 3.5 days after selective/superselective TACE (range = 2-56 days, P = 0.651); clinically significant fever (maximum temperature > 38°C) occurred in 20 cases after lobar TACE (74.

Remnant of the liver (REM) (%) was calculated by CT volumetry and

Remnant of the liver (REM) (%) was calculated by CT volumetry and the weight of resected specimens. In addition to general blood test, ICG elimination rate (ICG K) was measured preoperatively. PHLF was defined according to the criteria proposed by International Study Group of Liver Surgery (Surgery. 2011 May;149(5):713-24.) and gradad as A, B, or C. Liver fibrosis was graded as F0 to F4 by METAVIR score. The ability of SWV, ICG K, and general hematological/biochemical factors for the prediction of PHLF was compared by receiver operating characteristic (ROC) BMS-777607 purchase analysis. The mean SWV was 1.31, 1.40, 1.60, 1.80,

and 2.80 for F0 to F4, respectively. Grade A PHLF occurred in 21 patients (9%) whereas grade B in 16 patients (7%) and grade C in 4 patients (2%). The area under the curve (AUC) of the ROC curve (AUROC) for the prediction of PHLF was (in descending order) 0.704 for SWV, 0.698 for hyaluronic acid (HA), 0.674 for PT-INR, 0.673 for platelet count (PLT), 0.664 for T-bil and 0.619 for ICG K. AUROC for grade B or C PHLF was 0.783 for SWV, 0.754 for HA, 0.722 for PLT, 0.676 for ICG K, 0.636 for PT-INR and 0.621 for T-Bil. The stepwise variable selection with minimum BIC’s method identified 3 significant factors associated

with PHLF. They were 1/ SWV, 1/REM and T-Bil. By logistic regression analysis, we established a risk index for PHLF as (-2.23521458260909) + (-4.49647423960785) * 1/SWV + 1.24494777087502 * 1/REM + 1.91138407348298 * T-Bil. AUROC of the risk index for PHLF was 0.799 for all grade and 0.835 for grade B or C, which were better Aldol condensation than AUROC of any single preoper-ative factors. In conclusion, risk assessment incorporating LSM is useful

for the prediction of PHLF. Disclosures: The following people have nothing to disclose: Gen Yamamoto, Kojiro Taura, Yukinori Koyama, Kazutaka Tanabe, Takahiro Nishio, Yukihiro Okuda, Etsuro Hatano, Shinji Uemoto Background: Recent attention has focused on the impact of donor-specific HLA antibodies (DSA) in deceased donor liver transplantation (DDLT). With less ischemia, improved donor selection and more controlled procedures, living donor liver transplantation (LDLT) may speculatively lead to less DSA formation and/or impact on patient and graft outcomes. Aim: To compare the incidence and impact of DSA in LDLT vs. DDLT Methods: The A2ALL biorepository was probed for primary LDLT and DDLT recipients with available serum samples pre-(immediately prior to implantation) and post-LT (∼3 months). Samples positive for panel reactive antibodies were tested for DSA (class, titer) using the Luminex platform. We compared the incidence of pre- (preformed) and post- (de novo) LT DSA between LDLT and DDLT and correlated DSA with the following time-dependent endpoints: patient and graft survival, rejection, biliary/vascular complications, HCV recurrence.

19 It has been shown that HBx is able to inactivate GSK3β through

19 It has been shown that HBx is able to inactivate GSK3β through Akt activation.22 Thus, it is also possible that HBx inhibits the Fbw7α-mediated ubiquitination and degradation of AIB1 through the inactivation of GSK3β. However, our data showed that overexpression of HBx in 293T and HepG2 cells cannot further increase the levels of phosphorylated Akt (active form) as well as the levels of phosphorylated GSK3β (inactive form) (Supporting Fig. 2), indicating that the HBx-induced up-regulation Inhibitor Library screening of AIB1 protein is not the

result of the inactivation of GSK3β in this study. Because several oncogenic transcription factors, such as NF-κB, AP-1, and AR, can be activated by both AIB1 and HBx, we speculated that AIB1 and HBx may have synergistic effects on the activation of these transcription factors. In agreement with this notion, we found that the coexpression of AIB1 and HBx synergistically induced MMP-9 expression through enhancement of the transactivation activity of NF-κB and AP-1 and, subsequently,

promoted HCC invasion. In addition, we found that AIB1 and HBx could synergistically activate AR (Supporting Fig. 3), a nuclear receptor that plays an important role in promoting HCC progression,13, 23, 24 suggesting that AIB1 and HBx may cooperatively activate oncogenic transcription Maraviroc purchase factors other than NF-κB and AP-1 to promote HCC progression. Further study is needed to verify this implication. Cooperative effects of HBx and AIB1 on HCC progression may result in an earlier onset and diagnosis of the disease in patients with AIB1/HBx double-positive HCC. Indeed, we found that the rate of AIB1/HBx double-positive HCC in patients between the ages 30 and 45 (10 cases) was 80.0%, between 45 and 60 (11 cases) was 54.5%, and between 60 and 75 (9 cases) was 22.2%, suggesting that the rate of AIB1/HBx double-positive HCC in patients is inversely correlated with age. Furthermore, the average age of patients with AIB1/HBx double-positive HCC at the time of diagnosis (47.9 ± 12.3 years old) was dramatically lower than that of patients with AIB1-negative or HBx-negative HCC (59.0

± 16.4 years old) (Supporting Fig. 4). As in most cancers, multiple oncogenic pathways Protein kinase N1 have been implicated in HCC progression. Discovering the cross-talk between different oncogenic pathways in HCC not only helps to understand the molecular mechanisms of HCC progression, but also provides new clues for therapeutic intervention. In this study, for the first time, we revealed the cross-talk between two oncogenes (i.e., HBx and AIB1) during HCC progression, implicating that the simultaneous targeting of both HBx and AIB1 may stand for a therapeutic strategy for HBV-related HCC. Additional Supporting Information may be found in the online version of this article. “
“Microvillous inclusion disease (MVID) is a congenital disorder of the enterocyte related to mutations in the MYO5B gene, leading to intractable diarrhea often necessitating intestinal transplantation (ITx).

In the metabolic conditions group, impaired fasting glucose and/o

In the metabolic conditions group, impaired fasting glucose and/or diabetes mellitus was associated with 2.90- and 1.82-fold increased risks of HCC and ICC (P < 0.0001). Similarly, dyslipoproteinemia, hypertension, and obesity were each significantly (P < 0.0001) associated Dabrafenib nmr with increased risks, ranging from 1.35-1.93, of developing HCC and ICC. Combining the metabolic variables, metabolic syndrome was associated with a statistically significant 2.58- and 2.04-fold increased risk of HCC and ICC, respectively (95% CI = 2.4-2.76 [HCC] and 1.74-2.40 [ICC], P < 0.0001). To investigate whether the significant associations

between metabolic syndrome and risk of HCC and ICC were independent of other major liver cancer risk factors, we used a logistic regression model that adjusted for all demographic variables, as well as all risk factors that were significantly associated with HCC and ICC in the univariate analyses. As shown in Table 6, metabolic syndrome was associated with a significant 2.13-fold increased risk of HCC (95% CI = 1.96-2.31) and a significant 1.56-fold increased risk of ICC (95% CI = 1.32-1.83). Both associations were independent of all other major HCC or ICC risk factors. Several sensitivity analyses

were conducted. To minimize the possibility of diagnostic detection bias, the first analysis excluded conditions that were diagnosed in the year prior to cancer diagnosis. This limited the power to detect significant associations for some rare conditions (e.g., Wilson’s disease for HCC and choledochal Torin 1 datasheet cysts, infectious liver diseases and alcoholic liver disease for ICC). However, as in the main analysis, metabolic syndrome remained significantly associated with an increased Elongation factor 2 kinase and independent risk of both HCC and ICC (data not shown). To minimize the possibility of diagnostic misclassification, the analyses were also repeated, but restricted to histologically confirmed and well-differentiated or moderately differentiated tumors. In this analysis,

ORs remained similar to the main analysis; however, the power to detect statistically significant associations between HBV infection, alcoholic liver disease, biliary cirrhosis, and ICC risk were limited. In the adjusted analyses that excluded undifferentiated tumors, metabolic syndrome remained associated with a 2.07-fold increased risk of HCC and 1.80-fold increased risk of ICC (95% CI = 1.83-2.34, P < 0.0001 for HCC and 1.33-2.43, P < 0.0002 for ICC, respectively). This is the first large population-based study in the United States that investigated the association between metabolic syndrome and risk for both primary liver cancers: HCC and ICC. The results indicate that preexisting metabolic syndrome, as defined by the 2001 U.S. NCEP-ATP III criteria, confers a statistically significant 2.13- and 1.

There were positive correlation between

CML levels and SM

There were positive correlation between

CML levels and SMCs specific genes mRNA expression levels. Conclusion: Ultrastructural changes existed in colonic SMCs of diabetic patients, and these changes could be the basis of diabetic colonic motility disorders. There was an increased AGEs levels and smooth muscle cell specific protein expression in diabetic patients’ colonic muscle tissue. Correlation between AGEs and expression of smooth muscle cell specific proteins was positive, which suggested that AGEs may involve in diabetic colonic smooth muscle lesions. Key Word(s): 1. diabetes; 2. smooth muscle cells; 3. AGEs; 4. ultrastructure; Presenting Author: ZHOUJING WU Additional Authors: LINYAO GUANG Corresponding Author: LINYAO GUANG Affiliations: guangxi medical Selleck CHIR 99021 RO4929097 university Objective: Compared the clinical and pathological character-ristics of colorectal cancer (CRC) between the elderly and the non-elderly patients, to improve the awareness and diagnosis and treatment of the elderly CRC. Methods: A total number

of 1343 patients with CRC from June 1, 2009 to May 31, 2012 in our hospital were included in this retrospective study. We extracted data on gender, ethnicity, blood type, duration, length of hospital stay, clinical manifestations, comorbidity, biochemical tests, tumor markers, tumor location, tumor size, histological, depth of invasion, surgical situation. We compared differences between an older group (OG) (age ≥ 60 years) and a young group (YG) (age < 60 years), so as to arrive at the clinical and pathological characteristics of colorectal cancer in the elderly. Results: There 4-Aminobutyrate aminotransferase were 537 cases of OG in 1343 cases of CRC, accounted for 40% (537/1343). Single factor analysis show that OG patients were more proportion of Zhuang patients than YG, more proportion of disease duration less than 3 mouths, more likely to have a longer hospital stay, lower average BMI, less clinical symptoms, more

distant metastasis, more comorbidity, lower preoperative HB and ALB, batter pathologic type. OG patients were less likely than YG patients to receive surgery, and more likely to receive postoperative complications. Conclusion: In comparison with younger patients, elderly CRC patients were with a high incidence, and differences were observed between the groups in clinical symptoms, comorbidity, histological, metastasis, postoperative complications. Key Word(s): 1. colorectal cancer; 2. elderly; 3. young; Presenting Author: XU WEN-DA Additional Authors: CHEN JIANG, LIU XU, LI HONG-YU, GUO XIAO-ZHONG Corresponding Author: GUO XIAO-ZHONG Affiliations: General Hospital of Shenyang Military Area Command Objective: Accidental or intended radiation exposure in a mass casualty setting presents a serious and on-going threat. The development of mitigating and treating agents requires appropriate animal models.

The proliferation of ICC was identified by immunolabeling for Kit

The proliferation of ICC was identified by immunolabeling for Kit and Ki67, while the apoptosis of ICC was detected by TUNEL method. The ultrastructural alterations were reflected by transmission electron microscopy. Results: (1) The gastric emptying was severely delayed in DM group. LEA and HEA significantly promoted the delayed gastric emptying, but LEA induced more obvious effects than HEA. (2) Plentiful proliferated ICC forming bushy networks with only Kit+ cells could be observed in LEA and

HEA group, while Kit+/TUNEL+ cells could hardly be seen in LEA and HEA group. Conclusion: LEA and HEA at ST36 could renovate networks of ICC in the stomach of diabetic rats, resulting an improved gastric emptying. KPT-330 EA may have a check details novel therapeutic option for

diabetic gastroparesis. Key Word(s): 1. EA; 2. ICC; 3. Gastric Emptying; 4. Diabetic Rats; Presenting Author: YAN CHEN Additional Authors: JUANJUAN XU, SHI LIU, XIAOHUA HOU Corresponding Author: SHI LIU Affiliations: Huazhong University of Science and Technology Objective: Defects of interstitial cells of Cajal (ICC) may be an underlying mechanism of gastrointestinal motility disorders in diabetic patients. More evidence suggests that electroacupuncture (EA) at ST36 is an effective method to improve gastric motility, but the mechanism is not completely understood. The aim of this study was to investigate the effect of EA on gastric contraction and the related mechanism in diabetic rats whether ICC was involved. Methods: Male SD rats were randomized into normal control, DM, DM+SEA, DM+LEA and DM+HEA group. EA was performed everyday at certain time for 4 and 8 weeks persistently. Mechanical contraction of gastric antrum longitudinal strips was explored by organ bath technique. Western blot was employed to demonstrate c-kit and M-SCF expression in gastric antrum and the levels of S-SCF in serum were determined by ELISA. The distribution of ICC was further assessed by immunohistochemistry. Aldol condensation Results: (1) In DM group, contractions of gastric antrum longitudinal strips were attenuated in 4 weeks and severely weakened in 8 weeks. Low- and high-frequency

EA promoted the attenuated contractions in 4 and 8 weeks. (2) Western blot analysis suggested that the expression of c-kit was reduced apparently in 8 weeks in DM group, but was obviously upregulated in LEA and HEA group. Whereas the expression of M-SCF in DM group was slightly decreased in 4 weeks and dramatically reduced in 8 weeks, low- and high-frequency EA also markedly increased the expression of M-SCF in 8 weeks. (3) In normal group, abundant ICC distributed in muscular layer and intermuscular layer. In DM group, c-kit positive cells were not obviously altered in 4 weeks but significantly decreased in 8 weeks. However, c-kit+ cell in LEA and HEA group were rich both in muscular and intermuscular layer in 8 weeks.

, 2010), positional errors occur because of inclement weather, st

, 2010), positional errors occur because of inclement weather, steep topography, buildings or surrounding vegetation that limit communication with orbiting satellites (Börger, Dalziel & Fryxell, 2008). We used stationary units to estimate the bias that would result from positional error alone, and found that location imprecision would yield home-range sizes between 0.4 (outdoor) and 2.1 ha (indoor). Thus, estimates of home-range size <2 ha may not be meaningful for domestic cats tracked with the GPS loggers we used. In summary, our study shows that introduced cats on islands are generalist predators that can be expected to prey on both native

and introduced wildlife. Because of the availability of introduced rodents, cat predation pressure on native

species may be locally reduced, but rodents likely supplement cat populations and thus facilitate continuing cat predation of native wildlife. While only eradication of feral cats from islands will ensure conservation of native biodiversity, the confinement of domestic cats to owner’s homes and policies that preclude cat ownership within a 1-km radius around important native biodiversity aggregations may be useful to minimize the impact of domestic cats on threatened island biodiversity. The project LIFE07 NAT/P/000649 ‘Safe Islands for Seabirds’ made this work possible. We thank J. Benedicto, J. Katzenberger, J. Landschoff, S. Monforte, P. Domingos and cats’ owners for help with fieldwork. We are grateful to Vítor Paiva

and Pedro Geraldes for providing stimulating discussions on the design and analysis mTOR inhibitor of results and for the GPS units. The project was funded by the IMAR, RSPB and SPEA. The authors declare that this study complied with the current laws of Portugal. The associate of editor and two anonymous referees gave all kind of useful advices to improve the paper. Supporting Information Table S1. Number of prey (n P), percentage of different prey items (%RF), frequency of occurrence (%F), and of biomass (%B) of food items found in cats’ scats Felis catus, grouped into the four seasons, on the island of Corvo from September 2010 to August 2011. Supporting Information Table S2. Domestic cats Felis catus tracked with global positioning system (GPS) units once per season from July 2011 to November 2012 on Corvo Island, Azores. Home ranges were determined by minimum convex polygon areas (100% MCP) and 95% kernel density estimation (KE). Stationary GPS units were operational during the same period the cats were tracked, and reflect the home range that is estimated from positional error alone. Supporting Information Table S3. Model selection summary of 16 candidate models explaining variation in home-range size (n = 70 deployments) of domestic cats Felis catus tracked on the island of Corvo once per season from July 2011 to November 2012.