Stat Appl Genet Mol Biol 2004,3(1):Article 3 23 Smyth GK, Speed

Stat Appl Genet Mol Biol 2004,3(1):Article 3. 23. Smyth GK, Speed T:

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To date TAAs matching almost all of these criteria are the human

To date TAAs matching almost all of these criteria are the human papillomavirus (HPV) E6 and E7 proteins. The association of HPV with HNSCC and the utilisation of viral oncoprotein for immunotherapy has been reviewed elsewhere [6]. Briefly HPV is associated with approximately 20–25% of all HNSCC and up to 60–70% of those tumours localized to the oropharynx,

in Vorinostat in vivo particular tonsil [7]; the HPV type 16 has been found in more than 90% of HPV-positive HNSCC; the E6 and E7 proteins are constitutively expressed and maintained during the HPV-associated carcinogenesis; and the viral oncoproteins are foreign antigens and, therefore, are highly immunogenic. Beside the matching to an ideal TAA the HPV E6 and E7 proteins serve as model antigens for the development of immunotherapy and since HPV type 16 is also associated with cervical and anogenital cancers, the AP26113 clinical trial same vaccine strategies developed to prevent (already in clinical use) and/or to treat HPV-associated cervical and anogenital cancers can also be used in head and neck cancers [for review see [6, 8]]. Nevertheless these BMN 673 nmr oncoproteins account for only 20%

of HNSCC and enforces must be done to identify other TAAs in the remaining HNSCC matching closely all the above mentioned criteria. In this filed an enormous work has been done but before some of these TAAs becomes valid therapeutic vaccine other hurdles must be overcome, the tumour immune escape and tumour tolerance. Tumour immune escape and tolerance The discovery of so powerful TAAs in HNSCC is giving substantial basis 4-Aminobutyrate aminotransferase for efficacious and less toxic treatments, but in the mean time HNSCC as other tumours participates in tumour immune escape through various mechanisms: i) it disrupts antigen processing and presentation machinery by altering the MHC class I and TAP 1–2 expression;   ii) it recruits immunosuppressive Treg to dampen effector T-cell activity,   iii) by chemokine production it alters T-cell homeostasis

increasing the sensitivity of effector T cells to apoptosis.   Downregulation of antigen-processing machinery (APM) components, such as TAP 1/2 and MHC class I antigens, renders ineffective the recognition by CTL in HNSCC. More than 50% of primary and metastatic lesions showed MHC class I antigen loss [9]. Interestingly, interferon-γ (IFN-γ), which functions to up-regulate APM and MHC molecules, can restore in vitro the ability of specific CTLs to recognize their tumour cell targets and subsequently to lyse them [10, 11]. Thus in a therapeutic setting clinical efforts must be undertaken in order to restore APM and MHC class I antigen expression in HNSCC. The complex biology of CD4+CD25+FoxP3+ regulatory T cells (Treg), which function to downmodulate immune responses and have enormous implications on the development of cancer immunotherapies, is far to be fully understood.

N Engl J Med 2005, 353: 2012–2024 CrossRefPubMed 16 Barber TD, V

N Engl J Med 2005, 353: 2012–2024.CrossRefPubMed 16. Barber TD, Vogelstein B, Kinzler KW: Somatic,Hydrochloride-Salt.html mutations of EGFR in

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in advanced cervical cancer correlated with tumor progression and poor outcome after radiotherapy. Int J Oncol 2001, 18: 493–497.PubMed 22. Endoh H, Yatabe Y, Kosaka T: PTEN and PIK3CA expression is associated with prolonged survival after gefitinib treatment Selleck Ruboxistaurin in EGFR-mutated lung cancer patients. J Thorac Oncol 2006, 1: 629–634.CrossRefPubMed 23. Baselga J, Arteaga CL: Critical update and emerging trends in epidermal growth factor receptor targeting in cancer. J Clin Oncol 2005, 23: 2445–2259.CrossRefPubMed Alanine-glyoxylate transaminase 24. Russell Sambrook: olecular Cloning. Third edition. America: CSHL Press;

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Mullen JO, Mullen NL (1992) Hip fracture mortality A prospective

Mullen JO, Mullen NL (1992) Hip fracture mortality. A prospective, multifactorial study to predict and minimize death risk. Clin Orthop Relat Res 280:214–22PubMed 30. Nightingale S, Holmes J, Mason J, House A (2001) Psychiatric illness and mortality

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“Introduction A history of non-vertebral fracture (NVF) is associated with a doubling of the risk of a subsequent fracture, and the subsequent fracture risk is quadrupled after a vertebral fracture [1, 2]. This subsequent fracture risk is not constant over time and is driven by the high, three to fivefold increase in the years immediately after a first fracture, followed by a gradual waning off later on [3]. This has been shown for

repeat morphometric vertebral fractures [4], subsequent clinical spine, forearm and hip fractures in patients who were hospitalised with a vertebral fracture [5], repeat low-trauma fractures in subjects older than 60 years [6], repeat clinical vertebral and non-vertebral fractures from menopause onwards [3, 7, 8] and repeat hip fractures [9]. As a result, it has been shown in long-term follow-up studies that 40% isometheptene to 50% of HDAC inhibitors list all subsequent fractures occur within 3 to 5 years after a first fracture. The clinical implication is that patients older than 50 years presenting with a fracture need immediate attention to reduce reversible risk factors of a subsequent fracture. This indicates that to undertake immediate care in fracture patients is necessary, such as the Fracture Liaison Service, the involvement of a fracture nurse and other initiatives in the field of post-fracture

care [10–13]. It also indicates that treatment, which has been shown to reduce fracture risk within short term, should be started as soon as possible in patients with a high fracture risk [14]. An increased risk of Akt inhibitors in clinical trials mortality has been documented after hip, vertebral and several non-hip, non-vertebral fractures [15]. Similar to subsequent fracture risk, this increase in mortality is higher immediately after fracture than later on. In women and men older than 60 years, nearly 90% of excess deaths related to fracture over the 18 years of observation occurred in the first 5 years. Of the 5-year post-fracture excess mortality, approximately one third of deaths were associated to hip, vertebral and non-hip, non-vertebral fractures, respectively. The major causes of death were related to cardiovascular and respiratory comorbidity and infections [15].

Mol Cell Biol 2008, 28:397–409 PubMedCrossRef 6 Sharma GG, So S,

Mol Cell Biol 2008, 28:397–409.PubMedCrossRef 6. Sharma GG, So S, Gupta A, Kumar R, Cayrou C, Avvakumov N, Bhadra U, Pandita RK, Porteus MH, Chen DJ, Cote J, Pandita TK: MOF and histone H4 acetylation at lysine

16 are critical for DNA damage response and double-strand break repair. Mol Cell Biol 2010, 30:3582–3595.PubMedCrossRef 7. Rea S, Xouri G, Akhtar A: Males absent on the first (MOF): from flies to humans. Oncogene 2007, 26:5385–5394.PubMedCrossRef 8. Smith ER, Cayrou C, Huang R, Lane WS, Côtê J, Lucchesi BAY 73-4506 JC: A human protein complex homologus to the Drosophila MSL complex is responsible for the majority of histone H4 acetylation at lysine 16. Mol Cell Biol 2005, 25:9175–9188.PubMedCrossRef 9. Mendjan S, Taipale M, Kind J, this website Holz H, Gebhardt P, Schelder M, Vermeulen M, Buscaino A, Duncan K, Mueller J, Wilm M, Stunnenberg HG, Saumweber H, Akhtar A: Nuclear pore components are involved in the transcriptional regulation of dosage compensation in Drosophila. Mol Cell 2006, 21:811–823.PubMedCrossRef 10. Cai Y, Jin J, Swanson SK, Cole MD, Choi SH, Florens L, Washburn MP, Conaway JW, Conaway RC: Subunit composition and substrate specificity of a MOF-containing histone acetyltransferase distinct from the male-specific lethal (MSL) complex. J Biol Chem 2010, 285:4268–4272.PubMedCrossRef 11. Sykes SM, Mellert HS, Holbert MA,

Li K, Marmorstein R, Lane WS, McMahon SB: Acetylation of the p53 DNA-binding domain regulates apoptosis induction. Mol Cell 2006, 24:841–851.PubMedCrossRef 12. Taiple M, Rea S, Richter K, Vilar A, Lichter P, Imhof A, Akhtar A: hMOF histone acetyltransferase is required for histone H4 lysine 16 acetylation in mammalian cells. Mol Cell Epothilone B (EPO906, Patupilone) Biol 2005, 25:6798–6810.CrossRef 13. Mulligan

P, Yang F, Di Stefano L, Ji JY, Ouyang J, Nishikawa JL, Toiber D, Kulkarni M, Wang Q, Najafi-Shoushtari SH, Mostoslavsky R, Gygi SP, Gill G, Dyson NJ, Näär AM: A SIRT-LSD1 check details Co-repressor complex regulates notch target gene expression and development. Mol Cell 2011, 42:689–699.PubMedCrossRef 14. Orpinell M, Fournier M, Riss A, Nagy Z, Krebs AR, Frontini M, Tora L: The ATAC acetyl transferase complex controls mitotic progression by targeting non-histone substrates. EMBO J 2010, 29:2381–2394.PubMedCrossRef 15. Pfister S, Rea S, Taipale M, Mendrzyk F, Straub B, Ittrich C, Thuerigen O, Sinn HP, Akhtar A, Lichter P: The histone acetyltransferase hMOF is frequently downregulated in primary breast carcinoma and medulloblastoma and constitutes a biomarker for clinical outcome in medulloblastoma. Int J Cancer 2008, 122:1207–1213.PubMedCrossRef 16. Elsheikh S, Green AR, Rakha EA, Powe DG, Ahmed RA, Collins HM, Soria D, Garibaldi JM, Paish CE, Ammar AA, Grainge MJ, Ball GR, Abdelghany MK, Martinez-Pomares L, Heery DM, Ellis IO: Globle histone modifications in breast cancer correlate with tumor phenotypes, prognostic factors, and patient outcome.

294 SERP2428 arsA arsenical pump-driving ATPase 3 274 Protein syn

294 SERP2428 arsA arsenical pump-driving ATPase 3.274 Protein synthesis PI3K Inhibitor Library cell assay SERP0721 pheS Phe-tRNA synthetase alpha chain 2.036 SERP1809 infA translation initiation factor IF-1 0.5 SERP1812 rplO ribosomal protein L15 0.482 SERP1813 rpmD ribosomal protein L30 0.333 SERP1814 rpsE 30 S ribosomal protein S5 0.37 SERP1815 rplR 50 S ribosomal protein L18 0.323 SERP1816 rplF 50 S ribosomal protein L6 0.332 SERP1817 rpsH 30 S ribosomal protein S8

0.357 SERP1818 rpsN-2 30 S ribosomal protein S14 0.306 SERP1819 rplE 50 S ribosomal protein L5 0.324 SERP1821 rplN 50 S ribosomal protein L14 0.346 SERP1820 rplX 50 S ribosomal protein L24 0.356 SERP1822 rpsQ 30 S ribosomal protein S17 0.344 SERP1823 rpmC 50 S ribosomal protein L29 0.332 SERP1824 rplP 50 S ribosomal protein L16 0.438 SERP1825 rpsC 30 S ribosomal protein S3 0.345 SERP1826 rplV 50 S ribosomal protein L22 0.374 SERP1827 rpsS 30 S ribosomal protein S19 0.385 SERP1828 rplB 50 S ribosomal click here protein L2 0.421 SERP1829 rplW 50 S ribosomal protein L23 0.424 Nucleotide metabolism SERP0070 guaA bifunctional GMP synthase/glutamine amidotransferase protein 2.546 SERP0651 purC phosphoribosylaminoimidazole-succinocarboxamide

synthase 2.036 SERP0654 purL phosphoribosylformylglycinamidine synthetase 2.341 SERP0655 purF phosphoribosylpyrophosphate amidotransferase 2.164 SERP0656 purM phosphoribosylformylglycinamidine cyclo-ligase 2.369 SERP0657 purN IMP cyclohydrolase 2.111 SERP1003

thyA-1 thymidylate synthase 2.014 SERP1810 adk adenylate kinase 0.444 Energy metabolism SE0102-12228   carbamate kinase, putative 0.259 SE0104-12228   transcription regulator Crp/Fnr family protein 0.343 SE0106-12228 arcA arginine deiminase 0.301 SERP0672 cydA cytochrome d ubiquinol oxidase subunit II-like protein 13.85 SERP1985 narJ nitrate reductase delta Vildagliptin chain 0.441 SERP1986 narH nitrate reductase beta chain 0.327 SERP1987 narG nitrate reductase alpha chain 0.324 SERP1990 nirB nitrite reductase nitrite reductase 0.354 SERP2168 mqo-2 malate:quinone oxidoreductase 0.317 SERP2169   hypothetical protein 0.0165 SERP2261 manA-2 mannose-6-phosphate isomerase 0.479 SERP2312 mqo-3 malate:quinone oxidoreductase 0.451 SERP2352 arcC putative carbamate kinase 0.427 DNA replication, recombination and repair SERP0558   ISSep1-like transposase 4.66 SERP0599   site-specific recombinase, resolvase family 2.352 SERP0892   IS1272, transposase 2.774 SERP0909 lexA SOS regulatory LexA protein 2.227 SERP1023   DNA replication protein DnaD, putative 2.049 SERP2474 hsdR type I restriction-modification system, R subunit 46.79 Transcriptional regulator SERP0635   transcriptional regulator, MarR family 3.216 SERP1879   transcriptional regulator, AraC family 21.2 * The entire list of differentially expressed genes can be found on the National Center for Biotechnology Information Gene Expression Omnibus (GEO, available at http://​www.​ncbi.​nlm.​nih.

aureus has been demonstrated in a number of infection models such

aureus has been demonstrated in a number of infection models such as mastitis [23] and pneumonia [24]. It has also been proposed that α-haemolysin may play a role in colonisation of epithelia by attenuating bacterial clearance from the epithelial surface [25]; this could therefore be of relevance see more to the decontamination of nasal epithelia using PDT. In addition,

α-haemolysin has immunomodulatory properties, notably its ability to trigger the release of pro-inflammatory cytokines such as interleukin-1β [26]; thus inactivation of α-haemolysin by PDT may also protect against harmful inflammatory processes as well as eliminating infecting organisms. The treatment of S. aureus sphingomyelinase with laser light and methylene blue resulted in a significant, dose-dependent reduction in the

enzyme’s activity. Laser light alone also appeared to reduce the activity of sphingomyelinase; however this was found to be not statistically significant. Irradiation of sphingomyelinase with 1.93 J/cm2 laser light in the presence of the highest concentration of methylene blue tested (20 μM) achieved a highly significant reduction in the activity of the enzyme (76%), which was comparable to CH5424802 mouse the reduction in activity observed for the V8 protease when irradiated for the same time period. This reduction in activity was increased to 92% after irradiation of the enzyme for 5 minutes in the presence of 20 μM methylene blue. Production of sphingomyelinase (β-haemolysin) is thought to be of importance in severe, chronic skin infections, and strains of S. aureus producing high levels of this enzyme have been shown to cause more intense skin lesions than low-producing strains [27]. Inactivation of these toxins may therefore

be of notable relevance to the treatment of superficial staphylococcal skin infections. Sphingomyelinase has recently been shown to kill BIRB 796 mouse proliferating T lymphocytes, suggesting a role for this toxin in evasion of the host immune response [28]; hence inactivation of sphingomyelinase by PDT could also reduce the immunomodulatory properties of S. aureus. The photodynamic inactivation of α-haemolysin and sphingomyelinase was shown to be unaffected by the presence of human serum at concentrations resembling the protein content of an acute wound[29], indicating that photodynamic Ureohydrolase therapy may be effective in inactivating these virulence factors in vivo. Together with the data showing that PDT using methylene blue and 665 nm laser light is effective against a methicillin-resistant strain of S. aureus, this supports the potential of PDT as a treatment for superficial staphylococcal infections. The precise mechanism of inhibition of these virulence factors has not yet been determined; however it is possible that the reactive oxygen species formed during photosensitisation can oxidise proteins, thereby disrupting their function [13].

Nanotechnology 2007, 18:435504 CrossRef 10

Gordymova TA,

Nanotechnology 2007, 18:435504.CrossRef 10.

Gordymova TA, Davydov AA, Efremov AA: Ammonia and propylene complex formation on antimony oxide. React Kinet Catal Lett 1983, 22:143–146.CrossRef 11. Wang R, Zhang D, Sun W, Han Z, Liu C: A novel aluminum-doped carbon nanotubes sensor for carbon monoxide. J Mol Struct (THEOCHEM) 2007, 806:93–97.CrossRef 12. Omaye ST: Metabolic modulation of carbon monoxide toxicity. Toxicology 2002, 180:139–150.CrossRef 13. SB525334 ic50 Roberts GP, Youn H, Kerby RL: CO-sensing mechanisms. Microbiol Mol Biol Rev 2004, 68:453–473.CrossRef 14. Dong KY, learn more Ham DJ, Kang BH, Lee K, Choi J, Lee JW, Choi HH, Ju BK: Effect of plasma treatment on the gas sensor with single-walled carbon nanotube paste. Talanta 2012, 89:33–37.CrossRef 15. Kong J, Franklin NR, Zhou C, Chapline MG, Peng S, Cho K, Dai H: Nanotube molecular wires as chemical sensors. Science 2000, 287:622–625.CrossRef 16. Zhao K, Buldum A, Han J, Lu P: Gas molecule adsorption in carbon nanotubes and nanotube bundles. Nanotechnology 2002, 13:195–200.CrossRef 17. Poulin P, Vigolo B, Launois P: Films and fibers of oriented single wall nanotubes. Carbon 2002, 40:1741–1749.CrossRef 18. O’Connell MJ, Bachilo SM, Hoffman XB, Moore VC, Strano MS, Haroz

EH, Rialon KL, Boul PJ, Noon WH, Kittrell C, Ma J, Hauge RH, Weisman RB, Smalley RE: Band gap fluorescence from individual single-walled carbon nanotubes. Science 2002, 297:593–596.CrossRef 19. Kauffman DR, Star A: Carbon selleck chemicals llc nanotube gas and vapor sensors. Angew Chem Int Ed 2008, 48:6550–6570.CrossRef Megestrol Acetate 20. Wanna Y, Srisukhumbowornchai N, Tuantranont A, Wisitsoraat A, Thavarungkul N, Singjai P: The effect of carbon nanotube dispersion on CO gas sensing characteristics of polyaniline gas sensor.

J Nanosci Nanotechnol 2006, 6:3893–3896.CrossRef 21. Esumi K, Ishigami M, Nakajima A, Sawada K, Honda H: Chemical treatment of carbon nanotubes. Carbon 1996, 34:279–281.CrossRef 22. Hamon MA, Chen J, Hu H, Chen Y, Itkis ME, Rao AM, Eklund PC, Haddon RC: Dissolution of single-walled carbon nanotubes. Adv Mater 1999, 11:834–840.CrossRef Competing interest The authors declare that they have no competing interests. Authors’ contributions The work presented here was carried out in collaboration among all authors. KYD, HHC, and BKJ defined the research theme. KYD, JC, and YDL designed the methods and experiments, carried out the laboratory experiments, analyzed the data, interpreted the results, and wrote the paper. BHK and YYY worked on the associated data collection and their interpretation, and wrote the paper. KYD, HHC and BKJ designed the experiments, discussed the analyses, and wrote the paper. All authors read and approved the final manuscript.”
“Background Quantum dot-sensitized solar cells (QDSSCs) have attracted increasing attention due to their relatively low cost and potentials to construct high-efficiency energy conversion systems [1].

Figure 1 also shows that the coated mesh has the rough surface S

Figure 1 also shows that the coated mesh has the rough surface. Such hierarchical micro/nanostructure ZnO nanorods array can trap enough air in between substrate surface and water droplet. Therefore, the coated mesh is expected Roscovitine cell line to show superhydrophobicity. The wettability of the as-grown sample was evaluated via the water contact angle (WCA). Figure 3a presents that the WCA on the as-grown sample is about 157 ± 1°, which indicates that the coated mesh is superhydrophobic. Figure 3 The shape of

water and oil droplet on the as-prepared mesh film. (a) Water contact angle about 157 ± 1°, (b) oil contact angle about 0°, and (c) permeating behavior of oil on the mesh film. GS-9973 manufacturer According to the Wenzel equation [20], the oleophilicity of the oleophilic materials can be enhanced via increasing the roughness of the sample surface. The coated mesh is expected to show superoleophilicity because of the hierarchical micro/nanostructure ZnO nanorods array on the oleophilic stainless steel mesh. Figure 3b shows that the oil contact angle (OCA) on the as-grown film is about 0°, and

the oil droplet will penetrate freely through the coated mesh (Figure 3c). In order to confirm the feasibility of the coated mesh in practice, as shown in Figure 4, the mixtures of diesel oil and water (volume ratio 3:7) were slowly poured into the test tube; the oil permeated freely through the coated mesh and flowed into the beaker, while the water was repelled on the filter. Figure 4 Concrete experimental process of separation oil and water. (a) Before separation. (b) After separation. selleck screening library It has been reported that the pore sizes of the original stainless steel mesh are critically important to the wettability of the coated mesh [10]. Figure 5 shows the dependence of WCAs and the OCAs on the pore sizes of the original stainless steel mesh. The WCAs cAMP on the coated mesh increase with the increase of the pore sizes and have maximum value when the pore size is about 75 μm. Then, the

WCAs became smaller when the pore sizes increase further. The OCAs are always kept at 0° and do not change with the change of the pore sizes. It is generally considered that the larger the WCAs and OCAs distinction, the easier the filtration of water and oil. It can be shown that 75 μm is the optimum pore size for the filtration of water/oil mixtures. Figure 5 Relationship between the pore size of the original stainless steel mesh and the contact angles. Of water and oil on the corresponding coating film. The separation efficiency of the as-grown sample was studied by oil rejection coefficient (R %) [21]. (1) where C 0 is the oil concentration before filtration and C p is the oil concentration after filtration. Hexane, diesel oil, petroleum ether, and gasoline water/oil mixtures were used in the process of experiment. The specific separation efficiency is shown in Figure 6.

The resultant

nanomesh sectional geometries varied from v

The resultant

nanomesh sectional geometries varied from vertically erected nanobelts or nanowires depending on the size of the photomask patterns and the UV dose in the second photolithography process as shown in Figure 3e,f. The suspended carbon nanomeshes are designed to align obliquely to the bulk carbon post edges so that each junction, where four short carbon nanowires intersect, is supported evenly by the four nanowires. This robust mesh design avoids stiction between neighboring wires due to surface tension during development and breakage of the mesh structures during SHP099 molecular weight pyrolysis, and as a result, the nanowires can be spaced with a small gap. Figure 3 Scanning electron microscopy images of various types of suspended carbon nanomeshes. (a) A football-shape, (b,c) diamond shapes, (d) a hexagonal shape, (e) a vertically erected nanobelt type, (f) a nanowire type. The

CDK inhibitor microstructure of the pyrolyzed carbon structures Tucidinostat ic50 was analyzed using HRTEM and Raman spectroscopy. Figure 4a shows a HRTEM image at the edge of an approximately 190-nm-diameter carbon nanowire. Because the diameter of the suspended carbon nanowire is too large for electrons to be transmitted across the nanowire center, only the edge of a carbon nanowire as-made could be clearly observed in TEM (Figure 4a). The nature of the carbon nanowire is predominantly disordered but shows some short-range ordered nanostructures. The nature of the microstructure of the nanowire was also confirmed by a TEM diffraction pattern, as shown in Figure 4b. The ring shape diffraction pattern indicates a short-range crystalline order, and the foggy pattern

surrounded by the ring pattern is indicative of defects in the graphitic phase [23]. This short-range crystalline nature of the pyrolyzed carbon was confirmed by Raman spectroscopy. Due to the limited spatial resolution of the Raman spectroscopy, the carbon post instead of the suspended carbon nanowire was tested as shown in Figure 4c. The G-band at 1,590 cm−1 is representative of sp 2 hybridized graphitic material and the D-band Tangeritin shown at 1,350 cm−1 stems from disordered carbon [24, 25]. The overlapping shape of the D-band and the G-band and the relative intensity of the two bands are consistent with TEM results indicating that the pyrolyzed carbon is a mixture of ordered and disordered carbons. Figure 4 TEM image (a) and corresponding diffraction patterns (b) of a carbon nanowire and Raman spectrum from a carbon post (c). The TEM image was obtained at the edge of an approximately 190-nm-size bare carbon nanowire. The oxygen-to-carbon (O/C) ratio is often used to characterize the composition of carbonized materials. In Figure 5a,b, we show high-resolution XPS spectra in the C1s and O1s regions, respectively, of a pyrolyzed bulk carbon structure and a SU-8 precursor structure. The C1s spectrum of the SU-8 structure consists of peaks at 283.7 and 285.9 eV. The peak at 285.9 eV corresponds to carbon bound to oxygen and the peak at 283.