CrossRefPubMed 14 Shafikhani SH, Partovi AA, Leighton T: Catabol

CrossRefPubMed 14. Shafikhani SH, Partovi AA, Leighton T: Catabolite-induced repression of sporulation in Bacillus subtilis. Curr Microbiol 2003, 47:300–308.CrossRefPubMed 15. Sierro N, Makita Y, de Hoon M,

Nakai K: DBTBS: a database of transcriptional regulation in Bacillus subtilis containing upstream intergenic conservation information. Nucleic Acids Res 2008, 36:D93-D96.CrossRefPubMed 16. Gutierrez-Rios RM, Rosenblueth DA, Loza JA, Huerta AM, Glasner JD, Blattner PD-1/PD-L1 assay FR, et al.: Regulatory network of Escherichia coli: consistency between literature knowledge and microarray profiles. Genome Res 2003, 13:2435–2443.CrossRefPubMed 17. Moszer I, Jones LM, Moreira S, Fabry C, Danchin A: SubtiList: the reference database for the Bacillus subtilis genome. Nucleic Acids Res 2002, 30:62–65.CrossRefPubMed 18. Nakano MM, Zuber P: Anaerobic growth of a “”strict aerobe”" (Bacillus subtilis). Annu Rev Microbiol 1998, 52:165–190.CrossRefPubMed 19. Fujita M, Sadaie Y: Rapid isolation of RNA polymerase from sporulating

cells of Bacillus subtilis. Gene 1998, 221:185–190.CrossRefPubMed 20. Jedrzejas MJ, Huang WJ: Bacillus species proteins LY2835219 price involved in spore formation and degradation: from identification in the genome, to sequence analysis, and determination of function and structure. Crit Rev Biochem Mol Biol 2003, 38:173–198.CrossRefPubMed AZD8186 in vitro 21. Piggot PJ, Hilbert DW: Sporulation of Bacillus subtilis. Curr Opin Microbiol 2004, 7:579–586.CrossRefPubMed 22. Mekjian KR, Bryan EM, Beall BW, Moran CP Jr: Regulation of hexuronate utilization in Bacillus subtilis. J Bacteriol 1999, 181:426–433.PubMed 23. Yoshida K, Yamaguchi H, Kinehara M, Ohki YH, Nakaura Y, Fujita Y: Identification of additional TnrA-regulated genes of Bacillus subtilis associated with a TnrA box. Mol Microbiol 2003, 49:157–165.CrossRefPubMed

24. Eichenberger P, Fujita M, Jensen ST, Conlon EM, Rudner DZ, Wang ST, et al.: The program of gene transcription for a single differentiating cell type during sporulation in Bacillus subtilis. PLoS Biol 2004, 2:e328.CrossRefPubMed 25. Kroos L, Kunkel PLEK2 B, Losick R: Switch protein alters specifiCity of RNA polymerase containing a compartment-specific sigma factor. Science 1989, 243:526–529.CrossRefPubMed 26. Au N, Kuester-Schoeck E, Mandava V, Bothwell LE, Canny SP, Chachu K, et al.: Genetic composition of the Bacillus subtilis SOS system. J Bacteriol 2005, 187:7655–7666.CrossRefPubMed 27. Lozada-Chavez I, Janga SC, Collado-Vides J: Bacterial regulatory networks are extremely flexible in evolution. Nucleic Acids Res 2006, 34:3434–3445.CrossRefPubMed 28. Madan BM, Teichmann SA, Aravind L: Evolutionary dynamics of prokaryotic transcriptional regulatory networks. J Mol Biol 2006, 358:614–633.CrossRef 29. Gonzalez Perez AD, Gonzalez GE, Espinosa AV, Vasconcelos AT, Collado-Vides J: Impact of Transcription Units rearrangement on the evolution of the regulatory network of gamma-proteobacteria. BMC Genomics 2008, 9:128.CrossRefPubMed 30.

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M13KO7 bacteriophage functionalization Viruses are infectious age

M13KO7 bacteriophage functionalization Viruses are infectious agents that can cause disease in humans, plants, and animals; antibodies are typically used in immunoassays to detect viruses in biological

samples. The M13KO7 bacterial virus was used as a model system to determine if the large (approximately 2 μm in length; 16,400 kDa) M13KO7 could be directly bound to and detected on the PSi BSW/BSSW sensor surface. The M13KO7 bacteriophage is a low-cost, readily available, nonhazardous E. coli bacterial virus that can be readily detected using commercially available antibodies GDC-0449 mouse [18, 19]. The virus was covalently cross-linked to the PSi surface via APTES and GA linkers. APTES was attached IWP-2 research buy as described

above. GA is a homobifunctional cross-linker that can bind to and covalently link molecules through their free amines. A 2.5% GA in phosphate buffered saline (PBS) buffer solution was used to cross-link the APTES free amines on the sensor surface to the free amines on M13KO7 suspended in solution on the sensor surface. After a 30-min GA incubation step, a 1% sodium cyanoborohydride (Sigma-Aldrich, St. Louis, MO, USA) in PBS buffer solution was applied, followed by a 30-min incubation step to stabilize the Schiff base bonds formed during GA cross-linking [20]. The M13KO7 (0.32 mg/ml carbonate/bicarbonate buffer, pH ~ 10) was diluted to a final concentration of 32 μg/ml in PBS buffer (final pH ~ 9.5) and applied to the sensor surface for 20 min at room temperature. The device was thoroughly rinsed with DI water. Figure 2b shows a top view SEM image of the M13KO7 bacteriophage immobilized on the PSi surface. Coulombic interactions prevent a uniform self-assembled monolayer due to the negatively charged nature of the virus. Results and discussion A resonance condition is distinctly excited when the effective index of a BSW or BSSW mode is matched by the coupling conditions of either a prism or diffraction grating. Prism coupling is compatible with existing

surface plasmon resonance biosensing instrumentation. Grating coupling SAR302503 cell line allows for more compact devices, which could be Astemizole used for point of care diagnostics with microfluidics integration [21]. The BSW mode is confined by the band gap created by the Bragg mirror and by total internal reflection near the surface. Similarly, by reducing the optical thickness of one or more layers within the multilayer through the introduction of a step or gradient refractive index profile, BSSW modes with different effective indices can be supported within the multilayer. The implementation of a single step to break the periodicity of the Bragg mirror refractive index profile shifts the band edge of the Bragg mirror and gives rise to a single BSSW mode confined within the corresponding layer with reduced optical thickness.

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J Clin Endocrinol Metab

J Bone Miner Res 1998; 13:1431–1438 063 Yes   2 years 100 66.1 Bell NH, et al. J Clin Endocrinol Metab 2002; 87:2792–2797 072 Yes   2 years 100 61.3 Bone HG, et al. J Clin Endocrinol Metab click here 2000; 85:720–726 082 Yes   1 year 69.5 54.7 Saag KG, et al. N

Engl J Med 1998; 339:292–299 083 Yes   1 year 67.2 56.0 Saag KG, et al. N Engl J Med 1998; 339:292–299 087 Yes   6 months 100 78.5 Greenspan SL, et al. Ann PD-1/PD-L1 targets Intern Med 2002;

136:742–746 088 Yes   6 months 100 66.2 Bonnick SL, et al. Curr Med Res Opin 2007; 23:1341–1349 (INPACT) 095 Yes   1 year 43.9 46.0 van der Poest CE, et al. J Bone Miner Res 2002; 17:2247–2255 096 Yes   2 years 0 62.7 Orwoll E, et al. N Engl J Med 2000; 343:604–610 097 Yes   1 year 100 61.7 Lindsay R, et al. J Clin Endocrinal Metab 1999; 84:3076–3081 (FACET) 104 Yes   1 year 100 64 Downs RW Jr, et al. J Clin Endocrinol Metab 2000; 85:1783–1788 LY2835219 ic50 (FOCAS) 109 Yes   1 year 100 65 Data on file (inFOCAS) 112 Yes   2 years 51 50.5 Jeffcoat MK, et al. In: Davidovitch Z, Norton LA (eds) Biological mechanisms of tooth movement and craniofacial adaptation. Harvard Society for the Advancement of Orthodontics, Boston, 1996:365–373 117 Yes C-X-C chemokine receptor type 7 (CXCR-7)   6 months 36.6 63 Rubash H, et al. 50th annual meeting of the Orthopaedic Research Society [Abstract]. Transactions 2004; 29:1942 159 Yes   1 year 100 69.2 Hosking D, et al. Curr Med Res Opin 2003; 19:383–394 162 Yes   12 weeks 92.4 66.7 Greenspan S, et al. Mayo

Clin Proc 2002; 77:1044–1052 165 Yes   1 year 0 66.1 Miller PD, et al. Clin Drug Invest 2004; 24:333–341 193 Yes   1 year 58.4 52.9 Stoch S, et al. J Rheumatol 2009; 36:1705–1714 219 Yes   6 months 100 65.2 Cryer B, et al. Am J Geriatr Pharmacother 2005; 3:127–136 (OASIS) 901 Yes   1 year 100 62.8 Pols HA, et al. Osteoporos Int 1999; 9:461–468 (FOSIT) 902 Yes   1 year 100 57.3 Ascott-Evans BH, et al. Arch Intern Med 2003; 163:789–794 904 Yes   12 weeks 94.2 63.6 Eisman JA, et al. Curr Med Res Opin 2004; 20:699–705 056 No Paget’s disease 6 months 34.8 69.0 Siris E, et al. J Clin Endocrinol Metab 1996; 81:961–967 059 No Paget’s disease: alendronate dose above allowable range 6 months 43.6 69.9 Reid IR, et al. Am J Med 1996; 101:341–348 118 No No placebo comparator 2 years 100 66.5 Rizzoli R, et al. J Bone Miner Res 2002; 17:1988–1996 119 No No placebo comparator 1 year 100 56.2 Luckey MM, et al. Obstet Gynecol 2003; 101:711–721 189 No No placebo comparator 1 year 100 64.2 Luckey M, et al.

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Yi DK, Lee SS, Papaefthymiou GC, Ying JY: Nanoparticle architectu

Yi DK, Lee SS, Papaefthymiou GC, Ying JY: Nanoparticle architectures templated by SiO 2 /Fe 2 O 3 nanocomposites. Chem Mater 2006, 18:614–619.CrossRef 29. Parveen S, Sahoo SK: Evaluation of cytotoxicity and mechanism of apoptosis of doxorubicin using folate-decorated chitosan nanoparticles for targeted delivery to retinoblastoma. Cancer Nano 2010, 1:47–62.CrossRef 30. Li JC, Zheng LF, Cai HD, Sun WJ, Shen MW, Zhang GX, Shi XY: Polyethyleneimine-mediated synthesis of folic acid-targeted iron oxide nanoparticles for in

vivo tumor MR imaging. Biomaterials 2013, 34:8382–8392.CrossRef 31. Zhu YF, Fang Y, Kaskel S: Folate-conjugated Fe 3 O 4 @SiO 2 hollow mesoporous spheres for targeted anticancer drug delivery. J Phys Chem C 2010, 114:16382–16388.CrossRef 32. Wana A, Sun Y, Li HL: Characterization of folate-graft-chitosan as a scaffold for nitric oxide release. Int J Biol Macromol 2008, OSI-906 in vivo 43:415–421.CrossRef selleck products 33. Yang SJ, Lin FH, Tsai KC, Wei MF, Tsai HM, Wong JM, Shieh MJ: Folic acid-conjugated chitosan nanoparticles enhanced protoporphyrin IX accumulation in colorectal cancer cells. Bioconjugate Chem 2010, 21:679–689.CrossRef 34. Veiseh O, Sun C, Kohler GNJ, Gabikian P, Lee D, Bhattarai N, Ellenbogen R, Sze R, Hallahan A, Olson J, Zhang MQ: Optical and MRI multifunctional nanoprobe for targeting gliomas. Nano Lett 2005, 5:1003–1008.CrossRef 35. Wei W, Zhang Q, Zheng XW: Synthesis of chitosan/Fe 3 O 4

/SiO 2 nanocomposites and investigation into their check details catalysis properties. Acta Chim Sinica 2013, 71:387–391.CrossRef 36. Shen JM, Guan XM, Liu XY, Lan JF, Cheng T, Zhang HX: Luminescent/magnetic hybrid nanoparticles with folate-conjugated peptide composites for tumor-targeted drug delivery. Bioconjugate Chem 2012, 23:1010–1021.CrossRef 37. Bhattacharya D, Das M, Mishra D, Banerjee I, Sahu SK, Maiti TK, Pramanik P: Folate receptor targeted, carboxymethyl chitosan functionalized iron oxide nanoparticles: a novel ultradispersed nanoconjugates for bimodal imaging. Nanoscale 2011, 3:1653–1662.CrossRef 38. Lin YS, Haynes CL: Impacts of mesoporous silica nanoparticle size,

pore ordering, and pore integrity on hemolytic activity. J Am Chem ID-8 Soc 2010, 132:4834–4842.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions HL and YW conceived and designed the experimental strategy and wrote the manuscript. JZ and YC prepared andperformed the synthetic experiments. YH analyzed the data. ZH and BT performed the in vitro experiments. ZL helped with the editing of the paper. All authors read and approved the final manuscript.”
“Review Background Dilute nitrides are technologically important materials due to their promising physical properties and potential application in optoelectronic technology. The strong nitrogen dependence of the bandgap energy makes dilute nitrides promising candidate for device applications, operating in near infrared region [1–3].

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Chan et al documented decreases in mitogen (PHA)-stimulated

Chan et al. documented decreases in mitogen (PHA)-stimulated

IL-2 and IL-5 isolated peripheral blood mononuclear cells following resistance exercise [20]. We found plasma IL-5 significantly decreased at 90 min post exercise, and IL-2 was unchanged. These findings are puzzling, but may be explained in part by alterations in circulating cell numbers. IL-2 is secreted by T-Helper 1 (TH1) cells, IL-5 is secreted by T-Helper 2 (TH2) cells and Mast cells. Resistance exercise induces fluctuations in circulating immune cells, in P5091 order particular, a reduction of lymphocytes (including both TH1 and TH2) cells in the 30 min-6 h recovery period after exercise [18]. Thus the modest reduction in plasma IL-5 may simply reflect fewer circulating TH2 SB-715992 cells at that time. Additionally,

[12] found only a mild inflammatory response in untrained subjects following resistance exercise (in a circuit fashion) solely on ten Universal cable machines; however, the subjects only performed 30 min of total exercise. Koch et al. suggested that the resistance exercise SAR302503 cell line protocol be longer in duration, so our current study increased the duration of the resistance exercise from their 15 min protocol to 42 min [18]. As there are different types of muscle actions (i.e., isometric, isokinetic, concentric, eccentric), its been reported that exercises involving eccentric muscle contractions may induce greater muscular damage and thus a concomitant inflammatory response, which would include increased cytokine production [13]. We addressed equal time for concentric and eccentric muscle actions by having the subjects perform the exercises with a 2:2 cadence.

Also, in our Monoiodotyrosine study, we utilized resistance-trained athletes who performed exercises designed to be similar to that used in more typical athletic regimens and recruit and activate a large amount of muscle tissue. Despite the fact that RE trained athletes participated in the present study utilizing a whole body RE protocol, we did not observe changes in IL-2 and therefore a benefit from CHO supplementation. Conclusions In conclusion, this was the first study to report salivary immune responses using paired-exercises during an acute resistance training session. The paired-exercise format increased the acute exercise session duration to over 40 min in order to elicit a greater stress and immune response. The results of the present study suggest that IL-5 decreases after RE, but s-IgA and IL-2 levels remain stable. Furthermore, the present data suggest that CHO supplementation prior to-, during or following RE did not appear to alter salivary or cytokine immune responses. These findings are important, because as previously reported in the literature, CHO supplementation may assist in reducing exercise-induced suppression of various aspects of the immune system.

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Authors’ contributions AM participated in the study design, condu

Authors’ contributions AM participated in the study design, conducted the experimental work, analyzed and interpreted data, and wrote the manuscript. LS conducted the statistical analysis. KN and LA conceived the study, participated in the study design process and reviewed the manuscript. All authors read and approved the final manuscript.”
“Background The Gram-negative bacterium Shigella dysenteriae serotype 1 (SD1) is among the most virulent serotypes of the four Shigella (S.) species (S. dysenteriae, S. flexneri, NVP-BGJ398 S. sonnei and S. boydii). SD1 is a causative agent of shigellosis, a severe form of epidemic bacillary dysentery in humans and primates

[1, 2]. Shigellosis is most prevalent in underdeveloped countries, with a mortality rate of 10-15% when untreated, killing about 1.1 million people of the roughly 120 million cases each year http://​www.​who.​int/​vaccine_​research/​diseases/​diarrhoeal/​en/​index6.​html. SD1 has an extremely low infectious dose of 10-100 organisms which has contributed to causing pandemic Shiga dysentery in several continents including Asia, Africa and Central America [2]. In addition to having a low infectious dose, multi-drug antibiotic resistance to more than six types LY2874455 supplier of antibiotics (tetracycline, streptomycin,

chloramphenicol, etc.) has developed in several Shigella serotypes [3]. S. dysenteriae is also very closely related to Escherichia (E.) coli, with certain strains of E. coli (Shiga toxin-producing E. coli, or STEC) producing the potent Shiga toxins (Stx) of which Stx1 is produced by SD1 as well [4]. Shiga toxin causes cell death primarily in the microvascular endothelium. A vaccine that is protective against Shigella serotypes is of utmost importance, and several attenuated vaccines are currently being developed and tested in human volunteers. Components of the Type Three Secretion

System (TTSS) encoded by a virulence plasmid are also involved in the pathogenesis of shigellosis [5]. Also called the Mxi-Spa system in Shigella, the TTSS is responsible for triggering entry into host epithelial cells and apoptosis in macrophages [6, 7]. The TTSS is activated upon contact Aurora Kinase with host cells, leading to the integration of translocators in the host cell membranes which then promotes transit of effectors into host cells [8]. The TTSS and effector proteins thereby play an important role in infection and intra- and inter-cellular spreading of bacterial cells in the host intestinal epithelium [9]. O-antigens present in the cell surface lipopolysaccharide (LPS) of Shigella also contribute to its virulence [2]. The Shigella O-antigen comprises of a toxic lipid A moiety embedded in the bacterial outer membrane, a core sugar region and an exposed terminal O-polysaccharide. In SD1, the O-polysaccharide consists of tetrasaccharide repeats that contain repeat units of three rhamnose Quisinostat solubility dmso residues and one N-acetylglucosamine [2].

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Here, we showed a significant induction of apoptotic cell death f

Here, we showed a significant induction of apoptotic cell death following AZD8931 treatment in vitro in IBC cells. Most significantly, in current IBC models, we showed that AZD8931 monotherapy significantly inhibited tumor growth and the combination of paclitaxel + AZD8931 resulted in the highest levels of tumor growth inhibition in vivo in both cell lines (Figure  4). The most common treatment for IBC is multimodal involving neoadjuvant

combination chemotherapy followed by surgery, selleck adjuvant chemotherapy, or radiotherapy [5]. Conventional chemotherapy regimens are not sufficient for the treatment of IBC, particularly for TNIBC. Targeted therapy against HER2 is one promising strategy for the treatment of IBC patients with HER2 amplification. Several EGFR targeted therapies including small molecule inhibitors and anti-EGFR antibodies have been evaluated in preclinical and clinical studies [21–25]. Patients with EGFR expressing tumors did not respond to EGFR-targeted therapy, which suggests that EGFR expression alone does not indicate tumor cell growth dependence on the EGFR pathway.

One study indicated that the significant interactions between EGFR and other alternative signaling pathway kinases, such as c-MET and IGF-1R are linked to resistance to targeted therapies [26]. Thus, future studies are warranted to consider combining of EGFR-targeted therapy with drugs targeting other alternate signaling pathways to improve efficacy. Several antibodies targeting EGFR have also been investigated for their efficacy in patients with TNBC, some results have showed the clinical benefit in combination BIBW2992 purchase with chemotherapy drugs for patients with TNBC [27, 28]. Metastasis is the primary cause of breast cancer mortality. IBC is characterized by locally advanced disease and high rates of metastasis even after multimodality treatments [29]. In IBC, inflammation is associated with the invasion of aggregates of tumor

cells defined as tumor emboli, into the dermal lymphatics causing an obstruction of the lymph Phosphatidylinositol diacylglycerol-lyase channels [30]. Currently, the molecular pathways driving the early development of metastasis in IBC remain poorly characterized. EGFR family and its downstream signaling pathways are known to promote cell migration, angiogenesis, invasion, and metastasis [22]. Previous studies have shown that the EGFR inhibitor erlotinib (Tarceva™) significantly inhibited cell motility, invasiveness, tumor growth, and spontaneous lung metastasis in EGFR-expressing IBC models [31]. Further therapeutic studies are warranted to examine the effects of AZD8931 on the invasiveness and metastasis of IBC. Conclusions We demonstrate that EGFR/HER2/HER3-targeting with AZD8931 is associated with promising preclinical activity in EGFR-overexpressed and HER2 non-amplified IBC models, suggesting an important novel therapeutic approach for this aggressive disease.

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A 100 μL drop of MSgg was mounted on top of the biofilm and NO mi

A 100 μL drop of MSgg was mounted on top of the biofilm and NO microprofiles STA-9090 supplier were measured immediately with an NO microsensor as described previously [43]. For each experimental treatment, MSgg was supplied either with or without 300 μM of the NO donor SNAP. SNAP was mixed

to MSgg directly before the experiment. Experimental treatments were as followed: (i) wild-type: B. subtilis 3610 for which MSgg agar and drop were added without further supplementation; (ii) wild-type: B. subtilis 3610 for which MSgg agar and drop were supplemented with 100 μM L-NAME; and (iii) B. subtilis 3610 Δnos for which MSgg agar and drop were added without further supplementation. Acknowledgements We thank Bernhard Fuchs (MPI Bremen) for help with flow cytometry and Pelin Yilmaz (MPI Bremen) for help during initial Belinostat datasheet stages of swarming experiments. This study was supported by the Max Planck Society. Electronic supplementary material Additional file 1: Figure S1. Theoretical formation of NO from the NO donor Noc-18. The figure shows the calculated formation of NO over time for different starting concentrations of Noc-18. Figure S2. Theoretical formation of NO from the NO donor SNAP. The figure shows the calculated formation of NO over time for different starting concentrations of SNAP. (PDF 160 KB) References 1. Bredt DS, Snyder SH: Nitric-Oxide – a Physiological HTS assay Messenger Molecule. Annu Rev Biochem 1994, 63:175–195.PubMedCrossRef

2. Alderton WK, Cooper CE, Knowles RG: Nitric oxide synthases: structure,

function and inhibition. Biochem J 2001, 357:593–615.PubMedCrossRef 3. Stamler JS, Lamas S, Fang FC: Nitrosylation: The prototypic redox-based signaling mechanism. Cell 2001, 106:675–683.PubMedCrossRef 4. Sudhamsu J, Crane BR: Bacterial nitric oxide synthases: what are they good for? Trends Microbiol 2009, 17:212–218.PubMedCrossRef 5. Adak S, Aulak KS, Stuehr DJ: Direct evidence for nitric oxide production by a nitric-oxide synthase-like protein from Bacillus subtilis. J Biol Chem 2002, 277:16167–16171.PubMedCrossRef 6. Gusarov I, Nudler E: NO-mediated cytoprotection: Instant adaptation to oxidative stress Resminostat in bacteria. Proc Natl Acad Sci USA 2005, 102:13855–13860.PubMedCrossRef 7. Gusarov I, Shatalin K, Starodubtseva M, Nudler E: Endogenous Nitric Oxide Protects Bacteria Against a Wide Spectrum of Antibiotics. Science 2009, 325:1380–1384.PubMedCrossRef 8. Kers JA, Wach MJ, Krasnoff SB, Widom J, Cameron KD, Bukhalid RA, Gibson DM, Crane BR, Loria R: Nitration of a peptide phytotoxin by bacterial nitric oxide synthase. Nature 2004, 429:79–82.PubMedCrossRef 9. Spiro S: Regulators of bacterial responses to nitric oxide. Fems Microbiol Rev 2007, 31:193–211.PubMedCrossRef 10. Zumft WG: Nitric oxide reductases of prokaryotes with emphasis on the respiratory, heme-copper oxidase type. J Inorg Biochem 2005, 99:194–215.PubMedCrossRef 11. Aguilar C, Vlamakis H, Losick R, Kolter R: Thinking about Bacillus subtilis as a multicellular organism.

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FEMS Microbiol Ecol 2008, 66:567–578 CrossRefPubMed 3 Ritchie LE

FEMS Microbiol Ecol 2008, 66:567–578.Histone Acetyltransferase inhibitor CrossRefPubMed 3. Ritchie LE, Steiner JM, Suchodolski JS: Assessment of microbial diversity along the feline intestinal tract using

16S rRNA gene analysis. FEMS Microbiol Ecol 2008, 66:590–598.CrossRefPubMed 4. Suchodolski JS, Morris EM, Allenspach K, Jergens A, Harmoinen J, Westermarck E, Steiner JM: Prevalence and identification of fungal DNA in the small intestine of P505-15 concentration healthy dogs and dogs with chronic enteropathies. Vet Microbiol 2008, 132:379–388.CrossRefPubMed 5. Guarner F: Enteric flora in health and disease. Digestion 2006, 73:5–12.CrossRefPubMed 6. Frank DN, Amand ALS, Feldman RA, Boedeker EC, Harpaz N, Pace NR: Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases. PNAS USA 2007, 104:13780–13785.CrossRefPubMed 7. Marks SL, Kather EJ: Bacterial-associated diarrhea in the dog: a critical appraisal. Vet Clin North Am Small Anim Pract 2003, 33:1029–1060.CrossRefPubMed 8. Dethlefsen L, Huse S, Sogin ML, Relman DA: The pervasive effects of an antibiotic on the human gut microbiota, as revealed by deep 16S rRNA sequencing. PLoS Biol 2008, 6:e280.CrossRefPubMed 9. Collier CT, Smiricky-Tjardes MR, Albin DM, Wubben JE, Gabert VM, Deplancke B, Bane D, Anderson DB, Gaskins HR: Molecular ecological

analysis of porcine ileal microbiota responses to antimicrobial growth promoters. J Anim Sci 2003, 81:3035–3045.PubMed 10. Marks SL, Kather EJ: Antimicrobial susceptibilities of canine Clostridium difficile and Clostridium NVP-BSK805 perfringens isolates to commonly utilized antimicrobial drugs. Vet Microbiol 2003, 94:39–45.CrossRefPubMed 11. Suchodolski JS, Steiner JM: Laboratory assessment of gastrointestinal function. Clin Tech Small Anim Pract 2003, 18:203–210.CrossRefPubMed 12. Westermarck E, Skrzypczak T, Harmoinen J, Steiner JM, Ruaux CG, Williams DA, Eerola E, Sundbäck P, Rinkinen M: Tylosin-responsive chronic diarrhea in dogs. J Vet Int Med 2005, 19:177–186.CrossRef

13. Cao XY, Dong M, Shen JZ, Wu BB, Wu CM, Du XD, Wang Z, Qi YT, Li BY: Tilmicosin and tylosin have anti-inflammatory properties via modulation of COX-2 and iNOS gene expression and production MYO10 of cytokines in LPS-induced macrophages and monocytes. Int J Antimicrob Agents 2006, 27:431–438.CrossRefPubMed 14. Menozzi A, Pozzoli C, Poli E, Lazzaretti M, Cantoni A, Grandi D, Giovannini E, Coruzzi G: Effect of the Macrolide Antibacterial Drug, Tylosin, on TNBS-Induced Colitis in the Rat. Pharmacology 2005, 74:135–142.CrossRefPubMed 15. Blackwood RS, Tarara RP, Christe KL, Spinner A, Lerche NW: Effects of the macrolide drug tylosin on chronic diarrhea in rhesus Macaques (Macaca mulatta). Comp Med 2008, 58:81–87.PubMed 16. De La Cochetiere MF, Durand T, Lepage P, Bourreille A, Galmiche JP, Dore J: Resilience of the dominant human fecal microbiota upon short-course antibiotic challenge. J Clin Microbiol 2005, 43:5588–5592.CrossRef 17.

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CrossRef 4 Suárez S, Devaux A, Bañuelos J, Bossart O, Kunzmann A

CrossRef 4. Suárez S, Devaux A, Bañuelos J, Bossart O, Kunzmann A, Calzaferri G: Transparent zeolite–polymer hybrid

materials with adaptable properties. Adv Funct Mater 2007, 17:2298–2306.CrossRef 5. Althues H, Henle J, Kaskel S: Functional inorganic nanofillers for transparent polymers. Chem Soc Rev 2007, 36:1454–1465.CrossRef 6. Iskandar F: Nanoparticle processing for MI-503 supplier optical applications – a review. Adv Powder Technol 2009, 20:283–292.CrossRef 7. Ruiterkamp GJ, Hempenius MA, Wormeester H, Vancso GJ: Surface VRT752271 functionalization of titanium dioxide nanoparticles with alkanephosphonic acids for transparent nanocomposites. J Nanoparticle Res 2010, 13:2779–2790.CrossRef 8. Jeon I-Y, Baek J-B: Nanocomposites derived from polymers and inorganic selleck chemical nanoparticles. Materials 2010, 3:3654–3674.CrossRef 9. Lu C, Cui Z, Wang Y, Li Z, Guan C, Yang B, Shen J: Preparation and characterization of ZnS–polymer

nanocomposite films with high refractive index. J Mater Chem 2003, 13:2189–2195.CrossRef 10. Lu C, Cheng Y, Liu Y, Liu F, Yang B: A Facile route to ZnS-polymer nanocomposite optical materials with high nanophase content via gamma-ray irradiation initiated bulk polymerization. Adv Mater 2006, 18:1188–1192.CrossRef 11. Bhagat SD, Chatterjee J, Chen B, Stiegman AE: High refractive index polymers based on thiol-ene cross-linking using polarizable inorganic/organic monomers. Macromolecules 2012, 45:1174–1181.CrossRef 12. Jha G, Seshadri G, Mohan A, Khandal R: Sulfur containing optical plastics and its ophthalmic lenses applications. e-Polymer 2008, 035:1–27. 13. Kudo H, Inoue H, Inagaki T, Nishikubo T: Synthesis and refractive-index properties of star-shaped polysulfides radiating from calixarenes. Macromolecules 2009, 42:1051–1057.CrossRef 14. You N, Higashihara T, Suzuki Y, Ando S, Ueda M: Synthesis of sulfur-containing poly(thioester)s with high refractive indices and high Abbe numbers. Polym Chem 2010, 1:408–484.CrossRef 15. Okuda H, Seto R, Koyama Y, Takata T: Poly(arylene thioether)s containing 9,9′-spirobifluorene moieties in the main

chain: masked dithiol-based synthesis and excellent optical properties. J Polym Sci A Polym Chem 2010, 48:4192–4199.CrossRef 16. Nakagawa Y, Suzuki Y, Higashihara ifenprodil T, Ando S, Ueda M: Synthesis of highly refractive poly(phenylene thioether) derived from 2,4-dichloro-6-alkylthio-1,3,5-triazines and aromatic dithiols. Macromolecules 2011, 44:9180–9186.CrossRef 17. Li C, Cheng J, Yang F, Chang W, Nie J: Synthesis and cationic photopolymerization of a difunctional episulfide monomer. Prog Org Coat 2013, 76:471–476.CrossRef 18. Bain CD, Troughton EB, Tao YT, Evall J, Whitesides GM, Nuzzo RG: Formation of monolayer films by the spontaneous assembly of organic thiols from solution onto gold. J Am Chem Soc 1989, 111:321–335.CrossRef 19. Schlenoff JB, Li M, Ly H: Stability and self-exchange in alkanethiol monolayers. J Am Chem Soc 1995, 117:12528–12536.CrossRef 20.

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