3.5 (Excoffier and Lischer 2010). A Bonferroni correction was implemented to the P values. Genepop v. 4.0 (Rousset Trichostatin A chemical structure 2008) was used to test for linkage disequilibrium between all pairs of loci for each population (1,000 dememorization iterations, 1,000 batches, 10,000 iterations

per batch). Genetic diversity measures such as mean number of alleles per locus as well as observed and expected heterozygosities for each population were calculated in ARLEQUIN. The program FSTAT (Goudet 1995) was used to estimate another measure of genetic diversity, allelic richness, as well as to assess population differentiation between the putative populations by estimating the fixation index FST. Bonferroni correction was not applied (Narum, 2006). FSTAT was also used to analyze sex-biased dispersal among putative populations (Oceanic, Coastal, and Hauraki Gulf) by calculating FIS, HO, HE, and applying FST statistics to each sex independently. Jost estimated DEST (Jost 2008) was also calculated as a measure of pairwise population differentiation in SMOGD (Crawford 2010). A principal component analysis (PCA) was performed on a table of allele frequencies using the R packages ade4 (Thioulouse et al. 1997) and Akt inhibitor adegenet (Jombart 2008) as an exploratory

analysis to infer population differentiation (Jombart et al. 2009). The program STRUCTURE v.2.3.3 (Hubisz et al. 2009) was used to infer population structure 上海皓元医药股份有限公司 by assigning individuals (probabilistically) to clusters without a priori knowledge of population units and limits. The algorithm implemented in this program estimates the log-likelihood of the data for a given number of genetic clusters (K), under the assumption of Hardy-Weinberg and linkage equilibrium within clusters. We used the admixture model, which assumes that individuals have admixed ancestry. We performed 10 independent runs for each K from 1 to 6 using the correlated allele frequency with 1,000,000 repetitions and a burn in of 100,000. The estimated Ln probability for the data was averaged across the runs for each K. Structure Harvester (Earl and von Holdt 2012) was used to detect the most

likely K based on the Evanno method (Evanno et al. 2005). Population differentiation was additionally tested using a one level hierarchical analysis of molecular variance (AMOVA) in ARLEQUIN v. 3.5 using 10,000 randomizations, in which the existence of differentiation among the three populations was tested. Estimates of recent migration rates between putative populations were determined using a molecular assignment program that relies on a nonequilibrium Bayesian approach method through Markov Monte Carlo techniques, as implemented in BAYESASS (Wilson and Rannala 2003). This program estimates asymmetrical rates of migration between populations over the last several generations. The program was run using default settings.

Although disruption of PD-1 signaling after anti–B7-H1 monoclonal antibody treatment augmented hepatocellular damage, its stimulation following B7-H1 immunoglobulin (B7-H1Ig) fusion protected livers from IRI, as evidenced by low serum alanine aminotransferase levels and well-preserved liver architecture. The

therapeutic potential of B7-H1 engagement was evident by diminished intrahepatic T lymphocyte, neutrophil, and macrophage infiltration/activation; reduced cell necrosis/apoptosis but enhanced anti-necrotic/apoptotic Bcl-2/Bcl-xl; and decreased proinflammatory chemokine/cytokine gene expression in parallel with selectively increased interleukin (IL)-10. Neutralization of IL-10 re-created liver IRI and rendered B7-H1Ig–treated hosts susceptible to IRI. These findings

were confirmed in Carfilzomib mw T cell–macrophage in vitro coculture in which B7-H1Ig diminished tumor necrosis factor-α/IL-6 levels in an IL-10–dependent manner. Our novel findings document the essential role of the PD-1/B7-H1 pathway in liver IRI. Conclusion: This study is the first to demonstrate that stimulating PD-1 signals ameliorated liver IRI by inhibiting T cell activation and Kupffer cell/macrophage function. Harnessing mechanisms of negative costimulation by PD-1 upon T cell–Kupffer cell cross-talk may be instrumental in the maintenance of hepatic homeostasis by minimizing organ damage and promoting IL-10–dependent cytoprotection. (HEPATOLOGY 2010.) Liver ischemia and reperfusion injury (IRI), an exogenous antigen-independent inflammatory event, occurs Depsipeptide nmr in multiple clinical settings, including partial hepatectomy, trauma, and transplantation. IRI remains one of the most critical problems in liver transplant recipients, causing

up to 10% medchemexpress of early graft failure, in turn leading to a higher incidence of acute and chronic rejection and contributing to acute donor liver shortage.1, 2 Although its mechanism has not been fully elucidated, IR-triggered generation of reactive oxygen species inflicts tissue damage, which initiates circulatory disturbances, local inflammation, cell death, and organ failure. In 2003, we proposed that liver damage due to reperfusion following prolonged ischemia should be considered as an innate immunity-dominated inflammation response.2 Our group was among the first to document that activation of Toll-like receptor (TLR) 4 was required for the induction of IR-triggered hepatic inflammation and damage.3 By releasing inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and CXCL-10 downstream of TLR4 signaling, we have identified Kupffer cells as critical players in the mechanism of IRI.4, 5 In agreement with others,6 we have reported that T lymphocytes, particularly of the CD4 phenotype, represent the key mediators in IR-triggered liver IRI.

Although disruption of PD-1 signaling after anti–B7-H1 monoclonal antibody treatment augmented hepatocellular damage, its stimulation following B7-H1 immunoglobulin (B7-H1Ig) fusion protected livers from IRI, as evidenced by low serum alanine aminotransferase levels and well-preserved liver architecture. The

therapeutic potential of B7-H1 engagement was evident by diminished intrahepatic T lymphocyte, neutrophil, and macrophage infiltration/activation; reduced cell necrosis/apoptosis but enhanced anti-necrotic/apoptotic Bcl-2/Bcl-xl; and decreased proinflammatory chemokine/cytokine gene expression in parallel with selectively increased interleukin (IL)-10. Neutralization of IL-10 re-created liver IRI and rendered B7-H1Ig–treated hosts susceptible to IRI. These findings

were confirmed in Dabrafenib concentration T cell–macrophage in vitro coculture in which B7-H1Ig diminished tumor necrosis factor-α/IL-6 levels in an IL-10–dependent manner. Our novel findings document the essential role of the PD-1/B7-H1 pathway in liver IRI. Conclusion: This study is the first to demonstrate that stimulating PD-1 signals ameliorated liver IRI by inhibiting T cell activation and Kupffer cell/macrophage function. Harnessing mechanisms of negative costimulation by PD-1 upon T cell–Kupffer cell cross-talk may be instrumental in the maintenance of hepatic homeostasis by minimizing organ damage and promoting IL-10–dependent cytoprotection. (HEPATOLOGY 2010.) Liver ischemia and reperfusion injury (IRI), an exogenous antigen-independent inflammatory event, occurs Selleck Torin 1 in multiple clinical settings, including partial hepatectomy, trauma, and transplantation. IRI remains one of the most critical problems in liver transplant recipients, causing

up to 10% medchemexpress of early graft failure, in turn leading to a higher incidence of acute and chronic rejection and contributing to acute donor liver shortage.1, 2 Although its mechanism has not been fully elucidated, IR-triggered generation of reactive oxygen species inflicts tissue damage, which initiates circulatory disturbances, local inflammation, cell death, and organ failure. In 2003, we proposed that liver damage due to reperfusion following prolonged ischemia should be considered as an innate immunity-dominated inflammation response.2 Our group was among the first to document that activation of Toll-like receptor (TLR) 4 was required for the induction of IR-triggered hepatic inflammation and damage.3 By releasing inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and CXCL-10 downstream of TLR4 signaling, we have identified Kupffer cells as critical players in the mechanism of IRI.4, 5 In agreement with others,6 we have reported that T lymphocytes, particularly of the CD4 phenotype, represent the key mediators in IR-triggered liver IRI.

A total of 20 μg of S-100 MP protein from ST-treated Jurkat T cells and Huh-7 hepatoma cells was extracted and denatured with 0.1% (vol/vol) sodium dodecyl sulfate in phosphate-buffered saline, reduced and alkylated, digested with trypsin, and labeled with isobaric tags (4-plex iTRAQ; Applied Biosystems, Foster City, CA). The two digested extracts were

pooled and subjected to two-dimensional peptide fractionation and analyzed for their comparative proteomic signature by way of matrix-assisted check details laser desorption ionization/time of flight mass spectrometry.10 Subconfluent, serum-starved HSCs were preincubated with monoclonal blocking anti-human CD54 or isotype-matched (immunoglobulin G1 [IgG1]) control antibody (50 μg/mL; GeneTex Inc., Irvine, CA) for 120 minutes, washed, and incubated with Jurkat T cell–derived S100-MPs. S100-MPs were incubated with monoclonal blocking anti-human CD147 (Abcam, Cambridge, MA) or IgG1 control antibody (50 μg/mL; GeneTex Inc.) for 60 minutes prior to their addition to HSCs. HSCs were serum-starved for 24 hours, then washed with phosphate-buffered saline and fixed in cold methanol for 10 minutes. Nuclear translocation Selleckchem Y-27632 of p65 nuclear factor kappa B (NFκB) was detected by incubating cells

with polyclonal p65 antibody (1:100; Delta Biolabs) for 30 minutes followed by TRITC-conjugated anti-rabbit IgG (1:200, Dako, Germany). Representative images were documented using a scanning confocal microscope MCE (Carl Zeiss, Germany). Serum-starved HSCs were incubated with the inhibitors SB203580 (p38 MAPK), U0126 (extracellular signal-regulated kinases 1 and 2 [ERK1/2]), and LY294002 (phosphatidyl-inositol-3 kinase) (LC Labs, Woburn, MA) as described.11 The proteasome inhibitor MG132 (Rockland Inc.) was used to block NFκB nuclear translocation and activity. All data are presented as the mean ± SD. Differences between independent experimental groups were

analyzed using a two-tailed Student t test. P < 0.05 was considered statistically significant. Correlations of MP levels with histological grade and stage were calculated by best-fit linear regression analysis based on a 95% confidence interval. All calculations were performed with Prism 4 (GraphPad Software, Inc.). We searched for T cell–derived MPs in human plasma from normal controls and patients with chronic hepatitis. Pure S100-MPs that carried the MP marker Annexin V12, 13 and the T cell marker CD3 were present in human plasma (Fig. 1A). Their percentage increased significantly from 25% in healthy controls and patients with serologically mild hepatitis C (alanine aminotransferase [ALT] <40 IU/mL) to 31% in patients with serologically active hepatitis C (ALT >40 IU/mL and ALT >100 IU/mL) (Fig. 1B). The higher percentages were paralleled by a higher mean fluorescence intensity for CD3 (data not shown).

Frequent use (especially of caffeine-containing medications) can lead to an increase in headaches, resulting in “medication overuse headache” (MOH). To avoid this, OTC medication should be limited to no more than 2 days per week. In addition XL765 to MOH, prolonged overuse of acetaminophen can cause liver damage, while overuse of nonsteroidal anti-inflammatory drugs can lead to gastrointestinal bleeding.[5, 27-29] This recommendation is not intended to discourage appropriate intermittent use of OTC medications for headache. OTC medications are appropriate when they are reliably

effective and used sparingly. However, most medications that produce good short-term pain relief can paradoxically worsen headache over time when used too often, a situation termed medication overuse headache. Medication PI3K inhibitor overuse is a strong risk factor for the development of chronic forms of headache. One of the most important tasks of the physician is to help patients balance the desire for immediate relief of pain with longer term goals of preventing medication overuse

headache or other complications from medication use. In the case of OTC medications, it is difficult for physicians to monitor the frequency of medication use. It is easy for medication overuse to develop, especially when patients have frequent headache and perceive that medications sold without a prescription are likely to be safe. Thus, physician inquiry and advice about the frequency and type of medications patients are using to treat headache is very important.

Evidence is lacking about the type and amount of medication that can produce medication overuse headache, and individual susceptibility probably varies. Most experts believe, however, MCE公司 that limiting use of medication to 2 days per week makes medication overuse headache unlikely. Headache is among the principal reasons for physician visits and a common cause of emergency department visits. The costs of tests and treatments for headache are not insubstantial, and when unwarranted, they needlessly expose patients to potential harm. In a recent study of the treatments and procedures that contribute most to the $13 billion dollar annual cost of outpatient neurology visits, migraine alone was the diagnostic category with the second highest costs. For example, using data from the National Ambulatory Medical Care Survey, the authors estimated that CT scans ordered at neurology visits (many of which were probably done to evaluate headache) resulted in costs of roughly $358 million dollars (95% confidence interval $197–$519 million).[30] The American Headache Society encourages its members and all practitioners who treat people with headache disorders to help address the problem of low value care as we enter an age of medical scarcity and limited resources.

Each individual performed sequentially the congruent, neutral, and incongruent tasks, with 45

seconds per task. If a subject gives a wrong response, he or she must repeat the item. The number of items correctly named was quantified and adjusted by age, according to Spanish normality tables.34 The Map Search subtest version A of the everyday attention test was administered according to the manual to assess selective attention.35 The score is the number of items of 80 found in 2 minutes, and scaled-score equivalents of raw scores for four age bands are assigned to each subject.35 The Elevator Counting subtest version A was administered according Selleckchem JQ1 to the manual35 to evaluate sustained attention. This test consists of a board with a series of perforations of identical size arranged in six rows and six columns, perfectly aligned, but differently orientated, and a series of metal pieces that fits perfectly into the holes.36 The subject has to place the pieces, one by one, by rows into the perforations, until filling all the board. The test is performed twice, and total time is recorded. The test consists of moving a series

of metallic pegs, placed in one half of a pegboard, to the other half of the board, in order, by performing the movements symmetrically and simultaneously with both hands.37 The operation is repeated twice in each direction, and time is recorded as an index of bimanual coordination. The stimulation protocol and the MMN Alectinib research buy analysis were performed, as previously described,18 using a device for evoked potentials (NeuropackM1, 8-channels; Nihon-Kohden, Tokyo, Japan) and software for evoked potentials modified for MMN. Pure

sinusoidal tones (80-dB SPL, 5-ms rise/fall) were delivered binaurally via insert earplugs. A stimulus train consisted of a sequence of standard tones of one frequency and duration (10 ms), which were followed by an intertrain interval of 300 ms. The first tone of the next train (differing in frequency) corresponded to the “deviant.” Twelve frequencies, ranging in 50-Hz steps from 750 to 1,250 Hz, were used. MCE The number of tones in each stimulus train varied randomly and could be 2, 4, 8, 16, or 36. A total of 4,500 stimuli and 400 deviants were delivered. During the 45-minute EEG recording, subjects watched a silent self-selected video film. EEG was recorded continuously from electrodes Fz, F3, F4, Cz, and left and right mastoids placed according to the international 10-20 system. The vertical electrooculogram was recorded from electrodes placed above the right eye and the right outer canthus. System bandpass was 0-70 Hz, with a digital sampling rate of 500 Hz. The ground electrode was placed on the central forehead and reference on the bridge of the nose. Data were analyzed as previously described.18 Values are given as mean ± standard error of the mean.

Each individual performed sequentially the congruent, neutral, and incongruent tasks, with 45

seconds per task. If a subject gives a wrong response, he or she must repeat the item. The number of items correctly named was quantified and adjusted by age, according to Spanish normality tables.34 The Map Search subtest version A of the everyday attention test was administered according to the manual to assess selective attention.35 The score is the number of items of 80 found in 2 minutes, and scaled-score equivalents of raw scores for four age bands are assigned to each subject.35 The Elevator Counting subtest version A was administered according Venetoclax cell line to the manual35 to evaluate sustained attention. This test consists of a board with a series of perforations of identical size arranged in six rows and six columns, perfectly aligned, but differently orientated, and a series of metal pieces that fits perfectly into the holes.36 The subject has to place the pieces, one by one, by rows into the perforations, until filling all the board. The test is performed twice, and total time is recorded. The test consists of moving a series

of metallic pegs, placed in one half of a pegboard, to the other half of the board, in order, by performing the movements symmetrically and simultaneously with both hands.37 The operation is repeated twice in each direction, and time is recorded as an index of bimanual coordination. The stimulation protocol and the MMN selleck screening library analysis were performed, as previously described,18 using a device for evoked potentials (NeuropackM1, 8-channels; Nihon-Kohden, Tokyo, Japan) and software for evoked potentials modified for MMN. Pure

sinusoidal tones (80-dB SPL, 5-ms rise/fall) were delivered binaurally via insert earplugs. A stimulus train consisted of a sequence of standard tones of one frequency and duration (10 ms), which were followed by an intertrain interval of 300 ms. The first tone of the next train (differing in frequency) corresponded to the “deviant.” Twelve frequencies, ranging in 50-Hz steps from 750 to 1,250 Hz, were used. 上海皓元医药股份有限公司 The number of tones in each stimulus train varied randomly and could be 2, 4, 8, 16, or 36. A total of 4,500 stimuli and 400 deviants were delivered. During the 45-minute EEG recording, subjects watched a silent self-selected video film. EEG was recorded continuously from electrodes Fz, F3, F4, Cz, and left and right mastoids placed according to the international 10-20 system. The vertical electrooculogram was recorded from electrodes placed above the right eye and the right outer canthus. System bandpass was 0-70 Hz, with a digital sampling rate of 500 Hz. The ground electrode was placed on the central forehead and reference on the bridge of the nose. Data were analyzed as previously described.18 Values are given as mean ± standard error of the mean.

Each individual performed sequentially the congruent, neutral, and incongruent tasks, with 45

seconds per task. If a subject gives a wrong response, he or she must repeat the item. The number of items correctly named was quantified and adjusted by age, according to Spanish normality tables.34 The Map Search subtest version A of the everyday attention test was administered according to the manual to assess selective attention.35 The score is the number of items of 80 found in 2 minutes, and scaled-score equivalents of raw scores for four age bands are assigned to each subject.35 The Elevator Counting subtest version A was administered according selleck kinase inhibitor to the manual35 to evaluate sustained attention. This test consists of a board with a series of perforations of identical size arranged in six rows and six columns, perfectly aligned, but differently orientated, and a series of metal pieces that fits perfectly into the holes.36 The subject has to place the pieces, one by one, by rows into the perforations, until filling all the board. The test is performed twice, and total time is recorded. The test consists of moving a series

of metallic pegs, placed in one half of a pegboard, to the other half of the board, in order, by performing the movements symmetrically and simultaneously with both hands.37 The operation is repeated twice in each direction, and time is recorded as an index of bimanual coordination. The stimulation protocol and the MMN selleck compound analysis were performed, as previously described,18 using a device for evoked potentials (NeuropackM1, 8-channels; Nihon-Kohden, Tokyo, Japan) and software for evoked potentials modified for MMN. Pure

sinusoidal tones (80-dB SPL, 5-ms rise/fall) were delivered binaurally via insert earplugs. A stimulus train consisted of a sequence of standard tones of one frequency and duration (10 ms), which were followed by an intertrain interval of 300 ms. The first tone of the next train (differing in frequency) corresponded to the “deviant.” Twelve frequencies, ranging in 50-Hz steps from 750 to 1,250 Hz, were used. MCE公司 The number of tones in each stimulus train varied randomly and could be 2, 4, 8, 16, or 36. A total of 4,500 stimuli and 400 deviants were delivered. During the 45-minute EEG recording, subjects watched a silent self-selected video film. EEG was recorded continuously from electrodes Fz, F3, F4, Cz, and left and right mastoids placed according to the international 10-20 system. The vertical electrooculogram was recorded from electrodes placed above the right eye and the right outer canthus. System bandpass was 0-70 Hz, with a digital sampling rate of 500 Hz. The ground electrode was placed on the central forehead and reference on the bridge of the nose. Data were analyzed as previously described.18 Values are given as mean ± standard error of the mean.

Treating HBV-carrier mice with a dual-function short hairpin RNA (shRNA) vector, exerting both immunostimulatory and

HBx-silencing effects in vivo, efficiently inhibited HBV and increased type I IFN production. Most important, this therapy reversed HBV-induced hepatocyte-intrinsic immunotolerance and recovered systemic anti-HBV adaptive immunity by restoring hepatic CD8+ T-cell activation and proliferation as well as HBV-specific Ab responses. HepG2 cell lines were maintained in our laboratory and cultured in RPMI-1640 medium (GIBCO/BRL, Gaithersburg, MD) containing 10% fetal bovine serum (FBS). HepG2.2.15 cells (derived from HepG2 cells transfected with a plasmid carrying two head-to-tail copies of HBV genome DNA serotype ayw) were maintained in complete Dulbecco’s modified Eagle’s medium (DMEM) (GIBCO/BRL) supplemented selleck chemicals with 10% FBS. All cultures were incubated at 37°C and 5% CO2 in a humidified atmosphere. The TLR7 inhibitor was endotoxin-free oligodeoxyribonucleotide IRS661 (5′-TGCTTGCAAGCTTGCAAGCA-3′)15 (Takara, Japan). Neutralizing α-IFNR I Ab was from Millipore (Bedford, MA). HBV-carrier mice were established by hydrodynamic injection of pAAV/HBV1.2 plasmid (kindly provided by Pei-Jer Chen, National Taiwan University College) by way of the tail

vein into wild-type (WT) C57BL/6, IFN-γ−/− and Rag-1−/− mice. Four weeks later, hepatitis B surface antigen (HBsAg) was highly expressed in liver tissue, and HBV-carrier mice

(HBV+) were 上海皓元医药股份有限公司 defined as harboring serum HBsAg levels >500 ng/mL. For HBV vaccination, HBV vaccine (rHBs/CFA) was injected subcutaneously. All animal experiments and protocols were approved Raf inhibitor by the Committee on the Ethics of Animal Experiments of the Shandong University. Viral particles in supernatants and in mice sera were quantified by real-time polymerase chain reaction (PCR) according to the kit’s instructions (Da-An, Guangzhou, China). Primers detecting the HBV S region were 5′-ATCCTGCTGCTATGCCTCATCTT-3′ and 5′-ACAGGGGGAAAGCCCTACGAA-3′ as well as the 5′-FAM-TGGCTAGTTTACAGTGCCATTTG-TAMRA fluorescent probe. Quantitative PCR (qPCR) was performed in the iCycleriQ for 42 cycles. Multiparameter flow cytometry was performed according to a standard protocol. Surface or intracellular staining was performed using the following antimouse monoclonal Abs (mAbs) or Ab controls: FITC-conjugated immunoglobulin G (IgG) isotype, α-NK1.1, α-PD-1, α-PD-L1, α-CD8, and α-CD4; PE-conjugated IgG isotype, α-CD69, α-CTLA-4, α-IFN-γ, and α-perforin; PE-Cy5.5-conjugated IgG isotype, α-CD3, α-CD8, and α-CD25; allophycocyanin (APC)-conjugated IgG isotype, α-CD28, and α-CD107a. All Abs were purchased from eBioscience (San Diego, CA). Dimeric H-2Kb:Ig fusion protein (BD Biosciences, San Jose, CA) was complexed with HBc 93-100 peptide (AnaSpec, Fremont, CA). Lymphocytic choreomeningitis virus (LCMV) gp33-41 peptide was purchased from AnaSpec.

2010a), although SAR245409 datasheet most sightings in the area have taken place in waters off the shelf or on the shelf break. The prevalence of octopus in the diet of long-finned

pilot whales is also reported in a recent study based on analysis of 11 stomachs of pilot whales stranded in the Bay of Biscay (Spitz et al. 2011). The authors found benthic octopods to be the main prey in the stomachs analyzed (21.1% of prey biomass), followed by oceanic squids, such as Todarodes sagitattus and Histioteuthis reversa (17.2% and 10.7% of prey biomass, respectively). Cuttlefish (Sepia sp.) have also been recorded in the diet of long-finned pilot whales, being the most numerous prey in stomachs of two pilot whales that stranded on the French Atlantic coast, with E. cirrhosa representing only 14.3% of the total number of prey (Pierrepont

et al. 2005). The second most important prey family identified in our study is the squid family Ommastrephidae. Of the species present in the diet, Todarodes sagitattus has an oceanic distribution, while Illex coindettii and Todaropsis eblanae are also recorded in shelf waters (Guerra 1992). Long-finned pilot whales are widely distributed in the cold temperate waters selleck screening library of the northeast Atlantic but little is known on its population structure and movements in the area. Fullard et al. (2000) analyzed microsatellite DNA of whales from the East coast of the United States, West Greenland, the Faroe Islands, and the United Kingdom and the authors reported that their results did not support a simple isolation-by-distance 上海皓元 model of population differentiation. The authors explained the pattern found in their samples as possible if population differentiation occurs in areas of different sea surface temperature. Smaller-scale studies based on genetic

and stable isotope results, together with photoidentification studies carried out in the Strait of Gibraltar, suggest that at least some pilot whales are resident all year round and show a complex social structure constituted by several clans containing several pods each (De Stephanis et al 2008b). No information exists for other areas of the Northeast Atlantic. Desportes and Mouritsen (1993) noted that all prey species found in the stomach contents of pilot whales killed off the Faroes were common species in the area, but the authors also suggested that pilot whales showed a preference for the oceanic ommastrephid squid, Todarodes sagitattus, when this species was available in high numbers, information that these authors obtained from fishery data since this cephalopod species is also exploited commercially. As a mainly teuthophagous species, long-finned pilot whale is clearly in some respects a specialist feeder.