Cells were Dounce homogenized and nuclei were collected by centrifugation at 750 × g for 5 min. Cell

extracts were kept at 4°C for 5 min and the remaining intact nuclei were collected by a further centrifugation at 750 × g for 5 min. The supernatant was recovered and a crude membrane fraction was obtained by centrifugation at 43,000 × g for 20 min. The leftover supernatant represented the cytoplasmic fraction. Nuclear and membrane fractions were than separated on SDS-PAGE, transferred to nitrocellulose membrane (GE Healthcare) and analyzed by western blot with the appropriate antibodies. Statistics All experiment unless indicated were performed at least three times. All experimental results were expressed www.selleckchem.com/products/Nilotinib.html as the arithmetic mean ± standard deviation (s.d.). Student’s t-test was used for statistical significance of the differences between treatment groups. Statistical AZD1152 in vivo analysis was performed using analysis of variance at 5% (p < 0.05) or 1% (p < 0.01). Results and discussion KSHV-latent infection of monocytic cell line THP-1 results in an increase of AKT phosphorylation that persisted after bortezomib ICG-001 mouse treatment THP-1 monocytic cells, infected with KHSV for 48 hours, were subjected to immunofluorescence analysis

and, as shown in Figure 1A, the expression of latent associated nuclear antigen (LANA) was detected in about 35% of the cells, compared to mock infected cells. No expression of lytic antigens was found (data not shown), in accordance to previous reported studies [12], indicating that KSHV establishes a latent infection in THP-1 cells. Next, we investigated the impact of KHSV-infection on AKT phosphorylation in THP-1 cells. Western blot analysis showed that THP-1-infected cells displayed increased phosphorylation of AKT, in comparison to THP-1 mock-infected cells (Figure 1B). This is in agreement with other studies showing that KSHV proteins are able to activate PI3K/AKT pathway or down-regulate AKT phosphatases such as PTEN in several cell types [14, 20]. The activation of

AKT pathway has been also reported for other oncoviruses Teicoplanin [32]. As bortezomib has been shown to interfere with the activation status of AKT [27, 33], we then investigated if bortezomib-treatment could affect AKT phosphorylation in THP-1 cells. We observed that bortezomib (Bz, 10 nM for 48 hours) strongly down-regulated AKT phosphorylation in mock-infected cells, while KSHV infection impaired such effect (Figure 1B). This might be due to KSHV-induced inhibition of PTEN, demonstrated in other studies [20], that could counteract the bortezomib-mediated up-regulation of this phosphatase [34]. As expected, AKT phosporylation was completely abolished by pre-treatment with AKT inhibitor LY294002, both in mock and viral-infected cells (Figure 1B).

PubMedCrossRef 22. Lappin-Scott HM, Costerton JW: Microbial biofilms. Cambridge University Press; 1995.CrossRef 23. Allison DG: Community structure and Co-operation in biofilms. Cambridge University Press; 2000.CrossRef 24. Pierce GE: Pseudomonas

aeruginosa, Candida albicans , and device-related nosocomial infections: implications, trends, and potential approaches for control. J Ind Microbiol Biotechnol 2005,32(7):309–318.PubMedCrossRef 25. Senpuku H, Sogame A, Inoshita E, Tsuha Y, Miyazaki H, Hanada N: Systemic diseases in association with microbial species CX-6258 in oral biofilm from elderly requiring care. Gerontology 2003,49(5):301–309.PubMedCrossRef 26. Hogan DA, Vik A, Kolter R: A Pseudomonas aeruginosa quorum-sensing molecule influences Candida albicans morphology. Mol Microbiol 2004,54(5):1212–1223.PubMedCrossRef 27. El-Azizi MA, Starks SE, Khardori N: Interactions of Candida albicans with other Candida spp . and bacteria in the biofilms. J Appl Microbiol 2004,96(5):1067–1073.PubMedCrossRef 28. Hogan DA, Kolter R:

Pseudomonas-Candida interactions: an ecological role for virulence factors. Science 2002,296(5576):2229–2232.PubMedCrossRef 29. Kaleli I, Cevahir N, Demir M, selleck screening library Yildirim U, Sahin R: Anticandidal activity of Pseudomonas aeruginosa strains isolated from clinical specimens. Mycoses 2007,50(1):74–78.PubMedCrossRef 30. Grillot R, Portmann-Coffin V, Ambroise-Thomas P: Growth inhibition of pathogenic yeasts by Pseudomonas aeruginosa in-vitro : clinical implications in blood cultures. Mycoses 1994,37(9–10):343–347.PubMed 31. Hockey LJ, Fujita NK, Gibson TR, Rotrosen D, Montgomerie JZ, Edwards JE Jr: Detection of fungemia obscured by concomitant bacteremia: in-vitro and P505-15 in-vivo studies. J Clin Microbiol 1982,16(6):1080–1085.PubMed 32. Jin Y, Samaranayake

LP, Samaranayake Y, Yip HK: Biofilm formation of Candida albicans is variably affected by saliva and dietary sugars. 4-Aminobutyrate aminotransferase Arch Oral Biol 2004,49(10):789–798.PubMedCrossRef 33. Jin Y, Zhang T, Samaranayake YH, Fang HH, Yip HK, Samaranayake LP: The use of new probes and stains for improved assessment of cell viability and extracellular polymeric substances in Candida albicans biofilms. Mycopathologia 2005,159(3):353–360.PubMedCrossRef 34. Ramage G, Vandewalle K, Wickes BL, Lopez-Ribot JL: Characteristics of biofilm formation by Candida albicans . Rev Iberoam Micol 2001,18(4):163–170.PubMed Authors’ contributions LPS, LJJ, RMW and HMHNB conceived this research. HMHNB and JYYY designed and performed the experiments. HMHNB, LPS, LJJ contributed in data analysis and interpretation. HMHNB drafted the manuscript and it was reviewed by LPS, LJJ, RMW and JYYY. All authors read and approved the final manuscript.”
“Background Pseudomonas fluorescens is a highly heterogeneous species, as shown the extensive literature on the taxonomy and phylogeny of this species [1–4]. These studies include saprophytic, rhizopheric and phytopathogenic strains of P.

As a result, there is increasing interest for sports nutrition product manufacturers

to undertake specific research to validate or support marketing claims. check details VIPER®ACTIVE is a specific sports drink produced by Maxinutrition Ltd. The product is a carbohydrate-protein-electrolyte (CPE) formula designed to support click here exercise performance, energy production, stamina and short term recovery from intense training. The manufacturer guidelines indicate a dosage of 40 g of the product (mixed with 500 ml of water) for use during exercise bouts, equating to an 8.0% concentration (or 7.1% for total carbohydrate). It is widely established that the ingestion of carbohydrate (CHO) during exercise can improve time KU55933 supplier to exhaustion [1], through maintenance of plasma glucose concentrations, and increasing total carbohydrate oxidation (CHOTOT) rates [2]. Additional evidence exists that by increasing exogenous carbohydrate oxidation (CHOEXO) rates [3], beverages containing multiple CHO combinations may have further ergogenic potential [4]. The inclusion of essential electrolytes, namely sodium, into such beverages has also been shown to enhance or support higher hydration levels, or ingestion rates, during and post exercise [5–7]. There has been recent interest in the use of carbohydrate-protein (CP) combinations as a means to not only enhance time to exhaustion compared to a CHO beverage [8],

but also to improve post exercise recovery rates. It has been demonstrated [9] that the ingestion of a carbohydrate-casein hydrolysate beverage significantly enhanced late stage cycling time trial performance in comparison to CHO only; and attenuated post exercise creatine kinase concentrations along with subjective muscle soreness. The ergogenic potential of CP beverages firstly appears to be explained by the high CHO ingestion rates of ~60 g.hr-1, along with an independent caloric advantage though the co-ingestion of ~20 g.hr-1 of protein. The innovation of nutrient timing has also implied the need for early carbohydrate this website [10] and/or protein ingestion post exercise [11], particularly when repeated short term training

bouts are undertaken. Practical methods to support initial training bouts, as well as short term recovery are therefore warranted, including the assessment of specific formulas which utilise a complete array of essential nutrients, namely combined carbohydrates, essential amino acids and key electrolytes, that may enhance acute and repeated bouts of exercise. The aim of this study was therefore to undertake an independent assessment of the potential influence of a commercially available CPE beverage (VIPER®ACTIVE) on repeated submaximal physiological and work output parameters in comparison to a matched placebo (PL). A further aim was to assess the influence of both beverages on subsequent time trial performance following short term recovery.

bronchiseptica shedding in relation to the immune response and to use this finding to gain stronger insights into the epidemiology of a chronic infection. The strain of B. bronchiseptica used in this work was originally isolated from the nares of a 3 month old New Zealand White rabbit and it was assumed that it could be naturally transmitted between individuals [14]. Indeed, we found that rabbits were able to shed bacteria onto a BG blood agar plate by direct oro-nasal contact, which mimicked the natural Combretastatin A4 clinical trial contacts observed between free living individuals. Mean number of bacteria shed per second was 0.028 (± 0.001 S.E.) CFUs; shedding was high during the first month

post infection and again 15 weeks later but substantially dropped between the two peaks (Fig. 2). Based on the longitudinal data (weekly sampling of individuals for serum antibodies and blood cells), we found a significant negative effect of IgG on number of bacteria shed MK0683 order (coeff ± S.E: -0.092 ± 0.025 df = 88 P < 0.0001), once corrected by host variability. Blood cells did not contribute

to the pattern observed. The analysis was repeated using bacteria CFU counts from the nares of animals sampled at 60, 90, 120 and 150 post infection, and a weak but significant positive relationship was observed between bacteria shed at these sampling points and bacteria in the nasal cavity (coeff ± S.E.: 0.37e-7 ± 0.14e-7 d.f. = 8 P < 0.030). Together these results suggest that shedding is positively influenced by the level of infection in the oro-nasal cavity and negatively affected by serum IgG. Figure 2 Mean number of bacteria shed this website (CFUs/sec ± S.E.) by oro-nasal contact with a BG blood agar plate during the course of the infection. A total of 14 selleck chemicals llc infected rabbits were used and sacrificed at days 60, 90, 120 and 150 post-infection. Each individual

was weekly challenged by oro-nasal contact with a BG blood agar plate and time of interaction measured. Bacteria were enumerated after incubating for 36-48 hr at 37°C. For every week post infection (from WPI 2 to WPI 18) the number of plates positive for B. bronchiseptica after removal of contaminated cases and sacrificed individuals was: WPI 2 = 8, WPI 3 = 6, WPI 4 = 8, WPI 5 = N.D. (no data), WPI 6 = 11, WPI 7 = N.D., WPI 8 = 14, WPI 9 = 12, WPI 10 = 12, WPI 11 = 12, WPI 12 = 12, WPI 13 = 8, WPI 14 = 8, WPI 15 = 8, WPI 16 = 8, WPI 17 = 8, WPI 18 = 4. The overall average shedding pattern and the more specific three shedding groups (intermittent, fade-out and non-shedding) are reported. Three main patterns of shedding were identified during the course of the infection: i- bacteria were shed with variable intensities at irregular intervals (‘intermittent’ group, 46% of individuals), ii- intensity of bacteria shed fell with the progression of the infection (‘fade-out’ group, 31%) and iii- individuals never shed bacteria despite being infected (‘non-shedders’, 23%) (Fig. 2).

All obtained predicted proteins were analyzed with the TMHMM, ConPred II and HMMTOP algorithms [70–72] to test for the typical 7-transmembrane domain topology. For those few proteins exhibiting less than seven transmembrane domains, the respective encoding gene and flanking regions were retrieved from the genome database and examined manually. Wrongly predicted

intron-exon boundaries were mainly found and manually corrected resulting in the detection of the missing transmembrane domains. Protein alignments and phylogenetic analysis The classification system of Lafon et al. [1], which classifies fungal GPCRs into nine classes selleck compound according to their sequence similarity, was check details applied to all detected putative GPCRs of Trichoderma. In addition, members of the three additional classes identified in Verticillium spp. [36], and the GPR11 protein of Phytophtora sojae[35] were used to identify

and classify respective members of T. atroviride, T. virens and T. reesei. Multiple sequence alignments of the identified putative GPCR-like proteins and phylogenetic trees with a neighbor-joining approach were generated using ClustalX [73]. A bootstrap with 1000 repetitions was included. Cultivations and RT-qPCR analysis T. atroviride strain P1 (ATCC 74058; teleomorph Hypocrea atroviridis), T. virens strain IMI 206040 (teleomorph Hypocrea virens), this website and T. reesei strain QM6a (ATCC13631; teleomorph Hypocrea jecorina) were used in this study. The fungi were cultivated at 28°C on either complete medium (PDA, PDB) or minimal medium (MM, containing [g/l]: MgSO4 · 7H2O 1, KH2PO4 10, (NH4)2SO4 6, tri-sodium citrate 3, FeSO4 · 7H2O 0.005, ZnSO4 · 2H2O 0.0014, CoCl2 · 6H2O 0.002, MnSO4 · 6H2O Mirabegron 0.0017, glucose 10) on plates and in liquid culture, respectively. Plate confrontation assays were performed by cultivating Trichoderma together with Rhizoctonia solani on PDA plates covered with a cellophane membrane at 28°C. After direct contact between the two fungi, mycelium

of Trichoderma was harvested from the confrontation zone. For RNA isolation, 30 mg fungal mycelium was grinded in liquid nitrogen and RNA isolated using the peqGOLD TriFast Solution (PeqLab, Erlangen, Germany) according to the manufacturer´s instructions. For cDNA synthesis the Revert Aid H Minus First Strand cDNA Synthesis Kit (Fermentas, Vilnius, Lithuania) was used according to the manufacturer´s instructions with a combination of an oligo(dT)18 and a random hexamer primer. The sequences for the respective primer pairs for cDNA amplification of the reference gene sar1 and the genes encoding the putative receptors of class VIII identified in the Trichoderma genomes are given in Additional file 3.

Myers et al. [8] showed that purified VirR is able to bind the promoter of CPR_0761 and of CPF_0461. From our analysis it emerged that CPF_0461 in

str. ATCC1324 is the ortholog to CPR_0762 in str. SM101, for which too we predicted the presence of a VirR binding motif upstream. This motif is the same attributed to CPR_0761 and whose ability to bind VirR has been tested by Myers et al., 2006. Our comparative analysis, then suggests that the truly regulated gene could be the latter, because of the conservation of the site upstream of its homologs in two other organisms (ATCC3626 and ATCC1324), while we were not able to find sequences resembling CPR_0761 in any other C. perfringens strain by blasting both protein and nucleotide sequences against their genomes. Alternatively, the two genes can also form an operon, with CPR 0761 PD0332991 price performing an unknown function. The accessory VirR regulon We consider this dataset low confidence for two reasons: first of all this group of genes comprises only one experimentally verified target, i.e. virT (CPE0845, [7]) and moreover, all other genes have been found in draft genomes only. The list of all selleck putative targets of VirR is shown in Table 3. Notably, JGS1987 is characterized by an expansion of the VirR predicted regulon, while the accessory regulon of ATCC3626,

F4969 and SM101 strains learn more is composed of a single gene. The case of virT, a regulatory RNA, is particularly interesting. This sRNA implements a negative feed-back loop on some of the VirR targets i.e. pfoA and ccp [7]. Our analysis showed that virT is present in two strains only (strain 13 and strain ATCC3626). We can thus predict that the other strains lack this negative Amoxicillin control and express pfoA and ccp at different levels eventually by using additional

regulations. Actually, strains as ATCC 13124 produces large quantities of gangrene-associated toxins [9] and JGS1987 is a Type E strain which, tough containing an enterotoxin gene (cpe), did not show enterotoxin production [10]. The relatively large predicted regulon (10 genes) of JGS1987 may contain genes responsible for its peculiar pathogenicity profile. Within such regulon seven genes code for proteins of unknown function. One of them corresponds to a resolvase/recombinase (AC3_0180) suggesting a possible scenario in which host invasion is linked to gene mobilization. The other two genes with assigned function in the putative regulon of strain JGS1987 include a 2-keto-3-deoxygluconate kinase and a putative lipid A export permease. The first one has been associated with resistance to oxidative stress in C. perfringens mutants after transposon mutagenesis [11].

5). In contrast, the %TKV slope and log-TKV slope became smaller as age advanced (right panel of Table 3 and Fig. 5d). There was no significant correlation between

function-related slopes and age. The age-related results were not qualitatively different between baseline and final age. Discussion The present study confirmed the significant relationship between TKV and kidney function, which was reported check details by CRISP studies [4, 5, 14–16]. Among adjusted TKV parameters, log-TKV correlated with eGFR most significantly. As the CRISP study showed that TKV increased exponentially and GFR decreased linearly [4], it is reasonable that log-TKV correlates with kidney function better than the other adjusted TKV parameters [14]. Final eGFR but not baseline eGFR correlated with the eGFR slope. This observation is in agreement with our previous report [10], in which the eGFR slope had no correlation with baseline eGFR. The kidney

function remains well preserved for many years learn more but decreases rapidly at a later stage [1, 17]. This characteristic profile of renal function progression is explained by a compensatory adjustment for the loss of GFR. Compensatory adjustments make the decline in GFR slow or close to zero until certain stages [1]. GFR is maintained within the normal range despite decreased renal plasma flow Ketotifen in children and young adult patients with ADPKD [18–20]. In early stages, the decrease in renal plasma flow due to structural distortion in ADPKD is partially compensated for by an increased glomerular filtration fraction to renal plasma flow, but these adaptations eventually prove inadequate and kidney function starts to decline at a faster rate [21]. Those observations and hyperfiltration hypothesis are collectively

in accordance with the present finding that the eGFR slope becomes more negative as eGFR decreases (Table 2). The eGFR slope is relatively constant in relation to age (Fig. 4b). In our previous study, changes of reciprocal creatinine in 106 patients plotted against age showed that the progression patterns of renal function deterioration were different among patients [10]. Individual variation in renal functional progression might be a parallel characteristic to the wide distribution of kidney size growth, as shown in Fig. 3. Due to individual differences, the mean yearly change in eGFR (eGFR slope) as a whole patient group seemed to be constant, at least after ~30 years of age. Fig. 4 a Correlation coefficient (r) between eGFR and age is highly significant. Age and eGFR are those measured at the final time. b There was no significant correlation coefficient (r) between age and the slope of eGFR. Age is at the final measurement TKV increases each year in most patients with ADPKD (Fig.

Similarly, it was observed for all other clinical parameters analyzed. Surgery and prothrombotic markers Multivariate analysis demonstrated that only p-selectin was significantly correlated to the type of anesthesia and surgery (p = 0.01). It is very important to note that the TIVA-TCI patients undergoing LRP showed a significant reduction in p-selectin levels between T0 and T2 (p = 0.001) while no changes were observed Ilomastat concentration in the BAL group that did not use the robotic device (Figure 3).

In contrast, a significant increase of p-selectin value was observed in patients undergoing RALP, regardless of the type of anesthesia, both 1 and 24 hours after surgery. Figure 3 Changes of p-selectin levels between T0 (before the induction of anaesthesia) and T2 (24 hrs post-surgery) in patients undergoing conventional

laparoscopic radical prostatectomy (LRP) or robot-assisted laparoscopic prostatectomy (RALP). TIVA-TCI patients undergoing LRP showed a significant reduction click here in p-selectin levels between T0 and T2 (p = 0.001) while no changes were observed in the BAL group. In contrast, a significant increase of p-selectin value was observed 24 hours after surgery (T2) in patients undergoing RALP, regardless of the type of anaesthesia. Patients undergoing RALP showed also 24 hrs after surgery (T2), at univariate analysis, a greater reduction of PS, an inhibitor of haemostatic system, as compared Baf-A1 in vivo to patients undergoing LRP (p = 0.02) independent of the type of anaesthesia applied. Discussion Results of our study have demonstrated that both anaesthetic techniques seem to increase the risk of TED in prostate cancer patients undergoing

LRP, mainly when the robot device was utilized, suggesting, therefore, the utility of a peri-operative thromboembolic prophylaxis. In fact, both TIVA-TCI and BAL patients showed a marked and significant increase in pro-coagulant factors and consequent reduction in haemostatic system inhibitors in the early post operative period (p ≤ 0.004 for each markers). However, this effect could be linked also to surgical stress, although the latter seems to have an independent effect only for p-selectin, as demonstrated by multivariate analysis. Moreover, the significant reduction of p-selectin levels between T0 and T2 (p = 0.001) observed in TIVA patients undergoing LRP, although this group of patients was composed mainly of patients at high-risk prostate cancer (as reported in Table 1), demonstrated that general anaesthetic agents used for TIVA have a better protective effect on the platelet activation in this subgroup of patients. The evaluation of markers detecting activation of the hemostatic system represents a more sensitive way to assess the risk of thromboembolism as compared to the clinical assessment of TED.

Moreover, Zn-curc localized inside glioblastoma tissues suggesting its ability to cross the blood-tumor barrier. Materials

and methods Ethics statement All animals were handled in strict accordance with good animal practice as defined by the relevant national and/or local animal welfare bodies, and in accordance with the Italian and European legislation. All work was performed in accordance with the guidelines of the National Cancer Institute Regina Elena, where there is currently no active Ethical Committee for animal research, Akt phosphorylation and has been filed with the Veterinary Service Unit and the Italian Ministry of Health, in accordance with the Italian and European legislation. Cell culture and treatments The human colon cancer RKO (wtp53), glioblastoma U373MG (expressing R273H p53 mutation) and T98G (expressing M237I p53 mutation) cell lines were maintained in RPMI-1640 (Life Technology-Invitrogen), while human SKBR3 (expressing R175H p53 mutation), MD-MBA231 (expressing p53 mutation R280K) breast cancer cell lines and human fibroblasts (HF) (kindly provided by S. Soddu, Regina Elena National Cancer Institute, Rome, Italy) were maintained in DMEM (Life Technology-Invitrogen), all supplemented with 10% heat-inactivated fetal bovine serum plus glutamine and antibiotics. The following reagents were used: a heteroleptic pentacoordinated (bpy-9)Zn(curc, Cl) complex containing a

4,4′-disubstituted-2,2′-bipyridine as main ligand and curcumin (curc) and chloride (Cl) as ancillary ligands [13] was Etomidate dissolved in DMSO and used at the Nec-1s purchase indicated concentrations; curcumin was prepared as previously reported [17]; pifithryn-α (PFT-α) (ENZO Life Sciences, Lausen Switzerland) was dissolved in DMSO and used at 30 μM; adryamycin (ADR) was used at 2 μg/ml and ZnCl2 was used at 100 μM. Viability and colony assays Subconfluent cells were plated in triplicate in 60 mm Petri dishes and 24 h later treated with Zn-curc complex (20-50-100 μM) for 24 and 48 h. Both floating and adherent cells were collected and cell viability was determined by Trypan blue exclusion by direct counting with a haemocytometer, as reported. The percentage

of cell viability, as blue/total cells, was assayed by scoring 200 cells per well three times. For long-term cell survival, subconfluent cells were plated in 60 mm Petri dishes and 24 h later treated with Zn-curc complex (20-50-100 μM). Twenty-four hours later, plates were washed with PBS and fresh medium was added. Death-resistant colonies were stained with crystal violet 14 days later. Cell death/PI staining Cell death was detected by cytofluorimetric analysis of propidium iodide (PI)-stained cells staining. Briefly, cells floating were collected by centrifugation and pooled with adherent cells recovered from the plates, fixed in 80% ethanol and stained in a PBS solution containing PI (62.5 mg/mL; Sigma-Aldrich), and RNase A (1.125 mg/mL; Sigma-Aldrich).

AFM in a contact mode was also used to determine the film thickness by measuring the step height after lithography. X-ray photoelectron spectroscopy (XPS) measurements to analyze carbon bonding characteristics were done using a Kratos X-ray photoelectron spectrometer (Kratos Analytical Ltd, Manchester, UK) with Mg Kα X-ray source. C1s spectra were acquired at 150-W X-ray power with a pass energy of 20 eV and a resolution step of 0.1 eV. Results and discussion Figure 1 shows the Raman spectra from 3- to approximately 5-nm-thick carbon films grown on various fluorides by MBE. The characteristic peaks of graphitic carbon are well identified in all films: the D peak at approximately 1,350 cm−1 and the G peak at approximately 1,590 cm−1. These and previous studies show that MBE is an effective method selleck chemical for graphitic carbon growth on a wide range of

substrates [14–17]. The learn more degree of graphitization is, however, quite different depending on the cation. In fact, graphitic carbon refers to a wide range of disordered graphite, from NCG to mainly sp 2 amorphous carbon. As clarified by Ferrari [20], the relative strength of D and G peaks alone cannot determine the degree of disorder, and it is the 2D peak at approximately 2,700 cm−1 which distinguishes NCG from amorphous carbon. As shown in Figure 1, the Raman spectra of the carbon film on MgF2 show a clear 2D peak, indicating that successful NCG growth was accomplished on MgF2 by carbon MBE. In contrast, the carbon films grown on CaF2 and BaF2 can be ascribed to amorphous carbon. As far as we know, carbon MBE on a family of substrates having the same anion has not been reported. Clear understanding of this cation dependence Adenylyl cyclase is yet to come, but our results will stimulate systematic studies on other series of substrates and further theoretical investigations. Figure 1 Raman spectra

of carbon films. The films were grown by carbon MBE at 900°C on MgF2(100), CaF2(100), and BaF2(111). The pronounced 2D peak at approximately 2,700 cm−1 confirms that nanocrystalline graphite is formed on MgF2. We will focus on the growth on MgF2 from now on and compare the results with NCGs on oxides. For a quantitative comparison, the Raman spectra of NCG on MgF2 were fit by several Lorentzian functions as in [15] (Table 1). Interestingly, the intensity ratios of the D peak and 2D peak to the G peak (I D/I G and I 2D/I G) are larger than those from NCG on MgO. Furthermore, all the peaks are narrower, implying a better crystallinity on MgF2 (from the comparisons of the full width at half maximum (FWHM) in Table 1 and those in [15]). The average cluster size, L a, can be calculated from the relation I D/I G = C L a 2, where C = 0.0055 and L a in Å [20]. From I D/I G = 2.7 (Table 1), we get L a = 22 Å, a slight increase from those on oxides [15, 16]. Figure 2 shows a Raman map of the intensity ratio of I D/I G over 10 μm2. Most regions have I D/I G = 2.