Funding sources include NOAA Cooperative Agreement NA09OAR4320129, PO EA133F09SE4792, the M. S. Worthington Foundation, the North Pond Foundation, Sloan and Hardwick Simmons. The research and disentanglement was conducted under National Oceanic Atmospheric Administration Permit 932-1905-00/MA-009526 issued to Dr. Teresa Rowles. Appendix S1. Estimation of body weight from length. Table S1. Width-to-total body length ratios at intervals of 10% of the body for 10 mesomorphic right whales and Eg 3911. “
“Understanding the reproductive parameters of

very small or declining populations selleck inhibitor is of clear importance to conservation. From 1995 to 2011 we recorded calf production (n = 71) and calf survival for 27 breeding females in the bottlenose dolphin (Tursiops truncatus) population in Doubtful Sound, New Zealand; a population with a recent history of declining abundance. Overall, 67% of calves survived their first this website year, and 40% survived to 3 yr (or are 2 yr old and still alive). Most calves that died in the first year died in their first month (87%). Multiparous mothers (n = 18) showed high

variation in calf survival. The most successful six had all but one of their 20 calves (95%) survive to 1 yr. Fourteen of the 20 (70%) survived to 3 yr, and another four are still alive and are 1 or 2 yr old. In contrast, the least successful seven mothers produced a similar number of calves (21), eight of which (38%) survived to 1 yr, and none to 3 yr. Here we describe calving seasonality and calf survival, observed over 16 yr, and

show that large variation in reproductive success of individual females is an example of extreme demographic stochasticity in this small, endangered population. “
“Telomeres are the protective caps at the ends of all eukaryotic chromosomes. Because DNA replication of chromosome ends is incomplete, telomeres undergo sequence loss with each cell division resulting in the progressive shortening of their lengths. Telomere shortening with age is known from terrestrial mammals. We test whether this pattern is shared by marine mammals, by comparing telomere lengths between age classes in a pinniped species, the Australian sea PFKL lion (Neophoca cinerea). Telomere lengths were measured using a real-time quantitative polymerase chain reaction (PCR) method in specimens from three age classes: pup (<1.5 yr), juvenile (1.5–5 yr), and adult (>5 yr). Mean telomere lengths of the adults were significantly shorter than the juvenile and pup classes. However, we were unable to differentiate between pups and juveniles. These findings confirm that the Australian sea lion shares the general pattern of shortening telomere lengths with age as documented in terrestrial mammals.

In the trial, 548 patients were randomized to receive 90 mg/day of vitamin K2, 45 mg/day of vitamin K2, or placebo. The trial showed no difference in disease-free survival in the placebo group, compared with the combined treatment

group, nor any dose-dependent increase in disease-free survival between the two vitamin K2 treatment groups. The hypothesis of this trial was based on preclinical studies that suggest vitamin K2 or its analogs could inhibit the growth of HCC via suppression of cyclin D1,14, 15 and a previous randomized trial that suggested vitamin K2 might prevent the development of HCC in female patients with underlying cirrhosis.16 However, it has to be noted that the study in female cirrhosis patients was not initially designed see more to test the hypothesis that vitamin K2 could prevent the development

find more of HCC, but rather it was an extension of the follow-up of a study to investigate the effect of vitamin K2 on bone loss in female cirrhotic patients. The sample size was only 40 patients in total in that study, and it was possible that the reduction in HCC incidence in the group treated by vitamin K2 was just a chance event. Two subsequent small-scale randomized trials with 45 patients and 60 patients, respectively, failed to demonstrate a significant effect of vitamin K2 on the recurrence of HCC after resection or ablation.17, 18 Hence, the negative result demonstrated by this larger scale phase II/III trial of Yoshida et al. is not surprising. However, it remains questionable whether the trial is convincing enough to reject any potential benefit of vitamin K2 in HCC, as suggested in preclinical studies. The trial had a large sample size, but it was flawed by two problems in its design. First, it included patients with intrahepatic recurrence treated by reresection, in addition to treatment-naïve patients. There may be a higher risk of metastatic recurrence in patients who have already developed recurrence after previous treatment, compared PLEK2 with patients with newly diagnosed HCC. If the role of vitamin K2 is mainly inhibition of de novo hepatocarcinogenesis in cirrhosis, as suggested by the previous study on female cirrhotic patients,16 inclusion

of patients with a high risk of metastatic recurrence made it more difficult to demonstrate the benefit of vitamin K2 on de novo recurrence. Second, the study was terminated prematurely approximately 1.5 years after the start of the study. The short median follow-up of patients also made it difficult to detect any benefit of vitamin K2 on de novo recurrence, which tends to occur at least 1-2 years after resection. Nonetheless, it is unlikely that there will a further large-scale randomized trial on the effect of vitamin K2 on recurrence of HCC after resection, given the negative result of this study. The management of HCC has entered a new era of molecular targeted therapy after sorafenib has been demonstrated to improve the survival of advanced HCC patients in the SHARP trial.

angiodysplasia; 2. Meckel’s find more diverticulum; 3. gastrointestinal hemorrhage; 4. ectopic pancreas; 5. angiography Presenting Author: DONG KU KANG Additional Authors: DAE HWAN KANG, CHEOL WOONG CHOI, SU BUM PARK, JOUNG BOOM HONG, DONG JUN KIM, YOUNG SHIN SHIN, YU YI CHOI, MIN DAE KIM, EUL JO JEONG, HYUNG WOOK KIM Corresponding Author: DONG KU KANG Affiliations: Pusan National University Yangsan Hospital, Pusan National University Yangsan Hospital, Pusan National University Yangsan Hospital, Pusan National

University Yangsan Hospital, Pusan National University Yangsan Hospital, Pusan National University Yangsan Hospital, Pusan National University Yangsan Hospital, Bongseng Memorial Hospital, Jinju Bokum Hospital, Pusan National University Yangsan Hospital Objective: Performing emergency endoscopy is essential to diagnose and treat patients with acute GI bleeding. Early endoscopy (within 24 hours) is the standard treatment option for the patients with acute NVUGIB. According to several studies that analyzing the efficacy of emergency endoscopy, the need for urgent endoscopy (within 8 hours) is a matter of debate. This study compares

the outcomes of urgent endoscopy (within 8 hrs) with early endoscopy (from 8 to 24 hours). Methods: We have enrolled 434 patients who visited ER from January 2009 to December 2013 for hematemesis, melena, or/and hematochzia with blood or altered blood in the nasogastric aspiration. Patients with non-variceal Romidepsin research buy upper GI bleeding who previously underwent upper endoscopy within 24 hours were analyzed and received intravenous proton pump inhibitor (PPI). Based on the timing of the endoscopy, patients were classified into two groups; urgent (<8 hrs) and early (8–24 hrs). We defined positive endoscopic yield as the presence of definite bleeding sites and high-risk stigmata of recent bleeding such as adherent clots, non-bleeding visible vessels

Thiamet G and active bleeding. Results: We identified 224 patients who enrolled the inclusion criteria. There was no significant difference in outcomes between the two groups. The positive endoscopic yield for the urgent and early endoscopy groups were similar at 81/105(77.1%) and 100/119(84%), respectively (p = 0.17). There were no differences of outcomes between the urgent and early endoscopy groups with regard to in-hospital mortality (1.9% vs 2.5%, p = 0.75), need for repeat endoscopy within 72 hrs (10.5% vs 6.8%, p = 0.40), median packed red blood cell requirements (1.78 vs 1.73 unit, p = 0.84), need for hemostatic therapy (31% vs 43%, p = 0.05) and mean length of hospital stay (6.43 ± 5.61 vs 6.25 ± 6.42 days, p = 0.82). Conclusion: According to our retrospective study, there was no difference in the outcomes of performing urgent (<8 hrs) endoscopy compares to early (8–24 hrs) endoscopy. Therefore, we can conclude that the urgent endoscopy is not necessary for patients with acute upper gastrointestinal bleeding. Key Word(s): 1. gastrointestinal bleeding; 2.

Positional

cloning indicated that the hio mutation affects the raldh2 gene encoding retinaldehyde dehydrogenase type2 (RALDH2), the enzyme principally responsible for retinoic acid (RA) biosynthesis. Mutations of raldh2 in zebrafish preclude the development of pectoral fins. Interestingly, in hio mutants, expression of wnt2bb in the lateral plate mesoderm (LPM) directly adjacent to the liver-forming endoderm was completely lost. Conclusion: Our data reveal the unexpected finding that RA signaling positively regulates the wnt2bb gene expression required for liver specification in medaka. These results suggest that a common molecular mechanism may underlie liver and pectoral fin specification during piscine embryogenesis. (HEPATOLOGY 2009.) Embryonic liver development occurs in multiple stages that are governed by hormonal factors as well as by intercellular and matrix–cellular interactions. In mice, liver ontogeny initiates on approximately AZD2014 embryonic day 9 (E9), when epithelial cells of the foregut endoderm interact with the cardiogenic mesoderm and commit to becoming the liver primordium. The liver primordium proliferates and invades the mesenchyme of the septum transversum to give rise to the hepatic codes and bud at E9.5.1, 2 Over the last decade, studies in rats and mice have greatly expanded the list of molecules known to contribute to liver development; however, it is likely that many more factors are

involved in this complex process. In particular, the Neratinib cell line mechanism underlying the local induction of liver formation remains poorly understood. This gap in our knowledge is reflected in the dearth of reports on rodent mutations that specifically interfere with the initial specification of the liver anlage. Small fish are particularly suitable for mutational investigations because they are easy to rear in a relatively compact space, their generation times are reasonably short, and they produce transparent embryos. In many

fish species, embryos develop outside the mother’s body, 3-oxoacyl-(acyl-carrier-protein) reductase making it easy to inspect them visually and to manipulate their tissues and cells. Our group has previously used systematic mutagenesis in medaka to generate numerous mutations affecting various aspects of liver development and function.3–5 The focus of this paper is the recessive mutation hiohgi (hio). In wild-type (WT) medaka, the hepatic bud forms from the endoderm rod at stage 25 (50 hours post-fertilization at 27°C; 18–19 somite stage).6 In medaka hio embryos, the liver does not appear until stage 29 and is small and malformed. In addition to this liver defect, hio mutant embryos lack pectoral fins and die after hatching. These phenotypes suggested to us that the study of hio mutants might allow the dissection of various aspects of embryonic specification and perhaps the linking of liver formation to fin formation. The signaling pathway of vertebrate limb formation has been studied in detail.

In this issue of HEPATOLOGY, Kahraman et al.13 report that hepatic NK cells, expression of NK cell–associated cytotoxic mediators (such as tumor necrosis factor–related apoptosis-inducing ligand [TRAIL]), NKG2D, and MICA/B messenger RNAs in the liver are significantly elevated in nonalcoholic steatohepatitis (NASH) and, to a lesser extent, in nonalcoholic fatty liver (NAFL), when compared to normal healthy control livers. Immunohistochemical analyses reveal

that MICA/B proteins are detected from hepatocytes in patients with NASH and NAFL. Moreover, the expression of MICA/B messenger RNAs are positively correlated with NAS score and hepatocyte apoptosis in NASH. These findings suggest that the MICA/B protein levels are up-regulated in hepatocytes from patients with NASH through mechanisms that have yet to be identified. check details This is then followed by activation of hepatic NK cells that release TRAIL as a means of killing hepatocytes, and thereby inducing hepatocelluar damage in these patients. It is not clear whether NK cells only kill MICA/B-positive hepatocytes or if they also kill MICA/B-negative cells. This could be confirmed by performing double-staining to determine whether MICA/B protein and terminal deoxynucleotidyl transferase–mediated dUTP nick-end Epigenetic Reader Domain inhibitor labeling (TUNEL+) hepatocytes are colocalized. Whereas the molecular mechanism underlying up-regulation of hepatic MICA/B

in NASH and NAFL patients was not explored in the study by Kahraman et al.,13 it has been well documented that expression of NKG2D ligands are up-regulated through a variety of stimuli that have been collectively termed “cellular stress”, such as cellular transformation, viral infection, and/or DNA damage.2, 3 It is known that fat accumulation can generate oxidative stress-induced DNA damage in hepatocytes,14 which may contribute to the up-regulation of hepatic MICA/B Protein kinase N1 in patients with NASH and NAFL. Interestingly, Kahraman et al.13 also show that levels of MICA/B messenger RNAs correlate positively with stage of fibrosis, suggesting that MICA/B also contribute to the progression of liver fibrosis. However, recent studies using

murine models of liver fibrosis suggest that the NKG2D-ligand interaction triggers the killing of activated hepatic stellate cells (HSCs) by NK cells through a TRAIL-dependent mechanism, thereby inhibiting liver fibrosis.15, 16 Liver fibrosis is a common scarring response to virtually all forms of chronic liver injury and is characterized by HSC activation and accumulation of collagen in the liver. In normal healthy livers, HSCs are quiescent, storing large amounts of vitamin A (retinol). During liver injury or culturing on plastic dishes, HSCs become activated and differentiate into myofiboblast cells that produce collagen. Activated HSCs can also become senescent during chronic liver injury or after 9–15 passages in vitro.

The accuracy of CAP for the detection and quantification of hepatic steatosis was assessed based on histological findings according to the Nonalcoholic Steatohepatitis Clinical Research Network Scoring System. Data for 101 NAFLD patients (mean age 50.3 ± 11.3 years old, 51.5% male) and 60 non-NAFLD controls were analyzed. CAP was associated with steatosis grade (odds ratio [OR] = 29.16,

P < 0.001), body mass index (BMI; OR = 4.34, P < 0.001) and serum triglyceride (OR = 13.59, P = 0.037) on multivariate analysis. The median CAP for steatosis grades S0, S1, S2, and S3 were 184 dB/m, 305 dB/m, 320 dB/m, and 324 dB/m, respectively. The areas under receiver operating characteristics curves (AUROC) for estimation of steatosis grades ≥ S1, S2, and S3 were 0.97,

0.86, and 0.75, respectively. The optimal CAP cutoffs for estimation of steatosis grades ≥ S1, S2, and S3 were 263 dB/m, 281 dB/m, and 283 dB/m, respectively. Among non-obese patients, the AUROC for estimation of steatosis grades ≥ S1 and S2 were 0.99 and 0.99, respectively. Among obese patients, the AUROC for estimation of steatosis grades ≥ S1, S2, and S3 were 0.92, 0.64, and 0.58, respectively. CAP is excellent for the detection of significant hepatic steatosis. However, its accuracy is impaired by an increased BMI, and it is less accurate to distinguish between the different grades of hepatic steatosis. “
“Toll-like receptors (TLR) are the germline-coded pattern recognition receptors that sense microbial products. This signaling orchestrates complex signaling pathways that induce expression of inflammatory genes for host defense against invading microorganisms. Recent studies illustrate

the role of TLR on non-infectious inflammatory diseases. The liver Obeticholic Acid chemical structure has a unique anatomy bridging with the intestine by portal vein and bile ducts. This allows delivery of products from intestinal microflora directly into the liver. Subsequently, microbial products cause acute and chronic inflammation through TLR signaling in the liver. Not only exogenous products, but endogenous denatured products released from dying cells also facilitate inflammation even in sterile conditions. Consequently, these responses elicit tissue repairing including liver regeneration and fibrogenesis. An check details aberrant regenerative response may lead to hepatic carcinogenesis. In this review, we highlight the recently accumulated knowledge about TLR signaling in liver regeneration, fibrosis and carcinogenesis. “
“Although it is assumed that hemodynamic responders to pharmacological therapy after a variceal hemorrhage are adequately protected from rebleeding, there is no evidence that either this response or its protective effect extend beyond the usual 2-year follow-up featured in available studies. We aimed to assess the maintenance of hemodynamic response and its impact on outcomes in a large cohort of hemodynamic responders during a long follow-up.

25 To determine whether IL30 requires the other subunit, EBI3, to form a heterodimer for maximizing inhibition of IL12 toxicity, we compared the efficacy of IL30 to either EBI3 or IL27. Interestingly, IL30 is more potent

than IL27 or EBI3 in inhibiting IL12-induced toxicity in the liver, including the reduction of the number of liver lesions (Fig. 5A,B) and alanine aminotransferase (ALT) / aspartate aminotransferase (AST) levels (Supporting BEZ235 datasheet Fig. 4), suggesting that IL30 may act independently of IL27. To further this hypothesis, we used EBI3 knockout (EBI3−/−) mice. As expected, IL30 reverses IL12 hepatotoxicity in EBI3−/− mice, whereas reconstitution of IL27 or overexpression of EBI3 does not affect liver toxicity Ferroptosis mutation (Fig. 5A,B). One potential mechanism that explains the protective role of IL30 in the absence of EBI3 could be that IL30 competes or is more efficient than IL27 in occupying WSX1, therefore initiating downstream signaling independently of IL27. To confirm this hypothesis, the effect of IL30 on IL12-mediated toxicity was tested in WSX1−/− mice. If IL30 signals through WSX1 and competes with IL27 for signaling, then the lack of WSX1

would demolish the ability of IL30 to inhibit liver toxicity. The same as is found in wildtype mice, IL30 inhibits the number of liver lesions and the amount of the liver transaminases released in the serum in WSX1−/− mice (Fig. 5A,B; Supporting Fig. 4). These results confirm that the hepatoprotective selleck kinase inhibitor role of IL30 is independent of the IL27 pathway. Because IL12 induces IL30 expression by way of IFN-γ, we then asked whether IL30 might inhibit IL12 toxicity by way of inhibition of IFN-γ expression. As such, we determined whether IL30 inhibits IL12-mediated IFN-γ expression

in wildtype, EBI3−/−, and WSX1−/− mice. As expected, IL30 inhibits circulating IFN-γ levels (Fig. 6A). This observation once more confirms the IL27- and WSX1-independent function of IL30. Of interest here is that the number of lesions induced by IL12 is lower in the EBI3−/− and WSX1−/− when compared with wildtype mice (Fig. 5B), although the level of IL12-mediated IFN-γ induction is heightened in the absence of WSX1 or EBI3. This discrepancy could be explained by the increased induction of IL30 in these mice (Supporting Fig. 5), which counteracts the toxic effect from increased IFN-γ and reduces toxicity in livers. To further confirm that IFN-γ plays a key role in IL12-mediated liver injury and IL30 inhibits IFN-γ expression, both proinflammatory cytokines were coadministered into mice. As expected, coadministration of IL12 and IFN-γ enhanced toxicity of the liver when compared with IL12 alone (Fig. 6B,C), further demonstrating IFN-γ’s role in hepatotoxicity. Meanwhile, the addition of IL30 significantly reduced the number of lesions in the liver (Fig. 6C).

Recently, Scisciani and colleagues demonstrated that lipopolysaccharide, AZD1152-HQPA manufacturer lymphotoxin-α, and tumor necrosis factor-α inflammatory pathways activated miR-224 expression. In addition, these authors identified p65/NFκB as a direct transcriptional regulator of miR-224 expression.[36] In our study,

increased expression of miR-224 upon HCV reactivation is in accordance with the findings of Scisciani and colleagues,[36] as NFκB-dependent inflammatory pathway is a key process during HCV infection.[37] Increased expressions of miR-221, miR-224, and miR-217 were observed in samples taken after administration of IFN/RBV treatment as compared with the pretreatment samples. miR-224 was able to recognize OCLN as a target mRNA. miR-221 expression is dysregulated in HCC[38] and is suggested to be affected by HCV and IFN. Liu EGFR tumor and colleagues demonstrated that miR-221 was downregulated after HCV exposure, and the gain of miR-221 enhanced HCV RNA abundance in a dynamic in vitro HCV infection system.[9] Zhang and colleagues knocked down miR-221 and miR-222 in glioblastoma cells and reported that IFN-α was the most significantly affected signaling pathway.[39] Interestingly, we found that miR-221 expression level negatively correlated with HAI. miR-217 was previously shown to potentially predict therapy response in chronic HCV-infected patients[40] and was found to be related to tumor differentiation

as well.[14] We observed relevant alterations of microRNA expressions in the SVR group, whereas microRNA expression levels remained stable in non-responders after IFN/RBV treatment in comparison with pretreatment levels. Partial responders following completed antiviral therapy were only three patients; therefore, these patients were analyzed together within the NR group. It was recently revealed that hepatic microRNA expression could be associated with drug response[3]; however, our study did not reveal a predictive value of pretreatment microRNA levels, including miR-122, for the success of IFN/RBV treatment. Previously, Sarasin-Filipowicz and colleagues demonstrated markedly

decreased pretreatment miR-122 levels in patients who had no virological response during later IFN therapy.[31] Estrabaud and colleagues reported deregulated miR-99a*, miR-181a-2*, miR-23a, and selleck chemicals miR-217 in non-responders compared with patients with later SVR.[40] In contrast, our study revealed upregulated miR-96, miR-99a*, miR-122, miR-181a-2*, miR-217, and miR-221 expressions after IFN/RBV treatment in the SVR group when compared with the NR group. In addition, following antiviral treatment, miR-221 and miR-122 levels were higher in SVR when compared with pretreatment levels. This suggests that antiviral therapy restored miR-122 expression in SVR patients. miR-122 is considered a differentiation and homeostatis marker in hepatocytes.

Mismatch negativity (MMN) is an auditory event-related potential elicited when a sequence of repetitive standard sounds is interrupted infrequently by deviant “oddball” stimuli. The MMN is a measure of cortical activity in response to the deviant sound and reflects an automatic, memory-based, comparison process.17-22 It can be rapidly assessed, elicited while the individuals are performing other tasks or sleeping, and reflects preattentive sensory memory and involuntary attention.17 The area under the MMN wave in frontal electrodes is

reduced in patients with schizophrenia, compared to controls, and the area correlates with the degree of cognitive impairment.18 PF-562271 in vitro Histone Methyltransferase inhibitor Baldeweg et al.18 suggested that altered MMN in schizophrenia reflects an impaired attentional trigger, which would be a consequence of deficits in N-methyl-D-aspartate (NMDA) receptor-dependent neural processes underlying it. These and other studies19-22 support that, in schizophrenia, alterations in neurotransmission associated with NMDA receptors lead to impaired attention and cognitive

function, which are reflected in altered MMN, and result in impairment in everyday functioning, including sustained attention impairment. Patients with MHE also show impaired attention (including sustained attention) and cognitive function, which result in impairment in everyday functioning. Altered neurotransmission associated with NMDA receptors is a main contributor to cognitive impairment in animal models of HE.23-26 It is, therefore, likely that altered NMDA-receptor neurotransmission in the cortex could also contribute to attention deficits in MHE. This should be reflected in alterations in MMN. We hypothesized that patients with MHE, similarly find more to those with schizophrenia, should show alterations in MMN, which would be related with attention deficits. The aim of this work was to assess whether (1) MMN is altered in cirrhotic patients with MHE, compared to those

without MHE and to controls without liver disease, (2) MMN changes in parallel with performance in attention tests and/or with MHE in a longitudinal study; and (3) MMN predicts performance in attention tests and/or in the Psychometric Hepatic Encephalopathy Score (PHES). We performed MMN analysis and attention tests in 34 controls without liver disease, 37 patients with liver cirrhosis without MHE, and 23 with MHE. We used the Stroop and Map search tests to assess selective attention and the Elevator Counting test to assess sustained attention as well as visuomotor and bimanual coordination tests. We analyzed, in the same patients, the critical flicker frequency, proposed as an alternative method to detect MHE.

We applied this approach to geolocation tracking data on migration in three Eudyptes species, from three localities in the southern Indian Ocean (five populations). Sex had a subtle and consistent influence on the temporal activity of the 66 animals during their migratory journey. Males began migration to the breeding localities earlier than females, by an average of 9.1 (range: 4.5–13.5) days. This difference was statistically significant in 4 of 5 populations, and occurred among

all species, sites and years surveyed. Our study shows an original application of a recent modelling approach to detect change point in movement data. Our results suggest that sex-specific constraints related to breeding in migrating animals may also modify activity NVP-BGJ398 molecular weight schedules well before breeding commences. Understanding the interplay between successive periods of the life cycle in migratory animals has long been constrained by our inability to track individuals

across this website different phases (Sorensen et al., 2009). To track migrating animals’ movements over their complete non-breeding phase is difficult indeed, especially marine species such as seabirds, which are generally inaccessible when not breeding (Hamer, Schreiber & Burger, 2002). Consequently, our knowledge about their non-breeding phase has long remained poor (Warham, 1975; Stahl et al., 1985; Williams, 1995). However, over the last two decades, both animal-borne tracking and movement data analysis techniques have considerably improved and unravelling the behavioural adjustments taking place at sea may now be feasible (Wilson & Vandenabeele, 2012). In this study we therefore used some of the latest developments in both tracking and data analysis to investigate how the sex-specific adjustments on arrival date in their upcoming breeding season may affect migration patterns in penguins. We focused on the crested penguins (genus Eudyptes).

This is the most diverse penguin genus, and their complete selleck chemicals llc non-breeding phase while at sea is now well described for several species, thanks exclusively to the use of recently developed, ultra-miniaturized light-based geolocation loggers (GLSs). Penguins are very sensitive to instrumentation (Bannasch, Wilson & Culik, 1994), which precludes the use of large archival tags for extended periods at sea for both technical and ethical reasons. However, the size, shape and logging capacity of GLSs allowed us to collect data during their entire period of 5–7 months at sea, without major ethical considerations. Eudyptid penguins can venture thousands of kilometres from their colonies to reach their wintering areas, travelling ∼50 km per day (see Bost et al., 2009; Thiebot et al., 2011, 2012). Among studies on crested penguin species over the non-breeding season, no significant sex differences in foraging areas have been reported (Pütz et al., 2002, 2006; Raya Rey, Trathan & Schiavini, 2007; Bost et al.