The BIX 1294 concentration elemental composition of the Zr/CeO x /Pt was determined by energy dispersion. 05%), and Ce (3.83%). An oxygen peak at about 0.52 keV and Zr peaks at about 22.5 and 15.60 keV can be observed in the spectra. Figure 1 XRD pattern of the CeO x film and cross-sectional TEM selleck screening library and EDX images of the Zr/CeO x /Pt device. (a) XRD pattern of the CeO x film deposited on Si wafer at room temperature. (b) Cross-sectional TEM image of the Zr/CeO x /Pt device. (c) EDX image of the Zr/CeO x /Pt device. The ZrO y layer is also observed from XPS signals at the interface of Zr and CeO2 layers. XPS analysis

was carried out to examine the surface chemical composition and the valence/oxidation states of Ce and Zr species involved in the device by inspecting the spectral line shape and signal intensities associated with the core-level electrons. Figure 2a shows the depth profile of chemical composition in the Zr/CeO x /Pt device. The interdiffusion of O, Ce, and Zr atoms are evident from the spectra. This is an indication of the formation of an interfacial ZrO y layer between the CeO x and Zr top electrode. The formation of the ZrO y layer is further confirmed from the shifting of Zr 3d peaks from a higher binding energy PF477736 ic50 position to lower ones (Figure 2c). The CeO x 3d spectrum shown in Figure 2b consists of two sets of spin-orbit multiplets. These multiplets are the characteristics of 3d3/2 and 3d5/2 (represented 3-mercaptopyruvate sulfurtransferase as u and v, respectively) [15]. The spin-orbit splitting is about 18.4 eV. The highest peaks at around 880.2 and 898.7 eV, recognized as v 0 and u 0 respectively, correspond to Ce3+ with the highest satellites as v′ (885.1 eV) and u′ (903.3 eV). Low-intensity peaks, i.e., v (882.5 eV) and u (900.9 eV) along with satellite features represented as v″ (889.4 eV), v‴ (897.5 eV), u″ (905.4 eV), and u‴ (914.6 eV), are observed, corresponding to the Ce4+ state. Figure 2 XPS binding energy profiles. (a)

Depth profiles of Zr, Ce, O, Pt, and W for the W/Zr/CeO x /Pt structure, (b) Ce 3d, (c) Zr 3d, and (d) O 1 s in the Zr/CeO x /Pt device. In reference to the differentiation between the Ce3+ and Ce4+ species with different line shapes, the XPS spectra correspond to various final states: Ce(III) = v 0 + v′ + u 0 + u′ and Ce(IV) = v + v″ + v‴ + u + u″ + u‴ [16]. The presence of the Ce4+ state is normally supported by the intensity of the u‴ peak, which is known as a fingerprint of Ce(IV) states [16]. This result implies that both Ce4+ and Ce3+ ions coexist in the bulk as well as in the surface of the CeO x film. Concentrations of Ce4+ and Ce3+, as obtained from the deconvoluted XPS spectra, are 39.6% and 60.4%, respectively. The higher percentage of Ce3+ ions indicates that the film is rich of oxygen vacancies [17].

PubMedCrossRef 9. Valentine RJ, Saunders MJ, Todd MK, St Laurent TG: Influence of a carbohydrate-Batimastat protein beverage on cycling endurance and indices of muscle disruption. Int J Sport Nutr Exerc Metab 2008, 18:363–378.PubMed 10. Van Essen M, Gibala MJ: Failure of protein to improve time trial performance when added to a sports drink. Med Sci Sports Exerc 2006,38(8):1476–1483.PubMedCrossRef 11. Toone RJ, Betts JA: Isocaloric carbohydrate versus carbohydrate-protein ingestion and cycling time-trial performance. Int J Sport Nutr Exerc Metab 2010, 20:34–43.PubMed Ganetespib mouse 12. Saunders MJ: Coingestion of carbohydrate-protein during endurance exercise: influence on performance

and recovery. Int J Sport Nutr Exerc Metab 2007, 17:S87-S103.PubMed 13. Saunders MJ, Moore RW, Kies AK, Luden ND, Pratt CA: Carbohydrate and protein hydrolysate coingestion’s improvement of late-exercise time-trial performance. Int J Sport Nutr Exerc Metab 2009, 19:136–149.PubMed 14. Stearns RL, Emmanuel H, Volek JS, Casa DJ: Effects of ingesting protein in

combination with carbohydrate during exercise on endurance performance: a systematic review with meta-analysis. SHP099 price J Strength Cond Res 2010,24(8):2192–2202.PubMedCrossRef 15. Vegge G, Ronnestad BR, Ellefsen S: Improved cycling performance with ingestion of hydrolyzed marine protein depends on performance level. J Int Soc Sports Nutr 2012, 9:14.PubMedCrossRef 16. Calbet JA, Holst JJ: Gastric emptying, gastric secretion and enterogastrone response after administration of milk proteins or their peptide hydrolysates in humans. Eur J Nutr 2004, 43:127–139.PubMedCrossRef 17. Koopman R, Crombach N, Gijsen AP, Walrand S, Fauquant J, Kies AK, Lemosquet S, Saris WHM, Boirie Y, van Loon LJC: Ingestion of protein hydrolysate

is accompanied by an accelerated in vivo digestion and absorption rate when compared with its intact protein. Am J Clin Nutr 2009, 90:106–115.PubMedCrossRef 18. van Loon LJC, Kruijshoop M, Verhagen H, Saris WHM, Wagenmakers AJM: Ingestion of protein hydrolysate and amino acid-carbohydrate mixtures increases postexercise plasma insulin responses in men. J Nutr 2000, 130:2508–2513.PubMed 19. van Loon LJC, Saris WHM, Verhagen H, Wagenmakers AJM: Plasma insulin responses Lepirudin after ingestion of different amino acid or protein mixtures with carbohydrate. Am J Clin Nutr 2000, 72:96–105.PubMed 20. Kim S-K, Mendis E: Bioactive compounds from marine processing byproducts – a review. Food Res Int 2006, 39:383–393.CrossRef 21. Liaset B, Madsen L, Hao Q, Criales G, Mellgren G, Marschall H-U, Hallenborg P, Espe M, Froyland L, Kristiansen K: Fish protein hydrolysate elevates plasma bile acids and reduces visceral adipose tissue mass in rats. Biochim Biophys Acta 1971, 2009:254–262. 22. Jeacocke NA, Burke LM: Methods to standardize dietary intake before performance testing. Int J Sport Nutr Exerc Metab 2010, 20:87–103.PubMed 23.

Nature 1983,305(5936):709–712.PubMedCrossRef Stem Cells antagonist 55. Mack D, Siemssen N, Laufs R: Parallel induction by glucose of adherence and a polysaccharide learn more antigen specific for plastic-adherent Staphylococcus epidermidis: evidence for functional relation to intercellular adhesion. Infection and immunity 1992,60(5):2048–2057.PubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions TZ performed most of the experimental work and drafted the manuscript. QL carried out real time RT-PCR experiments. JH and FY participated in microarray analysis and corrected the manuscript. DQ and YW directed the project and analyzed data. All authors read and

approved the final manuscript.”
“Background Strains of non-typeable (NT) Haemophilus influenzae asymptomatically colonize the human pharynx, but are also opportunistic pathogens that cause localized respiratory tract infections such as otitis media, pneumonia, bronchitis, sinusitis, and COPD exacerbation [1, 2]. Bacterial factors that differentiate disease from commensal strains are largely unknown since the population structure of NT H. influenzae is genetically heterologous [3]. The association of bacterial factors with disease-causing strains can be inferred, however, by comparing the prevalence

of genetic traits between epidemiologically defined collections of disease Tariquidar concentration and commensal strains [4–7] or, alternatively, between the pathogenic species and a phylogenetically close but non-pathogenic relative [8–11]. Haemophilus haemolyticus is a phylogenetically close relative of NT H. influenzae, but has not been associated with disease [7, 12, 13]. The two species reside in the same host niche, overlap extensively by both taxonomic and phylogenetic analyses [10, 14, 15], and exchange DNA through natural transformation [10, 13, 16]. Given

their close relationship, but difference in disease potential, NT H. influenzae and H. haemolyticus likely possess common genes or genetic traits for commensal growth but differ in genes or traits that facilitate disease [10]. Historically, H. haemolyticus has been considered a rarely encountered commensal that was easily differentiated from NT H. influenzae by its hemolytic phenotype [17–19]. Recent studies, however, have shown that 20-40% of isolates in various Clostridium perfringens alpha toxin NT H. influenzae collections were miss-classified, and found to be non-hemolytic H. haemolyticus [7, 13]. These observations suggest that H. haemolyticus is significantly more prevalent in the pharynges than previously thought, and that clinical differentiation of the species from throat and sputum samples is inadequate [13]. Therefore, we recently sought to differentiate the species by their relative proportions of selected NT H. influenzae virulence genes and observed that a probe made to licA, a NT H. influenzae gene necessary for phosphorylcholine (ChoP) modification of LOS, hybridized to 96% of NT H.

A key part of the authors’ www.selleckchem.com/products/Ispinesib-mesilate(SB-715992).html argument was the double-blind analysis of the cells. As well as the usual laboratory-internal blind, a second blind was imposed by using a Xc1950 exposure device to expose the cells to electromagnetic rays or not without this choice being detectable.

The exposed/unexposed decoding was always done by an external service after the analysis was finished and the results documented. However, Wolf proved that this sophisticated system could easily be bypassed, simply by pressing a button. We conclude that an essential part of the FK228 in vitro Methods section (an externally imposed blind) of the Schwarz et al. paper is unreliable because of the undisclosed opportunity for fraud. Therefore, all subsequent parts of the paper (results, discussion) cannot safely be relied on. The editors of IAOEH wish to express their doubts about the results reported in the paper by Schwarz et al. (2008) in this EXPRESSION OF CONCERN and to apologize to the readers of IAOEH for publishing this paper. It was unfortunate that they did not learn of the contents of Wolf’s manuscript (published online on 31st July 2008) until 12th August 2008. At Selleck SN-38 this point we want to emphasize that laboratory-internal irregularities cannot be revealed in any review process and that the reviewers, editors and the publisher of a scientific journal always have to rely on the honesty of all persons involved in an experiment.

In the absence of new evidence or further action on the part of either the authors of the Schwarz et al. paper or the authors’ institution, the journal will not be publishing further statements

or Avelestat (AZD9668) communications on this matter. H. Drexler K. H. Schaller References Creutzfeldt W (1997) Die Aufgaben des Herausgebers einer medizinischen Zeitschrift: Manuskriptauswahl, Qualitätssicherung, Interessenskonflikte, ethische Fragen. In: Creutzfeldt, Gerock (Hrsg) Medizinische Publizistik. Georg Thieme Verlag, Stuttgart, New York, pp 10–17 Drexler H, Schaller KH (2008) Wissenschaftliche Objektivität und ethische Grundsätze bei der Herausgabe von Publikationen, 48. Jahrestagung der Deutschen Gesellschaft für Arbeitsmedizin und Umweltmedizin, Hamburg, p 12 Lerchl A (2008) Comments on “Radiofrequency electromagnetic fields (UMTS, 1,950 MHz) induce genotoxic effects in vitro in human fibroblasts but not in lymphocytes” by Schwarz et al., Int Arch Occup Environ Health. doi:10.​1007/​s00420-008-0305-5 Rüdiger HW (2008) Answer to comments by A. Lerchl on “Radiofrequency electromagnetic fields (UMTS, 1,950 MHz) induce genotoxic effects in vitro in human fibroblasts but not in lymphocytes” published by C. Schwarz et al., Int Arch Occup Environ Health. doi:10.​1007/​s00420-008-0330-4 Schwarz C, Kratochvil EA, Kuster N, Adlkofer F, Rüdiger H (2008) Radiofrequency electromagnetic fields (UMTS, 1,950 MHz) induce genotoxic effects in vitro in human fibroblasts but not in lymphocytes.

All transfected cells were exposed to G418 (800 μg/mL, Sigma Chemical Co., St. Louis, USA) for 3 weeks of selection. Resistant clones representing stably transfected cells were ring-cloned and expanded for further experiment. siRNAs against EGFR were transfected into T24 and Cilengitide research buy 5637 cells according to the transfection protocol of Lipofectamine2000

(Invitrogen). A nonspecific control siRNA strand was used as a negative control. Seventy-two hours after transfection, knockdown was assessed by western blot from a parallel transfection. After downregulation of EGFR, we detected the effect of LRIG1 cDNA on cell proliferation and EGFR signaling pathway by CCK-8 assays and western blot respectively. Quantitative real-time RT-PCR Total RNA was extracted from 45 cases of bladder cancer and 5 cases of respective non-neoplastic tissue samples and 2 bladder cancer cell lines with Trizol reagent. The expression of LIG1 and EGFR mRNA was done using quantitative real-time RT-PCR. RNA samples were run in triplicate using 20 ng of RNA perreaction. The resulting cDNA samples were amplified by real-time PCR using gene-specific primer sets in conjunction with the SYBR Premix Ex Taq (TaKaRa) in a Mx3000p instrument. The qPCR was performed with the following conditions: activation at 95°C for 5 min followed by 40 cycles of denaturation at 94°C for 15 s, amplification at 60°C for 30 s, elongation at 72°C for 30 s. In the

last, a cycle of solubility curve was added to examine the amplification quality. Expression of mRNA for GAPDH was used as an internal Vactosertib clinical trial standard. Reverse transcription products were amplified

by PCR using specific primers for human LRIG1 (forward 5′-GGTGAGCCTGGCCTTATGTGAATA-3′; reverse 5′-GGTGAGCCTGGCCT TATGTGAATA-3′) and human EGFR (forward 5′-TCCCTCAGCCACCCATAT GTAC-3′; reverse 5′-TCCCTCAGCCACCCATATGTAC-3′). Immunohistochemistry(IHC) Formalin-fixed and paraffin-embedded tissue sections (5 mm) were dewaxed with xylene and rehydrated through an ethanol gradient into water. Following blocking of endogenous peroxidase activity with 0.3% hydrogen peroxide for 10 min, the sections were washed with phosphate buffered saline(PBS) and incubated over-night with rabbit LRIG1 antibody or EGFR antibody at the dilution of 1:100 in a humidified chamber at 4°C. After of washing with PBS, sections were incubated with biotinylated secondary antibody for 30 min at 37°C and then with horseradish peroxidase labeled streptavidin for 30 min at 37°C. Diaminobenzidine(DAB) was used as chromogen and the sections were subsequently RAD001 cost counterstained with hematoxylin, then dehydrated, cleared and mounted. Western blotting analysis The transfected bladder cancer cells were collected and washed with 0.01 mol/L PBS for three times. Then the cells were added into 200ul pre-cold RIPA-PICT cell disruption liquor and centrifuged. All subsequent manipulations were performed on ice. After centrifugation, the supernatant was collected.

GVB contributed to overall study design, development of molecular methods and critical revision of the draft. NB contributed

to the overall study design, acquisition of clinical samples and data and drafting the manuscript. All authors read and approved the final manuscript.”
“Background Inorganic polyphosphate (polyP) is a chain of few or many hundreds of phosphate (Pi) residues linked by high-energy phosphoanhydride [1]. polyP has attracted considerable attention as a GRAS (generally recognized FHPI solubility dmso as safe) food additive by FDA with antimicrobial properties that can prevent spoilage of food [2,3]. polyP inhibits the growth of selleck inhibitor various gram-positive bacteria such as Staphylococcus aureus [4-8], Listeria monocytogenes [8,9], Sarcina lutea [7], Bacillus cereus [10], and mutans streptococci [11,12], and of fungi such as Aspergillus flavus [5]. The ability of polyP to chelate divalent cations is regarded as relevant

to the antibacterial effects, contributing to ABT-737 purchase cell division inhibition and loss of cell-wall integrity [5,13,14]. On the other hand, large numbers of gram-negative bacteria including Escherichia coli and Salmonella enterica serovar Typhimurium are capable of growing in higher concentrations, even up to 10% of polyP [5,7,15]. Periodontal disease is caused by bacterial infection which is associated with gram-negative oral anaerobes. In our previous study [16], polyP (Nan+2PnO3n+1; n = the number of phosphorus atoms in the chain) with

Niclosamide different linear phosphorus (Pi) chain lengths (3 to 75) demonstrated to have antibacterial activity against Porphyromonas gingivalis, a black pigmented, gram-negative periodontopathogen. polyP also showed antibacterial activity against other black-pigmented, gram-negative oral anaerobes such as Prevotella intermedia and Porphyromonas endodontalis [17,18]. However, the antimicrobial mechanism of polyP against gram-negative bacteria has not yet been fully understood. In the past decade, global genome-wide studies of changes in expression patterns in response to existing and new antimicrobial agents have provided us with a deeper understanding of antimicrobial action [19]. In the present study, we performed the full-genome gene expression microarrays of P. gingivalis, and gene ontology (GO) and protein-protein interaction network analysis of the differentially expressed genes were also performed for elucidating the mechanism of antibacterial action of polyP. Results and discussion The complete list of the average gene expression values has been deposited in NCBI’s Gene Expression Omnibus (GEO) (http://​www.​ncbi.​nlm.​nih.​gov/​geo/​) and is accessible through GEO Series accession number GSE11471. Using filtering criteria of a 1.5 or greater fold-change in expression and significance P-values of <0.05, 706 out of 1,909 genes in P. gingivalis W83 were differentially expressed by polyP75 treatment.

Glienke and Bergmann showed that siRNA-reduced WT1 mRNA expression was associated with a decreased cell proliferation

in K562 and HL-60 cells after transfection for 24 and 48 h [3]. Several studies indicated that pure curcumin downregulated the expression of WT1 in leukemic cell lines [9]. Moreover, combined treatment with curcumin and siRNA targeting WT1 resulted in a significant inhibition of cell proliferation compared to curcumin-treated cells alone in pancreatic cancer cells. All these data suggest that WT1 plays an important role in the anti-proliferative effects of curcumin. However, the mechanism by which pure curcumin downregulates H 89 clinical trial WT1 expression is still unknown. Our data show for the first time that pure curcumin downregulates WT1 expression via miRNAs pathway. The gene expression is regulated via a complicated network. Semsri et al. reported that pure curcumin decreased the mRNA and protein levels

of WT1 through attenuating WT1 auto-regulatory function and inhibiting PKCalpha signaling in K562 cells [21]. Our data showed that curcumin downregulated the expression of WT1 via miRNAs mediated pathway. However, whether other regulating factors are involved in the regulation is still not Doramapimod molecular weight completely delineated. Therefore it is difficult to accurately calculated how much of the down-regulation of WT1 in the curcumin- treated cells is attributable to the action of the miRNAs. Our previous data had showed overexpression of miR-15a/16-1 downregulated the protein level of WT1 but not mRNA level [19]. However, however in this report curcumin decreased the mRNA and protein levels of WT1 in leukemic

cells. Therefore, it is obvious that additional mechanisms [21] other than the induction of miR-15a/16-1 expression contribute to curcumin-induced WT1 downregulation. Taken together, as Additional file 1: Fedratinib nmr Figure S2 indicated pure curcumin inhibited the cell growth partly through miR-15a/16-1 mediated downregulation of WT1. Each miRNA typically targets mRNAs of hundreds of distinct genes by pairing to the mRNAs of protein-coding genes. Previous data had reported that Bcl-2 [18], WT1 [18], caprin-1 [22] and HMGA1 [22] were the target genes by miR-15a/16-1. WT1 and Bcl-2 are highly expressed in leukemic cells and function as oncogenes. The use of SiRNAs against WT1 and Bcl-2 in leukemic cells could effectively inhibit leukemic cells growth [3]. Overexpression of miR-15a/16-1 in leukemic cells suppressed cell growth probably through targeting WT1 and Bcl-2. However it is difficult to estimate how much of the inhibition of cell growth in leukemic cells is attributable to the downregulation of WT1 or Bcl-2. Recent studies have shown that natural agents, including curcumin, isoflavone, and EGCG, can regulate the expression of many miRNAs which increase the sensitivity of cancer cells to conventional agents and thereby suppress tumor cell proliferation [23, 24]. Zhang et al.

CrossRef 26. Wagner CD, Riggs WM, Davis LE, Moulder JF: Handbook of X-Ray Photoelectron Spectroscopy. Eden Prairie: Perkin-Elmer Corporation; 1979. Competing interests The authors declare that they have no competing interests. Authors’ contributions MQG and YLX designed the experiments. MQG, YB, and FX carried out the experiments and performed data analysis. MQG wrote the paper.

All authors read and approved Small molecule library cost the final manuscript.”
“EVP4593 mw Background High-brightness deep ultraviolet light-emitting diodes (UV LEDs) have attracted much attention in areas of air/water sterilization and decontamination, bioagent detection and natural light, identification, UV curing, and biomedical and analytical instrumentation [1]. To date, the maximum external quantum efficiency (EQE) for commercialization of deep UV LEDs is 3% at the wavelength of 280 nm [2, 3]. Various reasons can account for the poor EQE, mainly such as relatively low-resistance ohmic contacts, low hole concentration in p-type AlGaN layer, and the absence of transparent conductive learn more oxides (TCOs) electrode in the deep UV wavelength region [4, 5]. In particular, it is believed that the development of high-performance TCOs electrode in the deep UV region is a key to increase the EQE of UV LEDs.

Conventionally, indium tin oxide (ITO), which exhibits high conductance and good transparency in a visible region, has been widely used as the TCOs electrodes in LEDs and solar cells [6, 7]. However, it has an opaque property in the deep UV (<300 nm) region due to a small bandgap (approximately 3.2 eV), and hence, new TCO materials need to be explored for deep UV LEDs. The wide bandgap materials such as SiO2, Si3N4, HfO2 are attractive as TCOs for deep UV LEDs because of their high transmittance in deep UV regions, but it is difficult to provide electrical conductivity into these materials. In the meantime, the gallium oxide with β phase (β-Ga2O3) having a large optical bandgap of 4.9 eV has been reported as a deep-UV TCO material [8] because its conductivity Silibinin can be improved by thermal annealing, impurity doping,

or incorporating some conducting paths using SWNTs. The Ga2O3 film has also excellent adhesion to GaN surfaces [9]. For example, since undoped Ga2O3 film has insulating properties (i.e., conductivity (σ) <10-9 Ω-1 · Cm-1), it was doped with tin (Sn) atoms to increase the conductivity at the expense of optical transmittance. For 3 mol% Sn-doped Ga2O3 films, the conductivity was increased up to 375 Ω-1 · Cm-1 (42 Ω/square) but the transmittance decreased to approximately 15% in the deep UV region (280 nm) [10]. In order to improve the low optical properties, several groups have reported synthesized TCO layer by wet-based nanoparticles (NPs), such as ITO, indium zinc oxide (IZO), antimony zinc oxide (AZO), antimony tin oxide (ATO), etc. [11–14]. This small particle size (i.e.

It is worth to note that the fabrication approach, chemical composition, and microstructure of initial samples define strongly the effect of post-annealing processing. Conclusions In this paper, the first investigation by APT, to our knowledge, of the nanostructure of Er-doped silicon-rich silica layer was performed at the atomic level and correlated with photoluminescence properties. The phase separation

process between Si excess and the surrounding matrix was studied, and a formation of Si-rich or Er-rich phases was observed for samples annealed at high-temperature (1,100°C). this website The Si excess atoms precipitate in the form of pure Si nanoclusters in the silica matrix. Simultaneously, Er atoms form Er-rich clusters (about 30% of total Selonsertib ic50 amount), whereas 70% of the total Er atoms are free-dispersed in

the host, demonstrating a super-saturation state but with an increase of the Si-ncs-to-Er distances. The Er-rich clusters have complex shape and composition. They are localized at the Si-nc/matrix interface or in poor Si-nc regions, indicating a complicated precipitation mechanism. Diffusion coefficients for Si and Er have been deduced from APT experiments. We have directly evidenced the clustering of rare-earth ions upon high-temperature annealing in Er-doped Si-rich SiO2 films. selleck This process has been often expected but, to our knowledge, never observed and demonstrated directly for these materials fabricated

by different techniques. These results evidence the critical point to monitor the microstructure of Er-doped SRSO layers for the required inversion of 50% of the Er concentration to achieve a net gain in future Er-doped amplifier device. Acknowledgements This work was supported by the Upper Normandy Region and the French Ministry of Research in the framework of Research Networks of Upper Normandy. References 1. Fujii M, Yoshida M, Kanzawa Y, Hayashi S, Yamamoto K: 1.54 μm photoluminescence of Er3+ doped into HAS1 SiO2 films containing Si nanocrystals: evidence for energy transfer from Si nanocrystals to Er3+. Appl Physics Lett 1997,71(9):1198.CrossRef 2. Pacifici D, Irrera A, Franzo G, Miritello M, Iacona F, Priolo F: Erbium-doped Si nanocrystals: optical properties and electroluminescent devices. Physica E: Low-dimensional Syst Nanostructures 2003,16(3–4):331–340.CrossRef 3. Kenyon AJ, Trwoga PF, Federighi M, Pitt CW: Optical properties of PECVD erbium-doped silicon-rich silica: evidence for energy transfer between silicon microclusters and erbium ions. J Phys: Condensed Matter 1994,6(21):L319.CrossRef 4. Kik PG, Brongersma ML, Polman A: Strong exciton-erbium coupling in Si nanocrystal-doped SiO2. App Phys Lett 2325,76(17):2000. 5.