Methods The layer structure of a simulated deep UV LED is basical

Methods The layer structure of a simulated deep UV LED is basically similar to that of recently reported

deep UV LEDs [3, 4]. The layer structures are assumed to be grown on a sapphire substrate and consist of a 2-μm-thick n-Al0.6GaN layer, 50-nm-thick Al0.45GaN/Al0.56GaN multiple quantum well (MQW) active layers, a 50-nm-thick p-Al0.6GaN layer, and a p-GaN contact layer. see more It is assumed that the simulated UV LED chip is not encapsulated and thus exposed to air. In this work, we consider two types of LED structures: planar and nanorod structures. Figure  1 shows the cross section of the FDTD computational domain for simulated LED structures. In the nanorod LED structure, the AZD1080 ic50 sidewall of the nanorod is filled with SiO2 layers for passivation. The cross section of the nanorod is assumed to have a hexagonal shape as shown in Figure  1c because nanorod structures are mostly grown in the shape of a hexagon [16]. In the simulations, the dependence of LEE on the height (h) and diameter (d) of the nanorod structure will be investigated. Figure 1 Schematic diagram of FDTD computational domain. Side view of the simulated LED structure is shown for (a) the planar LED and (b) nanorod LED structures. PMLs are employed for the absorption boundary

condition of the FDTD simulation. The detection plane for extracted light is indicated as dotted red line. (c) Cross-sectional view of the simulated Emricasan price nanorod LED structure. In the FDTD simulation, a single dipole source is positioned in the middle of the MQW active region. The spectrum of the dipole source has a Gaussian shape. Center wavelength and full width at half maximum of the spectrum are assumed to be 280 and 10 nm, respectively. The dipole source is polarized in the direction either parallel to the MQW plane for the excitation of the TE mode or perpendicular to the MQW plane for the excitation

of the TM mode. In the computational domain shown in Figure  1, the dipole source for the TE and TM modes is set to be polarized 3-oxoacyl-(acyl-carrier-protein) reductase in the x and z directions, respectively. The propagating light is completely absorbed without reflection in the PML. The Poynting vectors are calculated on the surfaces near PMLs and used to determine LEE of LED structures. LEE is defined as the fraction of emitted power out of the LED structure to the total emitted power, which is determined by the ratio of Poynting vectors integrated over extraction surfaces to total integrated Poynting vectors [18]. The plane for detecting extracted light is shown as dotted red line of the computational domain in Figure  1. In order to obtain reliable simulation results, it is important to properly choose the refractive index and absorption coefficient of each material. The absorption coefficient of the GaN layer is chosen to be 170,000 cm-1[20, 21]. Light is strongly absorbed in the GaN layer due to the large absorption coefficient.

MVD was calculated by averaging the CD31+ microvessels of tumors

MVD was calculated by averaging the CD31+ microvessels of tumors in each group. As shown in Fig. 9E, tumor vessels formation was suppressed in CXCR7shRNA learn more tumors. Silencing of CXCR7 resulted in a significant reduction of MVD in CXCR7shRNA tumors compared with those of control and NC tumors (Fig. 9D). These results indicated that silencing of CXCR7 substantially suppressed angiogenesis and subsequently inhibited the tumor growth. To extend our in vitro findings and evaluate the contribution of CXCR7 to metastasis

formation in vivo, the effect of CXCR7 silencing on organ metastasis was next examined. We did not observe that HCC cells spontaneously metastasized to the lungs and other organs of mice (data not shown). None of the mice developed lung metastasis. In summary, results from the heterotopic models showed that silencing of

CXCR7 inhibited the tumor SNX-5422 growth but not the metastasis of HCC cells in vivo. Discussion The identification of new biomarkers for the early detection of HCC is critical in the development of tumor-targeted therapy, and would likely have an important positive effect on the prognosis of this disease. CXCL12 plays a well-recognized role in the process of tumor progression. Accumulating evidence indicates that CXCL12 and its receptors are involved in cancer development through the inhibition of apoptosis, and promotion selleck screening library of angiogenesis, cellular proliferation, invasion and metastasis [27, 28]. CXCR7 expression has been reported in various human cancers, including carcinomas of the lung, prostate, pancreas and breast, as well as HCC click here [4, 23–25]. In the present study, we observed that human hepatocellular carcinoma tissues exhibited increased expression of CXCR7 as compared to normal liver tissues.

We also found that expression of CXCR7 is elevated in all six HCC cell lines compared with HUVECs. In addition, we observed that high metastatic potential cell lines expressed significantly higher levels of CXCR7 than low metastatic potential cell lines. This finding implies that CXCR7 overexpression may be involved in invasion and metastasis nature of HCC. Considerable efforts have been made in recent years to elucidate the biological function of chemokine receptors in cancer invasion and metastasis. To date, the role of CXCR7 in regulating HCC cells invasion is unclear. In this study, we observed that treatment with CXCL12 enhanced invasion and silencing of CXCR7 significantly inhibited the invasive ability of SMMC-7721 cells. Our study indicated the significance of CXCR7 on HCC cells invasion. These results are consistent with recent studies showing that CXCR7 mediates chemotaxis of cancer cells towards CXCL12 [24, 26]. Some studies have shown that CXCR7 can not trigger chemotaxis and activate calcium mobilization and intracellular signaling cascades, such as PI3K and ERK pathways [19, 29].

In addition, the SiGe/Si MQW nanorod arrays are also shown to exh

In addition, the SiGe/Si MQW nanorod arrays are also shown to exhibit excellent antireflective characteristics over a wide wavelength range. Methods Our initial samples consist of 50-period Si0.4Ge0.6/Si (3.6/6.4 nm nominally) MQWs capped with a 50-nm-thick Si layer, which were grown on (001) Si wafers using a multi-wafer ultra-high vacuum chemical vapor deposition (UHV/CVD) system. Pure SiH4 and GeH4 were used as gas precursors for Si or SiGe epitaxy. MGCD0103 price The formation procedure of SiGe/Si MQW nanorod arrays from the SiGe/Si MQW samples is illustrated in Figure 1(a): (1) assembly of the polystyrene

(PS) nanosphere monolayer arrays, (2) etching of the SiGe/Si MQW samples by RIE, and (3) removal of the nanosphere template. For the formation of SiGe/Si MQW nanodot arrays,

Pritelivir PS nanosphere arrays were first resized and then used as an etching mask, as shown in Figure 1(b). The following is a detailed introduction of the fabrication procedure. Figure 1 Schematic of the experimental procedure. To fabricate uniform SiGe/Si MQW (a) nanorod and (b) nanodot arrays from the Si0.4Ge0.6/Si MQWs using NSL combined with the RIE process. It is crucial to obtain a hydrophilic surface to allow the self-assembly of PS nanosphere monolayer arrays. In the first step, the as-grown SiGe/Si MQW samples were ultrasonically cleaned in acetone and in a solution of 4:1 H2SO4/H2O2 at 80°C for 30 min to prepare a hydrophilic surface. The SiGe/Si MQW samples were then coated with 800-nm-diameter PS nanospheres to form highly ordered and close-packed nanosphere arrays. Subsequently, a mixture of SF6 and O2 was

used to etch the samples at a working pressure of 25 mTorr for various durations to form the SiGe/Si MQW nanorod arrays. During the RIE etching, the inductively coupled plasma (ICP) power and bias of the etcher were kept at 50 W and 25 V, respectively. Finally, the PS nanosphere template was removed by ultrasonically cleaning in acetone solution. In addition, for the nanosphere resizing, O2 plasma RIE was used to shrink the PS Metalloexopeptidase nanospheres, allowing Ralimetinib chemical structure postspin feature size control. The surface morphologies of the etched samples were examined by scanning electron microscopy (SEM; FEI Quanta 200F, Hillsboro, OR, USA). Transmission electron microscopy (TEM) was carried out with a JEOL 2100 TEM (Akishima, Tokyo, Japan) operating at 200 kV to reveal detailed information about the microstructures of the etched nanostructures. PL measurements were performed at 10 K to study the optical properties of the SiGe/Si MQW nanorod and nanodot arrays using a 514.5-nm line of an Ar+ laser. The PL spectra were recorded by a liquid nitrogen-cooled Ge photodetector with the standard lock-in technique. We also measured total hemispherical reflectance spectra in air on a spectrophotometer with an integrating sphere (300 to 2,000 nm, Hitachi U-4100, Chiyoda, Tokyo, Japan) for the etched SiGe/Si MQW nanostructures.

Results and discussion Influence of annealing temperature on surf

Results and discussion Influence of annealing temperature on surface passivation The effective lifetimes

of the samples annealed at different temperatures in air are shown in Figure 2. The effective lifetime change is the ratio of the effective lifetime after annealing to that of the effective lifetime before annealing. The ratio was used instead of the actual value because the effective lifetimes of the six as-deposited samples (before annealing) were not strictly identical, which rendered meaningless the observation of the absolute value of the effective lifetime after annealing. The effective lifetime change initially increased with increased annealing temperature and then rapidly decreased below unity. This result indicated that passivation collapsed at annealing temperatures higher than 700°C. The optimum annealing temperature was around 500°C in air, which was higher than the reported 400°C to 450°C when annealed Proteasome inhibitor in N2[15]. KU-60019 purchase learn more Figure 2 Influence of annealing temperature on Al 2 O 3 passivation. Corona charging measurement was performed to observe the field-effect and chemical passivation mechanisms. Q f and the lowest lifetime can be extracted from the resulting measurement curve, as described in the section ‘Corona charging measurement.’ Figure 3a shows the measured data, and Figure 3b shows the Q f and the minimum effective lifetime change (lowest lifetime after annealing

vs. as-deposited value) as a function of the annealing temperature. Q f significantly increased to 1012 cm-2 after annealing at 400°C compared with Q f of about 1011 cm-2 before annealing (Figure 1). Q f increases from 2.5 × 1011 cm-2 at 300°C, reaches the highest point of about 2.5 × 1012 cm-2 at 500°C, and thereafter decreases to 8 × 1011 Atorvastatin cm-2. Q f did not significantly change

when the annealing temperature was higher than 600°C. Meanwhile, the effective lifetime of the sample annealed at 300°C was slightly enhanced (Figure 2), i.e., 1.2 times greater than that of the as-deposited sample. This result indicated that Q f of 2.5 × 1011 cm-2 did not significantly affect surface passivation. The chemical passivation variation at 300°C to 500°C was similar to Q f based on the minimum lifetime in the corona charging measurement. The chemical passivation effect increased with increased annealing temperature before 500°C and quickly decreased thereafter. This variation was related to the hydrogen release from the film found by Dingemans [16]. Figure 3 Corona charging measurement of samples. (a) Before and after annealing. (b) Fixed charge density and minimum effective lifetime change after annealing at different temperatures. Notably, Q f reached 1012 cm-2 after annealing at 750°C, and this value was almost one magnitude higher than that of the as-deposited sample. However, the effective lifetime was low (Figure 2) because of the poor chemical passivation at 750°C in Figure 3b of the minimum lifetime change value.

Statistical analysis The significant difference of virulence (mor

Statistical analysis The significant difference of virulence (mortality) between low and high NADase activity groups was ascertained as follows. The mortality of mice infected with each GAS isolate, but not mean mortalities produced by pooling multiple isolates into the two groups, was determined. The four mortalities in the low NADase activity group and the four mortalities

in the high NADase activity group were compared using an unpaired t test http://​www.​graphpad.​com/​quickcalcs/​ttest1.​cfm. Survival times were assessed using a log-rank comparison. R software was used for statistical analysis http://​bioinf.​wehi.​edu.​au/​software/​russell/​logrank/​. P value ≤ 0.05 was considered significant. Results Correlation of NADase activity levels and virulence MM-102 mw The levels of detectable NADase activity produced by clinical isolates of M-1 GAS were divided into two groups (low-activity Pictilisib ic50 and high-activity) in our previous study [15]. It is possible that isolates belonging to the high-activity group are more virulent, possibly causing invasive infection at higher severity and/or with lower dose. To investigate this possibility, we

used a mouse model for the invasive soft-tissue infection, which is currently the most accepted available method for this type of in vivo experiment. As shown in Table 2, after skin inoculation with M-1 GAS isolates belonging to the high-activity group, 80%, 60%, 100% and 67% of the mice were dead within a week, respectively, whereas with the isolates belonging to the low-activity group, Amobarbital 29%, 33%, 67% and 17% of the mice died, respectively (P = 0.0272 for unpaired t test). The survival curves (Figure

1), based on the data of Table 2 showed that no mouse died after day 8 on the study. Table 2 Virulence (Mortality) to mouse of GAS isolates with different NADase activity NADase Isolate Mortalitya (Death/Trial) NADaseb Low activity 1529 KN01 MDYK MUY 29% (2/7) 33% (3/9) 67% (4/6) 17% (1/6) 3.37 ± 0.66 6.19 ± 0.52 2.95 ± 0.26 2.97 ± 0.95 High activity GT01 FI01 CR01 IYAT 80% (12/15) 60% (6/10) 100% (12/12) 67% (4/6) 57.03 ± 3.65 59.40 ± 4.76 114.30 ± 8.67 87.25 ± 5.22 No activityc GT01Δnga SF370 0% (0/8) 17% (1/6) 0.49 ± 0.13 -0.44 ± 0.80 a, Mortality was determined on Day 11. b, NADase activity (units) ± standard error are indicated. One unit of NADase activity is defined as the amount (μg) of β-NAD GSK461364 purchase cleaved per hour per μl culture supernatant as described previously [15]. c, Strain SF370, which encodes an inactive form of Nga [15] was added as negative control. Figure 1 Survival after skin inoculation with GAS isolates with different NADase activities. The survival times of 28 and 43 mice infected with GAS isolates belonging to low- and high-activity groups in Table 2, respectively, were shown.

e , to search for X-rich regions (where X stands for the kind of

e., to search for X-rich regions (where X stands for the kind of amino acid one is interested in). The algorithm just processes a list with the positions of the amino acids with the desired characteristics (X) and returns a list of MM-102 concentration protein regions rich in those amino acids (X-rich region). The version of the MS Excel macro included as supplementary material (Additional file 4) is able to analyze simultaneously up to 1500 proteins and is customized to search for hyper-O-glycosylated regions.

find more Basically, the application scans the data searching for regions of a given length, called Window (W), having a Density (%G) of the desired amino acid characteristic above a minimum value. These regions can either be reported as independent X-rich regions, or can be combined into a single, longer region if several of them are found that overlap or are separated from one another by a number of amino acids selleck compound which is less than the parameter Separator (S). The parameters W, %G, and S are set by the user. In any case, the beginning and end of X-rich regions are reported as the first and last amino acid with the

desired properties in the group, so that for example, for W = 20 and %G = 25% (at least 5 positive hits in the window of 20 residues), X-rich regions as small as 5 amino acids could be reported. The results of the analysis are reported as a pdf file containing the data for all the X-rich regions encountered for each protein, both graphically and as a table, as well as several graphics with statistics for the whole set of proteins loaded. The influence of different values of the parameters W and %G on the detection of pHGRs was studied with the set of B. cinerea proteins predicted to have signal peptide (Figure 5). Lower values for both parameters, by making the analysis less stringent, resulted in a higher number of pHGRs, distributed in a broader set of proteins. Likewise, lower %G values tend

to produce longer pHGRs, since the lower stringency permitted the pHGRs to be extended to neighboring regions Endonuclease displaying a not-so-high predicted sugar content. On the contrary, the average length of pHGRs increased with higher values of the parameter W, since this increase would eliminate the shorter ones as they would simply not be found. Figure 5 Influence of the parameters Window (W) and Density (%G) on the detection of pHGRs. The whole set of B. cinerea secretory proteins predicted by NetOGlyc to be O-glycosylated was scanned with the MS Excel macro XRR in search of pHGRs. A: results obtained with varying values of W and a fixed value for %G of 25%. B: results obtained with varying values of %G and a fixed value for W of 20.

Both for MPR and persistence rates, we found that the treatment r

Both for MPR and persistence rates, we found that the treatment regimen was a highly significant independent determinant of both MPR and persistence. With respect

to other variables independently associated with persistence or compliance, our findings were broadly consistent with previous reports. The influence of bone densitometry on reinforcing adherence has been a consistent finding of previous studies [16, 35], but is difficult to interpret here as the outcome of the evaluation (T-score) was not available. Calcium or vitamin D supplementation has previously been reported to be associated with better compliance and Fer-1 datasheet improved fracture outcome in the ICARO study [38]. Such Selleck PKC412 dietary supplementation may also be indicative

of higher motivation. Likewise, patients with a neurological disorder (notably epilepsy, Alzheimer or Parkinson’s disease) were more persistent than others, which may reflect awareness of physicians about the high risk of fracture in such patients [39–41], as well as, for patients with epilepsy, a history of treatment for which good adherence is critical. Topical products for joint and muscular pain mainly correspond to non-steroidal anti-inflammatory drugs. Those drugs could be prescribed for their analgesic effects on pain related to fractures, such as back pain with vertebral fractures. Relief of these symptoms may also lead patients ARRY-162 manufacturer to be less adherent to treatment of osteoporosis. Even

though the absolute number of patients was low (70 patients in all), a significant association between a diagnosis of comorbid rheumatoid arthritis and low MPR and poor persistence was observed. The interpretation of this finding is unclear, but in the absence of further information on rheumatoid pathology, it merits exploration in a dedicated study. It is noteworthy that it has been previously reported that patients with rheumatoid arthritis taking oral glucocorticoids did not routinely undergo ioxilan bone densitometry or receive prescription medications for osteoporosis [42]. An important determinant of the validity of our findings is the representativity of the source data. The Thales database has been demonstrated to be a reliable source of information in numerous previous studies in rheumatology [19, 24] and in other fields of medicine [43–46]. In addition, the proportions of patients with various comorbidities in our study sample are consistent with the known prevalence of these diseases in women over 45. This study has several limitations. Some of these are linked to the use of a primary care registry as the data source. The use of such databases for pharmacoepidemiological studies has become popular of recent years, since it allows access to information on a large number of patients gathered in real-world conditions [3, 47].

P21 (CIP1/WAF1) is a direct target of p53 [36], thus, p53 mediate

P21 (CIP1/WAF1) is a direct target of p53 [36], thus, p53 mediated induction of p21 (CIP1/WAF1) at least contributed to the inhibitory effect of BBR on cell proliferation and cell cycle arrest. On the other hand, our results suggested that activation of p38 MAPK mediated the BBR-induced Tozasertib FOXO3a protein expression and the latter also contributed to the BBR-inhibited cell growth and -induced apoptosis. It is possible that the inhibition of proliferation can be in part a consequence of increased cell apoptosis or vise versa. The FOXO3a is an important tumor suppressor and is

under-expressed in many cancers. There are a number of parallels between FOXO3a and p53, click here both play a pivotal role in regulating the cellular response to stress and damage signals, inducing cell cycle www.selleckchem.com/products/i-bet151-gsk1210151a.html arrest, apoptosis, and DNA repair [37]. Several studies showed that FOXO3a interacts with p53, and that FOXO3a is a p53 target gene [15, 38]. In this study, we demonstrated that the potential interaction and mutually exclusive events of p53 and FOXO3a may contribute to enhance BBR-induced apoptosis and -inhibited cell proliferation. However, the detailed mechanism underlining the regulation of these transcriptional networks in mediating the effect of BBR on the control of lung cancer cell survival

needs to be elucidated. Our results also demonstrated a causative role of FOXO3a in mediated the effect of BBR on p21 (CIP1/WAF1) expression. We showed that the knockdown of FOXO3a blocked, while overexpression of FOXO3a

augmented the increase in p21 (CIP1/WAF1) protein expression in BBR-treated cells. These, together with the observation from silencing of p53 experiments indicated that p21 (CIP1/WAF1) is not only the direct target of p53 but also function as FOXO3a downstream effector, which may be through the p53-independent the way [17]. p53 and FOXO3a share similar target genes including p21(CIP1/WAF1), FOXO factors bind to the promoter of p21 to induce cell cycle arrest at the G1/S transition [39]. Given the fact that p21 (CIP1/WAF1) is involved in regulation of fundamental cellular processes, such as cell proliferation, differentiation, regulation of gene transcription and apoptosis [40, 41]. BBR-induced FOXO3a expression may contribute to induce cell apoptosis, which could be in part a consequence of inhibition of NSCLC cell growth. Of note, the dual function of p21 (Cip1/Waf1) was observed in cancerogenesis. On the one hand, p21 (Cip1/Waf1) acts as a tumor suppressor; on the other hand, it prevents apoptosis and acts as an oncogene [40, 42]. Therefore, precise understanding the role of p21 (Cip1/Waf1) and relevant signaling pathways involved would help to develop better cancer-treatment strategies. Study showed that activation of p38 MAPK reduced protein expression of cyclin D1, another cell cycle regulator [43].

Appl Environ Microbiol 2007,73(5):1576–1585 PubMedCrossRef 34 Ja

Appl Environ Microbiol 2007,73(5):1576–1585.PubMedCrossRef 34. Jackson SR, Dryden M, Gillett P, Kearney P, Weatherall R: A novel midstream urine-collection

device reduces contamination rates in urine cultures amongst women. BJU Int 2005,96(3):360–364.PubMedCrossRef 35. Bekeris LG, Jones BA, Walsh MK, Wagar EA: Urine culture contamination: a College of American Pathologists Q-Probes study of 127 laboratories. Arch Pathol Lab Med 2008,132(6):913–917.PubMed 36. Ott SJ, Musfeldt M, Wenderoth DF, Hampe J, Brant O, Folsch UR, Timmis KN, Schreiber S: Reduction in diversity of the colonic mucosa selleck associated bacterial microflora in patients with active inflammatory bowel disease. Gut 2004,53(5):685–693.PubMedCrossRef 37. Carroll IM, Ringel-Kulka T, Siddle JP, Ringel Y: Alterations in composition and diversity of the intestinal microbiota in patients with diarrhea-predominant irritable bowel syndrome. Neurogastroenterol Motil 2012,24(6):521-e248.PubMedCrossRef 38. Turnbaugh PJ, Hamady M, Yatsunenko T, Cantarel BL, check details Duncan A, Ley RE, Sogin ML, Jones WJ, Roe BA, Affourtit JP, et al.: A core gut microbiome in obese and lean twins. Nature 2009,457(7228):480–484.PubMedCrossRef 39. Wilkins EG, Payne SR, Pead PJ, Moss ST, Maskell RM: Interstitial cystitis and the urethral syndrome: a possible answer. Br J Urol 1989,64(1):39–44.PubMedCrossRef

40. Haarala M, Jalava J, Laato M, Kiilholma P, Nurmi M, Alanen A: Absence of bacterial DNA in the bladder of patients with interstitial cystitis. J Urol 1996,156(5):1843–1845.PubMedCrossRef aminophylline 41. Lacroix JM, Jarvic K, Batrab SD, Heritze DM, Mittelman MW: PCR-based technique for the detection of bacteria in semen and urine. J Microbiol Methods 1996,26(1–2):61–71.CrossRef 42. Falagas ME, Betsi GI, Tokas T, Athanasiou S: Probiotics for prevention of recurrent urinary

tract infections in women: a review of the evidence from microbiological and clinical studies. Drugs 2006,66(9):1253–1261.PubMedCrossRef 43. Imirzalioglu C, Hain T, Chakraborty T, Domann E: Hidden pathogens uncovered: metagenomic analysis of urinary tract infections. Andrologia 2008,40(2):66–71.PubMedCrossRef 44. Darbro BW, Petroelje BK, Doern GV: Lactobacillus delbrueckii as the cause of urinary tract infection. J Clin Microbiol 2009,47(1):275–277.PubMedCrossRef 45. Maskell RM: The natural history of urinary tract infection in women. Med Hypotheses 2010,74(5):802–806.PubMedCrossRef 46. Maskell R, Pead L, Sanderson RA: Fastidious bacteria and the urethral syndrome: a 2-year clinical and bacteriological study of 51 women. Lancet 1983,2(8362):1277–1280.PubMedCrossRef Authors’ contribution HS, AJN, SLJ and KSJ were involved in study design; HS processed the samples and carried out the molecular techniques. KL and HS performed the bioinformatics and taxonomic analysis. HS interpreted the data and PD-0332991 cost authored the manuscript.

The good electro-optical properties of Cu2O make it used as photo

The good electro-optical properties of Cu2O make it used as photocatalyst in degradation of organic pollutants and H2 evolution from photoelectrolysis of water under visible light illumination [7–9]. By far, many deposited methods have been investigated to prepare Cu2O thin films, such as sputtering [10, 11], thermal oxidation [12], chemical vapor deposition [13], anodic oxidation [14], spray pyrolysis

[15, 16], chemical oxidation [17], electrodeposition [18, 19], and so on. Among these techniques, electrodeposition is an inexpensive, convenient, and effective way to prepare semiconductor oxide films over conductive substrates. The surface morphology and physical properties of the electrodeposition-derived films is mainly determined by deposition parameters such as applied potential, concentration of PXD101 mouse electrolyte, bath temperature, Sotrastaurin purchase and bath pH [20–23]. Yao et al. [24] reported the electrochemical deposition of Cu2O microcrystals on a glassy carbon (GC) electrode. When varying the deposition voltage at GC electrode, Cu2O nanocrystalline changed from superoctahedral to octahedron and then to microspheres. Jiang et al. [25] studied electronic structure of Cu2O thin films grown on Cu (110) by X-ray absorption spectroscopy (XAS) and X-ray photoelectron spectroscopy (XPS). Combined with XAS and XPS measurements,

accurate identification of the various chemical components has been determined. According to these observations, it can be concluded that the deposition conditions play an important PF-01367338 in vitro role in the physical properties of Cu2O thin films. And they also explained about the effect of deposition conditions on the microstructure and optical properties of Cu2O films. Recently, the electrodeposited Cu2O films prepared using potentiostatic method

and physical properties of the as-deposited Cu2O films have been reported. In this paper, Cu2O thin films were deposited by electrodeposition at different applied potentials. The effect of the applied potential on the morphological, microstructural, and optical properties of the as-deposited Cu2O films has been investigated in detail. Methods Preparation of Cu2O thin films The Cu2O thin films were prepared by electrodeposition on Ti sheets. Prior to the deposition, Ti sheets were ultrasonically cleaned in acetone, alcohol, and deionized water, sequentially. Then, they were chemically polished CYTH4 by immersing them in a mixture of HF and HNO3 acids (HF:HNO3:H2O = 1:1:2 in volume) for 20 s, followed by rinsing in deionized water. Electrodeposition of Cu2O was performed using a three-electrode system, in which a Ti sheet was used as a working electrode. A Pt plate and an Ag/AgCl in saturated potassium chloride aqueous solution were employed as counter and reference electrode. Cu2O films were grown on the surface of Ti sheets at bath temperature of 40°C using a solution consisting of 0.1 M sodium acetate (NaCH3COO) and 0.05 M cupric acetate (Cu(CH3COO)2).