Proc Natl Acad Sci USA 2004, 101:13306–13311 PubMedCrossRef 7 Pi

Proc Natl Acad Sci USA 2004, 101:13306–13311.PubMedCrossRef 7. Pirker R, Minar W, Filipits M: Integrating epidermal growth CB-839 cell line factor receptor-targeted

therapies into platinum-based chemotherapy regimens for newly diagnosed non-small-cell lung cancer. Clin Lung Cancer 2008,9(Suppl 3):S109–115.PubMedCrossRef 8. Pirker R, Filipits M: Targeted therapies in lung cancer. Curr Pharm Des 2009, 15:188–206.PubMedCrossRef 9. Lynch TJ, Bell DW, Sordella R, Gurubhagavatula S, Okimoto RA, Brannigan BW, Harris PL, Haserlat SM, Supko JG, Haluska FG, et al.: Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N Engl J Med 2004, 350:2129–2139.PubMedCrossRef 10. Fukuoka M, Yano S, Giaccone G, Tamura T, Nakagawa K, AR-13324 Douillard JY, Nishiwaki Y, Vansteenkiste J, Kudoh S, Rischin D, et al.: Multi-institutional randomized phase II trial of gefitinib for previously treated patients with advanced non-small-cell lung cancer (The IDEAL 1 Trial) [corrected]. J Clin Oncol 2003, 21:2237–2246.PubMedCrossRef 11. Kris MG, Natale RB, Herbst RS, Lynch TJ Jr, Prager D, Belani CP, Schiller JH, Kelly K, Spiridonidis H, Sandler A, et al.: Efficacy

of gefitinib, an inhibitor of the epidermal growth factor receptor tyrosine kinase, in symptomatic patients with non-small cell lung cancer: a randomized trial. Jama 2003, 290:2149–2158.PubMedCrossRef 12. Eberhard DA, Johnson BE, Amler LC, Goddard AD, Heldens SL, Herbst RS, Ince

WL, Janne PA, Januario T, Johnson DH, et al.: Mutations in the epidermal growth factor receptor and in KRAS are predictive and prognostic indicators in patients with non-small-cell lung cancer treated with chemotherapy alone and in combination with erlotinib. J Clin Oncol 2005, 23:5900–5909.PubMedCrossRef 13. Qin BM, Chen X, Zhu JD, Pei DQ: learn more Identification of EGFR kinase domain mutations among lung cancer patients in China: implication for targeted cancer therapy. Cell Res 2005, 15:212–217.PubMedCrossRef PIK3C2G 14. Zhang XT, Li LY, Mu XL, Cui QC, Chang XY, Song W, Wang SL, Wang MZ, Zhong W, Zhang L: The EGFR mutation and its correlation with response of gefitinib in previously treated Chinese patients with advanced non-small-cell lung cancer. Ann Oncol 2005, 16:1334–1342.PubMedCrossRef 15. Massarelli E, Varella-Garcia M, Tang X, Xavier AC, Ozburn NC, Liu DD, Bekele BN, Herbst RS, Wistuba II: KRAS mutation is an important predictor of resistance to therapy with epidermal growth factor receptor tyrosine kinase inhibitors in non-small-cell lung cancer. Clin Cancer Res 2007, 13:2890–2896.PubMedCrossRef 16. Perry MC, Ihde DC, Herndon JE, Grossbard ML, Grethein SJ, Atkins JN, Vokes EE, Green MR: Paclitaxel/ifosfamide or navelbine/ifosfamide chemotherapy for advanced non-small cell lung cancer: CALGB 9532. Lung cancer 2000,28(1):63–68.PubMedCrossRef 17.

skirrowii (Tables 1 and 2) Furthermore, the

expected amp

skirrowii (Tables 1 and 2). Furthermore, the

expected amplicons for A. butzleri and A. skirrowii in individual reactions were also obtained for the eight and three strains of A. CB-839 cibarius, respectively (Table 2). Nevertheless, no cross-reaction with non-targeted species occurred when using primers designed for A. cibarius that reacted only with the eight strains of this species. The combined method of Douidah et al.[9] and De Smet et al.[17], misidentified four of the non-targeted species (Arcobacter defluvii, Arcobacter ellisii, Arcobacter venerupis, and Arcobacter suis) as A. butzleri, and two of the three strains of A. ellisii as A. cryaerophilus (Table 2). The method performed correctly for the four remaining targeted species. Finally, the 16S rRNA-RFLP designed by Figueras et al. [18] was found to misidentify three species (A. trophiarum, A. thereius, and some A. cryaerophilus strains) as A. butzleri. Further to this, A. suis, and A. defluvii produced the same pattern, and two species (A. venerupis, and Arcobacter marinus)

a very PF-562271 chemical structure similar one (Table 2). Because of these limitations, this method has recently been updated selleck kinase inhibitor with new endonucleases; these produced specific results for all strains and species [19]. This updated protocol was the one used to identify all strains used in this study. Comparative evaluation of the targeted genes and designed primers When the results were evaluated in relation to genes used to identify the species, it was observed that the 23S rRNA gene regions targeted in the Kabeya et al.[15] method for A. butzleri, A. cryaerophilus, and A. skirrowii were Galeterone unreliable, as was the region employed in the Houf et al. method [14] for A. cryaerophilus (Tables 1 and Additional file 1: Table S2). However, the regions of the 23S rRNA gene targeted by the m-PCR method of Douidah et al. [9] were 100% reliable for the detection of A. skirrowii, A. cibarius, and A. thereius, but not for A. butzleri (Tables 1, 2 and Additional file 1: Table S2). With regard to the gyrA gene, the region used for the identification of A. cryaerophilus in the latter method, and the one in the method of Pentimalli et al. [16] were unreliable. Despite all strains of A. cryaerophilus being

correctly identified, A. ellisii was confused with this species when using the Douidah et al.[9] method, and with A. skirrowii when using the Pentimalli et al. [16] method (Tables 1 and 2). The main reason for the poor performance of the targeted regions of 23S rRNA or gyrA genes (Additional file 1: Table S2) is the limited amount of sequences used to derive the primers. For instance, the sequences of the 23S rRNA gene are, at the time of writing, only available for eight of the seventeen known Arcobacter species (A. butzleri, A. cryaerophilus, A. skirrowii, A. cibarius, A. nitrofigilis, A. thereius, Arcobacter mytili, and A. trophiarum), and the gyrA gene is only available for seven species (A. butzleri, A. cryaerophilus, A. skirrowii, A. cibarius, A. nitrofigilis, A.

J Exp Clin Cancer Res 2008, 27:49 PubMedCrossRef 15 Shekari M, S

J Exp Clin Cancer Res 2008, 27:49.PubMedCrossRef 15. Shekari M, Sobti RC, Tamandani DM, Malekzadeh K, Kaur P, Suri V: Association of genetic polymorphism of the DNA base excision repair gene (APE-1 Asp/148 Glu) and HPV type (16/18) with the risk of cervix cancer in north Indian population. Cancer Biomark 2008, 4:63–71.PubMed 16. Yoo DG, Song YJ, Cho EJ, Lee SK, Park JB, Yu JH, Lim SP, Kim

JM, Jeon BH: Alteration of APE1/ref-1 expression in non-small cell lung cancer: the implications of impaired extracellular Belinostat manufacturer superoxide dismutase and catalase antioxidant systems. Lung Cancer 2008, 60:277–284.PubMedCrossRef 17. van Baardwijk A, Dooms C, van Suylen RJ, Verbeken E, Hochstenbag M, Dehing-Oberije C, Rupa D, Pastorekova S, Stroobants S, Buell U, et al.: The maximum uptake of (18)F-deoxyglucose on positron emission tomography scan correlates with survival, hypoxia inducible factor-1alpha and GLUT-1 in non-small cell lung cancer. Eur J Cancer 2007, 43:1392–1398.PubMedCrossRef 18. Kaira

K, Oriuchi N, Shimizu K, Ishikita T, Higuchi T, Imai H, Yanagitani N, Sunaga N, Hisada T, Ishizuka T, et al.: Correlation of angiogenesis with (18)F-FMT and (18)F-FDG uptake in non-small cell lung cancer. Cancer Sci 2009, 100:753–758.PubMedCrossRef 19. Hodgkinson AD, Page T, Millward BA, Demaine AG: A novel polymorphism in the 5′ flanking region of the glucose transporter (GLUT1) gene is strongly associated with diabetic nephropathy in patients with Type Epigenetics Compound Library solubility dmso 1 diabetes mellitus. J Diabetes Complications 2005, 19:65–69.PubMedCrossRef 20. Matakidou A, el Galta R, Webb EL, Rudd MF, Bridle H, the GC, Eisen T, Houlston RS: Genetic variation in the DNA repair genes is predictive of outcome in lung cancer. Hum Mol Genet 2007, 16:2333–2340.PubMedCrossRef 21. Hanin FX, Lonneux M, Cornet J, Noirhomme P, Coulon C, Distexhe J, Poncelet AJ: Prognostic value of FDG uptake in Resminostat early stage non-small cell lung cancer. Eur J Cardiothorac Surg 2008, 33:819–823.PubMedCrossRef 22. Usuda K, Saito Y, Sagawa M, Sato M, Kanma

K, Takahashi S, Endo C, Chen Y, Sakurada A, Fujimura S: Tumor doubling time and prognostic assessment of patients with primary lung cancer. Cancer 1994, 74:2239–2244. PubMedCrossRef 23. Duhaylongsod FG, Lowe VJ, Patz EF Jr, Vaughn AL, Coleman RE, Wolfe WG: Lung tumor MLN4924 nmr growth correlates with glucose metabolism measured by fluoride-18 fluorodeoxyglucose positron emission tomography. Ann Thorac Surg 1995, 60:1348–1352.PubMedCrossRef 24. Liu ZH, Guan TJ, Chen ZH, Li LS: Glucose transporter (GLUT1) allele (XbaI-) associated with nephropathy in non-insulin-dependent diabetes mellitus. Kidney Int 1999, 55:1843–1848.PubMedCrossRef 25. Tarnow L, Grarup N, Hansen T, Parving HH, Pedersen O: Diabetic microvascular complications are not associated with two polymorphisms in the GLUT-1 and PC-1 genes regulating glucose metabolism in Caucasian type 1 diabetic patients. Nephrol Dial Transplant 2001, 16:1653–1656.PubMedCrossRef 26.

4a) The measuring chamber is thermostat controlled by a water ja

4a). The measuring chamber is thermostat controlled by a water jacket, and the liquid is continuously mixed by a magnetic stirrer. Light can be applied by a fiber optic illuminator (e.g., from Schott, Mainz, Germany; www.​schott.​com) (more detailed descriptions of the setup are given in references, Jouanneau et al. 1980; Lindberg et al. 2004). Fig. 4 a Schematic #click here randurls[1|1|,|CHEM1|]# of a measuring chamber connected to the vacuum of an MS as is set-up in the CEA Cadarache. An aliquot (ca. 1.5 ml) of the algal suspension is injected into

the measuring chamber of the Hansatech type where it is stirred by a little stir bar (not shown). Light can be applied by a fiber optic cable. Inhibitors such as DCMU can be applied by a syringe through the capillary of the lid. The bottom of the chamber is sealed by a thin gas-permeable Teflon membrane supported by a stainless steel frit. Gases dissolved in the cell suspension AZD8931 chemical structure (indicated by white circles) can diffuse through the membrane and enter

the ion source of the MS by a vacuum line. The addition of heavy isotopes can be applied to differentiate between respiration (uptake of 18O2) and oxygenic photosynthesis (production of 16O2), as well as between CO2 assimilation (uptake of 13CO2) and respiratory CO2 production (12CO2). The metabolism of D2 is an indicator of the hydrogen metabolism and the hydrogenase turnover rate. b Schematic graph of the effect of DCMU on the in vivo H2 -production rate of S-depleted C. reinhardtii cells as recorded utilizing the MS system depicted in (a). A stable H2 graph indicates the instantaneous H2 evolution rate PI-1840 of an illuminated, S-deprived algal culture. To define the contribution of photosynthetic water splitting to the electron supply of the hydrogenase, DCMU is

added. The difference of the H2-production rates before and after the addition of the PSII inhibitor is equivalent to the fraction of H2 which is generated with electrons provided by PSII. To determine the low rate of dark H2 production, light is turned off after the H2 graph has stabilized. The merit of this set-up is that changes of the concentrations of several gases can be recorded simultaneously. The spectrometer sequentially scans the abundance of the gases of interest while measuring one mass peak takes 0.5 s in the system described by Lindberg et al. (2004). Therefore, the concentrations of gases dissolved in a cell suspension within the measuring chamber are recorded in very short-time intervals and any change in gas abundance will be observable almost immediately. Thus, this MS system allows examining different metabolic processes in real time and in parallel, allowing a direct comparison without the need to take into account different measuring conditions and set-ups (e.g., light intensity, temperature, disturbance of the system by entry of air etc.).

The reason for this liberal

The reason for this liberal attitude of Buddhist ethics towards genetics is to be found in a general affinity of Buddhism and science as both see the need for the verification of truth by reason and experience. A less liberal attitude applies to the beginning of life. An embryo is human and thus possesses human dignity and human rights at the time of conception. In Buddhism, persons are interdependent. Germline cell therapy for instance is ethically questionable due to its potentially negative effects on humanity. Five parts and 13 chapters contain a diversity of issues for debate. In pluralistic societies

and within several religious groups, discussions on how to balance pros and cons of genetics and biotechnology find more are taking place. The book presents a kaleidoscope of these perspectives and shows that the challenges of the rapid progress of modern gene technology demand that religious ethics engages in new ideas and unorthodox ethical reflections. Open Access This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.”
“Background Over the last decade, basic

scientific research has led to a greater understanding of the contribution made by genes to present and future health (Guttmacher and Collins 2002). It is increasingly recognised that genetic information will need to be integrated into all aspects of health care delivery, including primary care (Department CX-5461 of Health 2003; Greendale and Pyeritz 2001; Harris and Harris 1995). Patient advocacy groups have lobbied to raise health professionals’ awareness of genetic issues (World Alliance of Organizations for the Prevention

of Birth Defects 2004), and the need for both patients and Tau-protein kinase professionals to have an appropriate level of familiarity with the new technologies has been recognised by the European Commission (McNally et al. 2004). Primary care providers have varying levels of involvement and confidence in genetics (Emery et al. 1999). We have demonstrated variable quality care provided for genetic conditions by non-geneticists (Harris et al. 1999). This has also been reported in Australia (Tyzack and Wallace 2003), the Netherlands (Baars et al. 2003; van Langen et al. 2003), Singapore (Yong et al. 2003), and USA (MCC950 solubility dmso Barrison et al. 2003; Batra et al. 2002; Schroy et al. 2002; Taylor 2003). Core competencies for all health professionals and particular professional groups are being developed by expert panels (Calzone et al. 2002; Core Competency Working Group of the National Coalition for Health Professional Education in Genetics 2001; Kirk et al. 2003), and we have recently reported the educational priorities of the healthcare providers themselves (Julian-Reynier et al. 2008).

Some studies, which combined data from

other genotypes, h

Some studies, which combined data from

other genotypes, have shown that the concurrent lack of GSTM1/GSTT1 and GSTP1 genes posed a significantly increased risk of prostate cancer [20, 28, 29]. However, these studies have not been confirmed by other authors [23]. One of the reasons for such discrepancy in the findings might lie in the difficulty of analyzing the impact of the modified GST activity on detoxification of known carcinogens. GST has overlapping substrate specificities; therefore, deficiency of a single GST isoenzyme may be compensated by other Selonsertib ic50 isoforms. Another important factor is the differential expression of genes for GST in different cells. The variation in published prostate cancer prevalence rates can be attributed partly to methodological differences in survey design, including age distribution of the population surveyed. It is also known that the incidence of prostate cancer is underestimated, buy LCZ696 maybe due to poor compliance of elderly with screening recommendations. Thus, regular follow-ups are difficult

to achieve and, as a consequence, many men never know they have prostate cancer. It has been reported that the calculated prevalence of prostate cancer at death (i.e. histological evidence) for a 60-year-old man is 32%, whereas but the prevalence in living men (clinically-defined disease) is approximately 4% [30]. In contrast to the possible role of GST in environmental carcinogenesis, next it has learn more been suggested that GST genotypes conferring lower enzyme activity may be of advantage for the patients who are undergoing chemotherapeutic treatment for neoplastic disease because reduced detoxification potentially enhances effectiveness of cytotoxic drugs [31]. Although somewhat speculative, the GST polymorphisms might be a protective factor during the

period of chemotherapy, as the carriers of GST null genotypes might better respond to the treatment. At present, it is difficult to confidently evaluate the GST polymorphisms impact on prostate cancer patients. Apparently, it would be far too simplistic to attribute a complex problem such as prostate cancer to any single cause. Although it is methodologically difficult to identify and separate all the factors that make it difficult to identify individual changes, it is nevertheless possible to conduct a carefully designed international and/or multicentric study, or of combining results of several independent studies on the topic. Conclusion Our results suggest a possible association between the GSTP1 Val/Val genotype and the occurrence of prostate cancer. However, broad confidence intervals indicate a naturally high variability in GST polymorphisms in the population, which has given less weight to the observed differences in GSTP1 Val/Val genotype frequencies between the patients and the control subjects.

BLAST atlas key for Additional files 3 and 4 (TIFF 14 KB) Additi

BLAST atlas key for Additional files 3 and 4. (TIFF 14 KB) Additional file 7: Evolutionary distance analysis of Vibrio sp. RC341. Evolutionary distance of strains used in this study from Vibrio sp. RC341 as determined by ANI between Vibrio sp. RC341 and all strains used in this study. (TIFF 81 KB) Additional file 8: Evolutionary distance analysis of Vibrio sp. RC586. Evolutionary distance of strains used in this study from Vibrio sp. RC586 as determined by ANI between Vibrio sp. RC586 and all strains

used in this study. (TIFF 83 KB) Additional file 9: Evolutionary distance analysis of V. mimicus MB451. Evolutionary distance of Vibrio sp. RC586 and Vibrio sp. RC341 from V. mimicus MB451 as determined by ANI between V. mimicus MB451 and all strains used in this study. (TIFF 84 KB) Additional file 10: Evolutionary distance analysis of V. cholerae BX 330286. Evolutionary BMS-907351 supplier distance of Vibrio sp. RC586 and GF120918 Vibrio sp. RC341 from strains V. cholerae BX 330286 as determined by ANI between V. cholerae BX 330286 and all strains used in this study. (TIFF 84 KB) Additional file 11: Putative Selleckchem MAPK inhibitor genomic islands of Vibrio sp. RC341. Putative genomic islands of Vibrio sp. RC341, showing insertion loci, homologous flanking loci in V. cholerae N16961, %GC, other carrier strains used in this study, ANI with homologous islands, δ*, direction of transfer, islands sharing same insertion

loci, and annotation. (XLS 32 KB) Additional file 12: Putative genomic islands of Vibrio sp. RC586. Putative genomic islands of Vibrio sp. RC586, showing insertion loci, homologous flanking loci in V. cholerae N16961, %GC, other carrier strains used in this study, ANI with homologous islands, δ*, SB-3CT direction of transfer, islands sharing same insertion loci, and annotation. (XLS 31 KB) Additional file 13: Strain legend. Legend for Additional files 10 and 11. (XLS 20 KB) Additional file 14: Phylogeny of the genomic island GI-2. Phylogeny of the genomic island GI-2 as determined by reconstructing a neighbor-joining tree using the Kimura-2 parameter as a nucleotide substitution

model. (TIFF 19 KB) Additional file 15: Phylogeny of the genomic island GI-41. Phylogeny of the genomic island GI-41 as determined by reconstructing a neighbor-joining tree using the Kimura-2 parameter as a nucleotide substitution model. (TIFF 6 KB) Additional file 16: Phylogeny of the genomic island GI-4. Phylogeny of the genomic island GI-4 as determined by reconstructing a neighbor-joining tree using the Kimura-2 parameter as a nucleotide substitution model. (TIFF 26 KB) Additional file 17: Phylogeny of VSP-I. Phylogeny of the genomic island VSP-I as determined by reconstructing a neighbor-joining tree using the Kimura-2 parameter as a nucleotide substitution model. (TIFF 11 KB) Additional file 18: Phylogeny of the genomic island GI-61. Phylogeny of the genomic island GI-61 as determined by reconstructing a neighbor-joining tree using the Kimura-2 parameter as a nucleotide substitution model.

90 ppm by 7 06 % what pointed at the 1,8-diazaphenothiazine syste

90 ppm by 7.06 % what pointed at the 1,8-diazaphenothiazine system and the derivative 7 (Scheme 3). Scheme 1 Synthesis if 10H-diazaphenothiazine 3 from disubstituted pyridines 2 and 3 and dipyridyl sulfide 5 Scheme 2 The NMR experiments for compound 7: a NOE and COSY, b HSQC and HMBC Scheme 3 Synthesis of 10-dialkylaminoalkyl-1,8-diazaphenothiazines

7–19 The full 1H NMR assignment of the RG-7388 chemical structure proton signals came from the homonuclear 1H–1H correlation (COSY). Three most deshielded proton signals at 7.90, 8.07, and 8.09 ppm were considered as the α-pyridinyl proton signals. The doublet of doublet signal at 6.90 ppm, considered as the β-pyridinyl proton, was intercorrelated (ortho-coupling) with the signals at 8.09 ppm and Adavosertib cell line at 7.26 ppm (γ-pyridinyl proton) with the coupling selleck compound constants of 4.9 and 7.2 Hz, respectively. The signal at 7.26 ppm was weak intercorrelated (para-coupling) with the signal at 8.09 ppm with the coupling constant of 1.8 Hz. The protons

were assigned as H3, H4, and H2, respectively. The α-pyridinyl proton signal at 8.07 ppm was correlated with the signal at 7.18 ppm (β-pyridinyl proton) with the coupling constant of 5.4 Hz. These protons were assigned as H7 and H6. The proton signal assignment was presented in Scheme 2. The new diazaphenothiazine system was also determined by the 13C NMR spectrum. The spectrum revealed eleven carbon signals: one primary, six tertiary, and four quaternary. The methyl group was observed at 32.8 ppm. The full assignment of carbon signals came from 2D NMR: HSQC (the tertiary carbon atoms connected with the hydrogen atoms) and HMBC (the tertiary and quaternary carbon atoms correlated with the hydrogen atoms via two and mainly three bonds). The proton-carbon correlation was presented in Scheme 2. The product structure as 10H-1,8-diazaphenothiazine 4 is the evidence for the Smiles

rearrangement of the S–N type of resulted dipyridinyl sulfide 5. Heating sulfide 5 in refluxing DMF gave 10H-1,8-diazaphenothiazine (4) in 88 % yield. The reaction run through the formation ID-8 of dipyridinyl amine 6 which (not isolated) very easily cyclized to diazaphenothiazine 4 (Scheme 1). The 1,8-diazaphenothiazine ring system was confirmed by X-ray analysis of the nitropyridyl derivative 12 (obtained by independent way from appropriate sulfide containing three nitropyridyl moieties via the double Smiles rearrangement), published separately (Morak-Młodawska et al., 2012). The parent 10H-1,8-diazaphenothiazine 4 was transformed into 10-derivative in one or three steps.

% cobalt acetate The precursors were rapidly heated to 310°C in

% cobalt acetate. The precursors were rapidly heated to 310°C in an electric furnace with an inert gas atmosphere for fast thermal decomposition (Figure 1). The syntheses were carried out using different ambient gases, including flowing inert Ar (99.999%), flowing air (99.999%) with a continuous oxygen supply, and closed air see more (99.999%) with oxygen inclusion only for the initial reaction (Table 1). The gas flow rate was maintained at 25 sccm. The nanowire length was manipulated from 500 nm to 3 μm by controlling the synthesis time between 30 min and 2 h. The synthesized nanowires were cleaned in ethanol and distilled water repeatedly, followed by annealing

in stages at 300°C for 10 h and 800°C MAPK inhibitor for 10 h under a vacuum (10-2 Torr) to remove organic residues. For comparison, ZnCoO nanopowder [13] and ZnCoO micropowder [20] were also prepared (see the

references for detailed information). Hydrogen injection was performed by plasma treatment using an Ar/H (8:2) mixed gas (99.999%), and all samples were exposed twice for 15 min to hydrogen plasma using an RF power of 80 W. Figure 1 Electric furnace for the synthesis of ZnCoO nanowires. Table 1 Controlling ambient gas by gas distinction Sample name Gas S1 Argon gas (99.999%, continuous flow) S2 Air gas (99.999%, continuous flow) S3 Air gas (99.999%, non-continuous) The change in nanowire morphology and the secondary phase were investigated by field-emission scanning electron microscopy (FE-SEM, S-4700, Hitachi, Tokyo, Japan) and X-ray diffraction (XRD, Empyrean series2, PANalytical, Almelo, The Netherlands). Magnetic properties such as magnetization were measured using a vibrating sample magnetometer (VSM, model 6000, Quantum Design, San Diego, CA, USA) attached to a physical property measurement system. Results and discussion Figure 2 shows the FE-SEM images of the ZnCoO nanowires synthesized using different ambient gases. Figure 2a shows the FE-SEM images of the samples labeled S1, which were fabricated using ambient Ar gas.

Figure 2b shows the same image magnified by a factor of three. ZnCoO nanowires were produced sporadically, and the average length was 700 nm. Figure however 2c shows the FE-SEM images of the samples labeled S2, which were fabricated using air continuously supplied with oxygen. Figure 2d shows the same image magnified by a factor of three. ZnCoO nanowires were produced sporadically, and the maximum length was approximately 2.5 μm. Figure 2e shows the FE-SEM images of the samples labeled S3, which were generated using a fixed air supply with restricted oxygen content. Figure 2f shows the same image magnified by 1.5. The ZnCoO nanowires were produced uniformly, and the average length was 2 μm. These results indicate that the morphology of the ZnCoO nanowires selleck chemicals llc depends on the ambient gas and, in particular, on the oxygen content.

In this study we use a techno-economic approach to examine the te

In this study we use a techno-economic approach to examine the technological feasibility of a global reduction of GHG emissions by 50 % relative to the 1990 level by 2050, a target that roughly corresponds to the AR-13324 climate target of 2 °C. We also perform a detailed analysis of the contribution of low-carbon technologies to GHG emission reduction in the mid- and long-term and evaluate the required technological cost.2 Methodology AIM/Enduse[Global] The analysis in this paper uses AIM/Enduse[Global], a techno-economic model for mid- to long-term climate change mitigation policy assessment. AIM/Enduse[Global]

is a dynamic recursive CBL0137 in vitro model with a 1-year time step and a detailed framework for technology selection. The model selects technologies by linear programming algorithms that minimize the

total system cost (including the initial investment, operation, and maintenance costs of technologies, energy cost, and other costs such as carbon tax) given fixed service demands such as steel production, passenger transport, space heating demand, Wnt inhibitor etc. The model estimates energy consumption and GHG emissions (e.g., CO2, CH4, N2O, HFC, PFC, and SF6) driven by technological change. Kainuma et al. (2003) provide a detailed formulation of the model. The version of AIM/Enduse[Global] used in this article splits the world into 32 regions over a time horizon from 2005 to 2050. It covers energy sectors through the phases of energy production to end-use, and non-energy sectors, including agriculture, waste, and F-gases (Fig. 1). Emission from land use change is treated as an exogenous scenario.3 A foremost feature of the model is its detailed description of technologies not only in energy supply sectors, but also in energy end-use sectors and non-energy sectors (Table 2). Fig. 1 Overview of AIM/Enduse[Global] Table 2 List of technologies

considered in AIM/Enduse[Global] Sector Category Technology options Power generation Coal Pulverized coal combustion (PCC), PLEKHM2 supercritical PCC (SC-PCC), ultra-supercritical PCC (USC-PCC), advanced ultra-supercritical PCC (AUSC-PCC), integrated gasification combined cycle (IGCC), SC-PCC with carbon capture and storage (CCS), USC-PCC with CCS, AUSC-PCC with CCS, IGCC with CCS Oil Combined cycle (CC) Gas Combined cycle (CC), advanced combined cycle (ACC) [level 1–2], ACC with CCS Renewables Hydropower, wind power [level 1–3], wind power with storage battery [level 1–3], photovoltaics [level 1–4], photovoltaics with storage battery [level 1–4], biomass power plant, biomass IGCC, biomass IGCC with CCS Hydrogen production   Coal, coal with CCS, natural gas, natural gas with CCS, biomass, biomass with CCS Industry Steel Coke oven (e.g., large-sized coke oven, coke gas recovery, automatic combustion, coal wet adjustment, coke dry type quenching, COG latent heat recovery, next generation coke oven), sinter furnace (e.g.