CrossRef 24. Yamada Y, Girard A, Asaoka H, Yamamoto H, Shamoto SI: Single-domain Si(110)-16×2 surface fabricated by electromigration. Phys Rev B 2007, 76:153309.CrossRef PLX3397 price 25. Yamamoto Y, Sueyoshi T, Sata T, Iwatsuki M: High-temperature scanning tunneling microscopy study of the ’16×2’⇔(1×1) phase transition on an Si(110) surface. Surf Sci 2000, 466:183.CrossRef 26. He Z, Stevens M, Smith DJ, Bennett PA: Dysprosium silicide nanowires on Si(110). Appl Phys Lett 2003, 83:5292.CrossRef 27. LeGoues FK, Reuter MC, Tersoff J, Hammer M, Tromp RM: Cyclic growth of strain-relaxed islands. Phys Rev Lett 1994, 73:300.CrossRef 28. Medeiros-Ribeiro G, Bratkovski

AM, Kamins TI, Ohlberg DAA, Williams RS: Shape transition of germanium nanocrystals on a silicon (001) surface from pyramids to domes. Science 1998, 279:353.CrossRef 29. Zhou W, Wang SH, Ji T, Zhu Y, Cai Q, Hou XY: Growth of erbium silicide nanowires on Si(001) surface studied by scanning tunneling microscopy. Jpn J Appl Phys 2059, 2006:45. 30. Weir RD: Thermophysics of advanced engineering materials. Pure Appl Chem 1999, 71:1215.CrossRef Competing interests click here The authors declare that they have no competing interests. Authors’ contributions ZQZ designed the project of experiments and drafted the manuscript. WCL and XYL carried out

the growth of MnSi~1.7 nanowires and STM measurements. GMS performed the SEM observations. All authors read and approved the final manuscript.”
“Background One-dimensional (1D) ZnO nanostructures (e.g., nanowires, nanorods,

and nanotubes) are promising with extensive applications in nanoelectronics and nanophotonics due to their efficient transport of electrons and excitons [1]. In recent years, increasing attention has been paid to three-dimensional (3D) hierarchical ZnO architectures which derived from 1D nanostructures as building blocks based on various novel applications [2–6]. To date, different kinds of hierarchical branched ZnO nanostructures, including nanobridges [7], nanoflowers [2, 8], rotor-like structures [9], and find more nanotubes surrounded by well-ordered nanorod structures [10], have been reported by using either solution-phase or vapor-phase method. However, these processes often require high temperature, complex multi-step process, or introduction of impurities by the templates or foreign catalysts in the reaction system. else Therefore, it is still a challenge to find a simple and controllable synthetic process to fabricate 3D hierarchical ZnO architectures with novel or potential applications. On the other hand, doping is a widely used method to improve the electrical and optical properties of semiconductors [11]. Copper, considered as a valuable dopant for the achievement of long-searched-for p-type ZnO [12], can serve not only as a luminescence activator but also as a compensator of ZnO [13]. In addition, Cu doping, leading to form donor-acceptor complexes, can induce a polaron-type ferromagnetic order in ZnO [14, 15].

This apparent better control implicates worsened CKD. CKD due to hypertension, if at an early stage, can be improved through strict blood pressure control. ACE inhibitors or ARBs are particularly used as first-line agents. In case of CKD at stage 1–2 find more caused by chronic glomerulonephritis, if urinary protein excretion is ≥0.5 g/day, a patient is referred to nephrologists, who might carry out renal biopsy if

feasible and determine a therapeutic approach based on histology of the biopsy specimen. Among CKD stage 3, cases with eGFR < 50 mL/min/1.73 m2 are referred to nephrologists for examination. Primary care physicians manage the case thereafter. Follow-up studies of CKD at stages 1–2 are delineated in Table 15-1. Table 15-1 Follow-up examinations at general physicians for stable patients with CKD stage 1 or 2 Variables Frequency Blood pressure Every visits Proteinuria, urine creatinine Every 3–6 months Serum creatinine, eGFR Every 3–6 months Blood chemistry (total protein, albumin, electrolyte, lipids) Every 3–6 months HbA1C (when DM) Every 1–3 months X-p (chest, abdomen including lateral view) Screening and annually Ultrasonography, Combretastatin A4 solubility dmso CT of the kidney Screening and as needed ECG Screening and annually A urine specimen is examined for protein (as well

as for microalbumin in diabetes) and is evaluated by urinary protein/urinary creatinine ratio. CKD progresses more rapidly as the amount of urinary protein increases. A CKD patient is examined for blood pressure at every visit, and also for HbA1c if diabetic. Blood pressure is lowered below 130/80 mmHg in general or below 125/75 mmHg in case of proteinuria ≥1 g/day. HbA1c is recommended to be less than 6.5% in diabetes. CKD progression is greatly affected by blood pressure and glycemic control.

Blood analysis of concentrations of the following components varies among CKD stages: electrolytes including Na, K, Cl, Ca, and P; urea nitrogen and uric acid; lipid including T-Chol, TG, LDL-C, and HDL-C; total protein and albumin. In CKD stages 4–5, electrolyte abnormalities such as hyperkalemia, hyperphosphatemia, and hypocalcemia emerge. It is noteworthy that hyperkalemia, in particular, may cause cardiac arrest due to ventricular arrhythmia. General blood Sclareol panel is necessary. Erythropoietin production by the kidney is reduced as kidney function declines, leading to normocytic normochromic anemia. Furthermore, since bleeding tendency may emerge in stage 4–5 CKD, anemia due to blood loss from the gastrointestinal tract must be differentiated from iron-deficiency anemia MK5108 purchase ascribable to appetite loss. The presence of anemia requires the determination of serum iron, transferrin saturation (TSAT), and ferritin. At stage 3 or later, blood gas analysis is performed. HCO3 can be measured in a venous blood sample. CKD, if complicated by metabolic acidosis, progresses faster and osteolysis is accelerated.

However, the exact mechanism of adhesion GW-572016 order has yet to be determined because of the complex combination of numerous other factors related to the bacteria itself, the in vivo environment and the particular artificial material involved. BioSelleckchem HKI-272 Materials used for clinical purposes are strictly regulated through standards such as the International

Organization for Standardization (ISO) and the American Society for Testing and Materials (ASTM). Biomaterials can be made of just a few kinds of standardized materials depending on their application, including titanium, stainless steel, and cobalt-chromium-molybdenum alloy (Co-Cr-Mo). Oxinium is an oxidized zirconium-niobium alloy commercialized as a new biomaterial in Japan in 2008. It is created by permeating

a zirconium-niobium alloy with oxygen at a high PCI-34051 ic50 temperature so that the surface is changed to a monoclinic zirconia ceramic with a depth of only 5 μm. As a result, Oxinium has the low abrasiveness on sliding surfaces of a ceramic, but has the strength of a metal. It also contains almost no toxic metals [21]. Steinberg et al. reported differences in bacterial adhesion to two different material surfaces, titanium and titanium alloy [22]. Recently, there have been a number of reports on the impact of the physical properties of the solid materials themselves on bacterial Montelukast Sodium adhesion [23-31] and a particularly strong relationship between bacterial adhesion and surface roughness has been highlighted [28-31]. Rougher surfaces have a greater surface area and the depressions in the roughened surfaces can provide more favorable sites for colonization. Some previous reports have shown that bacterial adhesion in vivo is primarily determined by a surface

roughness of Ra greater than 0.2 μm (200 nm) [32,33]. On the other hand, Lee et al reported in an in vitro study that the total amount of bacteria adherent on resin (Ra = 0.179 μm) was significantly higher than on titanium (Ra = 0.059 μm) or zirconia (Ra = 0.064 μm). However, they also demonstrated no significant difference between titanium and zirconia [34]. Öztürk et al indicated that the roughness difference of 3 to 12 nm Ra between as-polished and nitrogen ion-implanted Co-Cr-Mo contributes to bacterial adhesion behavior [35]. Thus, a general consensus has not been yet obtained in the literature regarding the minimum level of roughness required for bacterial adhesion. Furthermore, there are few studies that compare bacterial adherence capability on the same types of biomaterial that differ in surface roughness on the nanometer scale (Ra < 30 nm). To our knowledge, no other studies have been carried out to date that simultaneously evaluate the bacteriological characteristics of adhesion to five different types of material, including Oxinium.

Generally, the release mTOR inhibitor of drug from polymeric NPs will depend upon the FHPI diffusion rate of the drug from the NPs, NP stability, and the biodegradation rate of the copolymer. If the NPs are stable and the biodegradation rate of the copolymer is slow, the release rate will be most likely influenced by the following factors: the strength of the interactions between the drug and the core block, the physical state of the core, the drug-loaded content, the molecular volume of the drug, the length of the core block, and the localization of the drug within the NPs. As shown in Figure  5, PTX-PLA NPs and PTX-MPEG-PLA NPs both presented sustained drug release profiles with about 42.3% and 78.1% of the total PTX

released from NPs. The accelerated release may be explained by three factors. First, the particle size of the PTX-MPEG-PLA NPs was much smaller than that of the PTX-PLA NPs, reducing the total releasing time of the drug from the NPs. https://www.selleckchem.com/products/selonsertib-gs-4997.html Second, the presence of hydrophilic PEG in the polymer NPs reduced the hydrophobic interaction between the drug and matrix. Third, the outer PEG molecule could induce easier penetration of the water and facilitated the bulk erosion of the polymer matrix. All the factors, singly or in combination, could promote the release of PTX from the PTX-MPEG-PLA NPs. Figure 5 In

vitro release profiles of PTX-MPEG-PLA NPs versus PTX-PLA NPs in PBS (1/15 M, pH 7.4). The blue line represents the second phase of burst release. The purple arrows showed their burst start and endpoint. Of note, in the case of PTX-PLA NPs, a drug release behavior can be divided into two phases: the first one considered as a relatively fast release phase at the initial stage, commonly ascribing to the easy release of free PTX absorbed

on the surface of the NPs by simple diffusion, and subsequently, the Tryptophan synthase second one considered as a constantly prolonged release phase, which is most likely related to the slow transport of drug from the NPs driven by a diffusion-controlled mechanism. In the case of PTX-MPEG-PLA NPs, these release behaviors were different; the first abrupt release of PTX was minor from 0 to 12 h, which may have resulted from the steric effect of long PEG chain, which led to the low risk and reduced toxicity. Subsequently after the long sustained release by a diffusion-controlled mechanism, the second abrupt release of PTX from the NPs presented at 80 h, which was likely attributed to the deprotection of PEG as a result of the hydrolysis of MPEG-PLA, suggesting that the presence of hydrophilic PEG on the surface of NPs could eventually favor PTX to penetrate from the NPs. In vitro cellular uptake First, as may be seen from Figure  6, a predominant and strong accumulation of red signals in the cell cytoplasm was observed. The phenomenon demonstrated that rhodamine B-labeled PTX-PLA NPs and PTX-MPEG-PLA NPs could be uptaken into the cells.

Table 5 Descriptions on the selection of contrast media in CIN guidelines ACC(F) American College of Cardiology (Foundation), AHA American Heart Association, CIN contrast-induced nephropathy, LY333531 ESUR European Society of Urogenital Radiology, SCAI Society for Cardiovascular Angiography and Interventions High-osmolar contrast media have been used for a long period of time, and have caused adverse reactions due to their high osmolality. As low-osmolar contrast media became available in the 1980s and iso-osmolar contrast media were introduced thereafter, the incidence of adverse reactions to contrast media has decreased. In Japan, the

intravascular use of ionic high-osmolar contrast media has not been covered by the NHI since February 2001. Although the incidence of CIN has decreased as the use of low-osmolar contrast media has become common, CIN is still a major adverse reaction to contrast media. Considerable interest has been focused on the difference in incidence of CIN among currently available low- and iso-osmolar contrast media. The osmolarity of contrast media, when compared in iodine equivalent concentrations, is highest in high-osmolar contrast media followed by low-osmolar contrast

media and iso-osmolar contrast media. It also should be noted that the osmotic pressure ratio of low-osmolar contrast media to physiological saline ranges from 2–4, which is a higher ratio than that of iso-osmolar contrast media (1.0). Is the risk for developing CIN higher in patients receiving contrast media via invasive (intra-arterial) administration than in those receiving contrast media via non-invasive buy PD-1/PD-L1 Inhibitor 3 (intravenous) administration? Answer: Although there is no evidence

demonstrating that intra-arterial administration of contrast media is an independent risk factor for developing CIN, the incidence of CIN tends to be higher in patients receiving contrast media intra-arterially than in those receiving them intravenously. The majority of studies on CIN have been conducted in patients receiving contract media intra-arterially, and only a few studies have investigated a possible difference in the incidence of CIN by route of administration. The incidence of CIN tends to be lower in patients receiving contrast Methane monooxygenase media intravenously than in those receiving them intra-arterially (Table 6) [62–64], although this difference might be explained by other factors such as catheter techniques. In a review of 7 prospective observational studies, the overall incidence of CIN was 5.4 % in patients with CKD who intravenously IPI-549 mouse received low- or iso-osmolar contrast media, which suggested that intravenous administration of contrast media may pose a smaller risk of CIN as compared with that seen with intra-arterial administration [42]. Table 7 lists the incidence of CIN in patients with CKD after receiving different contrast media [5, 65–70]. Table 8 summarizes currently available iodinated contrast media and their osmolar pressure [71, 72].

62 FJ795447 FJ795490 FJ795464   Massarina eburnea CBS 473.64 GU301840 GU296170 GU371732 GU349040 Massarina igniaria CBS 845.96 GU301841 GU296171 GU371793   Massarina ricifera JK 5535 F GU479793 GU479759     Massariosphaeria phaeospora CBS 611.86 GU301843 GU296173 GU371794   Mauritiana rhizophorae BCC 28866 GU371824 GU371832 GU371796 GU371817

Mauritiana rhizophorae BCC 28867 GU371825 GU371833 GU371797 GU371818 Melanomma pulvis-pyrius CBS 124080 GU456323 GU456302 GU456350 GU456265 Melanomma pulvis-pyrius CBS 371.75 GU301845   GU371798 GU349019 Melanomma pulvis-pyrius SMH 3291 GU385197       Melanomma Acalabrutinib purchase rhododendri ANM 73 GU385198       Misturatosphaeria aurantonotata GKM1238 GU385173     GU327761 Misturatosphaeria aurantonotata GKM1280 GU385174     GU327762 Misturatosphaeria claviformis GKM1210 GU385212     GU327763 Misturatosphaeria kenyensis GKM1195 GU385194     GU327767 Misturatosphaeria kenyensis GKM L100Na GU385189     GU327766 Misturatosphaeria minima GKM169N GU385165     GU327768 Misturatosphaeria tennesseensis ANM911 GU385207     GU327769 Misturatosphaeria uniseptata selleck products SMH4330 GU385167     GU327770 Monascostroma innumerosum CBS 345.50 GU301850 GU296179   GU349033 Monotosporella tuberculata CBS 256.84 GU301851     GU349006 Montagnula anthostomoides CBS 615.86

GU205223 GU205246     Montagnula opulenta CBS 168.34 DQ678086 AF164370 DQ677984   Morosphaeria ramunculicola BCC 18405 GQ925854 BIX 1294 cell line GQ925839     Morosphaeria ramunculicola JK 5304B GU479794 GU479760 GU479831   Morosphaeria velataspora BCC 17059 GQ925852 GQ925841     Morosphaeria

velataspora BCC 17058 GQ925851 GQ925840     Massariosphaeria grandispora CBS 613 86 GU301842 GU296172 GU371725 GU349036 Massariosphaeria typhicola CBS 123126 GU301844 GU296174 GU371795   Neophaeosphaeria filamentosa CBS 102202 GQ387577 GQ387516 GU371773 GU349084 Neotestudina rosatii CBS 690.82   DQ384069     Neottiosporina paspali CBS 331.37 EU754172 EU754073 GU371779 GU349079 Ophiosphaerella herpotricha CBS CYTH4 240.31 DQ767656 DQ767650 DQ767645 DQ767639 Ophiosphaerella herpotricha CBS 620.86 DQ678062 DQ678010 DQ677958 DQ677905 Ophiosphaerella sasicola MAFF 239644 AB524599 AB524458 AB539098 AB539111 Paraconiothyrium minitans CBS 122788 EU754173 EU754074 GU371776 GU349083 Paraphaeosphaeria michotii CBS 591.73 GU456326 GU456305 GU456352 GU456267 Paraphaeosphaeria michotii CBS 652.86 GU456325 GU456304 GU456351 GU456266 Phaeosphaeria ammophilae CBS 114595 GU301859 GU296185 GU371724 GU349035 Phaeosphaeria avenaria CBS 602.86 AY544684 AY544725 DQ677941 DQ677885 Phaeosphaeria avenaria DAOM 226215 AY544684 AY544725 DQ677941 DQ677885 Phaeosphaeria brevispora MAFF 239276 AB524600 AB524459 AB539099 AB539112 Phaeosphaeria brevispora NBRC 106240 AB524601 AB524460 AB539100 AB539113 Phaeosphaeria caricis CBS 120249 GU301860     GU349005 Phaeosphaeria elongata CBS 120250 GU456327 GU456306 GU456345 GU456261 Phaeosphaeria eustoma CBS 573.

TGF-β1 levels were Selleck Sotrastaurin also higher in TDLNs draining TGF-β1-expressing tumors than tumors not expressing TGF-β1. B, Serum TGF-β1 levels measured in the same mice as in panel A. Serum TGF-β1 levels did not differ among the groups. *P < 0.05. n = 5 in each group. To begin assessing DC-mediated immunity in this model, we used flow cytometry to determine the

numbers and phenotypes of DCs within the TDLNs and non-TDLNs from wild SCCVII tumor-bearing mice on day 14 after tumor implantation. Figure 3A shows that TDLNs from these mice contained approximately 1.5 to 5 times as many CD11c+ DCs as non-TDLNs. Numbers of CD11c+CD86+ mature DCs were also increased 1.5 to 5 times within TDLNs, as compared to non-TDLNs (Figure 3B). Clearly, the PF-01367338 cost immune response to tumor antigen was higher in TDLNs than in non-TDLNs. ARS-1620 cell line Figure 3 Increases in the number and biological activity of DCs within TDLNs in wild SCCVII tumor-bearing mice. A, Numbers of CD11c+ DCs in TDLNs and non-TDLNs on day 14 after tumor inoculation. B, Numbers of CD11c+CD86+ mature DCs in TDLNs and non-TDLNs. The immune response of DCs to tumor antigen was higher in TDLNs than non-TDLNs. *P < 0.05. n = 10 in each group. To assess the inhibition of DC migration into TDLNs by tumor-derived TGF-β1, we used flow cytometry to count the numbers of DCs within TDLNs and non-TLDNs. We found that migration of DCs into TDLNs was

inhibited in mice inoculated with the three TGF-β1-expressing clones, resulting in a significant reduction in the numbers of CD11c+ DCs within TDLNs (Figure 4A). By contrast, there was no significant difference between the numbers of CD11+ DCs

in non-TDLNs from mice inoculated with mock or TGF-β1 transfectants. To identify the maturation status of the DCs within TDLNs, we also counted the numbers of CD11c+ and CD86+ DCs. We found that the TDLN/non-TDLN ratio for both CD11c+ cells and CD86+CD11c+ mature DCs was reduced in mice PLEK2 inoculated with TGF-β1-expressing clones (Figure 4B, C). Figure 4 Tumor-derived TGF-β1 reduces the number of DCs within TDLNs. A, Numbers of CD11c+ DCs in TDLNs and non-TDNLs from mice inoculated with TGF-β1-tranfected or mock-transfected tumor cells. B, TDLN/non-TDLN ratios for CD11c+ DCs in mice inoculated with TGF-β1-transfected or mock-transfected cells. C, To determine the maturation status of DCs within TDLNs, numbers of CD11c+ and CD86+ DCs were counted, after which the TDLN/non-TDLN ratio for CD11c+CD86+ DCs was calculated. * P < 0.05. To further clarify the mechanism underlying the reduction in the numbers of DCs within TDLNs, we injected the tumors with CFSE-labeled bmDCs and then counted the numbers of labeled cells within the TDLNs. With this method, we were able to distinguish migrated CFSE-labeled bmDCs from autologous DCs within TDLNs. Flow cytometric analysis of the TDLNs showed that significantly fewer immature (no added LPS) CFSE+ bmDCs migrated from TGF-β1-expressing tumors than from mock-transfected tumors (Figure 5A).

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These results suggest that the bacteria posed little damage to the epithelial cells

Selleck PRN1371 which infact may be beneficial for their long term survival within the host tissue. The effect of phage on the adherence and invasion pattern of MRSA 43300 was determined using the in vitro model of cultured murine nasal epithelial cells. Phage at both the MOI (1, 10) was able to show highly selleck chemicals significant reduction in all the three parameters as compared to untreated control. A pronounced decrease in the number of adhered bacterial population with negligible invasion and cytotoxicity was observed. Similarly phage was also able to significantly affect all the three parameters in clinical MRSA strains tested for these properties following interaction with phage. These results are in line with the findings of Clem [49] who showed that bacteriophages had protective effect on HEp-G2 cells from cellular damage and apoptosis induced by MRSA

isolates. A combination therapy with antimicrobials differing in their mechanisms buy Cediranib of action has been suggested to treat infections. This approach not only provides a broad spectrum of action due to synergistic effect but it also helps in preventing the emergence of drug-resistant subpopulation. It has been proposed that bacteria acquiring simultaneous resistance to both the phage and antibiotic is remote [13,14,50]. The results of this study suggest that when used in combination with phage, the frequency of emergence of spontaneous mutants towards mupirocin was effectively decreased to negligible levels (<10−9). To the best of our knowledge, the efficacy of lytic phage in decolonising the nares in an animal model has not been evaluated, though, the efficacy of phage born lytic enzymes has been assessed [51-53]. Hence, for assessing the therapeutic potential of phage MR-10 and mupirocin in eliminating

the nasal carriage of MRSA 43300, acute nasal colonization model (10 day) was experimentally established in healthy male BALB/c mice. MRSA colonisation was accomplished by putting a stress on the resident flora by increasing the inoculum load (106 CFU/ml, given twice) which helped in the dominance of MRSA 43300 in the nasal tissue over the resident flora. The treatment was started after allowing the Isotretinoin bacteria to colonise the nasal tissue of mice (in a period of 48 hours) in order to mimic the scenario prevalent in hospital and community settings, where the treatment is initiated in an already colonised person. Mice receiving two doses of phage MR-10 showed significant reduction (2.8 log cycles) on day 2 itself. Similarly, mupirocin given at a dose of 5 mg/kg (group 3) also showed significant reduction of 2 log cycles on day 2 and minimal bacterial load of 2.2 log CFU/gram on day 7. Both the agents given alone were able to significantly decrease the nasal load of MRSA 43300 by day 7.

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Caffeine supplementation and multiple sprint running performance. Med Sci Sports Exerc 2008, 40:1835–1840.PubMedCrossRef 13. Schneiker KT, Bishop D, Dawson B, Hackett LP: Effects of caffeine on prolonged intermittent-sprint ability in team-sport athletes. Med Sci Sports Exerc 2006, 38:578–585.PubMedCrossRef 14. Duvnjak-Zaknich DM, Dawson BT, Wallman KE, Henry G: Effect of caffeine on reactive agility time when fresh and fatigued. Med Sci Sports Exerc 2011, 43:1523–1530.PubMedCrossRef 15. Sökmen B, Armstrong LE, Kraemer WJ, Casa DJ, Dias JC, Judelson DA, Maresh CM: Caffeine use in sports: considerations for the athlete. J Strength Cond Res find more not 2008, 2:978–986.CrossRef 16. Lee CL, Cheng CF, Lin JC, Huang HW: Caffeine’s effect on intermittent sprint cycling performance with different rest intervals. Eur J Appl Physiol 2012, 112:2107–2116.PubMedCrossRef 17. Paton CD, Hopkins WG, Vollebregt L: Little effect of caffeine ingestion on repeated sprints in team-sport athletes. Med Sci Sports Exerc 2001, 33:822–825.PubMedCrossRef 18. Paton CD, Lowe T, Irvine A: Caffeinated chewing gum increases repeated sprint performance and augments increases in testosterone in competitive cyclists. Eur J Appl Physiol 2010, 110:1243–1250.PubMedCrossRef 19. Lorino AJ, Lloyd LK, Crixell SH, Walker JL: The effects of caffeine

on athletic agility. J Strength Cond Res 2006, 20:851–854.PubMed 20. Foskett A, Ali A, Gant N: Caffeine enhances cognitive function and skill performance during simulated soccer activity. Int J Sport Nutr Exerc Metab 2009, 19:410–423.PubMed 21. Stuart GR, Hopkins WG, Cook C, Cairns SP: Multiple effects of caffeine on simulated high-intensity team-sport performance. Med Sci Sports Exerc 2005, 37:1998–2005.PubMedCrossRef 22. Yeo SE, Jentjens RL, Wallis GA, Jeukendrup AE: Caffeine increases exogenous carbohydrate oxidation during exercise. J Appl Physiol 2005, 99:844–850.PubMedCrossRef 23. Van Nieuwenhoven MA, Brummer RM, Brouns F: Gastrointestinal function during exercise: comparison of water, sports drink, and sports drink with caffeine.