A network of game reserves and conservation areas are located to the west and east of Serengeti National Park (Fig. 1). This whole area is known as the Greater selleck kinase inhibitor Serengeti Ecosystem. The east of the national park boundary is settled by Maasai pastoralists who rarely hunt for wild meat and their lifestyles tend to be consistent with conservation of wildlife (Polansky et al. 2008). In contrast, human settlements to the west of the park boundary do consume game meat regularly (Holmern et al. 2006; Loibooki et al. 2002;

Nyahongo et al. 2005). Buffalo total counts Beginning in the early 1960s, buffalo populations were censused by aerial survey every few years. A detailed description of methods is given in Sinclair (1977). In 1970 all observations of buffalo (individuals and herds) in the Greater Serengeti

Ecosystem were Selleckchem BAY 11-7082 plotted on a map of the ecosystem. These observations were later incorporated into a GIS using the Universal Transverse Mercator (UTM) coordinates. From the 1992, 1998, 2000, 2003, and 2008 censuses similar data were obtained using global positioning system (GPS) technology. The buffalo population was close to its maximum in 1970 and this census was therefore used as the baseline with which we compared the following years. We determined the instantaneous rate of change in the buffalo population from 1970 Sclareol to

2008 by zone. Zones within the park (Fig. 1) represent distinct geographical and ecological areas. Buffalo herds are relatively sedentary, confine themselves to a home range of less than 20 km in diameter, and so rarely cross over zone boundaries (Sinclair 1977). These zones were the north, far east, far west, center, south and short grass plains. Because buffalo do not use the short grass plains we did not include this area in our analysis. We summed buffalo numbers within each zone for each year that we had census data and compared these numbers with those in 1970 to show the relative change. A major drought in 1993 affected all zones and caused a 40% mortality (Sinclair et al. 2007, 2008). Spatial population dynamics model We used a spatially structured population dynamics model to determine the trends in buffalo abundance in the five different regions between 1965 and 2008 (Hilborn et al. 2006). We examined a range of possible influences on abundance. These factors included carrying capacity, which is a function of size of zone times rainfall (a surrogate for food supply, Sinclair and Arcese 1995a), lion predation, and hunting effort.

The electrochemical deposition technique has been recently developed as a promising alternative means for the fabrication of nanomaterials under ambient condition due to the low cost, mild condition,

and accurate process control. Recently, Yang and co-workers [25] reported the synthesis of ultrathin ZnO nanorods/nanobelts arrays on Zn substrates by electrochemical deposition. Our group [26] reported an electrochemical route for the fabrication of highly dispersed composites of ZnO/carbon nanotubes. Herein, we report a tunable self-assemble strategy to selectively fabricate a series of ZnO with unique, pure, and larger quantity morphologies including petal-, flower-, sphere-, nest- and clew-shaped structures by electrochemical deposition. The size and morphology of the ZnO are systematically controlled by judiciously adjusting the concentration of the sodium AZD6738 ic50 citrate and the electrodepositing time in the self-assembly

process. Significantly, the nestlike structure dominates the further formation of hierarchical superstructure. The ZnO nestlike structure can be used as a container not only to hold several interlaced ZnO laminas, but also to fabricate Ag-ZnO heterostructures by growing silver nanoparticles or clusters in the center of nests by BIBW2992 cell line electrochemical deposition method. The multiphonon Raman scattering of as-fabricated Ag-ZnO Anacetrapib nestlike heterostructures is also largely enhanced by the strongly localized electromagnetic field of the Ag surface plasmon. Methods Synthesis of ZnO microstructures Zinc foils (99.9%, Sigma-Aldrich Corporation, St. Louis, MO, USA) with a

thickness of 0.25 mm were polished by sand paper then ultrasonically washed in absolute ethanol and dried in air before use. Electrochemical experiments with a CHI workstation were performed at room temperature in a two-electrode (Zn-Zn) system. For the production of nestlike ZnO, 0.01 mmol of sodium citrate and 14 μl of 30% H2O2 were added to 7 ml of deionized water under stirring at room temperature, adjusting the pH to 12. The two Zn foils (5 × 5 × 0.25 mm3) were put into the reaction solution in a parallel configuration with an interelectrode separation of 1 cm to apply a fixed electric potential of 3 V between the two Zn electrodes by using the electrochemical analyzer for the electrochemical deposition of ZnO nanostructures at room temperature. After being electrodeposited for 1 min, a whitish gray film was generated on the surface of Zn cathode. The Zn cathode with the deposited products was washed with distilled water for several times, dried at room temperature, and examined in terms of their structural, chemical, and optical properties.

Figure 3 shows the SEM images of the ZnO NRAs grown on Figure 3a, the bare CT substrate with the ultrasonic agitation; and in Figure 3b, the seed-coated CT substrate without the ultrasonic agitation For comparison, the external cathodic voltage and growth time were −2 V and 1 h, respectively, as the same condition of Figure 2. As shown in Figure 3a, the ZnO NRAs were grown on the seedless CT substrate. In fact, it was previously understood that the ZnO NRAs could be formed with no seed layer by the ED process [28, 29]. However, the size and distribution of ZnO nanorods were not selleck regular and the vertical

alignment was poor. Since the ZnO nuclei were randomly created and organized without seed layer, the ZnO nanorods were formed with different sizes and they were aligned obliquely along each growth direction. For the grown sample without the aid of ultrasonic agitation in Figure 3b, on the contrary, the ZnO NRAs were densely and vertically formed, but many microrods were attached to them. As explained in Figure 2, some zinc hydroxides were already formed in growth solution, and the microrods readily adhered to the ZnO NRAs when the ultrasonic agitation was not applied to the aqueous growth solution. Therefore, the seed layer and ultrasonic

agitation are crucial to obtain the well-integrated ZnO NRAs on CT substrates. Figure 3 FE-SEM HDAC inhibitors in clinical trials micrographs. ZnO NRAs grown on (a), the bare CT substrate with the ultrasonic agitation; and (b), the seed-coated CT substrate without the ultrasonic agitation. For comparison, the external cathodic voltage and growth time were −2 V and 1 h, respectively, as the same condition of Figure 2. Figure 4 shows the SEM images for the synthesized ZnO on the seed-coated CT substrate

at different external cathodic voltages of Figure 4a, −1.6 V; Figure 4b, −2.4 V; and Figure 4c, −2.8 V for 1 h under ultrasonic agitation; and Figure 4d, the current density as a function of growth time at different external cathodic voltages. The insets Baricitinib of Figure 4a,b,c show the magnified SEM images of the selected region of the corresponding samples. Below −1.6 V of external cathodic voltage, the ZnO NRAs could not be formed due to the insufficient electron supply under a low external cathodic voltage. In contrast, the size of ZnO was dramatically increased with increasing the external cathodic voltage to −2.4 and −2.8 V. In general, the ZnO nanorods may be grown anisotropically under ED conditions. While the Zn2+ ions diffuse rapidly into the polar plane, they cannot diffuse into the nonpolar plane relatively because the hexamine molecules were early attached to the ZnO pillars, thus blocking out the reaction between the Zn2+ and OH− ions [30]. Accordingly, the ZnO nanorods are grown along the polar planes corresponding to the c-axis of wurtzite crystal structure.

As such, initiatives to improve science-policy interfaces must reflect the multifaceted and multi–layered complexity of science and policy communication. There this website is little prospect of these becoming

less messy, or that the challenges will vanish simply by persevering in better presenting and packaging facts better (the current focus of much effort—Nutley et al. 2007). In this paper, we reframed the many existing critiques and insights (e.g. Dilling and Lemos 2011; Shaxson and Bielak 2012), stressing the importance of working across both scientific disciplines and policy sectors, in order to foster joint framing of issues, processes and outcomes. This will require creativity and resources, as well as a rethink in terms of ‘indirect’ science-policy links, namely the role of actors other than scientists and policy-makers in shaping the way biodiversity research is carried out and contributes to policy

processes. Whilst some others have touched on this (e.g. Juntti et al. 2009; Laurance et al. 2012; Roux et al. 2006; Sutherland Vorinostat research buy et al. 2009), we go further in recommending specific actions that will improve dialogue and ensuing action. In particular, we highlight the need for high-level changes to train, support and incentivise those scientists and policy actors enthusiastic about crossing boundaries and carrying out activities at the science-policy-public interface (Choi et al. 2005). These institutional and sectoral changes are needed in order that science and policy dialogue activities Phloretin are better supported and acknowledged as strengthening scientific excellence and policy decisions. The problem of loss and unsustainable uses of biodiversity is such that there is an urgent need for such improved dialogue. For the remainder of this section, we wish to focus on identifying the steps needed to achieve this, namely: (1) How to take into account

loss and unsustainable uses of biodiversity as a specific issue requiring improved science-policy conversations   (2) How research can help identify and reach the most relevant target groups regarding biodiversity; and   (3) How policy makers, economic interest groups, other stakeholders and the public can better acknowledge, understand and use biodiversity knowledge   The loss of biodiversity and ecosystem services poses particularly intractable challenges, that require improved science-policy conversations. A first challenge is that biodiversity, with the exception of charismatic species, is not always visible or salient to publics or policy makers. This may result in people considering the biodiversity issue as being irrelevant to them. Thus, we need to continue to spell out the relevance of biodiversity to both publics and policy sectors.

CrossRefPubMed 20. Cole SP, Harwood J, Lee R, She R, Guiney DG: Characterization of monospecies biofilm formation by Helicobacter pylori. J Bacteriol 2004, 186:3124–3132.CrossRefPubMed 21. Carron MA, Tran PARP inhibitor VR, Sugawa C, Coticchia JM: Identification of Helicobacter pylori biofilms in human gastric mucosa. J Gastrointest Surg 2006, 10:712–717.CrossRefPubMed 22. Lee EY, Choi DS, Kim KP, Gho YS: Proteomics in gram-negative bacterial

outer membrane vesicles. Mass Spectrom Rev 2008, 27:535–55.CrossRefPubMed 23. Park SR, Mackay WG, Reid DC: Helicobacter sp. recovered from drinking water biofilm sampled from a water distribution system. Water Res 2001, 35:1624–6.CrossRefPubMed 24. Davey ME, O’Toole GA: Microbial biofilms: from ecology to molecular genetics. Microbiol Mol Biol Rev 2000, 64:847–867.CrossRefPubMed 25. O’Toole GA, Kaplan HB, Kolter R: Biofilm formation as microbial development. Annu Rev Microbiol 2000, 54:49–79.CrossRefPubMed 26. Qin Z, Ou Y, Yang L, Zhu Y, Tolker-Nielsen T, Molin S, Qu D: Role of autolysin-mediated DNA release in biofilm formation of Staphylococcus epidermidis. Microbiology 2007, 153:2083–92.CrossRefPubMed 27. Götz F, Heilmann C, Cramton STI571 research buy SE: Molecular basis of catheter associated infections by staphylococci. Adv Exp Med Biol 2000, 485:103–11.CrossRefPubMed 28. Beveridge TJ: Structures of gram-negative cell walls and their derived membrane vesicles. J Bacteriol 1999, 181:4725–4733.PubMed

29. Fiocca R, Necchi V, Sommi P, Ricci V, Telford J, Cover TL, Solcia E: Release of Helicobacter pylori vacuolating cytotoxin by both a specific secretion pathway and budding of outer membrane vesicles. Uptake of released toxin and vesicles by gastric epithelium. J Pathol 1999, 188:220–226.CrossRefPubMed Microtubule Associated inhibitor 30. Keenan JI, Allardyce RA, Bagshaw PF: Dual silver staining to characterize Helicobacter spp. outer membrane components. J Immunol Methods 1997, 209:17–24.CrossRefPubMed 31. Danes PN, Pratt LA, Kolter R: Exopolysaccharide production is required for development of Escherichia coli K-12 biofilm architecture. J Bacteriol 2000, 182:3593–3596.CrossRef 32. Keenan JI, Davis KA, Beaugie CR, McGovern JJ, Moran AP: Alterations

in Helicobacter pylori outer membrane and outer membrane vesicle-associated lipopolysaccharides under iron-limiting growth conditions. Innate Immun 2008, 14:279–290.CrossRefPubMed 33. Costerton JW, Cheng KJ, Geesey GG, Ladd TI, Nickel JC, Dasgupta M, Marrie TJ: Bacterial biofilms in nature and disease. Annu Rev Microbiol 1987, 41:435–464.CrossRefPubMed 34. Williams JC, McInnis KA, Testerman TL: Adherence of Helicobacter pylori to abiotic surfaces is influenced by serum. Appl Environ Microbiol 2008, 74:1255–1258.CrossRefPubMed 35. Nakagawa S, Osaki T, Fujioka Y, Yamaguchi H, Kamiya S: Long-term infection of Mongolian gerbils with Helicobacter pylori : microbiological, histopathological, and serological analyses. Clin Diagn Lab Immunol 2005, 12:347–353.PubMed 36.

cDNA was synthesized using High CapaCity cDNA Reverse Transcription Kit (P/N 4368814, ABI, U.S.A.) for RT-PCR according to the manufacturer’s instruction. The sequence forward and reverse primers for Q-RT-PCR were designed using the primer

ExpressR Software provided by Applied Biosystems. A set of D. hansenii 18S ribosomal RNA primers was designed for use as an endogenous control. 18S forward: G’-CGTCCCTGCCCTTTGTACAC-3′ 18S reverse: G5′-GCCTCACTAAGCCATTCAATCG-3′ DhAHP target forward: G5′-GGAGCCCCAGGAGCATTTA-3′ DhAHP target reverse: GDC-0994 G5′-TGGGCCAAATAATCGGGAAT-3′ Real-time PCR assay was carried out in an ABI PRISM 7500 Sequence Detection System (ABI, U.S.A.). The amplification of the target genes was monitored every cycle by SYBR-Green fluorescence.

Rapid amplification of cDNA ends (RACE) The full-lengthed cDNA clone of DhAHP was obtained by rapid amplification of the cDNA ends using the GeneRacerTM Kit (Invitrogen, U.S.A.), as described in the manual provided by the manufacturer. The forward and reverse gene specific primers (GSPs) used for RACE were designed based on the DhAHP cDNA sequence. The universal primers for 5′ and 3′ Race were GeneRace 5′ and GeneRace 3′, respectively, provided in the kit. After PDK inhibitor PCR the DNA fragments were cloned into pGEMR-T Easy vector (Promega, U.S.A.) for sequencing. Forward (GSP): 5′- GTCAATGCTGCTTGGGGTAAAGCTTTA-3′ Reverse (GSP):5′- GGTCTCAGCACTGGAAATTTCAGTG-3′ GeneRace 5′:5′- CGACTGGAGCACGAGGACACTGA-3′ selleck inhibitor GeneRace 3′:5′- GCTGTCAACGATACGCTACGTAACG-3′ Bioinformatics analysis The deduced amino acid sequence of DhAHP was analyzed with the Expert Protein Analysis System http://​www.​expasy.​org/​.

Multiple sequence alignment was performed for sequence comparison and alignment of D. hansenii Ahp and two other reported AHPs (Swiss-Prot: P38013 and Q5AF44) from S. cerevisiae and C. albicans and peroxisomal membrane protein (Swiss-Prot: O14313) from S. pombe and three other structural homolog proteins (Swiss-Prot:Q8S3L0, B3GV28 and P30044) from P. tremula, P. sativum and H. sapiens. The alignment and phylogenetic analysis were carried out by the protein sequence alignment program CLUSTAL W. Southern and northern hybridization analysis Genomic DNA was isolated from yeast cells by the method of Hoffman and Winston [44]. Southern and northern hybridization analyses were performed using the DIG High Prime DNA Labeling and Detection Starter Kit (Roche Diagnostics, Switzerland). For Southern hybridization, 20 μg genomic DNA was digested with EcoRI and BamHI and electrophoretically separated on 0.7% (w/v) agarose gels in TBE buffer and DNA fragments blotted onto nylon membrane (Amersham Pharmacia Biotech, U.K.) by 20×SSC. The full-lengthed DhAHP DNA was labeled and used as a hybridization probe. For nothern hybridization analysis, RNA was extracted from D. hansenii that was not treated or treated with 2.

As reported from several other studies, both within Norway [17] and from other countries like UK [34] and the US [35], there was a significant seasonal variation in the occurrence of hip fractures in our study. In a study comparing and observing seasonal variation buy BIBW2992 of hip fractures in Scotland, Hong Kong and New Zealand [36] as well as in Taiwan [37], it was claimed evidence against a major influence of conditions underfoot causing extra falls and increased risk of fracture

during winter [36]. In our study, we had information about place of injury in 90% of all cases; 64% occurred indoors with no significant seasonal variation. For the fractures happening outdoors, there was a significant seasonal variation, which can be connected to falls on ice or slippery surfaces. Unfortunately, the data from the Harstad Injury Registry do not provide enough information for exact studies of the mechanisms leading to falls and fracture indoors. The mean age at hip fracture in persons above 50 years in Harstad, were not different from the mean age at hip fracture in Oslo, which

was 82.1 years in women and 76.6 years in men [8]. A lower mean age at fracture in men, compared to women, are also reported by others [26]. With 73% of the hip fractures occurring in women, the gender distribution of hip fractures in Harstad did not differ in comparison with Oslo (78%) or other comparable studies [12, 14]. Increased mortality risk up to 10 years find more has been reported for hip fractures

[38], although mortality is highest in the first year [3, 38]. A sex difference in mortality after hip fracture has also been indicated, with higher rates in men compared with women [2, 3, 38, 39]. In our study, mortality Mannose-binding protein-associated serine protease was higher in men than in women 3 months after fracture and persisted at 6 and 12 months after adjustment for age of hip fracture. This is in accordance with other Norwegian data showing higher mortality in men throughout the first year after hip fracture [40], and with a recent meta-analyses showing that, although the sex difference in mortality persists, the difference is greatest in the first 3 months after hip fracture, with reported relative all-cause mortality hazard of 5.75 (95% CI, 4.94–6.67) in women and 7.95 (CI, 6.13–10.30) in men [41]. One of the strengths of this study is the possibility to study the incidence of hip fractures in a well-defined municipality over a long time period and the accessibility of a well-established injury registry, which also provides the opportunity for quality assessment of the hip fracture registration. Furthermore, the injury registry provided valuable information on date and place of fracture and through the medical records we got access to mortality data. There are, however, several limitations in our dataset.

We also observed that overexpressed LATS1 caused the G2/M phase blockade in glioma U251 cells. Therefore, we investigated the expression change of CCNA1, a cell cycle factor in the Cdc2/ Cyclin A/B complex. This gene binds both CDK2 and CDC2 kinases and thus regulates the cell cycle transition at G2/M

[22–25]. We speculated CCNA1 might be involved in the cell cycle regulation pathway of LATS1 in glioma. Consistent with this presumption, we found that overexpression of LATS1 significantly reduced the expression of CCNA1 by western blot assay in glioma U251 cells. Further investigation Small molecule library is necessary to determine the exact role LATS1 plays in cell cycle pathway in glioma. Conclusions Our results indicate that the decreased expression of LATS1 appears to favor the development of glioma and might serve a suppressive role in glioma. Further, we applied a gain-of-function approach and to examine the biological processes regulated by LATS1 in glioma cells. We demonstrated the functional importance of LATS1 in suppressing glioma cell growth, buy EVP4593 migration, invasion and cell cycle transition from G2 to M phase. Finally, we observed that overexpression of LATS1 could inhibit the expression of cell cycle factor CCNA1, which might partly explain the mechanism by which LATS1 in controls cell proliferation. Acknowledgements

This study was supported by National Natural Science Foundation of P.R.China (30900559, 81101904) and Science and Technology Project of Xiamen (3502Z20104015;3502Z20124019). Electronic supplementary material Additional file 1: Figure S1.Cell cycle map of pLATS1-2, -4 cells and Control-vector cells. (DOC 28 KB) Additional file 2: Table S1.Overexpression of LATS1 reduced DNA content of G2 phase and

increased DNA content of G1 phase. (DOC 27 kb) (TIFF 191 KB) NADPH-cytochrome-c2 reductase References 1. Kleihues P, Cavenee WK: World Health Organization Classification of Tumours-Pathology and Genetics -Tumors of the Nervous System. Lyon. France: IARC Press; 2000:9–52. 2. Wu M, Chen Q, Li D, Li X, Li X, Huang C, Tang Y, Zhou Y, Wang D, Tang K, Cao L, Shen S, Li G: LRRC4 inhibits human glioblastoma cells proliferation, invasion, and proMMP-2 activation by reducing SDF-1 alpha/CXCR4-mediated ERK1/2 and Akt signaling pathways. J Cell Biochem 2008, 103:245–255.PubMedCrossRef 3. Louis DN, Ohgaki H, Wiestler OD, Cavenee WK, Burger PC, Jouvet A, Scheithauer BW, Kleihues P: The 2007 WHO classification of tumours of the central nervous system. Acta Neuropathol 2007, 114:97–109.PubMedCrossRef 4. Justice RW, Zilian O, Woods DF, Noll M, Bryant PJ: The Drosophila tumor suppressor gene warts encodes a homolog of human myotonic dystrophy kinase and is required for the control of cell shape and proliferation. Genes Dev 1995, 9:534–546.PubMedCrossRef 5.

Figure 9b shows the endurance characteristics Quisinostat chemical structure of the Ti x Zr y Si z O memory. The measurement conditions are V g = −6 V and V d = 6 V for programming and V g = V d = 6 V for erasing. Despite a small drift of the threshold voltage for both P/E operations, the memory window remained at around 2 V after 104 P/E cycles. No substantial window narrowing was observed.

selleck products The threshold voltage downward shift is mainly caused by the interface trap generation and hole trapping in the tunneling oxide. Figure 9 Reliability characteristics of the Ti x Zr y Si z O memory. (a) Retention characteristic of the memory at measurement temperatures of 85°C and 125°C. (b) Endurance characteristic of the memory up to 104 program/erase cycles. The electrical performance of the Ti x Zr y Si z O memory is summarized in Table 1 and compared with other sol–gel-derived memories [8, 13, 21]. As seen in the table, the Ti x Zr y Si z O memory in this study exhibits improved electrical performance, particularly in retention properties. The Ti x Zr y Si z O memory at either 600°C or 900°C annealing can be operated at much higher erase speeds compared to other materials. This is because the erase of the Ti x Zr y Si z O memory is operated by CHE. Moreover, the operation voltage of the sol–gel-derived Ti x Zr y Si z O memory can be decreased to only 6 V, without sacrificing its

performance. Table 1 Comparison of P/E speed and data retention of the sol–gel-derived Megestrol Acetate high- κ memory devices   This work (Ti x Zr y Si z O with 600°C annealing) Ti x Zr y Si z O NC with 900°C annealing[13] Zr x Hf y Si z O NC with 900°C annealing[6] HfSi x O y with 900°C annealing[21] Program speed (2-V shift) 1.6 × 10−5 s 2.4 × 10−5 s 3 × 10−5 s 2 × 10−2 s (V g = −8 V, V d = 8 V) 1.2 × 10−4 (V g = −8 V, V d = 8 V) (V g = 10 V, V d = 9 V) (V g = V d = 10 V) (V g = −6 V, V d = 6 V) Erase speed (2-V shift) 1.7 × 10−6 s 1.9 × 10−6 s 2 × 10−3 s 5 × 10−5 s (V g = V d = 8 V) 5.2 × 10−6 s (V g = V d = 8 V) (V g = −10 V, V d = 9 V) (V g = −10 V, V d = 10 V) (V g = V d = 6 V) Retention at 85°C 5% loss 12% loss 11% loss 20% loss (106 s) (106 s) (106 s) (only 104 s) Retention at 125°C 10% loss 22% loss 30% loss NA   (106 s) (106 s) (106 s)   NC nanocrystal. Conclusion We demonstrated a high-performance sol–gel-derived Ti x Zr y Si z O memory in this study. The memory exhibits a notable hot hole program characteristic, and hence, a much higher erase speed is achieved. The barrier height for the Ti x Zr y Si z O film to silicon oxide was estimated to be approximately 1.

JZ participated in the design of the study and revised manuscript. JS participated in the design 4EGI-1 molecular weight of the experiment, performed the analysis, and organized the final version of the paper. All authors read and approved the final manuscript.”
“Background Silicon nano-wires (SiNWs) have attracted the attention of many researchers due to their structural, optical, electrical and thermoelectric properties. They are expected to be

important building blocks in the future nano-electronic and photonic devices including solar cells, field-effect transistors, memory devices and chemical and biomedical sensors. Owing to their compatibility with the Si-base technology, SiNWs can be used not only as the functional units of the devices but also as the interconnects [1–6]. Various methods have been reported for SiNW fabrication, including both bottom-up and top-down techniques. Bottom-up growth methods include laser ablation, evaporation, solution-based methods and chemical vapour deposition (CVD). The CVD growth Dinaciclib purchase usually takes place via vapour-liquid-solid (VLS) route [7]. Many catalyst materials, mainly metals including Au, Al, Ni, Fe and Ag, have been used for the SiNW growth [1, 8]. Among these metals, Au as catalyst has been the most popular and most widely investigated due to its chemical inertness and low eutectic temperature of Au-Si system. However, Au introduces deep impurity levels in Si bandgap

and degrades the charge carrier mobility [8]. Therefore, alternative catalyst investigation is of crucial 4��8C importance. One of the important parameters when considering the nano-wire fabrication process is the growth temperature, as this can determine the variety of substrates that could be used, especially when there is a prefabricated layer of some temperature-dependent material. The nano-wire growth temperature is determined by the eutectic temperature of the catalyst-precursor alloy [9]; thus,

the low-temperature growth will depend on the appropriate catalysts choice. Considering the characteristics of Ga, including the Ga/Si alloy low eutectic point of 29.774°C, wide temperature range for silicon solubility and its non-reactivity to form solid compound with silicon, Ga has been suggested as a good alternative to Au to grow SiNWs at low-temperatures. It is important to note that Ga does not act as catalyst for the decomposition of precursor gas as it does not assist the dissociation of SiH4 below its thermal decomposition point. Therefore, Ga acts only as a solvent, and the decomposition is achieved by plasma treatment (by the use of plasma-enhanced chemical vapour deposition (PECVD) system) [10]. In this study, Ga catalyst is used with an aim to grow SiNWs at a lowest temperature using PECVD technique. The growth temperature was varied between 100°C and 400°C. The grown nano-structures were characterised using scanning electron microscopy (SEM), Ultra Violet Visible spectroscopy (UV-Vis) and Raman spectroscopy.