44 [95% CI, 1.12-1.87]) and migraine symptom severity score. Among those who were diagnosed, annual household income was the strongest predictor of currently using guideline-defined appropriate acute treatment (OR = 1.44 [95% CI, 1.07-1.93]) followed by a 10-point change in MIDAS score (OR 1.16 [95% CI, 1.02-1.35]). Conclusions.—

Among persons with migraine in need of medical care (MIDAS Grade II or greater), only one quarter traversed the 3 steps we proposed to be necessary to achieving minimally appropriate care (consulting, diagnosis, and treatment/medication use). Health insurance status was an important predictor of consulting. Among consulters, women were far more likely to be diagnosed than men, suggesting that gender bias in diagnosis may be an important barrier for men. There were economic barriers related to use of appropriate prescription medications. MG-132 cost Public health efforts should focus on improving consultation rates, particularly in the uninsured and diagnostic rates particularly in males with migraine. “
“(Headache 2011;51:237-245) Objective.— The aim of this study was to investigate the possible microstructural abnormalities of the corpus callosum (CC) in adult patients with migraine without aura complicated with depressive/anxious disorder. Background.— Emotional disorders, especially depression

and anxiety, are PD0332991 in vivo with relatively higher incidence in migraine population. However, the mechanism of migraine complicated with depressive/anxious disorder remains unclear. Methods.— Diffusion tensor magnetic resonance imaging was carried out in 12 adult patients Venetoclax mw with simple migraine (without aura and without depressive/anxious disorder) (S-M group), 12 adult patients with complicated migraine (without aura but complicated with depressive/anxious disorder) (Co-M group), and 12 age- and sex-matched healthy subjects (Control group). Fractional anisotropy (FA) and apparent diffusion coefficient were measured at genu, body, and splenium of the CC, respectively. Results.— There were

significant differences in FA values at all locations of the CC among the 3 groups. The FA values from both the SM and Co-M groups were significantly lower than the control (P < .05 and P < .01, respectively). The FA values from Co-M group were significantly lower than the SM group (P < .01). The apparent diffusion coefficient values of the above regions had no significant differences among these groups (P > .05). There were negative correlations between FA value of genu of the CC and disease course as well as FA value of genu and body of the CC and headache frequency (P < .05). Negative correlations were also found between FA values at all locations of the CC and Hamilton anxiety and Hamilton depression scores (both P < .05). Conclusions.

Apart from AVH, PUB may be another indication to administer nonselective beta-blocker in patients with cirrhosis if our finding is validated in clinical trials. This study has some limitations. First, the enrolled patients with cirrhosis were presumably more severe clinically selleck due to the stringent definition that was set to avoid misclassification of cohorts. Therefore, how the severity of portal hypertension affected rebleeding risk could not be evaluated. The indifferent association

between prior AVH and risk of future PUB should be comprehended carefully in the context of this limitation. Likewise, the study was limited in its exploration of different rebleeding risks among subgroups of patients with cirrhosis. Although we showed that alcoholic etiology appeared to incur a higher risk, how the etiological factor confounded the analysis could not be thoroughly appreciated. Risk stratification in patients with cirrhosis for predicting recurrent PUB is certainly interesting, but it was beyond the scope of the study. Also, the NHIRD did not include postnatal data for all study subjects, because this database was not established until 1995. Accordingly, we defined the index PUB episode as the first one occurring click here between January 1, 1997, and December 31, 2006,

but this episode may not have been the first in a patient’s lifetime. However, this limitation was unlikely to bias our results, because both cohorts were enrolled from the same PUB population during the same period. Furthermore, some variables had to be inferred indirectly from the administrative data. For example, the

status of H. pylori was inferred from the characteristic regimen instead of laboratory confirmation and drug exposure from the filled prescriptions without ascertainment of adherence. Finally, bleeding source can be difficult to determine in patients with cirrhosis with UGI bleeding, and PUB might be these insufficiently or erroneously coded. Such misclassification, nevertheless, would have underestimated the exact incidence of recurrent PUB in patients with cirrhosis and biased the results toward null difference. In conclusion, this nationwide population-based study revealed that cirrhosis is a risk factor for recurrent PUB in the long term, although the rebleeding risk diminishes with age because of the exceedingly high risk of mortality in patients with cirrhosis at advanced age. Regardless, our findings should inspire further research designed to explore effective therapy to reduce this excessive risk of rebleeding in patients with cirrhosis, particularly for those <60 years of age. The search for therapeutic intervention should target the pathophysiological consequences specific to liver cirrhosis, since its association with recurrent PUB is independent of H. pylori and ulcerogenic agents.

018 and P = .044, respectively) in reducing headache frequency, but only among those that completed the study. In the analysis including all treated patients, treatment groups did not differ significantly during follow-up. Feverfew Feverfew is an herbal preparation that was used for centuries in the treatment of fevers, headache, infertility, toothaches, inflammation and arthritis. Although the feverfew plant was originally native to the Balkan mountains in Eastern Europe, it now grows throughout Europe, North America, and South America. It is commercially available as the dried leaves of the weed plant Tanacetum parthenium,

and its anti-migraine action is probably related to the parthenolides within these leaves. Feverfew may act in migraine prophylaxis by inhibiting platelet aggregation as well as the release of BVD-523 clinical trial serotonin from platelets and white

blood cells. It may also act as an anti-inflammatory agent through the inhibition of prostaglandin synthesis and phospholipase A.68-71 The efficacy selleck screening library of feverfew in migraine prophylaxis has been controversial, as many RCTs72-77 conducted in the past 3 decades have yielded contradictory results. In addition, a 2004 Cochrane review78 of double-blind RCTs assessing the clinical efficacy and safety of feverfew in migraine prevention concluded that there was insufficient evidence to suggest that feverfew is more effective than placebo in migraine prophylaxis. No major safety or tolerability issues were identified, although side effects reported in the RCTs included gastrointestinal disturbances, mouth ulcers,

and a “post-feverfew syndrome” of joint aches. Inconsistent results from the above studies were attributed to wide variations in the strength of the parthenolides79 and differences in the stability of feverfew preparations80 and subsequently, a new, more stable feverfew extract (MIG-99) was created. In an initial RCT involving 147 patients,81 none of the MIG-99 doses were significant Axenfeld syndrome for the primary endpoint, although a subset of high-frequency migraineurs appeared to benefit from treatment. In a follow-up multicenter RCT with 170 subjects82 randomized to 6.25 mg t.i.d. of MIG-99 or placebo, a statistically significant and clinically relevant reduction in migraine frequency in the MIG-99 group compared to placebo was reported. Feverfew should not be used by pregnant women, as it may cause uterine contractions resulting in miscarriage or preterm labor. It can also cause allergic reactions; patients with allergies to other members of the daisy family, including ragweed and chrysanthemums, are more likely to be allergic to feverfew. Recreational Drugs Although controversial, the evidence for the use of recreational drugs such as marijuana, lysergic acid diethylamide (LSD) and psilocybin is worth mentioning for the insight it provides regarding the pathophysiology of migraine and cluster headache.

S7). However, SND1 inhibition (either by pdTp or by siRNA) did not affect increased Matrigel invasion activity conferred by AEG-1 (data not shown), indicating that SND1 primarily plays a role in regulating cell growth and proliferation. The observation that inhibition of SND1 can significantly inhibit cell growth and viability prompted us to probe deeper into SND1 involvement in HCC. At first we examined the SND1 expression

pattern by immunohistochemistry in tissue microarrays containing 86 primary HCC, 23 metastatic HCC, and 9 normal adjacent liver samples. SND1 expression was detected predominantly selleckchem in the cytoplasm (Fig. 6C). None of the normal liver and HCC samples stained negative for SND1 (Fig. 6C, Table 1). However, compared to normal liver there was a significant increase in SND1 expression in 81 out of 109 HCC patients (≈74%). SND1 expression gradually increased with the stages of the disease based on the Barcelona Liver Clinic

Cancer (BCLC) staging system that showed significant statistical correlation (Table 1). We next checked the consequence of stable overexpression of SND1 Ivacaftor mw in Hep3B and stable knockdown of SND1 in QGY-7703 human HCCs in the contexts of cell growth and tumorigenicity. Compared to the control neomycin-resistant cells (Hep3B-Con), Hep3B-SND1-17 clones had significant augmentation in cell growth and proliferation as observed by standard MTT and colony-forming assays (Fig. 7A,B, respectively). On the contrary, the QGY-SND1si-12 clone showed significantly slower cell growth and proliferation compared to QGY-Consi clone stably expressing control scrambled siRNA (Fig. 7A,B). In the in vivo nude mice xenograft assay,

the Hep3B-SND1-17 clone formed significantly larger subcutaneous tumors compared to the Hep3B-Con clone (Fig. 7C-E). As a corollary, the QGY-Consi clone formed significantly larger tumor compared to the QGY-SND1si-12 clone (Fig. 7C-E). Similar findings were observed in additional SND1-overexpressing clones of Hep3B cells and SND1-knockdown clones of QGY-7703 cells (Supporting Information Fig. S8). Nuclear SND1 functions as a transcriptional coactivator and helps in pre-mRNA splicing and AEG-1 also modulates transcription.6, Glycogen branching enzyme 7, 14, 19 However, we did not detect colocalization of AEG-1 and SND1 in the nucleus and we documented that AEG-1 interacts with SND1 in the cytoplasm, facilitating RISC activity. Cells lacking fragile X mental retardation protein, another component of RISC, have normal RISC activity,16 further supporting the contribution of AEG-1 in maintaining optimum RISC function. More important, we demonstrate that both AEG-1 and SND1 are overexpressed in HCC compared to normal liver, and human HCC cells exhibit higher RISC activity compared to normal immortal hepatocytes.

4-fold (Fig. 5A), whereas duodenal BMP6 mRNA expression was largely unaffected (Fig. 5B). The expression of ferroportin was markedly up-regulated in the duodenum of mice lacking hepatic Hjv (Fig. 5C). We conclude that hepatic Hjv is essential for preventing iron overload by way of appropriate signaling to hepcidin. Hfe2f/f:MCK-Cre mice bearing muscle-specific disruption of Hjv presented with

physiological serum iron indices (Table 2) and did not develop iron overload in the liver, pancreas, or, notably, in the heart (Fig. 4A; Supporting Fig. S1). Splenic macrophages contained stainable nonheme iron (Fig. S1), by analogy to Hfe2f/f controls. The expression of hepcidin mRNA (Fig. 4B), hepatic BMP6 mRNA (Fig. 5A), and duodenal BMP6 mRNA (Fig. 5B) did not significantly differ between Hfe2f/f:MCK-Cre and Hfe2f/f mice, whereas expression of duodenal ferroportin was undetectable

(Fig. 5C). Thus, the absence of muscle Hjv did not affect iron metabolism in the whole body and, apparently, also in the heart, a tissue that normally expresses Hjv. We compared the hepatic iron content and hepcidin mRNA expression levels among age- and sex-matched Hfe2f/f, Hfe2f/f:Alb-Cre, Hfe2f/f:MCK-Cre, and ubiquitous Hjv-/-7 mice; all lines shared a mixed 129S6/C57 genetic background, albeit with variable genomic ratios. The degree of hepatic iron overload (Fig. 4A), the deregulation of hepcidin expression (Fig. 4B), and the increase of hepatic BMP6 mRNA (Fig. 5B) were quantitatively similar among ubiquitous Hjv−/− and liver-specific Hjv−/− (Hfe2f/f:Alb-Cre) animals. Likewise, control floxed (Hfe2f/f) and muscle-specific Hjv−/− (Hfe2f/f:MCK-Cre) mice were phenotypically indistinguishable. Taken together, these results indicate that the absence of hepatic Hjv suffices to cause full-scale iron overload, whereas the lack of muscle Hjv does

not affect iron balance. Genetic studies in humans5 and mice6, 7 uncovered an important role of Hjv in the control of systemic iron homeostasis. Corroborating evidence was enough provided from biochemical data showing that Hjv activates the iron-dependent pathway for signaling to hepcidin by acting as a BMP coreceptor,8 whereas a circulating sHjv isoform is widely considered to antagonize this response.19, 20, 22, 31 We report here that the targeted disruption of Hjv in liver hepatocytes recapitulates the hemochromatotic phenotype of mice lacking Hjv ubiquitously.6, 7 Thus, the liver-specific ablation of Hjv leads to high transferrin saturation, hyperferremia, hyperferritinemia, hepatic iron overload, macrophage iron deficiency, and inappropriately low hepcidin expression, which are hallmarks of learn more hereditary hemochromatosis. In addition, it is associated with increased hepatic BMP6 mRNA expression, as in ubiquitous Hjv−/− mice.

2 (3–12)), Post-treatment Eckardt score was 0.3 (0–1). Complications related to operation included mucosa rupture in 1 (6.3%), mediastinal and subcutaneous emphysema in 4 (25%), asymptomatic pneumothorax in 2 (12.5%), gas under diaphram in 1 (6.3%). All the complications were cured by conservative treatments. ALL patients were follow-up, and no other post operation complications occurred. Conclusion: POEM is an effective, feasible and safe therapy

for achalasia, while the long-term efficacy and managements for complications are still to be elucidated. Key Word(s): 1. POEM; 2. Achalasia; Presenting Author: JINGJING WEI Additional Authors: ZEHAO Gefitinib in vivo ZHUANG, JIAYUAN ZHUANG, DUPENG TANG, YILIN ZENG, CHENGDANG WANG Corresponding Author: ZEHAO ZHUANG Objective: To investigate the prevalence of gastroesophageal reflux disease (GERD) in the Hakkas and to evaluate the practicability of two questionnaires, including Chinese gastroesophageal reflux disease questionnaire

(CGQ) and gastroesophageal reflux disease questionnaire (GerdQ) in this population. Methods: CGQ and GerdQ were used for GERD symptoms survey in a random sequence in a selected Hakkas community. Results: Paired questionnaires were collected from 203 subjects, including 104 males and 99 females. The positive rates were 12.3% and 4.9% by CGQ and GerdQ, respectively (P < 0.05). A male predominant trendcy was found in GERD symptom positive cases surveyed by GerdQ (P < 0.05), but not in those surveyed

by www.selleckchem.com/products/PD-98059.html CGQ (P > 0.05). The incidence of GERD showed an increasing tendency with the aging, through no significant difference was found in age-stratification analysis. The response time was 3.2 ± 0.8 min (CGQ) and 5.4 ± 0.6 min (GerdQ) respectively (P < 0.05). Conclusion: GERD symptoms were quite common in selected Hakkas community, while CGQ surveying showed a higher symptom positive rate than GerdQ surveying in this population. Key Word(s): 1. GERD; 2. GerdQ; 3. Chinese GerdQ; 4. hakka dialect; Presenting Author: LIULIU WEI Additional Authors: HONG CAI Corresponding see more Author: LIULIU WEI Affiliations: Ganzhou city people’s hospital; Objective: To investigate the clinical characteristics and risk factors of gastroduodenal damages induced by nonsteroidal anti-inflammatory drugs (NSAIDs). Strengthen to understand the disease. Methods: The sample consisted of 85 patients whose gastroduodenal damages were induced by nonsteroidal anti-inflammatory drugs (NSAIDs) at Ganzhou city people’s hospital from the January 2011 to April 2013. According to the endoscopic diagnosis, the patients were divided into two groups, erosive gastritis group and ulcer group. Record the patients’ age, sex, clinical symptoms, previous ulcer history, H. pylori infection, smoking history and kinds of NSAIDs. Results: ① Of 85 patients of gastroduodenal damages induced by NSAIDs, male 49, female 36, the male and female ratio 1.36 : 1, mean age (61.8 ± 13.

Remarkably, we revealed a significant down-regulation of the Mat1a protein specifically in the livers of Mdr2-KO/FVB mice (Fig. 6A,B). The Mat enzyme catalyzes the synthesis of S-adenosyl methionine, a universal donor of the methyl group for all methylation reactions in the cell. It is encoded by the genes Mat1a and Mat2a/2b; patients with liver cirrhosis have reduced activity of this enzyme.34 Mat1a

is highly expressed in the adult liver and keeps hepatocytes in a quiescent state. In human liver cancer, Mat1a expression is reduced, whereas Mat2a is increased; this switch facilitates cancer cell growth.35 We demonstrated previously that most hepatocytes of the Mdr2-KO/FVB strain undergo cell cycle arrest between the ages 3 and 9 months, www.selleckchem.com/products/Gemcitabine-Hydrochloride(Gemzar).html and this is characterized by a high level of cyclin D1 in hepatocyte nuclei.4, 36 Our current findings demonstrate that selectively in the Mdr2-KO/FVB mice, this stage of hepatocyte cycle arrest is characterized by a decreased level of the www.selleckchem.com/products/otx015.html Mat1a protein and up-regulation of the Mat2b transcript (Supporting Table 2). Despite the inverse differential expression of the Mbd1 transcript in the two Mdr2-KO strains (Supporting Table 2), protein expression

in both strains was increased in the mutant liver versus the control liver (Fig. 5). The Mbd1 protein binds methylated DNA and functions mainly as a transcriptional repressor;

its higher level in the Mdr2-KO/B6 strain versus the Mdr2-KO/FVB strain could be one of the factors responsible for a significantly lower number of up-regulated genes in the former mutant. Published data on the genotypic and phenotypic differences between the B6 and FVB strains are summarized in Supporting Table 4. There are several known differences between these strains that could be responsible check details for the different courses of chronic hepatitis and HCC development in the two Mdr2-KO mutants. The most prominent among them are (1) a deficiency of complement C5 protein in the FVB strain, (2) mutations in mitochondrial DNA in the FVB strain, and (3) a Tnfaip3 (A20) polymorphism that is responsible for the less effective feedback suppression of Tnf-α–induced NF-κB activation in the B6 strain (see the references in Supporting Table 4). In conclusion, we have demonstrated that the B6 murine strain has a remarkable resistance to both chronic hepatitis and HCC development caused by the Mdr2-KO mutation. By a comparative analysis of liver gene expression in the two Mdr2-KO strains, we determined a set of regulatory genes that could be responsible for affecting the severity of chronic hepatitis in these strains at an early age. The most prominent was the differential expression of multiple regulators of the NF-κB pathway, which is critical for manifestations of the Mdr2-KO phenotypes.

[30] In addition to inducing CD14 for innate immunity, 1,25-dihydroxyvitamin D can

also up-regulate antimicrobial peptides such as cathelicidin and beta-defensin by macrophages in the gastrointestinal track.[13, 31] In fact, activation of toll-like receptors in human macrophages can induce cathelicidin antimicrobial peptide, which is inhibited by either a VDR antagonist or C646 a non-specific inhibitor against 1-hydroxylase activity, suggesting that de novo synthesis of 1,25-dihydroxyvitamin D is required for cathelicidin induction.[32] Induction of beta-defensin expression by 1,25-dihydroxylvitamin D requires additional activation of NF-kappaB sites, which are adjacent to its VDRE via a mechanism involving IL-1, suggesting converge of inflammatory signals and immune regulation.[33] Thus, VD-induced antimicrobial

peptides in the gastrointestinal track may represent a typical example of host defense modulation of the innate immune system. Th1 cells secrete pro-inflammatory cytokines, including interferon-gamma (IFN-gamma) and IL-2, and activate B cells to produce immunoglobulin IgG2a. A large body of evidence has demonstrated that VD/VDR can suppress Th1 lymphocytes by mechanisms such as down-regulation of IL-2, a key cytokine for T cell proliferation and activation.[34] 3-deazaneplanocin A in vitro Moreover, 1,25-dihydroxyvitamin D also suppresses IL-12 and IFN-gamma, the two major Th1 cytokines for acute immune responses.[35] In contrast, Th2 cells secrete IL-4 and IL-10, and induce the production of IgG1 and immunoglobulin E (IgE) by B cells, in a manner skewed to immune regulation. Interestingly, activated monocytes and dendritic cells from the innate immune system, and B cells from the selleck chemicals adaptive immune system produce IL-12, which induces Th0 to become Th1 cells. Consequently, activated Th1 cells induce inflammation by generating IFN-gamma and TNF-alpha. For such regards, 1,25-dihydroxyvitamin D suppresses IL-12 production by

monocytes and B cells, thus consequently restraining Th1 activation.[36] Epidemiologic studies have shown that low blood VD levels are associated with autoimmune diseases. In particular, the potential role of VD in immune regulation by induction of T-regulatory cells (Tregs) is under extensive scrutiny. For example, bioactive VD was found to potentiate Treg activity,[37] and low levels of 25-hydroxy VD in the circulation are associated with compromised Treg function and high incidence of multiple sclerosis.[38] Accordingly, one study showed that high levels of 1,25-dihydroxyvitamin D are relevant to Th2 skew and increased Tregs in multiple sclerosis.[39] In a skin immune lesion model, topical application of 1,25-dihydroxlvitamin D can suppress antigen-induced CD8+ cell activation through induction of antigen-specific Tregs.

[30] In addition to inducing CD14 for innate immunity, 1,25-dihydroxyvitamin D can

also up-regulate antimicrobial peptides such as cathelicidin and beta-defensin by macrophages in the gastrointestinal track.[13, 31] In fact, activation of toll-like receptors in human macrophages can induce cathelicidin antimicrobial peptide, which is inhibited by either a VDR antagonist or Lorlatinib a non-specific inhibitor against 1-hydroxylase activity, suggesting that de novo synthesis of 1,25-dihydroxyvitamin D is required for cathelicidin induction.[32] Induction of beta-defensin expression by 1,25-dihydroxylvitamin D requires additional activation of NF-kappaB sites, which are adjacent to its VDRE via a mechanism involving IL-1, suggesting converge of inflammatory signals and immune regulation.[33] Thus, VD-induced antimicrobial

peptides in the gastrointestinal track may represent a typical example of host defense modulation of the innate immune system. Th1 cells secrete pro-inflammatory cytokines, including interferon-gamma (IFN-gamma) and IL-2, and activate B cells to produce immunoglobulin IgG2a. A large body of evidence has demonstrated that VD/VDR can suppress Th1 lymphocytes by mechanisms such as down-regulation of IL-2, a key cytokine for T cell proliferation and activation.[34] BMS-777607 clinical trial Moreover, 1,25-dihydroxyvitamin D also suppresses IL-12 and IFN-gamma, the two major Th1 cytokines for acute immune responses.[35] In contrast, Th2 cells secrete IL-4 and IL-10, and induce the production of IgG1 and immunoglobulin E (IgE) by B cells, in a manner skewed to immune regulation. Interestingly, activated monocytes and dendritic cells from the innate immune system, and B cells from the find more adaptive immune system produce IL-12, which induces Th0 to become Th1 cells. Consequently, activated Th1 cells induce inflammation by generating IFN-gamma and TNF-alpha. For such regards, 1,25-dihydroxyvitamin D suppresses IL-12 production by

monocytes and B cells, thus consequently restraining Th1 activation.[36] Epidemiologic studies have shown that low blood VD levels are associated with autoimmune diseases. In particular, the potential role of VD in immune regulation by induction of T-regulatory cells (Tregs) is under extensive scrutiny. For example, bioactive VD was found to potentiate Treg activity,[37] and low levels of 25-hydroxy VD in the circulation are associated with compromised Treg function and high incidence of multiple sclerosis.[38] Accordingly, one study showed that high levels of 1,25-dihydroxyvitamin D are relevant to Th2 skew and increased Tregs in multiple sclerosis.[39] In a skin immune lesion model, topical application of 1,25-dihydroxlvitamin D can suppress antigen-induced CD8+ cell activation through induction of antigen-specific Tregs.

We identified 26 groups; GSK3235025 in vitro nine were monitored in both years. Group size ranged from two to eight (mean±se=3.14±0.30, N=35) with 15 (42.86%) of 35 pairs accompanied by one to six subordinates. There were no inconsistencies between methods of identification (ear-tag vs. digital photographs). Group size increased significantly (F(1,33)=7.860, R2=0.165, P=0.008) (Fig. 3) and subordinates were more likely to be present (Wald χ2=6.995, P=0.008) further from the fur seal colony. Visual tracking and re-sightings of individually identifiable jackals confirmed that all groups travelled to the colony. Commuting distance varied from 0.45 to 20.03 km (mean±se=5.70 km±0.96,

N=35). We recorded 39 highways in eleven 1 km transects (mean±se=3.50 highways km−1±1.17). Highway density declined significantly with distance from the colony (F(1,9)=13.626, R2=0.602, P=0.005), (Fig. 4). We recorded agonistic and self-advertisement behaviour by all 12 dominant pairs. Agonistic behaviours involved chasing (N=86) of Topoisomerase inhibitor non-group, often same-sex, individuals at a run or trot

with ears pinned back, head down, back straight or arched and tail straight down or swishing. Intruders responded by moving away immediately or following display of submissive behaviour. Physical contact through fighting or biting was not recorded as part of territorial defence during the 6 week focal observations. We recorded 78 boundary displays in which neighbouring pairs would pace along their boundary in parallel, scent-marking frequently and emitting loud vocalizations. Self-advertisement through vocalizations (N=38) and tandem scent-marking (raised-leg urination, typically accompanied by scratching and rubbing) by the dominant pair (N=1419) was observed within or on the border of their territory. Additional, opportunistic observations during October to February confirmed self-advertisement and defence behaviour persisted outside of the 6-week focal observation

periods. Territory size was calculated for 12 different groups and for three in both years. Territory size ranged from 0.20 learn more to 11.11 km2 (mean±se=3.12 km2±0.98, N=15), increased significantly with distance from the colony (Wald χ2=46.140, P=<0.001) (Figs 1 and 5), but was independent of group size (Wald χ2=1.180, P=0.292) and presence of subordinates (Wald χ2=1.392, P=0.238). Among groups that were successful in breeding there was no relationship between number of dens and territory size (Wald χ2=0.624, P=0.430). For two of three groups for which territory size was estimated in both years, no substantial changes in territory size were observed. For one group, territory size declined by 64% in the second year of study (Fig. 1). Notably this group failed to breed in 2005. Although territory boundaries shifted over time there was consistency in space use by these three pairs between years, indicating site fidelity.