Cells used in PW calculations began at 4 layers and ran to 80 lay

Cells used in PW calculations began at 4 layers and ran to 80 layers; larger cells were not computationally tractable with this method. SZP and DZP models began at 40 layers to overlap with PW for the converging region and were then extended to their tractable limit (200 and 160 layers, respectively) to study convergence past the capability

of PW. Figure 2 Ball and stick model of a δ -doped Si:P layer viewed along the [110] Niraparib in vitro direction. Thirty-two layers in the [001] direction are shown. Si atoms (small gray spheres), P atoms (large dark gray spheres), covalent bonds (gray sticks), repeating cell boundary (solid line). For tetragonal cells, the k-point sampling was set as a 9 × 9 × N Γ-centred MP mesh as we have found that failing to selleck products include Γ in the mesh can lead to the anomalous placement of the Fermi level on band structure diagrams. N varied from 12 to 1 as the cells became more elongated (see Appendix 1). We note that, as mentioned in the work of Carter et al. [32], the large supercells involved required very gradual (<0.1%) mixing of the new density matrix with the prior step, leading to many hundreds of self-consistent cycles before convergence was achieved. Although it has been previously found PF299 that relaxing the positions of the nuclei gave negligible differences (<0.005 Å) to the geometry [31], this was for a 12-layer

cell and may not have included enough space between periodic repetitions of the doping plane for the full effect to be seen. Whilst a 40-layer model was optimised in the work of Carter et al. [32], this made use of a mixed atom pseudo-potential and is not explicitly comparable to the models presented here. We have performed a test relaxation on a 40-layer cell using the PW basis

(vasp). The maximum subsequent ionic displacement was 0.05 Å, with most being an order of magnitude smaller. The energy gained in relaxing the cell was less than 37 meV (or 230 μeV/atom). We therefore regarded any changes to the structure as negligibly second small, confirming the results of Carter et al. [31, 32], and proceeded without ionic relaxation. Single-point energy calculations were carried out with both software programs; for vasp, the electronic energy convergence criterion was set to 10−6eV, and the tetrahedron method with Blöchl correction [52] was used. For siesta, a two-stage process was carried out: Fermi-Dirac electronic smearing of 300 K was applied in order to converge the density matrix within a tolerance of one part in 10−4; the calculation was then restarted with the smearing of 0 K, and a new electronic energy tolerance criterion of 10−6 eV was applied (except for the 120- and 160-layer DZP models for which this was intractable; a tolerance of 10−4 eV was used in these cases).

Plant Physiol Biochem 2003, 41:828–832 CrossRef

Plant Physiol Biochem 2003, 41:828–832.CrossRef Mocetinostat ic50 6. Gouia H, Ghorbal M, Meyer C: Effects of cadmium on activity of nitrate reductase and on other enzymes of the nitrate assimilation pathway in bean. Plant Physiol Biochem 2000, 38:629–638.CrossRef 7. Mosulen S, Dominguez M, YH25448 purchase Vigara J, Vilchez C, Guiraum A, Vega J: Metal toxicity in Chlamydomonas reinhardtii . Effect on sulfate and nitrate assimilation. Biomol Eng 2003, 20:199–203.PubMedCrossRef 8. Rai LC, Tyagi B, Rai PK, Mallick N: Interactive effects of UV-B and heavy metals (Cu and Pb)

on nitrogen and phosphorus metabolism of a N2-fixing cyanobacterium Anabaena doliolum . Environ Exp Bot 1998, 39:221–231.CrossRef 9. Voigt J, Nagel K: The donor side of photosystem

II is impaired in a Cd2+−tolerant mutant strain of the unicellular green alga Chlamydomonas reinhardtii . J Plant Physiol 2002, 159:941–950.CrossRef 10. Permina EA, Kazakov AE, Kalinina OV, Gelfand MS: Comparative genomics of regulation of heavy metal resistance in Eubacteria. BMC Microbiology 2006, 6:49–49.PubMedCrossRef 11. Dominguez-Solis J, Lopez-Martin M, Ager F, Ynsa M, Romero L, Gotor C: Increased cysteine availability is essential TEW-7197 for cadmium tolerance and accumulation in Arabidopsis thaliana . Plant Biotechnol J 2004, 2:469–476.PubMedCrossRef 12. Houot L, Floutier M, Marteyn B, Michaut M, Picciocchi A, Legrain P, Aude J, Cassier-Chauvat C, Chauvat F: Cadmium triggers an integrated reprogramming

of the metabolism of Synechocystis PCC6803, under the control of the Slr1738 regulator. BMC Genomics 2007, 8:350.PubMedCrossRef 13. Kelly D, Budd K, Lefebvre DD: Mercury analysis of acid- and alkaline-reduced biological samples: identification of meta-cinnabar as the major biotransformed compound in algae. Appl Environ Microbiol 2006, 72:361–367.PubMedCrossRef 14. Kelly DJA, Budd K, Lefebvre DD: Biotransformation of mercury in pH-stat cultures of eukaryotic freshwater algae. Arch Microbiol Megestrol Acetate 2007, 187:45–53.PubMedCrossRef 15. Lefebvre DD, Kelly D, Budd K: Biotransformation of Hg(II) by cyanobacteria. Appl Environ Microbiol 2007, 73:243–249.PubMedCrossRef 16. Kelly DJA, Budd K, Lefebvre DD: The biotransformation of mercury in pH-stat cultures of microfungi. Can J Bot 2006, 84:254–260.CrossRef 17. Mendoza-Cozatl D, Loza-Tavera H, Hernandez-Navarro A, Moreno-Sanchez R: Sulfur assimilation and glutathione metabolism under cadmium stress in yeast, protists and plants. FEMS Microbiol Rev 2004, 29:653–671.CrossRef 18. Payne CD, Price NM: Effects of cadmium toxicity on growth and elemental composition of marine phytoplankton. J Phycol 1999, 35:293–302.CrossRef 19. Perales-Vela HV, Peña-Castro JM, Cañizares-Villanueva RO: Heavy metal detoxification in eukaryotic microalgae. Chemosphere 2006, 64:1–10.PubMedCrossRef 20.

095 when the Atlantic sample was included in the analysis) Blue

095 when the Atlantic sample was included in the analysis). Blue mussel Overall F ST is 0.47 (Table 2) with a strong barrier separating two southwestern samples and a second

barrier distinguishing island and mainland samples in the Baltic Proper West. High diversity at southern sampling sites contrasted with lower diversity and higher divergence in northern samples. The strikingly high F ST might reflect species mixture and introgression. M. trossulus is indigenous to the Baltic Sea but is closely related to M. edulis (common name also blue mussel), check details native to the North Sea. These taxa are known to hybridize and it is possible that our southern samples include very rare M. edulis specimens. The two species are difficult to distinguish even by genetic techniques, and geographic distribution and genetic characteristics of these species are continuously IWR 1 subject to revision (Riginos and Cunningham 2005; Steinert et al. 2012). Bladderwrack The three strongest barriers to gene flow occur in the northern part of the Baltic, although the high overall F ST (0.14; Table 2) indicated strong genetic structuring overall, with all sampling locations being significantly differentiated from each other (Table S2g). Discussion We conducted the first multi-species

study in the Baltic Sea where a large number of individuals and loci were collected from the same areas covering the full Baltic Sea. Surprisingly, we detected few shared genetic patterns in the seven species analyzed with respect to location of the three GSK621 manufacturer major genetic barriers to gene flow and diversity-divergence patterns (Fig. 2). An exception to this general lack of consistence is the genetic break between the Atlantic

and the Baltic Sea. We observe a variety of genetic patterns ranging from large and significant differences among sampling regions in both genetic variation and divergence, to very little differentiation within the Baltic Sea. The most pronounced, genetic breaks occurred almost individually for each species in different regions Org 27569 of the Baltic Sea, although several species showed significant pairwise differentiation between the majority of the samples (Table S2a–g). At the northern extreme, five of six samples from the Bothnian Bay showed high diversity, but no shared major genetic barrier was present in this region (Table 3; Fig. 2). Unlike previous studies of herring and perch (Jørgensen et al. 2005; Olsson et al. 2011) we found few shared major genetic breaks associated with the different sub-basins of the Baltic Sea, e.g. around the Åland Islands. Potential causes of variability patterns The species-specific genetic patterns in the Baltic Sea, including relative amount of genetic variation, location of major genetic breaks, and isolation by distance are likely dependent on a multitude of factors including salinity tolerance, oceanographic features, life history, and population history (Table 1).

In this study we have exposed wild-type and triazine-resistant pl

In this study we have exposed Selleck BMS202 wild-type and triazine-resistant plants of Canola to very high light intensities which caused photoinhibition. After one day the plants were transferred to a laboratory table with much less light. This cycle was repeated several days. The OJIP curve was each time measured after 1 day at high and after low light, respectively. The FIA analysis revealed that the photo-electrochemical component was suppressed Temozolomide after high light (and even completely abolished in the resistant biotype). There was a partial decrease of the photochemical component and a lower fluorescence parameter F o after high light. These effects were recovered after 1 day at the

low light of the laboratory. Materials and methods Plant material and growth conditions Canola (Brassica napus L.) seeds were planted on 18 September in a greenhouse at the University of Queensland, Brisbane, Australia. Sunrise was at about 5 am, sunset at about 6 pm. The roof of the greenhouse was cooled by water. Two plants of Vadimezan wild-type (S) and two of the resistant (R) biotype were used for the measurements. During day-time the temperature varied between 29 and 34°C; the photosynthetic photon flux density (PPFD) varied between 1,100 and 1,200 μmol photons m−2s−1 (HL). The fluorescence measurements were always performed at about 10 am and started on 23 October after the plants were exposed

to the high light. After 24 h in the greenhouse the plants were transferred to a table in the laboratory where the temperature varied between 21 and 23°C, and the PPFD was about 8 μmol photons m−2s−1 (LL). The plants were then transferred

several times from the laboratory to the greenhouse and back to the laboratory. Fluorescence measurements When following the effect of high light in the greenhouse and of low light in the laboratory, the same leaf of each individual plant under investigation was used. Measurements were performed at room temperature PJ34 HCl between 18 and 20°C. Induction curves of variable chlorophyll fluorescence were measured with a Plant Efficiency Analyzer (PEA, Hansatech Instruments Ltd, King’s Lynn, Norfolk, UK) using the standard clip for fixing the leaf in the proper position with respect to the optics of the instrument and kept in the dark for 20 min in the measuring unit. Fluorescence was excited with a 2 s pulse of red light (650 nm) obtained from light-emitting diodes at sub-maximal irradiance of about 280 W m−2 (approximately 1,500 μmol photons m−2s−1). Fluorescence data were recorded at a sampling rate of 10 μs in the lower time range between 0.01 and 0.2 ms, a sampling rate of 0.1 ms between 0.2 and 2 ms, a rate of 1 ms between 2 and 20 ms, and of 10 ms beyond 20 ms. Curves are plotted relative to F o which is the fluorescence level of the sample in the dark-adapted state.

We found that the electron transitions of the molecule occur via

We found that the electron transitions of the molecule occur via the excitation channels resulting from the learn more exciton-plasmon coupling. The results also show that the vibrational excitations assist the occurrence of the upconverted luminescence. Figure 1 Schematic diagram of mechanism for occurrence of the upconverted luminescence. Horizontal lines in each parabola denote vibrational

sublevels where |g〉 and |e〉 denote the electronic ground and excited states, respectively. The electronic excitation and de-excitation of the molecule are induced by the absorption and emission of the surface plasmon, respectively. These electron transitions are accompanied by the vibrational excitations, and the vibrational excitations assist the occurrence of the upconverted luminescence.

Methods We consider a model which includes the electronic ground (excited) state of the molecule |g〉 (|e〉). The electron on the molecule interacts with the molecular vibrations and the surface plasmons. The Hamiltonian of the system is (1) where and c m (m = e, g) are creation and annihilation operators for an electron with energy ϵ m in state |m〉. Operators b † and b are boson creation and annihilation operators for a molecular vibrational mode with energy ; a † and a are for a surface plasmon mode with energy , and and b β are for a phonon mode in the thermal phonon bath, with Q b  = b + b † and . The energy parameters M, V, and U β correspond to the coupling between electronic and vibrational degrees of freedom on the molecule (electron-vibration coupling), the exciton-plasmon Clomifene coupling, and the coupling between the molecular buy AZD1480 vibrational mode and a phonon mode in the thermal phonon bath. By applying the canonical (Lang-Firsov) transformation [15], H becomes (2) where X = exp[-λ(b † - b)], and . The luminescence spectra of the molecule are expressed in terms of Green’s function of the molecular exciton on the Keldysh contour [16], which is defined as (3) where 〈⋯ 〉 H and denote statistical average in representations by system evolution for H and , respectively. τ is the

Keldysh contour time variable, and T C is the time ordering along the Keldysh contour. By assuming the condition of stationary current, the distribution function N pl of the surface plasmons excited by inelastic tunneling between the tip and the Dibutyryl-cAMP substrate is given by (4) where T pl is a coefficient related to the current amplitude due to the inelastic tunneling [17]. We calculate L according to the calculation scheme previously reported by us [12]. The spectral function and the luminescence spectra of the molecule are defined by the relations, (5) (6) where L r and L < are the retarded and lesser projection of L. The parameters are given so that they correspond to the experiment on the STM-LE from TPP molecules on the gold surface [13]: , , and .

Sodium and chloride concentrations increased in both groups durin

Sodium and chloride Selleckchem BIIB057 concentrations increased in both groups during Ramadan. A chronic state of mild dehydration in both groups may explain the abovementioned increase of serum electrolytes

and renal function markers. Interestingly Ramadan fasting did not affect serum potassium concentrations in FED. Due to the dehydration and the elevations in serum sodium that occurred in FED, one might expect that increases in serum potassium concentrations would also be observed. However, a decrease in potassium intake may have offset any effects on serum potassium caused by dehydration [32]. HDL-C increased during Ramadan in FAST and FED, at variance with our previous work [2]. The rise in HDL-C was explained previously by change in body mass [2, 33] or fat intakes [34]. However, in the present study, selleck inhibitor body mass did not change in either group while fat intakes increased only in FED. Thus, the rise of proportion of fat intakes during Ramadan can explain the increase in HDL-C in FED; although mechanisms by which fasting increases HDL-C in FAST remain unclear. Further investigation is needed to resolve this issue. Whether Ramadan fasting affects cellular damage was also investigated in the present study. Serum CK, ALT, AST, ALT, AP and γ-GT were measured to assess the effect of Ramadan

fasting on cellular damage biomarkers of bodybuilders. Ramadan fasting did not affect any of these variables and is in accordance with previous reports observing sedentary Vildagliptin persons [35]. Nevertheless, to our knowledge, our study is the first to investigate the effect of Ramadan fasting on these parameters in men who undertake resistance training during Ramadan. Serum C-reactive PF-01367338 supplier protein concentrations reflect the activity of cytokine-mediated inflammatory processes and are roughly proportional to the extent of tissue injury [36]. C-reactive protein did not change in either group and this perhaps could be explained by the lack of effect of Ramadan

fasting on cellular damage biomarkers. Akin to previous studies in judokas [37], Ramadan had no impact on leukocyte count. Thus, in this context at least, continuation of resistance training whilst participation in Ramadan can be performed safely. It is worth noting that effect sizes of the parameters measured in the current study were consistent but rather low. This, and the small number of participants my have resulted in type II error for some of the parameters measured. With this in mind, replication of the study with more participants during Ramadan would be difficult because of recruitment, but may result in further significant findings. Nevertheless, we have previously observed metabolic changes with participation in Ramadan with similar numbers of subjects [28]. Conclusion In conclusion, hypertrophic resistance training, unlike aerobic training, was not affected, at least in terms of body composition and markers of immune and inflammatory systems, when performed in a fed compared to a fasted state during Ramadan.

Plasmid DNA was extracted from N315 cells (bearing the pN315 plas

Plasmid DNA was extracted from N315 cells (bearing the pN315 plasmid) cultured in 5.0 ml brain–heart infusion broth and purified by the Plasmid Mini kit (Qiagen, Tokyo, Japan). The average yield of DNA appeared to be ~50 ng. To confirm that the extracts contained the plasmid bearing the ß-lactamase gene, they were subjected to PCR amplification using the primer set K. Agarose gel Temsirolimus mouse electrophoresis clearly showed a single distinct large band corresponding to the size of the expected PCR product (similar to the result

in Figure 2, Ref. N315). Attempts have been made to extract the plasmid DNA from BIVR cells, such as K744 and five other strains, but the yield was consistently undetectable except for the K2480 cells, which showed a trace amount of DNA. PCR amplification of blaZ taking the K2840 extracts as the template yielded JNJ-26481585 no visible band. The BIVR cells, K744 and K2480, were transformed with plasmid

DNA extracted from N315 cells. Selection of the transformants for ß-lactam resistance was difficult because the recipient cells were ß-lactam-resistant beforehand to a certain extent. Thus, transformants were selected on agar plates impregnated with a 1.5-fold MIC equivalent of ampicillin and obtained from K744 and K2480 strains (K744-T and K2480-T, respectively). Presence of the blaZ gene in the K744-T and K2480-T cells was confirmed selleck chemicals by PCR using whole-cell extracts as the template, and subsequent agarose gel electrophoresis yielded a single DNA band corresponding

to that obtained from N315 cells (Figure 3). Note that the amount of PCR products using K744-T and K2480-T DNA as the template appeared low compared with that from N315 cells (Figure 3). The identity of untransformed and transformed cells was confirmed by pulse-field gel electrophoresis of the chromosomal DNA treated with SmaI. Unsuccessful attempts were made to transform FDA209P with the pN315 plasmid. The reasons for failure of this transformation experiment remain obscure. Figure 3 PCR products of the blaZ gene. The primer sets in alphabetical order correspond with that in Table 2. Agarose Calpain gel electrophoresis was carried out as described in the legend to Figure 2. Only a part of the electrophoretogram is shown. Arrow and bp, the amplicon size; N315, K744-T and K2480-T were the source of the template DNA. ß-lactamase activity was determined using N315, K744-T and K2480-T cells. The results showed that activity in N315 cells appeared to be 0.74 U, while the levels in K744-T and K2480-T cells were undetectable (Table 2). Plasmid DNA from K744-T was undetectable, but a trace amount was extracted from K2480-T comparable with the level from the untransformed parent cells. Attempts have been made to amplify the blaZ DNA using the column eluate of the extracts as the template.

They are under dark (filled symbols) or white light (empty symbol

They are under dark (filled symbols) or white light (empty symbols) conditions, in devices containing (a) 12- or (b) 2-nm a-Ge QWs. The used metal-insulator-semiconductor configuration is drawn in the figure. In order to quantitatively investigate the spectral response of the devices, we illuminated

them with different wavelengths and measured check details the external quantum efficiency ( where P is the power of incident photons per unit area), which gives the number of collected carriers per incident photon at a given wavelength. In Figure 5a, the EQE spectra are reported for both the devices biased at −3 V. The device with 2-nm a-Ge shows a fairly low and flat photoresponse in all the investigated spectral range. Such a response was expected

after the very low net photocurrent reported in Figure 4b. Actually, this behavior can be mainly attributed to the contribution of the carrier generation and extraction within the depleted region layer in the Si substrate, without a significant role of the Ge QW since (1) light absorption by the Ralimetinib molecular weight 2-nm a-Ge QW occurs only for photons with energy larger than 1.8 eV (λ ≤ 700 nm) and (2) even for λ ≤ 700 nm, the fraction of absorbed light is only a few percent of the total incident light (Figure 2a). Thus, a really small contribution of the 2-nm a-Ge QW is expected on the overall response of the photodetector, allowing for the consideration of the 2-nm a-Ge QW device as a reference for the substrate behavior. On the contrary, the device with 12-nm a-Ge QWs shows a much larger EQE, clearly indicating the paramount role of carrier photogeneration within a-Ge films. Even if the maximum EQE is only 14%, one should consider that the photoresponse in this device is mainly attributable to the photocarrier generation within the 12-nm Ge layer and their following extraction, since the Si substrate has only a minor contribution in this case. In particular, the fraction of absorbed light in the 12-nm-thick a-Ge QW is much lower than unity

in the entire spectral range investigated, since we have already reported the absorption spectrum of this same sample (Figure 2a). Therefore, we can extract the internal quantum efficiency (IQE), which gives the number of collected carriers per absorbed photon at a given wavelength by the Ge layer, Non-specific serine/threonine protein kinase . As reported in Figure 5b, the IQE shows values as high as 70% in the near-infrared region, close to the E G (approximately 0.9 eV) that we measured for this sample through an independent method in Figure 2b. This correlation further supports the main role of the a-Ge QW as active absorbing layer in the photodetector device. The IQE spectrum decreases for higher photon energy as the collection of the hotter carriers is less probable due to recombination PLX3397 issues. Figure 5 EQE and IQE spectra. (a) EQE spectra taken at −3-V bias for the 2- or 12-nm a-Ge QW devices. (b) IQE spectrum for the 12-nm a-Ge QW photodetector biased at −3 V.

Although the mechanism of this inhibition needs to be further inv

Although the mechanism of this inhibition needs to be further investigated, our results suggest that COX-2 may have a role in angiogenesis and may be a potential therapeutic target for the treatment of human osteosarcoma. Acknowledgements This research was supported by grants from the Shanghai Health Bureau Science Fund for Young Scholars (2009Y037), the https://www.selleckchem.com/products/sch-900776.html Technology Development Fundation of Shanghai Jiaotong University School of Medicine (09XJ21048). References 1. Bacci G, Longhi A, Versari M, Mercuri M, Briccoli A, Picci P: Prognostic factors for Gefitinib concentration osteosarcoma of the extremity treated with neoadjuvant chemotherapy: 15-year

experience in 789 patients treated at a single institution. Cancer 2006, 106:1154–1161.PubMedCrossRef 2. Naruse T, Nishida Y, Hosono K, Ishiguro N: Meloxicam inhibits osteosarcoma growth, invasiveness and metastasis by COX-2-dependent and independent routes. Carcinogenesis 2006, 27:584–592.PubMedCrossRef 3. Mirabello L, Troisi RJ, Savage SA: Osteosarcoma incidence and survival rates from 1973 to 2004: data from the Surveillance, Epidemiology,

and End Results Program. Cancer 2009, 115:1531–1543.PubMedCrossRef 4. Longhi A, Errani C, De Paolis M, Mercuri M, Bacci G: Primary bone osteosarcoma in the pediatric age: State of the art. Cancer Treatment Reviews 2006, 32:423–436.PubMedCrossRef 5. Yang G, Huang C, Cao J, Huang KJ, Jiang T, Qiu ZJ: Lentivirus-mediated shRNA interference targeting STAT3 inhibits human pancreatic cancer cell invasion. World J Gastroenterol 2009, 15:3757–3766.PubMedCrossRef 6. Brown JR, DuBois Repotrectinib in vitro RN: COX-2: a molecular target for colorectal cancer prevention. J Clin Oncol 2005, 23:2840–2855.PubMedCrossRef 7. Strillacci A, Griffoni C, Valerii Clomifene MC, Lazzarini G, Tomasi V, Spisni E: RNAi-based strategies for cyclooxygenase-2 inhibition in cancer. J Biomed Biotechnol 2010, 2010:828045.PubMedCrossRef 8. Denkert C, Kobel M, Berger S, Siegert A, Leclere A, Trefzer U: Expression of cyclooxygenase 2 in human malignant melanoma. Cancer

Research 2001, 61:303–308.PubMed 9. Masferrer JL, Leahy KM, Koki AT, Zweifel BS, Settle SL, Woerner BM: Antiangiogenic and antitumor activities of cyclooxygenase-2 inhibitors. Cancer Res 2000, 60:1306–1311.PubMed 10. Kulkarni S, Rader JS, Zhang F, Liapis H, Koki AT, Masferrer JL: Cyclooxygenase-2 is overexpressed in human cervical cancer. Clinical Cancer Research 2001, 7:429–434.PubMed 11. Kokawa A, Kondo H, Gotoda T, Ono H, Saito D, Nakadaira S: Increased expression of cyclooxygenase-2 in human pancreatic neoplasms and potential for chemoprevention by cyclooxygenase inhibitors. Cancer 2001, 91:333–338.PubMedCrossRef 12. Tsujii M, Kawano S, Tsuji S, Sawaoka H, Hori M, DuBois RN: Cyclooxygenase regulates angiogenesis induced by colon cancer cells. Cell 1998, 93:705–716.PubMedCrossRef 13.

However, due to the sophistication of the TEM technique, sometime

However, due to the sophistication of the TEM technique, sometimes, experimental artifacts could be erroneously interpreted or lead to controversy [6–10]. To date, most planar defect-related studies have

been focused on 1D nanostructures made of silicon, silicon carbide, III-V (e.g., GaAs, InP), or II-IV compounds (e.g., ZnO, CdSe) whose crystal structures are either cubic or hexagonal [8–15]. Boron carbide 1D nanostructures have attracted increasing attention in the last few years because of their potential applications in nanocomposites and thermoelectric energy conversion [16–25]. Most reported boron carbide 1D nanostructures were synthesized by carbothermal reduction or chemical vapor deposition at GSK461364 ic50 approximately GSK126 manufacturer 1,100°C [16–23]. Field emission [18, 23], photoluminescence [19], mechanical [21, 23], and thermal conductivity [22] properties of these 1D nanostructures were reported. However, due to the complicated rhombohedral crystal structure, detailed structural characterization especially on planar defects that could

greatly affect the properties of boron carbide 1D nanostructures has not yet gained enough attention, and the structure–property relations have not been established. In our previous study [22], about one hundred as-synthesized boron carbide nanowires were subjected to TEM study, during which each nanowire was examined throughout the full tilting range allowed by the configuration of our microscope. Approximately 75% examined nanowires were found to have planar defects, while the remaining 25% were planar defect-free-like. The defected nanowires were further categorized into two groups: transverse faults (TF) nanowires with planar defects perpendicular to the preferred growth direction of nanowires and axial faults (AF) nanowires with planar defects parallel to the preferred growth direction of nanowires. The determination of defects’ existence and fault orientations (TF or AF) within each nanowire was based on the characteristic features presented in TEM results, including modulated contrast in high-resolution TEM (HRTEM) images and

streaks in diffraction patterns. In this work, more extensive TEM examination and model simulation were performed to gain a deeper understanding MTMR9 of the nature of planar defects in the aforementioned boron carbide nanowires to answer two questions. (1) Do planar defect-free boron carbide nanowires really exist? Literature review shows that due to its relatively low stacking fault energy (75 mJ/m2) [26], planar defects have been frequently observed in bulk boron carbides independent of the synthesis Ispinesib in vivo methods [27–30]. It has also been reported that the density of planar defects decreases as the synthesis temperature increases [30]. However, the planar defects were still detectable by TEM from bulk samples synthesized at 2,100°C [30].