Virus Res 2008, 135:267–272.CrossRef 26. Lindenbach BD, Rice MC: Flaviviridae: the viruses and their replication. In Fields virology. 4th edition. Edited by: Knipe DM, Howley PM. Lippincott-Williams and Wilkins. New York; 2001:991–1041. 27. Wilson JR, de Sessions P, Leon MA, Scholle F: West Nile Virus Nonstructural Protein 1 Inhibits TLR3 Signal Transduction. J Virol 2008, 82:8262–8271.LY3023414 solubility dmso PubMedCrossRef 28. Chung K, Nybakken GE, Thompson BS, Engle MJ, Marri A, Fremont DH, Diamond this website MS: Antibodies

against West Nile Virus Nonstructural Protein NS1 Prevent Lethal Infection through Fcγ Receptor-Dependent and-Independent Mechanisms. J Virol 2006, 80:1340–1351.PubMedCrossRef 29. Volpina OM, Volkova TD, Koroev DO, Ivanov VT, Ozherelkov SV, Khoretonenko MV, Vorovitch MF, Stephenson JR, Timofeev AV: A synthetic peptide based on the NS1 non-structural protein of tick-borne encephalitis virus induced a protective immune response against fatal encephalitis in an experimental animal Autophagy screening model. Virus Res 2005, 112:95–99.PubMedCrossRef 30. Lin YL, Chen LK, Liao CL, Yeh CT, Ma SH, Chen JL, Huang YL,

Chen SS, Chiang HY: DNA immunization with Japanese encephalitis virus nonstructural protein NS1 elicits protective immunity in mice. J Virol 1998, 72:191–200.PubMed 31. Xu G, Xu X, Li Z, He Q, Wu B, Sun S, Chen H: Construction of recombinant pseudorabies virus expressing NS1 protein of Japanese encephalitis (SA14–14–2) virus and its safety and immunogenicity. Vaccine 2004, 22:1846–1853.PubMedCrossRef 32. Lin C-W, Liu K-T, Huang H-D, Chen W-J: Protective immunity of E. coli-synthesized NS1 protein of Japanese encephalitis virus. Biotechnol Lett 2008, 30:205–214.PubMedCrossRef 33. Amorima J, Porchiaa BFMM, Balanb A, Cavalcantea RCM, da Costac S, de Barcelos Alvesc A, de Souza

Ferreiraa L: Refolded dengue virus type 2 NS1 protein expressed in Escherichia coli preserves structural and immunological properties of the native protein. J Virol Methods 2010, 167:186–192.CrossRef 34. Sukupolvi-Petty S, Austin KS, Engle M, Brien JD, Dowd KA, Williams KL, Johnson S, Rico-Hesse R, Harris E, Pierson TC, Fremont DH, Diamond MS: Structure and Function Analysis of Therapeutic Monoclonal Antibodies against Dengue Virus Type 2. J Virol 2010, 84:9227–9239.PubMedCrossRef Loperamide 35. Shen X, Parks RJ, Montefiori DC, Kirchherr JL, Keele BF, Decker JM, Blattner WA, Gao F, Weinhold KJ, Hicks CB, Greenberg ML, Hahn BH, Shaw GM, Haynes BF, Tomaras GD: In Vivo gp41 Antibodies Targeting the 2F5 mAb Epitope Mediate HIV-1 Neutralization Breadth. J Virol 2009, 83:3617–3625.PubMedCrossRef 36. Denisova GF, Denisov DA, Yeung J, Loeb MB, Diamond MS, Bramson JL: A novel computer algorithm improves antibody epitope prediction using affinity-selected mimotopes: A case study using monoclonal antibodies against the West Nile virus E protein. Mol Immunol 2008, 46:125–134.PubMedCrossRef 37.

Among them were several genes involved in degrading polygalacturonic acid (Additional file 5: Table S2). In consequence, cell #selleck randurls[1|1|,|CHEM1|]# wall degradation by X. campestris pv. campestris is assumed to result in the release of a complex mixture of poly- and oligosaccharides to the surrounding medium. It

is in the best advantage of plants to recognize such signals of microbial pathogenicity as DAMPs in order to initiate suitable defense reactions. Plants are able to perceive diverse signal molecules such as the yeast elicitor in tobacco [70], bacterial flagellin [71, 72], harpin proteins [5–9], Hrp proteins from X. campestris[31], fungal proteins in parsley [73] and fungal exoenzymes in tobacco [74]. Rouet-Mayer et al. were also able to show that fungal lyase represents a different chemical stimulus than the OGAs produced from the cell walls by this enzyme’s activity and that both these elicitors despite their common origin activated at least partially differing signal transduction pathways. The fact that tobacco is not only able to perceive the products

of enzymatic digestion, but also the www.selleckchem.com/products/r428.html enzyme itself, shows how crucial it is for the plant to recognize the pathogenic fungus. Here we report on the release of elicitor-active compounds obtained from the co-incubation of C. annuum cell walls with X. campestris pv. campestris. The co-incubation was carried out using a crude cell wall extract from pepper leafs and the X. campestris pv. campestris strain Bac2. The use of crude cell wall extracts instead of complete Osimertinib datasheet plants or leafs has the advantage that all products resulting from the incubation can originate only from the plant cell wall material or the bacteria. Orientation

experiments indicated that cell wall-derived oligosaccharides were responsible for the elicitor activity. To identify the elicitor-active compound, HPAE chromatography [75] was employed. First hints on the origin of the elicitor-active molecules were obtained by analyzing the composition of neutral sugars and uronic acids. In comparison to the controls, an increased abundance of typical cell wall sugars was observed when X. campestris pv. campestris and cell-free pepper cell wall material were co-incubated. In the subsequent characterization of the oligosaccharide composition using HPAEC [76], UV absorption was measured in addition to the PAD signal in order to detect double-bonds in the newly formed oligosaccharides. This resulted in identifying the elicitor-active compounds as pectin fragments with a varying degree of polymerization (DP) by comparing the elution profile to a standard derived from pectin digested by a pectate lyase from a commercially supplier. MALDI-TOF MS was used as a valuable tool to obtain further structural information on the isolated oligosaccharides. These fragments with different DPs were then isolated with preparative HPAEC and tested for their elicitor activities.

In addition, transconjugants were tested for CI formation (PaiII_1rev/PaiII_53fw) and for site-specific integration of PAI II536 into the tRNA gene leuX (M803b/M805c). The latter two primer pairs find more also allowed the determination of the orientation of the integrated PAI (Figure 2). Remobilization experiments were carried out with two PAI II536-positive clones of E. coli K-12 as donors that derived from the mobilisation experiments and

a derivative of the wild type UPEC strain 536 as recipient. Donor and recipient strains were mixed in a 3 : 1 ratio and incubated at 20°C and 37°C, respectively. Experiments were divided into two sets according to the state of the mobilised PAI. In the first set, the donor strain SY327-77

harbored PAI II536 in the circular form. In the second set, clone SY327-23, harboring the chromosomally integrated PAI II536, served as donor strain. In both Pexidartinib chemical structure cases, strain 536-21, a non-hemolytic derivative of strain 536, which lacks the two islands encoding functional α-hemolysin determinants (PAI I536 and PAI II536) [2], served as the recipient. In the remobilisation experiments, the same PCR-based verification process as described above was carried out with exconjugants that grew on the Cm-lactose-M9 minimal agar plates. In addition, pulsed-field gel electrophoresis (PFGE) analysis of the randomly picked transconjugants was carried out. Genomic DNA for PFGE analysis was prepared and cleaved with NotI or SfiI as described before [2]. Gels were run for 21-24 h with pulse times of 0.5-50 s. Phenotypic characterisation of transconjugants PAI II536 comprises a α-hemolysin gene cluster. This determinant was used as a phenotypic marker in this study to verify the presence of PAI II536 in transconjugants after the mobilisation and remobilisation experiments. Therefore, transconjugants were screened post-experimentally on blood agar plates to FK228 datasheet analyse the hemolytic activity. UPEC strain 536 served as a positive control, while strains SY327 and 536-21 served as negative controls. Statistical analysis Statistical analysis of the conjugation rate was performed

by the Mann-Whitney U test. The ratio/distribution of integrated, cointegrated and partial transconjugant clones at 20°C and 37°C was compared by the chi-square test. The difference was considered significant if p < 0.05. Idoxuridine Acknowledgements and Funding This work was carried out within the European Virtual Institute for Functional Genomics of Bacterial Pathogens (CEE LSHB-CT-2005-512061) and the ERA-NET PathoGenoMics I consortium “”Deciphering the intersection of commensal and extraintestinal pathogenic E. coli”" (Federal Ministry of Education and Research (BMBF) grant no. 0313937A) and the Hungarian Research Foundation (OTKA 62092 and 78915). UD was also supported by the German Research Foundation (DO 789/4-1). The excellent technical assistance of K. Lotzl (Pécs) and B. Plaschke (Würzburg) is appreciated.

With over 80 % of water resources being used in agriculture, this strategy has led to rapidly diminishing groundwater resources across the region (Araus 2004; Comprehensive Assessment of Water Management in Agriculture 2007). Soil fertility losses due to erosion, soil salinisation, declining soil organic matter and nutrient mining (Pala et al. 1999; Lal 2002) have tightened the

dilemma of increasing production in an agro-ecological region where land and water resources are inherently scarce (Agnew 1995). Thus, to meet the imperative for ‘sustainable EPZ5676 price agricultural development in MENA’ (Rodríguez 1995; Chaherli et al. 1999), improved production systems are needed that maintain the resource base and increase the productivity per unit land and water. The intensification of rain-fed (non-irrigated) systems BIBW2992 purchase will play a key role for achieving these goals (Cassman 1999). Rationale for the sustainability goals The sustainability goals for wheat-based systems in the MENA region were chosen as “To increase the productivity of rain-fed cropping systems per unit (1) land and (2) water, (3) increase the profitability of production, and (4) maintain or enhance soil fertility”. Across MENA,

wheat (Triticum aestivum L. and Triticum turgidum ssp. durum) is the main staple food. Wheat-based systems dominate the zone delineated by the 350–600-mm isohyets. Typical rain-fed wheat-based rotations include food (Cicer arietinum, Lens AZD5363 research buy culinaris, Vicia faba) and feed legumes (Medicago sativa, Vicia sativa) (Cooper et al. 1987; Pala et al. 1999; Ryan et al. 2008). Fields are commonly left fallow over summer, as insufficient moisture prohibits the reliable production of rain-fed summer crops. Long fallows (winter plus summer) have been largely

replaced by cropping to increase production through intensified land use (Tutwiler et al. 1997; Pala et al. 2007). Conventional tillage includes deep ploughing (0.2–0.3-m depth) with a disc or mouldboard plough, followed by seed-bed preparation with tined implements (Pala et al. 1999, check details 2000). Some farmers may plough up to five times prior to planting. The rational is to obtain a fine, weed-free seed bed. Farmers also manage stubble loads by burning (Tutwiler et al. 1990; López-Bellido 1992). Reasons for stubble burning have been named as to control weeds, pests and diseases, and to facilitate seedbed preparation for the following crop (Pala et al. 2000; Virto et al. 2007). However, these tillage and residue management practices have been shown to degrade soil physical and chemical properties, as indicated by losses in structural stability and soil organic matter (Govaerts et al. 2006; Roldan et al. 2007; Verhulst et al. 2011). Stubble management further includes summer grazing by sheep and goats. Land is rented out to herders following the crop harvest in spring/early summer, which generates additional income for arable farmers in the traditional crop-livestock systems (Tutwiler et al. 1997).

The first plasmid, pJV853.1, encodes a MicA antisense sequence, thereby leading to partial buy MI-503 depletion of MicA in the cell due to formation of unstable double stranded RNA. The second plasmid,

pJV871.14, is a MicA overexpression construct, constitutively expressing MicA from a strong PLlacO promoter. The ampicillin resistant pJV300 plasmid used for both constructs, was included as a negative control. All plasmids were electroporated to wildtype S. Typhimurium SL1344 and the resulting strains were tested for biofilm formation using the peg system quantifying the formed biofilms with crystal violet [10]. The results are shown in Figure 3A. Interestingly, the presence of either the overexpression or the depletion construct had an impact on the biofilm forming capacity of S. Typhimurium although not to the same extent. Biofilm formation was almost completely abolished in the MicA overexpression strain while only slightly, but significantly decreased in the MicA depletion strain. This indicates that a tightly regulated balance of MicA expression is essential for proper biofilm formation in Salmonella Typhimurium. Note that all strains with the above plasmid constructs

VRT752271 purchase produce wildtype AI-2 levels (data not shown). Figure 3 Biofilm formation of Salmonella Typhimurium linked to sRNA. (A) Biofilm formation assay of S. Typhimurium SL1344 containing the control vector (pJV300), MicA depletion (pJV853.1) or overexpression (pJV871.14) constructs. (B) Biofilm formation assay of S. Typhimurium SL1344 rpoE (JVS-01028) and hfq (CMPG5628) deletion selleckchem mutants. Biofilm formation is expressed as percentage of wildtype SL1344 biofilm. Error bars depict 1% confidence intervals of at least three biological replicates. Further indirect evidence of small RNA molecules being involved in the regulation of biofilm formation was provided by the analysis of both hfq and rpoE mutants. Hfq is a prerequisite for the binding of many sRNAs to their trans-encoded targets [16, 17], while sigmaE, encoded by rpoE, has been shown to be involved in the transcription of several small RNAs, including MicA [18–20]. In the peg biofilm assay,

neither of these strains were able to form mature biofilms (Figure 3B). The phenotype could genetically be complemented by introducing the corresponding gene in trans on a plasmid carrying a ifenprodil constitutive promoter (data not shown). MicA targets involved in Salmonella biofilm formation Most likely, the impact of MicA on biofilm formation in Salmonella is through one of its Salmonella targets. To date, four trans encoded targets, all negatively regulated by MicA, have already been reported in Escherichia coli, i.e. the outer membrane porins OmpA [17, 21] and OmpX [22], the maltoporin LamB [23] and recently the PhoPQ two-component system [24]. Two of these targets, PhoPQ and OmpA, were previously shown to be involved in biofilm formation [25–27], i.e.

Figure 3 The effect of c-Myb on OPN expression of HCCLM6 cells. (A) OPN mRNA expression in HCCLM6 cells transfected with c-Myb siRNA was significantly decreased. (* P < 0.05, vs control). The mRNA expression of OPN in cells transfect with scramble siRNA was used as control. (B) OPN protein expression in HCCLM6 cells transfected with c-Myb siRNA was significantly reduced compared

with cells transfected with sramble siRNA. Blot was representative of three experiments. 3.4 Migration and invasion of HCCLM6 cells in vitro were inhibited by c-Myb siRNA As migratory and invasive behaviors are the indicators https://www.selleckchem.com/products/incb28060.html of the metastatic potential, we examined migration and invasion of HCCLM6 cells in vitro using the transwell assay after c-Myb expression was inhibited by c-Myb siRNA. The average numbers of HCCLM6 cells transfected with c-Myb siRNA migrating toward the conditioned medium

or invading through the Matrigel were significantly fewer than those transfected with scramble siRNA (Migration assay: 17.60 ± 4.04 vs 33.60 ± 4.67, P < 0.05; Invasion assay: 8.00 ± 2.55 vs 18.8 ± 4.15, P < 0.05, Figure 4), This result showed that the capability of migration and invasion in HCCLM6 cells was significantly XMU-MP-1 purchase decreased after inhibition of c-Myb, suggesting that c-Myb is an important contributor to the migration and invasion of HCC cells. Figure 4 Migration and invasion of HCCLM6 cells in response to transfection of c-Myb siRNA. The c-Myb siRNA could significantly inhibit the migration and invasion of HCCLM6 cells compared with cells treated with scramble siRNA (* P < 0.05). The migration and invasion assays were assessed by transwell chambers. Data were expressed as means ± SD of three experiments. 4-Aminobutyrate aminotransferase Discussion Metastasis remains one of the major challenges for HCC patients undergoing various therapies including liver resection, local ablation

and chemoembolization [2, 3]. Previous work at our institute has shown that OPN gene is over-expressed in the metastatic HCC [6]. In this study, we searched for transcription factors that were correlated with OPN expression in HCC cells and revealed that transcription factor c-Myb was positively associated with OPN expression in HCC cells, which can bind the OPN promoter and increase its transcription activity. Inhibition of c-Myb by siRNA decreased the transcription activity of the OPN promoter, reduced the expression of OPN, and compromised the ability for migration and invasion of HCC cells. AZD4547 Therefore, our results demonstrate that c-Myb plays an important role in regulating OPN expression in HCC cells, suggesting c-Myb might be a novel target for therapeutic intervention. OPN is known to mediate correlates of metastatic biology in a variety of cancers including HCC. Thus, modulating OPN expression might be a novel approach of suppressing tumor metastasis [17–19].

2001; Schmitt 2007; Pelc et al. 2009; Kelly and Palumbi 2010). In marine

habitats, common selleck locations of genetic discontinuities indicating shared barriers to dispersal have been found e.g. along the North American coasts (Pelc et al. 2009; Kelly and Palumbi 2010), in the Mediterranean (Patarnello et al. 2007), in the Caribbean (Taylor and Hellberg 2006), and at the entrance of the Baltic Sea (Johannesson and André 2006). Genetic similarities among species would be useful for management and conservation, for instance when marine reserves are established (Palumbi 2003). Alternatively, contrasting patterns of genetic differentiation among species could suggest that differences in life history or colonization history are major components in shaping the genetic structure of a species in a region (Kelly and Palumbi 2010). In such a situation, separate management for different groups of species, or even species-specific management would be required. In this study we focus on the Baltic Sea, which is a sub-basin

of the Atlantic Ocean formed less than 10,000 years ago as a postglacial marine environment (Zillén et al. 2008). The Baltic Sea is a highly suitable aquatic system to evaluate the presence or absence of common genetic diversity and differentiation patterns in multiple species. Environmental variation and potential barriers GM6001 in vivo to dispersal possibly affecting different species in similar manner include a temperature and salinity gradient (spanning 3–30 per mille; HELCOM 2010) reaching from the entrance of the Baltic Sea to the north of Adenosine triphosphate the Bothnian Bay (Gabrielsen et al. 2002), and several sub-basins between which water circulation is partially restricted by submarine sills (HELCOM 2010). Species with both freshwater and marine origin

have established populations which in many cases have undergone adaptations to the brackish water environment over the very short evolutionary history of the sea (Andersen et al. 2009; Gaggiotti et al. 2009; Papakostas et al. 2012). Marginal ecosystems such as the Baltic Sea can be of great conservation value because they may harbor unique genetic variation and even novel species (Lesica and Allendorf 1995; Johannesson et al. 2011). Indeed, a new species of macroalgae has evolved inside the Baltic Sea (Pereyra et al. 2009). At the same time, the dense human population of the Baltic drainage area imposes threats to its aquatic biota via eutrophication, CBL0137 ic50 habitat destruction, and overfishing (Ducrotoy and Elliott 2008). These factors indicate that high priority should be given to the management of genetic diversity as the eradication of locally adapted wild populations may result in severe effects to the ecosystem (Johannesson et al. 2011). Although a reasonable number of genetic studies have been carried out on Baltic species (see Johannesson et al.

Along with the implementation of ACCESS at VH, the performance of cancer operations not requiring inpatient

admission (such as breast cancer and melanoma) was shifted Torin 2 purchase to a Pifithrin-�� cost nearby ambulatory-care centre. During the study period, CCO also mandated a shift in the treatment of select malignancies (particularly hepatobiliary and colorectal cancer) away from community hospitals to high-volume tertiary-care centres such as VH. Consequently, there was a significant change observed in the composition of cancer surgeries performed at VH after the implementation of ACCESS, with fewer breast and melanoma surgeries, and increased proportions of colorectal and hepatobiliary cases. Interestingly, we observed a significant change in the distribution of cancer cases by priority post-ACCESS,

for all surgeons (including general surgeons) at Victoria Hospital: the proportion of P2 and P3 cases declined, while the proportion of P4 cases increased significantly. Since the general surgeons participating in ACCESS also perform cancer surgeries during their elective practices, they may have been performing P2 and P3 cancer cases on standby during ACCESS time (when there was a paucity of emergency general surgery cases), thereby contributing to the decline Eltanexor mw in P2 and P3 cases electively. If this was the case, surgeons may have had more time during their elective OR time to operate on patients with P4 cancers. This possible change may also partially explain the significant reduction in the number of general surgery cancer cases that exceeded the wait-time targets. Alternatively, surgeons at VH may have become more conservative in assigning priority levels for cancer

patients in order to avoid missing wait-time targets and the associated penalties. This explanation may be more likely given the down-grading present across all surgical specialties at VH, although a case–control analysis of cancer patients may determine if this has been occurring since the implementation of the Wait Time Strategy. One of the limitations of this study was our inability to accurately determine the number of cancer surgeries performed during ACCESS time because standby cancer operations were usually reported as emergency cases rather than elective surgeries. With the recent integration of operative databases Ergoloid for emergency and elective cases at our institution, however, future prospective analyses may provide this important information. Overall, there was no significant change in cancer surgery wait times pre- versus post-ACCESS. Therefore, the implementation of ACCESS, and the resultant reallocation of OR time from elective to emergency case loads, did not negatively impact wait times for elective cancer surgery. Additionally, wait-times remained unchanged despite the significant increase in the performance of hepatobiliary and colorectal surgeries post-ACCESS, which are typically longer and more complex than the breast cancer and melanoma cases that were moved off-site.

The 350-nm-wide EPZ015938 order computational cell used comprises a 63-nm-thick layer of a 100-nm-wide BARC stripe sandwiched between two 125-nm-wide Py stripes, atop a 2-μm-thick Lazertinib mouse Si substrate, with its bottom boundary fixed. It is to be noted that unlike the case of the 1D Py/Fe

nanostripe array of [7], no interfacial air gaps were considered in the calculations, as the fabrication process employed here precludes their formation. Elastic parameters used in the simulations for Py, BARC, and Si are Young’s moduli = 180, 6.26, and 169 GPa; Poisson ratios = 0.31, 0.34, and 0.064; and mass densities = 8600, 1190, and 2330 kg/m3, respectively [19–21]. The simulated dispersion relations for the lowest three SAW branches, below the

longitudinal bulk wave threshold [22, 23], presented in Figure  2a, accord well with the Brillouin measurements. Also shown in the figure are the dispersion relations of the vertically polarized transverse (T) and longitudinal (L) bulk waves, in the [110] direction, of the Si substrate. Simulated mode profiles for q = π/a, shown in Figure  2b, of the lowest two modes exhibit characteristics of the surface Rayleigh wave (RW). These RWs are standing Bloch waves satisfying the Bragg scattering condition. The mode profile of the third branch at the BZ boundary reveals that it is also a standing wave with most of its energy confined in the BARC stripes. Mode profiles for q = 1.4π/a displayed in Figure  2c indicate that at this wavevector, the first branch has the characteristics of the RW. In contrast, the higher two SAWs leak energy Foretinib clinical trial into the Si substrate as their dispersion curves extend beyond

the transverse bulk wave threshold [16, 22–24]. The dispersion relations of the RW and Sezawa wave (SW), modeled by treating the Py/BARC array as a homogeneous effective medium [25] on a Si substrate, are presented in Figure  2a. It can be seen that the gap opening arises from the zone folding of the RW dispersions and avoided crossings at the BZ boundary. A prominent feature of the phonon dispersion spectrum is the large hybridization bandgap. For a structure, such as ours, Amobarbital comprising a ‘slow’ film on a ‘fast’ substrate, Sezawa waves will exist only below the transverse bulk wave threshold, and over a restricted range of qh, where h is the film thickness [23, 26]. As shown in Figure  2a, within the first BZ, the SW and zone-folded RW do not cross, indicating that the measured bandgap does not originate from the hybridization of these waves. Instead, within the bandgap, the zone-folded RW crosses the transverse bulk wave threshold. Additionally, above but close to this threshold, attenuated SAWs called pseudo-Sezawa waves which exist as resonances with the substrate continuum of modes have been observed [23, 26, 27]. We thus attribute the origin of the bandgap to the hybridization and avoided crossing of the zone-folded RW and pseudo-Sezawa waves.

Österreichisches MLN2238 molecular weight J für Sportmedizin 2003, 33:11–18. 30. Knechtle B, Knechtle P, Rosemann T: No exercise-associated hyponatremia found in an observational field study of male ultra-marathoners participating in a 24-hour ultra-run. Phys Sportsmed 2010,38(4):94–100.PubMedCrossRef 31. Knechtle B, Wirth A, Knechtle P, Rosemann T, Senn O: Do ultra-runners in a 24-h run really dehydrate? Irish J Med Sci 2011,180(1):129–134.PubMedCrossRef 32. Kao WF, Shyu CL, Yang XW, Hsu TF, Chen JJ, Kao WC, Polun C, Huang YJ, Kuo FC, Huang CI, Lee CH: Athletic performance and serial weight changes during 12- and 24-hour ultra-marathons. Clin J Sports Med 2008,18(2):155–158.CrossRef 33. Knechtle B, Knechtle

P, Kohler G, Rosemann T: Does a 24-hour ultra-swim lead to dehydration? J Hum Sport Exerc 2011,6(1):68–79.CrossRef 34. Rüst CA, Knechtle B, Knechtle P, GS-4997 nmr Rosemann T: A comparison of anthropometric and training characteristics between recreational male marathoners and 24-hour ultra-marathoners. Open Access J Sports Med

2012, 3:121–129.PubMedCentralPubMed 35. Knechtle B, Knechtle P, Rosemann T: No association of skin-fold thicknesses and training with race performance in male ultraendurance runners in a 24-hour run. J Hum Sport Exerc 2011,6(1):94–100.CrossRef 36. Knechtle B, Knechtle P, Rüst CA, Rosemann T: Leg skinfold thicknesses and race performance in male 24-hour ultra-marathoners. Proc (Bayl Univ Med Cent) 2011,24(2):110–114. 37. Raschka C, Plath M: Body fat compartment and its relationship to food intake and clinical chemical parameters during extreme endurance performance. Schweiz Z Sportmed 1992,40(1):13–25.PubMed 38. Hoffman MD, Stuempfle KJ, Rogers IR, Weschler LB, Hew-Butler T: Hyponatremia in the 2009 161-km Western States Endurance Run. Int J Sports Physiol Perform 2012,7(1):6–10.PubMed 39. Noakes TD, Sharwood K, Speedy D, Hew T, Reid S, Dugas J, Almond C, Wharam P, Weschler L: Three independent biological mechanisms cause exercise-associated hyponatremia:evidence from 2, 135 weighed competitive athletic performances. Proc Natl Acad Sci USA 2005,102(51):18550–18555.PubMedCrossRef

40. Rosner MH: Exercise-associated hyponatremia. Semin Nephrol 2009,29(3):271–281.PubMedCrossRef 41. Reid SA, Speedy DB, Thompson JM, Noakes TD, Mulligan G, Page T, Campbell RG, Milne C: Study of hematological and biochemical eltoprazine parameters in runners competing a standard learn more marathon. Clin J Sport Med 2004,14(6):344–353.PubMedCrossRef 42. Noakes T: Waterlogged. The Serious Problem of Over Hydration in Endurance Sports. New Zealand: Human Kinetics; 2012. 43. Verbalis JG: Disorders of body water homeostasis. Best Pract Res Clin Endocrinol Metab 2003,17(4):471–503.PubMedCrossRef 44. Knechtle B, Duff B, Schulze I, Kohler G: A multi-stage ultra-endurance run over 1,200 km leads to a continuous accumulation of total body water. J Sports Sci Med 2008, 7:357–364.PubMedCentralPubMed 45.