Collegiate wrestlers also CFTRinh-172 nmr use moderate to high intensity resistance training with high work to rest ratios. In-season football training includes repeated bouts of short sprints and Olympic/power lifting with low work to rest ratios. Methods Twenty-two Divison II college wrestlers (19.9 ± 1.9 yr, age ± SD) and 15 football players (18.6 ± 1.5 yr) completed this double-blind, placebo controlled study. Each subject ingested either 4 g/day β-alanine or placebo in powdered capsule form. Subjects were tested pre and post 8-week treatment in timed 300 yd. shuttle, 90° flexed arm hang (FAH), body

composition, and blood lactate accumulation during 300 yd. shuttle. Wrestlers participated in 5 days per week training that included HIIT 3 days/week and resistance training with high work: rest ratios 2 days/week. Football players participated in 5 days/week training that included repeated sprints with low work: rest ratios 3 times/week and Olympic/power lifting 4 times/week. Results The subjects taking β-alanine achieved more desirable results on all tests compared to placebo (NS, p > 0.05). CYT387 Performance improvements were greatest in the football supplement group, decreasing 300 shuttle time by 1.1 sec (vs. 0.4 sec. placebo) and increasing FAH (3.0

vs. 0.39 sec.). The wrestlers, both placebo and supplement lost weight (as was the goal, i.e. weight bracket allowance); however, the supplement group increased lean mass by 1.1 lb., while the placebo group lost lean mass (-0.98 lb). Both football groups gained weight; however, the supplement group gained an average 2.1 lb lean mass compared to 1.1 lb for placebo. See Table 1. Table 1   Test Football

Placebo (n = 8) Mean (SD) Football Supplement (n = 7) Mean (SD) Wrestling Placebo (n = 12) Mean (SD) Wrestling Supplement (n = 10) Mean (SD) Δ bodyweight 2.8 (1.2) 2.6 (1.9) -3.2 (4.9) -0.43 (4.6) Δ bodyfat% 0.88 (1.5) 0.1 (1.1) -1.1 (1.4) -0.89 (0.66) Δ lean mass 1.1 (2.3) 2.1 (3.6) -0.98 (2.6) 1.1 (4.3) Δ 300 shuttle -0.4 (2.2) -1.1 (0.94) -1.3 (1.7) -1.6 (2.2) Δ 90° FAH 0.39 (6.5) 3.0 (5.4) 5.0 (3.9) 6.5 (7.3) Δ Lactate 1.5 (3.3) 0.03 (3.7) -2.3 (4.7) -2.6 (4.7) Conclusion Supplementation with beta-alanine appears Thiamet G to have the ability to augment performance and stimulate lean mass accrual in a short amount of time (8 weeks) in previously trained athletes. β-alanine may magnify the expected performance outcomes of training programs with different metabolic demands. Acknowledgements The products were donated by Athletic Edge Nutrition. No other funding was received. The authors declare that they have no competing interests.”
“Background We have recently reported that the dietary supplement Meltdown® (Vital Pharmaceuticals) increases plasma norepinephrine (NE), epinephrine (EPI), glycerol, and free fatty acids (FFA), as well as metabolic rate in healthy men [1].

Because of page limitations in CEN, we have decided to establish

Because of page limitations in CEN, we have decided to GW786034 chemical structure establish CEN Case Reports to facilitate publication of critical case reports and thereby contribute to clinical education. On behalf of the Japanese Society of Nephrology, we eagerly look forward to your submissions. Journal title: CEN Case Reports Published format: Electronic online edition only (separate orders for print edition accepted) Frequency of publication: twice a year (every 6 months) Contents: Case reports only Initial publication: May 2012 Submission and publication cost: No charge for three or fewer printed pages, including color pages Submission guidance: Use the online system Editorial Manager

starting 1 CCI-779 cost September 2011. For detailed instructions for submissions, please see the Instructions for Authors of CEN Case Reports.

http://​www.​springer.​com/​medicine/​nephrology/​journal/​13730 [Inquiries] CEN Case Reports, Editorial Office c/o Springer Japan KK No. 2 Funato Bldg. 1-11-11 Kudan-kita, Chiyoda-ku, Tokyo 102-0073, Japan Tel.: +81-3-68317009 Fax: +81-3-68317010 E-mail: [email protected] CEN Case Reports Editor-in-Chief Kenjiro Kimura, MD Co-Editor-in-Chief Tatsuo Sakai, MD Deputy Editors Toshiki Moriyama, MD Shunya Uchida, MD”
“Erratum to: Clin Exp Nephrol (2011) 15:226–234 DOI 10.1007/s10157-010-0390-0 The correct name of the sixth author should be given as Yoshihiro Arimura, not Yasuhiro Arimura.”
“Introduction There has been no national registry of renal biopsies in Japan. The Committee for the Standardization of Renal Pathological Diagnosis and the Working Group for Renal Biopsy Database in the Japanese LY2606368 order Society of Nephrology established the first nationwide, web-based, and prospective registry system, the Japan Renal Biopsy Registry (J-RBR), to record pathological, clinical, and laboratory data regarding all renal biopsies performed in 2007. To date, the epidemiological and clinical data of renal diseases are available from nationwide registries of renal biopsies from the United Kingdom [1], Italy [2],

Denmark [3], Spain [4], the Czech Republic [5], and Australia [6]. The role of a renal biopsy registry has been recently encouraged [7]. In Japan, several surveys were temporarily conducted for patients with restricted renal diseases, including primary glomerulonephritis [8], idiopathic membranous nephropathy (MN) [9], and immunoglobulin (Ig) A nephropathy (IgAN) [10]. However, there has been no web-based, nationwide, or prospective registry system of overall renal biopsies in Japan. The aim of the current study was to provide data to investigate the epidemiology and frequency of renal diseases with a histological diagnosis for patients registered in 2007 and 2008 on the J-RBR. Subjects and methods Registry system and patients The researchers on the Committee for the Standardization of Renal Pathological Diagnosis and the Working Group for Renal Biopsy Database in the Japanese Society of Nephrology participated in this study.

9; Figure 1) Receiver

9; Figure 1). Receiver GS-4997 operating characteristic curve A-1210477 analysis suggested the best cutoff point for CRP level in the diagnosis of AA was 27.1 mg/dL, which had a sensitivity of 97% and a specificity of 41% (area under curve [AUC]: 0.77; Figure 1). RDW was not correlated with CRP and leukocyte levels. However, we found a correlation between CRP and leukocyte levels (Table 2). Table 1 Comparison of the demographic features and leukocyte count, CRP, and RDW levels of

the subjects in the acute appendicitis and the control groups   Acute appendicitis (n = 590) Control group (n = 121) p Male/female 332/258 69/52 .82 Age (y)* 36.7 ± 12.2 35.2 ± 8.1 .67 Leukocyte (× 10 3 /mm3)* 13.5 ± 4.5 7.5 ± 2 <0.01 CRP (mg/L)* 48.8 ± 73.6 4.6 ± 4.7 <0.01 RDW (%)* 15.4 ± 1.5 15.9 ± 1.4 0.01 *Values see more are means±standard deviation. Abbreviations: CRP C-reactive protein, RDW red cell distribution width. Figure 1 Receiver operating characteristic (ROC) curve of red cell distribution width (RDW), leukocyte,

and C-reactive protein (CRP). Table 2 Correlation analysis of leukocyte, CRP, and RDW levels in patients with acute appendicitis Parameters Correlation coefficient (r) P value Leukocyte – RDW -0.031 .44 Leukocyte – CRP 0.21 <0.01 CRP – RDW -0.065 .11 Abbreviations: CRP C-reactive protein, RDW red cell distribution width. Discussion A parameter with ability to establish the diagnosis of acute appendicitis has always been a center of attention for physicians. Many different parameters have been examined or are under active investigation for that purpose. The pathophysiology of acute appendicitis

is characterized by the mucosal ischemia of the appendix that results from ongoing mucus secretion from the appendiceal mucosa distal to an obstruction of the lumen, elevating intraluminal and, in turn, venous pressures. Once luminal pressure exceeds 85 mmHg, venules that drain the appendix become thrombosed and, in Branched chain aminotransferase the setting of continued arteriolar in flow, vascular congestion and engorgement of the appendix become manifest [5]. Infection is added to the inflammation of appendicitis. WBC count is most frequently used to diagnose AA. Several reports have suggested that an elevated WBC count is usually the earliest laboratory measure to indicate inflammation of the appendix, and most patients with AA present with leukocytosis [14, 15]. We found that WBC count was significantly higher in AA. In various studies, the range of sensitivity and specificity of WBC in the diagnosis of AA have been reported 67%- 97.8% and 31.9%-80%, respectively [16]. Similar to the literature, the present study found that the sensitivity and specificity of leukocyte level were 91% and 74%, respectively. CRP is a sensitive acute phase protein that lacks specificity due to increased levels in all acute inflammatory processes. Its concentration increases with the duration and extent of the inflammation.

We found that in addition to activating tcpP, AphB was required f

We found that in addition to activating tcpP, AphB was required for full expression of ToxR in V. cholerae stationary growth phase. AphB regulated toxR directly as purified recombinant AphB binds to the toxR promoter. This study HSP inhibitor suggests that V. cholerae may use this additional layer of activation to turn on virulence factor production efficiently in optimal conditions. Results and Discussion Examination of toxR expression under different in vitro conditions using a transcriptional fusion reporter ToxR is one of two proteins, along with TcpP, shown to activate the expression of ToxT,

the master virulence activator in V. cholerae (Fig. 1). The expression of tcpP has been shown to be induced by AphA and AphB [11, 19], while toxR has been thought to be constitutively expressed and only modulated by temperature [16, 18]. To measure toxR expression, we placed the toxR promoter upstream of the luxCDABE operon on a plasmid [20] and transformed into wild type V. cholerae. We then grew the resulting cells at 37°C or 22°C. Expression of P toxR -luxCDABE was significantly increased at 22°C (Fig. 2A), consistent with the previous report [18] that the expression of toxR

is modulated by temperatures. Since the availability of 3-Methyladenine price oxygen concentrations is different during V. cholerae infection, we also examined the expression of toxR under varying oxygen concentrations (Fig. 2B). The lux expression was similar under each condition, suggesting that oxygen levels do not regulate toxR expression. Figure 2

The expression of toxR in wild type under selleck different conditions using a P toxR -luxCDABE transcriptional reporter. (A). The reporter strain was grown at 22°C or 37°C, and at successive time points, luminescence was measured. Units are arbitrary light units/OD600. The results are the average of three experiments ± SD. (B). The reporter strain was grown at 37°C aerobically, in an anaerobic chamber (Mini MACS Anaerobic workstation, Microbiology International) or in a BBL CampyPak Microaerophilic Myosin System. At different time points, samples were withdrawn and luminescence was measured. Units are arbitrary light units/OD600. The results are the average of three experiments ± SD. Influence of virulence regulatory proteins on toxR expression To investigate molecular influences on toxR expression, we introduced the P toxR -lux construct into various strains of V. cholerae with mutations in virulence regulator genes. We also included a tcpA mutant because a previous study showed that TcpA, the major subunit of TCP pilin [2], affects cholera toxin gene expression in vivo but not in vitro [21]. We grew these strains at 37°C for 12 hours and measured luminescence (Fig. 3A). We found that ToxR and ToxS did not affect toxR expression, indicating that ToxR does not autoregulate.


our study, we observed that edaravone displayed a line


our study, we observed that edaravone displayed a linear increase in the Cmax and AUCτ values over a dose range of 20–60 mg administered by intravenous infusion. The Cmax values were measured 30 minutes after the intravenous infusion of edaravone. The Cmax values (table II) were significantly higher than the values reported in a previous study (Cmax 222.53 ± 16.77 Ruxolitinib order ng/mL, dosage 0.2 mg/kg; Cmax 658.89 ± 96.88 ng/mL, dosage 0.5 mg/kg; Cmax 1727.19 ± 210.88 ng/mL, dosage 1.0 mg/kg; and Cmax 3060.73 ± 236.88 ng/mL, dosage 1.5 mg/kg).[20] The related explanations are as follows: 1. The intravenous infusion time in our study was 30 minutes, while in the previous study it was 40 minutes.   2. We selleck kinase inhibitor developed a simple, rapid, sensitive method for determination of the edaravone plasma concentration with HPLC, which took less than 10 minutes to obtain the supernatant, making it more convenient and stable. Edaravone is unstable in human plasma in air,[23] and the extraction method always takes more than 30 minutes,

meaning that edaravone is exposed to air for a long time.[20]   3. In a preliminary experiment, we found that edaravone in human plasma was unstable when stored at room temperature for more than 45 minutes.[24] This was consistent with the dramatic decrease in the edaravone plasma concentration. Thus we tested all plasma samples within 24 hours after administration of the drug.   The LC-MS/MS method, as another analytical method for measuring Selleck C225 the

plasma edaravone concentration, has also been used by another group. The calibration curve is linear in the range of 10–500 ng/mL but is not linear above 500 ng/mL.[19] In conclusion, edaravone parenteral solution is both well tolerated and safe when administered as a single dose or as multiple doses. Acknowledgments This study was supported by Nanjing Yudao Pharmaceutical Science & Technology Co. (Nanjing, China), Nanjing Hailing Pharmaceutical Co. Ltd. (Nanjing, China), the National Science and Technology Major Projects for “Major New Drugs Innovation and Development” (grant no. 2011ZX09302-003-02), Jiangsu Province Science and Technology Major Projects (grant no. BM2011017), the Foundation of the Health Bureau of Jiangsu Province (Nanjing, China; grant no. H201108), and the Foundation of the Nanjing Pharmaceutical Association (Nanjing, China; grant no. H2011YX001). References 1. Berliner JA, Heinecke JW. Review: the role of oxidized lipoproteins in atherogenesis. Free Radic Biol Med 1996; 20: 707–27.PubMedCrossRef 2. Breen AP, Murphy JA. Review: reactions of oxyl radicals with DNA. Free Radic Biol Med 1995; 18: 1033–77.PubMedCrossRef 3. Burdon RH. Review: superoxide and hydrogen peroxide in relation to mammalian cell proliferation. Free Radic Biol Med 1995; 18: 775–94.PubMedCrossRef 4. Markesbery WR.

In general, the C-terminal domain determines the type of bacterio

In general, the C-terminal domain determines the type of bacteriocin. The C-terminal nuclease domains are not only interchangeable but also lack species specificity [18]. Strikingly, the tRNase type of bacteriocin may accelerate exhaustion of tRNA in the cytoplasmic pool and thereby impair protein synthesis in vivo. Ogawa et al. have demonstrated that particular tRNA molecules can be digested

by colicin D as well as by colicin E5 [19, 20]. It has been suggested that phage-associated klebicin D is a tRNase type of bacteriocin based on similarity to the nuclease-like domain of colicin D [21]. Nguyen et al. Veliparib cell line reported production of a high-molecular-weight bacteriocin (carotovoricin Er) and Chuang et al. reported production of a low-molecular-weight

bacteriocin (LMWB; carocin) by Pectobacterium[22, 23]. The former has a bulky antenna-like tail, inner core, and contractile cylindrical structure, HDAC inhibitor and the carotovoricin-caused inhibition zone can be easily distinguished from that of carocin by its low diffusibility. Carocin S1 is a deoxyribonuclease type of LMWB (indicated by the letter S) and is secreted by Pcc strain 89-H-4. Additionally, export of Carocin S1 utilizes the type III secretion system in Pcc, which also controls the cell motility of the bacterium [24]. Pcc strain F-rif-18 is a spontaneous rifampin-resistant mutant of the wild-type 3F-3. Ultraviolet radiation can induce Pcc strain F-rif-18 to produce the LMWB Carocin S2. One of several sensitive cells, SP33, was selected as an indicator strain here. In the present study, the chromosomal bacteriocin gene, carocin S2, was introduced into an expression plasmid encoding two proteins, CaroS2K and CaroS2I. These proteins Anidulafungin (LY303366) were purified and characterized and their primary activities of killing (CaroS2K) and immunity (CaroS2I)

were investigated in vivo and in vitro. Results Isolation of Transposon Insertion Mutants Conjugation between F-rif-18 and E. coli 1830 resulted in ~3,500 colonies after selection on Modified Drigalski’s agar medium selleck chemicals containing rifampin and kanamycin. In bacteriocin assay, the size of the inhibition zone around each isolate was compared with that of F-rif-18. Mutant colonies were identified by smaller inhibition zones. This evidence of mutation suggested that transposon Tn5 had been inserted into LMW bacteriocin-related genes. The strain TF1-2, a putative insertion mutant, would no longer produce LMW bacteriocin (Figure 1). Figure 1 Bacteriocin assays of Tn 5 insertion mutants of Pcc strains. Strain number: 1, 3F3 (wild type); 2, 1830 (E. coli); 3, F-rif-18 (parent); 4, TF1-1 and 5, TF1-2 (insertion mutant). Other unlabelled strains are Tn5 insertion mutants of F-rif-18 strain. The indicator is Pcc strain SP33.

Materials and

methods Plant and seed material To test the

Materials and

methods Plant and seed material To test the effect of infection, host plant origin, and environmental factors (water and nutrient treatments), in August 2005, we CAL-101 manufacturer collected seeds from multiple natural tall fescue populations by the Baltic Sea in localities that were geographically separated from SBI-0206965 each other by approximately 500 km. These were the island of Åland (8 populations), the island of Gotland (9 populations), and the west coast of Sweden (6 populations). 10 to 50 individuals were collected from each population, and three seeds from each plant individual were stained for microscopic examination of the endophyte infection status (Saha et al. 1988). Neotyphodium coenophialum infectivity varied between 85–100% in all tall fescue populations from the three locations. Uninfected (E-) and infected (E+) seeds were combined separately from populations within each of the three study areas (Åland, Gotland, and coastal Sweden). In

other words, we pooled all E- seeds and then all E+ from the populations within each location to create three batches of E- seeds and three batches of E+ seeds that represented the three geographic origins. In addition to plants from natural tall fescue populations, we used E+ and E- K-31 (from T. selleck chemical Phillips, University of Kentucky) cultivar seeds in our experiment. To test the role of the endophyte on invertebrate communities while controlling for plant genotypic background, we Sitaxentan experimentally removed the endophyte from portion of E+ seeds (manipulatively endophyte-free plants = ME-). To kill the fungus while the seeds remained viable, the E+ seeds were heat–treated by keeping the seeds in warm water (56-57°C) for 10–20 min. All tall fescue seeds from natural populations, K-31 cultivar and endophyte-removed seeds were germinated on moist tissue paper in Petri-dishes in a greenhouse and planted 7 days after germination to individual

pots with sand and peat mixture. Field experiment To test the role of endophyte infection, plant geographic origin and environmental factors, a common garden field experiment was established at Botanical Garden, University of Turku, Finland in 2004. The study site is at the edge of the northern distribution range of natural tall fescue populations and has been in cultivation in the past. It was tilled in the summer 2004 without nutrient application. The experimental area was fenced to prevent large vertebrates (e.g., rabbits, deer) from browsing the plants. However, smaller vertebrates (e.g., voles) and invertebrates were allowed to freely access the area. The space between experimental plants was either mowed, hand weeded or sprayed with herbicide two times during the growing season to prevent interspecific competition in the field.

The AZO films AZO films with overall 1,090 cycles of ZnO plus Al2

The AZO films AZO films with overall 1,090 cycles of ZnO plus Al2O3 layers were alternatively deposited on quartz substrates

at 150°C. The ALD cycles in the ZnO/Al2O3 supercycles are 50/1, 22/1, 20/1, 18/1, 16/1, 14/1, 12/1, and 10/1, where monocycle Al2O3 doping layers were inserted between different cycles of ZnO sublayers. Since the real GSK2118436 Al concentration matches the ‘rule of mixtures’ formula well at lower Al concentration below 5%, in which the growth rate of the AZO is close to pure ZnO [19]. The Al concentration in the AZO films was calculated using the following formula: (1) where is the percentage of Al2O3 cycles, ρ Al, and ρ Zn are the densities of Al and Zn atoms deposited during each ALD cycle for the pure Al2O3 and ZnO films, respectively. The densities of Al2O3 and ZnO growth by ALD are 2.91 and 5.62 g/cm3[20], So ρ Al and ρ Zn were Dibutyryl-cAMP clinical trial calculated to be 5.89 × 10−10 mol/cm2/cycle and 1.27 × 10−9 mol/cm2/cycle, respectively. Figure  3 shows the XRD patterns of the AZO films grown on quartz substrate with different ZnO/Al2O3 cycle ratios that are varied

from 50:1 to 10:1 (corresponding to Al concentration from 0.96% to 4.42%). The diffraction pattern of the pure ZnO film without Al2O3 doping layer is also shown as a reference. The X-ray diffraction pattern from pure ZnO film exhibits multiple crystalline ZnO structure with (100), (002), and (110) peaks [17]. With increasing the Al doping concentration, the (002) and (110) diffraction peaks decrease strongly, thus the AZO films exhibiting (100) dominated the orientation. The intensity of the (100) diffraction peak

reaches a maximum at 2.06% (with the ratio of ZnO/Al2O3 layers is 22/1), and then it decreases at Evodiamine higher Al concentration above 3%. The preferred (100) orientation of the AZO films in our samples is consistent with the results reported by Banerjee et al. [18]. It is worthy to note that the Al2O3 layer by ALD is amorphous at the growth temperature of 150°C, so the decrease of the (100) peak at higher Al concentration can be explained that the amorphous Al2O3 doping layers destroy the crystal quality during the growth of AZO films. Figure  3 also shows that the (100) peak of ZnO shifts to larger diffraction angle with increasing the concentration of Al in AZO films. This can be interpreted as that the increase of the Al concentration will reduce the lattice constant by substitutions of Zn2+ ions (ion radius 0.74 Å) with smaller Al3+ (0.53 Å) ions; buy Entinostat therefore, the (100) peak of ZnO shifts to larger diffraction angle in AZO films. Figure 3 XRD patterns of the AZO films with different Al content from 0% to 4.42%. Figure  4 plots the resistivity of AZO films as a function of Al concentration, which was measured by four-point probe technique. As the Al concentration increases from 0% to 2.26%, the resistivity initially decreases from 1.11 × 10−2 to a minimum of 2.38 × 10−3 Ω·cm, and then increases at higher Al doping concentration.

Cells were derived from a single tumor, and subsequently

Cells were derived from a single tumor, and subsequently

induced to differentiate into the epithelioid (STAV-AB) and the sarcomatoid phenotype (STAV-FCS), respectively, by altering the serum composition [30]. Hence, STAV-AB cells were grown in Gibco RPMI 1640 medium (Invitrogen) and Alvocidib concentration 10% human AB serum, whereas STAV-FCS cells were grown in the same medium and 10% fetal calf serum. The specific differentiation of these cells has been evidenced by immunoprofiling showing that STAV-AB cells express more cytokeratin, whereas STAV-FCS cells have stronger reactivity to vimentin antibodies [21] as well as by morphometry. The elongated sarcomatoid cell INCB018424 supplier morphology of the STAV-FCS cells and the more round epithelioid morphology of the STAV-AB cells have been confirmed by average length:width ratios of 3.42 in the STAV-FCS cells and 1.58 in the STAV-AB cells [31]. Jurkat cells were obtained from the American

Type Culture Collection (ATCC) and grown in RPMI 1640 medium and 20% fetal calf serum. All cells were grown at 37°C with S3I-201 solubility dmso 5% CO2 and passaged approximately twice per week. Treatment of cell cultures and inhibition of signalling enzymes To investigate the contributions of several signalling pathways, inhibitors were used against key enzymes. Cells were washed, trypsinized and re-seeded with the respective inhibitors (specified in table 1) 24 h prior to selenite treatment, except for the JNK-inhibitor, with which they were pre-incubated for 1 h. Selenite was then added to the medium and the cells Celastrol were harvested 24 or 48 h later. Titrations were performed with all inhibitors based on the manufacturers’ instructions and concentrations reported in the literature. In all cases, the highest non-toxic doses tested were accepted. Table 1 Chemical inhibitors against apoptosis signalling enzymes Inhibitor Target Concentration Purchased

from SB 203580 p38 5 μM Merck SP 600125 JNK 10 μM A.G. Scientific Pifithrin p53 10 μM A.G. Scientific Pepstatin A Cathepsin D, E 5 μM Calbiochem Ca-074 Me Cathepsin B 10 μM SERVA Electrophoresis GmbH Cell viability assays Viability assays were performed in conjunction with flow cytometry experiments to obtain internal controls. Aliquots of cell suspensions prepared for flow cytometry were plated in triplicates in 96-well plates, with a density of approx. 5000 cells per well. They were then analysed using the WST-1 assay (Roche), whereby a tetrazolium salt is cleaved by mitochondrial enzymes to yield a coloured product, to measure viability. The plates were read in a Spectramax spectrophotometer at 450 nm with subtraction of background absorbance at 600 nm. Flow cytometric analyses Flow cytometric assays for detection of apoptosis were carried out using the Annexin V kit (Caltag Laboratories) according to the manufacturer’s protocol.

All symbols defined as in Figure 1 is the

All symbols defined as in Figure 1. is the Schottky barrier height from Equation 3. Three other commonly used metals for metal-assisted etching, all of which can be deposited by galvanic displacement deposition from solution, are Au, Pt, and Pd. These are all high work function metals compared to Si. In all three cases, the bands bend upward. As discussed by Tung [14], the Schottky-Mott relationships are an approximation to the true Schottky barrier height because the presence of surface states, reconstructions, or lack of an abrupt interface can lead to lower values. This is corroborated by comparison of the experimental values on n-type Si to the calculated values

in Table 1. The values for Ag are close to the ideal value. In all other cases, interfacial chemical and structural changes reduce the barriers below the ideal values. However, the shape of the band bending is always correctly predicted by the Schottky-Mott

relations. Therefore, they can be used to characterize the qualitative shape of the bands at the interface, and deviations from ideal character will not be important for hole injection into the valence band as discussed below. It is not the Schottky barrier itself that is of interest; rather, it is band bending and the energy of the Si valance band at the interface that are important. This is because a hole must be transferred from the metal to the Selleck BKM120 Si valence band to induce etching. The Schottky-Mott analysis allows us to calculate the energy of the Si valence band maximum at the interface, which is labeled E in Figures 1 and 2. Holes naturally relax to the highest available energy in a band, whereas electrons relax to the lowest energy in the band. The definition of the Schottky barrier height is the energy required to move a charge carrier from the metal to the Si interface; however, the carrier clonidine changes from p-type to n-type Si. On p-type material, the Schottky barrier height is the energy required to move a hole from

the metal to the Si valence band at the interface. Therefore, the Schottky barrier height is the same as the energy of the Si valence band maximum at the interface. On n-type material, the Schottky barrier height is the energy required to move a hole from the Si conduction band at the interface to the metal. This value is not directly relevant to the discussion of etching. Rather, it is again the energy of the Si valence band maximum at the interface E that is required. A nonideal interface may introduce gap states between the conduction and valence bands, which affects the Schottky barrier height. However, the introduction of gap states does not change E. Therefore, any inaccuracies in the Schottky-Mott relationships will not change the direction of band bending and should not affect the conclusions of the model presented here. Figures 1 and 2 show that Ag is clearly different than all other metals.