Despite the intensity of RSE being higher than ISE [3], CHO inges

Despite the intensity of RSE being higher than ISE [3], CHO ingestion affects the metabolic response to team sport exercise, with a significant increase in glucose concentration found throughout exercise [5, 51]. The mechanisms driving this increased blood glucose concentration are largely unknown. Blood glucose concentration initially increases after ingesting CAF + CHO or PLA + CHO and it may be suppressed by endogenous glucose production [52]. The blood glucose levels gradually decreased in the PLA + CHO trial during the RSE, suggesting that intense sprint exercise increases fuel requirements in working muscles and obligates more blood glucose to muscle cells during the RSE.

By contrast, the CAF + CHO exhibited higher blood glucose levels during the RSE, partly because caffeine is crucial for maintaining blood glucose concentration by enhancing glycolytic turnover [11]. Although Z-VAD-FMK the exact mechanisms of carbohydrate ingestion on exercise

performance, especially for exercise duration less than 1 hour, are not well understood, two major explanations are commonly used to interpret the possible ergogenic effects of carbohydrate. Firstly, the general metabolic response to prolonged intermittent exercise with CHO administration is an increase in plasma glucose concentration and higher rates of glucose oxidation during the later exercise stage [9]. Secondly, the presence of carbohydrate in the mouth Ixazomib mw has been shown to stimulate the receptors in the oral cavity, thus activating specific areas

of the brain associated with reward and the regulation of motor activity [27]. CHO ingestion may increase blood glucose concentrations, however, it should be noted that the improved performance in previous studies [45] might be attributed to the glycogen-depleted state prior to the intermittent sprint exercise. In this study, we asked participants to consume a standardized meal 2 hours before exercise test to mimic the real-life situation, e.g., fed athletes before competition, in each trial. The results indicate that ingestion of PLA + CHO provided a small but significant benefit on RSE performance in female athletes. Nevertheless, Colombani et al. [53] reported that CHO administration might PLEK2 not induce performance improvements in male athletes during exercise lasting less than 70-min in postprandial state. The increases in blood glucose levels and repeated sprint performance induced by CHO ingestion may also involve the central governor. Gastric empty rate of a CHO drink could be slowed by the hypertonic drink [54] and high-intensity intermittent sprint [55]. Jeukendrup et al. [56] reported that CHO ingestion has no effects on exogenous glucose uptake and total CHO oxidation during short-term (~1 hour) high-intensity cycling exercise.

Med Sci Sports Exerc 2006, 38:1650–1658 PubMedCrossRef 9 Hoffman

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This was caused by severe scoliosis (n = 17),

This was caused by severe scoliosis (n = 17), Mitomycin C inability to lay supine because of clinical condition (n = 23), severe adiposity (n = 5), and miscellaneous reasons (n = 31). In the remaining 2,424 patients, VFA was considered reliable. Image quality was subjectively scored as “good” in 2097 (87%), “moderate”

in 294 (12%), and “poor” in 33 patients (1%), and was based on assessment of the whole image. Despite “poor” or “moderate” VFA image quality results in those patients were considered sufficiently reliable to allow analysis. The levels that were adequately visualized by VFA were from vertebra L4 up through vertebra T4 in 1,991 (82%) patients,

from L4 through T5 in 2,247 (93%), and from L4 through T6 in 2,402 (99%). In total, around 30,000 vertebral bodies were analyzed. Vertebral Fracture Assessment results VFA demonstrated a vertebral fracture in 541 (22%) of the patients. An example is presented in Fig. 1. These 541 patients together had 954 vertebral fractures, which amounts to a mean of 1.8 fractures per patient with a fracture. In 375 patients (69% of those with a fracture, or 16% of the whole cohort), these fractures were not demonstrated earlier and were unknown according to the patient. Fig. 1 Example of a VFA study result with left the image after placing marker points, upper right the Genant classification and lower a table with the percentages of deformity. In this patient, one moderate vertebral fracture was detected: wedge shaped in L1 The distribution of the fractures over the individual vertebral levels showed the well-known dual-peak distribution with a peak

at T7 (119 fractures, 13% of total) and at T12 (169 fractures, 18% of total) (Fig. 2). The severity of the fractures was “mild” in 458 (48% of all fractures), “moderate” in 295 (31%), and “severe” in 201 (21%). Vertebral fractures were wedge shaped in 79% (n = 759), biconcave in 19% (n = 178) crotamiton and “crush” in 2% (n = 17). Mild fractures were often accompanied by moderate or severe fractures, and on a per patient analysis 219 patients (9% of all patients) had mild fractures only. Fig. 2 Frequency distribution of vertebral fractures assessed with VFA As there has been controversy in the definition of mild fractures we also analyzed the data for moderate and severe fractures only, after excluding mild fractures. The prevalence of moderate or severe vertebral fractures was 322 (13%) in this cohort, 180 (56%) were unknown.

Emerg Infect Dis 2002, 8:881–890 CrossRef 5 Donlan RM, Costerton

Emerg Infect Dis 2002, 8:881–890.CrossRef 5. Donlan RM, Costerton JW: Biofilms: survival mechanisms of clinically relevant microorganisms. Clin Microbiol Rev 2002, 15:167–193.CrossRef 6. Høibya N, Bjarnsholta T, Givskovb M, Molinc S, Ciofu O: Antibiotic resistance of bacterial biofilms. Int J Antimicr Agent 2010, 35:322–332.CrossRef 7. Nusbaum AG, Kirsner RS, Charles CA: Biofilms in dermatology. Skin

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12. Singh PK, Schaefer AL, Parsek MR, Moninger TO, Welsh MJ, Greenberg EP: Quorum-sensing signals indicate that cystic fibrosis lungs are infected with bacterial biofilms. Nature 2000, 407:762–764.CrossRef 13. Wu H, Song Z, Hentzer M, Andersen JB, Molin S, Givskov M, Hoiby N: Synthetic furanones inhibit quorum-sensing and enhance

bacterial clearance in Pseudomonas aeruginosa lung infection in mice. J Antimicrob Chemother 2004, 53:1054–1061.CrossRef 14. Rogan MP, Taggart CC, Greene CM, Murphy PG, O’Neill SJ, McElvaney NG: Loss of microbicidal activity and increased formation of biofilm due to decreased lactoferrin activity in patients with cystic fibrosis. J Infect Dis 2004, 190:1245–1253.CrossRef 15. Grumezescu AM, Chifiriuc MC, Marinas I, Saviuc C, Mihaiescu D, Lazar V: Ocimum basilicum and Mentha piperita essential oils influence the antimicrobial susceptibility of Staphylococcus aureus strains. Lett Appl Nano Bio Sci 2012, 1:14–17. 16. Marinas I, Grumezescu AM, Saviuc C, Chifiriuc C, Mihaiescu D, Lazar V: Rosmarinus officinalis essential oil as antibiotic potentiator Tolmetin against Staphylococcus aureus. Biointerface Res Appl Chem 2012, 2:271–276. 17. Saviuc C, Grumezescu AM, Bleotu C, Holban A, Chifiriuc C, Balaure P, Lazar V: Phenotypical studies for raw and nanosystem embedded Eugenia carryophyllata buds essential oil effect on Pseudomonas aeruginosa and Staphylococcus aureus strains. Biointerface Res Appl Chem 2011, 1:111. 18. Coimbra M, Isacchi B, van Bloois L, Torano JS, Ket A, Wu X, Broere F, Metselaar JM, Rijcken CJF, Storm G, Bilia R, Schiffelers RM: Improving solubility and chemical stability of natural compounds for medicinal use by incorporation into liposomes. Int J Pharm 2011, 416:433–442.CrossRef 19.

Based on the work of Ghani & Soothill [15] and Sriramulu et al [

Based on the work of Ghani & Soothill [15] and Sriramulu et al. [16], we utilized 0.5% mucin (1X) in our ASM+. But more recently, Henke et al. [36], showed that the concentrations of MUC5AC and MUC5B, the principal gel-forming mucins, are decreased in airway

secretions from CF patients with stable disease and greatly increased during pulmonary exacerbations (by 89% and 908%, respectively). When we reduced the mucin concentration of ASM+ by 50% (0.5X), the gelatinous mass still formed in the well, possibly through the contribution of other ASM+ components (DNA and lecithin) that add to the viscosity. However, the typical multilayered BLS was eliminated and replaced with a structure that appears Fludarabine in vitro to consist of small microcolonies amid individual cells and tiny cell clusters distributed throughout most of the gelatinous mass (Figure 4A, B). Surprisingly, the effect of increasing the concentration of mucin to 2X on the development of BLS was similar to that induced by reducing the mucin concentration. Rather than the distinct highly structured BLS architecture, PAO1 produced small microcolonies distributed throughout the ASM+ (Figure 4C). At this time, we do not know if the increase in the availability of mucin glycoprotein interferes with the development of microcolonies that coalesce to form the well-developed BLS. One of the hallmarks of the CF syndrome Selumetinib is the

overproduction of mucin within the lung alveoli [1, 3, 7]. Yet during P. aeruginosa infection of the CF lung alveoli, the level of mucin may vary [36].

P. aeruginosa LPS induces the production of reactive oxygen intermediates, which cause release of transforming growth factor α; TGF-α then up-regulates the expression of MUC-5 AC thereby causing excessive mucin production [37–39]. However, P. aeruginosa produces other factors that may reduce the amount of mucus within its immediate vicinity; alveolar mucin is degraded by P. aeruginosa extracellular serine proteases such as LasB [40]. Ultimately, the interaction of all these factors would produce a net mucin concentration suitable for the full development of the BLS, while any imbalance in the production of Sodium butyrate these factors that reduces or increases mucin concentration would prevent the establishment of the BLS. Alternatively, BLS may form in the initial stages of P. aeruginosa infection in the CF lung. Treatment that reduces the amount of mucin present would disperse the bacteria making them more susceptible to antibacterial treatment (stable disease). Alternatively, mucin may reduce the chances of forming new BLS. Extracellular DNA is another contributor to the viscosity of CF sputum [15, 16]. Within the CF lung, there are several sources for this extracellular DNA – dead host immune cells, lysed bacteria, QS-regulated release of P. aeruginosa DNA, and outer membrane vesicles that contain DNA [41, 42].

100 μL of samples of either serum or a standard solution or quali

100 μL of samples of either serum or a standard solution or quality control sample, were added to 200 μL of a solution of ethanol containing tocopheryl acetate (4 μM) that was used as an internal standard. After stirring the mixture for 30 seconds, the vitamins were extracted with 1000 μL of hexane (2 min of stirring). The organic phase was evaporated under nitrogen and the residues dissolved in 200 Quizartinib order μL of methanol and 50 μL were injected into the chromatograph. All procedures were performed in a room with glass windows that prevented penetration of direct sunlight. GSTM1, GSTP1, GSTT1 and hOGG1 genotyping analysis DNA was extracted

by the phenol-chloroform method using an aliquot out of the 20 ml venous blood samples of the subjects. Determination of GSTM1, GSTP1 and GSTT1 polymorphisms in the 60 subjects was performed as previously described [17]. Analysis of Selleck I BET 762 deletion polymorphism in GSTM1 and GSTT1 was performed by multiplex PCR and that of single nucleotide polymorphism in GSTP1 by a PCR-RFLP method as previously described [20]. In addition to these polymorphisms, subjects were also genotyped for the presence of either the serine or cysteine codon at position 326 (rs 1052133) of the hOGG1 gene by PCR-RFLP, using primers and conditions as previously described [21].

Briefly, the PCR amplification of the 293 bp fragment consisted of a 15-min denaturation at 95°C followed by 30 cycles of 95°C for 1 min, 50°C for 1 min and 72°C for 1 min. A final extension step of 72°C for 10 min was included. We used a simple RFLP method to identify the Ser 326 Cys by virtue of an Fnu 4HI restriction site. The hOGG1 PCR product was digested with Fnu 4HI overnight at 37°C. Recovery of two digested fragments (123/124bp

and 169/170bp) indicated presence of the Cys 326 allele, while an undigested amplicon indicated the Ser 326 allele. Statistical analysis All statistics and graphics have been performed with the SAS System release 9 (SAS Institute Inc., Cary, NC, USA). Distributions of 8-oxodG were normalised Ureohydrolase by logarithmic transformations. Mean values were compared by Student’s t-test or ANOVA and correlations between 8-oxodG and antioxidants were evaluated by Pearson correlation test. All statistical analyses were two-sided. Results Blood levels of 8-oxodG and vitamins A and E The mean serum concentrations of vitamin A were 2.77 μM and 2.74 μM, while those for vitamin E were 34.77 μM and 38.73 μM, in patients and controls respectively (Table 2). Table 2 Biochemical parameters of the study group Parameter Patients (mean ± s.d.) Controls (mean ± s.d.) P-value b patient vs. control 8-oxodG/10 6 2′dG c 7.2 ± 2.6 (n = 17) 4.9 ± 1.9 (n = 43) P < 0.001 Vitamin A (μM) 2.77 ± 0.94 (n = 15)a 2.74 ± 0.61 (n = 42)a P = 0.895 Vitamin E (μM) 34.77 ± 12.27 (n = 15)a 38.73 ± 9.47 (n = 42)a P = 0.204 PBMCs were collected and processed for measuring 8-oxodG. Vitamins were extracted from the serum samples for estimation.

coli strains only focused

on the identification of colici

coli strains only focused

on the identification of colicin production [30, 32]. While Šmarda and Obdržálek (2001) used five different indicator strains to detect colicin production in the fecal E. coli strain 1043 [32], Achtman et al. (1983) used 2 indicator strains for the detection of colicin producers in a sample of 234 fecal E. coli strains [30]. More recently, Gordon and O’Brien (2006) used PCR with 19 bacteriocin genes to screen 266 fecal E. coli strains (38% of which were bacteriocinogenic) [26], and Šmajs et al. (2010) detected 29 bacteriocin types in 411 fecal E. coli strains (55% of which were bacteriocin-encoding Akt inhibitor strains) [21]. Our results have revealed that the frequency of bacteriocinogeny in E. coli strains positively correlates with the detected number of virulence determinants. Bacteriocinogeny increased by as much as 75–80% depending on the number of encoded virulence factors. To our knowledge, this is the first time that the correlation between bacteriocinogeny frequency and the number of encoded virulence factors has been shown. This finding suggests that at least some bacteriocin-encoding genes should

be considered as factors which increase the virulence of E. coli strains. E. coli strains encoding only fimbriae type PCI-32765 price I did not show differences in the frequency of bacteriocinogeny compared to strains without genes for virulence factors. The role of fimbriae type I in development of human infections is not clear. Although deletion of the fim gene cluster from virulent E. coli strain O1:K1:H7 attenuated virulence in the urinary tract infection (UTI) model [33]; possession of fimbriae type 1 in E. coli strains from different sources was not found to correlate with the ability to cause UTIs [34–39]. Several virulence factors, typical for diarrhea-associated E. coli strains, including

pCVD432 (EAggEC), ial/ipaH (EIEC), eaeA/bfpA (EPEC) and afaI (DAEC) were not found to be associated with bacteriocin genes. Bacteriocin Epothilone B (EPO906, Patupilone) producers therefore appear to be mainly associated with ExPEC virulence factors (E. coli strains containing combinations of sfa, pap, aer, iucC, cnf1, α-hly determinants). The occurrence of these virulence factors were associated with both chromosomally (microcins H47 and M) and plasmid encoded colicin (E1, Ia and S4) and microcin types (B17, V). Presently, several bacteriocins including colicin E1, and microcins H47, I47, E492, M, and V are considered virulence factors in extraintestinal pathogenic E. coli strains [20–23]. Azpiroz et al.[20] and Budič et al.[22] found an association between production of microcins H47, I47, E492, M, and V and the distribution of virulence factors (i.e. hlyA, cnf1, usp, iroN, iroCD, fyuA, papC, papG and tcpC) in uropathogenic strains of E. coli; from these results they assumed that production of these bacteriocin types could contribute to development of bacteraemia.

Conclusions Interleukin-10 expression in tumor-associated macroph

Conclusions Interleukin-10 expression in tumor-associated macrophages correlates with disease aggressiveness of non-small cell lung cancer. We plan to conduct further studies to analyze the relationship between IL-10 in TAM and survival. The study concerning regulation of IL-10 in TAM is ongoing too. It will help to clarify and understand the possible mechanisms IL-10 secreted by TAM in the progression of NSCLC. Acknowledgements This work is supported,

in part, by National Natural Science Foundation of China (30800404), Shanghai Rising-Star Program (09QA1401200), Pujiang Talent Grant, (to J. Z), Young Investigator Grant from Shanghai Municipal Health Bureau.and Basic-clinical medicine grant (to H-Q C). We thank Shannon Wyszomierski for her editorial assistance. References 1. Pollard JW: Tumour-educated macrophages promote tumour progression and metastasis. Nat Rev Cancer 2004,4(1):71–78.PubMedCrossRef 2. Balkwill F, Mantovani find more A: Inflammation and cancer: back to Virchow?

Lancet 2001,357(9255):539–545.PubMedCrossRef 3. Joyce JA, Pollard JW: Microenvironmental regulation SRT1720 datasheet of metastasis. Nat Rev Cancer 2009,9(4):239–252.PubMedCrossRef 4. Ohno S, Ohno Y, Suzuki N, Kamei T, Koike K, Inagawa H, Kohchi C, Soma G, Inoue M: Correlation of histological localization of tumor-associated macrophages with clinicopathological features in endometrial cancer. Anticancer Res 2004,24(5C):3335–3342.PubMed 5. Takanami I, Takeuchi K, Kodaira S: Tumor-associated macrophage infiltration in pulmonary adenocarcinoma: association with angiogenesis and poor prognosis. Oncology 1999,57(2):138–142.PubMedCrossRef

6. Leek RD, Lewis CE, Whitehouse R, Greenall M, Clarke J, Harris AL: Association of macrophage infiltration with angiogenesis and prognosis in invasive breast carcinoma. Cancer Res 1996,56(20):4625–4629.PubMed 7. Lissbrant IF, Stattin P, Wikstrom P, Damber JE, Egevad L, Bergh A: Tumor associated macrophages in human prostate cancer: relation to clinicopathological variables and survival. Int J Oncol 2000,17(3):445–451.PubMed 8. Hanada T, Nakagawa M, Emoto A, Nomura T, Nasu N, Nomura Y: Prognostic value of tumor-associated macrophage Vitamin B12 count in human bladder cancer. Int J Urol 2000,7(7):263–269.PubMedCrossRef 9. Chen JJ, Lin YC, Yao PL, Yuan A, Chen HY, Shun CT, Tsai MF, Chen CH, Yang PC: Tumor-associated macrophages: the double-edged sword in cancer progression. J Clin Oncol 2005,23(5):953–964.PubMedCrossRef 10. Gocheva V, Wang HW, Gadea BB, Shree T, Hunter KE, Garfall AL, Berman T, Joyce JA: IL-4 induces cathepsin protease activity in tumor-associated macrophages to promote cancer growth and invasion. Genes Dev 2010,24(3):241–255.PubMedCrossRef 11. Lindahl C, Simonsson M, Bergh A, Thysell E, Antti H, Sund M, Wikstrom P: Increased levels of macrophage-secreted cathepsin S during prostate cancer progression in TRAMP mice and patients. Cancer Genomics Proteomics 2009,6(3):149–159.PubMed 12.

Black circles = GT group; White circles

Black circles = GT group; White circles mTOR inhibitor = PL group. Figure 3 Percent change scores from pre- to post-training for each individual

participant for (A) critical velocity, (B) anaerobic running capacity, (C) aerobic capacity, (D) percent body fat, (E) fat mass and (F) lean body mass. Black circles = GT group; White circles = PL group. A type I error rate that was less than or equal to 5% was considered statistically significant for all analyses. ANOVA models and t-tests were computed using SPSS (Version 14.0, SPSS Inc., Chicago, Ill), and the 95% confidence intervals and individual response graphs were calculated and created in Microsoft Excel (Version 2007, Microsoft Corporation; The Microsoft Network, LLC, Richmond, WA). Results Table 3 contains the means and standard errors for each of the dependent variables (CV, ARC, VO2max, %BF, FM, and LBM). In addition, there were no significant differences (p > 0.05) between the GT and PL groups at the pre-training testing session. Table 3 Mean ± SE values from pre- to post-training for critical velocity (CV), anaerobic running capacity (ARC), maximal oxygen consumption (VO2max), percent body fat (%BF), fat mass (FM) and lean body mass (LBM) for GT and PL.   CV (km/hr) ARC (km) VO2max (l·min-1) VO2max (ml·kg·min)   Pre Post Pre Post Pre Post Pre Post GT (n = 13) Autophagy Compound Library mouse 12.4 ± 0.8 12.8

± 0.8 0.2 ± 0.01 0.2 ± 0.02 3.1 ± 0.3 3.65 ± 0.2* 47.9 ± 3.4 56.2 ± 2.7* PL (n = 11) 10.7 ± 0.5 10.9 ± 0.6 0.2 ± 0.03 0.3 ± 0.04 3.1 ± 0.2 3.2 ± 0.3* 56.5 ± 2.1 45.3 ± 2.3*   %BF FM (kg) LBM (kg)       Pre Post Pre Post Pre Post     GT (n = 13) 18.9 ± 2.5 17.7

± 2.1 12.7 ± 1.9 12.0 ± 1.7 54.2 ± 3.5 55.4 ± 3.7     PL (n = 11) 19.1 ± 1.8 17.1 ± 1.9 12.4 ± 1.1 10.6 ± 1.1 53 ± 2.7 52.4 ± 3.2     *indicates a significant difference over time (p < 0.05). ANOVA Models For CV, there was no time × group interaction (p = 0.256) and no main effect for time (p = 0.507), but there was a main effect for group (p = 0.036). Prostatic acid phosphatase CV for the GT group was greater than the PL group at the pre- and post-training testing sessions. For ARC, there was no time × group interaction (p = 0.183) and no main effects for time (p = 0.093) or group (p = 0.053). For VO2max, there was no time × group interaction (p = 0.391) and no main effect for group (p = 0.258), but there was a main effect for time (p = 0.028). VO2max increased from pre- to post-training for the GT and PL groups. For %BF, there was no time × group interaction (p = 0.481) and no main effects for time (p = 0.178) or group (p = 0.864). For FM, there was no time × group interaction (p = 0.335) and no main effects for time (p = 0.305) or group (p = 0.583). For LBM, there was no time × group interaction (p = 0.386) and no main effects for time (p = 0.694) or group (p = 0.615).

Results and discussion Before the fabrication of metal/n-GaN cont

Results and discussion Before the fabrication of metal/n-GaN contacts, structural and morphological characterizations

of epitaxial layers have been see more done. The X-ray diffraction pattern of the GaN epitaxial layer using Cu-Kα radiation is shown below in Figure 2a. The X-ray diffraction pattern was taken in bulk mode. The orientation of the epitaxial layer was observed to be along the (002) which confirms the growth of the epitaxial layer along the [0001] direction having a hexagonal (wurtzite) crystal structure. Additional diffraction peaks from (102), (004), and (203) reflection planes of hexagonal GaN were also observed. The sharp diffraction peaks (FWHM value 432 arc sec for (002)) reveal the reasonably good crystalline quality of the GaN epitaxial layer [13]. The lattice constants ‘a’ and ‘c’ were found to be 0.320 and 0.518 nm, respectively, which matched well with the standard cell parameter values as given in JCPDS card 02–1078. GaN epitaxial layers were also examined under an atomic force

microscope (AFM) in the contact mode to measure the topography of the surface. Figure 2b shows the AFM images in a 2D view for the pristine samples. The surface area scanned was 10 × 10 μm2. The RMS roughness of the surfaces is around 1 nm for all samples. The result of the AFM measurement shows an overall smooth GaN surfaces. These samples have an average dislocation density value of about 5 × 108 cm-2, which is acceptable for GaN epilayers but poor as compared to Si and GaAs epilayers. VX-770 Figure 2 X-ray diffraction spectrum (a) and AFM image (b) of the GaN epitaxial layer. The asterisk ‘*’ indicates peaks from sapphire substrate. Electrical characterization of Schottky barrier devices was carried out in the temperature

range of 100 to Thymidine kinase 340 K measured at a temperature interval of 40 K. Figure 3 shows the experimental semilog forward and reverse bias I-V characteristics of the Pt/n-GaN Schottky barrier diodes (SBD). It should be mentioned here that for analysis, we have used diodes with 384-μm diameter and have almost identical electrical properties. The characteristics shown here demonstrate an average trend which was determined for a group of diodes. The current–voltage characteristics of SBD are given by the thermionic emission theory [14, 15]. For bias voltage V ≥ 3kT/q, the conventional diode equation is (1) (2) Figure 3 Semilog forward and reverse I-V characteristics for Pt/n-GaN Schottky diode at 100 to 340 K. Here, A** is the effective Richardson constant, ϕ ap is the apparent or measured barrier height, n is the ideality parameter, A is the diode area, and the other symbols have their usual meanings. Since image force is a very weak function of applied voltage, it could also be neglected [14–18].