Infect Immun 1996,64(8):3259–3266 PubMedCentralPubMed 45 Peters-

Infect Immun 1996,64(8):3259–3266.PubMedCentralPubMed 45. Peters-Golden M, McNish RW, Hyzy R, Shelly C, Toews GB: Alterations in the pattern of arachidonate metabolism accompany rat macrophage differentiation in the lung. J Immunol 1990,144(1):263–270.PubMed 46. Page B, Page M, Noel C: A new fluorometric assay for cytotoxicity measurements in-vitro. Int J Oncol 1993,3(3):473–476.PubMed Competing interests Tanespimycin The authors declare that they have no competing interests. Authors’ contributions

PAA: Conceived and designed the experiments; PAA, MSE, WMR, and PATP: Performed the experiments; PAA, MSE, and FWGPS: Analysed the data; LHF, SCL, and CLS: Contributed reagents/materials/analysis tools; PAA, MSE, FWGPS, and LHF: Wrote the manuscript. All authors read and approved the final manuscript.”
“Background Around 5.2 million children under five years old die yearly due to preventable

infectious diseases like pneumonia and diarrhoea [1, 2]. Among these infectious diseases, viral gastrointestinal infections belong to the most frequent diseases suffered in childhood, especially in the developing world. Rotavirus, a RNA virus, is the most common cause of severe dehydrating diarrhoea in children worldwide [3, 4]. Although there is already a successful rotavirus vaccine in the market, the epidemic in the developing world is far from being controlled [4, 5]. Apart from being not affordable for low-income population groups, it has also been shown that protection induced by natural infection and vaccination is reduced in developing areas, Dorsomorphin where among other factors, children are infected at an early age and high viral challenge loads are usual [6]. Moreover, Latin America in general and northern Argentina in particular, presents a significant population of malnourished children with its associated burden of otherwise preventable infectious

diseases such as rotavirus infections [2]. Several studies have demonstrated that certain lactic acid bacteria (LAB) strains can exert their beneficial effect on the host through their immunomodulatory activity. In this sense, some studies have centred on whether immunoregulatory probiotic LAB (immunobiotics) might sufficiently stimulate the intestinal immune Resveratrol system to provide protection against viral infections. It was reported that probiotics can exerts some beneficial effects in rotavirus intestinal infections such as shortening the duration of diarrhoea, reducing the number of episodes, lessening rotavirus shedding, normalizing gut permeability and increasing the production of rotavirus-specific antibodies [7–9]. In an attempt to find low-cost alternatives for the prevention of infectious diseases we have developed a new probiotic yogurt, containing the immunobiotic strain Lactobacillus rhamnosus CRL1505, able to improve resistance against respiratory and intestinal infections.

Genotyping The genomic DNA to be used was isolated for the previo

Genotyping The genomic DNA to be used was isolated for the previous study [1]. The genotype of OGG1 Ser326Cys [7] and MUTYH Gln324His [16] was determined by PCR-RFLP analysis, as described previously. Statistical analysis Statistical analysis was performed with the SPSS software package (version 14.0 for Windows; SPSS Ivacaftor Japan Inc., Tokyo, Japan). Hardy-Weinberg equilibrium was tested using the goodness-of-fit Chi-square test to compare the observed genotype frequencies with the expected genotype frequencies among the control subjects. Associations were expressed as odds-ratios (OR) with 95% confidence interval (95% CI) and p < 0.05 was considered statistically significant. Logistic regression analysis was

performed to assess the association between each genotype and lung cancer. ORs, which were computed to estimate the association between certain genotypes and lung cancer, were adjusted for age, gender, and smoking habit (number of pack-years smoked). The subjects were divided into two groups according to pack-years smoked: never-smokers (pack-years = 0) and ever-smokers (pack-years > 0). Results We present the characteristics of lung cancer in Table 1, including 108 patients and 121 controls. There

was no difference in the gender distribution (p = 0.491) between males (patients, 65.7%; controls, 61.2%) and females (patients, 34.3%; controls, 38.8%). There was no difference in the average ages (± SD) between patients (65.5 ± 9.4 years) and controls (67.4 ± 6.7 years) (p = 0.078). Non-smokers selleck comprised 29.6% of patients and 45.5% of controls and smokers comprised 68.5% of patients and 49.6% of controls. There was also no difference in the average pack-years (± SD) between Rucaparib chemical structure patients (33.8 ± 31.7) and controls (25.6 ± 35.1) (p = 0.069). Histological types of the patients were: 67 adenocarcinoma

(62.0%), 31 squamous cell carcinoma (28.7%) and 10 others (9.3%). Table 1 Characteristics of lung cancer case and control subjects     Patients Controls   Item n % n % P-value Number   108   121     Gender               males 71 65.7 74 61.2 0.491a   females 37 34.3 47 38.8   Age               ~64 40 37.0 50 41.3     65~69 17 15.7 29 24.0     70~74 30 27.8 20 16.5     75~ 19 17.6 22 18.2     unknown 2 1.9 0 0.0     Mean ± S.D. 65.5 ± 9.4   67.4 ± 6.7   0.078b Smoking status (Pack-years)               Never (Pack-years = 0) 32 29.6 55 45.5     Ever (Pack-years > 0) 74 68.5 60 49.6     unknown 2 1.9 6 5.0     Mean ± S.D. 33.8 ± 31.7   25.6 ± 35.1   0.069b Histological type               adenocarcinoma 67 62.0         squamous cell carcinoma 31 28.7         others 10 9.3       a: χ2 analysis b: Student’s T-test Genotyping results of OGG1 Ser326Cys and MUTYH Gln324His adjusted for gender, age, and smoking habit along with allele frequencies are shown in Table 2. The allele frequencies of the two gene polymorphisms in controls were consistent with the Hardy-Weinberg equilibrium.

This result matched the expectation of the priori statistical pow

This result matched the expectation of the priori statistical power calculation. Figure 2 Running time to exhaustion in the exercise (Ex) and exercise plus sweet cassava polysaccharide (ExSCP) groups. *Significantly differs from the Ex group at p > 0.05. The glycogen contents of the soleus muscle in the Ex group were significantly lower than in the ExSCP and C groups. In addition, those of the ExSCP group were significantly lower than the C group. The glycogen contents of the gastrocnemius muscle of the Ex group were significantly lower than those of Ensartinib mw the C and ExSCP groups,

but no significant difference was evident between the C and ExSCP groups (Figure 3, Table 1). Figure 3 Gastrocnemius and soleus muscle glycogen

content in each group. Notes: C, control group; Ex, exercise group; ExSCP, exercise plus sweet cassava polysaccharide group. #Significantly different from the C and ExSCP groups. ※Significantly different from the C group at p > 0.05. Table 1 The muscle glycogen content of the gastrocneminus and soleus selleck inhibitor muscles in the three groups (post-exercise in the Ex and ExSCP group)   C Ex ExSCP Gastrocnemius (mg/g) 2.1 ± 0.5 1.0 ± 0.3# 1.7 ± 0.2 Soleus (mg/g) 3.1 ± 0.9 1.1 ± 0.6# 2.2 ± 0.4※ #Signifinantly different from the C and ExSCP groups. ※Significantly different from the C group at p > 0.05. Notes: C, control group; Ex, exercise group; ExSCP, exercise plus sweet cassava polysaccharide group. Regarding the metabolites in the circulation, blood glucose levels in the Ex group were significantly lower than those in the ExSCP and C groups; no significant difference was found between the ExSCP and C groups (Figure 4). Similarly, the second FFA concentration of the Ex group was significantly lower than

that of the C and ExSCP groups, but no significant difference was evident between the C and ExSCP groups (Figure 5). In the case of insulin, no significant differences were found among the three groups, although the Ex group had lower concentrations compared to the other two groups (Figure 6, Table 2). Figure 4 Blood glucose concentrations in each group. #Significantly different from the C and ExSCP groups at p > 0.05. Figure 5 Free fatty acid concentrations in each group. #Significantly different from the C and ExSCP groups at p > 0.05. Figure 6 Insulin concentrations in each group. Table 2 The blood metabolites in the three groups (post-exercise in the Ex and ExSCP group)   C Ex ExSCP BG (mg/dL) 111.4 ± 5.6 100.1 ± 1.9# 109.1 ± 4.7 FFAs (mEq/L) 1.2 ± 0.1 0.8 ± 0.1# 1.2 ± 0.1 Insulin (μg/L) 0.064 ± 0.006 0.058 ± 0.006 0.064 ± 0.007 Notes: BG: blood glucose; FFAs: free fatty acids. #Significant different form the C and ExSCP groups.

49 Gauglianone P, Chan K, DelaFfor-Weiss E, Hanixh R, Jeffers S,

49. Gauglianone P, Chan K, DelaFfor-Weiss E, Hanixh R, Jeffers S, Sharma D, Muggia F: Phase I and pharmacologic study of liposomal daunorubicin (DaunoXome). Invest New Drugs 1994, 12:103–110.CrossRef find more 50. Eckardt JR, Campbell E, Burris HA, Weiss CR, Rodriguez CI, Fields SM, Thurman AM, Peacock NW, Cobb P, Rothenbeig ML: A phase II trial of DaunoXome, liposome-encapsulated daunorubicin,

in patients with metastatic adenocarcinoma of the colon. Am Clin Oncol 1994, 17:498–501.CrossRef 51. Schurmann D, Dormann A, Grunewald T, Ruf B: Successful treatment of AIDS-related pulmonary Kaposi’s sarcoma with liposomal daunorubicin. Eur Respir J 1994, 7:824–825.CrossRef 52. New RRC, Chance SM, Thomas SC, Peters W: Nature antileishmanial activity of antimonials entrapped buy LY2835219 in liposomes. Nature 1978, 272:55–58.CrossRef 53. Lopez-Berestein G, Fainstein V, Hopter R, Mehta KR, Sullivan M, Keating M, Luna M, Hersh EM: Liposomal amphotericin B for the treatment of systemic fungal infections in patients with cancer. J Infect Diseases 1985, 151:704–710.CrossRef 54. Lasic DD: Mixed micelles in drug delivery. Nature 1992, 355:279–280.CrossRef 55. Svenson CE, Popescu MC, Ginsberg RC: Liposome treatments of viral, bact and protozoal infections. Crit Rev Microbiol 1988, 15:S1-S31.CrossRef 56. Gabizon A: Liposomes as a drug delivery system in cancer therapy.

In Drug Carrier Systems. Edited by: Roerdink FHD, Kron AM. Chichester: Wiley; 1989:185–211. 57. Storm G, Roerdink FH, Steerenberg PA, de Jong WH, Crommelin DJA: Influence of lipid composition on the antitumor activity exerted by doxorubicin containing liposomes in a rat solid tumor model. Cancer Res 1987, 47:3366–3372. 58. Akbarzadeh A, Asgari D, Zarghami N, Mohammad R, Davaran S: Preparation and in

vitro evaluation of doxorubicin-loaded Fe 3 O 4 magnetic nanoparticles modified with biocompatible co-polymers. Int J Nanomedicine 2012, 7:511–526. 59. Akbarzadeh A, Zarghami N, Mikaeili H, Asgari D, Goganian AM, Khiabani HK, very Samiei M, Davaran S: Synthesis, characterization, and in vitro evaluation of novel polymer-coated magnetic nanoparticles for controlled delivery of doxorubicin. Nanotechnol Sci Appl 2012, 5:13–25. 60. Akbarzadeh A, Samiei M, Davaran S: Magnetic nanoparticles: preparation, physical properties, and applications in biomedicine. Nanoscale Res Lett 2012, 7:144.CrossRef 61. Valizadeh A, Mikaeili H, Samiei M, Mussa Farkhani S, Zarghami N, Kouhi M, Akbarzadeh A, Davaran S: Quantum dots: synthesis, bioapplications, and toxicity. Nanoscale Res Lett 2012, 7:480.CrossRef 62. Akbarzadeh A, Samiei M, Joo SW, Anzaby M, Hanifehpour Y, Nasrabadi HT, Davaran S: Synthesis, characterization and in vitro studies of doxorubicin-loaded magnetic nanoparticles grafted to smart copolymers on A549 lung cancer cell line. J Nanobiotechnology 2012, 10:46.CrossRef Competing interests The authors declare that they have no competing interests.

International variations in hip fracture risk have displayed a no

International variations in hip fracture risk have displayed a north–south gradient [6] which has been linked to the importance of sunlight exposure [22]. A study using national data from France showed substantial heterogeneity of hip fracture risk within the country, with higher hip fracture risk in the Southern France [23]. Other studies reporting regional differences in hip fracture rates within countries explain the differences by an urban–rural gradient [24]. In a study from Australia, the age-adjusted

incidence of hip fracture was 32% selleck products lower in rural compared to urban residents aged 60 years and above, 26% lower in women [25]. In comparison, the age-adjusted rates in women aged 65 years and above were 21% lower in Harstad than in the more urbanized capitol Oslo [8]. Unfortunately, with the registry data available, we do not have explanation for the indicated urban–rural difference, but another Norwegian study reported higher bone mineral density levels in rural versus urban dwellers at the hip [26], one factor which may explain differences in fracture risk. In a study by Ringsberg et al. [27], urban subjects had significantly poorer balance

compared with their rural counterparts, a difference which increased with increasing age, affected gait performance and Selleckchem Ceritinib risk of falls. With an extensive prevention program running in Harstad between 1988 and 1993 [18, 19] and part of this program still integrated in the community health service, this may also explain the differences in fracture rates between Harstad and Oslo. It could furthermore be expected Fossariinae that the extensive prevention program might have resulted in lower fracture rates especially in the first years after 1994. However, comparison of the two periods, 1994–1996 and 2006–2008, indicated no significant change in the age-adjusted incidence rates in any of the sexes during the time of the study. Interestingly, this stability of age-adjusted incidence rates is in accordance

with data from Oslo [8] and reports from several other countries including Finland, Denmark, Norway, Switzerland, Canada, US and Australia [10, 12–15, 28]. There are studies reporting increasing numbers of hip fracture rates in women and men in Germany and Austria [29, 30], in men in Switzerland [28], in the oldest age groups in Swedish [31] and Swiss [32] women. Conflicting results are also reported within countries where, for example, a recent paper from the Australian Capital Territory reported significant declining hip fracture rates after 2001 in women [13], while other data from Australia indicate no change in incidence [33]. The Australian report suggests that the declining hip fracture rates may be explained by increased use of anti-osteoporotic treatments [13].

Hence, this work includes all the results of both [4] (no power s

Hence, this work includes all the results of both [4] (no power source) and [6] (no resistances) as special cases. The fluctuations and uncertainty product in the DN and in the DSN are plotted in Figure 5. We can adjust the uncertainty (or fluctuation) of a quadrature to be small at the expense of broadening that

of another quadrature, or vice versa. The uncertainty in the case of this figure is larger than , while is smaller than due to the squeezing effect. Therefore, it is relatively difficult for us to know the precise value of charge q 1, while we can find out the conjugate current p 1 more precisely. However, the relevant uncertainty product in the DSN is nearly unaltered from see more that in the DN. Figure 5 Fluctuations. This inset shows fluctuations (dashed line) and (thick solid line) (a), and (dashed line) and (thick solid line) (b), and uncertainty product (dashed line) and (thick solid line)

(c) as a function of t where n 1=n 2=0, , R 0 = R 1 = R 2 = 0.1, L 0 = L 1 = L 2 = 1, C 1 = 1, and C 2 = 1.2. The values of squeezing parameters for the DSN are r 1 = 0.1, r 2 = 0.3, ϕ 1 = 1.2, and ϕ 2 = 0.6. Conclusions In summary, the time evolution of the DSN for the two-dimensional electronic circuit composed of nanoscale elements and driven Caspase inhibitor by a power source is investigated using unitary transformation method. Two steps of the unitary transformation are executed: We removed the cross term involving in the original Hamiltonian from the first step, and the linear terms represented in terms of in the firstly transformed Hamiltonian are eliminated by second unitary transformation.

We can see from Equation 6 that the original Hamiltonian is time-dependent. When treating a time-dependent Hamiltonian system dynamically, one usually employs classical solutions of the equation of motion for a given system (or for a system similar to a given system) [6, 7]. We also introduced such classical solutions in Equations 19 to 20 and in Equations 47 to 48. Among them, particular solutions q j p and p j p are important in developing quantum theory of the system involving most external power source since they are crucial factors that lead the transformed Hamiltonian to be simple so that we can easily treat it. Since the transformed system is just the same as the one that consists of two independent simple harmonic oscillators, provided that we can neglect the trivial terms in the transformed Hamiltonian, we easily identified the complete quantum solutions in the DSN in the transformed system. We also obtained the wave functions of the DSN in the original system via the technique of inverse transformation, as shown in Equation 50. If we regard the fact that the probability does not reflect the phase of a wave function, the overall phase of these states is relatively unimportant for many cases.

[38] This method combines a comparative genomic approach with ge

[38]. This method combines a comparative genomic approach with genome-specific distance models, and has shown some improvements in operon prediction [39]. System design and implementation MyBASE was developed using our established pipeline for biological databases [40–44]. It consists of three hardware components: a World Wide Web server, a database server, and a server for sequence analysis. The system buy LY2606368 is based on a MySQL

relational database and the front end consists of a set of JSP scripts running on a Tomcat web server. Hibernate, a high-performance object/relational persistence and query service for Java, was used for system development. The search engine, Multi-genome Comparison Viewer, was developed using Java. Genome Viewer was implemented using CGView [45]. Utility and discussion Database usage and the toolbox All the data in MyBASE can be easily explored using VX-770 manufacturer the toolbox. The keyword-based search engine enables a multiple keyword (e.g. gene name, COG number, etc.) search across MyBASE, while the BLAST-based sequence search engine allows user to quickly find similar genes to the query. LSP/RD data is a distinct feature of MyBASE. The Polymorphism-LSP/RD module was developed to explore and mine the LSP/RD datasets. Users can search for a genomic polymorphism

region by its name (e.g. RD1), the name of reference strain and query strain in the experiment, start/end positions within its genome, or by literature information. Users can also visualize the distributions of selected RDs in the genome

by using LSP/RD Viewer. RDs in the same dataset are present in one solid line according to its position along the genome (upper-left in Figure 1). Experimental information can be seen when users mouse over the LSP/RD region. To keep the data content in MyBASE most up-to-date, the “”LSP/RD upload”" module was designed for the user to upload their own LSP/RD data to MyBASE. Figure 1 Schematic representation of the data repository and the interrelation of functional modules in MyBASE. After the gene of interest Thymidine kinase is found, users can check whether it is in a genomic polymorphic region, compare the selected genome with MCV, explore the details of its genome segment with Genome Viewer or view its homolog distributions. The Multi-genome Comparison Viewer (MCV) allows users to rapidly align and compare mycobacterial genome synteny by selecting an anchor gene of interest. This module is helpful for genome structure and evolutionary analysis of mycobacteria. Users can select any number of genomes, zoom in or out and move upstream or downstream along the genome in the viewer. Genes in MCV with the same color-coding are predicted homologs via COG designation, while grey indicates that no homolog was detected. More importantly, MCV also displays various featured annotations in MyBASE with different legends.

pseudomallei specificity Figure 1 φX216 one-step growth curve φ

pseudomallei specificity. Figure 1 φX216 one-step growth curve. φX216 was adsorbed to B. mallei ATCC23344 cells for 15 min, inoculated into LB + 2% glycerol, and cultures were incubated at 37°C with shaking. Triplicate aliquots were removed at the SCH727965 solubility dmso indicated time intervals and used to inoculate plaque plates to determine pfu/mL. The pfu/mL values were divided by the means of the T0 and T1 (1 h) phage concentrations to adjust to pfu/input pfu. Of the 56 B. pseudomallei strains that could

be infected with φX216, 24 showed decreased relative plaquing efficiencies with the B. mallei lysate. However, when φX216 lysates were propagated two to three times on these initially low plaquing efficiency strains, lysates were obtained that then plaqued with titers of of 105 to 106 pfu/mL on those same strains. The reason(s) DAPT price for low plaquing efficiencies of B. mallei lysates on some B. pseudomallei strains remain unclear but probably reflect some kind of host restrictive mechanism(s). ϕX216 host receptor Experiments with B. mallei host strains indicated that B. pseudomallei phages φ1026b, φK96243 and φE202 use the lipopolysaccharide (LPS) O-antigen as a host receptor [8–10]. B. mallei O-antigen mutants cannot support infection by these phages and infection is restored if the O-antigen mutation is complemented. φX216 is also unable to infect B. mallei O-antigen mutants but, surprisingly, infection is not restored by complementing the mutation (see Additional

file 1). As opposed to B. mallei, B. pseudomallei O-antigen mutants Histamine H2 receptor still support infection by φX216. Both an engineered deletion of the wbiE gene in B. pseudomallei Bp82 as well as 10 mapped transposon insertions in the wbi genes of B. pseudomallei 1026b formed φX216 plaques with an efficiency comparable to their respective parent strains. Therefore, φX216 may use the wild-type B. mallei O-antigen as a host receptor but not in B. pseudomallei where it uses a different receptor that is absent from B. mallei[11]. ϕX216 genome characterization and chromosomal attachment site To ascertain genomic features of φX216, we initially

determined the entire φX216 genome sequence by low-coverage Sanger sequencing of plasmid clones generated by subcloning of φX216 DNA fragments and gap closing using sequence information obtained from PCR amplicons. This was supported by deep sequencing using the Illumina platform. Differences between Sanger and Illumina sequence runs were resolved by Sanger sequencing of specific phage DNA fragments obtained by PCR amplification using purified phage DNA and chromosomal DNA from φX216 lysogens as templates. The φX216 genome is 37,637 bases in length with a G + C content of 64.8% (GenBank: JX681814). GeneMark software predicted 47 open reading frames (Figure 2). The genome can be subdivided into predicted regions associated with capsid structure and assembly, host cell lysis, tail structure and assembly, and DNA replication and lysogeny (Figure 2).

Emerg Infect Dis 2002, 8:827–832 PubMedCrossRef 7 Annual Report

Emerg Infect Dis 2002, 8:827–832.PubMedCrossRef 7. Annual Report of Nosocomial Infections Surveillance System: Annual Report of Nosocomial Infections Surveillance System. Taiwan: Center for Disease Control; 2009. http://​www.​cdc.​gov.​tw/​english/​ 8. Dijkshoorn L, Nemec A, Seifert H: An increasing threat in hospitals: multidrug-resistant

Acinetobacter baumannii . Nat Rev Microbiol 2007, 5:939–951.PubMedCrossRef 9. Chang HL, Tang CH, Hsu YM, Wan L, Chang YF, Lin CT, Tseng YR, Lin YJ, Sheu JJ, Lin CW, et al.: Nosocomial outbreak of infection with multidrug-resistant Acinetobacter baumannii in a medical center in Taiwan. Infect Control Hosp Epidemiol 2009, 30:34–38.PubMedCrossRef 10. Sengstock DM, Thyagarajan R, Apalara J, Mira A, Chopra T, Kaye KS: Multidrug-resistant Acinetobacter baumannii : an emerging pathogen among older adults in community hospitals and nursing homes. see more GPCR Compound Library purchase Clin Infect Dis 2010, 50:1611–1616.PubMedCrossRef 11. Joseph NM, Sistla S, Dutta TK, Badhe AS, Rasitha D, Parija SC: Role of intensive care unit environment and health-care workers in transmission

of ventilator-associated pneumonia. J Infect Dev Ctries 2010, 4:282–291.PubMed 12. Wang CY, Wu HD, Lee LN, Chang HT, Hsu YL, Yu CJ, Yang PC, Hsueh PR: Pasteurization is effective against multidrug-resistant bacteria. Am J Infect Control 2006, 34:320–322.PubMedCrossRef 13. Rastogi VK, Wallace L, Smith LS: Disinfection of Acinetobacter baumannii -contaminated surfaces relevant to medical treatment facilities with ultraviolet C light. Mil Med 2007, 172:1166–1169.PubMed

14. Doidge M, Allworth AM, Woods M, Marshall P, Terry M, O’Brien K, Goh HM, George N, Nimmo GR, Schembri MA, et al.: Control of an outbreak of carbapenem-resistant Acinetobacter baumannii in Australia after introduction of environmental cleaning with a commercial oxidizing disinfectant. Infect Control Hosp Epidemiol 2010, 31:418–420.PubMedCrossRef 15. Donahue M, Watson LR, Torress-Cook A, Watson PA: Novel use of antimicrobial hand sanitizer in treatment of nosocomial Acinetobacter infection. Orthopedics 2009, 32:58.PubMedCrossRef 16. Martro E, Hernandez A, Ariza J, Dominguez MA, Matas L, Argerich MJ, Martin R, Ausina V: Assessment of Acinetobacter baumannii susceptibility Nutlin-3 in vivo to antiseptics and disinfectants. J Hosp Infect 2003, 55:39–46.PubMedCrossRef 17. Sharma M, Hudson JB: Ozone gas is an effective and practical antibacterial agent. Am J Infect Control 2008, 36:559–563.PubMedCrossRef 18. Wong MS, Sun DS, Chang HH: Bactericidal performance of visible-light responsive titania photocatalyst with silver nanostructures. PLoS One 2010, 5:e10394.PubMedCrossRef 19. Wisplinghoff H, Schmitt R, Wohrmann A, Stefanik D, Seifert H: Resistance to disinfectants in epidemiologically defined clinical isolates of Acinetobacter baumannii . J Hosp Infect 2007, 66:174–181.PubMedCrossRef 20.

Figure 7 SEM images of NW-NWL hybrid, ZnO NWL, and nanofin-NW hyb

Figure 7 SEM images of NW-NWL hybrid, ZnO NWL, and nanofin-NW hybrid. (a) Low magnification 52° side-view SEM image of the NW-NWL hybrid. Inset, higher magnification 52° SEM image shows the formation of NWL. Scale bar is 500 nm. (b) Top-view SEM image of ZnO NWL. Inset, higher magnification

52° side-view SEM image of the sample. Scale bar is 1 μm. (c) Top-view SEM image shows the presence of Au catalyst at the root and Zn cluster drift in random directions terminated with growth of NW. Inset shows higher magnification 52° side-view SEM image of the sample. Scale bar is 200 nm. (d) Low magnification 52° side-view SEM image of the nanofin-NW hybrid. Inset shows higher magnification 52° side-view SEM image of the sample. Scale bar is 500 nm. To follow the morphological evolution of the ZnO nanostructures, time-dependent growths were also carried out on the SiC substrates using the different Au nanoparticle densities. For this present investigation, the growth temperature was fixed at 900°C, while the growth times were either 90 or 180 min. Figure 7 presents the experimental results obtained for ZnO nanomaterial synthesis as a function of time. In Figure 7a, b, the growth of the ZnO NW-NWL hybrids and NWLs is obtained by varying time between

90 and 180 min, respectively, Selleckchem CHIR 99021 for the high-density Au nanoparticle case. Once again, the drifting was effectively halted by Zn clusters merging with other clusters and/or Au seed nanoparticles resulting in the formation of complete ZnO networks over large areas of the SiC substrates, as already shown in Figure 6b. When growing with low-density Au nanoparticles, the following Idoxuridine observations can be made: (i) the drift of the Zn cluster results in the formation of vertically oriented ZnO NWs at the Zn cluster drift sites and not at the seed particle site as shown in Figure 7c, and (ii) with increasing growth time (Figure 7d), a new form of nanostructure can be observed, in which NWLs are effectively terminated by NWs at one end. These observations were found to be consistent with the

so-called nanofins, reported in [19]. With longer synthesis time (180 min), we observed that the boundaries between ZnO NWs and horizontal trace of the Zn cluster were more favorable nucleation sites, forcing the growth of the observed ZnO nanofin-NW structures. Based on the experimental observations, the growth mechanisms for ZnO nanoarchitectures at 900°C are schematically illustrated in Figure 8. The first step of the process is the conversion of the Au thin film into spherical- and/or hexagonal-shaped nanoparticles, described by the ripening process [28]. The density of the Au nanoparticles, which can be controlled by the thickness of the sputtered Au layer, plays a key role in determining the final morphology of ZnO nanostructure.