Nature 2010,464(7285):59–65 PubMedCentralPubMedCrossRef 3 Human

Nature 2010,464(7285):59–65.PubMedCentralPubMedCrossRef 3. Human Microbiome Project: A framework for human microbiome research. Nature 2012,486(7402):215–221.CrossRef 4. Manichanh C, Rigottier-Gois

L, Bonnaud E, Gloux K, Pelletier E, Frangeul L, Nalin R, Jarrin C, Chardon P, Marteau P, Roca J, Dore J: Reduced diversity of faecal microbiota in Crohn’s disease revealed by a metagenomic approach. Gut 2006,55(2):205–211.PubMedCentralPubMedCrossRef 5. Versalovic J: The human microbiome and probiotics: implications for pediatrics. Ann Nutr Metab 2013,63(Suppl 2):42–52.PubMedCrossRef 6. Jeffery IB, O’Toole PW, Ohman L, Claesson MJ, Deane J, Quigley EM, Simren M: An irritable bowel syndrome subtype defined by species-specific alterations in faecal microbiota. Gut 2012,61(7):997–1006.PubMedCrossRef 7. Manichanh C, Eck A, Varela E, Roca J, Clemente JC, Gonzalez A, Knights CDK inhibitor D, Knight R, Estrella S, Hernandez C, Guyonnet D, Accarino A, Santos J, Malagelada JR, Guarner F, Azpiroz F: Anal gas evacuation and colonic microbiota in patients with flatulence: effect of diet . Gut 2013,63(3):401–408.PubMedCentralPubMedCrossRef 8. Lewis SJ, Heaton KW: Stool form scale as a useful guide

to intestinal transit time. Scand J Gastroenterol 1997,32(9):920–924.PubMedCrossRef 9. Fischer B, Hoh S, Wehler M, Hahn EG, Schneider HT: Faecal elastase-1: lyophilization of stool samples prevents false low results in diarrhoea. Scand J Gastroenterol 2001,36(7):771–774.PubMedCrossRef 10. Longstreth GF, Thompson WG, Chey WD, Houghton LA, Mearin F, Spiller RC: Functional bowel disorders. Gastroenterology 2006,130(5):1480–1491.PubMedCrossRef Enzalutamide 11. Tang Y, Forsyth CB, Keshavarzian A: New Phospholipase D1 molecular insights into inflammatory bowel disease-induced diarrhoea. Expert Rev Gastroenterol Hepatol 2011,5(5):615–625.PubMedCentralPubMedCrossRef

12. Wenzl HH, Fine KD, Schiller LR, Fordtran JS: Determinants of decreased fecal consistency in patients with diarrhoea. Gastroenterology 1995,108(6):1729–1738.PubMedCrossRef 13. Fujimoto S, Nakagami Y, Kojima F: Optimal bacterial DNA isolation method using bead-beating technique. Memoirs Kyushu Univ Dep Of Health Scis Of Medical Sch 2004, 3:33–38. 14. Cardona S, Eck A, Cassellas M, Gallart M, Alastrue C, Dore J, Azpiroz F, Roca J, Guarner F, Manichanh C: Storage conditions of intestinal microbiota matter in metagenomic analysis. BMC Microbiol 2012, 12:158.PubMedCentralPubMedCrossRef 15. Godon JJ, Zumstein E, Dabert P, Habouzit F, Moletta R: Molecular microbial diversity of an anaerobic digestor as determined by small-subunit rDNA sequence analysis. Appl Environ Microbiol 1997,63(7):2802–2813.PubMedCentralPubMed 16. Walters WA, Caporaso JG, Lauber CL, Berg-Lyons D, Fierer N, Knight R: PrimerProspector: de novo design and taxonomic analysis of barcoded polymerase chain reaction primers. Bioinformatics 2011,27(8):1159–1161.PubMedCentralPubMedCrossRef 17.

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tuberculosis invasion The confirmation of Rv0679c’s location in

tuberculosis invasion. The confirmation of Rv0679c’s location in mycobacterial surface, together with the identification of a binding region formed by HABPs 30985-30987, suggest that this protein may be related to adhesion and/or invasion processes. In addition, such surface localization could be facilitating contact between the bacilli and its host cell, thereby leading to triggering the host’s immune response via interaction with host cell surface receptors [16]. Conclusions The complexity of Mycobacterium tuberculosis as a pathogen and the variety of mechanisms that it uses for invading host cells

makes it necessary to develop an effective strategy to block the invasion of target cells. Our proposal is based on searching for fragments of different AUY-922 nmr proteins involved in the mycobacteria-host cell interaction. In our experience, sequences that bind specifically to target cells and that are capable of blocking invasion could be used as template to design peptides with ability to immunomodulate Selleckchem Midostaurin the protective response against tuberculosis. The immune response triggered against mycobacterial high-specific binding sequences could prevent invasion of target cells, either during a first encounter with the bacillum or during the reactivation of a latent infection. It has been reported that a considerable number of secreted proteins are

protective antigens and therefore have been considered as attractive candidates to develop subunit vaccines [43–46]. Moreover, they are hypothesized to mediate mycobacterial entry into the host cell [47]. Traditionally, vaccine development has been founded on the humoral immune response, which involves antibody production and is mainly targeted against extracellular microorganisms, whereas the immune response against intracellular microorganisms is mainly driven by cellular immune mechanisms. In addition, the distinction between the Th1 and Th2 cellular immune responses is complex for some of the antigens or immunogens included in vaccines that induce cellular as well as humoral immune responses, and it is not yet clear the degree of independence

between antibody-mediated many and cell-mediated immune responses under physiological conditions [48, 49]. Considering the variety of broad interactions of B lymphocytes with cellular immunity, B cells could have a significant impact on the outcome of airborne challenge with M. tuberculosis as well as the resultant inflammatory response [49]. Therefore, we expect for peptides of Rv0679c to induce an immune response where humoral and cellular immunity are not mutually excluded. The identification of Rv0679c HABPs capable of inhibiting target cell invasion by M. tuberculosis via host-cell receptor interactions supports their inclusion in further immunological studies in animal models aimed at evaluating their potential as components of a subunit-based antituberculous vaccine.

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06% of the original inoculum was obtained for non-stressed C jej

06% of the original inoculum was obtained for non-stressed C. jejuni. Pre-exposure of bacteria to heat, starvation or osmotic stresses exacerbated the bacterial susceptibility to intracellular killing, since a significant

decline of the number of surviving bacteria was observed upon pre-exposure to these stresses 5 h post-gentamicin treatment (Figure  3B). At 24 h post gentamicin Palbociclib cell line treatment, a few internalized bacteria (~1.5 × 103 CFU/ml) were observed with non-stressed inoculum. No bacteria that had been pre-exposed to heat, starvation or osmotic stress were detected. In contrast, pre-exposure to oxidative stress had no impact on internalization or intracellular survival of C. jejuni under the conditions and time frame studied. Effect of pre-exposure to stress on sub-cellular AZD6244 molecular weight location of internalized bacteria A detailed observation of C. jejuni cells internalized within the amoebae was carried out by confocal laser scanning microscopy (CLSM). In the absence of any stress, live C. jejuni cells were detected by CellTracker Red staining inside the trophozoites immediately after gentamicin treatment (Figure  4A, B). The intracellular bacteria were distributed as clusters within acidic vacuoles as

observed by the simultaneous staining of acidic vacuoles by LysoSensor Green DND-189 (Figure  4C, D). Pre-exposure of bacteria to low-nutrient, heat, osmotic or oxidative stresses did not qualitatively alter the sub-cellular location of internalized bacteria, as all were also recovered in acidic vacuoles (Figure  4E to T). Figure 4 Confocal microscopy

analysis of stressed and non-stressed C. jejuni cells within acidic organelles of A. castellanii observed immediately after gentamicin treatment. Control Thiamet G C. jejuni (A-D), C. jejuni pre-exposed to osmotic stress (E-H), heat stress (I-L), hydrogen peroxide (M-P), or starvation stress (Q-T). The multiplicity of infection was 100:1 (bacteria:amoeba). (A, E, I, M, Q) differential interference contrast image; (B, F, J, N, R) C. jejuni stained with CellTracker Red; (C, G, K, O, S) acidic amoeba organelles stained with LysoSensor Green; (D, H, L, P, T) corresponding overlay. Scale bar = 5 μm. In addition to the viable count assay for the quantification of intracellular bacteria and CLSM analyses reported above, TEM was also used to more precisely assess the effect of heat stress on intracellular location of C. jejuni within A. castellanii. Heat stress was selected for TEM studies because it decreased intracellular survival of C. jejuni, but it did not affect uptake. Therefore this heat stress allowed visualization of numerous internalized bacteria at early time points. As shown in Figure  5, sections of infected A. castellanii cells obtained right after gentamicin treatment showed that C. jejuni cells were confined to tight vacuoles within the amoebae, whether they had been heat-stressed or not prior to co-culture with amoebae (Figure  5A, C).

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5%, Sigma-Aldrich, St Louis, MO, USA), 4-nm Qdot® 525 ITK™ amino

5%, Sigma-Aldrich, St. Louis, MO, USA), 4-nm Qdot® 525 ITK™ amino (PEG) quantum dots (8-μM solution 5-Fluoracil in 50 mM borate, pH 9.0, Invitrogen, Life Technologies, Carlsbad, CA, USA), 16-mercaptohexadecanoid acid

(90%, HS(CH2)15COOH, Aldrich), and deionized (DI) water. N-(3-dimethylaminopropyl)-N′-ethylcarbodiimide hydrochloride (EDC; Sigma-Aldrich), N-hydroxysulfosuccinimide sodium salt (sulfo-NHS; 97%, Aldrich), and phosphate-buffered saline (PBS; pH 7.4, 10×, Invitrogen) were used for bioconjugation. Instruments This study used a NanoWizard® AFM (JPK Instrument, Berlin, Germany), MFP-3D-BIOTM AFM (ASYLUM RESEARCH, Goleta, CA, USA), HITACHI S-4800 field emission scanning electron microscope (FE-SEM; Chiyoda-ku, Japan), JEOL 2000 V UHV-TEM H 89 concentration (Akishima-shi, Japan), MicroTime 200 fluorescence lifetime systems with inverse time-resolved fluorescence microscope (PicoQuant, Berlin, Germany), and ULVAC RFS-200S RF Sputter System (Saito, Japan). We also employed 24 mm × 50 mm glass coverslips, a Lambda microliter pipette, and spin coating machine TR15 (Top Tech Machines Co., Ltd., Taichung, Taiwan) for the preparation of samples. Standard

silicon polygon-pyramidal tips (Pointprobe® NCH probes, tip radius of curvature <12 nm, resistivity 0.01 ~ 0.025 Ω cm, NanoWorld, Neuchâtel, Switzerland) supported by a cantilever with a spring constant k ~ 42 N/m were used for the attachment of Au-NPs. For Au-NP support during the attachment process, we used conductive n-type polished Si (100) wafers (resistivity 0.008 ~ 0.022 Ω cm), purchased from Swiftek Corp. (Hsinchu, Taiwan). An oscilloscope (LeCroy waveRunner 64Xi, 600 MHz, 10 GS/s, Teledyne LeCroy GmbH, Heidelberg, Germany) was used to measure the electric Ribonucleotide reductase potential. A waveform generator (WW2572A, 250 MS/s, Tabor Electronics, Tel Hanan, Israel) was employed to produce signals on demand. Sample preparation (Au-NPs) A diluted Au-NP solution was prepared by combining the initial Au-NP solution and ethanol at a volume ratio of 1:1,000. Au-NPs were then spread as a monolayer on

an n-type silicon wafer by spin-coating. The roughness of the silicon wafer surface had to be sufficiently low (on the order of 100 pm) to ensure that Au-NPs could be imaged using the NanoWizard® AFM. Sample preparation (QDs) A diluted solution of QDs was prepared by combining the initial Qdot® 525 solution with DI water at a volume ratio of 1:10,000. The diluted QD solution was then spread as a monolayer on a glass coverslip by spin-coating. The prepared sample was loaded into a fluorescence microscope. Homemade glass/Au film (65 nm) Half of the 24 mm × 50 mm glass coverslip area was exposed to a sputter source (Au) at a sputter rate of 3 Å/s. AFM images reveal an Au film thickness of 65 nm (see Additional file 1). Confocal examination To provide excitation, a picosecond diode laser (λ = 532 nm) was focused on a diffraction-limited spot using an oil-immersion objective lens (N.A. = 1.

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[24] No cases of penile/perianal/perineal cancer were reported in

[24] No cases of penile/perianal/perineal cancer were reported in either this website group.[25] The vaccine is also expected to be protective against genital warts in males aged 9–15 years, as the immune response in males of this age group was noninferior to that in males aged 16–26 years.[25] Efficacy of the quadrivalent HPV vaccine was also shown with regard to the prevention of persistent and incident HPV infection.[24] The quadrivalent HPV vaccine was generally well tolerated in males aged 9–26 years.[22–24] The most common adverse events reported were injection-site related,[22–24] and most of these were of mild to moderate severity.[11] Overall,

coadministration of the quadrivalent HPV vaccine with other vaccines was generally well tolerated.[26–29] Acknowledgments and Disclosures The full text article[1] from which this profile report was derived was reviewed by K. Kohl, Division of Global Migration and Quarantine, National Center for Emerging and Zoonotic Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA, USA; A. Moore, Arlington Center for Dermatology, Department of Dermatology, Baylor University Medical Center,

Dallas, Selleck Daporinad TX, USA, and Department of Dermatology, University of Texas Medical Branch at Galveston, Galveston, TX, USA. The manufacturer of the agent under review was offered an opportunity to comment on the original article during the peer review process. Changes based on any comments received were made on the basis of scientific and editorial merit. The preparation of the original article and this profile report was not supported by external funding.

A. Giuliano is on the Speaker’s Bureau of Merck and Co, Inc., and is a consultant to Merck and Co, Inc. References 1. Garnock-Jones KP, Giuliano Bumetanide AR. Quadrivalent human papillomavirus (HPV) types 6, 11, 16, 18 vaccine for the prevention of genital warts in males. Drugs 2011; 71(5): 591–602PubMedCrossRef 2. Hutchinson DJ, Klein KC. Human papillomavirus disease and vaccines. Am J Health Syst Pharm 2008 Nov 15; 65(22): 2105–12PubMedCrossRef 3. Hsueh PR. Human papillomavirus, genital warts, and vaccines. J Microbiol Immunol Infect 2009 Apr; 42(2): 101–6PubMed 4. Giuliano AR, Salmon D. The case for a gender-neutral (universal) human papillomavirus vaccination policy in the United States: point. Cancer Epidemiol Biomarkers Prev 2008; 17(4): 805–9PubMedCrossRef 5. Giuliano AR, Tortolero-Luna G, Ferrer E, et al. Epidemiology of human papillomavirus infection in men, cancers other than cervical and benign conditions. Vaccine 2008; 26 Suppl. 10: K17–28PubMedCrossRef 6. Miralles-Guri C, Bruni L, Cubilla AL, et al. Human papillomavirus prevalence and type distribution in penile carcinoma. J Clin Pathol 2009 Oct; 62(10): 870–8PubMedCrossRef 7. Kliewer EV, Demers AA, Elliott L, et al. Twenty-year trends in the incidence and prevalence of diagnosed anogenital warts in Canada.

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1990; McGettigan et al 1997; Bracchi et al 2005; Figueiras et a

1990; McGettigan et al. 1997; Bracchi et al. 2005; Figueiras et al. 2006; Bäckström and Mjörndal 2006; Smits et al. 2008). Since it was not possible

to change either the social security arrangements for occupational diseases or the registry system itself and since there were no means to supply financial incentives or accreditation points to reporting OPs, we chose to focus on attention, information and feedback to improve reporting behaviour. The key objective of the intervention is behavioural change: potential reporters should start reporting and should report more often. Programs aimed at changing (health) behaviour are often based on psychological models and theories such as the health belief model, the theory of reasoned action and the theory of planned behaviour. In these models, a person is considered to make decisions on a rational basis: BGJ398 people will change their behaviour as soon as they are convinced that

they can execute the change and that they will benefit from it. A psychological model that looks upon behavioural change as a process in time, influenced by many factors, is the stages of change model or Trans Theoretical Model (TTM). Since the aimed ODs reporting behaviour has to be maintained for a long small molecule library screening time and is influenced by many determinants, this model may provide a suitable theoretical base for the hypotheses of this study. TTM, introduced in the early 1980s (Prochaska and Diclemente 1984), distinguishes between several stages of behaviour. The first stage being precontemplation, in which there is no awareness of a problem and an individual does not consider a change in behaviour in the next 6 months. The second stage is contemplation, in which the individual does consider a change in behaviour, followed by a preparative stage, in which the individual makes cognitive preparations for a change in behaviour. In the action stage, the individual initiates a change in behaviour, and in the maintenance

stage he or she performs the behaviour for a longer period of time. Also relapse can occur. Each stage is influenced by its own relevant stage-specific factors, Alectinib datasheet like decisional balance that reflects the weighing of the importance of pro’s and con’s of a behaviour (precontemplation) or self-efficacy that reflects the situation-specific confidence people have in coping with a behaviour related situation (contemplation). Stage-specific interventions should match these stage-specific factors in order to produce progress through the stages. (Dijkstra et al. 1998, 2006; Gebhardt and Maes 2001; de Vet et al. 2005, 2007). Our first hypothesis is that supplying OPs, identified as precontemplators or contemplators, with personally addressed, stage-matched information on why and how to report occupational diseases, will persuade more OPs to report (more) occupational diseases to the national registry.

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*, P < 0 01 Expression of SOX9 protein and histological staging

*, P < 0.01. Expression of SOX9 protein and histological staging of NSCLC Immunostaining examination of tumor sections obtained from 142 patients showed that positive SOX9 BVD-523 expression was found to be correlated strongly with the clinicopathological stages of the patients’ cancer (P = 0.022), but no significant relationship was found between age (P = 0.382) or gender (P = 0.240), or pathology (P = 0.312) (Table 2). Spearman correlation analysis revealed a correlation coefficient of 0.200 (P = 0.017; Table 3) between SOX9 expression level and the

histological grading of NSCLC. Taken together, these observations support the notion that the progression of NSCLC is associated with increased SOX9 expression. Table 2 Correlation between the clinicalpathologic features and expressions of SOX9 Characteristics SOX9 P-value   Low or none High   Gender     0.382 Male Female 47 21 56 18   Age (years)     0.240 ≤ 65 >65 46 22 43 31   Pathology       Squamous cell carcinoma 26 21 0.312 Adenocarcinoma 32 36   Adenosquamous carcinoma 10 17   NSCLC histology (AJCC grade)     0.022 I and II III and IV 34 34 23 51   Survival (n = 89)     0.040 Alive Dead 21 23 12 33   Table 3 Spearman correlation analysis between SOX9 and clinical pathologic factors Variables SOX9   Spearman Correlation P -Value Gender -0.083 0.325 Age 0.098 0.247 NSCLC histology (AJCC grade) 0.200 0.017 Survival RG7204 chemical structure -0.239 0.024 Association between SOX9

expression and patient prognosis The statistical analysis presented in Table 2 revealed an inverse correlation between SOX9 level and patient survival (P = 0.040). Spearman

analysis also showed a correlation coefficient of -0.239 (P = 0.024; Table 3) between SOX9 and patient survival. Log-rank Rapamycin test and Kaplan-Meier analysis were also applied to evaluate further the effect of SOX9 expression and histological staging of lung cancer on survival. The log-rank test showed that the expression level of SOX9 protein in NSCLC was correlated significantly with patients’ survival time (P < 0.001), with a correlation coefficient of -0.262 (Figure 4; Table 4). As shown in Figure 4, the cumulative 3-year survival rate was 65.9% in the low-SOX9 expression group (n = 44), and 24.5% in the high-SOX9 expression group (n = 45). The multivariate survival analysis shown in Table 4 indicated that SOX9 expression level was an independent prognostic factor in the assessment of patient outcomes. Figure 4 Kaplan-Meier curves with univariate analyses (log-rank) for patients with low SOX9-expressing (bold line) versus high SOX9-expressing tumors (dotted line). The cumulative 3-year survival rate was 65.9% in the low SOX9 expression group (n = 44), whereas it was only 24.5% in the high SOX9 expression group (n = 45). Table 4 Univariate and multivariate analysis of different prognostic parameters in patients with NSCLC by Cox-regression analysis   Univariate analysis Multivariate analysis   No.

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With the increase of the magnetic field, the current amplitude in

With the increase of the magnetic field, the current amplitude in [110] crystallographic direction increased faster than that in [1 0] crystallographic direction, despite the magnetic field-independent background current in Figure 7b. Figure 7 The magneto-photocurrents J q in (a) [110] and (b) [1 0] crystallographic directions. IWR-1 concentration The red parabolic-shape lines are fitting curves of the

currents. Conclusions In summary, we have researched magneto-photocurrents in the InAs/GaSb superlattice when an in-plane and tilted magnetic field were applied respectively. The magneto-photocurrents in both conditions are insensitive to the polarization state of the incident light. A theoretical model involving anisotropic photo-excited carriers density is utilized to explain the in-plane magnetic field-induced MPE. Compared to the direct electron-photon interaction, the asymmetric electron-phonon interaction which contributes to the magneto-photocurrent may be more sensitive to the radiation polarization state. The quadratic magnetic field dependence of the magneto-photocurrents can be well illustrated by an additional Hall effect model. Acknowledgements The work was supported by the 973 Program (2012CB921304 and 2013CB632805) and the National Natural Science Foundation of China (Nos. 60990313, 61176014, 61307116 and 61290303). References 1. žutić I, Fabian J, Das Sarma S: Spintronics: fundamentals and applications.

Rev Mod Phys 2004, 76:323–410. doi:10.1103/RevModPhys.76.323CrossRef 2. Wolf SA, Awschalom DD, Buhrman

RA, Daughton JM, von Molnár S, Roukes ML, Chtchelkanova AY, Treger DM: Spintronics: a spin-based electronics vision for the future. Science Ivacaftor mw 2001,294(5546):1488–1495. doi:10.1126/science.1065389CrossRef 3. Ganichev SD, Prettl W: Spin photocurrents in quantum wells. J Phys: Condens Matter 2003,15(20):935. 4. Bel’kov VV, Ganichev SD: Magneto-gyrotropic effects in semiconductor quantum wells. Semiconductor Sci Technol 2008,23(11):114003.CrossRef 5. Dai J, Lu H-Z, Yang CL, Shen S-Q, Zhang F-C, Cui X: Magnetoelectric photocurrent generated by direct interband transitions in Meloxicam InGaAs/InAlAs two-dimensional electron gas. Phys Rev Lett 2010, 104:246601. doi:10.1103/PhysRevLett.104.246601CrossRef 6. Lechner V, Golub LE, Lomakina F, Bel’kov VV, Olbrich P, Stachel S, Caspers I, Griesbeck M, Kugler M, Hirmer MJ, Korn T, Schüller C, Schuh D, Wegscheider W, Ganichev SD: Spin and orbital mechanisms of the magnetogyrotropic photogalvanic effects in GaAs/Al x Ga 1− x As quantum well structures. Phys Rev B 2011, 83:155313. doi:10.1103/PhysRevB.83.155313CrossRef 7. Drexler C, Tarasenko SA, Olbrich P, Karch J, Hirmer M, Müller F, Gmitra M, Fabian J, Yakimova R, Lara-Avila S, Kubatkin S, Wang M, Vajtai R, Ajayan M, Kono J, Ganichev SD: Magnetic quantum ratchet effect in graphene. Nat Nano 2013,8(2):104–107.CrossRef 8. Ting DZ-Y, Cartoixà X: Resonant interband tunneling spin filter. Appl Phys Lett 2002,81(22):doi:10.1063/1.1524700.CrossRef 9.

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A goal we are proud to be part of Acknowledgements This article

A goal we are proud to be part of. Acknowledgements This article has been published as part of World Journal of Emergency Surgery Volume 7 Supplement 1, 2012: Proceedings of the World Trauma Congress 2012. The full contents of the supplement are available online at http://​www.​wjes.​org/​supplements/​7/​S1.

References 1. Carrasco CE, Godinho M, de Azevedo Barros MB, Rizoli S, Fraga GP: Fatal Motorcycle Crashes: A Serious Public Health Problem in Brazil. World Journal of Emergency Surgery 2012,7(Suppl 1):S5. 2. Zago TM, Pereira BM, Calderan TRA, Nascimento B, Fraga GP: Nonoperative management for patients with grade IV blunt hepatic trauma. World Journal of Emergency Surgery 2012,7(Suppl 1):S8. 3. Marttos AC, Kuchkarian FM, Pereira BM, Collet-Silva FS, Fraga GP: Enhancing Trauma Ibrutinib clinical trial Education Worldwide through Telemedicine. World Journal of Emergency Surgery 2012,7(Suppl 1):S4.CrossRef 4. Marttos AC, Kuchkarian FM, Palaios E, Rojas D, Abreu-Reis P, Schulman C: Surgical Telepresence: The Usability of a Robotic Communication Platform. World Journal of Emergency Surgery 2012,7(Suppl 1):S11.CrossRef 5. Abreu-Reis P, Oliveira GC, Curtarelli de Oliveira A, Sadique H, Nasr A,

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S, Cunha-Melo JR: Permissive hypotension does not reduce regional organ perfusion compared to normotensive resuscitation: animal study with fluorescent microspheres. World Journal of Emergency Surgery 2012,7(Suppl 1):S9.CrossRef 7. Morais PH, Ribeiro VL, Caetano de Farias IE, Almeida Silva LE, Carneiro FP, Veiga JPR, de Sousa JB: Alcohol acute intoxication before sepsis impairs the wound healing of intestinal anastomosis rat model of the abdominal trauma patient. World Journal of Emergency Surgery 2012,7(Suppl 1):S10. 8. Sankarankutty A, Nascimento FER B, da Luz LT, Rizoli S: TEG ® and ROTEM ® in trauma: similar test but different results? World Journal of Emergency Surgery 2012,7(Suppl 1):S3.CrossRef 9. Mamtani R, Nascimento B, Rizoli S, Pinto R, Lin Y, Tien H: The utility of Recombinant Factor VIIa as a Last Resort in Trauma. World Journal of Emergency Surgery 2012,7(Suppl 1):S7. 10. Gonsaga RAT, Brugugnolli ID, Fraga GP: Comparison between two systems of mobile prehospital care to trauma patients. World Journal of Emergency Surgery 2012,7(Suppl 1):S6.CrossRef 11. Fraga GP, de Andrade VA, Schwingel R, Neto JP, Starling SV, Rizoli S: The scientific production in trauma of an emerging country. World Journal of Emergency Surgery 2012,7(Suppl 1):S13.CrossRef Competing interests The authors declare that they have no competing interests.

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Phys Rev B 1994, 50:8699 CrossRef 39 Rodriguez-Vargas I, Gaggero

Phys Rev B 1994, 50:8699.CrossRef 39. Rodriguez-Vargas I, Gaggero-Sager LM: Sub-band and transport calculations in double n-type δ-doped quantum wells in Si. J Appl Phys 2006, 99:033702.CrossRef 40. Drumm DW, Hollenberg LCL, Simmons MY, Friesen M: Effective mass theory INCB024360 of monolayer δ doping in the high-density limit.

Phys Rev B 2012, 85:155419.CrossRef 41. Delley B, Steigmeier EF: Quantum confinement in Si nanocrystals. Phys Rev B 1993, 47:1397.CrossRef 42. Delley B, Steigmeier EF: Size dependence of band gaps in silicon nanostructures. Appl Phys Lett 1995, 67:2370.CrossRef 43. Ramos LE, Teles LK, Scolfaro LMR, Castineira JLP, Rosa AL, Leite JR: Structural, electronic, and effective-mass properties of silicon and zinc-blende group-III nitride semiconductor compounds. Phys Rev B 2001, 63:165210.CrossRef 44. Zhou ZY, Brus L, Friesner R: Electronic structure and luminescence of 1.1- and 1.4-nm silicon nanocrystals: oxide shell versus hydrogen passivation. see more Nano Lett 2003, 3:163.CrossRef 45. Barnard AS, Russo SP, Snook IK: Ab initio modelling of band states in doped diamond. Philos Mag 2003, 83:1163.CrossRef 46. Kresse G, Joubert D: From ultrasoft pseudopotentials

to the projector augmented-wave method. Phys Rev B 1999, 59:1758.CrossRef 47. Blöch PE: Projector augmented-wave method. Phys Rev B 1994, 50:17953.CrossRef 48. Artacho E, Anglada E, Dieguez O, Gale JD, Garcia A, Junquera J, Martin RM, Ordejon P, Pruneda JM, Sanchez-Portal D, Soler JM: The siesta method; developments and applicability. J Phys Condens Matter 2008, 20:064208.CrossRef 49. Troullier N, Martins JL: Efficient pseudopotentials for plane-wave calculations. Phys Rev B 1993, 43:1991. 50. Perdew JP, Burke K, Ernzerhof M: Generalized gradient approximation made simple. Phys Rev Lett 1996, 77:3865.CrossRef 51. Monkhorst HJ, Pack JD: Special points for Brillouin-zone integrations. Phys Rev B 1976, 13:5188.CrossRef 52. Blöchl PE, Jepsen O, Andersen OK: Improved tetrahedron method for Brillouin-zone integrations. Phys Rev B 1994, 49:16223.CrossRef 53. Wilson HF, Warschkow O,

Marks NA, Inositol monophosphatase 1 Curson NJ, Schofield SR, Reusch TCG, Radny MW, Smith PV, McKenzie DR, Simmons MY: Thermal dissociation and desorption of PH3 on Si(001): a reinterpretation of spectroscopic data. Phys Rev B 2006, 74:195310.CrossRef 54. Bradley CJ, Cracknell JP: The Mathematical Theory of Symmetry in Solids: Representation Theory for Point Groups and Space Groups. Oxford: Clarendon Press; 1972. 55. Chelikowsky JR, Cohen ML: Electronic structure of silicon. Phys Rev B 1974, 10:5095.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions DWD, SPR, and LCLH conceived the study. Density functional theory calculations were carried out by DWD, AB, and MCP. All authors contributed to the discussion of results and drafting of the the final manuscript. All authors read and approved the final manuscript.

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