Genome Biol 2008,9(4):R74 PubMedCrossRef 2 Jumaa PA, Sonnevend A

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: Mycobacterium tuberculosis Rv2536 protein implicated in specifi

: Mycobacterium tuberculosis Rv2536 protein implicated in specific binding to human cell lines. Protein Sci 2005,14(9):2236–2245.PubMedCrossRef 26. Chapeton-Montes JA, Plaza DF, Curtidor H, Forero M, Vanegas M, Patarroyo ME, Patarroyo MA: Characterizing the Mycobacterium tuberculosis Rv2707 protein and determining its sequences which specifically bind to two human cell lines. Protein Sci 2008,17(2):342–351.PubMedCrossRef 27. Chapeton-Montes JA, Plaza DF, Barrero CA, Patarroyo Alpelisib manufacturer MA: Quantitative flow cytometric monitoring of invasion of epithelial

cells by Mycobacterium tuberculosis . Front Biosci 2008, 13:650–656.PubMedCrossRef 28. Patarroyo MA, Plaza DF, Ocampo M, Curtidor H, Forero M, Rodriguez LE, Patarroyo ME: Gemcitabine cell line functional characterization of Mycobacterium tuberculosis Rv2969c membrane protein. Biochemical and biophysical research communications 2008,372(4):935–940.PubMedCrossRef 29. Matsuba T, Suzuki Y, Tanaka Y: Association of the Rv0679c protein with lipids and carbohydrates in Mycobacterium tuberculosis / Mycobacterium bovis BCG. Archives of microbiology 2007,187(4):297–311.PubMedCrossRef 30. Briken V, Porcelli selleck SA, Besra GS, Kremer L: Mycobacterial lipoarabinomannan and related lipoglycans: from biogenesis to modulation

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This leads to the necessity to focus on breast cancer follow-up p

This leads to the necessity to focus on breast cancer follow-up procedures for the high relevance they have for both patients and professional Vorinostat cost personnel [6]. The primary aim of routine post-operative surveillance after early stage breast cancer

surgery, referred to as ‘follow-up’, is to enhance survival, psychosocial and physical well-being of patients. The effectiveness of different breast cancer follow-up procedures for early detection of metastatic disease is an old issue, starting in the 1980s [7–10]. In the 1990s, evidences from phase III randomized trials (RCTs) demonstrated that intensive follow-up procedures do not improve outcome or quality of life when compared to patients’ Tucidinostat price educations about symptoms referral and regular physical VS-4718 chemical structure examinations [11–18]. Nowadays, there is a general agreement on the utility of yearly mammography for detecting local recurrences and/or second primary cancers while intensive follow-up practices by imaging techniques (i.e. chest radiograph, bone scan and liver sonography) are not recommended by current international guidelines [19, 20]. Nevertheless, the appropriateness of screening tests to be used as well as the frequency of follow-up procedures and the optimal follow-up duration

are still object of debate [21–24], which reflects in the wide use of intensive surveillance and in the long-term follow-up period in everyday clinical practice [6, 25–28]. Based on these premises, we conducted a systematic review of the surveillance procedures utilized in phase III RCTs of adjuvant treatments in early stage breast cancer in order to asses if a similar variance exists in the scientific world. Methods Literature mafosfamide search and eligibility criteria We searched PubMed (PubMed, available at URL: http://​www.​ncbi.​nlm.​nih.​gov/​pubmed) from January 1, 2002

to December 31, 2012 for phase III RCTs of early breast cancer medical adjuvant therapies with disease free survival (DFS) as primary endpoint of the study [29]. We selected only full text publications (not abstracts), written in English-language. Trials on neoadjuvant therapies, neoadjuvant followed by adjuvant therapies, adjuvant bisphosphonates alone, non medical treatments, radiation therapies, adjuvant chemotherapy for loco-regional relapses and non-phase III trials were excluded. When multiple publications of the same RCT were identified, the first publication was selected. We used as keywords: breast cancer adjuvant therapy, clinical trial, phase III, phase 3 and randomized. Data extraction Information extracted from each trial included: date of beginning of patients enrollment, geographic location, number of participating countries, sponsorship by pharmaceutical companies, number of participating centers, number of enrolled patients, follow-up description (modalities, frequency and duration).

Infect Immun 2006,74(1):488–496 PubMedCrossRef 21 Bassler BL: Ho

Infect Immun 2006,74(1):488–496.PubMedCrossRef 21. Bassler BL: How bacteria talk to each other: regulation of gene expression by quorum sensing. Curr Opin Microbiol 1999,2(6):582–587.PubMedCrossRef 22. Miller MB, Bassler BL: Quorum sensing in bacteria. Annu Rev Microbiol 2001, 55:165–199.PubMedCrossRef 23. De Keersmaecker SC, Sonck K, Vanderleyden J: Let LuxS speak up in AI-2 signaling. Trends Microbiol 2006,14(3):114–119.PubMedCrossRef

24. Surette MG, Miller MB, Bassler BL: Quorum sensing in Escherichia coli, Salmonella typhimurium, and Vibrio harveyi: a new family of genes responsible for autoinducer production. Proc Natl Acad Sci USA 1999,96(4):1639–1644.PubMedCrossRef 25. Schauder S, Shokat K, Surette MG, Bassler BL: The LuxS family of bacterial Nutlin-3a cost autoinducers: PCI-32765 solubility dmso biosynthesis of a novel quorum-sensing signal molecule. Mol Microbiol 2001,41(2):463–476.PubMedCrossRef 26. Chen X, Schauder S, Potier N, Van Dorsselaer A, Pelczer I, Bassler BL, Hughson FM: Structural identification of a bacterial quorum-sensing signal containing boron. Nature 2002,415(6871):545–549.PubMedCrossRef 27. Miller ST, Xavier KB, Campagna SR,

Taga ME, Semmelhack MF, Bassler BL, Hughson FM: Salmonella typhimurium recognizes a chemically distinct form of the bacterial quorum-sensing signal AI-2. Mol Cell 2004,15(5):677–687.PubMedCrossRef 28. Lupp C, Ruby EG: Vibrio fischeri LuxS and AinS: comparative study of two signal synthases. J Bacteriol 2004,186(12):3873–3881.PubMedCrossRef 29. Rader BA, Campagna SR, AMP deaminase Semmelhack MF, Bassler BL, Guillemin K: The quorum-sensing molecule Selleck 3-deazaneplanocin A autoinducer 2 regulates motility and flagellar morphogenesis in Helicobacter pylori. J Bacteriol 2007,189(17):6109–6117.PubMedCrossRef 30. Bansal T, Jesudhasan P, Pillai S, Wood TK, Jayaraman A: Temporal regulation of enterohemorrhagic Escherichia coli virulence mediated by autoinducer-2. Appl Microbiol Biotechnol 2008,78(5):811–819.PubMedCrossRef 31. Gonzalez Barrios AF, Zuo R, Hashimoto Y, Yang L, Bentley

WE, Wood TK: Autoinducer 2 controls biofilm formation in Escherichia coli through a novel motility quorum-sensing regulator (MqsR, B3022). J Bacteriol 2006,188(1):305–316.PubMedCrossRef 32. Shao H, Lamont RJ, Demuth DR: Autoinducer 2 is required for biofilm growth of Aggregatibacter (Actinobacillus) actinomycetemcomitans. Infect Immun 2007,75(9):4211–4218.PubMedCrossRef 33. Vidal JE, Ludewick HP, Kunkel RM, Zahner D, Klugman KP: The LuxS-dependent quorum-sensing system regulates early biofilm formation by Streptococcus pneumoniae strain D39. Infect Immun 2011,79(10):4050–4060.PubMedCrossRef 34. Auger S, Krin E, Aymerich S, Gohar M: Autoinducer 2 affects biofilm formation by Bacillus cereus. Appl Environ Microbiol 2006,72(1):937–941.PubMedCrossRef 35. Tannock GW, Ghazally S, Walter J, Loach D, Brooks H, Cook G, Surette M, Simmers C, Bremer P, Dal Bello F, et al.

Nat Rev Immunol 2009,9(5):313–23

Nat Rev Immunol 2009,9(5):313–23.PubMedCrossRef 7. Peterson DA, Frank DN, Pace NR, Gordon JI: Metagenomic approaches for defining the pathogenesis of inflammatory bowel diseases. Cell Host Microbe 2008,3(6):417–27.PubMedCrossRef 8. Hattori M, Taylor TD: The human intestinal microbiome: a new frontier of human biology. DNA Res 2009,16(1):1–12.PubMedCrossRef 9. Eckburg PB, Bik EM, Bernstein CN, Purdom E, Dethlefsen L, Sargent

M, Gill SR, Nelson KE, Relman DA: Diversity of the human intestinal flora. Science 2005, 308:1635–1638.PubMedCrossRef selleck inhibitor 10. Andersson AF, Lindberg M, Jakobsson H, Backhed F, Nyrén P, Engstrand L: Comparative analysis of human gut microbiota by barcoded pyrosequencing. PloS ONE 2008, 3:e2836.PubMedCrossRef 11. Claesson MJ, O’Sullivan O, Wang Q, Nikkila J, Marchesi JR, Smidt H, de Vos WM, O’Toole PW: Comparative analysis of pyrosequencing and a phylogenetic Selleckchem MS275 microarray for exploring microbial community structures in the human distal intestine. PLoS ONE 2009, 4:e6669.PubMedCrossRef 12. Turnbaugh Evofosfamide ic50 PJ, Hamady M, Yatsunenko T, Cantarel BL, Duncan A, Ley RE, Sogin ML, Jones WJ, Roe BA, Affourtit JP, Egholm M, Henrissat B, Heath AC, Knight R, Gordon JI: A core gut microbiome in obese and

lean twins. Nature 2009,457(7228):480–4.PubMedCrossRef 13. Turnbaugh PJ, Ley RE, Mahowald MA, Magrini V, Mardis ER, Gordon JI: An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 2006,444(7122):1027–31.PubMedCrossRef 14. Frank DN, St Amand AL, Feldman RA, Boedeker EC, Harpaz N, Pace NR: Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases. Proc Natl Acad Sci USA 2007,104(34):13780–5.PubMedCrossRef 15. Sokol H, Pigneur B, Watterlot L, Lakhdari O, Bermúdez-Humarán LG, Gratadoux JJ, Blugeon S, Bridonneau C, Furet JP, Corthier G, Grangette C, Vasquez N, Pochart P, Trugnan G, Thomas G, Blottière HM, Doré J, Marteau P, Seksik P, Langella P: Faecalibacterium prausnitzii is an anti-inflammatory

commensal bacterium identified by gut microbiota analysis of Crohn disease patients. Proc Natl Acad Sci USA 2008,105(43):16731–6.PubMedCrossRef 16. Stecher B, Robbiani R, Walker AW, Westendorf AM, Barthel M, Kremer M, Chaffron S, Macpherson AJ, Buer J, Parkhill J, Dougan G, von Mering C, Hardt WD: Salmonella enterica serovar typhimurium exploits Casein kinase 1 inflammation to compete with the intestinal microbiota. PLoS Biol 2007,5(10):2177–89.PubMedCrossRef 17. Pédron T, Sansonetti P: Commensals, bacterial pathogens and intestinal inflammation: an intriguing ménage à trois. Cell Host Microbe 2008,3(6):344–7.PubMedCrossRef 18. Mazmanian SK, Round JL, Kasper DL: A microbial symbiosis factor prevents intestinal inflammatory disease. Nature 2008,453(7195):620–5.PubMedCrossRef 19. Hamady M, Knight R: Microbial community profiling for human microbiome projects: Tools, techniques, and challenges. Genome Res 2009,19(7):1141–52.PubMedCrossRef 20.

[21], in which pvf and gac mutants were complemented by a wild-ty

[21], in which pvf and gac mutants were complemented by a wild-type extract. These results allow us to propose a putative regulatory role for the mgo operon in secondary metabolite production by P. syringae pv. syringae, in accordance with Vallet-Gely et al. [21]. To fully

characterise the functions of the mgo operon, more data concerning the chemical structure of mangotoxin and a characterisation of the other genetic traits that regulate mangotoxin biosynthesis by P. syringae pv. syringae UMAF0158 are required. PLX4032 Dibutyryl-cAMP mouse Conclusions In the present study, the organisation of the mgo operon in P. syringae pv. syringae UMAF0158 was characterised. The mgo operon is composed of four genes, mgoB, mgoC, mgoA and mgoD. Additionally, this operon possesses one active promoter and a terminator. The last three genes are essential for mangotoxin production, as insertional mutation of these genes results in a loss of mangotoxin production. This operon is only active in minimal medium, in agreement with the standard process for mangotoxin production.

Moreover, experiments performed to determine 4-Aminobutyrate aminotransferase the functional role of the mgo operon demonstrated a putative regulatory function in the production of mangotoxin. Methods Bacterial strains and plasmids used in this study The strains of Escherichia coli, Caspase Inhibitor VI supplier Pseudomonas fluorescens Pf-5 and Pseudomonas syringae pv. syringae as well as the vectors and plasmids used in this study are listed in Table 5. E. coli was grown in Luria-Bertani

medium (LB) at 37°C for 24 h. The Pseudomonas strains were grown routinely in King’s medium B (KB) at 28°C for 48 h. Derivative mutants of P. syringae pv. syringae UMAF0158 (Table 5) were grown and maintained in KB supplemented with the appropriate antibiotics (ampicillin, 50 μg/ml; streptomycin, 50 μg/ml; kanamycin, 50 μg/ml; and gentamicin, 20 μg/ml). Table 5 Bacterial strains and plasmids used in this study Strain or plasmid Relevant characteristicsa Reference or source Escherichia coli        DH5α recA lacZΔM15 [27]    CECT831 Indicator strain of mangotoxin production CECTb Pseudomonas fluorescens        Pf-5 Complete genome sequenced and free access. [28] Pseudomonas syringae pv.

J Microbiol Methods 2010, 80:281–286 PubMedCrossRef 16 Houf K, O

J Microbiol Methods 2010, 80:281–286.PubMedCrossRef 16. Houf K, On S, Coenye T, Debruyne L, De Smet S, Vandamme P: Arcobacter thereius sp. nov., isolated from pigs and ducks. Int J Syst Evol Microbiol 2009, Selleckchem 3 MA 59:2599–2604.PubMedCrossRef 17. De Smet S, Vandamme P, De Zutter L, On S, Douidah L, Houf K: Arcobacter trophiarum sp. nov. isolated from fattening pigs. Int J Syst Evol Microbiol 2011, 63:356–36118.CrossRef 18. Kim HM, Hwang CY, Cho BC: Arcobacter marinus sp. nov. Int J Syst Evol Microbiol 2010, 60:531–536.PubMedCrossRef 19. Collado L, Inza I, Guarro J, Figueras MJ: Presence of Arcobacter

spp. in environmental waters correlates with high levels of fecal pollution. Environ Microbiol 2008, 10:1635–1640.PubMedCrossRef 20. Collado L, Guarro J, Figueras MJ: Prevalence of Arcobacter in meat and Lonafarnib clinical trial shellfish. J Food Prot 2009, 72:1102–1106.PubMed 21. Collado L, Kasimir G, Perez U, Bosch A, Pinto R, Saucedo G, Huguet JM, Figueras JM: Occurrence and diversity of Arcobacter spp. along the Llobregat river catchment, at sewage effluents and in a drinking water treatment plant.

Water Res 2010, 44:3696–3702.PubMedCrossRef 22. Collado L, Levican A, Perez J, Figueras MJ: Arcobacter defluvii sp. nov., isolated from sewage. Int J Syst Evol Microbiol 2011, 61:1895–1901.CrossRef 23. Levican A, Collado L, Figueras MJ: Arcobacter cloacae sp. nov. and Arcobacter suis sp. nov., two new species isolated from food and sewage. Syst Appl Microbiol,. doi:10.1016/j.syapm.2012.11.003. in press. in press 24. Figueras MJ, Soler L, Chacón MR, Guarro JSH-23 nmr J, Martínez-Murcia AJ: Use of restriction fragment length polymorphism of the PCR-amplified 16S rRNA gene for the identification of Aeromonas spp. J Clin Microbiol 2000, 38:2023–2025.PubMed 25. Alperi A, Figueras MJ, Inza I, Martinez-Murcia AJ: Analysis of 16S rRNA gene mutations in a subset of Aeromonas strains and their impact in species

delineation. Int Microbiol 2008, 11:185–194.PubMed 26. Martínez-Murcia AJ, Benlloch S, Collins MD: Phylogenetic interrelationships of members of the genera Aeromonas and Plesiomonas as determined by 16S ribosomal DNA sequencing: lack of congruence with results of DNA-DNA hybridizations. Int J Syst Bacteriol 1992, 42:412–421.PubMedCrossRef CYTH4 27. Marshall SM, Melito PL, Woodward DL, Johnson WM, Rodgers FG, Mulvey R: Rapid identification of Campylobacter, Arcobacter, and Helicobacter isolates by PCR-restriction fragment length polymorphism analysis of the 16S rRNA gene. J Clin Microbiol 1999, 37:4158–4160.PubMed 28. Vincze T, Posfai J, Roberts RJ: NEBcutter: a program to cleave DNA with restriction enzymes. Nucleic Acids Res 2003, 31:3688–3691. http://​tools.​neb.​com/​NEBcutter2/​index.​php PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions MJF designed the research project, evaluated results and was principal author.

7) 15 (18 9) W 3 (4 3) 21 (26 6) FHA 0 0 FIA 0 0 FIB 32 (45 7) 23

7) 15 (18.9) W 3 (4.3) 21 (26.6) FHA 0 0 FIA 0 0 FIB 32 (45.7) 23 (29.1) Y 0 1 (1.3) I1 11 (15.7) 3 (3.8) Frep 1 (1.4) 17 (21.5) X 0 0 HI1 0 0 N 0 0 HI2 0 0 L/M 0 0 Our data show that the EPEC resistance

plasmid is found commonly in typical EPEC, and is uncommon in check details atypical EPEC, consistent with earlier data [27]. However, previous evaluation of the distribution of the EPEC multiresistance plasmid in a small collection of archival strains suggested that it was limited to O111:H2 and O119:H2 strains, which carry the EAF plasmid or vestiges of it NVP-BSK805 purchase [27]. In the current study, traI and traC markers from the resistance plasmid were identified in strains belonging to the serotypes O55:H6, O127:H6, and O119:H6, as well as O55 and O119 atypical strains that carry vestiges of the EAF plasmid (see Additional file 1). To determine whether this broader distribution among Brazilian isolates was a recent development, we screened 36 archival EPEC strains

that were isolated in the 1970s and 1980s from children with diarrhea in São Paulo [12], and the plasmid was predominately found in O111:H2, O119:H6 and O142:H6 strains (data not shown), which were among the most common circulating serovars at that time [2, 13, 31]. Although isolates that were susceptible to all tested agents were more likely to be traI and traC negative and strains that had these markers were to a higher degree multiple resistant, in contrast to the association seen with older isolates from other geographic locations [27], we did not find that the presence selleck kinase inhibitor of traI and traC markers in the EPEC isolates were absolutely or significantly associated with multiple resistance. The EPEC resistance plasmids of previously studied O111 and O119 strains bear class 1 integrons as well as one or more resistance genes identical to those on Salmonella enterica subsp. Typhi multiresistant plasmid pHCM1 [25]. Some typical strains and all atypical strains had fewer of these markers, even though antimicrobial resistance was just as common mafosfamide in these isolates (see Additional file 1).

Among isolates 12 of 39 strains carrying the EPEC resistance plasmid and one of 31 strains without it had a class 1 integron (p = 0.0025, Yates corrected Chi-squared test). None of the other markers screened showed significant association with the plasmid in strains. Combined with the resistance data, these findings suggest that the EPEC resistance plasmid plays less of a role in conferring resistance in these EPEC isolates, in particular atypical strains, and that there may be possible other genetic elements conferring resistance among those strains. EPEC strains bearing the EPEC resistance plasmid carry at least two, and sometimes more than three, large plasmids [27, 30]. We used a PCR-based replicon typing scheme to determine other possible plasmid types conferring antimicrobial resistance in the EPEC strains studied.

Potential phoBR mutants were then checked for their loss of alkal

Potential phoBR mutants were then checked for their loss of alkaline phosphatase activity (phoA, encoding alkaline phosphatase, is a Verteporfin cost conserved Pho regulon gene [1, 37]) and the sequence of the operon was determined, as described

in Methods. The phoB gene was predicted to encode a 229 amino acid (aa) protein with highest similarity to PhoB from Eca 1043 (96% identity/98% similarity). The phoR gene was located 28 bp downstream of phoB, and was predicted to encode a 440 aa protein sharing the highest degree of similarity to Eca 1043 PhoR (87% identity/90% similarity). PhoB regulates expression of pstC in Serratia 39006 In E. coli, the pst operon is activated via direct binding of PhoB to a conserved Pho box upstream of pstS [10–12]. As Serratia 39006 is a member of the Enterobacteriaceae, BIBF-1120 we identified potential Pho boxes based on the E. coli consensus sequence. A potential Pho box was identified within the pstS promoter region of Serratia 39006, centred 122 bp upstream of the pstS start codon (Fig. 1B). This suggested that, as could be expected based on regulation of the pstSCAB-phoU genes in other bacteria, the pstSCAB-phoU genes in Serratia 39006 may be regulated

by PhoB. A putative Pho box was also identified upstream of phoB (Fig 1B), centred 68 bp upstream of the phoB start codon, suggesting that phoBR may be auto-regulated via the putative Pho box. β-Glucuronidase

C-X-C chemokine receptor type 7 (CXCR-7) activity produced from selleck chemical a chromosomal pstC::uidA transcriptional fusion was measured in the presence or absence of a secondary mutation in phoB. The pstC::uidA fusion strain does not contain a functional Pst transporter and is therefore believed to mimic low phosphate conditions. These data showed that, in the presence of functional PhoB, pstC was expressed constitutively throughout growth (Fig. 1C). Expression was dramatically reduced following inactivation of phoB, indicating that PhoB activates expression of the pst operon in Serratia 39006 (Fig. 1C). Insertions within phoBR abolish upregulation of secondary metabolism and QS in the pstS mutant It was hypothesised that the upregulation of Pig, Car and QS in a Serratia 39006 pst mutant was mediated via the PhoBR two-component system. Assessment of Pig, Car and QS phenotypes in pstS, phoB and pstS, phoR double mutants confirmed that phoB and phoR were responsible for the upregulation of secondary metabolism in a pstS mutant background. The pstS mutant was increased for Pig (9-fold), Car (2-fold) and AHL (2.5-fold) production compared with the WT (Fig. 2). However, the pstS, phoB and pstS, phoR double mutants were restored to WT levels for Pig, Car and AHL production in LB (Fig. 2). Single phoB or phoR mutations had no effect on Pig, Car or AHL production (Fig. 2).

All authors read and approved the final manuscript “
“Backgr

All authors read and approved the final manuscript.”
“Background Participation in ultra-marathon running is of increasing popularity [1–5] AZD6244 mw where an ultra-marathon is a running race longer than the marathon distance of 42.195 km [5]. Within the ultra-marathons, there is a difference between single stage races [1, 2, 6, 7] and multi-stage races [3, 5], where the distance is split into daily stages. Running an ultra-marathon is associated with different problems such as a change in body mass [1, 8–10], dehydration [10], a loss of skeletal muscle mass [3, 7], an increase in total body water [3, 4, 6, 11], overuse injuries of the lower limbs with especially knee injuries

[5] and an impaired renal JNJ-64619178 cost function due to exertional rhabdomyolysis

[7], leading in extreme cases to a renal failure [12]. Among these ultra-running associated problems, an increase in total body water has been reported [3, 4, 6, 11] and the development of peripheral oedemas has been described in this context in endurance athletes [4, EPZ015938 research buy 13, 14]. In single stage ultra-distance races, Stuempfle et al. [15] reported a fluid overload caused by excessive fluid consumption during cold weather in a 161-km race in Alaska leading to both an increase in plasma volume and a decrease in serum sodium concentration ([Na+]). A decreased serum [Na+] as well as an increase in total body water has also been reported for male 100-km ultra-marathoners [6] and it was presumed that the increase in total body water led to the development of oedemas [6]. In contrast to male 100-km ultra-marathoners, total body water and serum [Na+] remained unchanged in female 100-km ultra-marathoners while drinking ad libitum [1]. Apart from ultra-running, also

Vitamin B12 after a Triple Iron triathlon, both total body water and plasma volume increased and clinically visible oedemas of the feet persisted until four days after the finish of the race [4]. An increase in total body water has also been reported for ten male multi-stage ultra-marathoners competing over 1,200 km with 17 consecutive stages [3]. Presumably, both the damage of skeletal muscle leading to rhabdomyolysis and an impaired renal function was the main factor for this accumulation of body water, since these ultra-runners suffered a decrease of skeletal muscle mass [3]. Exertional rhabdomyolysis due to exercise-induced myoglobinuria has been described before [7, 12]. In another multi-stage ultra-endurance exercise of five consecutive days of hill walking, an increase in leg volume in five male subjects due to fluid and sodium retention has been described [13]. These authors reported an increase in aldosterone activity leading to an increase in serum [Na+], fluid retention and an increased shift of fluid from the intracellular to the extracellular fluid compartment.