“
“The two omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) have been proven to have a wide range of beneficial effects, in particular on cardiovascular health [1], [2], [3], [4] and [5]. Fish and seafood

intake is considered too low in a large proportion of the population in the Western world, and to take omega-3 food supplements is a way to improve one’s daily need of these important fatty acids. To date, fish oils have been the most traditional omega-3 supplements, but new sources of omega-3 fatty acids, like algae and krill, are gaining popularity [6], [7] and [8]. Krill are shrimp-like crustaceans that are harvested commercially in the Antarctic Sea [9]. The estimated amount of krill (Euphausia superba) in Antarctica is EPZ5676 nmr between 125–750 million metric tons (http://www.fao.org/fishery/species/3393/en), being one of the most abundant animals on the planet. There are currently two main products produced from krill: krill oil and krill powder. Krill oil is sold as a food supplement and is characterized by a large proportion of phospholipids, especially

phosphatidylcholine TGF-beta inhibitor (PC) [10]. The majority of EPA and DHA in krill oil is esterified into PCs and omega-3 fatty acids in phospholipid form have been shown to be efficiently taken up by body tissues [11], [12], [13] and [14]. Also krill powder consists of a large fraction of phospholipids (20.2%) and it further contains proteins (41.7%) in addition to a lipid fraction (51.7%). Besides the high presence of phospholipids, krill also contains the red pigment molecule astaxanthin [15]. Astaxanthin is an antioxidant carotenoid that gives krill powder its reddish colour. The product has been used for both human and animal

from dietary supplementation [16], [17] and [18]. So far, krill powder has been tested in two pre-clinical [17] and [18] and one clinical study [16]. The pre-clinical studies investigated the effect of krill powder on hepatic gene regulation in healthy mice [17] and on inflammation and lipid metabolism in mice overexpressing TNFα [18]. The clinical study examined krill powder supplementation in mildly obese men and its effect on fat distribution, blood lipid levels and the endocannabinoid system [16]. The objective of the present study was to assess the safety of krill powder in a 13-week subchronic toxicity study in Wistar rats. Superba™ krill powder was provided by Aker BioMarine Antarctic AS (Oslo, Norway). The raw material was analysed for fatty acid composition, total lipid, lipid classes, proteins, ash, salt and astaxanthin content (Nofima AS, Bergen, Norway). The composition of the krill powder is shown in Table 1. The amino acis profile of krill powder has been analysed previously [17]. The subchronic toxicity study was designed and conducted based on the regulatory guidelines OPPTS 870.3100, OECD No.408 and US FDA Redbook. Twenty male and twenty female Han Wistar rats were obtained from Charles River UK Limited.

1 mmol/L phenylmethanesulfonylfluoride (PMSF), 5 μg/mL soybean trypsin inhibitor, and1 μg/mL of aprotinin, leupeptin,

and pepstatin, pH 7.4). Homogenate was stored at −80°C. The homogenized samples were frozen to −80°C and thawed 3 times to ensure complete membrane lysis. Samples were then spun down at 1000g for 10 minutes, the supernatant was collected, and protein concentration was determined by the bicinchoninic acid (BCA) method. Protein samples for electrophoresis were made using the Laemmli method. Proteins were separated by weight on Sodium Dodecyl Sulfate polyacrylamide gel electrophoresis (SDS-PAGE) gels. The gels were transferred to nitrocellulose or polyvinylidene difluoride (PVDF) membranes and incubated in 5% (wt/vol) milk or body Pictilisib mouse surface area–blocking solution for 1 to 1.5 hours. The Alectinib clinical trial membranes were then incubated in primary antibody at 4°C overnight or at room temperature for 1 hour. After a series of Tris-buffered saline with tween-20 (TBST) washes, the

membranes were incubated in secondary antibody suspended in a 1% (wt/vol) milk or body surface area–TBST solution for 1 hour. After the final washes, ECL (GE Healthcare, Cardiff, UK) was applied to cover the membrane. Membranes were then developed using autoradiographic film, and results were quantified using National Institutes of Health Bethesda, MD, USA software. Antibodies used in this study include the following: AMPK (2532 L; Cell Signaling, Beverly, MA, USA), phosphorylated AMPK (pAMPK) (4188 L; Cell Signaling), acetyl-CoA carboxylase (ACC) (3662; Cell Signaling), phosphorylated ACC (3661S; Cell Signaling), liver kinase B1 (LKB1) (no. 07-694; LKB1, Charlottesville, selleck inhibitor VA, USA), uncoupling protein 3 (UCP3) (AB3046; Millipore, Temecula, CA, USA), Cytochrome c (Cyt C) (C5723; Sigma-Aldrich, USA), and glucose transporter type 4 (GLUT4)

(2213; Cell Signaling). A power analysis was performed to determine the estimated number of animals that would be necessary to determine differences between groups. An SD estimated approximately 10% to 15% of the mean with difference of 25% considered a physiologically meaningful difference (α, .05; power of 0.7-0.8). A 2×2 factorial design was used ( Table 1). Data are presented as mean ± SE. All statistical analyses were performed using SigmaStat, San Jose, CA, USA 3.5 software. Two-way analysis of variance was performed with Bonferroni post hoc test. Significance was defined as P < .05. There was a main effect of SMSC supplementation on increasing serum Se concentration (P < .001). When the interaction with HIF and SMSC supplementation was examined, HIF Se group was showing higher levels than the LIF Se group (P < .05).

abyssorum abyssorum (Koren & Danielssen 1875). As Brotskaya & Zenkevich (1939) mentioned in their benthos research data, only G. m. margaritacea of the above species formed a significant biomass in the Barents Sea in the first half of the 20th century. However, its dense populations were basically concentrated in the central part of the Barents Sea and off the west coast of the Novaya Zemlya archipelago. The proportion of

sipunculans in the total benthic biomass in those areas reached 50%, whereas the mean biomass was 15–65 g m− 2. A second full-scale benthos survey in the Barents Sea undertaken by the Polar Research Institute of Marine Fisheries and Oceanography (PINRO) in 1968–1970 revealed a considerable decrease in the Gephyrea biomass. Its share of the total benthic biomass has decreased tenfold ( Denisenko 2007). Further reductions in the biomass and area of distribution of those species in the central GSK2118436 nmr Barents Sea were discovered during benthic research in the area in 2003 ( Denisenko 2007). Generally, despite Sipuncula being widespread in Arctic bottom communities, selleck products data on the numbers of species and their role in the Barents Sea’s benthos are quite fragmentary and scanty. The latest similar study of the quantitative distribution of Sipuncula in the Arctic was carried out off the west Spitsbergen

coast (Kędra & Włodarska-Kowalczuk 2008). Until recently, no dedicated research of the quantitative distribution of Sipuncula had been carried out in the Barents Sea as a whole, although in the last few years several publications by one of

the present authors have appeared describing the quantitative distribution of these invertebrates in particular parts of the Barents Sea (Central basin, the Novaya Zemlya archipelago, Franz Josef Land, the Pechora Sea) (Garbul, 2007, Garbul, 2009 and Garbul, 2010). The purpose Janus kinase (JAK) of this study is to give details of the contemporary diversity of sipunculans and their abundance in the southern and central Barents Sea. Material was collected during a multidisciplinary scientific expedition of PINRO on r/v ‘Romuald Muklevich’ in August–September 2003. samples of macrozoobenthos were taken from 63 benthic stations in central and southern Barents Sea (Figure 1). The data from two research cruises of the Murmansk Marine Biological Institute (MMBI) on the r/v ‘Dalnye Zelentsy’ in 1996 and 1997 were used for analysing the long-term dynamics of Sipuncula densities in the central Barents Sea (Garbul 2010). Primary data from the PINRO cruise on r/v ‘N. Maslov’ in 1968–70 and the literature data from the 2003 cruise of r/v ‘Ivan Petrov’ in the central Barents Sea were used (Denisenko, 2007 and Cochrane et al., 2009). Quantitative samples of macrozoobenthos were taken with a 0.1 m2 van Veen grab in five replicates at each station. The material was washed through a soft 0.5 mm mesh sieve and fixed with 4% formaldehyde buffered by sodium tetraborate.

Figure 9 shows the time series of wind speed and direction at the position of the ship’s failure as well as the symbols

for the labelled terms of the hypothetical onset of the oil spill. Figure 10 shows the wind fields for the model spatial domain during periods shortly after the hypothetical oil spill. At station 1 (13°29.477E, 45°24.999 N) current measurements were performed using an ADCP 600 kHz Workhorse Sentinel unit manufactured by Teledyne RDI, at 9 levels (6 m to 22 m bins) with a vertical spatial resolution of 2 metres, and a sampling interval of 15 minutes. The most significant spectral energies at station 1 (Figure 8) were observed during semidiurnal and diurnal tidal periods, and during long periods (gradient currents and synoptic atmospheric disturbances, periods E7080 in vivo longer than 40 h). It is interesting that during diurnal

tidal periods, the energies of subsurface and near-bottom currents are of the same order of magnitude, while for semidiurnal periods the energy of the Nutlin-3a supplier subsurface current is an order of magnitude larger. In addition, energy peaks were also detected at 16.8 h, representing the inertial period, and during the period of the fundamental Adriatic seiche (21 h). Subsurface currents (at a depth of 4 m) were somewhat more pronounced than near-bottom currents (22 m depth). Figure 11, Figure 12, Figure 13, Figure 14 and Figure 15 show the plumes of oil pollution for the 240th and 480th hours after the onset of the spill. The presentation of oil pollution (Figure 11, Figure 12, Figure 13, Figure 14 and Figure 15) is given in

the form of oil slick thickness [μm] and oil concentration per unit sea surface area [g m− 2]. The figures also give an insight into the time exposure for the first 480 hours after the onset of the spill. Time exposure should be interpreted as the time taken for a particle to be advected and dispersed from the source point to a certain location. Furthermore, the oil thickness exceeds the threshold value of 10 m throughout the simulation period of two months after the start of the oil spill, indicating the area with a longer oil Tangeritin retention period. In the first situation analysed, with the oil spill starting at 18:00 hrs on 11 January 2008, the predominant circulation is under the influence of the tidal signal with the periodic exchange of NW and SE coastal circulation along the eastern coast of the area affected. The result of such a circulation is a smaller absolute shift of the oil slick and higher concentrations in the first 20 days (see Figure 11) than in the other situations addressed. An oil slick of thickness > 10 m occupies an area a little more to the north of the spill position during 15% of the simulation period of 60 days (see Figure 11f). The oil slick reaches the coast only after 45 days, on the stretch of coastline between Rovinj and Poreč, with a maximum thickness of 5 μm.

Experiments were performed

at least in triplicates. Results are presented as means ± standard deviation. The One-way ANOVA followed by Tukey’s post test was performed to analyse the reporter gene data. For the statistical analysis of the gene expression data the Two-way ANOVA followed by the Bonferroni post test was applied. For graphs and statistics the software GraphPad Prism 5 for Windows was used. HepG2 were transiently co-transfected with ERE-TK-LUC and the hERα expression vector. E2 (10 nM) resulted in a significant induction of reporter gene activity. TCDD (1 nM) significantly decreased E2-induced ERE-mediated activity by about 50%, whereas TCDD alone had no effect on ERE-mediated transcription (Figure 1). The partial AhR antagonist α-naphthoflavone reversed TCDD’s anti-estrogenic action SB203580 mouse and the pure estrogen antagonist ZK 191 703 completely blocked the selleck chemicals estrogenic action of E2. In cells lacking the transfected ERα none of the tested compounds had any effect on reporter gene expression (data not shown). In the same way, XRE-luc reporter was co-transfected or not with hERα into HepG2 cells (Figure 2). E2 (10 nM) significantly enhanced TCDD-induced AhR-regulated transcription up to 1.6-fold in co-transfected

cells, whereas E2 alone had no effect on transcriptional activity via the AhR. By adding the anti-estrogen ZK 191 703, this enhancement by the co-treatment was abolished, while the XRE-driven increase by TCDD was still observed.

The AhR-mediated action of TCDD was partially inhibited by the AhR antagonist α-naphthoflavone, while addition of E2 to TCDD/α-naphthoflavone further enhanced this inhibitory effect. Application of the anti-estrogen Idoxuridine ZK 191 703 or experiments with XRE-luc without exogenous ERα reversed the potentiating effect by E2. In any case basal levels of reporter plasmid (ERE or XRE)-mediated activity were not influenced by transfection of ERα or solvent treatment. Receptor transcript levels for ERα and AhR were not changed with treatments (Figure 3). With regard to relative CYP expression (normalized to respective controls) there was no difference in response to TCDD between non-transfected and ERα-transfected HepG2 cells. TCDD (1 nM) induced both CYP1A1 and CYP1B1 mRNA, whereas the latter response was less pronounced. E2 alone had no impact on CYP1A1 and CYP1B1 mRNA compared with solvent control. Furthermore, E2 showed no modulating effect on TCDD-induced CYP expression. The treatments had no significant influence on COMT mRNA levels (Figure 3). However, transcript levels were significantly different in the TCDD treatment and the co-treatment with and without ERα transfection. In this study a well-known in vitro human liver cancer cell model, the HepG2 hepatoma cell line, was used to investigate the mode of action of the cross-talk between ERα and AhR following treatment with E2 and/or TCDD.

“
“Event Date and Venue Details from 2012 1st INTERNATIONAL WORKSHOP ON BAC-TERIAL DISEASES OF STONE FRUITS AND

NUTS 14–17 FebruaryZurich, SWITZERLAND B. Duffy, Agroscope FAW, Schloss, Postfach 185, 8820 Waedenswil, SWITZERLANDE-mail: [email protected]. 25th GERMAN CONFERENCE ON WEED BIOLOGY AND CONTROL 13–15 MarchBraunschweig, GERMANY Info: www.unkrauttagung.de 7th INTERNATIONAL IPM SYMPOSIUM 2012 – March USA, in planning phase E. WolffE-mail: [email protected] 4th EUROPEAN WORKSHOP ON THE STANDARDIZED PROCEDURE FOR THE INSPECTION OF SPRAYERS GSK2126458 cost IN EUROPE 27–29 March Lana, ITALY Info: http://tinyurl.com/6wolvs2 *8th CONGRESO ARGENTINO DE ENTOMOLOGIA 17–20 AprilBariloche, ARGENTINA

Info: http://tinyurl.con/659gqpz 64th INTERNATIONAL SYMPOSIUM ON CROP PROTECTION 22 May Ghent, BELGIUM Info: B. Vandekerkhove, Fac. of Biosci., Ghent Univ., Coupure Links 653, BE-9000 Gent, BELGIUM Fax: 32-09-264-6223 Voice: 32-09-264-6145 E-mail: [email protected] Web: www.iscp.ugent.be. INTERNATIONAL FUSARIUM LAB WORKSHOP 03–08 June Bari, ITALY Info: www.mycotox-society.org/fusarium-2012 VI INTERNATIONAL WEED SCIENCE CONGRESS 17–22 JuneDynamic Weeds, Diverse Solutions, Hangzhou CHINA H.J. Huang, IPP, CAAS, No. 2 West Yuanmingyuan Rd., Beijing 100193, CHINA Fax/voice: 86-10-628-15937 E-mail: [email protected] Web: www.iwss.info/coming_events.asp 2nd MEETING OF THE TEPHRID WORKERS OF EUROPE AFRICA AND THE MIDDLE EAST 02–06 July Kolymbari Crete, GREECE Info: [email protected] 2nd INTERNATIONAL SYMPOSIUM–TEPHRITID WORKERS OF EUROPE, AFRICA, AND THE MIDDLE GSK2118436 mw EAST 03–06 July Kolymbari, Crete,

GREECE N. Papadopoulos E-mail: [email protected]: www.diptera.info/news.php *8th MEETING OF TEPHRID WORKERS OF THE WESTERN HEMISPHERE 30 July–03 AugustPanama City, PANAMA Info: www.8twwh.org *JOINT MEETING ENTOMOLOGICAL SOCIETIES OF CANADA and ALBERTA 04–07 NovemberEdmonton, ALB, CANADA Info: www.esc-sec.ca/annmeet.html 2013 INTERNATIONAL HERBICIDE RESISTANCE CONFERENCE 18–22 February Perth, AUSTRALIA S. Powles, AHRI, School of Plant Biol., Univ. of Western Australia, 35 Stirling Hwy., Crawley, Perth 6009, WA, AUSTRALIA selleck kinase inhibitor Fax: 61-8-6488-7834 Voice: 61-8-6488-7870 E-mail: [email protected] AMERICAN PHYTOPATHOLOGICAL SOCIETY ANNUAL MEETING 10–14 August Providence, RI, USA Info: APS, 3340 Pilot Knob Rd., St. Paul, MN 55121, USAFax: 1-651-454-0755 Voice: 1-651-454-3848 E-mail: [email protected] Web: www.apsnet.org Full-size table Table options View in workspace Download as CSV “
“Inflammatory bowel disease (IBD) refers essentially to 2 different but closely related chronic intestinal disorders: Crohn disease and ulcerative colitis. Although much progress has been made in understanding the pathogenesis of human IBD, its etiology has not yet been defined.