To ascertain whether the SSF-induced upregulation

of NPQ involved similar photoprotective mechanisms in different accessions, photosynthetic pigment composition was analyzed in mature leaves on day 0 and 7. Three accessions, Col-0, C24, and Eri, were chosen for the analysis because they exhibited distinct responses of leaf RGR (Fig. 7): a moderate decrease (Col-0), a strong decrease (Eri, Northern European accession), and an increase (C24, Southern European accession) in SSF 1250/6. In the C50 condition, dark-adapted plants (sampled at the end of the night) of the three accessions were comparable in terms of leaf Chl content (Fig. 8a), Chl a to Chl b ratio (Chl a/b; Fig. 8b) and pool size of the xanthophyll-cycle pigments V, A and Z (V + A + Z; Fig. 8c). A 5-min exposure of the dark-adapted plants to ca.

1,000 μmol photons m−2 s−1 (as was applied for the measurements of DAPT solubility dmso the maximal NPQ in Fig. 6) strongly 3-deazaneplanocin A supplier increased the de-epoxidation state of the xanthophyll-cycle pigments (DPS = (A + Z)/(V + A + Z); Fig. 8d) in all plants. These pigment parameters change in leaves of a variety of Selleck EPZ5676 species during HL acclimation (Demmig-Adams and Adams 1992; Matsubara et al. 2009), including Arabidopsis (Ballottari et al. 2007; Kalituho et al. 2007), or tropical rainforest plants under sunfleck/gap conditions (Logan et al. 1997; Watling et al. 1997b; Adams et al. 1999; Krause et al. 2001). Fig. 8 Changes in leaf pigment composition of Col-0, C24 and Eri. a Total chlorophyll content. b Chlorophyll a to chlorophyll b ratio. c Pool size of the xanthophyll-cycle pigments. Leaf samples for a–c were harvested at the end of the night Chorioepithelioma period on day 0 (all plants under C 50) and day 7 (C 50 or SSF 1250/6). None of the leaves contained A or Z except a single SSF sample of Col-0 in which a small amount of A was detected on day 7. d De-epoxidation state (DPS) of the xanthophyll-cycle pigments after 5-min exposure to 1,000 μmol photons m−2 s−1. The DPS was calculated as (A + Z)/(V + A + Z). For

each accession, asterisks indicate significant differences (**P < 0.01; *P < 0.05) between day 0 (C 50) and day 7 of SSF 1250/6; plus signs indicate significant differences (++ P < 0.01; + P < 0.05) between C 50 and SSF 1250/6 on day 7. Data are means of 3~4 plants (±SE) The SSF 1250/6 treatment decreased the Chl content in all three accessions (Fig. 8a), which was accompanied by somewhat increased Chl a/b for Col-0 and C24, but not for Eri (Fig. 8b). The levels of V + A + Z relative to Chl increased by 20, 27, and 17 % in Col-0, C24, and Eri, respectively (Fig. 8c). The concentrations of other carotenoids (β-carotene, lutein, and neoxanthin) were similar in the three accessions and did not change significantly in SSF 1250/6 by day 7 (data not shown).

Separation of this PCR by gel electrophoresis revealed two products that were approximately 250 and 410 base

pairs (Fig. 6A; lane 3). The bands were gel extracted and sequenced. Sequence analysis of the lower band showed this product was from mispriming of the oligo dC-anchor primer to three guanosines located 160 to 162 base pairs downstream of the chbC translational start site (data not shown). Comparison of the sequences from the upper dG-tailed product (Fig. 6C) and the dA-tailed product (Fig. 6B) revealed the chbC transcriptional start site 42 base pairs upstream of the translational start site. Figure 6 Determination of the chbC transcriptional start site. The chbC transcriptional start site was determined by 5′ RACE analysis. (A) One percent TAE agarose gel of the 5′ RACE products. A 1 kb ladder was used as a size standard (lane 1) for comparison of 5′ RACE products (lane Selleck MM-102 2, dA-tailed

product; lane 3, dG-tailed product). (B) DNA sequence of the dA-tailed 5′ RACE product showing the ambiguous chbC transcriptional start site (enlarged font). (C) DNA sequence of the dG-tailed 5′ RACE product showing the chbC transcriptional start site (enlarged font). Sequences were determined using the anti-sense primer BBB04 5′ RACE R2. Identification of the chbC transcriptional start site allowed us to identify FG-4592 purchase the -10 and -35 promoter regions by visual inspection of the upstream sequence (Fig. 7). Further analysis of the promoter region was conducted

by comparing the putative chbC promoter to previously described B. burgdorferi promoters controlled by RpoD, RpoS and RpoN (Fig. 7). Recently, EPZ004777 molecular weight Caimano et al [21] evaluated the RpoS regulon in B. burgdorferi by microarray and qRT-PCR expression analysis and identified genes that were absolutely RpoS-dependent as well as genes that were dually transcribed by RpoS and at least one of the other sigma factors in B. burgdorferi. Analysis of the promoter region from ten absolutely RpoS-dependent genes allowed them to identify a putative RpoS consensus -10 and -35 sequence (Fig. 7). In addition, they attempted to identify the promoter regions for Endonuclease 10 dually transcribed genes, but were only able to find putative promoter elements for five of the genes which were highly similar to the consensus sequence generated from the absolutely RpoS-dependent genes. We used these five putative promoters to generate a dually transcribed -10 and -35-consensus sequence for comparison to our newly identified chbC promoter region (Fig. 7), as results presented above strongly suggest that this gene is dually regulated by RpoS and RpoD. Additionally, we generated a consensus RpoD-dependent promoter sequence for comparison (Fig. 7) based on seven genes identified in the literature [22–27]. Figure 7 Identification of the chbC promoter.

Iijima R, Kurata S, Natori S: Purification, characterization, and cDNA cloning of an antifungal protein from the hemolymph of Sarcophaga peregrina (flesh fly) larvae. J Biol Chem 1993, 268:12055–12061.PubMed 15. Lüders T, Birkemo GA, Fimland G, Nissen-Meyer J, Nes IF: Strong synergy between a eukaryotic antimicrobial peptide and bacteriocins from lactic acid bacteria. Appl Environ Microbiol 2003, 69:1797–1799.PubMedCrossRef 16. Kobayashi S, Hirakura Y, Matsuzaki K: Bacteria-selective synergism between the antimicrobial peptides

alpha-helical magainin 2 and cyclic beta-sheet tachyplesin I: toward cocktail therapy. Biochemistry 2001, 40:14330–14335.PubMedCrossRef 17. Chalk R, Albuquerque CM, Ham PJ, Townson H: Full sequence and characterization of two insect Selumetinib defensins: immune peptides from the mosquito Aedes aegypti . Proc Biol Sci 1995, 261:217–221.PubMedCrossRef 18. Yan H, Hancock REW: Synergistic interactions between mammalian antimicrobial defense peptides. this website Antimicrob Agents Chemother 2001, 45:1558–1560.PubMedCrossRef 19. Polak J, Della Latta P, Blackburn P: In vitro activity of recombinant lysostaphin-antibiotic combinations toward methicillin-resistant Staphylococcus aureus . Diagn Microbiol Infect Dis 1993, 17:265–270.PubMedCrossRef 20. Graham S, Coote PJ: Potent, synergistic inhibition of Staphylococcus aureus upon exposure https://www.selleckchem.com/products/8-bromo-camp.html to a combination

of the endopeptidase lysostaphin and the cationic peptide ranalexin. J Antimicrob Chemother 2007, 59:759–762.PubMedCrossRef 21. Pillai A, Ueno S, Zhang

H, Lee JM, Kato Y: Cecropin P1 and novel nematode cecropins: a bacteria-inducible antimicrobial peptide family through in the nematode Ascaris suum . Biochem J 2005, 390:207–214.PubMedCrossRef 22. Ueno S, Kusaka K, Tamada Y, Minaba M, Zhang H, Wang PC, Kato Y: Anionic C-terminal proregion of nematode antimicrobial peptide cecropin P4 precursor inhibits antimicrobial activity of the mature peptide. Biosci Biotechnol Biochem 2008, 72:3281–3284.PubMedCrossRef 23. Kato Y, Komatsu S: ASABF, a novel cysteine-rich antibacterial peptide isolated from the nematode Ascaris suum: purification, primary structure, and molecular cloning of cDNA. J Biol Chem 1996, 271:30493–30498.PubMedCrossRef 24. Zhang H, Yoshida S, Aizawa T, Murakami R, Suzuki M, Koganezawa N, Masuura A, Miyazawa M, Kawano K, Nitta K, Kato Y: In vitro antimicrobial properties of recombinant ASABF, an antimicrobial peptide isolated from the nematode Ascaris suum . Antimicrob Agents Chemother 2000, 44:2701–2705.PubMedCrossRef 25. Pillai A, Ueno S, Zhang H, Kato Y: Induction of ASABF ( Ascaris suum antibacterial factor)-type antimicrobial peptides by bacterial injection: novel members of ASABF in the nematode Ascaris suum . Biochem J 2003, 371:663–668.PubMedCrossRef 26. Sims PJ, Waggoner AS, Wang CH, Hoffman JF: Studies on the mechanism by which cyanine dyes measure membrane potential in red blood cells and phosphatidylcholine vesicles. Biochemistry 1974, 13:3315–3329.PubMedCrossRef 27.

Although the virus has not been linked to illness in humans, GSK2118436 order many studies have suggested that the virus is a latent pathogen of humans causing a fever of unknown origin. GETV could cause illnesses in humans and livestock animals and, indeed, antibodies to GETV have been detected in many species of animals around the world [4–6]. Analysis of all sequences

included in this study showed that the nsP3 non-structural protein gene and the capsid protein gene nucleotide sequence identity between YN08 isolates and other Chinese isolates (GETV_M1 [12], ALPV_M1, HB0234 and YN0540) ranged from 98.0 to 99.31% and 97.56 to 99.31%, respectively. Multiple alignments showed that the S_Korea isolate does not possess the 92 nt sequence from 11341–11433 in the virus genome and there was a low level of identity (92.19–93.75%) between S_Korea and other GETV strain at the 3’-UTR sequences. Despite possessing 3’-UTR sequences of different lengths, GETV isolates contain various numbers of an identical sequence element that could have originated Dibutyryl-cAMP mouse from a large ancestral 3’-UTR [26, 27]. Phylogenetic trees constructed using viruses sequence data are the best indication of the evolutionary

relationships between viruses and genetic changes associated with antigenic drift. To provide further insight into the evolutionary relationship of YN08 and other alphaviruses, phylogenic analysis was performed based on the capsid protein gene and the 3’-UTR sequence of YN08 and other 9 alphaviruses. These analyses showed that YN08 is a member of the GETV and was most Fulvestrant datasheet closely related to HB0234 and S_Korea and then with YN0540 and GETV_LEIV_17741_MPR to form a distinguishable branch based on nsP3 and capsid protein genes. Thus, the phylogenetic analysis clearly showed that YN08 is more closely related to Hebei HB0234 strain than YN0540 strain and

more genetically distant to the MM2021 Malaysia primitive strain. Present methods rely on prior genetic knowledge but are not effective for the identification of unknown viruses. Thus, we developed the simple VIDISCR method based on the cDNA-RAPD technique [8, 9]. The RAPD technique is a type of PCR but random segments learn more of DNA are amplified. Unlike traditional PCR analysis, RAPD does not require any specific knowledge of the DNA sequence of the target organism by the use of 10-mer primers for the amplification of DNA. However, the resolving power of the VIDISCR method is prone to interference from DNA or RNA from the lysed host tissues and cells (or bacteria). Since VIDISCR relies on a large, intact DNA template sequence, it has some limitations in the use of degraded DNA samples. Therefore, the intact DNA template sequence of virus genomes required and chromosomal DNA, mitochondrial DNA, and cellular RNA must be removed from the preparation to perform VIDISCR.

Firstly, we focused on the effect of different substrate temperatures as shown in the SEM images of Figure 1a,b,c,d. Figure 1a shows the case with the substrate temperature of 750°C ~ 800°C, where many nanoparticles and few nanowires were found on silicon substrates. AC220 Figure 1b

shows the case with the substrate temperature of 800°C ~ 850°C, where there were many nanoparticles larger in size than those found in Figure 1a and few nanowires on silicon substrates. When we increased the substrate temperature to 850°C ~ 880°C as shown in Figure 1c, lots of nanowires of about 15 ~ 20 μm in length and few larger nanoparticles appeared. Figure 1d shows the case with the substrate temperature of 880°C ~ 900°C, where on silicon substrates, we can see many nanowires as well but they are of different morphologies as compared in Figure 1c. For further investigation on the atomic PRT062607 research buy structures of the nanowires, we conducted TEM analysis as shown in Figure 2. It has been confirmed that the

nanowires on 850°C ~ 880°C Avapritinib substrates are single-crystal CoSi nanowires with 10 ~ 20 nm SiOx as an outer layer as shown in Figure 2a. The high-resolution TEM image in Figure 2b and the corresponding selected area diffraction pattern in its inset show that the single-crystal CoSi nanowire has a cubic B20-type structure with a lattice constant of 0.4446 nm; also, the growth direction is [211], and the interplanar distance of (211) is 0.1816 nm. Figure 2c is an energy-dispersive X-ray spectroscopy (EDS) spectrum for the nanowires showing that in addition to cobalt and silicon, there is also oxygen and that the atomic percentage ratio for Co/Si/O = 5:8:12. Since the

core structure has been identified to be CoSi, all these results reasonably indicate that the shell material click here is amorphous silicon oxide. On 880°C ~ 900°C substrates, Figure 2d shows a single-crystal Co2Si nanowire without surface oxide. The high-resolution TEM image in Figure 2e and the corresponding selected area diffraction pattern in its inset show that the single-crystal Co2Si nanowire has an orthorhombic structure with [002] growth direction and lattice constants of a = 0.4918 nm, b = 0.7109 nm, and c = 0.3738 nm and that the interplanar distances of plane (002) and plane (310) are 0.187 and 0.213 nm, respectively. Figure 2f shows an EDS spectrum indicating that the ratio of Co and Si is close to 2:1. Figure 1 SEM images of as-synthesized nanowires. At silicon substrate temperatures of (a) 750°C ~ 800°C, (b) 800°C ~ 850°C, (c) 850°C ~ 880°C, and (d) 880°C ~ 900°C, respectively. Figure 2 TEM images and EDS spectra of cobalt silicide nanowires. (a) Low-magnification, (b) high-resolution TEM images and (c) EDS spectrum of CoSi nanowires grown at 850°C ~ 880°C. The inset in (b) shows the corresponding selected area diffraction pattern with a zone axis of [0-11].

Zhang and colleagues [22] identified MNT, a known MYC antagonist, as a miR-210 target. Overexpression of miR-210 can override hypoxia-induced cancer cell cycle arrest and promote cell proliferation by down-regulating MNT directly and activating PX-478 molecular weight c-MYC indirectly. Similarly but in a different way, Yang and colleagues [27] demonstrated that downregulation of miR-210 in hypoxic

human hepatoma cells induced cell cycle arrest in the G0/G1, resulting in reduced cancer cell proliferation. However, functional targets of miR-210 contributing to such effect require further researches. miR-210 inhibits apoptosis and protects cancer cell Hypoxic cancer cells are notorious for their resistance to radiotherapy and many conventional chemotherapeutic agents, of which the underlying mechanisms remain to be revealed [3]. As the master HRM, the association

of miR-210 and apoptosis as well as cell survival was intensively investigated. Its antiapoptotic and cytoprotective effects have been demonstrated in many studies involving not only cancer cells [27, 60, 61] but also normal cells Savolitinib such as human pulmonary artery smooth muscle cells (HPASMC) [32], cardiomyocytes [24, 33], bone marrow-derived mesenchymal stem cells (MSCs) [31], as well as neural progenitor cells [36]. Many functional targets of miR-210 associated with apoptosis have been identified, as shown in Table 1. By downregulating the expression of caspase-8-associated protein-2 (Casp8ap2), miR-210 promoted the survival of MSCs that underwent ischemic preconditioning [31]. Through repressing the expression of regulator of differentiation 1 (ROD1), which is also named polypyrimidine Methocarbamol tract binding protein 3 (PTBP3), miR-210 reduced the apoptosis of hypoxic cells and increased the survival of hypoxic cells [61]. E2F3, a member of the E2F family of transcriptional factors and a well-known cell cycle regulator, was identified as a direct target of miR-210 in hypoxic HPASMC, its downregulation was shown to be responsible in part for the antiapoptotic effect of miR-210 [32]. Knock down

of miR-210 in hypoxic HPASMC, which resulted in concomitant upregulation of E2F3, induced apoptosis without significant change of cell proliferation, indicating the proapoptotic effect of E2F3 as well as the antiapoptotic effect of miR-210 in HPASMC under 3-MA research buy hypoxia stress [32]. The cytoprotective effect of miR-210 against radiotherapy was also investigated. Overexpression of miR-210 in A549 cell line (non-small cell lung carcinoma-derived cell line) under normoxia can protect cancer cells from radiation [57], while downregulation of miR-210 in hypoxic human hepatoma cells led to increased radiosensitivity, both in vitro and in vivo [27, 62]. As elucidated by Grosso et al., A549 cells stably expressing miR-210 in normoxia exhibited similar radioresistance to A549 cells expressing miR-control in hypoxia, and hypoxia can further increase this resistance.

CD44 is a key receptor for hyaluronan, critical for cell signalling and drug resistance. We investigated the expression of CD147, CD44, and transporter (MDR1) and MCT proteins in CaP progression. Methods: CD147, CD44s and v3-10, MDR1, MCT1 and MCT4 expression was studied in human metastatic CaP cell lines (PC-3 M-luc(MDR), PC-3 M-luc, Du145, LN3, click here DuCaP) and primary CaP tumours, lymph node metastases and normal prostate, using immunoperoxidase, immunofluorescence and microscopy. Cell line dose-response and sensitivity (IC50) to docetaxel was measured with

MTT, and correlated with CD147, CD44, MDR1, and MCT expression. Results: PC-3 M-luc (MDR), PC-3 M-luc and Du145 cells expressed high level CD147, CD44, MDR1 and MCT. In contrast, DuCaP cells showed no CD147 or CD44, but weak MCT immunostaining. LN3 cells expressed

strong CD147 and MCT, weak CD44v and MDR1, and no CD44s. Docetaxel sensitivity was positively related to CD44, CD147, MDR1 and MCT expression. Strong heterogeneous CD147, CD44, MDR1, MCT expression was found in high grade primary tumours (Gleason score >7). Heterogeneous co-localization of CD147 with CD44, MDR1 and MCT was found in PC-3 and Du145 cells, and in high grade tumours. Conclusions: Metastatic CaP cell lines and primary CaP displayed overxpression of CD147, CD44, MDR1, MCT proteins. Interactions between Regorafenib purchase these proteins could contribute to the development of CaP drug resistance and metastasis. Selective targeting of CD147 and CD44 to block their activity (alone or combined) may limit tumour metastasis, and increase drug sensitivity by modifying expression of MDR and MCT proteins. Poster No. 185 Metallic Ion Composition Discriminates between Normal Esophagus, Dysplasia, and Carcinoma Daniel Lindner 1 , Derek Raghavan1, Michael Kalafatis3, Charis Eng2, Gary Falk4 1 Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA, 2 Genomic Medicine Institute, Cleveland Clinic, Cleveland, OH, USA, 3 Department of Chemistry, Cleveland State University, Cleveland, OH, USA,

4 Digestive Disease Institute, Cleveland Clinic, Cleveland, OH, USA Subtractive hybridization, and more recently, whole genome expression arrays pentoxifylline have advanced our understanding of differential gene expression in neoplastic compared to normal tissues, leading to identification of several important oncogenes as well as tumor suppressor genes. We hypothesized that such changes in gene expression would not only result in differential protein expression profiles, but would also ultimately result in detectable differences in the ionic composition of normal, dysplastic, and neoplastic tissues. In a blinded fashion, we utilized SU5402 nmr atomic absorption (AA) to analyze the metallic ion composition (iron, zinc, copper, chromium, magnesium, and manganese) in normal human esophagus, low grade dysplasia, intestinal metaplasia (Barrett’s esophagus), high grade dysplasia, and carcinoma.

Following exposure to human monocyte-derived macrophages, M. genitalium was killed rapidly and elicited a potent pro-inflammatory 3-deazaneplanocin A response including secretion of cytokines associated with enhanced HIV-1 replication. These are the first data showing that cultured human vaginal and cervical ECs are susceptible and immunologically responsive to M. genitalium infection likely inducing cellular immune responses to infected tissues. Continued investigation of whether intracellular

localization in reproductive tract ECs provides protection from the cellular immune response is warranted but rapid invasion of vaginal ECs, combined with the low immunological response, provides evidence for how M. genitalium might efficiently establish reproductive tract infection. Acknowledgements The authors thank Dr. Tonyia Eaves-Pyles and Michelle Kirtley from the UTMB Department of Microbiology and Immunology for their assistance with macrophage isolation. We also thank Violet Han and Julie Wen for their assistance in sample preparation for electron microscopy. We are grateful to Nicole Arrigo for critical reading of the manuscript. This work was supported by the Gulf South Sexually

Transmitted Infection/Topical Microbicide Cooperative Research Center grant Epigenetics inhibitor NIH-NIAID; U19 AI061972. References 1. Hjorth SV, Bjornelius E, Lidbrink P, Falk L, Dohn B, Berthelsen L, Ma L, Martin DH, Jensen JS: Sequence-based typing of Mycoplasma genitalium reveals PRIMA-1MET sexual transmission. J Clin Microbiol 2006,44(6):2078–2083.CrossRefPubMed Atezolizumab 2. Manhart LE, Holmes KK, Hughes JP, Houston LS, Totten PA: Mycoplasma genitalium among young adults in the United States: an emerging sexually transmitted infection. Am J Public Health 2007,97(6):1118–1125.CrossRefPubMed 3. Martin DH: Nongonococcal Urethritis: New Views through the Prism of Modern Molecular Microbiology.

Curr Infect Dis Rep 2008,10(2):128–132.CrossRefPubMed 4. Haggerty CL: Evidence for a role of Mycoplasma genitalium in pelvic inflammatory disease. Curr Opin Infect Dis 2008,21(1):65–69.CrossRefPubMed 5. Falk L, Fredlund H, Jensen JS: Signs and symptoms of urethritis and cervicitis among women with or without Mycoplasma genitalium or Chlamydia trachomatis infection. Sex Transm Infect 2005,81(1):73–78.CrossRefPubMed 6. Manhart LE, Critchlow CW, Holmes KK, Dutro SM, Eschenbach DA, Stevens CE, Totten PA: Mucopurulent cervicitis and Mycoplasma genitalium. J Infect Dis 2003,187(4):650–657.CrossRefPubMed 7. Pepin J, Labbe AC, Khonde N, Deslandes S, Alary M, Dzokoto A, Asamoah-Adu C, Meda H, Frost E: Mycoplasma genitalium: an organism commonly associated with cervicitis among west African sex workers. Sex Transm Infect 2005,81(1):67–72.CrossRefPubMed 8. Uno M, Deguchi T, Komeda H, Hayasaki M, Iida M, Nagatani M, Kawada Y: Mycoplasma genitalium in the cervices of Japanese women. Sex Transm Dis 1997,24(5):284–286.CrossRefPubMed 9.

This experiment proved the absence of the fmt gene and showed that polypeptide deformylase, which has no substrates in the mutant is downregulated in OICR-9429 price Δfmt (Table  1). In addition, genes from several metabolic pathways were downregulated in Δfmt indicating that the absence of formylated proteins has pleiotrophic effects on transcription, which results probably either from dysfunctional regulatory proteins or from regulatory feedback events in metabolic pathways depending on formylated enzymes (see below). Table 1

Genes involved in metabolic processes differentially regulated by fmt deletion in S. aureus RN4220 under (A) aerobic or (B) anaerobic growth conditions Gene IDa,b Nameb Gene productb x-fold change A Reduced expression in Δ fmt compared to wild type: Amino acid metabolism 01452 ald alanine dehydrogenase 103.1 00008 hutH histidine ammonia-lyase 67.1 01451 ilvA threonine dehydratase 39.8 00899 argG argininosuccinate synthase 22.5 00435 gltB glutamate synthase, large subunit, putative 21.8 02468 alsS acetolactate synthase 14.1 00558   acetyl-CoA acetyltransferase, putative 12.2 01497 ansA L-asparaginase, putative 7.6 01450   amino acid permease* 6.4 00081   HPCH-HPAI aldolase family protein* 4.6 02287 leuC 3-isopropylmalate dehydratase, Cobimetinib manufacturer large subunit

4.4 02574   NAD-NADP octopine-nopaline dehydrogenase family protein* 3.8 01450   amino acid permease* 3.2 02281 ilvD dihydroxy-acid dehydratase 3.2 02839   L-serine dehydratase, iron-sulfur-dependent, alpha subunit 2.9 00510 cysE serine acetyltransferase, putative 2.8 00147   acetylglutamate kinase, putative 2.5 02563 ureF Fossariinae urease accessory protein, putative 2.3 02723   glycerate kinase, putative 2.2 Protein biosynthesis 01183 fmt methionyl tRNA formyltransferase 585.8 01182 def2* polypeptide deformylase (def2*) 6.3 01839 tyrS tyrosyl-tRNA synthetase 2.8 00324   ribosomal-protein-serine acetyltransferase, putative 2.4 01738 hisS histidyl-tRNA synthetase 2.4 Folic acid metabolism 01183 fmt methionyl tRNA formyltransferase 585.8 02374   aminobenzoyl-glutamate utilization protein B, putative 4.5 02610 hutG

formiminoglutamase 3.4 Fermentation 00188 pflA formate acetyltransferase activating enzyme 604.5 02830 ddh D-lactate dehydrogenase, putative 263.6 00187 pflB formate acetyltransferase (pyruvate-formate-lyase) 99.0 00608 adh1 alcohol dehydrogenase I, putative 74.0 00113 adhE alcohol dehydrogenase, iron-containing 40.8 02467 budA2 alpha-acetolactate decarboxylase 2.6 02875   L-lactate dehydrogenase, putative 2.3 Purine metabolism 02553   inosine-uridine preferring nucleoside hydrolase* 3.3 00211   inosine-uridine preferring nucleoside hydrolase* 3.3 Lipid biosynthesis 01278 glpD aerobic glycerol-3-phosphate dehydrogenase 14.7 Transport Pritelivir in vitro systems 00748   iron compound ABC transporter, ATP-binding protein, putative* 15.0 03019   ABC transporter, ATP-binding protein, putative 7.2 01991   ABC transporter, permease protein, putative 7.

CrossRef 7. Hassan NK, Hashim MR, Allam NK: Low power UV photodetection characteristics of cross-linked ZnO nanorods/nanotetrapods grown on silicon chip. Sens Actuator A Phys 2013, 192:124–129.CrossRef 8. Shinde SS, Rajpure KY: Fabrication and performance of N-doped ZnO UV photoconductive detector. J Alloy Compd 2012, 522:118–122.CrossRef 9. Mehrabian M, Azimirad R, Mirabbaszadeh K, Selleckchem Sapitinib Afarideh H,

Davoudian M: UV detecting properties of hydrothermal synthesized ZnO nanorods. Phys E 2011, 43:1141–1145.CrossRef 10. Chang SP, Chuang RW, Chang SJ, Lu CY, Chiou YZ, Hsieh SF: Surface HCl treatment in ZnO photoconductive sensors. Thin Solid Films 2009, 517:5050–5053.CrossRef 11. Jandow NN, Yam FK, Thahab SM, Abu Hassan H, Ibrahim K: Characteristics FHPI of ZnO MSM UV photodetector with Ni contact electrodes on poly propylene carbonate (PPC) plastic substrate. Curr Appl Phys 2010, 10:1452–1455.CrossRef 12. Gupta V, Menon R, Sreenivas K: Enhanced ultraviolet photo-response of nanostructure Buparlisib zinc oxide (ZnO) thin film irradiated with pulsed laser. In Proceedings of the Conference on Optoelectronic and Microelectronic Materials and Devices: July 28–Aug 1 2008; Sydney, Australia. Edited by: IEEE. Piscataway: IEEE; 2008:55–88.CrossRef 13. Zhang CY: The influence of post-growth annealing on optical and electrical

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connected ZnO rods grown on porous silicon substrate. Sens Actuator A Phys 2012, 180:11–14.CrossRef 16. Chai GY, Chow L, Lupan O, Rusu E, Stratan GI, Heinrich H, Ursaki VV, Tiginyanu IM: Fabrication and characterization of an individual ZnO microwire-based UV photodetector. Solid State Sci 2011, 13:1205–1210.CrossRef 17. Abbasi MA, Ibupoto ZH, Khan A, Nur O, Willander M: Fabrication of UV photo-detector based on coral reef like p-NiO/n-ZnO nanocomposite structures. Mater Lett 2013, 108:49–152.CrossRef 18. Chao LC, Ye CC, Chen YP, Yu H-Z: Facile fabrication of ZnO nanowire-based UV sensors by focused ion beam micromachining and thermal oxidation. Appl Surf Sci 2013, 282:384–389.CrossRef 19. Chen KJ, Hung FY, Chang SJ, Young SJ: Optoelectronic characteristics of UV photodetector based on ZnO nanowire thin films. J Alloy Compd 2009, 479:674–677.CrossRef 20. Lupan O, Chow L, Chai G: A single ZnO tetrapod-based sensor. Sens Actuator B Chem 2009, 141:511–517.CrossRef 21. Panigrahi S, Basak D: Morphology driven ultraviolet photosensitivity in ZnO–CdS composite. J Colloid Interface Sci 2011, 364:10–17.CrossRef 22. Xu Z-Q, Deng H, Xie J, Li Y, Zu X-T: Ultraviolet photoconductive detector based on Al doped ZnO films prepared by sol–gel method. Appl Surf Sci 2006, 253:476–479.CrossRef 23.