AmJTrop Med Hyg 2009, 81:67–74. 22. Willems H, Thiele D, Frolich-Ritter R, Krauss H: Detection of Coxiella burnetii in cow’s CB-839 research buy milk using the polymerase chain reaction (PCR). Zentralbl Vet B 1994, 41:580–587. 23. Berri M, Laroucau K, Rodolakis A: The detection of Coxiella burnetii from ovine genital swabs, milk and fecal samples by the use of a single touchdown polymerase chain reaction. Vet Microbiol 2000, 72:285–293.PubMedCrossRef 24. Barandika JF, Hurtado A, García-Esteban C, Gil H, Escudero R, Barral M, Jado I, Juste RA, Anda P, García-Pérez AL: Tick-borne Stattic zoonotic bacteria in wild and domestic small mammals in northern Spain. Appl Environ Microbiol

2007, 73:6166–6171.PubMedCrossRef 25. Jado I, Escudero R, Gil H, Jiménez-Alonso MI, Sousa R, García-Pérez AL, Rodríguez-Vargas M, Lobo B, Anda P: Molecular method for identification of Rickettsia species in clinical and environmental samples. J Clin Microbiol 2006, 44:4572–4576.PubMedCrossRef 26. Montejo-Baranda M, Corral-Carranceja J, Aguirre-Errasti C: SHP099 nmr Q fever in the Basque Country: 1981–1984. Rev Infect Dis 1985, 7:700–701.PubMedCrossRef 27. Montes M, Cilla G, Vicente D, Nieto V, Ercibengoa M, Perez-Trallero E: Gipuzkoa, Basque Country, Spain (1984–2004): a hyperendemic area of Q fever. Ann N Y Acad Sci 2006, 1078:129–132.PubMedCrossRef 28. Alarcón A, Villanueva JL, Viciana P, López-Cortés L, Torronteras R, Bernabeu

M, Cordero E, Pachón J: Q fever: epidemiology, clinical features and prognosis. A study from 1983 to 1999 in the South of Spain. J Infect 2003, 47:110–116.PubMedCrossRef 29. Bolaños M, Santana OE, Pérez-Arellano PIK-5 JL, Ángel-Moreno A, Moreno G, Burgazzoli JL, Martín-Sánchez AM: Fiebre Q en Gran Canaria: 40 nuevos casos. Enferm Infecc Microbiol Clin 2003, 21:20–23.PubMedCrossRef

30. Lepe JA, Guerrero FJ, Ruiz-Calderón A, del Castillo E, Gómez-Salvago S, Jiménez-Alonso MA, Palomo S, Perea R: Epidemiología de la fiebre Q en la zona norte de Huelva. Enferm Infecc Microbiol Clin 1999, 17:65–68.PubMed 31. Pascual-Velasco F, Borobio MV, González Z, Carrascosa M: Clinical presentation of acute Q fever in Lanzarote (Canary Islands): a 2-year prospective study. Scand J Infect Dis 1996, 28:533–534.PubMedCrossRef 32. Rivero A, Zambrana JL, Pachón J: Fiebre de duración intermedia. Enferm Infecc Microbiol Clin 2003, 21:147–152.PubMed 33. Romero-Jiménez MJ, Suárez-Lozano I, Fajardo JM, Benavente A, Menchero A, de la Iglesia A: Hepatitis como manifestación única de la fiebre Q: características clínicas y epidemiológicas en 109 pacientes. Enferm Infecc Microbiol Clin 2003, 21:193–195.PubMedCrossRef 34. Millán Mon A, Argany Fajardo A, Febles Bethencourt J, González Caloca C, Vento Remedios TE, Fernández Cabrera M: Fiebre Q en la isla de La Palma. Revisión de 35 pacientes. An Med Interna 1989, 6:527–530.PubMed 35.

Most species within the Salmonella and Shigella genera do not have the check details ability to ferment lactose. However, Shigella sonnei may ferment lactose, but only after extended incubation [31]. ChromID ESBL, Brilliance ESBL and BLSE agar are available as “ready to use” plates from the producers, while CHROMagar ESBL is sold as a powder base. Statistical analyses The calculation of the sensitivity for detecting ESBL-carrying isolates for each screening agar was based on a total of 87 isolates, Palbociclib 51 isolates carrying ESBLA genotypes and 36 carrying AmpC genotypes. The single isolate which was

both ESBLA – and AmpC positive was counted as an AmpC in the statistical analysis. For each agar plate the total sensitivity was calculated (ESBLA + AmpC) (n = 87), as well as the sensitivity for ESBLA and AmpC alone (n = 51 and n = 36, respectively). A 95% confidence interval (95% CI) for each value was manually calculated using binomial proportions’ confidence interval. Results The ESBL genotyping results are shown in Tables 2 and 3. The genotypic characterisation enabled prediction of growth and color JQ-EZ-05 mouse of the colonies growing on the various media. The expected outcome was compared with the observed results. The expected colony colours for Salmonella spp. and Shigella sonnei on each ESBL screening agar are shown in Figure 1. The grading of growth for the 87 isolates is presented in Tables 4 and 5, respectively. The calculated sensitivity is presented

in Table 6. Table 2 Distribution of ESBL-genes in the 87 isolates   ESBL A ESBL A + AmpC AmpC Total   CTX-M SHV-12 CTX-M −15 + SHV-12 TEM-63 + CMY-2 CMY-2 DHA-1   Salmonella 26 3 4 1 33 1 68 Shigella 18 0 0 0 1 0 19 Total 44 3 4 1 34 1 87 Table 3 Genotypes within the CTX-M-isolates   Salmonella Shigella CTX-M-1 1 0 CTX-M-3 ADP ribosylation factor 0 1 CTX-M 3/22 1 0 CTX-M-9 1 0 CTX-M 14/17/18 7 1 CTX-M 15 16 15 CTX-M-27 0 1   26 18 Figure 1 Picture of normal

growth of Salmonella (left) and Shigella sonnei (right) with ESBL genotypes. All ESBL positive isolates were mixed with a fecal suspension controlled for the absence of Salmonella, Shigella and any other ESBL-producing bacteria, before being inoculated onto the screening agars. The Lactose and XLD agars (top) were used as controls. a = Salmonella, b = Shigella sonnei, 1 = Lactose + XLD (control agars), 2 = BLSE agar, 3 = Brilliance ESBL, 4 = ChromID ESBL, 5 = CHROMagar ESBL. Table 4 Grading of growth of 68 ESBL A – and/or AmpC-producing Salmonella isolates (n=68) Growth Excellent Good Poor No growth   ESBL A AmpC ESBL A AmpC ESBL A AmpC ESBL A AmpC Brilliance ESBL 31 9 1 5 1 17   4 BLSE agar* – Drigalski 31 35 1       1   BLSE agar* – Mac Conkey 31 34   1 1   1   CHROMagar ESBL 32 4 1 4   14   13 ChromID ESBL 33 12   16   4   3 All ESBL-producing isolates were mixed with a fecal suspension controlled for the absence of Salmonella, Shigella and any other ESBL-producing bacteria, before being inoculated on the screening agars.

If we can control the z-distance between the

nanoemitter and the Au nanoarray, it is possible to manipulate the LDOS enhancement as well as the light emission rate. Moreover, the large field and LDOS enhancement can also be demonstrated by the PL measurement [33, 45], and these detailed experimental results can be found in Additional file 1: Figure S4. Since the emission rate selleck chemicals of nanoemitters is proportional to the LDOS, the increase of LDOS greatly confirms the utilization of the Au GDC-0941 mouse nanoarray for light emission-manipulating nanoantennas. The light emission rate manipulation experiment was set up using a time-correlated single-photon counting system [45], and the normalized time-resolved PL spectra are shown in Figure 4. The nanoemitters were commercial quantum dots with emission peak located at 655 nm, and the wavelength of incident laser was tuned to 400 nm with the excitation power of 2 mW. Figure 4a shows the LDOS enhancement in the presence of a dipole with an emission wavelength of 655 nm at 10 nm above the Au nanoarray. An average enhancement of 64 times can be found

I-BET-762 price from the calculation results. Compared with the average LDOS enhancement of 75 times at the emission wavelength of 792 nm, it can be seen that the LDOS enhancement region of the Au nanoarray is quite large, which can make the Au nanoarray find useful applications in the design of functional plasmonic devices. In Figure 4b, the PL decay trace of the QDs on SiO2 substrate and pure AAO are single exponential

with the corresponding emission rate τ = 0.0429 ns−1 on SiO2 and τ = 0.0559 ns−1 on pure AAO. The single-exponential decay trace indicates that the cooperative effects caused by the assembling of QDs can be neglected [18]. On the contrary, the time-resolved PL curve of QDs on Au nanoarray decays in a two-component exponential form: where A f and A s are the weight factors of the fast and slow decay processes, Glutamate dehydrogenase respectively, and t f and t s are the corresponding lifetimes (emission rate τ = 1/t). The two-component exponential decay form suggests the strong interaction between QDs and Au nanoarrays. Figure 4 LDOS enhancement and the normalized time-resolved PL spectra of QDs on Au nanoarray. (a) The x-position dependence of LDOS enhancement at the wavelength of 655 nm. An average LDOS enhancement of 64 times can be achieved. (b) The normalized time-resolved PL spectra of QDs with emission peak located at 655 nm. The emission rate of QDs increases from 0.0429 to 0.5 ns−1 by the existence of the Au nanoarray, showing an enhancement of 10.7 times. From the data in Figure 4, t s is 23.3 ns, while t f is 2.0 and 3.4 ns for QDs on uniform and nonuniform Au nanoarrays, respectively.

More fluid is absorbed, increasing the size and pressure within the injured liver parenchyma until a breaking point is reached, tearing the tissue and causing bleeding. Such bleeding

may either be sustained and form a pseudoaneurysm, create an arteriovenous fistula, or break into the peritoneal cavity. In the latter case, bleeding may be life threatening. Our patient developed all three possible types of late vascular complications. The first event of active intraperitoneal bleeding occurred two weeks after the accident. A review of the literature revealed only one description of such a late bleeding in adults [7]. In this case the patient received 51 units of PC in order to deal with combined liver and spleen hemorrhage. In contrast to our case the patient, eventually, selleck chemicals llc died. To our knowledge, there

was no report of successful treatment after two weeks delayed bleeding from blunt liver trauma in adults and therefore our should be the first case to be published. Goettler et al. [8] published a case in 2002 describing delayed bleeding after blunt liver trauma in a pediatric patient. They reviewed the literature and found 11 such cases in children. The delay ranged from 8 hours to one month post trauma. The presentation included abdominal pain, hemodynamic instability and decreased hematocrit. A significant resulting problem that we encountered was the handling of liver parenchyma during laparotomy. Usually, the trauma surgeon handles the liver parenchyma during laparotomy relatively early, within hours from the injury. At that time the consistency of the https://www.selleckchem.com/products/bms-345541.html liver parenchyma is relatively normal. In our case, 15 days post trauma, we found a spongy, soft and very fragile liver parenchyma

which was torn very easily and was difficult to handle. In consequence, we had to perform a damage control laparotomy only with packing of the liver. It appears that the first angiography performed shortly after this operation was prompted by a false alarm, as it did not detect ADAMTS5 any signs of active bleeding. Kazar et al. [2] who reviewed the treatment of blunt liver trauma in adults, offered an algorithm that summarized the treatment. Based on the possible great delay in bleeding, we suggest that patients with complex blunt liver trauma (grades IV and V) who are managed nonoperatively, be followed by frequent US examinations, starting soon after the patient is stable. Such examinations may detect an increase in the size of the intrahepatic clots and GW-572016 datasheet parenchymal damage, indicating that a delayed bleeding may occur. Increased amounts of intraperitoneal fluid and suspicious changes in the liver texture should alert the surgeon and promote further imaging and angiographic studies. Such patients should be kept hospitalized to allow immediate surgery, should sudden massive intraperitoneal bleeding occur.

5×105 cells/well. Total RNA was extracted from CCA cell lines using

TRIzol® reagent following the manufacturer’s instructions (Invitrogen). Total RNA was isolated using a previously Verteporfin described method [20]. Total RNA (1 μg) was reverse transcribed in a 20 μL reaction mixture, containing 0.5 μg of oligo(dT)15 primer, 20 U of RNasin® ribonuclease inhibitor, and 200 U of ImProm-II™ reverse transcriptase in BIBF 1120 price 1× PCR buffer, 3 mmol/L MgCl2, and 1 mmol/L dNTPs. The first-strand cDNA was synthesized at conditions of 42°C for 60 min. The reverse transcription products served as templates for real-time PCR. PCR amplification was performed using specific primers for the NQO1, wild type p53 and the internal control using β-actin. The primer sequences were as follows: 1) NQO1 (NM_000903.2): forward primer 5’-GGCAGAAGAGCACTGATCGTA-3’ and reverse primer 5’-TGATGGGATTGAAGTTCATGGC-3’;

2) wild type p53 (NM_005256778.1) [25]: forward primer 5’-ATGGAGGAGCCGCAGTCAGATCC-3’ and reverse primer 5’-TTCTGTCTTCCCGGACTGAGTCTGACT-3’; 3) β-actin: forward primer 5’-TGCCATCCTAAAAGCCAC-3’ and reverse primer 5’-TCAACTGGTCTCAAGTCAGTG-3’. The real-time fluorescence PCR, based on EvaGreen® dye, was carried out in a final volume of 20 μL containing 1x SsoFast™ EvaGreen® supermix (#172-5200; Bio-Rad, CA, USA), 0.5 μmol/L see more of each NQO1 or wild type p53, and 0.25 μmol/L of β-actin primer. Thermal cycling was performed for each gene in duplicate on cDNA samples in 96-well reaction plates using the ABI 7500 Sequence Detection system (Applied Biosystems). Nintedanib A negative control was also included in the experimental

runs. The negative control was set up by substituting the template with DI water. Real-time PCR was conducted with the following cycling conditions: 95°C for 3 min, followed by 40 cycles of 95°C for 15 s and 60°C for 31 s. To verify the purity of the products, a melting curve analysis was performed after each run. Upon completion of 40 PCR amplification cycles, there was a dissociation step of ramping temperature from 60°C to 95°C steadily for 20 min, while the fluorescence signal was continually monitored for melting curve analysis. The concentration of PCR product was calculated on the basis of established standard curve derived from serial dilutions of the positive control for NQO1, wild type p53 and β-actin in the CCA cell lines. Western blot analysis After treatment with chemotherapeutic agents, CCA cells were washed with PBS, collected, and lysed at 4°C with 1x cell lysis buffer with 1 mmol/L dithiothreitol and 0.1 mmol/L phenylmethylsulfonyl fluoride (PMSF) with vigorous shaking. After centrifugation at 12,000 g for 30 min, supernatant was collected and stored at -80°C until use. Thirty microgram of the protein samples were mixed with 5x loading-dye buffer, heated at 90°C for 10 min, and proteins were then separated by electrophoresis in 10% SDS-polyacrylamide gel.

This finding

suggests that the full virulence of E. coli RS218 requires both chromosomal and plasmid-located genes. Further studies including in depth CP673451 analysis of RS218 chromosome will advance our understanding of NMEC pathogenesis. Conclusions Incomplete understanding of NMEC pathogenesis is a major hindrance that has been identified and pointed this website out by many scientists particularly in relation to formulation of novel therapeutic and prevention strategies for neonatal meningitis. The plasmid pRS218 in NMEC RS218 strain belongs to IncFIB/IIA subset of virulence plasmids in pathogenic E. coli. These plasmids harbor many virulence traits that are required for bacterial survival inside the host. The nucleotide sequence of pRS218 showed selleck screening library a greater similarity to the plasmids of E. coli associated with acute cystitis than the plasmids from NMEC. However, the prevalence of pRS218 virulence-related

genes was significantly higher in NMEC strains tested than fecal commensal E. coli. We have also demonstrated that the pRS218 is involved in NMEC pathogenesis using both in vivo and in vitro experiments. Future studies on pRS218 transcriptome analysis, identification of plasmid-located genes responsible for current observations and in-depth analysis of E. coli RS218 whole genome will likely broaden our knowledge of NMEC pathogenesis. Methods Bacterial strains and media The prototype NMEC strain E. coli RS218 (O18: H7: K1) and NMEC strain EC10 (O7: K1) were kindly provided Dimethyl sulfoxide by Dr. James Johnson (Department of Medicine, University of Minnesota, Minneapolis, MN). Both E. coli RS218 and EC10 strains have been isolated from cerebrospinal fluid of neonates diagnosed with bacterial meningitis (15). A total of 51 NMEC strains which were isolated from neonatal meningitis cases were also obtained from Dr. K.S. Kim

(School of Medicine, John Hopkins University, Baltimore, MD) and 49 fecal E. coli strains isolated from feces of healthy individuals were obtained from the E. coli Reference Center (Pennsylvania State University, University Park, PA). All E. coli were stored in Luria Bertani broth (LB) at -80°C until further use. Bacteria were grown in MacConkey agar or LB broth. All bacteriologic media were purchased from Becton, Dickinson and Company (BD), Sparks, MD. Plasmid isolation, sequencing, assembly and annotation Sequencing of pRS218 was performed as a part of a project that sequenced the whole genome of E. coli RS218. The genomic DNA including the plasmid DNA was extracted using phenol-chloroform method as described previously [33]. The DNA preparation was further cleaned using Genomic Tips (Qiagen, Valencia, CA) [33]. Whole genome sequencing was performed using Ion Torrent PGM Technology (Life Technologies, Carlsbad, CA) at the Genomics Core Facility (Pennsylvania State University, University Park, PA).

Genotypes connected by a shaded background differ by a maximum of 2 of the 10 VNTR markers and could be considered a “”clonal complex”". Thick connecting lines represent one marker difference; regular connecting lines represent two marker differences; thick interrupted lines represent three differences; thin interrupted lines represent four or more differences. The length of each branch is also proportional to the number of difference. Each epidemiological CYC202 cost situation is represented by a specific colour: red for isolates collected during an epidemiological survey conducted in the same duck farm in 2007 and 2008 in

Sarthe region, France; salmon pink for isolates collected during an epidemiological survey conducted in another single duck farm in 2007 and 2008 in Sarthe region, France; navy blue for isolates collected during an epidemiological survey in a chicken farm in 2008 in Guangxi province, China; light blue for isolates collected during an epidemiological survey in a duck farm in 2008 in Guangxi province, China; green

for environmental isolates collected in 2009 in a turkey hatchery in Maine et Loire region, France and yellow for unrelated isolates. Large ellipses correspond to the three major clusters (with the colour of the majority LB-100 order of the genotypes). Discussion Typing A. fumigatus isolates may help to improve the understanding of the distribution of this major pathogen in different situations and environments, including susceptible birds in poultry farms. This molecular approach may also give a deeper understanding of the colonization pattern of putative hosts. To date, it is still a matter of controversy

find more whether certain isolates are more virulent and genetically distinct from other isolates, or whether infection by A. fumigatus is simply a matter of contracting infection from any environmental source. www.selleck.co.jp/products/cobimetinib-gdc-0973-rg7420.html The choice of a specific typing technique depends on the scientific questions and the equipment of the laboratory. Many different techniques have already been described for A. fumigatus: Random Amplified Polymorphic DNA (RAPD) [19], Restriction Enzyme Analysis (REA) [20], Restriction Fragment Length Polymorphism (RFLP) [21], Amplified Fragment Length Polymorphism (AFLP) [22], Microsatellite Length Polymorphism (MLP) [23–27] and Multilocus Sequence Typing (MLST) [28]. CSP typing is a recently developed typing strategy that involves DNA sequence typing of a repetitive region of the A. fumigatus AFUA_3G08990 gene coding for a Cell Surface Protein, designated the CSP locus [29, 30]. All of these typing techniques were developed in order to resolve closely related isolates for the purposes of outbreak investigation in hospitals and disease surveillance in humans. RFLP (with Afut1 probe) and MLP typing methods were proved to be highly discriminant. Furthermore MLP showed high reproducibility because of the unambiguous data.

Z Kinderchir 1984, 39:46–49.PubMed 11. Jansen PL, Sturm E: Genetic cholestasis, causes and consequences for hepatobiliary transport. Liver Int 2003, 23:315–322.PubMedCrossRef 12. Trauner M, Crenigacestat chemical structure Wagner M, Fickert P, Zollner G: Molecular regulation of hepatobiliary transport systems: clinical implications for understanding and treating cholestasis. J Clin Gastroenterol 2005, 39:S111-S124.PubMedCrossRef 13. Paulusma CC, Kool M, Bosma PJ, Scheffer GL, ter Borg F, Scheper RJ, Tytgat GN, Borst P, Baas F, Oude Elferink RP: A mutation in the human canalicular multispecific organic anion transporter gene causes the Dubin-Johnson syndrome. Hepatology 1997, 25:1539–1542.PubMedCrossRef

14. Sookoian S, Castaño

G, Burgueño A, Gianotti TF, Pirola CJ: Association of the multidrug-resistance-associated protein gene AZD1480 chemical structure Nutlin3a (ABCC2) variants with intrahepatic cholestasis of pregnancy. J Hepatol 2008, 48:125–132.PubMedCrossRef 15. Oswald M, Kullak-Ublick GA, Paumgartner G, Beuers U: Expression of hepatic transporters OATP-C and MRP2 in primary sclerosing cholangitis. Liver 2001, 21:247–253.PubMedCrossRef 16. Yamada T, Arai T, Nagino M, Oda K, Shoda J, Suzuki H, Sugiyama Y, Nimura Y: Impaired expression of hepatic multidrug resistance protein 2 is associated with posthepatectomy hyperbilirubinemia in patients with biliary Selleckchem Venetoclax cancer. Langenbecks Arch Surg 2005, 390:421–429.PubMedCrossRef 17. Fardel O, Jigorel E, Le Vee M, Payen L: Physiological, pharmacological and clinical features of the multidrug resistance protein 2. Biomed Pharmacother 2005, 59:104–114.PubMedCrossRef 18. Nies AT, Keppler D: The apical conjugate efflux pump ABCC2 (MRP2). Pflugers Arch 2007, 453:643–659.PubMedCrossRef

19. Wagner M, Zollner G, Trauner M: New molecular insights into the mechanisms of cholestasis. J Hepatol 2009, 51:565–580.PubMedCrossRef 20. Geier A, Wagner M, Dietrich CG, Trauner M: Principles of hepatic organic anion transporter regulation during cholestasis, inflammation and liver regeneration. Biochim Biophys Acta 2007, 1773:283–308.PubMedCrossRef 21. Denson LA, Auld KL, Schiek DS, McClure MH, Mangelsdorf DJ, Karpen SJ: Interleukin-1beta suppresses retinoid transactivation of two hepatic transporter genes involved in bile formation. J Biol Chem 2000, 275:835–8843.CrossRef 22. Denson LA, Bohan A, Held MA, Boyer JL: Organ-specific alterations in RAR alpha: RXR alpha abundance regulate rat Mrp2 (Abcc2) expression in obstructive cholestasis. Gastroenterology 2002, 123:599–607.PubMedCrossRef 23. Roelofsen H, Schoemaker B, Bakker C, Ottenhoff R, Jansen PL, Elferink RP: Impaired hepatocanalicular organic anion transport in endotoxemic rats. Am J Physiol 1995, 269:G427-G434.PubMed 24.

There is therefore a strong rationale for using PND-1186 price anti-CTLA-4 therapy to treat elderly patients with metastatic melanoma in order to enhance adaptive immunity AZD0530 concentration against this disease. Most data regarding the use of ipilimumab in older patients are provided by

EAP analyses. The EAPs are a valuable source of information regarding the efficacy and safety of ipilimumab outside of clinical trials, but they are also subject to limitations due to their retrospective, nonrandomised nature and the specific data collected. For example, the effect of patient comorbidities on the efficacy and safety of ipilimumab in elderly patients treated in the Italian EAP could not be assessed, as only limited comorbidity data were collected as part of the programme. In addition, it was not possible to stratify patients by activities of daily learn more living (ADL) and instrumental ADL scales, which would have better characterised the patient population. However, these preliminary results suggest that ipilimumab is a safe and effective treatment option for elderly patients with metastatic melanoma. Continued follow-up in this patient population will

provide long-term efficacy and safety results. Conclusions Results from this analysis of elderly patients with advanced melanoma treated as part of an EAP in Italy suggest that ipilimumab 3 mg/kg is a well-tolerated treatment option, providing clinical benefit and extending survival in these patients. In addition, the clinical

activity and safety profiles of ipilimumab in patients aged > 70 years were consistent with those observed in the wider population of the EAP. Although this analysis is subject to limitations, these results suggest that age should not be a deciding factor when considering whether to use ipilimumab to treat patients with advanced melanoma. Acknowledgements The authors would like to thank the patients and investigators who participated in the European EAP. Funding This work was supported in part by the Associazione Italiana per la Ricerca sul Cancro, why the Italian Ministry of Health, via the Ricerca Finalizzata 2010. The EAP was sponsored by Bristol-Myers Squibb (BMS). Editorial and writing assistance was provided by StemScientific, funded by BMS. Statistical support was provided by Clinical Research Services, funded by BMS. References 1. Balch CM, Gershenwald JE, Soong SJ, Balch CM, Gershenwald JE, Soong SJ, Thompson JF, Atkins MB, Byrd DR, Buzaid AC, Cochran AJ, Coit DG, Ding S, Eggermont AM, Flaherty KT, Gimotty PA, Kirkwood JM, McMasters KM, Mihm MC Jr, Morton DL, Ross MI, Sober AJ, Sondak VK: Final version of 2009 AJCC melanoma staging and classification. J Clin Oncol 2009, 27:6199–6206.PubMedCentralPubMedCrossRef 2.

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