C) Relative hGM-CSF and hIL-12 expression in A549 cells D) Relat

C) Relative hGM-CSF and hIL-12 Torin 2 solubility dmso expression in A549 cells. D) Relative hGM-CSF and hIL-12 expression in Hep3B cells. HT: heating treatment. N = 5 repeated experiments. The effect of heat treatments on hGM-CSF and hIL-12 expression As shown in Figure 3A in non-heated A549 cells, first heat

treatment significantly increased hIL-12 levels in A549 cells infected with 100 vp 500 vp, 1000 vp virus, respectively, while the second heat treatment was more efficient in increasing hIL-12 levels in A549 cells (p < 0.05 at all 3 viral dosages). In non-heat treated Hep3B cells, first heat treatment significantly increased hIL-12 expressions in Hep3B cells 24 hrs after first heat treatment. The second heat treatment was also more efficient in increasing hIL-12 levels in Hep3B (p < 0.05 at all 3 viral dosages). These results suggest JAK inhibitor that hIL-12 expression is heat-inducible. In contrast, first heat treatment significantly increased hGM-CSF expression in A549 cells infected with 500 vp and 1000 vp virus in non-heat treated A549 cells shown in Figure 3B; however, second heat treatment did

not significantly increase hGM-CSF expression in A549 cells (p > 0.05). Selleckchem MEK inhibitor In non-heat treated Hep3B cells, first heat treatment increased hGM-CSF levels in Hep3B cells but showed no statistical difference (p > 0.05). After second heat treatment, significant difference was observed in Hep3B cells infected with 1000 vp virus. These results suggest that heat treatment can increase hGM-CSF

expression, but hGM-CSF expression is not heat-dependent. Figure 3 The time dependence Fenbendazole of hGM-CSF and hIL-12 expression in heat treated A549 and Hep3B cells. Cells were infected and heated as described in Figure 2. Medium was collected at 24 and 48 hrs after heating treatment. A) hIL-12 expression in A549 and Hep3B cells. B) hGM-CSF expression in A549 and Hep3b cells. C) Comparison of hIL-12 expression between cells heated for 24 hrs and cells without heating for 24 and 48 hrs. D) Comparison of hGM-CSF expression between cells heated for 24 hrs and cells without heating for 24 and 48 hrs. N = 5 repeated experiments. We further compared the expression of hIL-12 (Figure 3C) and hGM-CSF (Figure 3D) in A549 and Hep3B cells infected with the virus underlying heat treatment for 24 hrs and no heat treatment for 24 and 48 hrs. Results showed that there were no significant differences in hIL-12 levels between 24 and 48 hrs in both A549 and Hep3B cells infected with 3 different viral doses underlying no heat treatment, but a significant increase in A549 and Hep3B cells was observed after 24 hrs of heat treatment. These results suggest that hIL-12 expression is heat-inducible, but not time-dependent. In contrast, significant differences in hGM-CSF levels were observed in A549 and Hep3B cells infected with 500 vp and 1000 vp virus underlying no heat treatment for 24 and 48 hrs.

Antimicrob Agents Chemother 2013,57(3):1428–1433 PubMedCrossRef 4

Antimicrob Agents Chemother 2013,57(3):1428–1433.PubMedCrossRef 42. Andreas H, Diacon AH, Rodney D, Von Groote-Bidlingmaier F, Gregory S, Amour V, Donald PR: 14-day bactericidal activity of PA-824, bedaquiline,

pyrazinamide, selleck kinase inhibitor and moxifloxacin combinations: a randomised trial. Lancet 2012,380(9846):986–993.CrossRef Competing interests The authors declare that they have no competing of interests. Authors’ contributions CNP, SS have designed the work. SS and RSA carried out the experiment. PV analyzed the data and contributed for the statistical analysis. SS and RSA wrote the manuscript and CNP reviewed the manuscript critically. All the authors have read the article and approved the final manuscript.”
“Background Integrative and conjugative elements (ICEs) are self-transmissible mobile genetic elements that mediate horizontal gene transfer between bacteria [1]. ICEs share certain features of phages, transposons and plasmids. But unlike these elements, ICEs integrate into and replicate as part of their host chromosomes, and can be transferred

via conjugation [1, 2]. ICEs and related elements can constitute a large proportion of bacterial chromosomes [3], and bestow a wide range of phenotypes upon their host with carried gene cassettes [4]. The first described ICEs-related elements were Tn916 from Enterococcus faecalis in 1980 [5] and CTnDOT from Bacteroides thetaiotaomicron in 1988 [6]. To date, a variety of ICEs have been classified into several families, and have been reported in diverse Tozasertib concentration Gram-positive and Gram-negative bacteria [1, 7], among which the SXT/R391 family were identified in Vibrionaceae isolates of clinical and environmental origins [8–10]. Vibrionaceae are Gram-negative, mesophilic and chemoorganotrophic

bacteria, which belong to γ-proteobacteria. They are virtually ubiquitous in aquatic environments, including estuaries, marine coastal waters and sediments, and aquaculture settings worldwide [11]. Globally water-borne infectious diseases are one of the major contributors to disease burden and mortality [12]. Pathogenic selleck Vibrio cholerae and Vibrio parahaemolyticus are serious human food-borne pathogens, causing cholera epidemics and diarrheal disease, respectively, and continue to be prevalent particularly in developing countries with disputable sanitary conditions [13]. The Farnesyltransferase SXT element was originally discovered in V. cholerae O139, the first non-O1serogroup of V. cholerae, which gave rise to epidemic cholera in India and Bangladesh in early 1990s [14]. Unlike E1 Tor O1 strains of V. cholerae, the O139 stain was identified to harbor characteristic pattern of resistance to sulfamethoxazole, trimethoprim, streptomycin and furazolidone, which was carried on a ~100 kb self-transmissible SXT element [14]. Comparative sequence analysis revealed closer genetic relationship between the SXT and R391 element (89 kb) that was identified in Providencia rettgeri isolate in South Africa in 1972 [15, 16].

Bradley L (2007) Lamm, Paley D Charcot neuroarthropathy of the f

Bradley L (2007) Lamm, Paley D. Charcot neuroarthropathy of the foot and ankle in limb lengthening and reconstruction surgery. In: Rozbruch SR, Ilizarov S (eds) Limb lengthening and reconstruction surgery, vol 1. Informa Healthcare, London, pp 221–232 9. Axelrad T, Kakar S, Einhorn TH (2007) New technologies for the enhancement of skeletal repair. Injury

38S1:S49–S62. doi:10.​1016/​j.​Smoothened Agonist order injury.​2007.​02.​010 CrossRef 10. Jiang Y, Zhao JJ, Mitlak BH, Wang O, Genant HK, Eriksen EF (2003) Recombinant human parathyroid hormone (1–34) [teriparatide] improves Selleck U0126 both cortical and cancellous bone structure. J Bone Miner Res 18:1932–1941. doi:10.​1359/​jbmr.​2003.​18.​11.​1932 PubMedCrossRef 11. Rubin MR, Cosman F, Lindsay R, Bilezikian JP (2002) The anabolic effects of parathyroid hormone. Osteoporos Int 13:267–277. doi:10.​1007/​s001980200026 PubMedCrossRef 12. Knecht TP (2004) Teriparatide and

fracture healing in cortical bone. Endocr Pract 10:293PubMed 13. Puzas JE, Houck J, Bukata SV (2006) Accelerated fracture healing. J Am Acad Orthop Surg 14:S145–S151PubMed 14. Resmini G, Iolascon G (2007) 79-year-old post-menopausal woman with humerus fracture during teriparatide treatment. Aging Clin Exp Res 19:30–31PubMed 15. Rubery PT, Bukata SV (2010) Teriparatide may accelerate healing in delayed unions of type III odontoid fractures: Tariquidar cost a report of 3 cases. J Spinal Disord Tech 23:151–155. doi:10.​1097/​BSD.​0b013e31819a8b7a​ PubMedCrossRef 16. Oteo-Alvaro A, Moreno E (2010) Atrophic humeral shaft nonunion treated with teriparatide

(rh PTH 1–34): a case report. J Shoulder Elbow Surg 19:e22–e28. doi:10.​1016/​j.​jse.​2010.​05.​005 PubMedCrossRef 17. Lee YK, Ha YC, Koo KH (2012) Teripatratide, a nonsurgical solution for femoral nonunion? A report of three cases. Ostheoporos Int 23:2897–2900. doi:10.​1007/​s00198-012-2172-x CrossRef”
“Introduction Metformin is widely prescribed as a first-line therapy for patients with type 2 diabetes mellitus (T2DM) as an anti-hyperglycaemic agent which acts primarily by suppressing glucose production by the liver [1]. In contrast to thiazolidinediones (TZD), another T2DM therapy Clostridium perfringens alpha toxin which has adverse effects on the skeleton [2, 3], several studies have documented that metformin is osteogenic in vitro. It was reported that metformin can induce MC3T3-E1 osteoblastic cells differentiation and bone matrix synthesis via adenosine 5′-monophosphate-activated protein kinase (AMPK) activation and subsequent induction of endothelial nitric oxide synthase (eNOS) and bone morphogenetic protein-2 (BMP-2) expression [4, 5]. Metformin was also found to regulate Small Heterodimer Partner (SHP) in MC3T3-E1 cells, an orphan nuclear receptor which stimulates osteoblastic bone formation by interacting with the transcription factor Runx2 [6].

However, the validity of this single-item

However, the validity of this single-item question in subjects with different cultural backgrounds has been questioned (Agyemang et al. 2006). Differences in self-concepts between ethnic groups may influence the results of the single item general health question. The observation that after adjusting for the well-established socio-demographic www.selleckchem.com/products/mm-102.html determinants of health inequalities, still systematic differences in occurrence of poor health in ethnic groups relative to the Dutch group were observed may indicate over-estimation of poor health. In the current

study similar conclusions on unemployed, ethnicity, and health were drawn when using the single question on perceived general health question and the other 35 questions on physical and mental health dimensions of the selleck chemicals llc SF-36. This corroborates the opinion that the general health question provides a good summery of the mental and physical health in migrant groups and the indigenous population. This finding is, of course, also supported by the high correlations

between perceived general health and all health dimensions in the SF-36. A high proportion of persons with a poor health among ethnic groups has been observed in various studies in different countries (Bos et al. 2004; Chandola 2001; Smith et al. 2000; Nazroo 2003; Sundquist 1995). Different explanations have been put forward. A Swedish study among immigrants from Poland, Turkey, and Iran found that acculturation (defined by the knowledge of the Swedish language) was an important mediator in the pathway between ethnicity and poor health (Wiking et al. 2004). Indeed, in our study population differences in mastering the Dutch GSK1120212 ic50 language may have influenced health. For Surinamese MRIP and Antilleans Dutch is usually a first or second language, whereas for Turks and Moroccans knowledge

of the Dutch language is often limited or absent, especially among older women. Language problems may hamper effective communication with physicians and also inhibit access to information on health and health care (Uniken Venema et al. 1995). In the current study, mastery of the Dutch language was not included in the analyses, but the observation that the health status of homemakers with a Turkish or Moroccan background was worse than the health status of homemakers with another ethnic background may reflect a lower acculturation. Differences in migration experiences may also contribute to the differences in health between the ethnic minority groups. Refugees have a different migration history than Turks, Moroccans, Surinamese, and Antilleans. For refugees, experiences of violence, the flight to asylum and forced broken social networks may have affected health (Sundquist 1995).

Either 5 or 10 μL of the supernatant was injected for tissue or p

Either 5 or 10 μL of the supernatant was injected for tissue or plasma samples, respectively. Calibration curves and QC samples were prepared

in both brain and liver, for tissue sample analysis. The A-1210477 concentration working ranges for liver and brain were 0.125–100 and 0.125–25 ng/mL, respectively. Equipment High performance liquid chromatography was carried out on an Agilent 1100 system (Agilent Technology, Palo Alto, CA), coupled with a single-quadrupole mass spectrometer, utilizing electrospray ionization in positive mode. Samples were cooled to 4°C in a thermostated autosampler and the column compartment, containing a Waters SymmetryShield RP8 column (2.1 × 50 mm, 3.5 μm), was maintained at 35°C. Samples were eluted using a gradient mobile phase, comprised of 10 mM ammonium acetate with 0.1% formic acid and methanol, XAV939 running at a flow rate of 0.35 mL/min for 10 min, including re-equilibration. Mass spectrometric conditions were as follows: fragmentor, 150 V; gain, 2; drying gas flow, 10 L/min; drying gas temperature, 300°C; nebulizer pressure, 40 Repotrectinib in vitro psi; and capillary voltage, 1500 V. Selected-ion monitoring

was accomplished at m/z 494.2 for imatinib and m/z 213.1 for the internal standard. The chromatographic data were acquired and analyzed using the Chemstation software package (Agilent). Validation procedures Calculation of accuracy and precision was carried out according to procedures reported in detail previously [17]. Calibration samples were prepared fresh each

day in the relevant matrix and frozen QC samples were defrosted and analyzed. A 1/x2 weighting scheme was employed in the generation of standard curves to account for concentration dependent variance. Detector response for plasma was found to be linear in the imatinib concentration range of 10–1000 ng/mL. Plasma accuracy and precision were evaluated with QC samples. Overall, the assay was found to be accurate (deviation of less than 10% for QCs) and precise (within run precision <10%, between run precision <12.6%) for plasma, liver, and brain. Animals All experiments were performed on six-week old, male, tuclazepam Balb/C mice obtained from Charles River Laboratories (Wilmington, MA). The mice weighed approximately 15 to 20 g at the time of study. All mice were allowed unlimited access to water and rodent chow prior to, and during the experiment. Blank mouse liver and brain samples were harvested from surplus mice following euthanasia. NCI-Frederick is accredited by AAALAC International and follows the Public Health Service Policy for the Care and Use of Laboratory Animals. Animal care was provided in accordance with the procedures outlined in the “”Guide for Care and Use of Laboratory Animals”" (National Research Council; 1996; National Academy Press; Washington, DC). The study design and protocol were approved by the NCI Animal Care and Use Committee (Bethesda, MD).

: Molecular pathogenesis of Salmonella enterica

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regulation of the aconitase genes ( acnA and acnB ) of Escherichia coli . Microbiology UK 1997, 143:3795–3805.CrossRef 53. Levanon SS, San KY, Bennett GN: Effect of oxygen on the Escherichia coli ArcA and FNR regulation systems and metabolic responses. Biotechnol Bioeng 2005, 89:556–564.PubMedCrossRef 54. Jeong JY, Kim YJ, Cho N, Shin D, Nam TW, Ryu S, et al.: Expression of ptsG encoding the major glucose transporter is regulated by ArcA in Escherichia Idelalisib solubility dmso coli . J Biol Chem 2004, 279:38513–38518.PubMedCrossRef 55. Cotter PA, Gunsalus RP: Contribution of the Fnr and ArcA gene-products in coordinate regulation of cytochrome-o and cytochrome-d oxidase ( cyoABCDE and cydAB ) genes in Escherichia coli . FEMS Microbiol Lett 1992, 91:31–36.CrossRef 56. Kato Y, Sugiura M, Mizuno T, Aiba H: Effect of the arcA mutation on the expression of flagella genes in Escherichia coli . Biosci Biotechnol Biochem

2007, 71:77–83.PubMedCrossRef 57. Lu S, Killoran PB, Fang FC, Riley LW: The global regulator ArcA controls resistance to reactive nitrogen and oxygen intermediates in Salmonella enterica serovar Enteritidis. Infect Immun 2002, 70:451–461.PubMedCrossRef 58. Gao H, Wang X, Yang ZK, Palzkill T, Zhou J: Probing regulon of ArcA in Shewanella oneidensis MR-1 by integrated BIBW2992 molecular weight genomic analysis. Bmc Genomics 2008, 9:42.PubMedCrossRef 59. Wong SMS, Alugupalli KR, Ram S, Akerley BJ: The ArcA regulon and oxidative stress resistance in Haemophilus influenzae . Mol Microbiol 2007, 64:1375–1390.PubMedCrossRef 60. Gralnick JA, Brown CT, Newman DK: Anaerobic regulation by an atypical Arc system in Shewanella oneidensis . Mol Microbiol 2005, 56:1347–1357.PubMedCrossRef 61. Romeo T: Global regulation by the small RNA-binding protein CsrA and the non-coding RNA molecule CsrB. Mol Microbiol 1998, 29:1321–1330.PubMedCrossRef 62.

Nat Nanotechnol 2010, 5:722–726 CrossRef 13 Lee KH, Shin HJ, Lee

Nat Nanotechnol 2010, 5:722–726.CrossRef 13. Lee KH, Shin HJ, Lee J, Lee IY, Kim GH, Choi JY, Kim Selleckchem AZD6244 SW: Large-scale synthesis of high-quality hexagonal boron nitride nanosheets for large-area graphene electronics. Nano Lett 2012, 12:714–718.CrossRef 14. Shi Y, Hamsen C, Jia X, Kim KK, Reina A, Hofmann M, Hsu AL, Zhang K, Li H, Juang ZY, Dresselhaus MS, Li L-J, Kong J: Synthesis of few-layer hexagonal boron nitride thin film by chemical vapor deposition. Nano Lett 2010, 10:4134–4139.CrossRef 15. Auwärter W, Suter HU, Sachdev H, Greber T: Synthesis of one monolayer

of hexagonal boron nitride on Ni(111) from B-trichloroborazine (ClBNH) 3 . Chem Mater 2004, 16:343–345.CrossRef 16. Lee Y-H, Liu K-K, Lu Tucidinostat mw A-Y, Wu C-Y, Lin C-T, Zhang W, Su C-Y, Hsu C-L, Lin T-W, Wei K-H, Shi Y, Li L-J: Growth selectivity of hexagonal-boron nitride layers on Ni with various crystal orientations. RSC Adv 2012, 2:111–115.CrossRef 17. Kim KK, Hsu A, Jia X, Kim SM, Shi Y, Hofmann M, Nezich D, Rodriguez-Nieva JF, Dresselhaus

M, Palacios T, Kong J: Synthesis of monolayer hexagonal boron nitride on Cu foil using chemical vapor deposition. Nano Lett 2012, 12:161–166.CrossRef 18. Song L, Ci L, Lu H, Sorokin PB, Jin C, Ni J, Kvashnin AG, Kvashnin DG, Lou J, Yakobson BI, Ajayan PM: Large scale growth and characterization of atomic hexagonal boron nitride layers. Nano Lett 2010, 10:3209–3215.CrossRef 19. Guo N, Wei J, Fan L, Jia Y, Liang D, Zhu H, Wang K, Wu D: Controllable growth of triangular hexagonal boron nitride domains on copper foils by an improved low-pressure chemical vapor deposition method. Nanotechnology 2012, Tangeritin 23:415605.CrossRef 20. Yan K, Peng H, Zhou Y, Li H, Liu Z: Formation of bilayer Bernal graphene: layer-by-layer epitaxy via chemical

vapor deposition. Nano Lett 2011, 11:1106–1110.CrossRef 21. Shi Y, Zhou W, Lu AY, Fang W, Lee YH, Hsu AL, Kim SM, Kim KK, Yang HY, Li LJ, Idrobo JC, Kong J: Van der Waals epitaxy of MoS 2 layers using graphene as growth templates. Nano Lett 2012, 12:2784–2791.CrossRef 22. Hwang J, Kim M, Campbell D, Alsalman HA, Kwak JY, Shivaraman S, Woll AR, Singh AK, Hennig RG, Selleck MK-8931 Gorantla S: Van der Waals epitaxial growth of graphene on sapphire by chemical vapor deposition without a metal catalyst. ACS Nano 2012, 7:385–395.CrossRef 23. J-s L, C-r Z, Li B, Cao F, Wang SQ: An investigation on the synthesis of borazine. Inorg Chim Acta 2011, 366:173–176.CrossRef 24. J-s L, C-r Z, Li B, Cao F, Wang SQ: An improved synthesis of borazine with aluminum chloride as catalyst. Eur J Inorg Chem 2010, 2010:1763–1766. 25. Lima MP, Fazzio A, da Silva AJR: Edge effects in bilayer graphene nanoribbons: ab initio total-energy density functional theory calculations. Phys Rev B 2009, 79:153401.CrossRef 26.

Various concentrations of NH3 gases, ranging from 5 to 100 ppm, w

Various concentrations of NH3 gases, ranging from 5 to 100 ppm, were purged into the chamber in order to probe the sensing performance of the optimal Py-rGO sensor. As shown in Figure  8a, the plots of normalized resistance change versus time for the sensing selleck products device based on assembled Py-rGO upon exposure to NH3 PFT�� nmr gases with different concentrations were illustrated. The results revealed that the sensing device exhibited an excellent and highly reversible response to different concentrations of NH3 gases. When the NH3 gases were introduced into

the chamber, the resistance of the sensing device increased significantly over a period of 12 min, and the increase of the concentration of NH3 gas can result in the increase of the resistance of the device, and all of the resistance variations can be distinctly observed when the devices expose to the NH3 gas with the concentration

ranging from 5 ppb to 100 ppm. When the concentration of NH3 gas is 100 ppm, ca. 22% of the resistance change can be observed. As the concentration of NH3 gas decreases, the resistance change of the device decreases accordingly, and ca. 4.2% of the resistance change can be also observed when the concentration of NH3 gas was as low as 5 ppb. This is fascinating since the Py-rGO-based sensing devices exhibit much better response to NH3 gas than many other rGO-based devices Carbohydrate VX-689 [47, 48]. Furthermore, the relationship of response variation of the Py-rGO sensor as a function of NH3 concentration has also been studied as shown in Figure  8b. The sensing signal changed linearly with the concentration of ammonia when the concentration is above 50 ppb. The linear relationship between the response of Py-rGO and the concentration of NH3 is in

accordance with the work we reported before [29]. When the concentration is below 50 ppb, the sensing signal dropped rapidly (as shown in Figure  8b), which might be due to the PPy molecules covered on the surface of rGO sheets, and blocked the gas molecules interact with the rGO sheets, leading to a worse response to the NH3 gas molecules. Figure 8 The response performance of sensing devices based on assembled Py-rGO sheets. (a) Plot of normalized resistance change versus time for the sensing device based on assembled Py-rGO upon exposure to NH3 gas with concentrations ranging from 5 ppb to 100 ppm: a, 5 ppb; b 50 ppb; c, 10 ppm; d, 50 ppm; and e, 100 ppm. (b) Relationship of response variation of the Py-rGO sensor as a function of NH3 concentration. Furthermore, the sensor response exhibits an excellent recovery characteristic (as shown in Figure  8a). As illuminated with IR lamp together with flushed with dry air over the periods ranging from 134 to 310 s, the resistance of the device decreased and essentially recovered to the initial values.

The bbk32 gene was amplified from B31 genomic DNA, however, PCR p

The bbk32 gene was amplified from B31 genomic DNA, however, PCR product was not detected in the N40D10/E9 strain. (B) Southern blot of EcoR1-digested genomic DNA of both strains (top) was hybridized with the probe prepared

using the bbk32 PCR product from B31. An approximately 1.8 kb size fragment was detected only in B31, as expected, but not in the N40D10/E9 genomic DNA containing lane. In another study, we see more compared two important, highly variable virulence factors of B. burgdorferi, OspC and DbpA. As expected, both of these selleck molecules are present in both spirochete strains but showed high sequence variation [29]. Therefore, irrespective of the phylogenetic grouping of these strains using RST and OspC categorization, the presence of known virulence factors in both strains suggests that B31 and N40D10/E9 could possibly exhibit similar levels of pathogenicity. Furthermore, although BBK32 is an adhesin [41], previous

studies showed that its absence results in a subtle infectivity defect, exhibiting disease attenuation only at low dose of infection [45, 102, 103]. Divergence of fibronectin-binding adhesin gene bbk32 in N40D10/E9 strain BBK32 could possibly Compound C supplier contribute to the adherence-mediated tissue colonization in B31 as compared to N40D10/E9 strain but a negative PCR result is not sufficient to demonstrate this difference. Since sequence divergence at the priming sites may lead to unsuccessful PCR amplification, Southern hybridization was conducted to determine the presence of a homolog of bbk32 gene in the N40D10/E9 strain. Absence of a band in N40

even under low stringency conditions (data not shown) indicated that either bbk32 homolog in the N40D10/E9 strain was absent or had substantial DOK2 DNA sequence divergence from that in the B31 strain (Figure 3B). Therefore, irrespective of the presence of BBK32, the two B. burgdorferi strains examined here (B31 and N40D10/E9) show similar levels of binding to most cells, indicating redundancy of function. However, BBK32 may contribute to the binding of Lyme spirochetes to specific cell line(s), such as Vero cells, and potentially to epithelial cells in vivo. B31 and N40D10/E9 showed remarkably different protein expression profiles Although known virulence factors are present in both B31 and N40D10/E9 strains (Figure 3A), they only represent the molecular profile of previously identified virulence factors and molecules associated with infectivity. Therefore, it would be erroneous to conclude that they represent the full repertoire of the virulence factors of B. burgdorferi that play important roles during pathogenesis in the mammalian host.

Toxicol Lett 2009, 191:1–8 CrossRef 41 Li N, Ma L, Wang J, Zheng

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nanoparticles: role of deposited dose and solubility. Inhal Toxicol 2011, 23:95–103.CrossRef 46. Cao H, Wang Y, Wang Y, Chen G, Ge S: The influence of the liver and kidney induced by large doses of nano-TiO 2 in mice. Chin J Misdiagn 2010, 10:4332. 47. Guo L, Liu X, Qin D, Gao L: Effects of nanosized titanium dioxide on the reproductive system of male mice. Nat J Androl 2009, 15:517–522. 48. Han Y, Yin L, Long L, Liu R: Distribution STI571 concentration of nano-Fe 3 O 4 and nano-TiO 2 in tissues of mice. Chin J Publ ic Health 2009, 25:835–836. 49. Liu Q, Xue X, Ye J, Zhang H: The influence of brain, liver and lung tissue

induced by nano TiO 2 in mice. J Huaqiao Univ (Nat Sci) 2009, 30:179–182. 50. Song W, Zhang W, Zhang J, Liu Y, Ding F, Gao M, Hu W: The effect study of the lungs induced by nano TiO 2 in mice. Acta Sci Nat Univ Nankaiensis 2008, 41:14–18. 51. Liu X, Guo L, Qin D, Gao L: Effects of titanium dioxide nanoparticles on main organs of female mice in vivo . Jiang su Med J 2009, 35:549–551. 52. OSBPL9 Wang Y, Kang X, Ding S, Mu S, Wang Y, Cao H: Acute toxicity of nanometer titanium dioxide to liver and kidney of mice. J Environ Health 2008, 25:112–113. 53. He P, Tao J, Zhang Y, Tang Y, Wang Y: Effect of inhaled nano-TiO 2 on lung and serum biochemical indexes of mice. Trans Nanjing Univ Aeronaut Astronaut 2010, 27:338–343. 54. Xiao G, Xu X, Cai W, Fu C, Wu Q, Ding S, Yuan J, XI Z, Yang X: DNA damage of liver cells and kidney cells of mice induced by nanosized TiO 2 . Asian J Ecotoxicol 2008, 3:590–595. 55. Zhang SH, Mei QB, Yang CM: The acute toxicity study induced by nano TiO 2 Ro 61-8048 through the oral route. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi 2009, 27:355–356. 56.