Int J Food Microbiol 2006, 108:164–171.PubMedCrossRef 38. Costafreda MI, Bosch A, Pinto RM: Development, evaluation and standardization of a real time TaqMan reverse transcription-PCR THZ1 solubility dmso assay for quantification of hepatitis A virus in clinical and shellfish samples. Appl Environ Microbiol 2006, 72:3846–3855.PubMedCrossRef 39. Di Pasquale S, Paniconi M, De Medici D, Suffredini E, Croci L: Duplex real time PCR for the detection of hepatitis A virus in shellfish using feline calicivirus as a process control. J Virol Methods 2010, 163:96–100.PubMedCrossRef

40. Di Pasquale S, Paniconi M, Auricchio B, Orefice L, Schultz AC, De Medici D: Comparison of different concentration methods for the detection of hepatitis A virus and calicivirus from bottled natural mineral waters. J Virol Methods 2010, 165:57–63.PubMedCrossRef 41. Pang XL, Lee B, Boroumand N, Leblanc B, Preiksaitis JK, Yu Ip CC: Increased detection of rotavirus using a real time reverse transcription-polymerase buy MGCD0103 chain reaction (RT-PCR) assay in stool specimens from children with diarrhea. J Med Virol 2004, 72:496–501.PubMedCrossRef 42. Tichopad A, Dilger M, Schwarz G, Plaffl MW: Standardized determination of real-time PCR efficiency from a single reaction set-up. Nucleic Acids Res 2003,31(20):e122. Erratum in: Nucleic Acids Res 2003, 31 (22), 6688PubMedCrossRef 43. Geeraerd AH, Valdramidis VP, Van Impe JF: GInaFiT, a freeware tool to assess non-log-linear

microbial survivor curves. Int J Food Microbiol 2005, 102:95–105. Erratum in: 2006. Int J Food Microbiol 110: 297PubMedCrossRef Competing interests The authors declare 17-DMAG (Alvespimycin) HCl that

they have no competing interests. Authors’ contributions CC and AF performed these experiments. LG performed statistical study. All authors wrote, read and approved the final manuscript.”
“Background It is estimated that one-third of the world’s population is infected with M. tuberculosis and 8.7 million suffer from active TB and 1.4 million deaths occur due to it every year [1]. M. tuberculosis is able to evade the human immune response in part by triggering formation of insulating hypoxic granulomas following infection of pulmonary macrophages. Bacilli within this environment have adapted themselves to slowly replicate and respire, making them tolerant of many drugs. This resistant state is thought to contribute to the prolonged combination chemotherapy required to cure patients [2, 3]. Lack of compliance with treatments lasting up to 9 months contributes to the emergence of resistant strains [4]. To contain this situation, new anti-tuberculosis drugs and lesser duration of treatment are of immediate requirement. The discovery of new drugs involves several constraints that discourage many companies from investing in novel anti-TB drugs. The research is expensive, slow and difficult, and it requires specialized facilities for handling M. tuberculosis.

Figure 3 Mean serum antibody response (OD index ± S.E.) in infected and control rabbits by sampling week (WPI). Serum was collected twice from all individuals prior to infection (48 rabbits sampled at week -1) and weekly thereafter. Number of samples decreased with time of infection as groups of 6 individuals (4 infected and 2 controls) were regularly sacrificed. Sera were assayed individually. The neutrophil concentration in

the blood decreased with the duration of the infection (coeff ± S.E.: -0.011 ± 0.002 d.f = 334 P < 0.0001) and was similar between infected and controls except in the first 2 weeks post-infection, where a significant neutrophilia was observed in infected compared to controls (coeff ± S.E.: 0.159 ± 0.075 d.f. = 27 P < 0.05). These findings Protein Tyrosine Kinase inhibitor further support the short-lived and early involvement of neutrophils in B. bronchiseptica clearance [15, 27]. Cytokine response in the lungs As shown in fig. 4 and based on the 2-ΔΔct transformation, a high IL-10 expression was observed in the lungs of infected rabbits in the first 30 days post infection, this was followed by a short-lived peak in IFN-γ at 60 days post infection, and a general decrease in cytokine expression thereafter. IL-4 showed consistent baseline expression. Overall and using the raw Ct values

for analysis tractability, results confirmed the important anti-inflammatory role of IL-10 in B. bronchiseptica infected rabbits (interaction between infected-controls and sampling time, coeff ± S.E.: 0.001 ID-8 ± 0.0001 d.f. = 41 P AZD5582 < 0.05,

corrected for the random effect of the host). IFN-γ and IL-4 Ct values significantly changed among sampling time but not between infected and controls (respectively, coeff ± S.E.: 0.001 ± 0.0003 and -0.001 ± 0.0003 for both d.f. = 42 P < 0.05). Through its anti-inflammatory properties and involvement in the recruitment and activation of other anti-inflammatory cells [28, 29], IL-10 probably facilitated the establishment of bacteria in the respiratory tract and the subsequent persistence in the nares, while the peaks at 7 and 60 days post infection in IFN-γ confirmed its important role in bacteria clearance from the lungs and possibly trachea. In summary, the dynamics of cytokine expression in the lungs of infected rabbits was in line with previous studies [20, 21]. Figure 4 Cytokine gene expression profiles in the lungs at days 3, 7, 14, 30, 60, 90, 120 and 150 post-infection (DPI). Cytokine data are presented using the 2-ΔΔCt ± S.E approach. Briefly, for each rabbit cytokine expression was scaled relative to the housekeeping gene HPRT (Ct), Ct values from infected individuals were then scaled over the controls. Discussion This study showed that rabbits infected with Bordetella bronchiseptica strain RB50 were able to shed bacteria by oro-nasal contact for at least 128 days post infection.

The degree of difficulty of the 3D MIVAT technique was graded by the surgeon using a 5-point subjective scale, ranging from 5 (very easy) to 1 (very difficult) in order to recognize the upper and lower vascular pedicles, the parathyroids, the superior and inferior laryngeal nerves. Patients were asked to report their opinion according to the cosmetic results and postoperative pain. Cosmetic results were graded using a 4-point Citarinostat ic50 scale,

ranging from 1 (very happy) to 4 (unhappy), while postoperative pain was evaluated by a visual analogue scale (VAS) from 1 (no pain ever) to 10 (worse pain). Results Two female and 1 male with a mean age (±SD) of 44.5 years (±8.4) underwent 3D MIVAT. Mean operative time for the total thyroidectomy was 80 minutes (range 72-90). Conversion into conventional technique was never required. Neither intra-nor postoperative complications were observed during the study. A suction drain was placed at the end of surgery and it was removed when blood loss was <2 mL/hour. All patients were discharged 24 hours after surgery. Table  1 summarizes clinical, pathologic and operative findings. The surgical team noticed a good perception of depth and easy recognising of anatomic structures, especially concerning Caspase inhibitor the upper and lower vascular

pedicles, the parathyroids, the superior and inferior laryngeal nerves (Figure  2). The recognition of these anatomic structures worsened in presence of blood in the surgical field. This PRKD3 new perception of depth and volume allowed an easy use of the endoscope during the procedure and an intuitive manipulation of critical structures, making comfortable and safe surgical maneuvres using instrumentation. The negligible weight of the handle and the absence of lateral cables made the device light and easy to manage. The surgeons wore polarizing glasses without any problem even during the open part of the surgery. No user side-effects

related to the dual-camera device were reported. Two surgeons considered the technique as very easy, while one surgeon as easy. All patients were very happy about the cosmetic results. Pain VAS at 1, 3 and 7 postoperative day ranged from 1 to 2 in all cases. Table  2 summarizes the subjective qualitative evaluation of 3 D endoscopic system. Table 1 Clinical, pathologic and operative findings of the patients Patients Goiter volume (mL) Dominant nodule major diameter (cm) Operative time (min) Intraoperative blood loss (mL) Postoperative blood loss (mL) Pathologic findings Hositaliztion (days) No. 1 20 2.8 90 45 30 Follicular adenoma 1 No. 2 18 1.4 78 35 25 Multinodular goiter 1 No. 3 22 1.1 72 35 10 Multinodular goiter 1 Figure 2 An intraoperative 3D view of the operative field. The upper vascular pedicle (white arrow) and the superior laryngeal nerve (black arrow) on the right side are easily recognized with good depth perception by the surgical team.

The properties of graphene, including a high intrinsic mobility [1, 2], a large theoretical specific surface area, and a high chemical stability, are potentially useful in

applications ranging from chemical sensors to transistors [3–8]. Toward exploiting Angiogenesis inhibitor these unique properties of graphene, several research groups have attempted to fabricate large-scaled graphene oxide sheets [9–12]. Graphene oxide (GO) is a layered material consisting of hydrophilic oxygenated graphene oxide sheets bearing oxygen functional groups on their basal planes and edges [13]. It is a useful platform for fabricating functionalized graphene that can potentially confer improved mechanical, thermal, or electronic properties. The numerous chemical functionalities on a GO surface are expected to readily lend themselves to further chemical Selleckchem Autophagy inhibitor functionalization. Graphene-based materials, therefore, show promise in a variety of technological applications. The use of GO surfaces as catalysts of synthetic transformations is a relatively new research area

with outstanding potential. Current efforts are directed toward harnessing the oxygen carriers present on GO surfaces as heterogeneous catalysts [14–16]. In this study, we systematically compared and investigated the oxidation of aniline to form azobenzene on monolayer graphene (EG) or graphene-oxide-like (GOx) surfaces fabricated with benzoic acid. Moreover, we focus on examining the difference between EG and GOx surfaces in one substrate, simultaneously.

Raman spectroscopy and high-resolution photoemission spectroscopy (HRPES) were used to characterize the surface-bound products. The carboxyl groups introduced onto the graphene surface upon oxidation Loperamide by benzoic acid to GOx allowed aniline to react with the oxygen carriers. The oxidation of aniline proceed via a reaction between the aniline amine groups and the oxygen groups on the GOx surface under ultra-high vacuum (UHV) conditions maintaining a 365-nm UV light exposure. Generally, it is hard to distinguish the difference between EG and GOx surfaces in one substrate due to the large size of the HRPES beam. Hence, no previous systematic experimental studies have examined the oxidation of aniline on a GOx surface. However, this study is meaningful with regards to indicating this distinctive difference using the feature of micro Raman spectroscopy. Methods A Si-terminated 6H-SiC(0001) substrate (Cree Research, Durham, NC, USA) was used to fabricate EG. The substrate was degassed, annealed at 1,200 K under a Si flux (1 Å/min), and graphitized at temperatures up to 1,500 K (for 2 min) to produce a monolayer of graphene (EG). The annealing temperature was monitored using an infrared pyrometer (with an emissivity of 0.9). A GOx surface was fabricated by exposing the EG surface to benzoic acid (Sigma Aldrich, purity, 97%, St. Louis, MO, USA).

The increase of SodM level was also observed, but only when cells were exposed to externally generated oxidative stress (xanthine/xanthine oxidase) [16]. Summarizing, although we did observe some differences of the basic Sod activity levels in PDI-susceptible vs. PDI-resistant strains, their statistical relevance is not obvious and does not explain the huge differences in PDI-based bactericidal efficacy (Table 2). The reports previously published by our group showed that the bactericidal effect of PpIXArg2-based photokilling was almost completely abolished, when PS was washed away after incubation (before light exposure) [25]. This indicated

that externally generated ROS are responsible for bacterial JNK-IN-8 cell destruction. In regard to our currently presented results we also noticed that some amount of PS enters the cell and influences the transcription of certain genes, eg. sodA and sodM. We observed an increase Cell Cycle inhibitor in sodA and sodM transcript levels but only in 472 and 80/0, PDI-susceptible strains (Table 2). The strains recognized as PDI-resistant, namely 1397 and 2002, did not demonstrate higher sodA nor sodM transcript levels. These results correlate very well with Sod activity measurements observed in these strains. However, Sod activity increase in only susceptible cells proves that this is probably not the only factor

affecting S. aureus vulnerability to porphyrin-based PDI. Conclusions We confirmed in the presented study that the protoporphyrin-based photokilling efficacy is a strain-dependent phenomenon. We showed that oxidative stress sensitivity caused by the lack of both Sod enzymes can be relieved in the presence of Mn ions and partially in the presence of Fe ions. The fact that Sod activity increase Liothyronine Sodium is observed only in PDI-susceptible cells emphasizes that this is probably not

the only factor affecting S. aureus vulnerability to porphyrin-based PDI. Methods Light source BioStimul Lamp which emits polarized (96% level of polarization) monochromatic light (624 nm ± 18 nm) (BIOTHERAPY, Czech Republic) was used for all irradiation experiments. The power of the lamp was measured using a light power meter (model LM1, CARL ZEISS, Jena, Germany). The delivered light energy was approx. 0.2 J/cm2 per minute. Photosensitiser Protoporphyrin IX (MP Biomedicals) stock solution was prepared in 100% dimethyl sulfoxide (DMSO) (Sigma-Aldrich) to the final concentration of 10 mM and kept in the dark at room temperature. Bacterial strains In this investigation we used the reference S. aureus strains: RN6390, RN6390 sodA:: tet (lack of SodA activity), RN6390 sodM::erm (lack of SodM activity), RN6390 sodM::erm sodA:: tet (lack of SodA and SodM activities). These strains were obtained from the collection of Dr. Mark Hart from University of Arkansas, USA [8]. We also investigated eight S. aureus clinical strains isolated from patients from the Provincial Hospital in Gdansk, Poland.

For individuals with abnormal urine findings at a recent health examination, kidney dysfunction, abnormal

morphology of the kidney, habitual intake of drugs, such as NSAIDs, or acute kidney injury, modifications in lifestyle are encouraged, and regular follow-up examinations of kidney function and urine tests are needed to detect CKD at an earlier stage. Hypertension is a treatable risk factor in many cases and should be adequately managed in a high-risk group of CKD. The higher the blood pressure, the greater the risk of proteinuria and the higher the incidence of end-stage kidney disease (ESKD). Adequate control of blood pressure is one of the most effective approaches to managing CKD. Although diabetic nephropathy is the leading cause of ESKD in Japan, Selleckchem ARRY-438162 adequate control of the blood glucose level may prevent the development of CKD or improve the severity (stage). The Kumamoto SB202190 order Study and UKPDS suggest that a good control of blood glucose prevents diabetic nephropathy. It is noted that pancreas transplantation improves diabetic nephropathy. Obesity is a significant risk factor for proteinuria and ESKD development, especially

in males. Dyslipidemia is a risk factor of atherosclerosis. Although based on very little evidence, it has been suggested that a complication of dyslipidemia may promote ESKD. Increases in urinary protein excretion are associated with increased incidence of dyslipidemia. Hyperuricemic patients suffer frequently from kidney disorders and, vice versa, CKD patients tend to have hyperuricemia. However, it is controversial whether hyperuricemia is an independent

risk factor for atherosclerosis, since hyperuricemic patients have hypertension and other risk factors for atherosclerosis. Fig 3-1 Risk factors for the development of stages 1–2 chronic kidney disease. GFR Glomerular filtration rate, DM diabetes mellitus. The data are quoted, with modification, from: Yamagata K et al. (Kidney Int. 2007;71:159–166) Fig. 3-2 Risk factors for the development of stages 3–5 CKD. HDL High-density lipoprotein. The data are quoted, with modification, from: Yamagata K et al. (Kidney Int. 2007;71:159–166)”
“A. Evaluation L-gulonolactone oxidase method for kidney function Kidney function is evaluated by estimated GFR (eGFR), which is calculated using an estimation formula based on serum creatinine value. eGFR can be calculated for Japanese people using a Japanese eGFR formula based on serum creatinine value as determined by an enzymatic method. The estimation formula for GFR is a simplified method. For more accurate kidney function evaluation, inulin clearance or creatinine clearance (Ccr) is recommended. A-1. eGFR (estimated GFR) The gold standard method for GFR determination is inulin clearance. However, the procedure is complicated, so eGFR is suitable in clinical settings. For Japanese over 18 years old, eGFR is widely calculated by GFR equation based on serum creatinine, with the use of the simple MDRD formula in many cases.

Rather than opening a gap in bilayer graphene, this tuned the magnitude of overlap in TGN. Based on the energy dispersion of biased TGN, wave vector relation with the energy (E-k relation) shows overlap between the conduction and valence band structures, which can be controlled by a perpendicular external electric field [6, 39]. The band overlap increases with Fosbretabulin in vitro increasing external electric field which is independent of the electric field polarity. Moreover, it is shown that the effective mass remains constant when the external electric field is increased [3, 33].

As an essential parameter of TGNs, density of states (DOS) reveals the availability of energy states, which is defined as in [40, 41]. To obtain this amount, derivation of energy over the wave vector is required. Since DOS shows the number of available states at each energy level which can be occupied, therefore, DOS, as a function of wave vector, can be modeled as [39]

(2) where E is the energy band structure and A, B, C, D, and F are defined as A = −6.2832α, B = 14.3849α 2 β, , D = −9β 2, and . As shown in Figure 4, the DOS for ABA-stacked TGN at room temperature is plotted. As illustrated, the low-DOS spectrum exposes two prominent peaks around the Fermi energy [39]. Figure 4 The DOS of the TGN with ABA stacking. The electron concentration is calculated by integrating the Fermi probability distribution function over the energy as in [42]. Biased ABA-stacked TGN carrier concentration is modified as [43] (3) where , the normalized Fermi energy is , and M and N are SCH772984 order defined as and . Based on this model, ABA-stacked TGN carrier concentration is a function Enzalutamide of normalized Fermi energy (η). The conductance of graphene at the Dirac point indicates minimum conductance at a charge neutrality point which depends on temperature. For a 1D TGN FET, the GNR channel is assumed to be ballistic. The current from source to drain can be given by the Boltzmann transport equation

in which the Landauer formula has been adopted [44, 45]. The number of modes in corporation with the Landauer formula indicates conductance of TGN that can be written as [32] (4) where the momentum (k) can be derived by using Cardano’s solution for cubic equations [46]. Equation 4 can be assumed in the form G = N 1 G 1 + N 2 G 2, where N 1 = 2αq 2/lh and N 2 = −6βq 2/lh. Since G 1 is an odd function, its value is equivalent to zero. Therefore, G = N 2 G 2[32], where (5) This equation can be numerically solved by employing the partial integration method and using the simplification form, where x = (E − Δ)/k B T and η = (E F − Δ)/k B T. Thus, the general conductance model of TGN will be obtained [32] as (6) It can be seen that the conductivity of TGN increases by raising the magnitude of gate voltage. In the Schottky contact, electrons can be injected directly from the metal into the empty space in the semiconductor.

Consequently, more effective nutritional strategies need to be discovered. In the present study, the effects of eFT-508 concentration BCAA supplementation combined with taurine on a highly intense ECC-induced DOMS and muscle damage were investigated via a randomized, placebo-controlled, and double-blind trial, because taurine was reported to decrease oxidative stress induced by ECC [16]. In ECC-induced DOMS and muscle damage, subjective and objective parameters including VAS scores, CIR, and serum levels of LDH and 8-OHdG were significantly improved by the combination of

BCAA and taurine supplementation. This combined supplementation also tended to improve serum CK and aldolase activities, but not significantly. These parameters, especially serum CK activity, have a high degree of individual biological variability, and it is difficult to demonstrate a statistically significant difference between the small number of subjects [3]. Overall, the present study demonstrated that combined supplementation with BCAA and taurine is beneficial for see more reducing ECC-induced DOMS and muscle damage. However, it was impossible to determine whether the combined effects were due to the

synergistic effect of both BCAA and taurine or the sum of the individual effects. Compared with the effectiveness of BCAA supplementation on exercise-induced muscle soreness and damage reported in previous studies [4, 7, 9, 22, 25], BCAA supplementation alone was not sufficient to effectively inhibit muscle soreness and damage in the present study. This discrepancy might be due to differences in the exercise protocol (intensity and type) and the supplemental regimen (duration and dose). In a previous study by Shimomura et al., the authors recognized that the intensity was low in a squatting exercise where subjects used only their body weight because the changes in the levels of serum muscle damage markers, including CK and myoglobin, were very small over the three days following exercise [7, 8]. On the other hand, repeated arm extensions with

weight loads of 90% MVC in the present study caused a significant increase in serum muscle damage markers in the placebo group, thereby implying higher exercise intensity. Fludarabine The present findings with this higher intensity suggest that a combination of BCAA and taurine taken during high-intensity exercise may prevent severe muscle soreness and damage that cannot be attenuated by BCAA alone. In addition to exercise intensity, the amount of oral BCAA intake is one of the important factors for preventing exercise-induced muscle soreness and damage. Shimomura et al. suggested that the BCAA dose should be adjusted according to body mass to at least 92–100 mg/kg because the inhibitive effects of BCAA on DOMS and muscle damage were greater in females than in males [7, 8]. The BCAA dose in the present study should be sufficient because daily BCAA supplementation at 9.6 g/day worked out to 145.67 ± 5.3 mg/kg.

3. Results 3.1. Inhibition of JAK1/STAT3 and JAK1/STAT6 signal pathways does not affect HSV-1-induced KSHV lytic cycle

replication We have previously demonstrated that the production of IL-10 and IL-4 from HSV-1-infected BCBL-1 cells partially contributed to HSV-1-induced KSHV replication [6]. Commonly, Stem Cells inhibitor IL-10 exerts its function via JAK1, TYK2/STAT3 signal pathway, and IL-4 through JAK1, JAK3/STAT6 pathway [15–17]. To determine whether these signal pathways were altered in HSV-1-infected BCBL-1 cells, Western blot analysis was performed. As shown in Figure 1A, HSV-1 infection of BCBL-1 cells did not display any effect on phosphorylation of STAT3 or STAT6 at 3, 6, 12, and 24 h when compared to Mock-infected groups. Similar results were also observed when BCBL-1 cells were infected with HSV-1 or Mock at 15, 30, 45, and 60 min (data not shown). To confirm these results, BCBL-1 cells were transfected with STAT3-DN or STAT6-DN construct followed by HSV-1 infection. RT-qPCR demonstrated that transfection of either STAT3-DN or STAT6-DN did not affect KSHV ORF26 mRNA transcripts induced by HSV-1 in BCBL-1 cells (Figure 1B and 1C). To further extend above results, piceatannol, a JAK1 tyrosine kinase-specific inhibitor, was added to BCBL-1 cells culture before selleck chemicals HSV-1 infection. The results from RT-qPCR indicated that inhibition of JAK1 did not influence KSHV replication by HSV-1 (data

not shown). These data collectively suggest that either IL-10/JAK1/STAT3 or IL-4/JAK1/STAT6 signal pathway is not involved in HSV-1-induced KSHV replication. Figure 1 Either JAK1/STAT3 or JAK1/STAT6 signal pathway does not mediate HSV-1-induced KSHV replication. (A) Western blot analysis for phosphorylation of STAT3 and STAT6. BCBL-1 cells were infected with Mock (M) or HSV-1 (H) for 3, 6, 12, and 24 h. Cells were collected and cell lysates were subjected to SDS-PAGE, transferred to membrane, and then immunoblotted

with the indicated antibodies. (B) RT-qPCR was used to detect relative quantities of ORF26 mRNA in STAT3-DN (pST3-DN) or control vector transfected and HSV-1 infected BCBL-1 cells as indicated. ** p < 0.01 and *** p < 0.001 for Student's t-test versus Mock + pMSCV group; n.s., not significant for Student's t-test versus HSV-1 + pMSCV group. (C) RT-qPCR was used to detect relative quantities of ORF26 mRNA in STAT6-DN (pST6-DN) or control vector transfected Pyruvate dehydrogenase and HSV-1 infected BCBL-1 cells as indicated. ** p < 0.01 and *** p < 0.001 for Student’s t-test versus Mock + pRed group; n.s., not significant for Student’s t-test versus HSV-1 + pRed group. 3.2. Suppression of PI3K/AKT signal pathway inhibits HSV-1-induced KSHV replication Besides signal pathways from JAK1/STAT3 by IL-10 and JAK1/STAT6 by IL-4, both IL-10 and IL-4 can also induce activation of PI3K/AKT pathway [18–20]. To examine whether PI3K/AKT signaling was activated in HSV-1-infected BCBL-1 cells, Western blot analysis was carried out.

Petersburg State Polytechnical University. MP holds PhD degree at St. Petersburg Academic University. OSh is a PhD student at St. Petersburg State Polytechnical University. YuS holds DrSci degree and professor position at the University of Eastern Finland. AL holds DrSci degree and professor positions at St. Petersburg Academic University

and St. Petersburg State Polytechnical University. Acknowledgments This study was supported by Russian foundation for Basic Research (project no. 12-02-91664), Russian Ministry for Education and Science, Joensuu University Foundation, Academy of Finland (project nos. 135815 and 137859) and EU (FP7 projects ‘NANOCOM’ and ‘AN2’). References 1. Zayats buy MGCD0103 AV, Smolyaninov II, Maradudin AA: Nano-optics of surface plasmon polaritons. Phys Rep 2005, 408:131–314.CrossRef 2. Smith CLC, Desiatov B, Goykmann I, Fernandez-Cuesta I, Levy U, Kristensen A: Plasmonic V-groove waveguides with Bragg grating filters via nanoimprint lithography. Opt Express 2012, 20:5696–5706.CrossRef 3. de Ceglia D, Vincenti MA, Scalor M, Akozbek N, Bloemer MJ: Plasmonic band edge effects on the transmission properties of metal gratings. AIP Adv 2011,1(032151): 1–15. 4. Genov DA, Shalaev VM, Sarychev AK: Surface plasmon excitation and correlation-induced

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