Th1 cells probably exert a tumor suppressive effect in bladder cancer [13]. In fact, in bladder

tumor patients, a marked polarization exists towards the expression of Th2-type cytokines, whereas Th1 remains suppressed. Th1 cytokines play an important role in bacillus Calmette-Guérin (BCG)-induced macrophage cytotoxicity, and the combination of BCG with select Th1-stimulating cytokines may enhance the effect of BCG in the treatment of bladder cancer patients [41]. In patients undergoing BAL anesthesia, a significant eFT508 clinical trial reduction in Treg levels of 30% was observed in the early peri-operative period (T1) (p = 0.03; Table 3) and remained constant up to T2, showing values similar to those measured in healthy controls. This is the first study to evaluate the effect on circulating levels of Tregs due to various types of anesthesia. Earlier evidence suggested that Tregs accumulate in tumors and in the peripheral blood of patients with cancer and through suppression of the anti-tumor immune response these cells promote tumor growth and disease progression in a variety of human malignancies, including

bladder cancer [18, 19, 42]. The role of Tregs in metastasis is just beginning to emerge, and circulating Tregs are ATM Kinase Inhibitor in vitro associated with poor prognosis in some human cancers [43]. In vivo expansion of Tregs is mediated by glucocorticoid-induced tumor necrosis factor receptor family-related (GITR) proteins [44]. Interestingly, Tregs detected in tumor tissues express high levels of GITR molecules. Depletion of Tregs by anti-GITR mAb represents a novel mechanism for cancer immunotherapy [45]. Therefore, the reduction in Tregs we observed in the BAL group appears particularly remarkable in patients with bladder cancer, a type of neoplasm that is responsive to immunotherapy. Conclusions The increase in the Th1 response observed in the TIVA-TCI group and the reduction in Tregs observed in BAL patients seem to balance

the putative immunosuppressive effect induced by IL-6 and supports the hypothesis that TIVA-TCI and BAL techniques can be both used during major surgery in patients with bladder cancer without worsening the Capmatinib price outcome. Funding This work these was supported by a grant from “Istituto Nazionale Tumori Regina Elena” and “Ministero della Salute” for the Research project “Anesthesia and Immunity.” References 1. Grivennikov SI, Greten FR, Karin M: Immunity, inflammation, and cancer. Cell 2010, 140:883–899.PubMedCrossRef 2. Rakoff-Nahoum S, Medzhitov R: Toll-like receptors and cancer. Nat Rev Cancer 2009, 9:57–63.PubMedCrossRef 3. Margel D, Pevsner-Fischer M, Baniel J, Yossepowitch O, Cohen IR: Stress proteins and cytokines are urinary biomarkers for diagnosis and staging of bladder cancer. Eur Urol 2011, 59:113–119.PubMedCrossRef 4. Kurosawa S, Kato M: Anesthetics, immune cells, and immune responses. J Anesth 2008, 22:263–277.PubMedCrossRef 5. Homburger JA, Meiler SE: Anesthesia drugs, immunity, and long-term outcome.

Firstly,

the clinical recognition and effective management of fungal infections in surgical settings is challenging and the strategy to reduce damages needs a multistep diagnostic approach to establish a certain diagnosis. Secondly, the study underlines the importance of culture and histological examination of surgical specimens, which could detect the presence of fungi even when blood cultures are negative. Finally, histological examination allows us to observe the quantity and the morphological aspects of budding Proteases inhibitor hyphae which can suggest a real overgrowth and a pathogenic role. More consideration needs to be given to selecting the appropriate antifungal agent for high-risk surgical patients. Consent Written informed consent was obtained from patients for publication of these Case Reports and any accompanying images. Geneticin purchase A copy of the written consent is available for review by the Editor-in-Chief of this journal. References 1. Chahoud J, Kanafani ZA, Kanj SS: Management of candidaemia and invasive candidiasis

in critically ill patients. Int J Antimicrob Agents 2013, 8:134–139. 2. Sartelli M, Catena F, Ansaloni L, Moore E, Malangoni M, Velmahos G, Coimbra R, Koike K, S63845 Leppaniemi A, Biffl W, Balogh Z, Bendinelli C, Gupta S, Kluger Y, Agresta F, Di Saverio S, Tugnoli G, Jovine E, Ordonez C, Augusto Gomes C, Pereira GA, Yuan KC, Bala M, Peev MP, Cui Y, Marwah S, Zachariah S, Sakakushev B, Kong

V, Ahmed A, et al.: Complicated intra-abdominal infections in a worldwide context: an observational prospective study (CIAOW Study). World J Emerg Surg 2013, 8:1.PubMedCrossRef 3. Di Carlo P, Pantuso G, Cusimano A, D’Arpa F, Giammanco A, Gulotta G, Latteri AM, Madonia S, Salamone G, Mammina C: Two cases of monomicrobial intraabdominal abscesses due to KPC-3 Klebsiella pneumoniae ST258 clone. BMC Gastroenterol 2011, 11:103.PubMedCrossRef 4. Tortorano AM, Peman J, Bernhardt H, Klingspor L, Kibbler CC, Faure O, Biraghi E, Canton E, Zimmermann K, Seaton S, Grillot R, ECMM Working Group on Candidaemia: Epidemiology of candidaemia in Europe: results of 28-month European Confederation out of Medical Mycology (ECMM) hospital-based surveillance study. Eur J Clin Microbiol Infect Dis 2004, 23:317–322.PubMedCrossRef 5. Ables AZ, Blumer NA, Valainis GT, Godenick MT, Kajdasz DK, Palesch YY: Fluconazole prophylaxis of severe Candida infection in trauma and postsurgical patients: a prospective, double-blind, randomized, placebo-controlled trial. Infect Dis Clin Pract 2000, 9:169–175.CrossRef 6. Sartelli M, Viale P, Koike K, Pea F, Tumietto F, van Goor H, Guercioni G, Nespoli A, Tranà C, Catena F, Ansaloni L, Leppaniemi A, Biffl W, Moore FA, Poggetti R, Pinna AD, Moore EE: WSES consensus conference: Guidelines for first-line management of intra-abdominal infections. World J Emerg Surg 2011, 6:2.PubMedCrossRef 7.

Importantly, the majority of Vietnamese strains (77%; 80/103) had the 18-bp deletion, irrespective of geographical location (80% in Ho Chi Minh and MLN4924 cell line 76% in Hanoi) (Table 1). In contrast, only 13% (13/103) of the isolates carried the 39-bp deletion. In this study, we designated the 18-bp deletion type as the Vietnamese pre-EPIYA type, and the 39-bp deletion type as the East Asian pre-EPIYA type. Three types of pre-EPIYA region were distinguishable by simple PCR (data not shown) using primer sets covering the cagA pre-EPIYA region, as described in Methods. However, there was no relationship between

pre-EPIYA types and clinical outcome in this Vietnamese population (data not shown). Figure 1 Alignment of cagA pre-EPIYA region sequences from Vietnamese H. pylori. An 18-bp deletion, a 39-bp deletion, and no deletion were found at about 300 bp upstream of the first EPIYA region. The first EPIYA sequence is indicated in the clear square. Numbers were input from the first EPIYA motif. Genotypes of the cag right-end junction It has been reported that the cag right-end junction motif can be classified into five groups [18]. We found that type II was the most common (84%), followed by type I (9%) and type III (4%)

(Table 1). The remaining Savolitinib ic50 three strains could not be categorized into any genotype. This result was consistent with previous data showing that type II was the most common among H. pylori isolates from East Asian countries [13, 18]. Interestingly, Avelestat (AZD9668) type I, which was considered to be AG-14699 specific for Western strains, was significantly more common in strains isolated in Ho Chi Minh (16%) than in those originating from Hanoi (2%) (p

< 0.05). In contrast, type II was significantly more common in Hanoi (93%) than in Ho Chi Minh (76%) (p < 0.05). There was no significant relationship between the cag right-end junction types and clinical outcome in this Vietnamese population (data not shown). Type II was very common in H. pylori strains carried by Vietnamese (86%: 69/80) and also in the East Asian pre-EPIYA type (100%: 13/13) (Table 2). In contrast, among strains with a Western pre-EPIYA type, type II accounted for 40% (2/5) and type I for the remaining 60% (3/5). Table 2 Relationship between cagA pre-EPIYA type and cag right-end junction types or vacA genotypes.     cag right-end junction type vacA m type     I II III N.D. m1 m2 (-) cagA pre-EPIYA type Vietnamese (n = 80) 6 69 4 1 35 40 5   East Asian (n = 13) 0 13 0 0 6 7 0   Western (n = 5) 3 2 0 0 1 4 0   cagA (-) (n = 5) 0 3 0 2 2 3 0 N.D.: not determined Genotypes of the vacA genotypes All Vietnamese strains possessed the vacA s1 genotype and only one case from Hanoi possessed both the s1 and s2 genotypes, suggesting mixed infection with two strains. The m1 genotype was significantly more common in strains isolated in Hanoi than in those originating from Ho Chi Minh (54% vs. 31%) (p < 0.05) (Table 1).

The text summarizes genes with a log fold change (log FC) over 0.8 in beginning of regeneration, whereas all genes towards Entospletinib molecular weight termination of regeneration are discussed. For time contrast 3–0 weeks one gene was up-regulated (log FC 0.9); Insulin-like growth factor binding protein

7 (IGFBP-7). It is involved in regulation of cell proliferation [16]. One gene was down-regulated (log FC −1.8); Cytolytic granule protein APR-246 chemical structure (TIA1) which functions potentially as an inducer of apoptosis [17]. For time contrast 6–0 weeks two genes were down-regulated (log FC −1.1): BAG3 potentially prevents FAS-mediated apoptosis [18] while Tumor protein p53 inducible nuclear protein 1 (TP53INP1), (log FC −0.9) potentially Alpelisib purchase induces apoptosis

[19]. Towards end of regeneration, one gene found differentially expressed in both time contrasts 6–0 and 6–3 has a potential negative effect on cell cycle progression and promotes apoptosis; Zinc finger protein 490 (ZNF490) [20]. By comparing the log fold change for genes in the resection group, this gene had the highest rate of 2.0 at t = 1, and 2.4 at t = 2. For time contrast 6–3 weeks, one gene was down-regulated (log FC −1.1), that is Fas associated factor 1 (FAF1) which potentially increases cell death [21]. Caspase recruitment domain family, member 11 (CARD11) was up-regulated (log FC 0.4). Parathyroid hormone-like hormone (PTHLH) was also up-regulated in termination of liver regeneration (log FC 0.4), and has been reported to regulate cell why proliferation [22]. General trends of apoptosis, cell cycle and cell proliferation within the sham group For time contrast 3–0 weeks, one gene was up-regulated (log FC 0.9): Uromodulin (UMOD) which is a potential negative regulator of cell proliferation [23]. By comparing the first time contrast that is from 0 until 3 weeks, with the second,

6–0, we found one common up-regulated gene, MDM4, (log FC 1.9 and 2.0, respectively). This gene potentially inhibits the G1 phase of the cell cycle [24] in both time-contrasts. For time contrast 6–0 weeks, one gene regulating cell proliferation was down-regulated: SOCS2 (log FC −0.9). This gene suppresses cytokine signalling and inhibits STAT and thereby terminating the transcription activity [25]. For time contrast 6–3 weeks, one gene was down-regulated, BTG3 (log FC −0.9). This gene is an anti-proliferative gene and ANA is a member of this family. It has been shown that an over expression of ANA impaired serum-induced cell cycle progression from the G0/G1 to S phase [26]. General trends of apoptosis, cell cycle and cell proliferation within the control group For time contrast 3–0 weeks, we found one down-regulated gene (log FC −2.8).

Although Staphylococcus strains isolated from meat samples showed low-level of linezolid selleck products resistance in the present study, emergence of the multiresistance gene cfr in meat poses a potentially significant threat to the public health, considering that the cfr-mediated linezolid resistance can rapidly and widely spread among different bacterial

species. Conclusions To the best of our knowledge, this is the first study to report a surprisingly high occurrence of cfr in retail meat samples in Chinese markets. Animal meat harboring bacteria containing the transmissible cfr would be a serious threat to the public health as these bacteria may act as reservoirs for spreading cfr to bacteria that infect humans, particularly in environments with a large microbial community. Recently, cfr was detected in human isolates in China [20, 25]. Thus, more attention needs to be paid to the possibility that cfr can find its way through the food chain to commensal or pathogenic bacteria of humans. Considering that a limited number of meat samples were used and that to from only one city in China, www.selleckchem.com/products/AZD8931.html the results of the present study regarding dissemination of cfr among staphylococcal species from

animal food sources in China is not conclusive. Thus, continuing the surveillance of cfr gene in meat distributed in China is critical to limit its dissemination, which could potentially threaten the human health. Methods Sample collection, identification of species, and cfr detection In February 2012, 72

pork samples and 46 chicken samples were collected from five free markets and one supermarket in Guangzhou. The meat samples were incubated in Luria–Bertani (LB) broth for enrichment. Then, the cultured broth was streaked onto selective media plates of Baird–Parker agar supplemented with 10 mg/L florfenicol. One isolate per sample was selected for further analysis. Whole-cell DNA was prepared according to a previously described protocol [26]. The presence of cfr was screened by PCR with previously described primers [5]. Species identification of the cfr-carrying strains was performed by the API-Staph System (bioMérieux, France) and further confirmed by 16S rRNA sequencing [27]. Molecular typing and transformation PFGE of selleck all cfr-positive Staphylococcus isolates was performed by using the CHEF Mapper System (Bio-Rad Laboratories, Hercules, CA), according to the previously described protocol [10]. All the plugs of genomic DNA were digested with SmaI (TaKaRa Biotechnology, Dalian, China). The PFGE patterns were interpreted according to the criteria described by Tenover et al. [28]. The location of cfr was determined by Southern blotting. Cfr-carrying plasmids of the isolates were extracted by using the selleck chemical Qiagen Plasmid DNA Midi Kit (Qiagen, Hilden, Germany) and then transferred into S. aureus RN4220 by electrotransformation, as described previously [29].

All authors made critical revision of the manuscript for important intellectual content.”
“Background Expression

profiling can be used for Cilengitide in vitro disease classification, predictions of clinical outcome or the molecular dissection of affected pathways in hereditary or acquired diseases. Animal models for human diseases facilitate cause-effect studies under controlled conditions and allow comparison with untreated or healthy individuals. Especially the latter can be an ethical or logistic problem in human medicine. More than 300 genetic human disorders are described in dogs http://​www.​ncbi.​nlm.​nih.​gov/​sites/​entrez. Many of these diseases occur in one or just a few of around 400 dog breeds. Single gene

diseases are easy to characterize in inbred dog populations, and research of complex diseases profits from the fact that dogs share the human environment. In addition to similarities between dogs and humans with respect to physiology, pathobiology, and treatment response, research of breed-related canine behaviour and phenotypic diversity is promising. Therefore dogs were advocated as a model animal in translational research [1]. Molecular genetic tools available for such comparable research between dogs and humans include the in-depth sequencing of the complete dog genome [2, 3], a single-nucleotide polymorphism (SNP) data base, containing 2.5 million SNPs [4], and easy access to genetic information of several generations of dogs. In addition, the high degree of inbreeding, buy EX 527 which founded the present dog breeds the last few hundreds years, further facilitates the investigations in inheritable gene defects [5–7]. Dog specific micro-arrays are available to perform functional genomic studies. This kind of high-throughput gene expression profiling requires the use of high quality mRNA. Likewise is the quality of mRNA of major impact on the reliability of the results in quantitative RT-PCR (Q-PCR). So far the Janus kinase (JAK) emphasis in canine molecular biology was put on the use of internal controls for proper Q-PCR measurements and subsequent data analysis [8–10]. However,

little information is available that compares different methods of retrieval, isolation and storage of canine Compound C in vivo tissues for molecular research purposes. Especially liver, but also heart and jejunum, are difficult tissues for retrieval of high quality mRNA [11]. Liver biopsies, taken for medical and research purposes, are processed for histopathology including immunohistochemistry and RNA and protein isolation. Since these diverse intentions require different fixation and storage methods, clinicians and researchers are often faced with a multitude of different vials, and fluids in order to retain biopsies. In addition, the applications of specific fixation protocols can be necessary, which might require additional training, time and sophisticated laboratory equipment.

g. due to providing nutrients, while S-symbionts have LY333531 in vitro a beneficial but not essential role for host insect survival (for reviews see [3] and [6]). In many insects, endosymbionts are located in PD-1/PD-L1 Inhibitor 3 solubility dmso specialized organs (referred to as bacteriomes or mycetomes) and their inheritance usually follows a strict vertical transmission from mother to offspring. Understanding

relationships between insect hosts and their endosymbiotic bacteria is not only relevant from an evolutionary point of view, but can also aid in the identification of new targets for insect pest control [7] as well as for biotechnology and biomedicine [3]. Yet, since many of the relevant microorganisms cannot be cultured, their identification and functional characterization was so far difficult or not possible at all. Lately, the accessibility

of novel genomic techniques, in particular next generation sequencing (NGS) technologies represent new, cost-efficient and fast strategies to depict microbial diversity without the need for culturing click here the respective organisms [8]. With these techniques thousands of sequence reads can be analysed in parallel allowing an extensive assessment of bacterial diversity within insects. As a target for bacterial NGS projects, ribosomal DNA genes (rDNA) like the 16S rDNA, also used for the taxonomic classification of bacterial species [9], have frequently been applied for analysing the bacterial microbial community in metagenomic studies of soil [10, 11], mines [12], the deep sea [13] or oral human microflora [14]. In this study, we used high-throughput tag-encoded FLX amplicon pyrosequencing [15] to characterise bacterial communities associated with four

different weevil species of the genus Otiorhynchus Germar (Coleoptera: Curculionidae). Members of this genus are polyphagous and are regarded as pests of a variety of ornamental and nursery plants worldwide. Their soilborne larvae feed on the host plants’ roots which may be lethal in particular for younger plants or recently transplanted cuttings. Further, feeding damage of adults on the plants foliage may reduce the market value of ornamentals. For these reasons weevils are often controlled by intensive insecticide applications [16]. Moreover, Otiorhynchus spp. can serve Isoconazole as a model genus for understanding the evolution of asexual reproduction, since it includes species both reproducing mostly parthenogenetically (like O. sulcatus and O. rugosostriatus) as well as sexually (like O. salicicola and O. armadillo) [17, 18]. Here, by applying 454 sequencing technology, we show that weevils of the genus Otiorhynchus are associated with several endosymbiotic bacteria. This study is the first to report Rickettsia and “Candidatus Nardonella” endosymbionts – the ancestral endosymbiont of weevils – in Otiorhynchus spp..

Eur J Cell Biol

1988, 47: 121–31.PubMed 25. Chaudhary N, Cance WG, Worman HJ, Blobel G, Cordon-Cardo C: Nuclear lamin expression in normal and neoplastic human tissues. J Cell Biol 1990, 111: 375a. 26. Ozaki T, Saijo M, Murakami K, Enomoto H, Taya Y, Sakiyama S: Complex formation between lamin A and the retinoblastoma gene product: identification of the domain on lamin A required for its interaction. Oncogene 1994, 9: 2649–53.PubMed 27. Dreuillet C, Tillit J, Kress M, Ernoult-Lange M: In vivo and in vitro interaction between human transcription factor MOK2 and nuclear lamin A/C. Nucleic Acids Res 2002, 30: 4634–42.CrossRefPubMed 28. Lloyd DJ, Trembath RC, Shackleton S: A novel interaction between lamin A and SREBP1: implications for partial lipodystrophy

and other laminopathies. Hum Mol Genet 2002, 11: 769–77.CrossRefPubMed 29. Johnson BR, Nitta RT, Frock RL, Mounkes L, Barbie DA, Stewart CL, Selleckchem Geneticin Harlow E, Kennedy check details BK: A-type lamins regulate retinoblastoma protein function by promoting subnuclear localization and preventing proteasomal degradation. Proceedings of the National Academy of Sciences of the United States of America 2004, 101: 9677–9682.CrossRefPubMed 30. Nitta RT, Jameson SA, Kudlow BA, Conlan LA, Kennedy BK: Stabilization of the retinoblastoma protein by A-type nuclear lamins is required for INK4A-mediated cell cycle arrest. Molecular and Cellular Biology 2006, 26: 5360–5372.CrossRefPubMed 31. Pekovic V, Harborth J, Broers JL, Ramaekers FC, van Engelen B, Lammens M, von Tideglusib concentration Zglinicki T, Foisner R, Hutchison C, Markiewicz E: Nucleoplasmic LAP2alpha-lamin A complexes are required to maintain a proliferative state in human fibroblasts. J Cell Biol 2007, 176: 163–72.CrossRefPubMed 32. Johnson BR, Nitta RT, Frock RL, Mounkes L, Barbie DA, Stewart CL, Harlow E, Kennedy BK: A-type lamins regulate retinoblastoma

protein function by promoting subnuclear localization and preventing proteasomal degradation. Proc Natl Acad Sci USA 2004, 101: 9677–82.CrossRefPubMed 33. Nitta RT, Smith CL, Kennedy BK: Evidence that proteasome-dependent degradation of the retinoblastoma protein in cells lacking A-type lamins occurs independently of gankyrin and MDM2. PLoS Selleckchem Erastin ONE 2007, 2: e963.CrossRefPubMed 34. Plass C: Cancer epigenomics. Hum Mol Genet 2002, 11: 2479–88.CrossRefPubMed 35. Sugimura T, Ushijima T: Genetic and epigenetic alterations in carcinogenesis. Mutat Res 2000, 462: 235–46.CrossRefPubMed 36. Ogi K, Toyota M, Ohe-Toyota M, Tanaka N, Noguchi M, Sonoda T, Kohama G, Tokino T: Aberrant methylation of multiple genes and clinicopathological features in oral squamous cell carcinoma. Clin Cancer Res 2002, 8: 3164–71.PubMed 37. Kang GH, Shim YH, Jung HY, Kim WH, Ro JY, Rhyu MG: CpG island methylation in premalignant stages of gastric carcinoma. Cancer Res 2001, 61: 2847–51.PubMed 38. Ding Y, Le XP, Zhang QX, Du P: Methylation and mutation analysis of p16 gene in gastric cancer.

Standardized cost prices were used where available, or else real costs or tariffs were used to estimate the costs. Medication costs were calculated using Mdivi1 solubility dmso prices based on the Defined Daily Dose which is defined by the Health Care Insurance

Board as the buy S63845 assumed average maintenance dose per day for a drug used for its main indication in adults [33, 34]. Prices of paid domestic help were based on tariffs for unpaid work. With respect to costs of hospital admissions, the cost price of a non-teaching hospital was used because hip fracture surgery does not require the expertise of a teaching hospital, and the Maastricht University Medical Centre has both the function of a non-teaching and teaching hospital. Costs of surgery were not included in the cost calculation because previous research by Haentjens et al. [35] showed that the costs of the different types of surgery are comparable. Incremental cost-effectiveness ratios, cost-effectiveness planes and cost-effectiveness acceptability curves To evaluate cost-effectiveness,

incremental cost-effectiveness ratios (ICERs) were calculated. ICERs were calculated by dividing the difference in the mean costs (between two treatments or interventions) by the differences in the mean outcomes. In this study, ICERs were calculated for weight change and for QALYs. The ICERs were interpreted as the incremental cost per unit of additional outcome [29, 36]. These ICERs were plotted learn more in a cost-effectiveness plane (CEP), in which the x-axis showed the difference in effect between the interventions and the y-axis the the differences in costs between the interventions [29, 36, 37]. In the

CEP, four quadrants were shown; ICERs located in the North East (NE) indicated that the intervention was more effective and more costly as compared with usual care. ICERs in the South East (SE), the dominant quadrant, indicated that the intervention is more effective and less costly. ICERs in the South West (SW) indicated that the intervention was less effective and less costly, and ICERs located in the North West (NW) indicated that the nutritional intervention was less effective but more costly. Based on the CEPs, cost-effectiveness acceptability curves (CEAC) were plotted [29, 36–38]. In the CEAC, the probability that the nutritional intervention is more cost-effective as compared with the usual care (y-axis) was presented for several ceiling ratios (x-axis), which were defined as the amount of money the society is willing to pay to gain one unit of effect [29, 36–38]. Within The Netherlands, the value the society is willing to pay to gain one QALY ranges from 20,000 to 80,000 Euro, depending on the severity of the disease [39]. Sensitivity analyses Sensitivity analyses were performed for age categories (55–74 vs.

At the desired growth temperature (900°C), carbothermally reduced Zn vapors are generated and efficiently captured by Au nanoparticles. The capturing processes occur on the Au droplets since Zn vapor #EPZ 6438 randurls[1|1|,|CHEM1|]# trapping is energetically more favorable at these sites than at the SiC surface. The supply of Zn vapors is expected to either condense directly into the Au nanoparticle or be transported from adjacent regions on

the growth substrate into the Au droplets/clusters to form clusters of Au-Zn alloys. The eutectic temperature of Au-Zn systems was estimated to be around 683°C [29] with a Zn maximum solubility in Au of 33.5 at%. However, throughout this present investigation, the growth temperatures (850 or 900°C) were well above the eutectic temperature for Au-Zn systems. As such, Au and Zn can be expected to be molten alloy droplets on the substrates. The formation of such droplets can be well described by the following expression [30]. Figure 8 Schematic of growth mechanism for ZnO nanoarchitectures. Schematic of the growth mechanism for ZnO nanoarchitectures at 900°C with (a) high density of Au nanoparticles and (b) low density of Au nanoparticles. (1) With increasing growth time, the continual supply of Zn vapors results in an increase in Zn concentration in Au-Zn alloy clusters. The process of Zn condensation/dissolution within the Au-Zn alloy system continues until

the supersaturation point, where click here a solid crystal of ZnO nucleates check details out of the molten alloy droplet [30]. However, the present experimental work shows that depending on the system (growth) temperature, ZnO nucleation can occur either on the Au-Zn alloy droplets (850°C, Figure 6c) or away from the Au-Zn alloy droplet (900°C). At 900°C, Zn-rich clusters that are precipitated on Au-Zn alloy droplets experience a drift as a result of the high thermal energy [19]. In our system, it was observed that at 700

sccm of Ar flow, the Zn cluster drift phenomenon can be significant above 850°C. As can be seen in Figure 8b (ii), the Zn cluster appears to drift with no preferential direction. The Zn cluster drift was subsequently halted either by (1) merging with other moving Zn cluster traces and/or Au-Zn alloy droplets (Figure 8a (ii) for the high density of Au nanoparticle case), (2) sticking on a substrate defect site, and/or (3) reduction in the local substrate temperature (Figure 8b (ii) for the low density of Au nanoparticle case). With continual supply of Zn vapors and residual oxygen atoms inside the growth chamber, precipitation of ZnO NWs via self-catalyzed VLS process is established (Figure 8 (iii)). Beyond this stage, NW growth is effectively controlled by a non-catalytic-assisted VLS mechanism and the Au nanoparticles play no further role in the evolution of the growth process [16, 22].