This variant is significantly different from those isolated during previous cholera outbreaks in the 1990s in the same geographic area. Indeed, it holds a peculiar CTXΦ array and the SXT-like element ICEVchAng3. Ribotype analysis suggests that this strain might have spread to West Africa from the Indian Subcontinent. Methods Bacterial strains, susceptibility tests and transfer of drug resistances MRT67307 We

analyzed V. cholerae strains isolated in Angola or India between 1992 and 2006 (Table 1). All strains were isolated from stool samples and/or rectal swabs from patients, and after isolation on thiosulfate citrate bile sucrose agar and biochemical identification, bacterial strains were routinely grown in Luria-Bertani (LB) or agar plates at 37°C and maintained at -80°in LB broth containing 30% (vol/vol) glycerol. Table 1 V. cholerae O1 strains analyzed in this study   Isolation             Strain Place Year Antibiotic resistance profile Antibiotic resistance genes ICE content CTXΦ array Ribotype Reference VC175 Angola (Luanda) 2006 Ap, Pn, Sm, Su, Tp floR, strA, strB, dfrA1, sulII b ICEVchAng3 B R1 This study VC189 Angola (Luanda) 2006 Ap, Pn, Sm, Su, Tp floR, strA, strB, dfrA1, sulII b ICEVchAng3 B R1 This study VC582 Angola (Luanda) 1992 Ap, Cm, Kn, Pn, Sm, Sp, Su, Tc, Tpa aph, tetG, cat1, blaP1, dfrA15, aadA8, sul2 c – A R2 [11] VC1383 Angola (Benguela) 1994 Ap, Cm, Kn, Pn, Sm, Sp, Su, Tc, Tpa aph, tetG, cat1, blaP1, dfrA15, aadA8, sul2 c

– A R3 [11] VC547 Angola (Bengo river) 1994 Ap, Cm, Kn, Pn, Sm, Sp, Su, Tc, Tpa aph, tetG, cat1, blaP1, dfrA15, aadA8, sul2 c – A R4 [11] VC7452 India (Sevagram) 1995 Ap, Nx, Pn, Sm, Sp, Su, Tp floR, strA, strB, dfrA1, Histone Methyltransferase inhibitor sulII b ICEVchInd5d B R1 [16] VC15699 India (Sevagram) 1999 Ap, Nx, Pn, Sm, Sp, Su, Tp floR, strA, strB, dfrA1, sulII b ICEVchInd5

B R1 [16] VC9258 India (Sevagram) 1999 Ap, Nx, Pn, Sm, Sp, Su, Tp floR, strA, strB, dfrA1, sulII b ICEVchInd5 B R1 [16] aResistance profile conferred by conjugative plasmid p3iANG [11]; blocated on the ICE; clocated on p3iANG; dICE fully sequenced. Abbreviations: Ap, ampicillin; Cm, chloramphenicol; Kn, kanamycin; Nx, nalidixic acid; Pn, penicillin; Sm, streptomycin; Sp, spectinomycin; Su, sulfamethoxazole; Tc, tetracycline; Epothilone B (EPO906, Patupilone) Tp, trimethoprim. Antimicrobial susceptibility was tested at the following concentrations: ampicillin (Ap), 100 μg/ml; chloramphenicol (Cm), 20 μg/ml; kanamycin (Km), 50 μg/ml; nalidixic acid (Nx), 40 μg/ml; penicillin (Pn), 20 μg/ml; rifampin (Rf), 100 μg/ml; spectinomycin (Sp), 50 μg/ml; streptomycin (Sm), 50 μg/ml; sulfamethoxazole (Su), 160 μg/ml; tetracycline (Tc), 12 μg/ml; and trimethoprim (Tm), 32 μg/ml. Antibiotic concentrations were defined according to their MIC breakpoints as previously described [18, 20] and were included in ISO sensitest (Oxoid) agar plates. Bacterial strains were spotted onto the plates as previously described [11]. Conjugation assays were used to transfer ICEVchAng3 from V.

The completed first-dimensional strip was subjected to 2-D SDS-PAGE with 12.5% acrylamide gel. Separated proteins were stained by silver staining as mentioned above. Cloning and expression

of recombinant HADH A 1311-bp LIC13300 DNA fragment was amplified using oligomers LIC13300-F 5′-GGAATTCCATATGAGAGAAATCAAAACAGTAACAG-3′ and LIC13300-R 5′-CCGCTCGAGTCCTTTGAAAAGTGAACGAGC-3′ designed based on L. interrogans serovar Copenhageni genome sequences (GenBank accession YP_003205). PCR was performed with KOD plus ver. 2 PCR kit (Toyobo, Osaka, Japan) from strain K64. Cycling conditions were: 95°C, 5 min, followed by 40 cycles at 95°C, 1 min, 50°C, 1 min, 68°C, 2 min, and a final extension cycle of 5 min, 68°C. PCR product was digested with NdeI and IACS-10759 mouse XhoI (Roche, Basel, Schweiz), ligated to NdeI- and XhoI- digested expression vector, pET-28a (+) (Novagen, San Diego, CA). The ligated plasmid was amplified in E. coli DH5α and purified using Midi PlusTM Ultrapure Plasmid Extraction System (Viogene, Taipei, Taiwan). After confirming the presence of correct inserts by sequence analysis, the plasmid was transformed

in E. coli (DE3). Cultures were grown MK 8931 ic50 to OD600 = 0.5 and protein expression was induced with 1 mM isopropyl-beta-D-thiogalactopyranoside selleck screening library (IPTG), and incubated at 25°C overnight. His-tagged LIC13300 recombinant protein (rHADH) was purified under native

conditions with TALON® Metal Affinity Resin (Clontech) as previously described [59]. Antiserum against rHADH One female Japanese white rabbit (Biotek. Co.,Ltd., Japan) weighing 1.5 kg was immunized subcutaneously with 30 μg of the recombinant protein. The rHADH was mixed with an equal volume of complete Freund’s adjuvant (Sigma-Aldrich, St. Louis, MO) to make an emulsion. Four subsequent booster injections were given at two-week intervals in the same way, by using incomplete Freund’s adjuvant (Sigma-Aldrich, St. Louis, MO). One week after the final immunization, the blood of rabbit was collected through cardiac puncture and the serum was analyzed by immunoblotting. Immunoblotting Proteins separated by SDS-PAGE were transferred to an Immobilon-P transfer membrane (Merck Millipore, Billerica, MA, USA) and blocked with 1% (wt/vol) nonfat dry milk (WAKO, Osaka, Japan) in TBS-0.05% Tween 20 (TBS-T). The membranes were incubated overnight at 4°C with polyclonal antibody produced against live whole cells of L. interrogans serovar Manilae (anti-L.

A loss-of-function mutation in zwf allows for YS873 to grow well in LB broth at a pH of 6.6 (Figure 7A). 5% CO2 inhibited the growth of YS873 and YS873 zwf in LB pH 6.6 and GDC-0994 solubility dmso 7.6 (Figure 7B). Although zwf protects against 5% CO2 in LB broth pH 6.6 (Fig 7B), it does not significantly improve survival in the presence of 5% CO2 in LB broth pH 7.6 (Figure

7B), suggesting that an acidic pH is a component for zwf to suppress msbB-mediated sensitivity to 5% CO2. Figure 7 zwf suppresses sensitivity to acidic pH in LB broth in air, and to 5% CO 2 in LB broth pH 6.6, but not pH 7.6. Strains were grown in LB broth buffered to pH 6.6, or pH 7.6, in either air (A and C) or 5% CO2 (B and D). β-galactosidase assays confirm cell lysis in LB broth, pH 6.6, in air find more To test if the loss of growth of YS873 in

LB broth pH 6.6 was the result of cell death or simply the result of inhibition or delay of cell division, β-galactosidase release was measured. As shown in Figure 8A, significant cell lysis occurs after growth of YS873 for 8 hours in LB broth, pH 6.5 but not pH 7.5 (pH shifted slightly [+/-0.1 units] during autoclaving). Furthermore, a loss-of-function mutation in zwf significantly reduces cell lysis of YS873 grown in LB broth pH 6.5. This reduction in cell lysis, as measured by release of the cytoplasmic enzyme β-galactosidase, correlates with increased CFU/ml numbers observed in YS873 zwf (as compared to YS873) grown in LB broth, pH 6.6 (Figure 7A). Figure 8 β-galactosidase release assays confirm cell lysis in LB broth, pH 6.6,

in air; zwf inhibits cell lysis in LB broth, pH 6.6, in air and in LB broth, pH 6.6, but not pH 7.6, in the presence of 5% CO 2 . Release of β-galactosidase Resveratrol from the cytosol of the bacteria was used to test if the growth defects observed in YS873 and YS873 zwf resulted from cell lysis. Strains grown in LB broth at either pH 6.5, or pH 7.5, under either ambient air (A) or 5% CO2 (B) conditions. zwf reduces YS873 cell lysis in the presence of 5% CO2 in LB broth pH 6.6, but not pH 7.6 Since we observed that YS873 lysed when there was no net growth in LB broth pH 6.5 while maintaining a relatively constant CFU/ml, we investigated if cell lysis occurs in YS873 zwf, which also exhibits little net growth with a relatively constant CFU/ml in the presence of 5% CO2 in LB broth pH 6.6 or 7.5 (Figure 7B). Growth curves for these strains indicated that there was a decrease in CFU/ml when YS873 was grown in LB broth pH 6.6 in the presence of 5% CO2, but that CFU/ml remained relatively constant if a loss-of-function mutation in zwf was present or if the pH of LB broth was 7.

PubMedCrossRef 18. Goh BK, Wong AS, Tay KH, Hoe MN: Delayed presentation of a patient with

a ruptured diaphragm complicated by gastric incarceration and perforation after apparently minor Blunt trauma. Canadian Journal of Emergency Medicine GS-9973 2004, 6:277–280.PubMed 19. Matsevych OY: Blunt diaphragmatic rupture: four year’s experience. Hernia 2008, 12:73–8.PubMedCrossRef 20. Bergeron E, Clas D, Ratte S, Beauchamp G, Denis R, Evans D, Frechette P, Martin M: Impact of deferred treatment of Blent diaphragmatic rupture: a 15-year experience in six trauma centers in Quebec. J Trauma 2002, 52:633–40.PubMedCrossRef 21. Brasel KJ, Borgstrom DC, Meyer P, Weigelt JA: Predictors of outcome in Blent diaphragm rupture. J Trauma 1996, 41:484–7.PubMedCrossRef 22. Shapiro MJ, Heiberg E, Durham RM, Luchtefeld W, Mazuski JE: The unreliability of CT scans and initial chest radiographs in evaluating blunt trauma induced diaphragmatic rupture. Clin Radiol 1996, 51:27–30.PubMedCrossRef 23. Montresor E, Mangiante G, Vassia S, Barbosa A, Attino M, Bortolasi L, Nifosi F, Modena S, Puchetti V: [Rupture of the diaphragm caused by closed trauma. Case contributions and review of the literature.]. Ann Ital Chir 1997, 68:297–303. discussion 303–5. Italian.PubMed 24. Esme H, Solak O, Sahin DA, MK0683 nmr Sezer M: Blunt and penetrating traumatic ruptures of the diaphragm. Thorac

Cardiovasc Surg 2006, 54:324–7.PubMedCrossRef 25. cAMP Athanassiadi K, Kalavrouziotis G, Athanassiou M, Vernikos P, Skrekas G, Poultsidi A, Bellenis I: Blunt diaphragmatic rupture. Eur J Cardiothorac Surg 1999, 15:469–74.PubMedCrossRef 26. Gwely NN: Outcome of blunt diaphragmatic rupture. Analysis of 44 cases. Asian Cardiovasc Thorac Ann 2010, 18:240–3.PubMed 27. Yalçinkaya I, Kisli E: Traumatic diaphragmatic rupture: results of the chest surgery clinic. Ulus Travma Acil Cerrahi Derg 2008, 14:221–5.PubMed Competing

interests Dr. Ramon Vilallonga is president of the Dr. Vilallonga Foundation. The rest of authors, declare that they have no competing interests. Authors’ contributions VR has take care of the patient and has draft the manuscript. PV, AL, CR helped to the clinical assessment and draft of the manuscript. CR, AM and NS have been involved in drafting the manuscript or revising it critically for important intellectual content. All authors read and approved the final manuscript.”
“Introduction A World Society of Emergency Surgery (WSES) Consensus Conference was held in Bologna on July 2010, during the 1st congress of the WSES, involving surgeons, infectious disease specialists, pharmacologists, radiologists and intensivists with the goal of defining recommendations for the early management of intra-abdominal infections. This document represents the executive summary of the final recommendations approved by the consensus conference.

1) demonstrated that treatment with 1 μM and 2 μM for 48 hours insignificantly triggered cell death (P > 0.05 VS control). However, concentrations from 5 μM to 30 μM could markedly inhibit tumor cells (P < 0.01 VS control). The bivariate correlation analysis confirmed the negative relationship between PTL concentrations and cell survival rates and the positive relationship between PTL concentrations and cell inhibition rates. In BxPC-3 cells, EC50 was estimated to be 14.5 μM. Figure 1 PTL inhibited BxPC-3 proliferation. MTT assay demonstrated that PTL can inhibit BxPC-3 cell growth in vitro. Besides, this effect was in a dose-dependent manner. The cell viability and inhibition rates were calculated by comparing with

the control group (100%) Selleck BB-94 Selleckchem Necrostatin-1 after 48 hours treatment. Data were presented as mean ± SD (n = 3). Points, mean; bars, + SD. *, P > 0.05; **, P < 0.01 compared with the control group. PTL induced significant apoptosis in human pancreatic cancer cell To investigate the effect of inducting apoptosis by PTL in BxPC-3 cells, the flow cytometry and DNA fragmentation analysis were preformed. Annexin-V/PI-FACS analysis (Fig. 2A) was applied to quantify the apoptotic phenotype. Annexin-V-positive cells (right quadrant in the density dot plot) were summarized, including early apoptotic and late apoptotic cell death. PTL-treated cells revealed morphologic events of apoptosis more significantly than cells treated with DMSO alone. The inductive

effect of apoptosis presented as a concentration-dependent manner. The apoptosis induced was further confirmed using DNA fragmentation analysis (Fig. 2B). Disintegrated nuclei and nonrandom DNA fragmentation were found on gels. More apoptotic internucleosomal DNA fragmentation was observed after higher concentrations of PTL treatment. These results revealed that PTL effectively induced a dose-dependent apoptosis in human pancreatic cancer cell. Figure 2 PTL induced BxPC-3 apoptosis. BxPC-3 cells were

treated with the indicated concentrations of PTL for 48 hours. (A) The quantification of apoptosis was estimated by Annexin-V/PI-FACS analysis. As apoptotic events Annexin-V-positive cells (right quadrant in the density dot plot) were summarized. (B) DNA Fragmentation Thiamet G Analysis indicated that the cells treated with higher concentrations of PTL showed higher proportions of apoptotic internucleosomal DNA fragmentation. These results revealed that PTL-induced apoptosis in BxPC-3 cells was in a dose-dependent manner. The data was described as mean ± SD (n = 3) and the representative figures are shown. PTL suppressed BxPC-3 cell migration Increased migration rate is one of the characteristics in metastatic cancer cells [13]. Pancreatic cancer is a major health problem due to its high risk of metastasis. Accordingly the wound closure assay (Fig. 3) was used to investigate if PTL influenced migration ability of BxPC-3 cells. Wound gap of similar size was created in monolayer BxPC-3 cells at 0 hour.

Clin Ther 2005, 27: 588–593.CrossRefPubMed

8. Yang HW, Xie YQ, Guo QL: Clinical observation of propofol combined with flurbiprofen axetil for induced abortion anesthesia. Zhong Nan Da Xue Xue Bao Yi Xue Ban 2006, 31: 752–755.PubMed 9. Ou Yang X, Wang W, Peng Y, et al.: Analgesic effect of flurbiprofen axetil injection on cancer pain. Chinese Journal of Pain Medicine 2005, 11: 281–283. 10. Wong DL, Baker CM: Pain in children: comparison of assessment scales. Pediatr Nurs 1988, 14: 9–17.PubMed 11. World Health Organization: Cancer pain relief and palliative care. Geneva: World Health Organization 1990. 12. NCI: Cancer Therapy Evaluation Program, Common Terminology Criteria for Adverse Events. [http://​ctep.​cancer.​gov] Version 3.0 2003. 13. Mizushima Y, Shoji Y, Kato T, Fukushima M, Kurozumi S: Use of lipid microspheres as a drug carrier for antitumour drugs. J Pharm Pharmacol 1986, 38: 132–134.PubMed 14. Washinton C: Stability Selleck BI 10773 of lipid emulsions for drug deliver. Adv Drug Delivery Rev 1996, 20: 131–145.CrossRef 15. Park KM, AG-881 Lee MK, Hwang KJ, Kim CK: Phospholipid-based microemulsions of flurbiprofen by the spontaneous emulsification process. Int J Pharm 1999, 183: 145–154.CrossRefPubMed 16. Yamazaki Y, Sonoda H, Seki S: Effects of preoperatively administered flurbiprofen axetil

on the action of inhaled anesthesia and postoperative pain. Masui 1995, 44: 1238–1241.PubMed 17. Xu G, Li X, Duan L, Zhu T, Xie Q, Zhou Y, Wang B, Deng Y, Shen L, Yuan X: Phase II clinical study for flubiprofen axetil injection in treatment of moderate postoperative pain. Chinese New Drugs Journal 2004, 13: 846–848. 18. Duan L, Li X: Clinical application these of flurbiprofen axetil injection. Chinese New Drugs Journal 2004, 13: 851–852. Competing interests The authors declare

that they have no competing interests. Authors’ contributions HW collected the data and drafted the manuscript, ZC designed this study and modified the manuscript, GS, KG, YP, JH, YD, JN participated in its design and coordination. All authors read and approved the final manuscript.”
“Background Prostate cancer is the most common cancer among men in industrialized countries with the main risk factor being the age of over 50. Prostate cancer is uncommon in men younger than 45, but becomes more common with increasing age. The average age at the time of diagnosis is 65 [1–4]. Since early detection increases the chance of successful treatment, the prostate-specific antigen (PSA) test and the digital rectal examination should be offered to men annually beginning at age 50. Men with high risk should begin testing at age 45. The only well-established risk factors for prostate cancer are age, ethnicity, geography and family history of prostate cancer. However, research in the past few years has shown that genetic, socioeconomic and environmental factors, particularly diet and lifestyle, likely have an effect as well.

CrossRef 4. Baxter JB, Aydil ES: Nanowire-based dye-sensitized solar cells. Appl Phys Lett 2005, 86:053114.CrossRef 5. Huynh AZD4547 chemical structure WU, Dittmer JJ, Alivisatos AP: Hybrid nanorod-polymer solar cells. J Sci 2002, 295:2425.CrossRef 6. Grätzel M: Photoelectrochemical cells.

Nature 2001, 414:338–344.CrossRef 7. Perez M: Iron oxide nanoparticles: hidden talent. Nat Nanotechnol 2007,2(9):535–536.CrossRef 8. Rajeev P, Bagchi A, Kumar G: Nanostructures, local fields, and enhanced absorption in intense light–matter interaction. Optic Letter 2004,29(22):2662–2664.CrossRef 9. Nakayama K, Tanabe K, Atwater H: Plasmonic nanoparticle enhanced light absorption in GaAs solar cells. Appl Phys Lett 2008, 93:121904.CrossRef 10. Kume T, Hayashi S, Yamamoto K: Light emission from surface plasmon polaritons mediated by metallic fine particles. Phys Rev B 1997,55(7):4774–4782.CrossRef 11. Seung H, Choi K, David J, Grigoropoulos CP: Nanosecond laser ablation of gold nanoparticle films. Appl Phys Lett 2006, 89:141126.CrossRef 12. Westin P-O, Zimmermann U, Ruth M, Edoff M: Next generation interconnective laser patterning of CIGS thin film modules. Sol Energy Mater Sol Cells 2011,95(4):1062–1068.CrossRef 13. Compaan AD, Matulionis I, Nakade S: Optimization of Laser Scribing for Thin-Film PV Modules. National

Renewable Energy Laboratory: Golden; 1997. 14. Novotný M, Fitl P, Sytchkova A, Lancok A, Pokorný P, Najdek D, Bocan J: Pulsed laser treatment of gold and black gold thin films fabricated by thermal evaporation. J Phys 2009,7(2):327–331. 15. Hairen T, Rudi S, Smets

AHM, Miro Z: Plasmonic light trapping in thin film silicon cells with improved self assembled silver nanoparticles. 4SC-202 order Nano Lett 2012,12(8):4070–4076.CrossRef 16. Jiang W, Mangham SC, Reddy VR, Manasreh MO, Weaver BD: Surface plasmon enhanced intermediate band based quantum dots solar cell. Sol Energy Mater Sol Cells 2012, 102:44–49.CrossRef 17. Manickam S, Venkatakrishnan K, Tan B, Venkataramanan V: Study of silicon nanofibrous structure formed by laser irradiation in air. Opt Express 2009,17(16):13869–13874.CrossRef 18. Tan B, Venkatakrishnan K: Synthesis of fibrous nanoparticle aggregates by femtosecond laser ablation in air. Opt Exp 2009,17(2):1064–1069.CrossRef 19. Amirkianoosh K, Palneet Singh W, Venkatakrishnan K, Tan B: Synthesis of 3D nanostructured metal alloy this website of immiscible materials induced by megahertz repetition femtosecond laser pulses. Nanoscale Res Lett 2012,7(1):518.CrossRef 20. Mahmood A, Sivakumar M, Venkatakrishnan K, Tan B: Enhancement in optical absorption of silicon fibrous nanostructure produced using femtosecond laser ablation. Appl Phys Lett 2009, 95:034107.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions At the time of this work, ASM was a Ph.D. candidate at Ryerson University. He conducted the experiment, developed the theory, and drafted the manuscript. KV was ASM’s supervisor.

4th edition. Edited by: Perez CA, Brady LW, Halperin

EC, Schmidth-Ullrich RK. Philadelphia, USA: Lippincott Williams and Wilkins Press; 2004:1502–1553. 4. Cho BC, Hurkmans CW, Damen EM, Zijp LJ, Mijnheer BJ: Intensity modulated versus non-intensity modulated radiotherapy in the treatment of the left breast and upper internal mammary lymph node chain: a comparative click here planning study. Radiother Oncol 2002, 62: 127–136.CrossRefPubMed 5. Sonnik D, Selvaraj RN, Faul C, Gerszten K, Heron DE, King GC: Treatment techniques for 3D conformal radiation to breast and chest wall including the internal mammary chain. Med Dosim 2007, 32: 7–12.CrossRefPubMed 6. Thoms WW Jr, McNeese MD, Fletcher GH, Buzdar AU, Singletary SE, Oswald MJ: Multimodal treatment for inflammatory breast cancer. Int J Radiat Oncol Biol Phys 1989, 17: 739–745.CrossRefPubMed 7. Recht A, Edge SB, Solin LJ, Robinson DS, Estabrook A, Fine RE, Fleming GF, Formenti

S, Hudis C, Kirshner JJ, Krause DA, Kuske RR, Langer AS, Sledge GW Jr, Whelan TJ, Pfister DG, American Society of Clinical Oncology: Postmastectomy radiotherapy: clinical practice guidelines of the American Society of Clinical Oncology. J Clin Oncol 2001, 19: 1539–1569.PubMed 8. ICRU 50: Prescribing, recording, and reporting photon beam therapy. Bethesda, MD: International Commission on Radiation Units and Measurements Press; 1993. 9. Thomsen MS, Berg M, Nielsen HM, Pedersen AN, Overgaard M, Ewertz M, Block

T, Brodersen HJ, Caldera C, Jakobsen E, Kamby STI571 solubility dmso C, Kjaer-Kristoffersen F, Klitgaard D, Nielsen MM, Stenbygaard L, Zimmermann SJ, Grau C, Danish Breast Cancer Cooperative Group: OSBPL9 Post-mastectomy radiotherapy in Denmark: from 2D to 3D treatment planning guidelines of The Danish Breast Cancer Cooperative Group. Acta Oncol 2008, 47: 654–661.CrossRefPubMed 10. Pierce LJ, Butler JB, Martel MK, Normolle DP, Koelling T, Marsh RB, Lichter AS, Fraass BA: Postmastectomy radiotherapy of the chest wall: dosimetric comparison of common techniques. Int J Radiat Oncol Biol Phys 2002, 52: 1220–1230.CrossRefPubMed 11. Ung YC, Sixel KE, Bell C: The influence of patient geometry on the selection of chest wall irradiation techniques in post-mastectomy breast cancer patients. Radiother Oncol 2000, 57: 69–77.CrossRefPubMed 12. Vu TT, Pignol JP, Rakovitch E, Spayne J, Paszat L: Variability in radiation oncologists’ opinion on the indication of a bolus in post-mastectomy radiotherapy: an international survey. Clin Oncol (R Coll Radiol). 2007, 19: 115–119. 13. Quach KY, Morales J, Butson MJ, Rosenfeld AB, Metcalfe PE: Measurement of radiotherapy X-ray skin dose on a chest wall phantom. Med Phys 2000, 27: 1676–1680.CrossRefPubMed 14. Hsu SH, Roberson PL, Chen Y, Marsh RB, Pierce LJ, Moran JM: Assessment of skin dose for breast chest wall radiotherapy as a function of bolus material. Phys Med Biol 2008, 53: 2593–2606.CrossRefPubMed 15.

Mod Rheumatol 2007, 17:54–56. 10.3109/s10165-006-0529-8PubMedCrossRef 4. Magill HL, Hixson SD, Whitington G, Igarashi M, Hannissian A: Duodenal perforation in childhood dermatomyositis. Pediatr Radiol

1984, 14:28–30. 10.1007/BF02386727PubMedCrossRef 5. Wang IJ, Hsu WM, Shun CT, Chiang BL, Ni YH: Juvenile dermatomyositis complicated with vasculitis and duodenal perforation. J Formos Med Assoc 2001,100(12):844–846.PubMed 6. Thompson JW: Spontaneous perforation of the esophagus as a manifestation of dermatomyositis. Ann Otol Rhinol Laryngol 1984, 93:464–467.PubMed 7. Niizawa M, Maie O, Asanuma Y, Saito T: Adult dermatomyositis with angiopathy and cecum perforation and panniculitis. Nihon Hifuka Zasshi 1991, 101:447–451. 8. Suwa A, Hirakata M, Hama N, Ishiyama K, Amano K, Tanaka H, Fujimaki J, Mimori T, Inada S, Akizuki M: An adult case of dermatmyositis MK-2206 clinical trial complicated with cecum perforation and panniculitis. Nihon Rinsho Gakkai Kaishi 1997, 20:60–66. 10.2177/jsci.20.60CrossRef 9. Mamyrova G, Kleiner DE, James-Newton L, Shaham B, Miller FW, Rider LG: Late-onset gastrointestinal pain in juvenile dermatomyositis Pritelivir mouse as a manifestation of ischemic ulceration from chronic endarteropathy. Arthritis

Rheum 2007, 57:881–884. 10.1002/art.22782PubMedCrossRefPubMedCentral 10. Zarbalian Y, von Rosenvince EC, Twadell W, Mikdashi J: Recurrent pneumatosis intestinalis in a patient with dermatomyositis. BMJ Case Rep 2013, 23:2013. 11. Chiu SK, Yang YH, Wang LC, Chiang BL: Ten-year experience of juvenile dermatomyositis:

a retrospective study. J Microbiol Immunol Infect 2007,40(1):68–73.PubMed 12. Chen GY, Liu MF, Lee YJJ, Chen WC: Combination of massive mucinosis, dermatomyositis, pyoderma gangrenosum-like ulcer, bullae and fatal intestinal vasculopathy in a young female. Eur J Dermatol 2005,15(5):396–400.PubMed 13. Ghayad E, Tohme A, Ingea H: Digestive manifestastions of juvenile dermatomyositis. A case report and review of the literature. J Med Liban 1993,41(4):240–243.PubMed 14. Downey EC Jr, Woolley MM, Hanson V: Required surgical theraphy in the pediatric patient with dermatomyositis. Arch Surg 1988,123(9):1117–1120. 10.1001/archsurg.1988.01400330093014PubMedCrossRef 15. Miller LC, Michael AF, Kim Y: Childhood dermatomyositis. Rebamipide Clinical course and long-term follow-up. Clin Pediatr (Phila) 1987,26(11):561–566. 10.1177/000992288702601101CrossRef 16. Shullinger JN, Jacobs JC, Berdon WE: Diagnosis and management of gastrointestinal perforations in childhood dermatomyositis with particular reference to perforations of the duodenum. J Pediatr Surg 1985,20(5):521–524. 10.1016/S0022-3468(85)80479-6CrossRef 17. Kaplinsky N, Hod C, Gal-Semo R, Frankl O: Spontaneous duodenal perforation during fulminant dermatomyositis. J Am Med Womens Assoc 1978,33(5):213–214.PubMed 18.

Note that the identification of Al2O3 using XRD is evidential from the previous study [51]. In addition to those solid products, gaseous species such as O2 was also possibly formed. It is interesting to reveal the production of AlNi from the Al/NiO GSK1120212 MIC. As a comparison, the formation of Ni was shown with lower and fewer XRD peaks, while Al still existed as a relatively large amount. Based on these observations, the following reaction was responsible: (7) Figure 5 XRD patterns measured from the reaction product of sample D, 33 wt.% NiO. Note that in this study, MIC Φ = 3.5 contained abundant

Al nanoparticles and thus made the reaction R7 feasible. The propagation of R7 does not necessarily require the completeness of R2 since the decomposition of NiO may occur first and be followed by the reaction between Al and Ni. A further study on elementary reactions related to R2 and R7 is needed in order to gain more insights on this issue. To further characterize these microstructures of the products, the SEM and EDAX analyses were performed on the same product examined

by XRD. Figure 6 shows two typical structures observed from MIC Φ = 3.5: (Figure 6a,c) a sphere which was rich in Ni and Al, and (Figure 6b,d) a bunch of Al2O3 crystalline structures. The coexistence of Ni Capmatinib clinical trial and Al in the sphere is possibly in the form of AlNi. Figure 6 SEM images (a, b) and respective EDX patterns (c, d). They were obtained from the reaction products of sample D, 33 wt.% NiO. In order to further examine the possible formation pathway of the AlNi phase,

ab initio MD simulation Edoxaban was conducted for scoping the reaction time scale and identifying the equilibrium product of the thermite reaction of the Al/NiO MIC. For this simulation, the initial temperature was set to 0 K. At this temperature, the thermodynamic equilibrium structure of an Al crystalline nanoparticle and a NiO nanowire was obtained, as shown in Figure 7a. The system temperature was then increased to 1,000 K (or 726°C) to ignite the reaction. After ignition, the simulation was done under adiabatic condition. It was found that after 5 ps, as shown in Figure 7b, Al atoms diffused through the Al-NiO interface and met with O atoms (while the diffusion of O atoms into the Al nanoparticle was possible but with a much smaller chance, as observed from the image where only one O atom was found in the Al nanoparticle). Meanwhile, Ni atoms were grouped together and were intended to form the pure Ni phase. It was also observed that the AlNi phase exists at the interface between the Al nanoparticle and the NiO nanowire. Accompanying this fast thermite process, the system temperature was increased up to 3,500 K within 5 ps. This MD simulation confirmed the possibility of forming the AlNi phase from the Al-NiO thermite reaction and revealed the diffusion paths of Al and Ni atoms during the thermite reaction.