1987; Lavergne and Leci SBE-��-CD clinical trial 1993; Schansker and Strasser 2005). These instruments can also be used to study the S-states (oxidation states S0, S1, S2, S3 and S4) of

the oxygen evolving complex of PSII. A series of STFs induces period-4 oscillations in the F O-level as a function of the S-states (see Delosme 1972; Delrieu 1998; Ioannidis et al. 2000 for examples of such measurements). To probe the oxidation of reduced Q A following a saturating flash, there are two possible approaches: (1) The easiest method makes use of low-intensity modulated light, which excites only a small fraction of the PSII RCs per unit of time. Figure 2 shows an example of such a measurement. For control samples, in which re-oxidation of Q A − via forward electron transport can occur, this approach works well. However, when the sample is inhibited, e.g., by an electron transfer inhibitor such as DCMU (3-(3,4-dichlorophenyl)-1,1-dimethylurea), which displaces Q B from its binding site (Velthuys 1981; Lavergne 1982b), the low-intensity modulated light leads to the accumulation of a LY411575 price considerable population Epacadostat chemical structure of Q A − complicating the analysis of the experiment,

because re-oxidation of Q A − by recombination with the donor side is much slower than forward electron transport to Q B.   (2) The second method uses a combination of a STF followed by a probe flash that probes the redox state of Q A at the time of the probe flash (this is called a pump–probe experiment) (Mauzerall

1972; Robinson and Crofts 1983). The intensity of the probe flash is much lower than that of the STF. In this case, the experiment is repeated many times and each time at a variable time Dipeptidyl peptidase t after the STF, a probe flash is given to probe the redox state of Q A. In this way, the re-oxidation kinetics are constructed point by point. The actinic light problem, described above for DCMU inhibited samples, does not exist in this case. On the other hand, identical samples do not exist, and therefore, the biological variability between samples will lead to experimental noise and the need for repetitions to obtain smooth kinetics. To make different phases in the re-oxidation kinetics visible, the use of a logarithmic time scale has been introduced (see e.g., Cser and Vass 2007). Commercial equipment to make this type of measurements is the superhead fluorometers (Photon Systems Instruments, Brno, Czech Republic), which can also be used to measure OJIP transients and saturating pulse protocols (see below).   Complementary techniques for flash fluorescence measurements are thermoluminescence (TL) (reviewed by Vass and Govindjee 1996; Misra et al. 2001a, b; Ducruet and Vass 2009) and delayed fluorescence (DF) (recently reviewed by Goltsev et al. 2009) measurements that provide specific information on recombination reactions within PSII RCs. Flash fluorescence measurements are frequently used to study PSII mutants (e.g., Etienne et al. 1990; Nixon et al.

In keeping with this, the statistical analysis showed a significant day*group interaction (P = 0.0045). Table 4 Salivary IgA and PHA-Stimulated lymphocyte proliferation during exercise tests before and after 30 days of selleckchem supplementation Variable Day 0 Inmunactive Placebo Day 30 Inmunactive Placebo Salivary IgA (mg · L-1)         Basal 1.87 ± 0.38 2.59 ± 1.16 2.32 ± 0.96 2.31 ± 0.61

150 min 2.43 ± 1.06 2.13 ± 0.70 1.91 ± 0.54 1.35 ± 0.45 PHA-Stimulated lymphocyte proliferation (cpm · 1000-1)     Basal 29.3 ± 3.5 35.5 ± 4.4 29.1 ± 2.1 25.9 ± 3.9 24 h 21.4 ± 3.6 35.9 ± 53.8* 34.5 ± 5.4 20.6 ± 5.1* Values are means ± SE (n = 10). An asterisk indicates significant differences between groups at specified time point (P < 0.05). Discussion Scientific evidence from placebo-Pritelivir concentration controlled trials of nutritional compounds having a positive enhancing effect on the immune function in the healthy population is scarce [32]. High-intensity

exercise has been classically associated to immune disturbances in healthy individuals [2] and thus could be considered as a model to study the efficacy of nutritional interventions in populations during periods of immune suppression [33]. Exposure to cold environments has been claimed to elicit a stress response impacting immune cell function [10], but find more evidences from controlled studies are also scarce [13]. Research on the potential for dietary nucleotides to enhance the human immune response is wide but human trials are mainly

restricted to critically ill patients [34] and to supplementation of infant formula [35]. To our knowledge, this is the first controlled study in which the efficacy of nucleotide supplementation has been evaluated in healthy individuals under multiple stressors such as strenuous exercise and cold environment. The exercise protocol was designed to elicit an immune disturbance according to previously published data [4, 36]. Subjects were instructed to perform a controlled physical work corresponding to Obatoclax Mesylate (GX15-070) 90% of the VO2max for more than 20 minutes, in an exercise bout of more than 45 minutes in total. The described workload led to exhaustion as demonstrated by the maximum heart rate, lactate concentration and Borg values. On the second exercise test, Borg values were lower and HRmax and lactate concentration tended to be lower than in the previous exercise test, probably due to the effect of the training during the month of the trial. Levels of salivary IgA were unaffected by the exercise. Although falls in saliva IgA can occur during intense exercise [37–39], levels are generally unchanged with exercise lasting less than 1 h [40] and also not affected by environmental temperature [41–43], as observed in the present trial.

30 g/kg lean mass) followed by a 42 days Selleck PRIMA-1MET maintenance phase (0.075 g/kg lean mass) of CM or ethyl ester both combined with a resistance training program in 30 novice males with no previous resistance training experience. The results of this study [65] showed that ethyl ester was not as EX 527 nmr effective as CM to enhance serum and muscle creatine stores. Furthermore creatine ethyl ester offered no additional benefit for improving body composition, muscle mass, strength, and power. This research did not support the claims of the creatine ethyl ester manufacturers. Polyethylene glycol is a non-toxic, water-soluble polymer

that is capable of enhancing the NVP-BGJ398 order absorption of creatine and various other substances [66]. Polyethylene glycol can be bound with CM to form polyethylene glycosylated creatine.

One study [67] found that 5 g/d for 28 days of polyethylene glycosylated creatine was capable of increasing 1RM bench press in 22 untrained young men but not for lower body strength or muscular power. Body weight also did not significantly change in the creatine group which may be of particular interest to athletes in weight categories that require upper body strength. Herda et al [68] analyzed the effects of 5 g of CM and two smaller doses of polyethylene glycosylated creatine (containing 1.25 g and 2.5 g of creatine) administered over 30 days on muscular strength, endurance,

and power output in fifty-eight healthy men. CM produced a significantly greater improvement in mean power and body weight meanwhile both CM and polyethylene glycosylated form showed a significantly (p < 0.05) greater improvement for strength when compared with control group. These strength increases were similar even though the dose of creatine in the polyethylene glycosylated creatine groups was up to 75% less than that of CM. These results seem to Phosphatidylinositol diacylglycerol-lyase indicate that the addition of polyethylene glycol could increase the absorption efficiency of creatine but further research is needed before a definitive recommendation can be reached. Creatine in combination with other supplements Although creatine can be bought commercially as a standalone product it is often found in combination with other nutrients. A prime example is the combination of creatine with carbohydrate or protein and carbohydrate for augmenting creatine muscle retention [5] mediated through an insulin response from the pancreas [69]. Steenge et al [70] found that body creatine retention of 5 g CM was increased by 25% with the addition of 50 g of protein and 47 g of carbohydrate or 96 g carbohydrate when compared to a placebo treatment of 5 g carbohydrate.

Infect Immun 2009, 77:1842–1880.PubMedCrossRef 13. Kulesus RR, Diaz-Perez K, Slechta ES, Eto DS, Mulvey MA: Impact of the RNA chaperone Hfq on the fitness and virulence potential of uropathogenic BAY 80-6946 mouse Escherichia coli . Infect Immun 2008, 76:3019–3026.PubMedCrossRef 14. Sittka A, Pfeiffer V, Tedin K, Vogel J: The RNA chaperone Hfq is essential for the virulence of Salmonella typhimurium . Mol Microbiol 2007, 63:193–217.PubMedCrossRef 15. de Fernandez MT F, Eoyang L,

August JT: Factor fraction required for the synthesis of bacteriophage Qbeta-RNA. Nature 1968, 219:588–590.CrossRef 16. Moller T, Franch T, Hojrup P, Keene DR, Bachinger HP, Brennan RG, Valentin-Hansen P: Hfq: a bacterial Sm-like protein that mediates RNA-RNA interaction. Mol Cell 2002, 9:23–30.PubMedCrossRef 17. Hajnsdorf E, Boni IV: Multiple activities of RNA-binding proteins S1 and Hfq. Biochimie 2012, 94:1544–1553.PubMedCrossRef 18. Masse E, Gottesman S: A small RNA regulates the expression of genes involved in iron metabolism in Escherichia coli . Proc Natl Acad Sci U S A 2002, 99:4620–4625.PubMedCrossRef learn more 19. Masse E, Salvail H, Desnoyers G, Arguin M: Small RNAs controlling iron metabolism. Curr Opin Microbiol 2007, 10:140–145.PubMedCrossRef 20. Mellin JR, McClure R, Lopez D, Green O, Reinhard B, Genco C: Role of Hfq in Iron Dependent and Independent Gene Regulation in Neisseria meningitidis . Microbiology

2010, Casein kinase 1 156:2316–2326.PubMedCrossRef 21. Chao Y, Vogel J: The role of Hfq in bacterial pathogens. Curr Opin Microbiol 2010, 13:24–33.PubMedCrossRef 22. Nizet V, Colina KF, Almquist JR, Rubens CE, Smith AL: A virulent nonencapsulated see more Haemophilus influenzae.

J Infect Dis 1996, 173:180–186.PubMedCrossRef 23. Bakaletz LO, Kennedy B-J, Novotny LA, Duquesne G, Cohen J, Lobet Y: Protection against Development of Otitis Media Induced by Nontypeable Haemophilus influenzae by Both Active and Passive Immunization in a Chinchilla Model of Virus-Bacterium Superinfection. Infect Immun 1999, 67:2746–2762.PubMed 24. Morton DJ, Seale TW, Bakaletz LO, Jurcisek JA, Smith A, VanWagoner TM, Whitby PW, Stull TL: The heme-binding protein (HbpA) of Haemophilus influenzae as a virulence determinant. Int J Med Microbiol 2009, 299:479–488.PubMedCrossRef 25. Poje G, Redfield RJ: General methods for culturing Haemophilus influenzae . Methods Mol Med 2003, 71:51–56.PubMed 26. Whitby PW, Morton DJ, Stull TL: Construction of antibiotic resistance cassettes with multiple paired restriction sites for insertional mutagenesis of Haemophilus influenzae . FEMS Microbiol Lett 1998, 158:57–60.PubMedCrossRef 27. Morton DJ, Smith A, Ren Z, Madore LL, VanWagoner TM, Seale TW, Whitby PW, Stull TL: Identification of a haem-utilization protein (Hup) in Haemophilus influenzae . Microbiology 2004, 150:3923–3933.PubMedCrossRef 28.

Although ATG2 is not preceded by a classical Shine Dalgarno sequence, MM-102 this deletion was suspected to affect the efficiency of ribosome binding to the cpoA transcript [7]. However, the possibility remained that translation actually starts at an alternative start codon (ATG1 in Figure 1) 27 bp upstream of ATG2 which is preceded by a perfect −10 region. In this case, the deletion in P106 would lead to a frameshift in the

5th codon and thus to the production of a nonsense peptide. Figure 1 Genes, transcription and deletions in the cpoA-spr0985 region of S. pneumoniae R6. (A) Wide horizontal arrows indicate genes apparently co-transcribed with cpoA (black), and flanking genes (white). spr0983.1 has not been annotated in the R6 genome [20], but its presence has been predicted from other S. pneumoniae genomes such as TIGR4 [56]. The positions and extend of in-frame deletions are shown as white boxes below the respective genes. Lines above the genetic map represent DNA products obtained by RT-PCR with total RNA and gene-specific primers. The positions of the promoter P cpoA and of learn more putative ρ-independent terminators (T1 [ΔG = −10.4 kcal/mol], T2 [ΔG = −10.1 kcal/mol]) are given by angled and vertical arrows, respectively. (B) The nucleotide sequence upstream of S. pneumoniae R6 cpoA and

putative 3′-coding sequences is shown together with the predicted peptide sequence (Sp). The −10 element of P cpoA is underlined, and Meloxicam the transcription start

site (+1) is indicated with an angled arrow. The position of an adenine nucleotide, deleted in the mutant strain P106 [7] is marked with *Δ. Two potential start codons of the cpoA gene (ATG1, ATG2; see text for detail) are underlined. The respective cpoA sequences of S. mitis B6 (Sm) and S. oralis Uo5 (So) are shown below. To first clarify this issue, the expression signals of cpoA were mapped. The 5′ end of cpoA mRNA was determined by RACE, and shown to be located 27 bp upstream of ATG2 (Figure 1B). Since this is exactly the position of the alternative start codon ATG1, translation initiation at ATG1 would imply that the cpoA transcript is leaderless [16]. In order to see whether ATG1 is indeed functional or whether ATG2 is required for translation, three plasmids were constructed in which the inferred promoter P cpoA together with either both, ATG1 and ATG2 (P cpoA -ATG12), ATG1 plus a mutated ATG2 (P cpoA -ATG1ATA2), or ATG1 only (P cpoA -ATG1), was Emricasan ic50 translationally fused with the lacZ reporter gene. After single-copy integration of the resulting reporter constructs at the bgaA locus of R6, the expression of lacZ was determined in two transformants in up to three experiments.

In addition, similar

to FasL and RCAS1, CD70 overexpressed on RCC promotes lymphocyte apoptosis by binding to its receptor CD27, indicating a proapoptotic role of CD70 in the elimination of TICs as well [82]. All these observations suggest that the direct induction of TIC apoptosis by persistent expression of FasL, RCAS1 see more or perhaps other apoptosis-inducing ligands (e.g. CD70) on carcinoma cells plays a role in the ability of carcinoma cells to escape from the anti-carcinoma immunity. Suppression of TIC activity by molecular and cellular factors Immunoregulatory cytokine/cytokine-like: Transforming growth factor (TGF)-β1 and Galectin-1 (Gal-1) TGF-β1 is a multifunctional cytokine involved in immunosuppression. Numerous clinical studies have demonstrated that a higher level of TGF-β1 expression is significantly

associated with an invasive phenotype of tumors or metastases in patients [83–86]. In vitro a significant amount of TGF-β1 is produced in the poorly differentiated prostate carcinoma cell lines but not in well-differentiated cells [87]. These data imply that TGF-β1 may increase metastasis by a paracrine matter, such as suppression of local immune response or increased angiogenesis. Indeed, in the biopsies of cervical carcinoma tumors, an inverse relationship between TGF-β1 expression in tumor cells and the extent of TICs is demonstrated [88]. GS-1101 research buy This clinical observation is further confirmed by several experimental studies. In a mouse skin explant model, TGF-β1 is produced by progressor types but not regressor squamous cell carcinoma PAK5 lines, and this tumor-derived cytokine inhibits migration of professional APCs, Langerhans cells (LCs), and keeps them in an immature

form [89], or transgenic expression of TGF-β1 enhances growth of regressor squamous carcinoma cells in vitro and in vivo just like progressor phenotype, and reduces the number of infiltrating LCs, CD4+ and CD8+ T cells [90]. A further study with invasive colon carcinoma U9A cell line shows that decreasing TGF-β1 expression by antisense reduces the invasive activity and metastasis of tumor cells to the liver [91]. All these studies suggest that carcinoma-derived TGF-β plays an important role in the tumor metastasis, which may be caused by its immune suppressive function. Gal-1 is a member of β-galacosidess binding protein family (galectins), and is a recently identified immunoregulatory RXDX-101 clinical trial cytokine-like molecule in cancer [92]. It has been documented that Gal-1 exhibits immunoregulatory effects by which it controls immune cell trafficking, regulates activation of dendritic cells (DCs) and induces T-cell apoptosis [93].

fumigatus ΔAfcrzA strain to caspofungin [26]. Interestingly, some of these genes are involved in stress response, such as: (i) the Scf1 homologue (Afu117370), a plasma membrane localized protein that protects membranes

from desiccation and it is induced by heat shock, oxidative stress, osmostress, stationary phase entry, glucose depletion, oleate and alcohol, and is regulated by the HOG and Ras-Pka pathways http://​www.​yeastgenome.​org[27]; (ii) TipA (Afu2g07540), a component of the TOR (target of rapamycin) signaling pathway, that interacts physically and genetically with Tap42p, which regulates protein phosphatase 2A [28]; and (iii) a protein phosphatase KPT-8602 chemical structure 2C (Afu4g00720), important physiological regulator of cell growth and of cellular stress signaling [29]. The increased mRNA accumulation of these genes could mean that they are directly or indirectly repressed by AfCrzA and can open new frontiers for studying biochemical pathways that are under influence of the A. fumigatus selleck chemicals llc calcineurin-CrzA pathway. We then PXD101 used RT-PCR, both to assess the reliability of the microarray hybridizations and to document mRNA expression from selected genes of interest in the wild type, ΔAfcalA and ΔAfcrzA mutant backgrounds, choosing five

genes (three and two with decreased and increased mRNA accumulation in the microarray experiments, respectively) to analyze after 10 and 30 minutes in the presence of 200 mM CaCl2. We had previously shown that five

other genes (such as Afu8g05010, C2H2 finger domain protein; Afu4g03960, C6 transcription factor; Afu2g16520, phospholipase D; and Afu2g05330, vacuolar H+/Ca+2 exchanger; and Afu2g13060, calcineurin binding protein), identified here in this screening had induced mRNA accumulation in the presence of calcium, but reduced in ΔAfcrzA mutant background [16]. Expressing the results as fold induction relative to expression prior to calcium exposure, all values were in strong agreement with array hybridisation data (Figure 1). Comparisons between the gene expression variation estimated by microarray and real-time RT-PCR were performed by calculating both Pearson’s (R P) and Spearman’s (R S) correlation coefficients for the log2 ratios obtained by these two approaches. Tenofovir clinical trial Positive correlation was observed for both R P and R S in all nine genes (Figure 1) [16]. Furthermore, the value of either R P or R S was above 0.70 (indicating moderate-to-strong correlation). Thus, these data suggest that our approach was able to provide information about A. fumigatus gene expression modulation with a considerably high level of confidence. Figure 1 Validation of the genes observed as more or less induced in the A. fumigatus ΔAfcrzA mutant. Fold increase in mRNA levels after the incubation with 200 mM CaCl2 for 10 and 30 minutes of (A) AfrcnA (Afu2g13060), (B) AfrfeF (Afu4g10200), (C) Af BAR adaptor protein (Afu3g14230), (D) Af AAA ATPase (Afu4g04800), and (E) AfScf1 (Afu1g17370).

Our study found no significant differences among the expressions of P-gp, MRP and LRP in GC of different pathological types, in agreement with findings by Shi et al [20], who found that the ATM Kinase Inhibitor concentration positive rates

of P-gp and LRP were 49.2% and 58%, respectively, and such expression was closely related to clinicopathological staging but not related to tumor differentiation. In our study, MRP and LRP expression was not related to tumor invasion depth or lymphatic metastasis. Based on these findings, we propose that innate resistance may exist in those 59 GC patients even without prior chemotherapy. P-gp confers resistance to cytotoxicity by chemotherapy drugs, cytokine TNF-alpha, and ultraviolet light [21]. Faggad et al. [22] found that MRP1 expression EPZ-6438 research buy was as an independent negative prognostic factor CB-839 chemical structure for overall survival in ovarian cancer. As the patients in our group had mixed postoperative

treatment, it is impossible to correlate these findings with clinical outcomes. This is the limitation of the current study, and future work should be done to elaborate on this issue. The expression of P-gp, MRP and LRP confers different drug resistance profiles [23], including P-gp conferring resistance to doxorubicin, vincristine, vinblastine, actinomycin-D and paclitaxel, MRP conferring resistance to etoposide and epirubicin, and LRP conferring resistance to carboplatin and Melphalan. Our study found these molecules

are interrelated, and P-gp is correlated with LRP (r = 0.803), especially for moderately differentiated adenocarcinoma (r = 0.915). The finding suggests that both two resistance mechanisms exist in most patients. As the resistance mechanisms of P-gp, MRP and LRP are clarified, suggestions are proposed if we can block all the ABC transporters at once [24]? Recent studies revealed some new methods to overcome MDR, such as specific PI3K inhibitors to reduce P-gp [25, 26]. Du [27] showed that RP L6 could regulate MDR in GC cells by suppressing drug-induced apoptosis. Robey [28] reported an initial phase I studies of CBT-1, an orally-administered, bisbenzylisoquinoline plant alkyloid as P-gp inhibitor. CBT-1 at 1 μM completely reversed P-gp-mediated resistance Clomifene to vinblastine, paclitaxel and depsipeptide. Although the value of systemic chemotherapy for GC is controversial, several studies have demonstrated that GC could benefited for chemotherapy [29], although MDR remains a major challenge to effective chemotherapy [30]. Combined determination of P-gp, MRP and LRP may help tailor the chemotherapy regimes and predict the outcomes of treatment. Conclusion There are high percentages of innate expressions of P-gp, LRP and MRP in GC without prior chemotherapy, which may contribute to the poor response to chemotherapy of GC.

For the marginal means (collapsed across condition), *PRE > POST, 24 h, 48 h, and 72 h (p < 0.05); †POST < PRE, 24 h, 48 h, and 72 h (p < 0.05); #PRE < POST, 24 h, 48 h, and 72 h (p < 0.05). There were no condition x time (p > 0.05) interactions and no main effects for condition (p > 0.05) or time (p > 0.05) for systolic blood pressure (Figure 4a), diastolic MK5108 order blood pressure (Figure 4b), or resting heart rate (Figure 4c). Figure 4 Heart rate

and blood pressure. Data presented are means ± standard error of the mean for (a) systolic blood pressure (mmHg), (b) diastolic blood pressure (mmHg), and (c) heart rate (bpm) during the supplement (dashed line, open circles; ANA) and placebo (solid line, closed circles; PLA) conditions assessed Givinostat at baseline (visits 1 or 6)and 72 h after the bout of maximal eccentric exercise.

Discussion The results of the present study did not support our original hypotheses that ANA would improve the PFT�� chemical structure recovery of PT, hanging joint angle, relaxed arm circumference, or subjective pain ratings compared to PLA in response to eccentric-induced muscle damage. The protocol used in the present study has been used to elicit muscle damage in previous studies [6, 13, 19, 20]. For example, Beck et al. [13] demonstrated 21-43% decreases in PT of the forearm flexors, while Cockburn et al. [20] reported 15-20% decreases in leg flexion PT. The 23-44% decreases in PT observed in the present study were consistent with Beck et al. [13], but greater than Cockburn et al. [20], which may have been related to the muscle group Suplatast tosilate studied. Nevertheless, Warren et al. [2] suggested that PT is the single best non-invasive indicator of muscle damage resulting from eccentric exercise, therefore,

the results of the present study suggested that the magnitude of muscle damage that occurred was consistent with or greater than previous studies using the same protocol. Interestingly, these previous studies [13, 20] and others [10] have also demonstrated that this muscle damage protocol has elicited decreases in PT that were sensitive to dietary supplement interventions to improve recovery. However, in the present study there were no differences between ANA and PLA conditions during the recovery of PT, hanging joint angle, relaxed arm circumference, or subjective pain rating within 72 h after eccentric exercise. Thus, our conclusion was that ANA supplementation had no effect on recovery of muscle strength, joint stiffness, arm swelling, or pain using this model of muscle damage. Connelly et al.

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