14 encapsulated and 307.14 nonencapsulated) were taken. The serotype was confirmed by Quellung reaction. Electron microscopy Bacteria were cultured as described above for the FITC-dextran exclusion assay, grown to OD600nm of 0.2–0.25 in CDM, pH 7, 5.5 mM glucose and harvested by centrifugation. Serotype was confirmed by Quellung reaction after overnight incubation at 37°C with 5% CO2 atmosphere on CSBA plates. Bacteria were cryopreserved by high-pressure freezing

as described before [52]. Acetone containing 2% osmium tetroxide, 0.1% SAR302503 mouse uranyl acetate, 0.2% ruthenium hexamine trichloride (RHT) and a total of 4% H2O served as medium for freeze substitution. The RHT added improves capsule resolution [53]. Electron micrographs from cross-sectional bacterial preparations were taken at a magnification of 53 000×. The buy STA-9090 polysaccharide capsule thickness was measured perpendicular

to the bacterial cell wall from at least 30 randomly selected bacterial cell bodies in 15 pictures using the free software ImageJ v1.45 l (National Institutes of Health, USA, http://​imagej.​nih.​gov/​ij). One to four measurements were taken at distinct positions of a given cell body. Growth assays Strains were streaked onto CSBA plates and incubated at 37°C in 5% CO2 overnight and then subcultured in the semi-defined, nutritionally relatively rich Lacks medium [49-51] supplemented with 20 mM glucose and with the following modifications: 14.7 mM C2H3NaO2 · 3H2O, 5.41 μM CaCl2, 0.89 μM MnSO4 · H2O (all Merck, Germany) and ≥ 12 800 U catalase (Sigma, C40) per liter Lacks medium, no NaC2H3O2 and no bovine albumin. For growth assays, CDM [54] representing a nutritionally limited environment was used. Since pH may affect growth and competence, CDM was stabilized using Sørensen click here buffer (KH2PO4, Na2HPO4 · 2H2O), pH 7 instead of double-distilled water (Additional file 1: Table S2). Half-loopfuls of colonies were used to inoculate 10 ml Lacks supplemented

with 20 mM glucose. The bacteria were grown to OD600nm of 0.5 and frozen at -80°C in aliquots in 15% glycerol. Thawed bacterial suspensions were diluted in PBS pH 7.4 and plated on CSBA to determine the number of colony forming units (CFU) per ml the next day. The serotype was confirmed by Quellung reaction. For growth assays an inoculum of 5 × 107 CFUs was used for subculture in 20 ml CDM, 5.5 mM glucose. Bacteria were grown for 10 hours at 37°C in a water bath and the OD600nm measured every 30 minutes. Growth assays were repeated on three different days. Transformation frequency To compare transformation frequencies between the two phenotypes the bacteria were cultured as described for the FITC-dextran exclusion assay and grown to OD600 = 0.15 in CDM, 5.5 mM glucose, pH 7. 0.5 ml of the culture were transferred to 9.5 ml TSB competence medium pH 8.0 prewarmed to 30°C and incubated for 15 min at 30°C.

aureus in Nigeria is based on phenotypic testing especially the disk diffusion technique but recent studies have relied on the PCR detection Semaxanib research buy of the mecA gene for the identification and confirmation of MRSA [23–26]. However, no information is available on the nature of antibiotic resistance genes of S. aureus

in Nigeria. Our present study provides baseline information on antibiotic resistance and molecular epidemiology of MSSA and MRSA in Nigeria. Results Antibiotic susceptibility testing and detection of antibiotic resistance genes in S. aureus isolates The 68 S. aureus isolates obtained between January and April 2009 were analyzed for antimicrobial resistance (Table 1). All the isolates were susceptible to teicoplanin, vancomycin, phosphomycin, fusidic acid, rifampicin, daptomycin, mupirocin, linezolid and tigecycline, and two isolates were susceptible to all the antibiotics tested. In addition to the antibiotics stated above, all MSSA isolates (84%) were susceptible to clindamycin and moxifloxacin and less than 4% were resistant to erythromycin, 21.1% to ciprofloxacin, 47% to tetracycline, 68% to cotrimoxazole and 86% to penicillin. The predominant antibiotypes among the MSSA isolates

were resistance to penicillin, tetracycline and cotrimoxazole (15 isolates), and resistance to penicillin and cotrimoxazole (13 isolates). A total of 11 isolates were resistant to oxacillin and

confirmed Selleckchem CB-839 as MRSA based on the detection of the mecA gene (Table HSP90 1). The ermA gene was identified in all erythromycin-resistant MRSA isolates, while two erythromycin-resistant MSSA isolates possessed the msrA gene. All the gentamicin-resistant isolates carried the aacA-aphD gene. Moreover, the tetM gene was detected in 11 isolates (7 MRSA and 4 MSSA) and the tetK gene was present in 4 MRSA and 23 MSSA isolates. SCCmec typing The SCCmec type V was identified in four MRSA isolates obtained in Ile-Ife, Ibadan and Lagos, while one MRSA isolate from Ile-Ife possessed the SCCmec type IV element (Table 2). The MRSA isolates from Maiduguri were non-typeable for the SCCmec element based on established protocols [9, 27], and no amplification was observed for the ccrA, ccrB, and ccrh genes. However, these MRSA isolates possessed the ccu gene. The comparison and analysis of the ccu sequences from two selected MRSA isolates in this group with sequences in the GenBank suggested that the MRSA isolates possessed an SCCmec type III element of uncommon organization, which had not been identified using standard protocols.

Once again, following caffeine supplementation times to exhaustion were significantly increased. Results indicated subjects were able to cycle for 96 min during the caffeine trial, as compared to 75 min for placebo [18]. Recently McNaughton et al. [72] reported the effects of a moderate dose of caffeine (6 mg/kg) on 1-hour time trial performance. Captisol cost This investigation is unique to the research because, while

continuous, the protocol also included a number of hill simulations to best represent the maximal work undertaken by a cyclist during daily training. The caffeine condition resulted in the cyclists riding significantly further during the hour-long time trial, as compared to placebo and control. In fact, time trial performance was improved 4-5% by the caffeine treatment over the other two treatments [72]. The use of caffeine in anhydrous form, as compared to a cup of caffeinated

coffee, seems to be of greater benefit for the purpose of enhancing endurance performance. In addition, a low-to-moderate dose of caffeine between 3 and 6 mg/kg appears to be sufficient for enhancing performance in a maximal sustained endurance effort. Caffeine: High-Intensity and Team Sport Exercise It is evident that caffeine supplementation provides an ergogenic response for sustained aerobic efforts in moderate-to-highly trained endurance athletes. The research is more varied, however, TPCA-1 manufacturer when pertaining to bursts of high-intensity maximal efforts. Collomp et al. [46] reported results for a group of untrained subjects, who participated in only 2-3 hours per week of non-specific sport activity. In a fasted state, and in a crossover design, subjects consumed caffeine at a dose of 5 mg/kg as well as a placebo condition, and performed a 30-second Wingate test. Compared to a placebo, caffeine did not result Interleukin-3 receptor in any significant increase in performance for peak power or total work performed [46]. These results are in agreement with Greer and

colleagues [45], where in addition to a lack of performance enhancement with caffeine supplementation (6 mg/kg), subjects classified as non-trained experienced a decline in power, as compared to placebo, during the last two of four Wingate bouts [45]. As previously stated, Crowe et al. [47] reported significantly slower times to reach peak power in the second of two bouts of 60-s maximal cycling. Subjects in that study were untrained in a specific sport and consumed caffeine at a dose of 6 mg/kg [47]. Finally, Lorino et al. [47] examined the effects of caffeine at 6 mg/kg on athletic agility and the Wingate test. Results were conclusive in that non-trained males did not significantly perform better for either the pro-agility run or 30-s Wingate test [73]. In contrast, a study published by Woolf et al.

PubMed 21. Di Bonaventura G, Pompilio A, Picciani C, Nicoletti M, Zappacosta R, Piccolomini R: Adhesion to and biofilm formation on IB3–1 bronchial cells by Stenotrophomonas maltophilia : implications in cystic fibrosis [abstract]. Clin Microbiol Infect 2008, 14:s178. 22. de Oliveira-Garcia D, Dall’Agnol M, Rosales M, Azzuz AC, Martinez MB, Girón JA: Characterization of flagella produced by clinical strains of Stenotrophomonas maltophilia . Emerg Infect Dis 2002, 8:918–923.PubMed 23. O’Sullivan BP, Freedman SD: Cystic fibrosis.

Lancet 2009, 373:1891–1904.PubMedCrossRef 24. Ryan RP, Monchy S, Cardinale M, Taghavi S, Crossman L, Avison MB, Berg G, Lelie D, Dow JM: The versatility and adaptation of bacteria from the genus Stenotrophomonas . High Content Screening Nat Rev Microbiol 2009, 7:514–525.PubMedCrossRef 25. Graff GR, Burns selleckchem JL: Factors affecting the incidence of Stenotrophomonas maltophilia isolation in cystic fibrosis. Chest 2002, 121:1754–1760.PubMedCrossRef 26. Goss CH, Otto K, Aitken ML, Rubenfeld GD: Detecting Stenotrophomonas maltophilia does not reduce survival of patients with cystic fibrosis. Am J Respir

Crit Care Med 2002, 166:356–361.PubMedCrossRef 27. Nicodemo AC, Paez JI: Antimicrobial therapy for Stenotrophomonas maltophilia infections. Eur J Clin Microbiol Infect Dis 2007, 26:229–237.PubMedCrossRef 28. Kirisits MJ, Parsek MR: Does Pseudomonas aeruginosa use intercellular signalling to build biofilm communities? Cell Microbiol 2006, 8:1841–1849.PubMedCrossRef 29. Ewig S, Soler N, Gonzalez J, Celis R, El-Ebiary M, Torres A: Evaluation of antimicrobial treatment in mechanically ventilated patients with severe chronic obstructive pulmonary disease exacerbations. Crit Care Med 2000, 28:692–697.PubMedCrossRef 30. Valdezate S, Vindel A, Maiz L, Baquero F, Escobar H, Cantón R: Persistence and variability of Stenotrophomonas maltophilia in

C-X-C chemokine receptor type 7 (CXCR-7) cystic fibrosis patients, Madrid, 1991–1998. Emerg Infect Dis 2001, 7:113–122.PubMedCrossRef 31. Sampaio SC, Gomes TA, Pichon C, du Merle L, Guadagnini S, Abe CM, Sampaio JL, Le Bouguènec C: The flagella of an atypical enteropathogenic Escherichia coli are required for efficient interaction with and stimulation of IL-8 production by enterocytes in vitro. Infect Immun 2009,77(10):4406–13.PubMedCrossRef 32. Yonekura K, Maki-Yonekura S, Namba K: Growth mechanism of the bacterial flagellar filament. Res Microbiol 2002, 153:191–197.PubMedCrossRef 33. Stepanoviæ S, Vukoviæ D, Hola V, Di Bonaventura G, Djukiæ S, Cirkoviæ I, Ruzicka F: Quantification of biofilm in microtiter plates: overview of testing conditions and practical recommendations for assessment of biofilm production by staphylococci. APMIS 2007, 15:891–899.CrossRef 34. Pompilio A, Piccolomini R, Picciani C, D’Antonio D, Savini V, Di Bonaventura G: Factors associated with adherence to and biofilm formation on polystyrene by Stenotrophomonas maltophilia : the role of cell surface hydrophobicity and motility. FEMS Microbiol Lett 2008, 287:41–47.PubMedCrossRef 35.

Rather after 28 d GPLC at 4.5 g/d there was a significantly greater rate of power decline within individual sprints with reduced mean power output. In contrast, 28 d at a lower dosage, 1.5 g/d, provided increased mean values of power similar

to those exhibited acutely with 4.5 g. The increases in NO reported after 28 d GPLC at 4.5 g/d are apparently associated with the extreme leg pump that limited cycling power in the present study. Similarly, with 4.5 g/d there was a significant reduction in net lactate accumulation per unit power acutely – with like reductions also observed after 28 d at 1.5 g/d, but not but not after 28 d at 4.5 g/d. Apparently, the long-term effects SB431542 purchase of GPLC are related to the timed effects of different individual mechanisms. The vasodilatory effects are certainly directly related to NO levels while the increased power output may be related to increased cellular supply of the propionate unit which when converted to succinate provides an anaplerotic energy substrate. Greater carnitine supply may

be responsible for the reduced lactate accumulation due to buffering of the Coenzyme A pool thereby reducing the rate of fatigue and enabling a higher rate of power output. It would appear that both check details the vasodilatory effects and power output enhancement effects increased in magnitude over the 28 d period of the present study. The present study is limited by several factors including a modest sample size which restricted the statistical analyses. Some variability dipyridamole within groups could be associated with the lack of control of the study supplement. Study participants

were provide with 28 days of GPLC in the respective group levels and directed to take six capsules daily. However, there were no means available to ensure daily intake of the respective supplements. This investigation applied three absolute dosage levels (1.5, 3.0, 4.5 g/d) in all research participants. The absolute dosing regardless of body mass likely increased the variability of response within supplementation groups thereby limiting the findings of the present study. It is recommended that future investigations examine GPLC dosing relative to body mass. Regardless of these potential limitations, the total subject pool in this study did not display the same main effects for enhancement of power output with reduced lactate accumulation as had been observed with acute supplementation. While the lower intake group (1.5 g/d) did display improvements in mean values of power output with significantly lower net lactate accumulation per unit power output, the higher intake groups (3.0 and 4.5 g/d) actually produced lower mean values of power output. From the participant reports and the relatively crude thigh girth measurements, it would appear that the higher intake levels produced greater levels of leg pump which acted as a hindrance during high speed, high intensity cycle sprints.

PubMedCentralPubMedCrossRef 8. Gonza M, Heidelberg JF, Whitman WB, Kiene RP, Brinkac L, Lewis M, Johri S, Weaver B, Pai G, Miller TR, Carlton J, Rasko DA, Paulsen IT, Ren Q, Daugherty Selleck Erismodegib SC, Deboy RT, Dodson RJ, Sullivan SA, Rosovitz MJ, Haft DH, Selengut J: Genome sequence of Silicibacter pomeroyi reveals adaptations to the marine environment. Nature 2004,432(December):910–913. 9. Sebastian A, Larsson L: Characterization of the Microbial Community in Indoor Environments: a Chemical-Analytical Approach. Appl Environ Microbiol 2003, 69:3103–3109.PubMedCentralPubMedCrossRef 10. Martínez JA, Ruthazer R, Hansjosten K, Barefoot L,

Snydman DR: Role of environmental contamination as a risk factor for acquisition of vancomycin-resistant Enterococci in patients treated in a medical intensive care unit. Arch Intern Med 2003, 163:1905–1912.PubMedCrossRef 11. Hayden MK, Blom DW, Lyle EA, Moore CG, Weinstein RA: Risk of hand or glove contamination after contact with patients colonized with vancomycin-resistant Enterococcus or the colonized patients’ environment. Infect Control Hosp Epidemiol 2008, 29:149–154.PubMedCrossRef 12. Sehulster L, Chinn R: Guidelines for Environmental Infection Control in Health-Care Facilities. Center for Disease Control (CDC); 2003. [http://​www.​cdc.​gov/​ncidod/​hip/​enviro/​guide.​htm]URL 13. WHO: Report on the Burden of Endemic Health

NSC23766 solubility dmso Care-associated Infection Worldwide. 2011, 1–34. 14. Wiener-Well Y, Galuty M, Rudensky B, Schlesinger Y, Attias D, Yinnon AM: Nursing and physician attire as possible source of nosocomial infections. Am J Infect Contro 2011, 39:555–559.CrossRef 15. Perry C, Marshall R, Jones E: Bacterial contamination of uniforms.

J Hosp Infect 2001, 48:238–241.PubMedCrossRef Tangeritin 16. Brady RRW, Verran J, Damani NN, Gibb AP: Review of mobile communication devices as potential reservoirs of nosocomial pathogens. J Hosp Infect 2009, 71:295–300.PubMedCrossRef 17. Datta P, Rani H, Chander J, Gupta V: Bacterial Contamination of Mobile Phones of Health Care Workers. Indian J Med Microbiol 2009, 27:279.PubMedCrossRef 18. Marinella MA, Pierson C, Chenoweth C: The Stethoscope A Potential Source of Nosocomial Infection? Arch Intern Med 2013, 786:790. 19. Doğan M, Feyzioğlu B, Ozdemir M, Baysal B: Investigation of microbial colonization of computer keyboards used inside and outside hospital environments. Mikrobiyol Bul 2008, 42:331–336.PubMed 20. Safdar N, Drayton J, Dern J, Warrack S, Duster M, Schmitz M: Telemetry leads harbor nosocomial pathogens. Int J Infect Control 2012, 8:10–12. 21. Livornese LL, Dias S, Samel C, Romanowski B, Taylor S, May P, Pitsakis P, Woods G, Kaye D, Levison ME: Hospital-acquired infection with vancomycin-resistant Enterococcus faecium transmitted by electronic thermometers. Ann Intern Med 1992, 117:112–116.PubMedCrossRef 22. Myers MG: Longitudinal evaluation of neonatal nosocomial infections: association of infection with a blood pressure cuff. Pediatrics 1978, 61:42–45.PubMed 23.

J Clin Oncol 2008, 26:3176–3182.PubMedCrossRef 47. Pujade-Lauraine E, Hilpert F, Weber B, Reuss A, Poveda A, Kristensen G, Sorio R, Vergote IB, Witteveen P, Bamias A, Pereira D, Wimberger P, Oaknin A, Mirza MR, Follana P, Bollag DT, Ray-Coquard I, AURELIA Investigators AURELIA: A randomized phase III trial evaluating bevacizumab (BEV) plus chemotherapy (CT) for platinum (PT)-resistant recurrent ovarian cancer (OC) [abstract]. J Clin Oncol 2012,30(Suppl): LBA5002. 48. Ikeda Y, Takano M, Oda K, Kouta

H, Goto T, Kudoh K, Sasaki N, Kita T, Kikuchi Y: Weekly administration of bevacizumab, gemcitabine, and oxaliplatin in patients with recurrent and refractory ovarian cancer: a preliminary result of 19 cases. Int J Gynecol Cancer 2013, 23:355–360.PubMedCrossRef 4SC-202 49. Itamochi H, Kigawa J: Clinical trials and future potential of targeted therapy for ovarian cancer. Int J Clin Oncol 2012, 17:430–440.PubMedCrossRef 50. Eckstein N: Platinum resistance in breast and ovarian cancer cell lines. J Exp Clin Cancer Res 2011, 30:91.PubMedCrossRef 3-Methyladenine ic50 Competing interests The authors declare that they have no competing interests. Authors’ contributions LDL and PV conceived and designed

the study, DS, LP, LM, MGA, MB, MMS, CV, EV, GC, GP, FT, ST collected and assembled the data, DG performed the statistical analysis, PV wrote the manuscript. All authors read and approved the final manuscript.”
“Introduction Epithelial ovarian cancer (EOC), a tumor originating Amino acid from ovarian epithelial surface, includes different histological subtypes [1–3]. In 2013, there will be an estimated 22,240 new diagnoses and 14,030 deaths from this neoplaia in the United States [4, 5]. It is the fifth most frequent cause of death from cancer in females and the most lethal cancer among gynecological

tumors, with severe impact on public health and social costs [6–9]. Unfortunately, unlike other gynecologic cancers, etiology of EOC is still unkown [10]; and for biological and clinical reasons EOC is still diagnosed and treated at a very advanced stage; still now an early diagnosis is very difficult and infrequent and a validated program of screening for this tumor is still lacking [11–13]. Furthermore, despite the improved surgical approach and the novel active drugs that are available today in clinical practice, at the time of diagnosis about 80% of women have an advanced disease, with a 5-year survival rate of only 30% [12]; probably, one of the possible reasons could be the ovarian cancer cells ability to develop resistance mechanisms to the drugs through congenital and acquired genetic characteristics [14].

J Epidemiol Commun Health 56:294–300CrossRef

Siegrist J, Strake D, Chandola T, Godin I, Marmot M, Niedhammer I, Peter R (2004) The measurement of effort-reward imbalance at work: European comparisons. Soc Sci Med 58:1483–1499CrossRef Steenland K, Burnett C, Lalich N, Ward E, Hurrell J (2003) Dying for work: the magnitude of US mortality from selected causes of death associated with occupation. Am J Ind Med 43:461–482CrossRef SBE-��-CD Sultan-Taïeb H, Lejeune C, Drummond A, Niedhammer I (2011) Fractions of cardiovascular diseases, mental disorders, and musculoskeletal disorders attributable to job strain. Int Arch Occup Environ Health 84:911–925CrossRef”
“Introduction Firefighting is a universal profession, with rather similar work features across countries, i.e., extinguishing fires, performing rescue operations and often also medical first aid. Firefighting work has considerable physical as well as psychological demands, causing high loading of both the body and mind. However, firefighters’ health problems, especially musculoskeletal disorders, have rarely been reported in epidemiological studies. (Sluiter and Frings-Dresen 2007). Early retirement due to disability is frequent among firefighters. WH-4-023 supplier In Finland, for example, little <70 % of operative firefighters are able to work until their normal

retirement age (63‒68 years). In 2008‒2010, the mean age of disability retirement among Finnish firefighters’ was 53. The most common reasons for early retirement are musculoskeletal (43 %), mental (14 %) and cardiovascular (14 %) disorders. The most common medical diagnoses (16 % of all diagnoses) for early retirement are related to low back (e.g., degeneration of lumbar disk). (A Koski-Pirilä, The Local Government Pensions Institution, personal communication,

2011). The number of full-time workers in the fire Grape seed extract and rescue sector (including firefighters and paramedics/ambulance drivers) in Finland is approximately 5,000. In addition, about 14,000 part-time employees and voluntary fire brigade members are available for emergency situations (Ministry of the Interior of Finland 2006). Each year in Finland, some 85,000 emergency operations are carried out by firefighters, and this number has doubled over the last 10 years. In addition, approximately 200,000 urgent ambulance call-outs are also answered by firefighters in Finland each year (Ministry of the Interior of Finland 2006). Most of the above-mentioned firefighting and rescue tasks require extremely good musculoskeletal health. Increasing problems in daily work tasks at fire stations, due to firefighters’ musculoskeletal problems, may occur among the aging workforce in particular.

Final results, expressed as N-fold differences in target gene expression relative to the reference gene GAPDH, termed ‘Ntarget’, were determined as follows:Ntarget = 2(delta Ct sample – delta Ct reference gene). Where delta Ct values of the sample and reference were determined by subtracting the average Ct value of the test gene from the average Ct value

of the β-actin gene. The sequence of primer for three known human transketolase genes and β-actin were from reference.4. β-actin gene was amplified as internal control. The sequences of primers for TKT, TKTL1, TKTL2 were obtained by referring to Coy et al [9]. EPZ015938 The sequences of primers for β-actin gene: 5′-GTG CGT GAC ATT AAG GAG-3′(sense), 5′-CTA AGT CAT AGT CCG CCT-3′(antisense) were designed by using Primer Premier Lazertinib in vivo 5.0 software package. The amplification conditions: denaturing at 94°C for 3 min, 40 cycles at 94°C for 5 s and at 57°C for 5 s. The amplification products were visualized by electrophoresis on a 1.5% agarose gel stained with ethidium bromide. Measurements of transketolase activity In order to prepare the extract of HeLa and End1/E6E7 cells, cells were sonicated and centrifuged. The resulting supernatant was filtered to remove some endogenous

metabolites. TK activity was determined by using enzyme-linked method [4]. Samples were added to a cuvette containing buffer (50 mM Tris/HCl, pH 7.6), 2 mM ribose 5-phosphate, 1 mM xylulose 5-phosphate, 5 mM MgCl2, 0.2 U mL-1 of TPI, 0.2 mM NADH and 0.1 mM TPP. Reactions were initiated by the addition of HeLa or End1/E6E7 cells extract at 37°C. TK activity was expressed as ng product per min per mg total protein. Total protein content of cell extracts was determined by the Bradford method. Each experiment was repeated three times. Cell cycle analysis 104 cells of each group were seeded into a 6-well culture

plate. Then cells were harvested after cultured for 72 hours. The harvested cells were washed with PBS, fixed with 70% alcohol, treated with RNase A and then stained with propidium iodide. The analysis of cell cycle distribution was performed by FAC-Scan Flow Cytometer (Becton Dickinson, USA) and analyzed by CellQuest software package. Each experiment was repeated three times. Cell proliferation assay Cell proliferation Benzatropine was measured by the MTT assay. HeLa and End1/E6E7 cells (cells without transfection, cells transfected with control plasmid and cells transfected with siRNA), at 2 × 103 per well, were seeded into five 96-well culture plates, respectively. Each plate has three kinds of cells (without transfection, transfected with control plasmid or siRNA plasmid) and each group consisted of 12 parallel wells. Absorption value of one of five culture plates was determined by MTT at 490 nm after 24-hour cultivation. Then, absorption value of every culture plate was detected in the following four days. The growth curve of each group was plotted on the basis of absorption values.

Several researchers have investigated the effect of these various forms of Cr in terms of Cr retention, uptake into

the muscle cell, and effects on performance [11–15], confirming CrM as the most effective formulation [10]. (For review of alternative forms see [10]) Previous research has also shown that the addition of certain nutrients to Cr may improve Cr retention [16–19]. For example, researchers have found that the co-ingestion of 5 g of CrM with 93 g of glucose significantly increased Cr retention by 60% compared to CrM alone after 5 days of 20 g · d-1[17]. Similarly the addition of certain macronutrients have also been shown to improve Cr retention [18]. Steenge et al. [18] found that the addition of 96 g of carbohydrates and/or 47 g of carbohydrates with 50 g of protein check details to 20 g of CrM daily improved Cr retention

by roughly 25% (p < 0.05) compared to 5 g carbohydrates. Results of the study suggest that higher insulin levels, in response to the additional macronutrients, may augment Cr uptake into the muscle. While co-ingesting large amounts of carbohydrate and/or protein with Cr has been reported to augment muscle and/or whole body Cr retention, some athletes or recreationally active individuals may be interested in lower-calorie strategies to improve Cr uptake. Recently there has been an interest in the effects of combining Cr with additional ingredients to Metalloexopeptidase improve Cr uptake and retention. For example, Greenwood and associates [16] found that the co-ingestion Doramapimod ic50 of 1 g of D-pinitol (a plant extract with insulin-like properties) per day with CrM (20 g/d) for 3 days significantly improved Cr absorption and retention compared to CrM alone and a placebo. Ethanolic or aqueous extracts

of Russian Tarragon (RT) (artemisia dracunculus) have been purported to have anti-hyperglycemic effects. Theoretically, co-ingestion of RT with Cr may help augment Cr uptake [20, 21]. To support this theory, Jäger et al. [20] found that plasma Cr levels were reduced when RT was combined with CrM compared to CrM alone, suggesting an increase in Cr uptake. Therefore, the purpose of this study was to examine whether a low dose aqueous RT extract ingested 30 minutes prior to CrM intake during a 5-day loading phase significantly affected whole body Cr retention and/or anaerobic capacity in healthy, recreationally active males when compared to CrM ingestion alone. Methods Experimental design The study was conducted in a double-blind, randomized, and crossover manner. The independent variable was RT extract supplementation. Dependent variables included intramuscular Cr concentration, whole body Cr retention, and anaerobic sprint performance capacity. Participants who qualified for the study participated in a familiarization session in which the study was explained following written consent.