All children were recruited from the northwest of England, and all came from homes where English was spoken as the first Sunitinib concentration language. The children with SLI obtained a Core Language Score (CLS) of −1.25 SD or less on the Clinical Evaluation of Language Fundamentals-4th Edition, UK Standardisation (CELF-4 UK, Semel et al., 2003), and a Performance IQ (PIQ) score no less than 1 SD below the mean on the Wechsler Abbreviated Scale of Intelligence (WASI, Wechsler, 1999). TD children obtained standardised scores within one standard deviation (SD) of the mean on both the CELF-4 UK and WASI. The SLI and TD groups differed on

the CLS and CELF (Expressive Language Index – ELI, Receptive Language Index – RLI) language measures, but not on age or PIQ. Working memory, declarative memory, procedural memory and lexical and grammatical abilities were all assessed with well-studied measures of these domains. Working memory functioning was assessed with the Working Memory Test Battery for Children (WMTB-C, Pickering and Gathercole, PR-171 research buy 2001). This test comprises eight subtests, which were designed to assess the central executive, phonological loop, and visuo-spatial sketchpad components

of Baddeley’s (2003) model of working memory (for validation study see Gathercole et al., 2004). All subtests from the WMTB-C are standardised to a mean of 100 and SD of 15. The central executive component is assessed by the Listening Recall, Counting Recall, and Backward Digits Recall subtests, all of which require the short-term storage and processing of information. On Listening Recall, children are presented with a series of sentences. For each sentence, they must first provide true/false judgements on the sentence’s semantics, and then recall the sentence-final word. The Listening Recall subtest is an adaptation of the Competing Language Task (Gaulin and Campbell, 1994). On the Counting Recall task, children are presented with pictures of randomly presented dots, and are asked to count and then recall the

dots. Counting Recall is based on the counting span task developed by Case et al. (1982). The Backward Digit Recall subtest, in which children are asked to repeat a string of digits in reverse order, Vasopressin Receptor is similar to the Backward Digit Span Task in the Wechsler Intelligence Scales (e.g., Wechsler, 2003 and Wechsler, 2008). These subtests are likely to probe not only Baddeley’s central executive, but also Cowan’s focus of attention. Note that while all these subtests are designed to measure central executive (and likely attentional) working memory functioning, as they require both the short-term storage and processing of information, it is important to emphasise that all have a verbal component, and thus likely depend more generally on verbal aspects of working memory. The WMTB-C does not include central executive tasks which can be considered non-verbal.

For experimental groups, the effect of saliva on the polar component and the total surface free energy varied depending on type of coating, with this effect being more significant for rough surfaces. As observed for the non-coated specimens, significant differences were also found mainly for the polar component of rough surfaces treated with S and HP coatings. However, for the S coating, saliva decreased the polar component, and the values became similar to the polar component

of the control group; for the HP coating, an increase in the polar component was observed after incubation with saliva. Thus, the effect of saliva on the surface free energy varied depending on substrate characteristics, particularly the chemical Belnacasan purchase composition and surface roughness. These findings suggest that the nature of

the surface-exposed chemical groups after coating applications may influence the formation of the salivary pellicle (adsorbed salivary proteins). Other authors have also reported that small differences in the chemical composition of acrylic resins changed the adsorption of salivary proteins and, consequently the nature of the adsorbed salivary pellicle.47 and 48 In this study, this phenomenon was particularly evident for rough surfaces due to a larger surface area and more exposed chemical groups available to interact with saliva. In the present investigation, XTT assay results showed that, for the specimens fabricated in contact with the stone, the adhesion of C. albicans in S30, S35 and HP30 groups was lower as compared with the control.

One factor that might have contributed to these Metalloexopeptidase findings would Afatinib datasheet be the hydrophilicity of the coated surfaces. 21, 27 and 28 As mentioned before, the rough surfaces coated with S30, S35 and HP30 exhibited significantly higher mean surface free energy values as compared with the control group, suggesting a decreased hydrophobic character. Hence, in this study, the decrease in C. albicans adhesion in the S30, S35 and HP30 groups may be partially related to the hydrophilicity of the rough surfaces treated with these coatings. Changes in chemical compositions of the coated acrylic surfaces may also have contributed to the findings as demonstrated by the XPS analysis. There were changes in the carbon and oxygen content with special relevance for S and HP coatings. In addition, surfaces modified with the S coating also exhibited an additional peak for the presence of sulphur. The S coating contains sulfobetaine, a member of the zwitterionic betaine family of compounds, 5, 10, 11, 13, 14, 15, 16, 18, 21 and 49 which have a mixture of anionic and cationic terminal groups with an overall neutral charge. Surfaces with zwitterionic groups resist non-specific interaction with plasma proteins and cells via a bound hydration layer from solvation of the charged terminal groups in addition to hydrogen bonding.

1% BSA for 1 h at room temperature on a horizontal shaker. After being washed three times with PBS plus 0.05% Tween-20, the membranes were incubated with rabbit anti-horse IgG conjugated to alkaline phosphatase (whole molecule) diluted 1:7500 in PBS plus 0.1% BSA and 0.05% Tween-20. Then, the membranes were incubated for 1 h at room temperature on a horizontal shaker. The membranes were washed three times with PBS plus 0.05% Tween-20 and placed in developing solution for Western blotting.

The reaction was terminated by washing with distilled water. Polystyrene, high-affinity ELISA plates (96 wells) were coated with 1.0 μg of crude C. d. terrificus, C. d. collilineatus, C. d. cascavella or C. d. marajoensis venom in 100 μL of PBS buffer and kept overnight at 4 °C. In some assays, crotoxin or PLA2 purified from C. d. terrificus was used as the antigen. The wells were

blocked for 2 h at 37 °C Anti-cancer Compound Library concentration with 200 μL of PBS plus 5% BSA. The wells were washed with 200 uL Carfilzomib manufacturer of PBS. Serial dilutions of horse IgG or F(ab′)2 preparations (1:4000 to 2,048,000) in PBS plus 0.1% BSA were prepared, and 100 μL of each dilution was added to individual wells. The plates were then incubated at 37 °C for 1 h, and then, the wells were washed three times with the wash buffer. Rabbit peroxidase-conjugated anti-horse IgG (whole molecule) (Sigma Aldrich, St. Louis, MO) diluted (1:20,000) in PBS plus 0.1% BSA and 0.05% Tween-20 (100 μL/well) was added to the plates. The plates were incubated for 1 h at 37 °C. After three washes with the wash buffer, 50 μL of substrate buffer were added to each well, and plates were incubated at room temperature for Grape seed extract 15 min. The reaction was terminated with 50 μL of 4 N sulfuric acid per well. Absorbance was recorded at 492 nm using an ELISA plate reader (Labsystems Multiskan Ex, Thermo Fisher Scientific Inc., Walthan, MA). IgG from horses collected before immunization was always used as a negative control. The IgG dilution giving an optical density of 0.2 was used to calculate the U-ELISA per milliliter of the undiluted IgG solution. One U-ELISA was defined as

the smallest dilution of antibody that presented an O.D. of 0.2 under conditions of the ELISA assay, as described previously ( Almeida et al., 2008). The value was then multiplied by 10 to correspond to milliliters. The affinity of anti-Crotalus antibody was measured by ELISA, as described above, with the inclusion of a potassium thiocyanate (KSCN) elution step ( Pullen et al., 1986; Romero-Steiner et al., 2005). After the serum incubation step, dilutions of KSCN (0.0–5.0 M, in intervals of 0.50 M) in PBS were added to the wells and incubated for 30 min at room temperature. The remaining bound antibodies were detected with rabbit peroxidase-conjugated anti-horse IgG (whole molecule) (Sigma Aldrich, St. Louis, MO) diluted (1:20,000) in PBS plus 0.

5% of the contigs (Table 2). These data generated from the mantle of P. maximus form a valuable addition to those generated from hemocytes of the same species ( Pauletto et al., 2014) and, in a

more general context, to the transcriptomes generated for other molluscs including the Yesso scallop Patinopecten yessoensis ( Hou et al., 2011), Mytilus galloprovincialis ( Craft et al., 2010), Laternula elliptica ( Clark et al., 2010), Meretrix PLX4032 meretrix ( Huan et al., 2012), Ruditapes philippinarum ( Milan et al., 2011), Haliotis midae ( Franchini et al., 2011), several pearl oysters ( Huang et al., 2013) and the oyster genome data ( Zhang et al., 2012), thus increasing the sequence resource available for commercially important shellfish species and for researchers investigating shell deposition processes in molluscs. The sequence data for this transcriptome has been deposited in the GenBank SRA, accession number: SRP040427. The contigs, and the annotation for those contigs with a match of 1e − 10 and lower, are available from http://ramadda.nerc-bas.ac.uk/repository/entry/show/Polar+Data+Centre/NERC-BAS+Datasets/Genomics/. This study was funded by grants from the Région Bretagne, i.e. the

Pemadapt project (ref. 6368) and a doctoral fellowship to S.A. (Protmar project, ref. 6197). This study was also supported by a Natural Environment Research Council (NERC) grant to Lloyd Peck (NE/G018) and the British Antarctic Survey Polar Sciences for Planet Earth programme, which is also funded by the Natural Environment Research Council. Two French National Research Agency Olaparib in vivo (ANR) programmes also supported our research: COMANCHE (ANR-2010-STRA-010) and LabexMER (ANR-10-LABX-19-01). “
“Three congeners of the salmonid fish family with high commercial value were under study Lck to identify species-specific markers for a validated species determination: Oncorhynchus mykiss, Salmo salar and Salmo trutta. The latter ones are common in Polish marine waters, whereas O. mykiss is only represented in this region in hatcheries. Difficulties in species identification may result in non-sustainable

salmon fisheries leading to imbalances in the ecosystem. The development of easy tests by means of molecular markers will therefore help in monitoring fishery activities as well as natural stock development. Single nucleotide polymorphisms (SNPs) have been used for ecological and conservational studies and have proven very useful for differentiating individuals, populations and species. A species-specific SNP-microarray initially comprised of 15163 loci was constructed and then optimized to 7000 markers for functional genes of S. salar in CIGENE, Norway. It has been used in studies of differences between farmed and wild Atlantic salmon ( Karlsson et al., 2011), genetic architecture of North Atlantic populations ( Bourret et al., 2013), and characterization of SNPs in S. trutta populations from the Southern Baltic Sea ( Drywa et al., 2013).

1G–I. Enhanced ALP staining was anticipated, but not

verified, in the OVX group. ALP expression, while expressed consistently seen throughout osteoblastic differentiation, has been demonstrated to be condition sine qua non for mineralization as demonstrated in ALP knockout mice [34]. OVX animals suffer from accelerated bone turnover, showing stimulated osteoclastic bone resorption and reactive osteoblastic bone formation with a net result of bone loss. Even though eldecalcitol activates mature osteoblasts and induces minimodeling, the activated osteoclastic status in OVX animals may conceal any surplus in bone formation. Osteoblasts may compensate for the abnormal bone destruction by frantically synthesizing osteoid, check details while mineralization seems to be slowed down. After ovariectomy, Parameters that refer to non-mineralized bone matrix such as osteoid surface and mineralizing surface show two- and three-fold increases, respectively, when compared to Sham animals. Osteoblasts in the OVX group, therefore, may not show enhanced expression of ALP because their main function, in a scenario of untamed bone destruction, is rapid bone matrix synthesis, not its mineralization. The histological picture seen after eldecalcitol treatment is quite different from the one obtained with an intermittent PTH regimen, in which we

showed the clear proliferative and osteoblastic activation effects of that hormone [35]. Alternatively, Okuda et al. [23] have shown that ED-71, the former denomination of eldecalcitol, was capable of promoting enhancement of ALP activity and bone nodule formation in bone marrow cells in vitro,

where the influence Navitoclax mouse of osteoclastic Tyrosine-protein kinase BLK bone resorption does not exist. Under our experimental circumstances, it seems that eldecalcitol drives osteoblastic differentiation in vivo with consequent bone minimodeling without noticeable differences in the pattern of ALP staining. The histological data in this study unveiled the consistent presence of a rather particular type of bone formation after eldecalcitol treatment: bone minimodeling. Minimodeling is termed so because magnification is needed to visualize it [36], and it basically consists of bone formation not preceded by osteoclastic bone resorption with cement lines that are typically smooth [37]. Minimodeling in bone has been reported after treatment with bone anabolic agents like PTH [38] and prostaglandin E2[39]. It has been hypothesized that the mechanism guiding minimodeling-based bone formation is the resumption of osteoblastic activity of bone lining cells [40]. In our histological samples, we did observe a dominant presence of plump osteoblasts compared to that of resting bone lining cells in eldecalcitol-treated specimens (Figs. 2C–D). The absence of numerical data regarding the amount of minimodeling-based bone formation and the number of active osteoblasts as opposed to bone lining cells are limitations of this study.

These enable the live monitoring of gene expression and protein localization in vivo, and in real time. The traditional approach of collecting “static” images of fixed or post mortem cells and tissues provides a snapshot view of events at a single fixed point in time. However, this inherently overlooks the dynamic aspects of the biology being examined. In contrast, live cell imaging enables the visualization of temporal changes in living specimens and can reveal novel aspects of the biology that may not otherwise have been appreciated. Additionally, the datasets generated from time-lapse imaging are information rich and can be interrogated quantitatively to enable measurement of cellular,

subcellular and tissue dynamic events as a function of time (reviewed in [37]). Although these approaches are leading to exciting discoveries click here that are advancing our understanding of biological systems, there are several limitations that need to be acknowledged. Firstly, the use of any fluorescent probe has the potential to perturb or alter the biology being examined and this must always be taken into account when interpreting live imaging data. For example, fusion of GFP sequences, which are approximately 27 kDa in size, with the protein of interest may disrupt the normal function of the protein. Therefore, validation studies are needed

to make sure that the fusion protein still functions similarly to the wild type form. It is also advantageous to confirm findings with more than one type of imaging probe if possible. For example, a GFP fusion protein can be used for in selleck chemicals llc vivo localization of a specific protein and key data can be confirmed using a fluorescence-conjugated antibody against the same protein. When developing live cell imaging protocols, there is always a compromise between obtaining a high enough signal-to-noise ratio to enable quantitative measurements and to obtain sufficient image resolution, while at the same time avoiding phototoxic effects to the cells (reviewed in [36] and [38]). Therefore, to ensure cell

viability, the researcher may have to accept a lower image quality and resolution than would be acceptable for equivalent images of fixed specimens. Light microscopy based live Adenosine triphosphate cell imaging approaches that use widefield or confocal microscopy are also limited by issues such as signal attenuation with depth of penetration into the tissue, as mentioned earlier in this review. For a more extensive discussion of the advantages and limitations of live cell imaging methods in relation to imaging of bone cells, please refer to Dallas and Veno 2012 [36]. Technologies such as multiphoton fluorescence microscopy can increase the depth of tissue penetration for live cell imaging applications and reduce phototoxicity by using a longer wavelength light to excite the fluorophores.

Similarly, single incubation with DHA showed concentration-dependent reductions in cell survival, and PFT significantly

inhibited the cytotoxic effects of DHA in both cell types ( Fig. 2). Thus, PFT abrogated DHA-induced cytotoxicity Angiogenesis inhibitor independently of p53 expression. We examined the effects of PFT on DHA-induced oxidative stress, as indicated by DCF fluorescence (Fig. 3). Induction of oxidative stress by DHA at 120 μM was significantly elevated after 1 h of incubation (126.8 ± 12.8%; p < 0.05), and increased further at 2, 4 and 6 h (154.2 ± 8.1%, 196.6 ± 32.8% and 229.8 ± 20.3%, respectively), as compared to controls (p < 0.01). These DHA-induced increase in oxidative stress were abrogated by pretreatment with PFT after incubation for 1 h (110.8 ± 3.6%; p < 0.05), selleck products and were further blocked by longer incubation for 2, 4 and 6 h (113.8 ± 12.4%, 106.5 ± 2.3% and 103.9 ± 12.2%, respectively; p < 0.01). To confirm the inhibitory effects of PFT on DHA-induced oxidative stress and whether PFT has antioxidant capacity, we performed TAC assay.

As shown in Fig. 4, PFT does not show antioxidant capacity when compared with Trolox, even at 2000 μM. In order to explore the inhibition mechanisms of PFT on DHA-induced cytotoxicity, we focused on the induction of autophagy (Fig. 5). Levels of LC3A-II, which is an LC3-phosphatidyl-ethanolamine conjugate and a promising autophagosomal marker (Asanuma et al., 2003), showed concentration-dependent increases in incubation with DHA on Western blotting (Fig. 5A and B). Expression was completely blocked by PFT. This inhibitory effect of PFT was also observed in both Hep3B and Huh7 by incubation with high concentrations of DHA at 200 μM (Fig. 5C and D). On immunofluorescence, PFT incubation for 24 h Aurora Kinase showed no changes when compared with control groups, but the DHA-treated group showed increased numbers of LC3-positive cells, and this effect

was apparently blocked by pretreatment with PFT (Fig. 5E). Similarly, after transfection with pAcGFP-LC3 in HepG2 cells, PFT blocked the formation of LC3 puncta in cells on incubation with DHA (see Supplementary data 1). Next, we examined the release of cytochrome c from mitochondria to cytosol by DHA ( Fig. 6). Cytochrome c is a critical mediator of mitochondrial cell death. COX IV, a specific mitochondrial marker, was detected in mitochondrial fractions, indicating good-quality mitochondrial preparations ( Fig. 6A). Cytochrome c decreased in the mitochondrial fraction and increased in the cytosol fraction after incubation with DHA. On densitometric measurement of bands on Western blotting (ratio is expressed as cytosol/mitochondria fraction), single incubation with DHA for 1 or 4 h gave ratios of 0.95 ± 0.15 or 1.33 ± 0.29 when compared with controls, and this release of cytochrome c was significantly suppressed by pretreatment with PFT (0.56 ± 0.

Clinical reports have shown a range BTK inhibition of effects of vestibular stimulation on somatic sensory systems. Recently, it has been demonstrated that left cold CVS interacts not only with tactile perception (Vallar et al., 1990, 1993) but also with chronic pain in brain-damaged patients (Ramachandran et al., 2007; McGeoch et al., 2008), and with higher-order body representation

(Bisiach et al., 1991). However, to our knowledge, no clinical study has studied effects of vestibular stimulation on diverse aspects of somatic processing in the same individuals. Here we extend previous clinical findings to healthy volunteers, and show that vestibular inputs have widespread functional effects on different somatosensory submodalities. Because CVS has strong effects on spatial attention, particularly in right brain-damaged patients (Rubens, 1985), many previous clinical studies interpreted effects of CVS on tactile perception in terms of general arousal or shifts of supramodal attention towards the side of the space contralateral to the vestibular organs stimulated (Vallar et al., 1990, 1993). However, several lines of evidence suggest that our Vorinostat cost data may reflect a direct vestibular-somatosensory interaction, and not just indirect

effects mediated by attention. First, some clinical reports demonstrated PLEK2 an impairment of the VOR with reduced leftward slow-phase and rightward fast-phase in neglect patients (Doricchi et al., 2002; Ventre-Dominey et al., 2003). These results highlight the inter-relation between eye movements, attention, and the vestibular system. Oculomotor effects of vestibular stimulation suggest a direct influence of vestibular signals in the neural activity of brain-damaged areas in the right hemisphere (Ventre-Dominey et al., 2003). Moreover, evidence from healthy

volunteers found no modulation of covert visuo-spatial attention following vestibular stimulation (Rorden et al., 2001). Additionally, CVS selectively affected somatosensory detection but not visual detection in a previous study (Ferrè et al., 2011). Finally, neuroanatomical overlap between vestibular and somatosensory cortical projections is widespread, and not confined to ‘attentional’ brain areas. The present results provide further evidence for a direct vestibular-somatosensory interaction, in addition to any attentional aspect. Our results cannot easily be reconciled with the attentional interpretation of CVS derived from patient studies. First we found that vestibular modulation of both touch and pain was bilateral, and not unilateral as a spatial attentional account would predict.

After 8–10 days of decalcification, the paws were embedded in paraffin and 7 μm tissue sections were cut and stained with hematoxylin/eosin. For each group, four stained paw sections were analyzed. Mice (n = 4) were injected in the right hind paw (i.pl.) with 15 μg of protein of SpV in 30 μL of PBS or only PBS (control-group). After 0.5, 2, 6, 12, 24 and 48 h of venom injection, mice were sacrificed and the paws were removed at the level of the tibiotarsal joint. The tissue was disrupted with scissor and homogenized with a polypropylene piston using a Potter homogenizer (100 rpm, 30 s)

in Antiinfection Compound Library research buy PBS pH 7.4, containing aprotinin 0.1 mM, benzothium 0.1 mM, EDTA 10 mM, tween 20 0.05% and phenylmethylsulfonyl fluoride 0.1 mM. Following centrifugation for 20 min at 4 °C/14.000 g, the supernatants were recovered and stored at −80 °C until use. Cytokines (TNF and IL-6) and a chemokine (MCP-1) levels were measured in the supernatants by flow cytometry using Cytometric Bead Array – Mouse Inflammation Kit, according to the manufacturer’s instructions (BD Biosciences,

San Diego, CA, USA). For these analyses, a typical forward and side scatter gate was set to exclude buy Venetoclax aggregates; a total of 1800 events in the gate were analyzed using FACScalibur cytometer and Cell questPro Software (BD Biosciences, San Jose, CA, USA). Samples were quantified by comparison with standard curves of recombinant mice cytokines and chemokines. The results were expressed Leukocyte receptor tyrosine kinase as mean ± SEM. To the investigation of the edema provoked by SpV, different groups of mice received the venom (15 μg of protein in 30 μL of PBS, i.pl.) 30 min after each one of following treatments by intraperitoneal route (i.p.): i) cyclooxygenase (COX) non-selective inhibitor, diclofenac sodium (Voltaren®, 1 mg/kg); ii) histamine H1 receptor antagonist, promethazine (Phenergan®, 1 mg/kg); iii) serine-proteases inhibitor, aprotinin (Trasylol®,

8 mg/kg); iv) bradykinin B2 receptor antagonist, icatibant (100 nmol/kg) and; v) PBS, according to Bohrer et al. (2007). Local edema was quantified (see item 2.2) periodically after 0.5, 2 and 6 h of SpV injection (n = 4). Mice injected with PBS were considered as control. Results were expressed as mean ± SEM of percentage increase of paw thickness after venom administration. In order to verify the presence of kinin-releasing enzymes in the crude venom, amidolytic activity was measured using Pro-Phe-Arg-pNA (S-2302) p-nitroanilide substrate, specific for plasma kallikrein. Assays were performed in 50 mM Tris–HCl, pH 9.0, containing 0.80 mM NaCl and 0.32 mM Pro-Phe-Arg-pNA, in a final volume of 250 μL. The reactions were initiated by the addition of the samples (SpV and chromatographic fractions) and incubated at 37 °C by 5 h.

Die kontroversen Aspekte dieser this website Hypothese werden im Folgenden beleuchtet. Selen ist essentiell für die Biosynthese und Funktion der etwa 25 bekannten selenocysteinhaltigen Selenoproteine [4]. Die Biosynthese der 21. Aminosäure, Selenocystein, und ihr kotranslationaler Einbau in bestimmte Proteine werden

streng reguliert [5]. Selenocystein befindet sich im katalytischen Zentrum der meisten Selenoenzyme. Eines der am besten bekannten und charakterisierten Redox-Systeme ist das Glutathion-System, das aus den selenabhängigen Peroxidasen (GPx) [6] and [7] und den Thioredoxinreduktasen besteht [8]. Diese reduzieren nicht nur Wasserstoffperoxid, Lipid- und Phospholipidhydroperoxide und verringern so die Bildung von freien Radikalen und reaktiven Sauerstoffspezies, sondern auch die Hydroperoxid-Intermediate im Cyclooxygenase- und Lipoxygenase-Signalweg

und die Bildung von inflammatorischen Prostaglandinen und Leukotrienen [7]. Außerdem modulieren sie durch die Pexidartinib Reduktion von Wasserstoffperoxid und die Produktion von Superoxid den oxidativen Stress. Durch die mit einem niedrigen Selenspiegel assoziierte erniedrigte GPx-Aktivität bei kritisch kranken Patienten [9] erhöht sich möglicherweise in einigen Kompartimenten der oxidative Stress, was letztlich zum Multiorganversagen mit beiträgt. In Tierversuchen wurde darüber hinaus gezeigt, dass eine Selensupplementierung die intrazelluläre GPx- und Thioredoxinreduktaseaktivität normalisiert und den oxidativen Stress, die intranukleäre Translokation von NF-κB, die Bildung von Zytokinen sowie die Schädigung von Geweben

verringert [10]. Einer der wichtigsten anti-inflammatorischen Effekte von Selen ist die Verringerung der Translokation von NF-κB in Makrophagen und die daraus resultierende reduzierte Freisetzung von Zytokinen [11]. Außerdem ist der Spiegel von Selenoprotein P (SePP), dem wichtigsten zirkulierenden Selenoprotein, das allein 70 % des Plasmaselens enthält, bei Sepsis-Patienten signifikant erniedrigt [12]. SePP ist nicht nur ein Transportprotein zur Verteilung von Selenocystein an verschiedene Organe, es bindet auch an aktivierte Endothelzellen Aldehyde dehydrogenase und kann die oxidative Schädigung dieser Zellen verhindern [13]. Daher ist ein niedriger Plasmaselenspiegel nicht notwendigerweise die Folge eines niedrigen Selengehalts im Körper insgesamt, sondern gibt nur die Kompartimentierung von SePP aus dem Plasma wieder, das an die Endothelzellen gebunden wurde. Diese Annahme wird gestützt durch den Befund, dass sich der Plasmaselenspiegel auch ohne Selensupplementierung normalisiert, wenn sich Patienten von ihrer Krankheit erholen [14]. Jedoch könnte auch der Bedarf an Selenoenzymen und damit an Selen als dem Hauptsubstrat bei allen kritischen Krankheitszuständen erhöht sein.