Specific capacitance of NiO-Film (S2): the specific capacitance of the supporting NiO film is measured at different scan https://www.selleckchem.com/products/Fludarabine(Fludara).html rates (Figure S2) to estimate the maximum contribution of the supporting NiO film. (DOCX 226 KB) References 1. Winter M, Brodd RJ: What are batteries, fuel cells, and supercapacitors? Chem Rev 2004, 104:4245–4270.CrossRef 2. Kuperman A, Aharon I: Battery–ultracapacitor hybrids for pulsed current loads: a review. Renewable Sustainable Energy Rev 2011, 15:981–992.CrossRef 3. Miller JR, Simon P: LY3039478 clinical trial electrochemical capacitors for

energy management. Science 2008, 321:651–652.CrossRef 4. Simon P, Gogotsi Y: Materials for electrochemical capacitors. Nat Mater 2008, 7:845–854.CrossRef 5. Lota G, Centeno TA, Frackowiak E, Stoeckli F: Improvement of the structural and chemical properties of a commercial

activated carbon for its application in electrochemical capacitors. Electrochim Acta 2008, 53:2210–2216.CrossRef 6. Fang B, Binder L: A modified activated carbon aerogel for high-energy storage in electric double layer capacitors. J Power Sources 2006, 163:616–622.CrossRef 7. Conway click here BE: Transition from “supercapacitor” to “battery” behavior in electrochemical energy storage. J Electrochem Soc 1991, 138:1539–1548.CrossRef 8. Sarangapani S, Tilak BV, Chen C-P: Materials for electrochemical capacitors theoretical and experimental constraints. J Electrochem Soc 1996, 143:3791–3799.CrossRef 9. Conway BE: Electrochemical Supercapacitors: Scientific Fundamentals and Technological Applications. New York: Plenum; 1999.CrossRef 10. Zheng JP, Cygan PJ, Jow TR: Hydrous ruthenium oxide as an electrode material

for electrochemical capacitors. J Electrochem Soc 1995, 142:2699–2703.CrossRef 11. Ke YF, Tsai DS, Huang YS: Electrochemical capacitors of RuO 2 nanophase grown on LiNbO 3 (100) and sapphire(0001) substrates. J Mater Chem 2005, 15:2122–2127.CrossRef 12. Zheng JP, Jow TR: A new charge Reverse transcriptase storage mechanism for electrochemical capacitors. J Electrochem Soc 1995, 142:L6-L8.CrossRef 13. Lang JW, Kong LB, Wu WJ, Luo YC, Kang L: Facile approach to prepare loose-packed NiO nano-flakes materials for supercapacitors. Chem commun 2008, 4213–4215. doi:10.1039/B800264A. 14. Liang K, Tang X, Hu W: High-performance three-dimensional nanoporous NiO film as a supercapacitor electrode. J Mater Chem 2012, 22:11062–11067.CrossRef 15. Fisher AE, Pettigrew KA, Rolison DR, Stround RM, Long JW: Incorporation of homogeneous, nanoscale MnO 2 within ultraporous carbon structures via self-limiting electroless deposition: implications for electrochemical capacitors. Nano Lett 2007, 7:281–286.CrossRef 16.

Gene expressions Epacadostat order in

the early stage of PRV infection In the first 2 h of infection, the viral DNA replication has not yet been initiated, and the copy number of viral genomes in a cell therefore corresponds with the infectious dose. In this analysis, we found that the mRNA levels of most examined PRV genes were higher in the cells infected with the high MOI than in those infected with the low MOI (Additional file 2a) at both 1 h and 2 h pi. This was not unexpected since in the former case viral DNAs were represented in an approximately 10-fold higher proportion in an GDC-0994 in vivo average infected cell. Exceptions to this were the transcripts ul1, ul33, and ul51 mRNAs at 1 h pi, and ul36, ul38, ul43, and ul48 mRNAs at 2 h pi, and at both 1 h and 2 h: ie180 and ul30 mRNAs, as well as, LAT and AST. However, the expression levels normalized to the genome copy number (i.e. using R/10 values in the high-MOI infection) MI-503 manufacturer showed an inverse pattern: only a few genes were expressed at higher abundance in the high-MOI than

in low-MOI infection (Additional file 2a). AST was expressed at a considerably higher quantity in the cells infected with the low MOI than in those infected with the high MOI (Rlow MOI/Rhigh MOI = 111-fold at 1 h, and 298-fold at 2 h pi). The expression rate of a single genomic region encoding the AST was even 10 times higher (1 h: 1110-fold and 2 h: 2980-fold) in the low-dose infection experiment Resveratrol (Additional file 2a). In the high-dose infection 6 of the 37 genes (ie180, ul36, ul50, ul54, us1, and ul24) exhibited higher expression levels at 1 h than at 2 h pi. It should be noted that 3 of them (ie180, us1 and ul54) are regulatory genes. The fourth regulatory PRV gene, ep0, is expressed at a very high level during the first 2 h in the high-MOI infection (R1 h = 1.87, R2 h = 2.05). Apart from ep0, ul5 (R2 h = 1.2) was the only gene that was expressed at a higher extent in the early stages of infection than at 6 h pi in the high-MOI experiment. The ie180 gene is the only one that was expressed in a higher amount at 1 h than at 2 h pi under both experimental

conditions (Additional file 2). Overall, it appears that the 4 regulatory genes were expressed at relatively high levels before the onset of DNA replication in the high-MOI infection, which was not the case in low-MOI infection, with the exception of the ie180 gene. We think that the reason for the higher expression of regulatory genes at the onset of viral DNA replication in the high-MOI infection is that more regulatory proteins are needed to carry out the multiplication of a higher copy number of the viral genome. The rate of change in gene expression within the 1 h to 2 h interval (R2h/R1h) was higher in more than two-thirds of the PRV genes (25/37) in the low-MOI than in the high-MOI infection (Additional file 2c). The proportion of AST to ie180 mRNA molecules (RAST/Rie180) was 0.47 at 1 h pi, and 4.

Figure 6 Caspase-3 activation as determined by flow cytometry. Top four panels: flow cytometric analyses of procaspase-3. Sarcomatoid and 3-Methyladenine clinical trial epithelioid VX-661 clinical trial cells showed a similar baseline expression. In both cell types, a

subpopulation lost expression after selenite treatment. Gray histograms show the negative controls for the immunostaining. Bottom four panels: flow cytometric analyses of caspase-3 activation. Selenite treatment caused the appearance of a distinctly positive subpopulation in the epithelioid cells, whereas the sarcomatoid cells showed a small positive subpopulation that was not distinctly separated from the main peak. Three independent experiments were performed. All eight panels are derived from the same experiment. Divergent data have been published regarding the role of caspases in selenite-induced apoptosis. Several studies have shown that selenite causes a caspase-independent apoptotic cell death [6, 18, 40], whereas others have shown caspase-dependence [9, 17, 36, 57]. We report that caspase-3 was activated in a sub-population of epithelioid cells, but little reactivity was seen in sarcomatoid cells. The limited caspase activation in sarcomatoid cells was surprising. A possible explanation could be an upregulation of Inhibitor of Apoptosis (IAP) family members such as survivin and XIAP. Earlier studies

have found that overexpression of IAP family members is common in mesothelioma cells [58–61]. Inhibition of cathepsin Staurosporine supplier B but not of cathepsins D and E caused increased loss of δΦm Cathepsins are a group of proteases that are physiologically present in lysosomes, and may be released upon stimuli such as oxidative stress [62]. Cells that were pretreated

with cathepsin B inhibitor CA-074 Me showed slightly less apoptosis after selenite exposure (Figure 1). In the sarcomatoid cells, this was reflected in correspondingly increased viability. In the epithelioid cells, the viable proportion decreased slightly instead. Interestingly, when selenite mafosfamide was combined with the cathepsin B inhibitor, the loss of δΦm was greater than with any other inhibitor (Table 2). Cathepsin D and E inhibitor Pepstatin A did not affect the induction of apoptosis by selenite, nor did it alter the loss of δΦm. Signs of autophagy were not detected Autophagy is a form of programmed cell death in which cells do not exhibit apoptotic characteristics. Kim et al have shown that selenite induces autophagy in glioma cells [38]. We wanted to investigate whether some of the cell death that we observe could be due to autophagy. Cells were stained with monodansyl cadaverine and analysed with confocal microscopy for the appearance of granules that might represent autophagic vesicles.

J Plant Physiol 157:307–314CrossRef Hakala M, Tuominen I, Keränen M, Tyystjärvi T, Tyystjärvi E (2005) Evidence for the role of the oxygen-evolving manganese complex in photoinhibition of Photosystem II. PLX3397 datasheet Biochim Biophys Acta 1706:68–80PubMedCrossRef Herlory O, Richard P, Blanchard GF (2007) Methodology of light response curves: application see more of chlorophyll fluorescence to microphytobenthic biofilms. Marine Biol 153:91–101CrossRef Jakob T, Schreiber

U, Kirschesch V, Langner U, Wilhelm C (2005) Estimation of chlorophyll content and daily primary production of the major algal groups by means of multiwavelength-excitation PAM chlorophyll fluorometry: performance and methodological limits. Photosynth Res 83:343–361PubMedCrossRef Kirilovsky selleck chemical D (2007) Photoprotection in cyanobacteria: the orange carotenoid protein (OCP)-related non-photochemical-quenching mechanism. Photosynth Res 93:7–16PubMedCrossRef Klughammer C, Schreiber U (2008) Complementary PS II quantum yields calculated from simple fluorescence parameters measured by PAM fluorometry and the Saturation Pulse method. PAM Application Notes, vol 1, pp 27–35. http://​www.​walz.​com/​downloads/​pan/​PAN11001.​pdf Koblizek M, Kaftan D, Nedbal L (2001) On the relationship between the non-photochemical quenching of the chlorophyll fluorescence and the Photosystem II light harvesting efficiency. A repetitive flash

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light to biosphere, vol V. Kluwer, Dordrecht, pp 825–828 Krall JP, Edwards GE (1990) Quantum yields of Photosystem II electron transport and carbon dioxide fixation in C4 plants. Aust J Plant Physiol 17:579–588CrossRef Kramer DM, Johnson G, Kiirats O, Edwards GE (2004) New fluorescence parameters for the determination of QA redox state and excitation energy fluxes. Photosynth Res 79:209–218PubMedCrossRef Lavergne J, Leci E (1993) Properties of inactive PS II centers. Photosynth Res 38:323–343CrossRef L-NAME HCl Lavergne J, Trissl HW (1995) Theory of fluorescence induction in photosystem II: derivation of analytical expressions in a model including exciton-radical-pair equilibrium and restricted energy transfer between photosynthetic units. Biophys J 68:2474–2492PubMedCrossRef Ley AC, Mauzerall DC (1982) Absolute absorption cross-sections for Photosystem II and the minimum quantum requirement for photosynthesis in Chlorella vulgaris. Biochim Biophys Acta 680:95–106CrossRef Matsubara S, Chow WS (2004) Populations of photoinactivated Photosystem II characterized by chlorophyll fluorescence lifetime in vivo.

Using this system we routinely identify more than 100 click here recombinants per experiment in both laboratory and pathogenic E. coli strains, using short regions of homology to the chromosome, thus maintaining both a high-throughput and broad-range compatibility system. G-DOC plasmids The pDOC plasmids are derived from pEX100T, a medium copy number plasmid which carries ampicillin resistance and the B. subtilis sacB gene [19]. We have introduced different DNA sequences into the pEX100T I-SceI restriction sites to create a suite of plasmids, schematic diagrams of which are shown in Figure 1. The

cloning plasmid, pDOC-C, has a large cloning region (CR) flanked by two I-SceI recognition sites. The DNA sequence of pDOC-C, from 100 bp upstream of the left-hand I-SceI site to 100 bp downstream of the right-hand I-SceI site is shown in Figure 2, panel A. The template plasmid, pDOC-K, carries a kanamycin resistance cassette flanked by Flp recombinase GSK2118436 cell line recognition sites (Flp1 and Flp2). On either side of this region are 2 cloning regions (CR1 and CR2). The

other template plasmids, pDOC-H, pDOC-F, pDOC-P and pDOC-G are derivatives of pDOC-K that have the coding sequence for a 6 × His, 3 × FLAG, 4 × Protein A and GFP tag respectively, immediately downstream of CR1. Figure 2; panel B, shows the DNA sequence common to all of the pDOC template plasmids, from 100 bp upstream of the left-hand I-SceI site to 100 bp downstream Chloroambucil of the right-hand I-SceI site. The template plasmids differ between the CR1 and FLP1 sequences: this region is outlined by an open box in the figure. The DNA sequence 4SC-202 molecular weight proceeds through CR1, along the respective DNA sequence for each plasmid

within the open box, and into the FLP1 sequence below. The plasmid pDOC-K has 30 bp of DNA sequence prior to FLP1. The plasmid pDOC-H has the coding sequence for the 6 × His tag and a stop codon followed by a short DNA sequence leading into the FLP1 site. The first 10 codons of the 3 × FLAG, ProteinA and GFP tags are shown, followed by the stop codon and short DNA sequences leading into FLP1 site. Other features indicated on the DNA sequences of the pDOC plasmids in Figure 2 are described in the G-DOC recombineering protocol below. The full DNA sequence of each pDOC plasmid is provided in Additional file 1 and is also available from GenBank, accession numbers GQ88494-GQ889498. Figure 1 The pDOC donor plasmids. Circular representation of the pEX100T plasmid showing the location of the origins of replication, the sacB gene and the ampicillin resistance gene. Below is a linear representation of the pDOC plasmid inserts, showing the I-SceI restriction sites, cloning regions (CR, CR1 and CR2), the Flp recognition sites flanking the kanamycin resistance cassette (KanR) and the location of the epitope tags in plasmids pDOC-H, pDOC-F, pDOC-P and pDOC-G. Figure 2 DNA sequences of the pDOC plasmids.

J Appl Phys 2005,98(7):074904.CrossRef 25. Deal BE, Grove AS: General relationship for the thermal oxidation of silicon. J Appl Phys 1965,36(12):3770–3778.CrossRef NU7026 26. Brunner K: Si/Ge

nanostructures. Rep Prog Phys 2002, 65:27–72.CrossRef 27. Medeiors-Ribeiro G, Williams RS: Thermodynamics of coherently-strained GexSi1-x nanocrystals on Si(001): alloy composition and island formation. Nano Lett 2007,7(2):223–235.CrossRef 28. Plummer JD, Deal MD, Griffin PB: Silicon VLSI Technology: Fundamentals, Practice and Modeling. New Jersey: Prentice Hall; 2000. 29. Enomoto T, Ando R, Morita H: Thermal oxidation rate of a Si 3 N 4 film and its masking effect against oxidation of silicon. Jpn J Appl Phys 1978, 17:1049–1058.CrossRef 30. Flint PS: The rates of oxidation of silicon. PF-4708671 Los Angeles: Paper presented at the Spring Meeting of The Electrochemical Society, Abstract No. 94; 1962. Competing interests The authors declare that they have no competing interests. Authors’ contributions CW carried out the TEM experimentation and analysis. PL and MK carried out the Ge QD growth and kinetics analysis. TG conceived the mechanism of Ge QD explosion

and drafted the manuscript. PL conceived the study, supervised the work, contributed to data analysis and the manuscript preparation. All authors read and approved the final manuscript.”
“Background With the development of nanotechnology, complex micro/nanodevice assembly would gradually be a reality in the future. The various explorations in the aspects www.selleck.co.jp/products/obeticholic-acid.html of nanomaterial preparation and performance at present provide the base for nano-engineering, in which the controllable preparation and unique performance of nanomaterials have been the keys of exploration. With the aim of exploiting new coupling phenomena and potential applications, nanocomposites have attracted much attention over the past decade [1–5]. The typical preparation way is through an in situ fabrication; the different components are integrated together to form a nanocomposite at the same time. For example,

metallic nanocrystals could be incorporated into one-dimensional (1D) carbons to form a metal-carbon nanocomposite via an organometallic precursor-controlled thermolysis approach. Unprecedented physical and chemical properties become available due to the effects of spatial confinement and synergetic electronic interactions between metallic and carbonaceous components [6]. This type of nanocomposite has shown unique properties in some aspects including magnetic, catalytic, electronic, and thermoelectric properties [7–10]. Another preparation way is the surface recombination of several different individual nanomaterials using a physical or chemical MCC950 cell line method. Due to the complexity and importance of the nanomaterial surface property, this type of nanocomposite can more easily show the new phenomenon and unique performance.

The participants were then assigned to the following groups: <1 L/day (14.5 %), 1–1.9 L/day (51.5 %), 2–2.9 L/day (26.3 %), and ≥3 L/day (7.7 %). As water intake increased, the percentage annual eGFR decline turned out to be 1.3, 1.0, 0.8, 0.5 %, respectively. Hebert et al. reported that high fluid intake resulted in Captisol cost an increased urine volume, and low urine osmolality (Uosm) was not associated with slower renal disease progression. In a randomized control trial performed by Spigt et al., one group was advised to increase their daily fluid intake by 1.5 L of water, and the other group was given placebo medication. Most subjects did not manage to increase their fluid intake by 1.5 L. The average

increase in the intervention group was approximately 1 L. Twenty-four-hour water turnover in the intervention group was

359 mL (95 % CI 171–548) higher than that of the control group at the 6-month follow-up. Blood pressure, sodium level, TPCA-1 cell line GFR, and QOL did not change significantly in either group during the intervention period. Increased water intake is effective for maintaining kidney function in CKD Selleckchem BTK inhibitor patients at stage G1 and G2, but it could be a risk factor for worsening kidney function in CKD patients at stage G3 and higher. Dehydration can exacerbate kidney function at any CKD stage. It is important to maintain an appropriate water intake based on the CKD stage. Bibliography 1. Clark WF, et al. Clin J Am Soc Nephrol. 2011;6:2634–41. (Level 4)   2. Hebert LA, et al. Am J Kidney

Dis. 2003;41:962–71. (Level 4)   3. Spigt MG, et al. J Am Geriatr Soc. 2006;54:438–43. (Level 2)   Is vaccination recommended for CKD? CKD patients have a weakened immune system and are at risk of higher morbidity and mortality rates from infections compared to healthy subjects. It is recommended that CKD patients should be given vaccinations against high risk pathogens. Pneumococcal and Influenza vaccines are inactivated, hence both have a low potential for adverse events related to the administration of the vaccination. Influenza is a common and widespread infection causing morbidity and mortality in the general population, and regular vaccinations are recommended to prevent the Tau-protein kinase associated comorbidities. Influenza may be significantly exacerbated to pneumonia, especially in the elderly. Therefore, influenza vaccination is related to the prevention of pneumonia. The report from the United States Renal Data System (USRDS) in 2007 showed that influenza vaccination for CKD patients aged over 66 years decreased total mortality and hospitalization rates from January to March compared to that of unvaccinated patients. Pneumonia is the 4th leading cause of death in patients aged over 65 years in Japan, and 95 % of deaths from pneumonia occur in patients aged over 65 years. Pneumococcus is the most common pathogen in community-acquired pneumonia of the elderly, and it is reported that 30–50 % of Pneumococcus is drug-resistant. Viasus et al.

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Stress 16(1):79–87CrossRef Harkness TGF beta inhibitor EF, Macfarlane GJ, Nahit ES, Silman AJ, McBeth J (2003) Risk factors for new onset low back pain amongst cohorts of newly employed workers. Rheumatology 42:959–968CrossRef Hartvigsen J, Lings S, Leboeuf-Yde C, Bakketeig L (2004) Psychosocial factors at work in relation to low back pain and consequences of low back pain; a systematic, critical review of prospective cohort studies. Occup Environ Med 61(1):e2 Hayden JA, Chou R, Hogg-Johnson S, Bombardier C (2009) Systematic Selleck BI-2536 reviews of low back pain prognosis had variable methods and results: guidance for future prognosis reviews. J Clin Epidemiol 62(8):781–796CrossRef Helmhout

PH, Staal JB, Heymans MW, Harts CC, Hendriks EJ, de Bie RA (2010) Prognostic factors for perceived recovery or functional improvement in non-specific low back pain: secondary analyses of three randomized clinical trials. Eur Spine J 19(4):650–659CrossRef Heymans MW, de Vet HC, Knol DL, Bongers PM, Koes BW, van MW (2006) Workers’ beliefs and expectations affect return to work over 12 months. J Occup Rehabil 16 (4):685–695 Hoogendoorn WE, van Poppel MN, Bongers PM, Koes BW, Bouter LM (2000) Systematic review of psychosocial factors at work and private life as risk factors for back pain. Spine 25(16):2114–2125CrossRef Hoogendoorn WE, Bongers PM, de Vet HCW, Houtman ILD, Ariens GAM, van Mechelen W, Bouter LM (2001) Psychosocial work characteristics and psychological

strain in relation to low-back pain. Scand J Work Environ Health 27(4):258–267CrossRef Cobimetinib nmr Ijzelenberg W, Burdorf A (2005) Risk factors for musculoskeletal symptoms and ensuing health care use and sick leave. Spine 30(13):1550–1556CrossRef Iles RA, Davidson M, Taylor NF (2008) Psychosocial predictors of failure to return to work in non-chronic non-specific low back pain: a systematic review. Occup Environ Med 65(8):507–517CrossRef Johnson JV, Hall EM (1988) Job strain, work place social support, and cardiovascular GDC-0973 research buy disease: a cross sectional study of a random sample of the Swedish working population. Am J Public Health 78:1336–1342CrossRef Josephson M, Vingard E (1998) Workplace factors and care seeking for low-back pain among female nursing personnel.

J Phys Chem C 2009, 113:8143–8146.CrossRef 13. Wu Y, Xiang J, Yang C, Lu W, Lieber CM: Single-crystal metallic nanowires and metal/semiconductor nanowire heterostructures. Nature 2004, 430:61–65.CrossRef 14. Weber WM, Geelhaar L, Graham AP, Unger E, Duesberg GS, Liebau M, Pamler W, Cheze C, Riechert H, Lugli P, Kreupl F: Silicon-nanowire transistors with intruded nickel-silicide contacts. Nano Lett 2006, 6:2660–2666.CrossRef 15. Lu KC, Wu WW, Wu HW, Tanner CM, Chang JP, Chen LJ, Tu KN: In situ control of atomic-scale Si layer with huge strain in the nanoheterostructure NiSi/Si/NiSi through point contact reaction. Nano

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LT, Hsin CL, Wu WW: Copper silicide/silicon nanowire heterostructures: in situ TEM observation LY2835219 research buy of growth behaviors and electron transport properties. Nanoscale 2013, 5:5086–5092.CrossRef 18. Hsin CL, Yu SY, Wu WW: Cobalt silicide nanocables grown on Co films: synthesis and physical properties. Nanotechnology 2010, 21:485602.CrossRef 19. Lee CY, Lu MP, Liao KF, Lee WF, Huang CT, Chen SY, Chen LJ: Free-standing single-crystal NiSi 2 nanowires with excellent electrical transport and field emission properties. J Phys Chem C 2009, 113:2286–2289.CrossRef 20. Lee CY,

Lu MP, Liao KF, Wu WW, Chen LJ: Vertically well-aligned epitaxial Ni 31 Si 12 nanowire arrays with excellent field emission properties. Appl Phys Lett 2008, 93:113109.CrossRef 21. Decker CA, Solanki R, Freeouf JL, Carruthers JR, Evans DR: Directed growth of nickel silicide nanowires. Appl Phys Lett 2004, 84:1389–1391.CrossRef 22. Dong LF, Bush J, Chirayos V, Solanki R, Jiao J, Ono Y, Conley JF, Ulrich about BD: Dielectrophoretically controlled fabrication of single-crystal nickel silicide nanowire interconnects. Nano Lett 2005, 5:2112–2115.CrossRef 23. Song YP, Jin S: Synthesis and properties of single-crystal β 3 -Ni 3 Si nanowires. Appl Phys Lett 2007, 90:173122.CrossRef 24. Song YP, Schmitt AL, Jin S: Ultralong single-crystal metallic Ni 2 Si nanowires with low resistivity. Nano Lett 2007, 7:965–969.CrossRef 25. Tsai CI, Yeh PH, Wang CY, Wu HW, Chen US, Lu MY, Wu WW, Chen LJ, Wang ZL: Cobalt silicide nanostructures: synthesis, electron transport, and field emission properties. Cryst Growth Des 2009, 9:4514–4518.CrossRef 26. Foll H, Ho PS, Tu KN: Transmission electron microscopy of the formation of Nickel silicides. Philos Mag A 1982, 45:31–47.CrossRef 27. Dheurle F, Petersson CS, Baglin JEE, Laplaca SJ, Wong CY: Formation of thin-films of NiSi – metastable structure, diffusion mechanisms in intermetallic compounds. J Appl Phys 1984, 55:4208–4218.CrossRef 28.

Märgen, shortly after Glashütte coming from Hexenloch, MTB 8014/2, 47°59′37″ N 08°07′32″ E, elev. 750 m, on hymenium of Fomitopsis pinicola on Picea abies, 2 Sep. 2004, H. Voglmayr & W. Jaklitsch, W.J. 2666 (WU 29431). Schramberg, Heiligenbronn, Schwarzwald, Spitalwald, on basidiome of Fomitopsis pinicola, 4 Oct. 2006, W. Gams, W.J. 3055 (WU 29436, culture CBS 120643). Bavaria, Starnberg, Tutzing, Hartschimmel, Goaslweide, MTB 8033/3/1, 47°56′35″ N 11°11′02″ E, elev. 735 m, on hymenium of Fomitopsis pinicola, 22 Oct. 2003, P. Karasch, W.J. 2488 (WU 29430, culture C.P.K. 1992). Hessen, Eltville am Rhein, Hattenheim, forest at Geis, on Polyporus resinosus, identified as Fomitopsis pinicola, L. Fuckel, autumn,

Fungi Rhenani 2467 (M!). Italy, MI-503 cell line Südtirol, Pustertal, Sexten, Porzenwald, near Moos, MTB 9340/1, 46°40′34″ N 12°23′08″ E, elev. 1470 m, on Fomitopsis

pinicola, 1 Sep. 2000, W. Jaklitsch & H. Voglmayr. Sweden, Uppsala Län, Österbybruk, 3–4 km north from the town, right from the road to Forsmark, MTB 4373/4, 60°14′10″ N 17°55′41″ E, elev. 40 m, on hymenium of Fomitopsis pinicola on Picea abies, soc. Melanospora sp., Ophiostoma polyporicola, Cyclosporin A scant material, 5 Oct. 2003, W. Jaklitsch, W.J. 2439 (WU 29427, culture C.P.K. 2395). Stockholms Län, Nothamn, forest at the east coast, MTB 4179/3, 60°01′45″ N 18°50′43″ E, elev. 10 m, on hymenium and upper part of Fomitopsis pinicola on Picea abies, 7 Oct. 2003, W. Jaklitsch, W.J. 2446 (WU 29428, culture C.P.K. 2397). Switzerland, Neuchatel, Lac de la Gruère, on basidiome of Fomitopsis pinicola, 10 Oct. 2006, Farnesyltransferase W. Gams, W.J. 3056 (WU 29437, culture CBS 120640 = C.P.K. 2862). United Kingdom, Buckinghamshire, Slough, Burnham Beeches,

51°33′39″ N 00°37′55″ W, elev. 30 m, on hymenium of Piptoporus betulinus 23 cm diam, 15 Sep. 2007, W. Jaklitsch & H. Voglmayr, W.J. 3166 (WU 29439). Herefordshire, Leominster, Queenswood Country Park, Dinmore Hill, 52°09′13″ N 02°43′38″ W, elev. 150 m, on Piptoporus betulinus 2 m above ground on a standing trunk of Betula pendula, 11 Sep. 2007, W. Jaklitsch & H. Voglmayr, W.J. 3152 (WU 29438). Notes: This species is common and easily identified by ecological (growth on polypores) and morphological characteristics (unevenly distributed pigment, monomorphic ascospores, verrucose surface hairs, and lanceolate ostiolar cells). On Fomitopsis pinicola, H. pulvinata is often accompanied by H. protopulvinata; for differentiation see also under that species. To verify whether the Omipalisib fungus occurs on Laetiporus sulphureus (Polyporus sulphureus) and Ischnoderma resinosum (Polyporus resinosus), the lectotype from FH and the part of Fungi Rhenani 2467 from M were examined. In both specimens the host has a light to medium brown context and a resinous crust that melts in heat. This latter trait occurs only in basidiomata of Fomitopsis pinicola and uncommon species of Ganoderma, viz. G. pfeifferi and G. resinosum. The latter genus differs from Fomitopsis by a dark brown context.