Eukaryot Cell 6:1656–1664PubMed Sikora RA, Pocasangre L, zum Feld

Eukaryot Cell 6:1656–1664PubMed Sikora RA, Pocasangre L, zum Felde A, Niere B, Vu TT, Dababat AA (2008) Mutualistic endophytic fungi and in-planta

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Finkelstein EA, Trogdon JG, Cohen JW, Dietz W: Annual medical spe

Finkelstein EA, buy EPZ-6438 Trogdon JG, Cohen JW, Dietz W: Annual medical spending attributable to obesity: payer- and service-specific estimates. Health Aff (Millwood) CB-839 research buy 2009, 28:822–831.CrossRef 2. Hogan P, Dall T, Nikolov P: Economic costs of diabetes in the U.S. in 2002. Diabetes Care 2003, 26:917–932.PubMedCrossRef 3. World Health Organization:

World Health Organization Consultation on Obesity. WHO, Geneva; 2000. 4. Boyle J, Honeycutt A, Narayan K, Hoerger T, Geiss L, Chen H, Thompson T: Projection of diabetes burden through 2050: impact of changing demography and disease prevalence in the U.S. Diabetes Care 2001, 24:1936–1940.PubMedCrossRef 5. Mokdad A, Bowman B, Ford E, Vinicor F, Marks J, Koplan J: The continuing epidemics of obesity and diabetes in the United States. J Am Med Assoc 2001, 286:1195–1200.CrossRef 6. Dommarco selleck products JR, Cuevas Nasu L, Shamah Levy T, Villalpando Hernández S, Avila Arcos MA, Jiménez Aguilar A: Nutrición. In Encuesta Nacionalde Saludy Nutrición. Instituto Nacional de Salud Pública, Cuernavaca, Mexico; 2006. 7. Villalpando Hernandez S, Cruz V, Rojas R, Shamah Levy T, Ávila MA, Berenice

Gaona B, Rebollar Hernández L: Prevalence and distribution of type 2 diabetes mellitus in Mexican adult population. A probabilistic survey. Salud Pública de México 2010, 52:19–26.CrossRef 8. DeFronzo RA: Lilly Lecture: The triumvirate: cell, muscle, liver: a collusion responsible for NIDDM. Diabetes 1988, 37:667–687.PubMed 9. Reaven GM: Role of insulin resistance

in human disease. Diabetes 1988, 37:1595–1607.PubMedCrossRef ifenprodil 10. Abdul-Ghani M, DeFronzo RA: Inhibition of renal glucose reabsorption: a novel strategy for achieving glucose control in type 2 diabetes mellitus. Endocr Pract 2008, 14:782–790.PubMed 11. Boden G, Shulman GI: Free fatty acids in obesity and type 2 diabetes: defining their role in the development of insulin resistance and β-cell dysfunction. Eur J Clin Invest 2002,32(Suppl 3):14–23.PubMedCrossRef 12. DeFronzo RA: From the triumvirate to the ominous octet: A new paradigm for the treatment of type 2 Diabetes Mellitus. Diabetes 2009, 58:773–795.PubMedCrossRef 13. Matsuda M, DeFronzo RA, Glass L, Consoli A, Giordano M, Bressler P, Del Prato S: Glucagon dose response curve for hepatic glucose production and glucose disposal in type 2 diabetic patients and normal individuals. Metabolism 2002, 51:1111–1119.PubMedCrossRef 14. Matsuda M, Liu Y, Mahankali S, Pu Y, Mahankali A, Wang J, DeFronzo RA, Fox PT, Gao JH: Altered hypothalamic function in response to glucose ingestion in obese humans. Diabetes 1999, 48:1801–1806.PubMedCrossRef 15. Reaven GM, Chen YD, Golay A, Swislocki AL, Jaspan JB: Documentation of hyperglucagonemia throughout the day in nonobese and obese patients with noninsulin-dependent diabetes mellitus. J Clin Endocrinol Metab 1987, 64:106–110.PubMedCrossRef 16. Unger RH: Lipotoxic diseases. Annu Rev Med 2002, 53:319–336.PubMedCrossRef 17.

Identification of the resistant mechanisms, particularly a novel

Identification of the resistant mechanisms, particularly a novel mechanism, is

important for the development of surrogate markers that can be combined with other known resistance determinants to improve the rapid detection of drug-resistant M. tuberculosis strains. Methods Mycobacterial strains and culture conditions Mycobacterium tuberculosis clinical strains (one strain per Belinostat mouse patient) were obtained from the Drug-Resistant Tuberculosis Research Laboratory, Drug-Resistant Tuberculosis Research Fund, Siriraj Foundation, Faculty of Medicine Siriraj Hospital, Mahidol University. They were isolated between 2004 and 2011 from new and previously treated patients with both known and unknown HIV status. This study was approved by the Siriraj Ethics Committee, Mahidol University, Bangkok, Thailand (Certificate of Approval No. Si 208/2005). The mycobacteria were cultured on Löwenstein-Jensen (LJ) medium (BBL, Epigenetics Compound Library USA) and incubated

buy Poziotinib at 37°C for 3-4 weeks. Species identification and antimycobacterial susceptibility testing were performed using in-house one-tube multiplex PCR [39] and the standard proportion method [40, 41], respectively. Isolation of genomic DNA One loop of mycobacterial cells grown on solid medium was scraped and suspended in 500 μl of TE buffer (10 mM Tris-HCl (pH8.0), 1 mM EDTA). The cells were inactivated by heating at 80°C for 20 min and subsequently harvested by centrifugation at 6,000xg at 4°C for 10 min. The cells were resuspended in 400 μl of Tris-EDTA-Tween-lysozyme solution (10 mM Tris-HCl (pH 8.0), 1 mM EDTA, 0.5% (v/v) Tween 80, 2 mg/ml lysozyme (Amresco, USA)), and the mixtures were then incubated at 37°C for 3 h. SDS and proteinase K were added to the cell suspension to generate final concentrations of 1% (w/v) and 1 mg/ml, respectively, prior to incubation at 37°C for 1 h. Then, 80 μl of 5 M NaCl and 80 μl of 10% (w/v) cetyl trimethyl ammonium bromide (CTAB) (Sigma, USA) were added to the suspension, and the suspension was immediately heated at 65°C for 15 min. An equal volume of chloroform-isoamyl

L-NAME HCl alcohol (24:1) (v/v) was added to the suspension. The aqueous DNA phase was separated by centrifugation at 12,000xg for 5 min and mixed again with an equal volume of chloroform-isoamyl alcohol (24:1) (v/v). DNA was precipitated by adding 0.1 volume of 3 M sodium acetate (pH 5.3) and 2.5 volumes of ice-chilled absolute ethanol, followed by incubation at -70°C for 30 min. DNA was separated by centrifugation at 12,000xg at 4°C for 15 min. Total nucleic acid was washed once with 500 μl of ice-chilled 70% ethanol, dried, and resuspended in 20 μl of TE buffer. RNaseA (Qiagen, Germany) was added to the total nucleic acid solution to generate a final concentration of 0.5 μg/μl, and the tube was subsequently incubated at 37°C for 1 h.

Lnd Eng Chem 1936, 28:988–990 21 Xue ZX, Wang ST, Lin L, Chen L

Lnd Eng Chem 1936, 28:988–990. 21. Xue ZX, Wang ST, Lin L, Chen L, Liu MJ, Feng L, Jiang L: A novel superhydrophilic

and underwater superoleophobic hydrogel-coated mesh for oil/water separation. Adv Mater 2011, 23:4270–4273.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions HL participated in the design of the study, carried out the experiments, performed the statistical analysis, and drafted the manuscript. YSL participated in the design of the study. QZL revised the manuscript. All authors read and approved the final manuscript.”
“Background Metastable intermolecular composites (MICs) are often composed of aluminum mTOR inhibitor review nanoparticles (the fuel is usually manufactured with a shell of alumina on each particle) and some oxidizer nanoparticles including CuO [1–12], Fe2O3[13–15], Bi2O3[5, 16],

MoO3[5, 17, 18], and WO3[5, 19, 20]. These MICs have drawn much attention recently in developing reliable SRT1720 in vivo and high-performance power selleck chemical generation systems due to their nanosized components which allow for the tuning of ignition temperature, reaction propagation rate, and volumetric energy density [12, 17, 21–24]. Applications include gas generators, micro-heaters, micro-thrusters, micro-detonators, and micro-initiators [25]. MICs can be used to fabricate an insert element which is assembled into the conventional solid propellants. This approach helps adjust ignition timing and enhance combustion propagation. However, the challenge remains in identifying a suitable MIC candidate for providing an optimal energetic performance which matches with the properties

of the solid propellants. Generally speaking, better control of the initiation process requires a sufficient heat production rate from the MIC core and a relatively slow pressure increase at the interface between the MIC core and the solid propellant. Gasless thermite reactions are desired for this reason. Gas generation from the thermite reactions is mainly attributed to the formation of vapors of metals (such as Cu, Fe, and Ni), the elemental oxygen (formed from the decomposition of the oxidizer), the gas of metal oxides if the combustion temperature is high enough, and other gaseous Fossariinae reaction products. While the metal vapor forms at a temperature which is above the boiling temperature of the metal, the release of elemental oxygen from the decomposition of the oxidizer component of MICs can be significant as well. Recently, Sullivan and Zachariah characterized the reaction mechanism of a variety of MICs [26], and they found that, while most oxidizers such as CuO and SnO2 decompose before the thermite reactions occur, which possibly indicates solid-state reactions, the decomposition of Fe2O3 becomes rate-limiting for igniting its thermite reaction. More investigations are needed in order to understand the cause of these different ignition mechanisms. Among the bulk scale thermite reactions, the Al-NiO system was reported to produce less gas [27].

And third, phenotype prediction in female foetuses with a full mu

And third, phenotype prediction in female foetuses with a full mutation is difficult, if not impossible. Cascade screening may be a more acceptable approach to identify female carriers of FXS (De Jong and De Wert 2002; De Wert 2005). An important advantage being that one starts from (a patient with)

a disease-causing allele, allowing for more straightforward genetic counseling. With regard to PCS for CF, the apparent lack of international buy CH5183284 consensus is reflected in a recent European consensus document that only provides a template for further debate (Castellani et al. 2010). The reasons behind this include the fact that due to the large number of CFTR mutations, CF carrier tests have a less than perfect sensitivity and also that for many mutations the genotype–phenotype correlation is weak. However, in a Dutch study, it was found that PCS for CF would in principle fulfil the requirements of the normative framework (Henneman et al. 2002). Screening in the

context of reproduction is especially sensitive as it may affect decision making with regard to having or avoiding to have children with a disease or disability. It is far from imaginable that as a result of offering such screening, these choices will come under pressure as to what professionals or society would like to see happen. That is indeed the concern behind the charges of eugenics and medicalization

briefly discussed in the beginning of this section. As suggested, the Proteasome inhibitor only way to answer this is through safeguards that protect reproductive freedom. Some of those safeguards will need to be integrated in the set-up of the programme. These include adequate provisions for ensuring voluntary, well-informed decision making regarding participation in PCS, the availability of non-directive counseling (within the limits earlier referred to), and a systematic evaluation aimed at identifying and removing elements of unjustified directivity. Other safeguards will have to crotamiton be of a societal nature, including the continued availability and funding of proper health care services for children born with the diseases targeted in PCS, also when their parents had the option to choose to avoid their birth (Human Genetics Commission 2011). Modes of offering carrier screening Carrier screening may be offered either in pregnancy or preconceptionally, and if preconceptionally, either to couples with possible reproductive plans or to all individuals of (pre-)reproductive age. Which of these learn more approaches is more in line with the proportionality requirement of the normative framework will to a large extent also depend on whether prevention or autonomy is taken as the overarching objective. In terms of enabling reproductive choices, carrier screening in pregnancy is clearly suboptimal.

The dark and photocurrent values were 7 35 and 22 89 μA, respecti

The dark and photocurrent values were 7.35 and 22.89 μA, respectively, which clearly indicate a threefold increase in the dark current value. Figure 4 I – V curves of the area-selective deposited ZnO nanorods in dark and UV light environments. The sensor mechanism is based on Equations (1) to (3) [35, 36]; the reactions on the ZnO nanorod surface during UV illumination can be explained as follows: when the adsorbed

oxygen Pitavastatin chemical structure molecules capture the electron from the conduction band, a negative space charge layer is created, which results in enhanced resistivity [37]. (1) When the photon energy is greater than the bandgap energy (Eg), the incident radiation is adsorbed in the ZnO nanorod UV sensor, which results in electron–hole pairs. (2) The positively charge holes that were created due to the photogeneration neutralize the chemisorbed oxygen that was responsible for higher resistance that revealed conductivity increment, and as a consequence, the photocurrent increases. where O2 is the oxygen molecule, e – is the free electron and the photogenerated electron in the conduction band, is the adsorbed oxygen, hv is the photon energy of the UV light, and h + is the photogenerated hole in the valence band. After the UV light is switched

on, the number of oxygen molecules on the ZnO nanorod surface rapidly reaches the maximum value in response to the ultraviolet light [38]. When the ultraviolet learn more light is switched off, the oxygen molecules are reabsorbed

on the ZnO nanorod surface. Thus, the sensor reverts to its initial mode [39]. An important parameter used to evaluate the suitability of the sensor for MRT67307 mouse UV-sensing applications is spectral responsivity as a function of different wavelengths. This parameter yields the internal photoconductive gain. Generally, the sensor responsivity can be calculated as [40] (3) where λ, q, h, c, and η show the wavelength, electron charge, Planck’s constant, light velocity, external quantum efficiency, and internal gain of the sensor. As Exoribonuclease shown in Figure 5, the sensor responsivity shows a linear behavior below the bandgap UV region (300 to 370 nm) and a sharp cutoff with a decrease of two to three orders of magnitude at approximately 370 nm. The maximum responsivity of our sensor at an applied bias of 5 V was 2 A/W, which is higher than the values reported in the literature [41–43]. Figure 5 Spectral responsivity of area-selective deposited ZnO nanorods between the microgap electrodes. Another important parameter for UV sensor is the current-to-time (I-t) response in the switched on/off states of UV light. Figure 6 shows the I-t response curves at different voltages of area-selective deposited ZnO nanorods on microgap electrodes with UV illumination. The rise time was 72 s, whereas the decay time was 110 s.


Additional data file 1 is a excel spreadsheet listing the 268 organisms used in this

study, and a table listing all orthologs obtain by the Bidirectional Best Hit. (XLSX 65 KB) Additional file 2: The following additional data are available with the online version of this paper. Additional data file 2 is a table listing PcoC proteins in 8 organisms caspase inhibitor harboring the full copper homeostasis repertoire, indicating location and presence of mobile elements. (XLS 14 KB) References 1. Crichton RR, Pierre JL: Old iron, young copper: from Mars to Venus. BioMetals 2001, 14:99–112.PubMedCrossRef 2. Gunther MR, Hanna PM, Mason check details RP, Cohen MS: Hydroxyl radical formation from cuprous ion and hydrogen peroxide: A spin-trapping study. Arch Biochem Biophys 1995, 316:515–522.PubMedCrossRef 3. Macomber L, Rensing C, Imlay Selleckchem Trichostatin A JA: Intracellular copper does not catalyze the formation of oxidative DNA damage in Escherichia coli . J Bact 2007, 189:1616–1626.PubMedCrossRef 4. Robinson NJ, Winge DR: Copper metallochaperones. Annu Rev Biochem 2010, 79:537–562.PubMedCrossRef 5. Pontel LB, Soncini FC: Alternative periplasmic copper resistance mechanisms in Gram negative bacteria. Mol

Microbiol 2009, 73:212–225.PubMedCrossRef 6. Zhu YQ, Zhu DY, Lu HX, Yang N, Li GP, Wang DC: Purification and preliminary crystallographic studies of CutC, a novel copper homeostasis protein from Shigella flexneri . Protein Pept Lett 2005, 12:823–826.PubMedCrossRef 7. Rensing C, Grass G: Escherichia coli mechanisms of copper homeostasis in a changing environment. FEMS Microbiol Rev 2003, 27:197–213.PubMedCrossRef 8. Munson GP, Lam DL, Outten FW, O’Halloran TV: Identification of a copper-responsive two-component system on the chromosome of Escherichia coli K-12. J Bact 2000, 182:5864–5871.PubMedCrossRef 9. Rensing C, Fan B,

Sharma R, Mitra B, Rosen BP: CopA: an Escherichia coli Cu (I)-translocating P-type ATPase. Proc Natl Acad Sci USA 2000, 97:652–656.PubMedCrossRef GABA Receptor 10. Grass G, Rensing C: CueO is a multi-copper oxidase that confers copper tolerance in Escherichia coli . Biochem Biophys Res Commun 2001, 286:902–908.PubMedCrossRef 11. Outten FW, Huffman DL, Hale JA, O’Halloran TV: The Independent cue and cus Systems Confer Copper Tolerance during Aerobic and Anaerobic Growth in Escherichia coli . J Biol Chem 2001, 276:30670–30677.PubMedCrossRef 12. Kim EH, Nies DH, McEvoy MM, Rensing C: Switch or funnel: how RND-type transport systems control periplasmic metal homeostasis. J Bact 2011, 193:2381–2387.PubMedCrossRef 13. Brown NL, Barrett SR, Camakaris J, Lee BTO, Rouch DA: Molecular genetics and transport analysis of the copper-resistance determinant (pco) from Escherichia coli plasmid pRJ1004. Mol Microbiol 1995, 17:1153–1166.PubMedCrossRef 14. Rouch D, Camakaris J, Lee BTO: Copper transport in E. coli . In Metal Ion Homeostasis:Molecular Biology and Chemistry. Edited by: Hamer DH, Winge DR. New York: Alan R.Liss; 1989:477. 15.

Using this system we routinely identify more than 100 recombinant

Using this system we routinely identify more than 100 recombinants per experiment in both laboratory and pathogenic E. coli strains, using short regions of homology to the chromosome, thus maintaining both a high-throughput and broad-range compatibility system. G-DOC plasmids The pDOC plasmids are derived from pEX100T, a medium copy number plasmid which carries ampicillin resistance and the B. subtilis sacB gene [19]. We have introduced different DNA find more sequences into the pEX100T I-SceI restriction sites to create a suite of plasmids, schematic diagrams of which are shown in Figure 1. The

cloning plasmid, pDOC-C, has a large cloning region (CR) flanked by two I-SceI recognition sites. The DNA sequence of pDOC-C, from 100 bp upstream of the left-hand I-SceI site to 100 bp downstream of the right-hand I-SceI site is shown in Figure 2, panel A. The template plasmid, pDOC-K, carries a kanamycin resistance cassette flanked by Flp recombinase CFTRinh-172 ic50 recognition sites (Flp1 and Flp2). On either side of this region are 2 cloning regions (CR1 and CR2). The

other template plasmids, pDOC-H, pDOC-F, pDOC-P and pDOC-G are derivatives of pDOC-K that have the coding sequence for a 6 × His, 3 × FLAG, 4 × Protein A and GFP tag respectively, immediately downstream of CR1. Figure 2; panel B, shows the DNA sequence common to all of the pDOC template plasmids, from 100 bp upstream of the left-hand I-SceI site to 100 bp downstream through of the right-hand I-SceI site. The template plasmids differ between the CR1 and FLP1 sequences: this region is outlined by an open box in the figure. The DNA sequence Selleckchem BAY 63-2521 proceeds through CR1, along the respective DNA sequence for each plasmid

within the open box, and into the FLP1 sequence below. The plasmid pDOC-K has 30 bp of DNA sequence prior to FLP1. The plasmid pDOC-H has the coding sequence for the 6 × His tag and a stop codon followed by a short DNA sequence leading into the FLP1 site. The first 10 codons of the 3 × FLAG, ProteinA and GFP tags are shown, followed by the stop codon and short DNA sequences leading into FLP1 site. Other features indicated on the DNA sequences of the pDOC plasmids in Figure 2 are described in the G-DOC recombineering protocol below. The full DNA sequence of each pDOC plasmid is provided in Additional file 1 and is also available from GenBank, accession numbers GQ88494-GQ889498. Figure 1 The pDOC donor plasmids. Circular representation of the pEX100T plasmid showing the location of the origins of replication, the sacB gene and the ampicillin resistance gene. Below is a linear representation of the pDOC plasmid inserts, showing the I-SceI restriction sites, cloning regions (CR, CR1 and CR2), the Flp recognition sites flanking the kanamycin resistance cassette (KanR) and the location of the epitope tags in plasmids pDOC-H, pDOC-F, pDOC-P and pDOC-G. Figure 2 DNA sequences of the pDOC plasmids.

4D–F) These cords appeared to be embedded in aggregates of bacte

4D–F). These cords appeared to be embedded in aggregates of bacteria that did not label with Con A. The structures that labeled with Con A in other regions of the biofilm appeared diffuse and were not easily identified (data not shown). Discussion A bacterial species from an extreme environment rich in toxic compounds was isolated into axenic culture and grown in the laboratory. During the course of these studies, it was observed that the isolate produced atypical growth curves and formed a macroscopic structure tethered to the bottom of the culture tubes. These biofilms were unusual as they did not consist of the typical mucoidal material,

but were made up of well-defined solid structures. Confocal laser scanning microscopy confirmed that these mature structures contained significant NCT-501 zones of physiological Trichostatin A activity. Physical and chemical characterization of the mature biofilms was carried out and is discussed below.

When examined by light microscopy, bacterial cultures reproducibly contained similar structural motifs that were composed of viable bacteria as well as dead cells and extracellular material. At the macroscopic level, delicate flocculent material of what appeared PF 01367338 to be bacterial aggregates was enveloped by a network of fibers. Smaller fibers branched from this central core in a microscopic analogue to tree branches emanating from a trunk and surrounded by foliage (i.e., the bacterial aggregates). Each culture tube also contained one complex three-dimensional structure that resembled a parachute. At higher magnification using the confocal microscope, the thick fibers in the flocculent material appeared tightly coiled. The tightly coiled structures contained bacteria and had an affinity for fluorescently-labeled concanavalin A (conA).

These results suggest that there are specialized zones within the biofilm consisting of bacteria associated with extracellular proteins. The presence of bacterial aggregates in the biofilm that did not label with con A suggests that at least part of the extracellular material contains glycoproteins. Rapid freezing of biofilms followed by freeze substitution aminophylline and epoxy resin embedding of the specimens enabled examination of thin sections through biofilms that had been minimally disturbed [35, 36]. Cryofixation followed by freeze-substitution has been shown to be a highly effective method for preserving biofilm organization for EM examination [37]. It is well known, however, that freezing can lead to structural artifacts [38] and that highly hydrated structures such as biofilms will collapse to some extent during sample preparation that involves dehydration. These distinct features must be recognized to avoid misinterpretation of the images.

On the other hand, it should be considered that MeNP biosynthesis

On the other hand, it should be considered that MeNP biosynthesis starts in healthy cells, which then rapidly undergo a progressive alteration until they are completely disrupted due to Ag toxicity. Thus, it could be that MeNP biosynthesis is initiated within the chloroplasts in a healthy cell and ends in the cytoplasm of the same cell, which has been damaged. Conclusions The synthesis of AgNPs in living plants was confirmed in B. juncea and M. sativa and demonstrated for the first time in F. rubra. We assessed the subcellular localization of AgNPs in the plant fractions demonstrating that AgNPs had a similar distribution SB-715992 molecular weight but different sizes. Regarding promotion agents, the presence of AgNPs within the

chloroplasts suggested that primary sugars, at least in the beginning phase, could have a role in the in vivo synthesis of AgNPs. However, while the effects of these substances are usually studied individually, it is very unlikely that they have an exclusive role. On the contrary, given the complexity of plant metabolism, it is most likely that there are synergistic effects between

different substances. We did not verify a clear quantitative relationship between the amount of GLU, FRU, AA and PP and the quantity of AgNPs formed. To evaluate if plants can be efficiently exploited for their ability to synthesize in vivo MeNPs, further experiments are needed not only to define more precisely the mechanism of metal nanoparticle formation in living plants but also to better understand if differences in plant behaviour, due to molecular Tobramycin selleck chemicals mechanisms, result in differences in the amount, forms, dimensions and 3-D structures of the in vivo synthesized

MeNPs. Acknowledgements The authors thank Dr. Laurence Cantrill (Out of Site English, Sydney) for the English revision. References 1. Klaine SJ, Alvarez PJJ, Batley GE, Veliparib in vitro Fernandes TF, Handy RD, Lyon DY, Mahendra S, McLaughlin MJ, Lead JR: Nanomaterials in the environment: behavior, fate, bioavailability, and effects. Environ Toxicol Chem 2008, 27:1825–1851.CrossRef 2. Hernandez-Viezcas JA, Castillo-Michel H, Andrews JC, Cotte M, Rico C, Peralta-Videa JR, Ge Y, Priester JH, Holden PA, Gardea-Torresdey JL: Mapping and speciation of CeO 2 and ZnO nanoparticles in soil cultivated soybean ( Glycine max ). ACS Nano 2013, 7:1415–1423.CrossRef 3. Kawazoe Y, Meech JA: Welcome to IPPM’03—nanotechnology: do good things really come in small packages? In Intelligence in a Small Materials World. Edited by: Meech J, Kawazoe Y, Kumar V, Maguire JF. Lancaster: DSEtech; 2005:3–11. 4. Kowshik M, Ashataputre S, Kharrazi S, Kulkarni SK, Paknikar KM, Vogel W, Urban J: Extracellular synthesis of silver nanoparticles by a silver-tolerant yeast strain MKY3. Nanotechnology 2003, 14:95–100.CrossRef 5. Mohanpuria P, Rana KN, Yadav SK: Biosynthesis of nanoparticles: technological concepts and future applications. J Nanopart Res 2008, 10:507–517.CrossRef 6.