The rate of recurrence in patients undergoing conventional EMR is higher than ESD. The aim of our study was to compare the safety, cost and efficacy of esophageal EMRL and ESD. Methods: A total of 152 patients were enrolled from our database on the basis of the following criteria: (1) histologically confirmed ESCC or HGIEN in the EMR or ESD specimens,

(2) tumor invasion depth of epithelium to muscularis LEE011 supplier mucosae, (3) no prior therapy for ESCC. They were divided into two groups: an ESD group and an EMRL group. ESD and EMRL have been performed for superficial squamous cell cancer and HGIEN since Dec 2006 and Dec 2008, respectively. Follow-up was done at 1, 3, 6, 12 months after resection, then annually. Rates of complications, devices cost, procedure time,

Doxorubicin concentration and recurrence rate in the two groups were compared. Statistical analysis done by Mann Whitney U-test and chi-square. Results: There was no significant difference between the two groups in age or sex, in mean size of the lesions (28 mm vs. 25 mm; p > 0.05), and in recurrence rate. The rates of complications were 9.3% (bleeding), 3.5% (perforation), 5.8% (stenosis) in ESD group and 1.5% (bleeding), 0% (perforation), 6.0% (stenosis) in EMRL group, respectively. The mean procedure time and devices cost were 46 min and 8650 ¥ in ESD group and 21 min and 2300 ¥ in EMRL group, respectively. There was no significant difference between the rates of recurrence and stenosis in the two groups., but the rates of bleeding and perforation, selleck products mean procedure time and devices cost were significantly higher in the ESD group. Conclusion: The efficacy of EMRL method is similar as ESD method for esophageal superficial lesions. And EMRL is a safer, easier and cheaper method for esophageal superficial lesions. Key Word(s): 1. EMRL; 2. ESD; 3. Esophagus; 4. Cancer;   ESD (n86) EMRL(n66) P value HGIEN: high-grade intraepighelial neoplasia, M: intraucosal carcinoma,

“Bleeding” was difined as bleeding volume >20 ml Presenting Author: JIN MYUNG PARK Additional Authors: JI KON RYU, JAE MIN LEE, JOO KYUNG PARK, SANG HYUB LEE, YONG-TAE KIM Corresponding Author: JI KON RYU Affiliations: Seoul National University Hospital Objective: The advantage of EUS-guided fine needle biopsy (EUS-FNB) is an acquisition of histologic core tissues. There have been some studies using EUS-FNB with 19-G Procore needle to find out its feasibility and safety for histopathologic diagnosis, however, technical difficulties were encountered with transduodenal biopsy. The aim of this study was to compare diagnostic accuracy and safety of 22-G FNB Procore device to those of 22-G FNA device for pancreatic solid lesion. Methods: The patients who underwent EUS-FNA or FNB with 22G needle for pancreatic solid lesion were retrospectively reviewed between October 2011 and July 2012, and clinicopathologic data was acquired. Sensitivity and specificity were compared along with safety as well between the FNA and FNB groups.

The rate of recurrence in patients undergoing conventional EMR is higher than ESD. The aim of our study was to compare the safety, cost and efficacy of esophageal EMRL and ESD. Methods: A total of 152 patients were enrolled from our database on the basis of the following criteria: (1) histologically confirmed ESCC or HGIEN in the EMR or ESD specimens,

(2) tumor invasion depth of epithelium to muscularis selleck compound mucosae, (3) no prior therapy for ESCC. They were divided into two groups: an ESD group and an EMRL group. ESD and EMRL have been performed for superficial squamous cell cancer and HGIEN since Dec 2006 and Dec 2008, respectively. Follow-up was done at 1, 3, 6, 12 months after resection, then annually. Rates of complications, devices cost, procedure time,

find more and recurrence rate in the two groups were compared. Statistical analysis done by Mann Whitney U-test and chi-square. Results: There was no significant difference between the two groups in age or sex, in mean size of the lesions (28 mm vs. 25 mm; p > 0.05), and in recurrence rate. The rates of complications were 9.3% (bleeding), 3.5% (perforation), 5.8% (stenosis) in ESD group and 1.5% (bleeding), 0% (perforation), 6.0% (stenosis) in EMRL group, respectively. The mean procedure time and devices cost were 46 min and 8650 ¥ in ESD group and 21 min and 2300 ¥ in EMRL group, respectively. There was no significant difference between the rates of recurrence and stenosis in the two groups., but the rates of bleeding and perforation, learn more mean procedure time and devices cost were significantly higher in the ESD group. Conclusion: The efficacy of EMRL method is similar as ESD method for esophageal superficial lesions. And EMRL is a safer, easier and cheaper method for esophageal superficial lesions. Key Word(s): 1. EMRL; 2. ESD; 3. Esophagus; 4. Cancer;   ESD (n86) EMRL(n66) P value HGIEN: high-grade intraepighelial neoplasia, M: intraucosal carcinoma,

“Bleeding” was difined as bleeding volume >20 ml Presenting Author: JIN MYUNG PARK Additional Authors: JI KON RYU, JAE MIN LEE, JOO KYUNG PARK, SANG HYUB LEE, YONG-TAE KIM Corresponding Author: JI KON RYU Affiliations: Seoul National University Hospital Objective: The advantage of EUS-guided fine needle biopsy (EUS-FNB) is an acquisition of histologic core tissues. There have been some studies using EUS-FNB with 19-G Procore needle to find out its feasibility and safety for histopathologic diagnosis, however, technical difficulties were encountered with transduodenal biopsy. The aim of this study was to compare diagnostic accuracy and safety of 22-G FNB Procore device to those of 22-G FNA device for pancreatic solid lesion. Methods: The patients who underwent EUS-FNA or FNB with 22G needle for pancreatic solid lesion were retrospectively reviewed between October 2011 and July 2012, and clinicopathologic data was acquired. Sensitivity and specificity were compared along with safety as well between the FNA and FNB groups.

For example, osteopontin MLN8237 cell line negatively regulates PPARα, so that inhibition of osteopontin increases PPARα.90 PPARα agonists suppress synthesis of osteopontin in macrophages and circulating levels in patients.94 However, osteopontin gene-deficient animals exposed to chronic alcohol exhibit increased steatosis, a finding that is counterintuitive to this proposed role of osteopontin.95 It therefore seems likely that osteopontin has other mechanisms of action in the pathogenesis of ALD. Interestingly, osteopontin is upregulated in animal models of AS, ASH96,97 and NASH,98,99 as well as in human ALD77,100–102 and its other roles are

discussed later. In contrast, adiponectin, a hormone produced by adipocytes, positively regulates Kinase Inhibitor Library PPARα DNA binding,103 thereby increasing fat accumulation,104 via AMPK signaling, that is suppressed with chronic alcohol.105 However, the role of adiponectin in ALD

remains controversial. PPARα also suppresses SREBP-1 activity and its downstream lipogenic targets via liver X receptor (LXR),106,107 while chronic alcohol upregulates SREBP-1c and steatosis in an experimental model.108 Hepatocyte-specific signal transducer and activator of transcription 3 (STAT3) knockout animals exposed to chronic alcohol exhibit significantly higher liver expression of SREBP-1c and steatosis, indicating STAT3 may act as a negative regulator of SREBP-1c.109 Other PPARs (PPARδ and PPARγ) are also involved in liver injury but studies are limited and inconclusive. In leptin

deficient ob/ob mice, disrupted PPARγ was associated with decreased triglyceride showing PPARγ to be pro-lipogenic;110 however, other reports suggest PPARγ to be protective against liver injury.105,111,112 These lines of evidence suggest that steatosis and its injurious consequences in ALD may involve multiple levels of regulation and sophisticated interactions/feedback loops, particularly actions exerted on and by PPARα. Alcohol see more impairs both innate and adaptive immunity. The immune effects of alcohol are context-dependent. They can be direct, through production of ROS, or indirect, by way of increased gut permeability, release of endotoxin and enhanced susceptibility to infections due to compromised immunity.113 Acute alcohol (24 h) inhibits pro-inflammatory signals generated predominantly by Kupffer cells, such as IL-1, TNF-α and NFκB, while chronic alcohol (>4 weeks) exacerbates these processes through the LPS-TLR4-CD14 pathway described earlier.114,115 TLR4 is one of the multiple pattern recognition receptors, that recognizes both pathogen- and host-derived factors to modulate inflammatory signals.116 It is widely expressed by macrophages/monocytes, leukocytes and natural killer (NK) cells. These components of innate immunity also produce cytokines, chemokines and ROS for surveillance and as the first line of defence.

Key Word(s): 1. Chronic hepatitis B; 2. Cirrhosis; 3. serum p53; 4. HBx; Presenting Author: MOHAMMADMEHDI MIR-NASSERI Additional Authors: HOSSEIN POUSTCHI, SIAVOSH NASSERI-MOGHADAM, ASHRAF MOHAMMADKHANI, REZA MALEKZADEH Corresponding Author: MOHAMMADMEHDI MIR-NASSERI Affiliations: NVP-LDE225 supplier – Objective: BACKGROUND: Hepatitis C

(HCV) is increasing worldwide including Iran. HCV is more prevalent among intravenous drug abusers (IDU), especially if imprisoned, mostly due to needle sharing. We determined the rate of HCV seropositivity among IDU prisoners and compared it with those of non-prisoners. Methods: METHODS: A cross-sectional study was conducted on consenting IDUs inhabiting

two prisons and attending three rehabilitation centers in Tehran, Iran. A questionnaire was completed for each subject and 5 ml blood was drawn. The samples were kept at 2–8°C until the sera were separated and stored at −70°C. HCVAb (ELISA) was checked by a single technician. Chi-square, Fisher’s exact test and multivariate analysis were used where appropriate. Results: RESULTS: Five-hundred and eighteen subjects were enrolled. About 74.5% were prisoners and 89.6% were male. Overall, 59.5% were positive for HCVAb (93.2% males and 6.8% Gemcitabine solubility dmso females, P < 0.02). HCV seropositivity was higher among prisoners compared to selleck chemicals llc non-prisoners (78.3% vs. 30.6%, respectively, P < 0.001). Also, it was higher in IUD older than 45 year-old compared to those younger than 30 year-old (77.8% vs. 54.2%, respectively, P = 0.002). Multivariate analysis showed significant association of HCV seropositivity with imprisonment (OR: 9.32, 95% CI: 5.60–15.51), sharing syringes (OR: 2.00, 95% CI: 1.26–3.17) and duration of intravenous drug use (OR: 0.86, 95% CI: 0.80–0.92). Conclusion: CONCLUSIONS:

HCV is rather common among IDU prisoners. Imprisonment is an independent risk factor for HCV and the infected IDUs going back to the society could be an important source of HCV. Taking effective strategies (education of high risk groups, provision of sterile syringes, identification and treatment of infected IDUs) to reduce the risk of this public health problem is needed urgently. Key Word(s): 1. Hepatitis C; 2. IV drug abuse; 3. prison; Presenting Author: YOUN HEE CHO Additional Authors: YOUNG SEOK KIM, MIN JIN KIM, HEE YOON JANG, YUN NAH LEE, SANG GYUNE KIM, SAE HWAN LEE, JAE YOUNG JANG, HONG SOO KIM, BU SUNG KIM Corresponding Author: YOUNG SEOK KIM Affiliations: Digestive Disease Center and Research Institute, Department of Internal Medicine, Soon Chun Hyang University School of Medicine Objective: Chronic hepatitis B accounts for most of causes of liver cirrhosis and hepatocellular carcinoma in Korea.

The emergence of hIPSCs (human Induced Pluripotent Stem Cells) and differentiation protocols to generate hepatocyte-like cells has opened the possibility of addressing these issues. Here we discuss the recent progress and potential in the production of various cell types constituting the liver and their applications to model liver diseases and test drug toxicity in vitro. This article is protected by copyright. All rights reserved. “
“The plight of liver disease is often complicated by bleeding and thrombotic diathesis. The forces of procoagulation and

anticoagulation, fibrinolysis and antifibrinolysis are in constant flux as a result of impaired liver function and insults that complicate PF-02341066 research buy liver disease. Our standard methods for assessing coagulation support the notion that liver disease is a bleeding disorder. The prothrombin time (PT) and activated partial Nutlin-3a clinical trial thromboplastin time (APTT) are prolonged, with the former being an important prognostic indicator in liver disease. However, these

and other conventional measures of individual protein levels are poor at estimating bleeding and thrombosis risk in this group of patients. Alternative testing, which takes into account the interplay between the various coagulant forces, can predict thrombosis and bleeding risk in patients with hepatic dysfunction. While

the basis for understanding coagulopathy has its roots in the traditional clotting cascade, this rigid pathway is now more complex than once thought. A number of coagulation proteins are synthesized by the liver and their synthesis is variably impaired in liver disease (see Table 1). Factor VII is the first protein to decrease when there is hepatocyte damage, likely due to its short half-life (approximately 2 h)1 and serum levels are inversely correlated with the degree of cirrhosis.2 Factors II, V and X are also reduced in acute liver injury, with additional deficiencies of factors IX and XI in chronic liver injury.3 Fibrinogen levels are within the normal range in stable selleck kinase inhibitor liver disease, but decreases occur as liver disease progresses, with concurrent dysfibrinogenemia.4 Conversely, plasma factor VIII levels are elevated in liver disease, despite decreased mRNA expression within the liver. This is likely secondary to enhanced vWF synthesis, which binds VIII and results in increased plasma vWF–VII complexes.5 These procoagulant protein deficiencies are counterbalanced by a deficit in anticoagulant proteins. These proteins are also synthesized within the liver, and their diminished circulating levels swing the coagulopathy pendulum in favor of clotting.

Methods: We analyzed 118 consecutive patients with ALD who performed colonoscopy between January 2000 and December 2013. For each case, age – (±5 years) and sex-matched controls were identified from patients with non-alcoholic fatty liver disease (NAFLD) and healthy controls. Clinical characteristics were reviewed through medical records, colonoscopic finding, pathologic finding, images. Results: The prevalence of colorectal cancer was Decitabine in vivo 6 (5.1%) in ALD patients, 5 (2.5%) in

NAFLD patients, 0 (0.0%) healthy control (P = 0.007). In addition, the prevalence of advanced colonic adenoma was 18 (15.3%) in ALD patients, 17 (8.6%) in NAFLD, in 6 (2.8%) healthy control (P < 0.001). A case-control study showed that odds for detecting a colorectal advanced neoplasm among ALD patients without decompensated liver cirrhosis were approximately 10.1 times greater than in healthy controls [OR,10.095; 95% Confidential interval (CI),

3.638-28.014; P < 0.001) ]. There was no significant difference in the prevalence of colorectal cancer (P = 0.428) and advanced colonic adenoma (P = 0.876) according to the presence of decompensated liver cirrhosis (LC) in ALD patients. RAD001 mw Age is an independent risk factor for detecting advanced colonic neoplasm in patients with ALD [OR, 1.091; 95% CI, 1.025-1.162; P = 0.007] Conclusion: The yield for detecting advanced neoplasm was significantly higher in patients with ALD than in healthy control. Screening for colorectal neoplasm using colonoscopy is warranted in ALD patients without decompensated LC. Key Word(s): 1. alcoholic liver disease; 2. advanced colonic neoplasm; 3. decompensated

liver cirrhosis Presenting Author: MYUENG GUEN OH Additional Authors: MAN WOO KIM, CHAN GUK PARK, YOUNG DAE KIM, JUN LEE, MI AH HAN Corresponding Author: MYUENG GUEN OH Affiliations: selleck chemical Chosun University Hospital, Chosun University Hospital, Chosun University Hospital, Chosun University Hospital, Chosun University Objective: This study was performed to investigate the association between coffee and serum aminotransferase in Korean adults. Methods: Data were obtained from the 4th and 5th Korea National Health and Nutrition Examination Survey. Elevated alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were defined as >30 IU/L for men and >19 IU/L for women, respectively. Proportion of elevated ALT and AST according to general characteristics and coffee consumption frequency were tested by chi-square tests. Adjusted odds ratios (aOR) and 95% confidence interval (CI) for elevated ALT and AST by coffee consumption frequency were calculated after adjusting for sex, age, smoking status and body mass index.

[5] Using anatomical and histological techniques, they showed that the dura of the middle cranial fossa is innervated Tofacitinib purchase by nerve fibers of the mandibular and maxillary trigeminal divisions, while the dura of the anterior cranial fossa and the tentorium cerebelli are innervated by nerve fibers of the ophthalmic division. Due to the seminal intraoperative experiments of Ray and Wolff during

this time, the essential role for the generation of headaches of trigeminal nerve fibers innervating meningeal blood vessels was published and widely accepted,[6] later confirmed by additional studies of other groups.[7, 8] A number of animal experiments during the last decades widened our knowledge about the trigeminovascular system of the meninges as morpho-functional basis for the pathogenesis of headaches. Further studies clarified details of the structure9-12 and the functional characteristics of meningeal afferents innervating the rodent dura mater,13-16 and identified their central projections.[17, 18] Through immunohistochemical examinations, we know that a considerable proportion of these meningeal afferents contains neuropeptides like substance P and calcitonin gene-related peptide.[10, 19, 20] This could also be demonstrated for the human dura mater, confirming the homology of the nociceptive innervation

between mammals.[21] Despite this knowledge, the pathogenesis of headaches is still full of unresolved problems, which applies particularly to primary PD-1/PD-L1 assay headaches such as migraine. While a central origin of primary headaches has been intensely discussed during recent see more years, clinical and experimental observations provide evidence for an essential contribution of peripheral, intracranial

as well as extracranial, nociceptive processes.[22] The intracranial and pericranial trigeminal innervation may partly form a functional unit, a concept that is supported by recent histological and functional data that show collateral afferent connections between the dura mater and deep pericranial tissues in rodents.[23, 24] In the light of these recent findings, old anatomical studies on the primate and human meningeal innervation reporting about nerve fibers that penetrate the skull become again highly important.[2, 3, 5] These nerve fibers, in addition to their originally supposed function to innervate the skull, eg, in the region of the mastoid,[5] can indeed supply extracranial tissues. The present postmortem anterograde tracing study in rat and human skulls completes and extends our recent in vivo anterograde tracings.[24] They show that in the area of the middle cranial fossa, intracranial (meningeal) and extracranial (deep muscular) tissues are innervated by trigeminal nerve fibers passing through the cranial dura mater.

Results were presented as fold induction, normalized to hypoxanthine-guanine phosphoribosyltransferase, which was selected as the most stable reference gene as described.14 Hygromycin phosphotransferase was used as a transfection marker, encoded within the pCB7-ATP8B1 construct. U2OS cells were grown on coverslips and co-transfected with pCB7-ATP8B1 and pcDNA3-CDC50A using polyethylenimine. After 2 days, cells were fixed using

paraformaldehyde and ATP8B1 and the ER-marker protein disulfide isomerase (PDI) or CDC50A were visualized using rabbit Selleck Palbociclib anti-VSV-G and Cy3 coupled secondary antibody together with mouse anti-PDI and AlexaFluor 488–coupled secondary antibody or FITC-conjugated mouse anti-V5. Images were acquired using a LSM710 Meta confocal microscope (Carl Zeiss, Jena, Germany). Two days after transfection, U2OS cells were washed with phosphate-buffered

saline supplemented with 0.5 mM CaCl2 and 1.0 mM MgCl2 (PBS-CM), and proteins present at the cell surface were biotinylated using sulfo-NHS-SS-biotin and solubilized as described.15 Biotinylated proteins were precipitated for 2 hours using neutravidin-coupled beads (Pierce) and analyzed by immunoblot analyses. Cytosolic proteins were undetectable in the precipitated fraction, and no precipitated protein was detected when sulfo-NHS-SS-biotin was omitted, demonstrating the specificity of the procedure. All figures represent at least three independent experiments. Protein expression was measured by densitometry using ImageJ (http://rsbweb.nih.gov/ij/). Background intensity was subtracted Cilomilast and values were compared using Mann-Whitney after testing for overall significance using the Kruskal-Wallis test (P < 0.05 was considered significant). Data are provided as mean ± standard deviation (SD). To study the effect of cholestasis-associated mutations in ATP8B1 on selleck compound protein expression, HEK293T cells were cotransfected with CDC50A and ATP8B1 wild-type (WT) and mutants. ATP8B1 WT protein was readily detectable at approximately 140 kDa, and endogenous expression in HEK293T cells was very low. The protein expression of ATP8B1 mutations G308V,

D454G, D554N, I661T, G1040R, and R1164X was significantly reduced, whereas the p.L127P mutation did not affect ATP8B1 expression levels (Fig. 1B). Identical results were obtained using U2OS cells, strongly suggesting cell type independence, and data of both cell types are averaged in Fig. 1C. ATP8B1 R1164X migrated faster than ATP8B1 WT, in agreement with the absence of the carboxyl-terminus (Fig. 1B), and also exhibited reduced expression. In contrast, the messenger RNA (mRNA) expression of all mutants with reduced protein expression was unaffected (Fig. 1D). Protein expression of ATP8B1 WT, I661T, and G1040R was increased 1.1-fold to 2-fold upon treatment with the proteasomal inhibitors MG132 or epoxomycin (Fig. 2A). ATP8B1 mutants with lowest protein expression in control conditions, i.e., p.G308V, p. D454G, p.D554N, and p.

37, 38 However, because we did not evaluate children of other ethnic groups with NAFLD, we cannot exclude the idea that the PNPLA3 I148M SNP has a different histological expression according to the genetic background. Importantly, in line with previous

findings in adults, the association between the PNPLA3 148M allele and NASH-related fibrosis was independent of confounding factors such as the age at presentation, adipose tissue mass and distribution, presence of diabetes or IGT,19, 27, 32, 39 and ALT levels, and this indicates that the evaluation of the rs738409 genotype may provide additional useful information find more for clinical identification of patients at risk of progressive disease. However, because of the limited number of subjects considered, the lack of an association between the

PNPLA3 SNP and liver enzymes, despite increased liver damage in children, should be further confirmed in larger series. The effect of the rs738409 genotype on fibrosis progression check details should be evaluated in prospective studies enrolling young patients with NAFLD.40 Nevertheless, the unexpectedly striking association between the PNPLA3 148M variant and liver damage reinforces the suggestion that liver biopsy29 and aggressive treatment should be indicated for pediatric patients carrying the rs738409 GG genotype. However, although it was previously observed in a multiethnic US population that the same rs738409 SNP explained a good part of

the increased susceptibility to steatosis of Hispanics versus subjects of European descent,19 we should note that the present results apply selleck chemical only to Caucasian children with NAFLD. In conclusion, the PNPLA3 rs738409 SNP is associated with steatosis severity and the presence of NASH and fibrosis in pediatric Italian patients with NAFLD. Individuals carrying the GG allele have a very high risk of progressive liver disease. Screening analysis of the PNPLA3 rs738409 SNP could be a useful tool for discriminating among the at-risk pediatric subjects who require continuous monitoring over time because they are extremely susceptible to NASH and fibrosis. “
“Taurolithocholate (TLC) acutely inhibits the biliary excretion of multidrug-resistant associated protein 2 (Mrp2) substrates by inducing Mrp2 retrieval from the canalicular membrane, whereas cyclic adenosine monophosphate (cAMP) increases plasma membrane (PM)–MRP2. The effect of TLC may be mediated via protein kinase Cϵ (PKCϵ). Myristoylated alanine-rich C kinase substrate (MARCKS) is a membrane-bound F-actin crosslinking protein and is phosphorylated by PKCs. MARCKS phosphorylation has been implicated in endocytosis, and the underlying mechanism appears to be the detachment of phosphorylated myristoylated alanine-rich C kinase substrate (pMARCKS) from the membrane.

It is likely that seabird species smaller than Cory’s shearwater formed a large part of the diet of cats on Corvo in the past (Monteiro, Ramos & Furness, 1996). As these seabird

species were not found in cat scats in our study, cats likely exterminated accessible colonies of these species (Fitzgerald et al., 1991). Without the availability of introduced rodents as alternative prey, the feral cat population would not have survived the extermination of an important food source, highlighting the adverse effect of introduced learn more rodents in supplementing predator populations on islands. We found no evidence that seasonally varying abundance of prey taxa explained variation in the home-range size of domestic cats. Instead, home-ranges were

extremely variable among individuals and seasons as has been found elsewhere (0.3–69.0 ha; Metsers, Seddon & van Heezik, 2010, 0.5–21.8 ha; van Heezik et al., 2010). While confined cats that receive sufficient food from human buy Anti-infection Compound Library owners may not need to adjust their roaming behaviour to prey availability, even the unconfined cats in our study did not display a consistent response to the availability of prey that we measured. Because cats appear to be generalist predators, the roaming behaviour may be controlled by factors other than food requirements, such as temperature, photoperiod, precipitation or territoriality (Goszczynski, Krauze & Gryz, 2009). Overall, we found high individual variation in home-range size, and all our covariate subgroups therefore had small sample

sizes, rendering their mean size estimates less robust. selleck kinase inhibitor We found a small positive effect of age on home-range size, possibly because young cats show reduced dispersal behaviour until they are 1–3 years old (Liberg, 1980). Confined cats had generally smaller home-ranges than unconfined cats, and tended to roam less far from their home (Fig. 3), therefore cat owners could be encouraged to confine the cat to the immediate vicinity of the house. If individual cats display consistent individual roaming behaviour, identifying and constraining the widest roaming cats may be easier to implement than other generally applicable cat constraint approaches (Calver et al., 2011). Another potential management option is to restrict cat ownership in human settlements that are too close to vulnerable native wildlife congregations such as seabird colonies. Our study shows that confined cats are less likely to roam very far, but that some unconfined cats can move >10 km in a single night. On average, however, movements were within a 1-km radius around the owner’s house, and impacts on native wildlife are presumably greatest within this radius. The tracking of cats with GPS loggers provided a great opportunity to assess the spatial impact of domestic cats on native wildlife.