(2010), using tandem mass spectrometry in 10 type 2 DM and 14 obese patients, demonstrated the accumulation of plasmatic long-chain AC in the Z-IETD-FMK in vivo mitochondria and its relationship to selleck screening library insulin resistance after an overnight fast and four hours on an euglycemic clamp [22]. Studies with thiazolidinediones, on the other hand, have shown that these consequences of lipotoxicity can be prevented or reversed in subjects with type 2 DM [23, 24]. Hiatt et al. (1989) demonstrated that a change occurred in the patterns of AC when they evaluated the influence

of an episode of aerobic exercise (AE) of variable intensity in six healthy volunteers [25]. However, it is unknown whether this effect on the pattern of AC in a single episode of AE can be repeated or modified when carrying out a long term AE program. The influence of an AE program on the pattern of AC has not been studied in non-diabetic overweight or obese individuals. The identification of favorable changes in the ACs pattern of these populations, when subjected to an AE program, could be useful to modify the consequences of lipotoxicity. We designed a randomized, prospective, longitudinal, experimental study in a group of obese or

overweight individuals who underwent a 10-week AE ATR inhibitor program. Our main purpose was to define the influence of an AE program on beta-oxidation and fatty acid transport in mitochondria according to changes in total carnitine and short, medium, and long-chain ACs. We were also interested in studying the behavior of essential and nonessential amino acids, and analyzing the correlation of these changes with the determination of metabolic and anthropometric markers that can be modified with a controlled AE program. Subjects and methods Subjects After obtaining approval from the Research and Ethics Committee and informed consent from each subject, we began the study. Participants were recruited through advertisements placed in different parts of the health campus of the Universidad Autónoma de Nuevo León. A total of 36 women, aged 18 to 24 years with a body mass index (BMI) greater

than or equal to 27 kg/m2 were included. We excluded individuals who had exercised periodically in the last 3 months, subjects who had a 5-FU concentration weight change greater than 10% in the last 6 months or who were taking medications that alter insulin sensitivity, or lipid lowering or antihypertensive drugs during this period. We also excluded individuals with DM, hypertension, dyslipidemia or who smoked in the last 6 months. Study protocol The participants were consecutively and randomly assigned to one of two groups: cases and controls. In order to prevent a change in calorie intake that would lead to a modification in body weight, which in turn would indirectly affect the effects of exercise, all participants received individual and group nutrition education.

Overview of R. eutropha transcriptomes Clustering of the four transcriptomes (F16, F26, F36, and O26) based on the calculated RPKM values detected global changes in the transcription levels of a number of genes, which depended on the cellular phases (Figure 2). However, the clustering analysis indicated the strong resemblance of the A-1155463 clinical trial O26 transcriptome to that of F36. In particular, there are almost no Apoptosis inhibitor significant differences between F36 and O26 in terms of the expression

levels of genes encoding β-oxidation enzymes, including the two gene clusters previously identified by Brigham et al. [18]. These facts implied that the transcriptional changes related to fatty acid

metabolism had already fulfilled 2 h after the stepwise addition of octanoate at 24 h. Thus, the O26 transcriptome was not ICG-001 examined in detail in the present study. Further optimization of the time point for RNA isolation should be considered to obtain the transcriptomes of R. eutropha grown on fatty acids. The medium-chain-length (mcl)-(R)-3-hydroxyacyl-CoA molecules are provided through β-oxidation in several PHA-producing bacteria, including R. eutropha[9, 11–14, 24], therefore, the

transcriptomic changes that depended on the chain length of fatty acids would be valuable information. Figure 2 Heatmaps of transcriptomes in R. eutropha H16 Fossariinae in different phases. The expression pattern is shown by the color scale based on RPKM value of each gene on chromosome 1 (left), chromosome 2 (center), and pHG1 (right), except for rRNA- and tRNA-coding genes and non-significant genes in expression (P > 0.05). The arrows A-P indicate highly expressed clusters. Table 2 summarizes highly expressed gene clusters during cultivation on fructose (indicated by arrows in Figure 2). Gene clusters that encoded a number of ribosomal proteins and RNA polymerase subunits (H16_A3457-A3484 and H16_A3490-A3505), and membrane-bound hydrogenase subunits along with the accessory proteins (PHG001-PHG023) were highly expressed throughout cultivation.

We have used two different kinds of commercial GNRs in order to compare their photothermal transduction efficiency. Both are tuned to the laser source and have their maximum surface plasmon resonance (SPR) at 808 nm (longitudinal band). The first commercial GNRs used are bare GNRs (B-GNRs) MNK inhibitor A12-10-808-100 Nanorodz (Nanopartz, Salt Lake City, UT, USA). B-GNRs are dispersed in deionized water (DI-H2O) with <0.1% ascorbic acid and <0.1% cetyltrimethylammonium bromide (CTAB) surfactant

capping agent. B-GNRs have an axial diameter of 10 nm and a length of 41 nm. The other commercial GNRs used are PEGylated GNRs (PEG-GNRs) PEG-10-808-50 (Nanoseedz, China). PEG-GNRs are functionalized by thiol-terminated methoxypoly(ethylene glycol) (mPEG-PH) and are also dispersed in DI-H2O. The

dimensions of PEG-GNRs are equal to the dimensions of B-GNRs (axial diameter = 10 nm, length = 41 nm). The laser is connected to the system via Selleckchem BI 10773 a multimode optical fiber with a core diameter of 600 μm, a length of 1.5 m, and a power transmission of 90% to 99% (600-μm MM fiber, Changchun New Industries, China). The laser light from AG-881 supplier the fiber irradiates the samples through a collimation lens (78382, Newport Corporation, Irvine, CA, USA), which is in direct contact with a 4-well plate containing the samples, which have a total volume of 500 μl, and is located on a Teflon support. A temperature sensor (F100 Precision Thermometer, Automatic Systems Laboratories, Redhill, UK) is fixed vertically with the aid of a tripod stand and

a burette clamp and remains in contact with the samples during the experiments (Figure 1). Figure 1 Experimental setup: complete view (A), fiber-lens connection details (B), and sample and temperature these sensor details (C). Thermal parameters In order to determine the parameters that characterize and describe the thermal behavior of our hyperthermia device, it is needed to develop a thermal model, which can be raised from the resolution of an equivalent electric circuit (Figure 2). Figure 2 Electrical equivalent circuit used to obtain the thermal parameters of the optical hyperthermia device. In this circuit, P is the delivered power, T(t) is the sample temperature which is time dependent, and C d (W/K) and C t (J/K) are the thermal conductance and the thermal capacitance of our experimental enclosure, respectively. Solving the circuit, we can formulate the equation that describes the power distribution, obtaining that the delivered power (P) is equal to the sum of the stored power in the capacitor (P s) and the dissipated power in the resistor (P d): (1) In this equation, T ref – m is the reference temperature (the subscript m refers to the thermal model), that is to say, the initial temperature of our sample before the laser irradiation that should match the environment temperature.

3%. In LY2835219 solubility dmso addition, Tn2010 is a composite element of adding the mefE gene on the basis of Tn6002, with a proportion of 28.9% in the present study. Tn3872 results from the insertion of the ermB-containing Tn917 transposon [30] into Tn916[31]. Tn1545 and Tn6003 have similar compositions; they both contain the kanamycin resistance gene aph3’-III aside from the erythromycin- and tetracycline-resistance determinants ermB and tetM. In this study, the transposons Tn3872 and Tn1545/Tn6003

were rare at approximately 11.1%, indicating that Tn3872 and Tn1545/Tn6003 were not the main factors for erythromycin and tetracycline resistance in Beijing children. Moreover, we also found five pneumococcal isolates without transposon determinants that carried the ermB and tetM genes or only ermB gene. Further studies are necessary to verify if these five isolates contain unknown transposons. Three conjugate vaccines, namely, PCV7, PCV10, and PCV13, were introduced to prevent pneumococcal infections in children. PCV13 included serotypes 1, 3, 5, 6A, 7F, and 19A plus the PCV7 serotypes 4, 6B, 9V, 14, 18C, 19F, and 23F. In this study, the serotypes 23F, 19F, 14, and 6B were common among S. pneumoniae from Beijing children younger than five years. This result was similar with the previous AZD8186 studies

in China [20, 32, 33], but different from that of the other European countries, in which the serotypes 1, 3, 6A, 7F, and 19A were common among pneumococcal isolates [34]. Since the introduction of PCV7, the incidence of pneumococcal disease because of PCV7-serotypes has significantly declined in many countries. However, several countries have reported an increased rate of pneumococcal disease in non-PCV7 serotypes. This phenomenon, termed ‘replacement’, is associated with specific pneumococcal serotypes or clones [35]. In China, the PCV7-serotypes were more popular among children for two reasons: first, PCV7 has been on the market for only four years in China since 2008. Second, only about 1% of Chinese

children use PCV7 for their routine pneumococcal immunization. We found that the PCV13 coverage of the erythromycin-resistant isolates was higher than that of PCV7 PLEK2 among all children younger than five years as well as the children aged 0 to 2 years because of the high rates of serotypes 3, 6A, and 19A. Moreover, the PCV7 coverage of children aged 2 to 5 years was also significant higher than that of children aged 0 to 2 years. All these results indicate that PCV13 controls the pneumococcal diseases Bucladesine purchase caused by the erythromycin-resistant isolates better than PCV7 for children, especially those younger than two years. Maiden et al. [36] introduced the MLST approach to monitor the epidemiology of bacteria based on multi locus enzyme electrophoresis. Enright and Spratt were the first to apply MLST for pneumococcal studies [14].

Discussion In this report, we present evidence showing that the peptide S20-3, corresponding to the Ig-like domain of the Fas-targeting K1 protein of HHV-8, selectively kills hematological cancer cells, and the mechanism involves the Fas and TNFRI receptors. The cell-killing effect appears to be selective for cancer cells in vitro. In vivo, even a single intratumoral dose of peptide was active against the growth of xenograft tumors. From the array of K1 Ig-like domain peptides tested (Table 1), only the S20-3 peptide demonstrated strong and reproducible cell-killing

activity (Figure 1 and Figure 2) in all 6 hematological cell lines tested but not in PBMC controls (Figure 2). While it is not clear as to why S20-3, and also less reproducibly S20-2, but not other K1 Ig-like domain-derived A-1210477 price peptides, possess cell-killing activity, the structural features of the predicted Ig-domain (Figure 5B) reveal a unique feature Wnt inhibitor of the S20-3 peptide; a loop (centered at conserved glycine residue) linking 2 beta sheets, which are predicted to be destabilized or absent in the rest of peptides tested (Table 1). A truncated version of the S20-3 peptide, S10-1, representing

the first beta sheet and the loop (Figure 5B), as well as S8-2 peptide, representing the second beta sheet (Figure 5B), lack cell killing properties (Figure 1B). On the other hand, a TCR-derived peptide sharing 5 structure-defining residues with S20-3 (Figure 5A) also showed cell-killing effect (Figure 5C), suggesting that the biological effect of S20-3 is related to its structure. A seemingly contradictory effect

of the whole Ig-like domain in K1 protein and S20-3 peptide on Fas signaling may also be explained by the structure-function relationship. The fact that peptide S10-1, Thalidomide but not S20-3 or any other K1 peptide, was able to disrupt the K1-Fas complex (Additional file 1: Figure S2) suggests that first beta sheet is involved in K1-Fas interaction. This is further supported by the fact that peptide S10-2, lacking 3 residues from the first beta sheet, failed to displace K1 (Additional file 1: Figure S2) and did not show any enhancement of FasL activity (Figure 1A). Additionally, peptide S20-2, which also contains S10-1 residues, showed cell-killing properties similar to peptide S20-3, but with reduced reproducibility, suggesting that the second beta sheet in peptide S20-3 increases structural stability of the peptide and the additional residues, preceding (S20-2) or following (S20-3) S10-1 region, affect peptide behavior. selleck chemicals Taking all this into account, we hypothesize that the smaller size and possible flexibility of the loop within S10-1peptide as compared to S20-3 peptide (Figure 5B) allow access of this peptide to the K1 binding site and, thus, displacement of K1 from Fas (Additional file 1: Figure S2).

J Pharmacol Exp Ther. 2000;292:288–94. http://​www.​ncbi.​nlm.​nih.​gov/​pubmed/​10604960. 3. Gheorghiade M, Niazi I, Ouyang J, et al. Vasopressin V2-receptor blockade with tolvaptan in patients with chronic heart failure: results from a

double-blind, randomized trial. Staurosporine concentration Circulation. 2003;107:2690–6. http://​www.​ncbi.​nlm.​nih.​gov/​pubmed/​12742979. 4. Gheorghiade M, Gattis WA, O’Connor CM, et al. Effects of tolvaptan, a vasopressin antagonist, in patients hospitalized with JAK inhibitor worsening heart failure. JAMA. 2004;291:1963–71. 5. Gheorghiade M, Orlandi C, Burnett JC, et al. Rationale and design of the multicenter, randomized, double-blind, placebo-controlled study to Evaluate the Efficacy of Vasopressin Antagonism in Heart Failure: Outcome Study with Tolvaptan (EVEREST). J Card Fail. 2005;11:260–9.PubMedCrossRef 6. Blair JEA, Pang PS, Schrier RW, selleck inhibitor et al. Changes in renal function during hospitalization and soon after discharge in patients admitted for worsening heart failure in the placebo group of the EVEREST trial. Eur Heart J. 2011;32:2563–72. 7. Vaduganathan M, Gheorghiade M, Pang PS, et al. Efficacy of oral tolvaptan in acute heart failure

patients with hypotension and renal impairment. J Cardiovasc Med (Hagerstown). 2012;13:415–22. http://​www.​ncbi.​nlm.​nih.​gov/​pubmed/​22673023. 8. Costello-Boerrigter LC, Smith WB, Boerrigter G, Ouyang J, Zimmer CA, Orlandi C, Burnett JC Jr. Vasopressin-2-receptor antagonism augments water excretion without changes in renal hemodynamics or sodium and potassium excretion in human heart failure. Am J Physiol Renal Physiol. 2006;290:F273–8. 9. Okada T, Sakaguchi T, Hatamura I, et al. Tolvaptan, a selective oral vasopressin V2 receptor antagonist, ameliorates podocyte injury in puromycin aminonucleoside nephrotic rats. Clin Exp Nephrol. 2009;13:438–46. http://​www.​ncbi.​nlm.​nih.​gov/​pubmed/​19452240.

10. Onogawa T, Sakamoto Y, Nakamura S, Nakayama S, Fujiki H, Yamamura Y. Effects of tolvaptan on systemic and renal hemodynamic function in dogs with congestive heart failure. Cardiovasc Drugs Ther. 2011;25 Suppl 1:S67–76. http://​www.​ncbi.​nlm.​nih.​gov/​pubmed/​22120095. 11. Matsue Y, Suzuki M, Seya M, et al. Tolvaptan Mirabegron reduces the risk of worsening renal function in patients with acute decompensated heart failure in high-risk population. J Cardiol. 2012. http://​www.​ncbi.​nlm.​nih.​gov/​pubmed/​23159210. 12. Mullens W, Abrahams Z, Francis GS, et al. Importance of venous congestion for worsening of renal function in advanced decompensated heart failure. J Am Coll Cardiol. 2009;53:589–96. http://​www.​ncbi.​nlm.​nih.​gov/​pubmed/​19215833. 13. Peacock WF, Costanzo MR, De Marco T, et al. Impact of intravenous loop diuretics on outcomes of patients hospitalized with acute decompensated heart failure: insights from the ADHERE registry. Cardiology. 2009;113:12–9. http://​www.​ncbi.​nlm.​nih.​gov/​pubmed/​18931492. 14.

8, 2.2 and 3-fold (P < 0.05) increase in cleaved caspase-3-positive cells over that of control group. These results confirmed the apoptotic effect of Mesothelin shRNA in tumors, which could have been mediated by the caspase-3 pathway. Our results shown buy C188-9 in Capan-2 cells with wt-p53, mesothelin regulated PUMA, bax and bcl-2 through wt-p53 dependent pathway. In Capan-1, MIA PaCa-2 and ASPC-1 cells with mt-p53, mesothelin regulated PUMA, bax and bcl-2 through wt-p53 independent pathway (Figure 6D). Discussion Mesothelin is a glycoprotein to be largely restricted to mesothelial cells or to epithelial cells of the trachea,

tonsils, fallopian tube, and kidneys [21]. Mesothelin has been reported to be a tumour-associated marker in several types of human cancers, including ovarian carcinomas and adenocarcinomas arising from the pancreatico-biliary tract, endometrium, and lungs [22]. Mesothelin has also been reported to interact with CA125 to mediate cell adhesion [23]. Although the biological functions of mesothelin remain largely unknown, there is evidence that mesothelin has the potential as a new cancer biomarker [10] and as a target molecule for gene therapy [24]. Some investigators have reported that mesothelin can be a new

Belinostat supplier marker for the diagnosis of ovarian carcinoma [25] and as a target in mesothelin-expressing tumours [18], including pancreatic cancer [11]. However,the signal transduction pathways induced by mesothelin resulting in cell survival is unclear. In the present study, we have shown that mesothelin was overexpressed in the human pancreatic cancer cell lines. Increased mesothelin is associated with increased cell proliferation of pancreatic cancer cells in vitro and contributes to tumor progression in the nude mouse xenograft model. Silencing of mesothelin expression significantly decreased cell proliferation and promoted apoptosis in pancreatic cancer cells in vitro and inhibited tumor see more growth in vivo. We also shown mesothelin mediated cell survival Prostatic acid phosphatase and apoptosis by

p53-dependent and independent conditions. p53 is a critical regulator of the response to DNA damage and oncogenic stress. Loss of p53 function, through mutation or deletion, is a frequent occurrence in human malignancies. Previous experimental works have converged to indicate that the wt-p53 protein would act as a negative regulator of cell growth [26–28] and a suppressor of transformation and tumonigenesis [29]. In the study reported here, we chose HPAC cells which expressed wt-p53 with less endogenous mesothelin, and Capan-2 cells which expressed wt-p53 with moderate endogenous mesothelin. We found that mesothelin overexpression in HPAC and Capan-2 cells is associated with increased cell proliferation followed by decreased wt-p53. p53 re-inhibition by siRNA in stable mesothelin sliencing Capan-2 and HPAC cells promoted cell survival and proliferation.

When cultured in TSB as free-living cells, wild type and all mutant strains showed the similar growth rates, as reported in previous FK228 study [20]. In contrast, when incubated in PBS for 24 h, wild type and mutants lacking long and/or short fimbriae formed distinct biofilms (Figure

1 and Table 1). Wild type strain 33277 formed biofilms with a dense basal monolayer and dispersed microcolonies. Compared with the wild type, the long fimbria mutant KDP150 formed patchy and sparser biofilms with a significantly greater distance between fewer peaks, although mean peak height was almost the same as that of the wild type strain. In contrast, the short fimbria mutant MPG67 developed cluster and channel-like selleck products biofilms consisting of significantly taller microcolonies compared to the wild type. Similar to MPG67, the mutant (MPG4167) lacking both types of fimbriae also formed thick biofilms with significantly taller microcolonies than the wild type. Viability of the cells in biofilms of each strain was tested by colony count and confirmed at 24 h (data not shown). These results suggest that the long fimbriae are involved in initial attachment and organization of biofilms by P. gingivalis, whereas the short fimbriae have a suppressive regulatory role for these steps. Figure

1 Homotypic biofilm formation by P. gingivalis wild-type strain and mutants in PBS. P. gingivalis strains were stained with CFSE (green) and incubated in PBS for 24 hours. After washing, the biofilms that developed on the coverglass ID-8 were observed with a CLSM equipped with a 40× objective. Optical sections were obtained along the z axis at 0.7-μm intervals, and images of the x-y and x-z planes were reconstructed

with an imaging software as described in the text. Upper panels indicate z stacks of the x-y sections. Lower panels are x-z sections. P. gingivalis strains used in this assay are listed in Table 4. The experiment was repeated independently three times with each strain in selleck compound triplicate. Representative images are shown. Table 1 Features of biofilms formed by P. gingivalis wild-type strain and mutants in PBS   Peak parametersa) Strain Number of peaks Mean distance between peaks (μm) Mean peak height (μm) ATCC33277 (wild type) 28.5 ± 3.3 3.0 ± 0.2 2.8 ± 0.4 KDP150 (ΔfimA) 14.7 ± 2.4** 5.4 ± 1.0** 2.7 ± 0.8 MPG67 (Δmfa1) 29.3 ± 2.0 3.6 ± 0.2 16.6 ± 0.8** MPG4167 (ΔfimAΔmfa1) 30.5 ± 1.9 3.1 ± 0.2 12.7 ± 0.5** KDP129 (Δkgp) 25.5 ± 2.1 3.6 ± 0.3 12.7 ± 1.3** KDP133 (ΔrgpAΔrgpB) 13.0 ± 2.6** 8.4 ± 1.3** 23.2 ± 2.8** KDP136 (ΔrgpAΔrgpBΔkgp) 30.5 ± 2.4 3.2 ± 0.2 12.7 ± 0.7** a) Number of peaks was evaluated in an area sized 90 (x axis) × 2 (y axis) μm. The mean ± SE of 10 areas was shown. **p < 0.

Positive but weak congruence between trees, and birds and bats is also found in the distribution of

endemic species. Lowland dipterocarp 17DMAG nmr forest has the highest proportion of endemic tree species, for birds and bats this forest type ranks third in endemism following ultrabasic and montane forest. Whereas mangrove forest is still a relatively important forest type for endemic birds and bats, no endemic trees are found there. At country level, congruence between Philippine plant and vertebrate endemism as a proportion of global species richness is 100% (Myers et al. 2000), but our results show that there is much more heterogeneity in cross-taxon relations in endemic species richness at finer spatial scale levels. The distribution of globally Pitavastatin cost threatened species seems incongruent. Lowland dipterocarp forest has the highest relative occurrence of threatened tree species, whereas for birds and bats montane forest is the most important forest type in this respect. Within the two survey plots in lowland dipterocarp forest, nine endemic dipterocarp tree species were recorded that are listed as Critically Endangered

(Table 5), of these only two also occur in ultrabasic forest. Lowland dipterocarp and ultrabasic forest have comparable numbers Ruboxistaurin molecular weight of threatened tree species within the lower threat categories. In mangrove forest and montane forest no tree species listed as globally threatened

were recorded. No globally threatened birds were recorded in mangrove forest either but montane forest is an important forest type for threatened Alanine-glyoxylate transaminase birds. This is largely due to the fact that endemic montane species have small ranges and are thus more vulnerable to even small changes in montane forest cover (Brooks et al. 1999) and as a result qualify easier as threatened under the area change criteria of the IUCN Red List. Montane forest in the NSMNP has several enigmatic bird species, among which the Critically Endangered Philippine Eagle Pithecophaga jefferyi, the conservation icon of the Philippines. In this study, only one globally threatened species was recorded in mangrove forest, the Endangered fruit bat Acerodon jubatus. Cross-taxon congruence between the proportions of threatened trees and bats across the four forest types correlated negatively. It must be noted however that trees have not been completely assessed for the IUCN Red List, possibly explaining the lack of tree species classified as threatened in montane forest.

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cardiac troponin T assay during and after a 216 km ultra-endurance marathon run in Death Valley. Clinical Research in Cardiology 2007, 96:359–364.PubMedCrossRef 6. Skenderi KP, Kavouras SA, Anastasiou CA, Yiannakouris N, Matalas AL: Exertional rhabdomyolysis during a 246-km continuous running race. Medicine and Science in Sports and Exercise 2006, 38:1054–1057.PubMedCrossRef 7. Reid SA, King MJ: Serum biochemistry and morbidity among runners presenting for medical care after an Australian mountain ultramarathon. Clinical Journal of Sport Medicine 2007, 17:307–310.PubMedCrossRef 8. Uberoi HS, Dugal JS, Kasthuri AS, Kolhe VS, Kumar AK, Cruz SA: Acute renal failure in severe exertional rhabdomyolysis. The Journal of the Association of Physicians of India 1991, 39:677–679.PubMed 9. Fellmann N, Sagnol M, Bedu M, Falgairette G, Van Praagh E, Gaillard G, Jouanel P, Coudert J: Enzymatic and hormonal responses following a 24 h endurance run and a 10 h triathlon race. European

Journal of Applied Physiology 1988, 57:545–553.CrossRef 10. Dohm GL, Tapscott EB, Kasperek GJ: Protein degradation during endurance exercise Selleck Forskolin and recovery. Medicine and Science in Sports and Exercise 1987, 19:S166-S171.PubMed 11. Knechtle B, Kohler G: Running 338 kilometres within five days has no effect on body mass and body fat but reduces skeletal muscle mass – the Isarrun 2006. Journal of Sports Science and Medicine 2007, 6:401–407. 12. 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. Journal of Sports Science and Medicine 2008, 7:357–364. 13. Romano-Ely BC, Todd MK, Saunders MJ, Laurent TS: Effect of an isocaloric carbohydrate-protein-antioxidant drink on cycling performance. Medicine and Science in Sports and Exercise 2006, 38:1608–1616.PubMedCrossRef 14. Saunders MJ, Moore RW, Kies AK, Luden ND, Pratt CA: Carbohydrate and protein hydrolysate coingestions improvement of late-exercise time-trial performance.