Petersburg State Polytechnical University MP holds PhD degree at

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’). see more References 1. Zayats selleck screening library 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

localization-delocalization transition in semicontinuous metal films. Phys Rev B 2005,72(113102): 1–4. 5. Chen W, Thoreson MD, Kildishev AV, Shalaev VM: Fabrication and optical characterizations of smooth silver-silica nanocomposite films. Laser Phys Lett 2010, 9:677–684.CrossRef 6. Sardana N, Heyroth F, Schilling J: Propagating surface plasmons CFTRinh-172 molecular weight on nanoporous gold. J Opt Soc Am B 2012, 29:1778–1783.CrossRef 7. Stockman MI, Kurlayev KB, George TF: Linear and nonlinear optical susceptibilities of Maxwell-Garnett composites: dipolar spectral theory. Phys Rev B 1999, 60:17071–17083.CrossRef 8. Thoreson MD, Fang J, Kildishev AV,

Prokopeva LJ, Nyga P, Chettiar UK, Shalaev VM, Drachev VP: Fabrication and realistic modeling of three-dimensional metal-dielectric composites. J Nanophotonics 2011,5(051513): 1–17. 9. Lu D, Kan J, Fullerton EE, Liu Z: Tunable surface plasmon polaritons in Ag composite films by adding dielectrics or semiconductors. Appl Phys Lett 2011, 98:243114–243117.CrossRef 10. through Shi Z, Piredda G, Liapis AC, Nelson MA, Novotny L, Boyd RW: Surface plasmon polaritons on metal-dielectric nanocomposite films. Opt Lett 2009, 34:3535–3537.CrossRef 11. Kelly KL, Coronado E, Zhao LL, Schatz GC: The optical properties of metal nanoparticles: the influence of size, shape, and dielectric environment. J Phys Chem B 2003, 107:668–677.CrossRef 12. Kreibig U, Vollmer M: Optical Properties of Metal Clusters. Berlin: Springer; 1995.CrossRef 13. Agranovich VM, Mills DL: Surface Polaritons. Amsterdam: North-Holland Publishing Co; 1982. 14. Maxwell Garnett JC: Colours in metal glasses and in metallic films. Philos Trans R Soc Lond A 1904, 203:385–420.CrossRef 15.

9 (3 × 108 CFU/mL) L plantarum MB452 caused an increase in TEER

9 (3 × 108 CFU/mL) L. plantarum MB452 caused an increase in TEER of 42-51% compared to the untreated controls from 4 to 10 hours. The effect of L. plantarum MB452 on TEER was 19-27% higher at an OD600 nm of 0.9 compared to OD600 nmof 0.6 (P < 0.05 from 4 to 8 hours). Similarly, the effect of L. plantarum MB452 on TEER was 23-33% higher at an OD600 nm of 0.6 compared to OD600 nm of 0.3 (P < 0.05 from 4 to 8 hours). Figure 1 Change in trans-epithelial electrical resistance (TEER) across confluent Caco-2 VX-809 chemical structure monolayers (5 days old) over time in the presence of different optical densities of L. plantarum MB452. The change in TEER is the percentage change compared to the initial TEER for each monolayer.

selleck compound The values plotted are the means for four monolayers and the error bars show the SEM. OD = the starting optical density of the L. plantarum cultures at 600 nm. The drop in TEER for all treatments between 0 and 2 hours observed in all assays was likely due to the Caco-2 cell monolayers being disturbed by the change in media during the sample addition after the initial readings. The increase in TEER over time for the control Caco-2 cells was likely due to an increase in nutrient availability after the fresh media was added at the beginning of the experiment. The increases in

TEER caused by L. plantarum MB452 were additional to those observed with JQEZ5 supplier fresh media. L. plantarum MB452 was also able to increase the TEER by 20 at 2 hours to 64% at 10 hours across differentiated Caco-2 cells (18 days old; Figure 2) in the same manner as for confluent, undifferentiated cells (5 days old; Figure 1). A differentiated, polarised Caco-2 cell monolayer better represents the human intestinal barrier than confluent undifferentiated Caco-2

cells. The tight junctions between the differentiated Caco-2s were better formed than the undifferentiated Caco-2s (higher initial TEER readings), were less affected by the media addition (no initial drop in TEER) and had less variation between replicates (lower SEM values). Figure 2 Change in trans-epithelial electrical resistance (TEER) across differentiated Caco-2 monolayers (18 days old) in the presence of L. plantarum MB452 (OD 600 nm 0.9). The change Dichloromethane dehalogenase in TEER is the percentage change compared to the initial TEER for each monolayer. The values plotted are the means for four monolayers and the error bars show the SEM. L. plantarum MB452 altered the expression of genes involved tight junction formation The ability of L. plantarum MB452 to alter gene expression in intestinal epithelial cells was measured using global gene expression analysis. The analysis indicated that 1,181 Caco-2 cell genes were differentially expressed (fold change > 1.2, modified-P < 0.05) when co-cultured with L. plantarum MB452; the expression levels of 554 genes were increased and 627 genes were decreased. The relatively low fold-change cut-off of 1.

2009 [3], Hotter et al 2010 [15], Revez et al 2011 [16]; p<0 05

2009 [3], Hotter et al. 2010 [15], Revez et al. 2011 [16]; p<0.05/# p<0.001 Semaxanib cell line significance level in comparison to the remaining isolates belonging not to the corresponding group, additionally the values in subgroups with above average numbers of positive isolates are given in bold numbers; in the case of ceuE and pldA the NCTC 11168 typical allele presence is given in bold if the isolate numbers were above average. Figure 1 MLST-sequence based UPGMA-tree and the arrangement of the six different marker genes within the six defined groups (twelve subgroups). On the left side the MLST-sequence based UPGMA-tree of 266 C. jejuni isolates

is depicted. The numbers shown on the branches of the tree indicate the linkage distances. The right side of the table lists all isolates in the order of the UPGMA-tree depicting the source of the isolate, the presence or absence of the six marker genes and their belonging to one of the groups listed in Table1.

Source: Human isolates are marked blue, chicken isolates yellow, bovine isolates red, and turkey isolates green. Marker genes: Presence of a genetic marker is marked with a light red shade, absence with a light green shade. The marker genes from left to right are: cjj1321-6 : O-linked flagellin glycosylation locus; fucP: L-fucose CB-839 permease gene (cj0486); cj0178: outer membrane siderophore receptor; cj0755: iron uptake protein (ferric receptor cfrA); ceuE: enterochelin uptake binding protein; pldA: outer membrane phospholipase A; cstII: LOS sialyltransferase II; cstIII: LOS sialyltransferase III; The last column gives the group according to Table1:

light grey (1A), light yellow (1B*) intense yellow (1B**), dark yellow (1B***) cyan blue (2A), bondi blue (2B), carrot-orange (3A*), orange-red (3A**); rust-red (3B), turquoise [4], red [5], steel-blue [6] and white (singeltons). The flagellin O-glycosylation locus cj1321-cj1326 as marker for livestock-associated strains could be detected in the majority of the isolate groups: 1A, 1B*, 1B**, 3A and 4, assuming their livestock association. In contrast to that, especially the groups 2A + B as well as 1B***, 3B and 5 were negative for this HSP90 marker gene. A comparable distribution pattern could be demonstrated for the fucP gene. The isolate groups 1A, 1B*, 1B**, 3A* and 6, are positive for this marker gene, whereas the fucP genes was nearly absent in the groups 1B***, 2A + B, 3A** + B and 4. Feodoroff and coworkers identified a subpopulation in which they were not able to detect ceuE using ceuE-primers derived from the NCTC 11168 genome sequence [7]. The same STA-9090 phenomenon was described by them for pldA using NCTC 11168 genome based primers, but here the differences were not significant [7].

These subsystems (except “Benzoate transport and degradation clus

These subsystems (except “Benzoate transport and degradation cluster”) were also considerably more abundant in Tplain and Tpm1-2 than in the other Troll metagenomes (Figure 6). This was also seen in the PCA analysis, where the level I SEED subsystem “Ro 61-8048 clinical trial Metabolism of Aromatic Compounds” was contributing to the separation of Tplain and Tpm1-2 from the Oslofjord samples (Figure 3). Figure 6 Significant differences in potential for nitrogen and aromatic compound metabolism between Troll and Oslofjord metagenomes. The figure shows differences in level III SEED subsystems involved in metabolism of nitrogen and aromatic compounds where at least one Troll metagenomes was significantly different from both Oslofjord

metagenomes in the STAMP analysis. Troll metagenomes significantly different from the Oslofjord metagenomes are marked by red arrows. Identification of selected key enzymes for hydrocarbon degradation further supported a CX-5461 molecular weight higher potential for hydrocarbon degradation AZ 628 purchase in Tplain and Tpm1-2 compared to the other samples (Figure 7). Anaerobic degradation of several aromatic compounds is often funneled through benzoate and benzoyl-CoA by benzoate-CoA ligase and subsequent dearomatization by benzoyl-CoA reductase [34]. The anaerobic activation step of

toluene and several other aromatic hydrocarbons with fumarate addition can be catalyzed by benzylsuccinate synthase. We searched for these anaerobic key enzymes as well as for several dioxygenases involved in aerobic ring-cleavage of the aromatic intermediates catechol, protocatechuate, gentisate and homogentisate. Figure 7 Key genes Carnitine palmitoyltransferase II for hydrocarbon degradation detected. The figure shows reads assigned to a selection of key genes for hydrocarbon degradation

detected in the metagenomes. The reads were identified by search in MG- rast 3; and against a reference library for alkane monooxygenase. Both benzoate-CoA ligase, and several dioxygenases (e.g. protocatechuate 3,4-dioxygenase and homogentisate 1,2-dioxygenase) were overrepresented in the metagenomes from Tplain and Tpm1-2. Alkane 1-monooxygenase (alkB), the key enzyme in alkane degradation, was also seen to be more abundant in Tplain and Tpm1-2 than in the other metagenomes. A few reads assigned to the key genes in anaerobic (methyl-coenzyme M reductase) and aerobic (particulate and soluble methane monooxygenase) methane oxidation were also detected in the Tpm1-2 metagenome. The soluble methane monooxygenase was identified in the metagenomes from Tplain and OF2 as well. An inspection of the level 3 SEED subsystems sorting under “Nitrogen Metabolism” (Figure 6) revealed that “Ammonia assimilation” was overrepresented in all Troll metagenomes, although the difference was only significant for Tplain. This fits well with the overrepresentation of autotrophic nitrifiers in the Troll metagenomes.

Contributions to nephrology Basel: Karger; 2011 vol 170, p 13

Contributions to nephrology. Basel: Karger; 2011. vol. 170, p. 135–44. 9. Warner FJ, Lubel JS, McCaughan GW, Angus PW. Liver fibrosis: a balance of ACEs? Clin Sci (Lond). 2007;113:109–18.CrossRef 10. Velez JC. The importance of the intrarenal renin-angiotensin

system. Nat Clin Pract Nephrol. 2009;5:89–100.PubMedCrossRef 11. Rüster C, Wolf G. GSK126 concentration angiotensin II as a morphogenic cytokine stimulating renal fibrogenesis. J Am Soc Nephrol. 2011;22:1189–99.PubMedCrossRef 12. Mustafa MR, Dharmani M, Kunheen NK, Sim MK. Effects of des-aspartate-angiotensin I on the actions of angiotensin III in the renal and mesenteric vasculature of normo- selleck inhibitor and hypertensive rats. Regul Pept. 2004;120:15–22.PubMedCrossRef 13. Santos RA, Simoes e Silva AC, Maric C, Silva DM, Machado RP, de Buhr I, et al. Angiotensin-(1–7) is an endogenous ligand for the G protein-coupled receptor Mas. Proc Natl Acad Sci USA. 2003;100:8258–63.PubMedCrossRef 14. Chai SY, Fernando R, Peck G, Ye SY, Mendelsohn FA, Jenkins TA, et al. The angiotensin IV/AT4 receptor. Cell Mol Life Sci. 2004;61:2728–37.PubMedCrossRef 15.

Nguyen G, Delarue F, Burcklé C, Bouzhir L, Giller T, Sraer JD. Pivotal role of the renin/prorenin Vadimezan receptor in angiotensin II production and cellular responses to renin. J Clin Invest. 2002;109:1417–27.PubMed 16. Nguyen G, Muller DN. The biology of the (pro)renin receptor. J Am Soc Nephrol. 2010;21:18–23.PubMedCrossRef 17. Ferrario CM, Varagic J. The ANG-(1–7)/ACE2/mas axis in the regulation of nephron function. Am J Physiol Ren Physiol. 2010;298:F1297–305.CrossRef 18. Kriz W, LeHir M. Pathways to nephron loss starting from glomerular diseases—insights from animal models. Kidney Int. 2005;67:404–19.PubMedCrossRef 19. Qian Y, Feldman E, Pennathur S, Kretzler M, Brosius FC 3rd. From fibrosis to sclerosis: mechanisms of glomerulosclerosis in diabetic nephropathy. Diabetes. 2008;57:1439–45.PubMedCrossRef 20. Brenner BM. Remission of renal disease: recounting the challenge, acquiring the goal. J Clin Invest. 2002;110:1753–8.PubMed 21. Taal MW, Brenner BM. Renoprotective benefits Niclosamide of RAS inhibition: from ACEI to angiotensin II antagonists.

Kidney Int. 2000;57:1803–17.PubMedCrossRef 22. Wühl E, Schaefer F. Therapeutic strategies to slow chronic kidney disease progression. Pediatr Nephrol. 2008;23:705–16.PubMedCrossRef 23. Seikaly MG, Arant BS Jr, Seney FD Jr. Endogenous angiotensin concentrations in specific intrarenal fluid compartments of the rat. J Clin Invest. 1990;86:1352–7.PubMedCrossRef 24. Atiyeh BA, Arant BS Jr, Henrich WL, Seikaly MG. In vitro production of angiotensin II by isolated glomeruli. Am J Physiol. 1995;268(2 Pt 2):F266–72.PubMed 25. Lai KN, Leung JC, Lai KB, To WY, Yeung VT, Lai FM. Gene expression of the renin-angiotensin system in human kidney. J Hypertens. 1998;16:91–102.PubMedCrossRef 26. Del Prete D, Gambaro G, Lupo A, Anglani F, Brezzi B, Magistroni R, Graziotto R, Furci L, Modena F, Bernich P, Albertazzi A, D’Angelo A, Maschio G.

Of the

Of the various criteria used to initiate full trauma activations, severe head injuries denoted by a depressed Glasgow Coma Scale (GCS) have long been the most controversial at our institution and the most problematic in terms of adherence to protocols and standards. Routine trauma quality assurance (QA) activities in our center note that this criterion represents the majority of failures to activate the trauma team [9]. While trauma surgeons from a general surgery specialty practically do not operate on severe head injuries it

is perceived that they both contribute to resuscitative care and expedite the work-up. However, there is limited information regarding the time factors and efficiency of different trauma systems in triaging and optimizing the prompt attainment of CT imaging in the critically injured 7-Cl-O-Nec1 chemical structure [10]. This prompted us to review the association between the type of trauma response and the efficiency of obtaining a CT scan in seriously head injured patients. Methods The Alberta Health Services Calgary Region (AHSCR) is a fully integrated, selleckchem publicly funded health system that provides virtually all medical and surgical care to the residents of the city of Calgary and a large surrounding area including smaller towns and communities (population ~ 1.2 million). In the AHSCR, adult trauma services are regionalized to the Foothills Medical Centre (FMC), and pediatric

trauma services (age mandate ≤14 years) to the Alberta Children’s selleck compound Hospital. These are the only accredited tertiary trauma care centers providing trauma services for Southern Alberta, Canada (~35% of the population of the Province of Alberta). Patients may also be transported to Calgary from trauma care services in neighboring provinces. At FMC, full trauma activations (FTAs) involve an expedited response by an attending trauma surgeon and trauma team (TT), residents from critical care medicine, respiratory therapists, and other dedicated trauma resources including anesthesia and the operating room, in addition

to emergency physicians MRIP and nurses who are the typical responders to initial non-trauma team responses (NTTR) (Table 1). Patients with an initial NTTR are often seen after the initial assessment by the emergency medicine team in the format of a trauma consult by the TT if admission or ongoing care is required. A FTA may be initiated by the emergency physician based on changing patient status, updated prehospital information, or clinical judgment. The response performance of trauma personnel is a trauma quality assurance audit filter and is assessed and reported annually in the Trauma Services Annual Report noting that recent audit revealed the attending trauma surgeons are typically always present within 20 minutes at a FTA [9]. Table 1 Alberta health services – Calgary Region trauma activation criteria 1. Shock defined by BP systolic < 90 mmHg or Temperature ≤ 30°C 2.

Adsorption experiments Of the samples, 5 mg was re-dispersed in 1

Adsorption experiments Of the samples, 5 mg was re-dispersed in 10 mL of the organic dyes (concentration 10 mg/L) and the mixed solution was stored in the dark for 45 min with gentle stirring. The reaction solution was sampled every 15-min intervals at room temperature; 2 mL solution was sampled and centrifuged to remove the adsorbents, and the corresponding UV-visible

spectra were recorded to monitor the progress of the degradation of organic dyes by a Shimadzu 2550 UV-visible spectrophotometer. Results and discussion Figure 1a shows the representative XRD patterns of the as-obtained hollow SnO2 and hollow SnO2@C nanoparticles. All of the diffraction peaks can be well indexed to the tetragonal rutile phase of SnO2 (JCPDS card No. 41-1445). The absence of characteristic

peaks corresponding to impurities selleck kinase inhibitor indicates high purity of the products [17]. The result reveals that the carbon coating process and annealing treatment will not change the structure of the SnO2. To prove the generation of the carbon layer on the as-prepared hollow SnO2 seeds, the two samples were characterized by Raman spectroscopy. As shown in Figure 1b, the two peaks of 1,585 and 1,360 cm−1 can be observed in the hollow SnO2@C sample, which can be attributed to the E2g vibration mode of the ordered carbon layer (G band) and the A1g vibration mode of the disordered carbon BMS-907351 cost layer (D band), PR-171 ic50 respectively. The peak intensity ratio (I D/I G) (ca. 0.76) calculated is a useful index for comparing the degree of crystallinity of various carbon materials; a smaller value ratio reflects a higher degree of check details ordering in the carbon material. The peaks at 560 and 629 cm−1 can be observed, respectively. The peak at 560 cm−1 can be assigned to the Sn-O surface vibrations; the peak at 629 cm−1 can be indexed to the A1g mode of SnO2. The above results reveal that the carbon has been successfully coated on the surface of the SnO2 nanoparticles, and the structure of SnO2 was not change. Figure 1 XRD patterns (a) and Raman

spectra (b) of the as-obtained hollow SnO 2 and hollow SnO 2 @C nanoparticles. The structure and morphology of the as-prepared hollow SnO2 nanoparticles are investigated by TEM and HRTEM. As shown in Figure 2a, the as-prepared samples mainly consist of uniform flower-like nanoparticles. The contrast (dark/bright) between the boundary and the center of the nanoparticles confirms their hollow nature. The histogram of the particle diameters (inset in Figure 2a) demonstrates that the average diameter of the as-prepared hollow SnO2 nanoparticles is 53 nm. The bright rings in the selected-area electron diffraction (SAED) pattern (Figure 2b) can be well indexed to the rutile-phase SnO2. Figure 2c shows the TEM image at high magnification of the hollow SnO2 nanoparticles.

Conversely, Buckley et al , [13] showed whey

protein hydr

Conversely, Buckley et al., [13] showed whey

protein hydrolysate ingestion in the days following an intense exercise bout (100 maximal knee extensions of the knee extensors) improved muscle strength recovery. The authors suggested that the use of partially hydrolysed (pre-digested) form of whey protein isolate may provide quicker delivery of amino acids to the muscle, and ultimately, more rapid recovery of force-generating capacity following muscle injury. The administration of whole proteins in the study by White et al. [12], may explain the lack of improvement in force recovery following damage. Furthermore, only a single dose was given to participants, whereas Buckley et al. [13] continued supplementation following the exercise bout and during the recovery period.

It could be suggested that for Alisertib concentration optimal ergogenic effects and recovery within the muscle, a hydrolysed form of whey Selleck SB273005 protein (or free amino acids) needs to be ingested both immediately following the exercise bout, and in the days during recovery. However, this concept, particularly with eccentric contractions, has not been extensively investigated, as Buckley et al. [13] only followed recovery for 24 hours post-exercise. BKM120 As such, whether the effects observed were related to muscle damage/regeneration, or simply faster recovery from fatigue, are difficult to determine. Jackman and colleagues [14] supplemented a controlled diet with BCAA and ameliorated the soreness following eccentric exercise. While they did not observe changes in strength measurements, ingestion was on the day of damage and for another 3 days afterwards, rather than for the whole regeneration process. In our previous study [15], ingestion of creatine monohydrate prior to and following a resistance exercise session indicated a possible attenuation of the amount of damage, and an increase in the rate of functional Montelukast Sodium recovery,

compared to a CHO placebo. Similarly, in the current study, given the equivocal data on protein supplementation and muscle recovery, we were interested in establishing whether a commercially available protein supplement can improve recovery from exercise-induced muscle damage, and thus used a CHO placebo as the comparison group. Thus, we supplemented the diet of a group of participants with a hydrolyzed whey protein isolate for 14 days during recovery from an identical resistance training session as used in our previous study [15]. We hypothesized that supplementation with hydrolyzed whey protein isolate will accelerate muscle strength recovery compared to an iso-energetic CHO control after a single bout of eccentric exercise. Methods Participants Seventeen healthy, untrained males (23 ± 5 yrs, 180 ± 6 cm, 80 ± 11 kg) volunteered for this study. Descriptive characteristics of the participants are presented in Table 1. Participants fulfilled the inclusion criteria as described in our previous study [15].

The platinum islands were annealed in the furnace for 10 min at 1

The platinum islands were annealed in the furnace for 10 min at 1,000°C in nitrogen flow to protect them from oxidation. Cubooctahedral facetted particles form on (100) STO

substrate [2]. Figure 4 shows SEM image of arrays of platinum Duvelisib chemical structure nanoparticles click here prepared with 450- and 150-nm silica bead masks. The larger and smaller silica masks produced approximately 100-nm and approximately 20-nm platinum nanoparticles, respectively. The entire process is schematically shown in the Figure 5. Figure 2 AFM images of monolayers from silica beads with diameter (a) 150 nm and (b) 450 nm. Imaged areas are 8 × 8 μm2 and 25 × 25 μm2, respectively. Figure 3 AFM image of platinum nanoislands deposited through voids in template from hexagonally packed 450-nm silica beads. Scanned area is equal to 3.5 × 3.5 μm2. Figure 4 SEM images of platinum nanocrystals. The crystals are arranged in hexagonal patterns produced using 450-nm (a) and 150-nm (b) silica bead templates. Insets: top right corner, rendered particle; bottom right corners, digital zooms of actual cubooctahedral nanocrystals with

clearly visible top 100 facets and four 111 facets on the sides. Distortion of hexagonal arrangement of nanocrystals in (b) is caused by the sample drift at high magnifications. Figure 5 Schematic diagram summarizing production of arrays of platinum cubooctahedral nanoparticles on STO substrates. X-ray characterization of Pt arrays on STO We performed X-ray diffraction (XRD) characterization of prepared nanoparticle arrays in order to prove the epitaxial relationship between Proteasome inhibitor particles and the STO substrate. The X-ray diffraction results for Pt nanoparticle arrays made using 150- and 450-nm silica bead templates are shown in Figure 6a,b, respectively. In both

cases, there exists a Pt (004) reflection on the shoulder of specular STO (004); thus, the Pt nanocrystals have a surface normal to (001) facet, which agrees with Pt nanoparticles prepared by e-beam lithography [2] on STO (100). Because the peaks sit on the shoulder of strong reflection from STO, it is difficult to precisely estimate the width of the platinum peak. crotamiton Figure 6 θ -2 θ scans. θ-2θ scans of Pt (004) for (a) 150-nm and (b) 450-nm samples showing that Pt (004) is parallel to the substrate’s normal reflection. Insets show SEM images of the platinum particles after annealing (the hexagonal grids are guides to the eyes). In order to show in-plane epitaxial orientation of Pt nanoparticles, we performed scans in the HK directions. Figure 7 shows Pt (113) peak on the shoulder of the STO (113). The ϕ scans (constant L) shown in the insets of Figure 7a,b show that equivalent Pt (113) peaks occur every 90°, as expected, and no other Pt peaks are found in the ϕ scans. Figures 6 and 7 together show that the Pt nanocrystals are indeed epitaxially deposited onto the STO substrate. Figure 7 ϕ scans.

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