All authors read and approved the final manuscript “

All authors read and approved the final manuscript.”
“Background Botrytis cinerea is a pathogen ascomycete, which causes gray mold on a large number of economically important agricultural and horticultural crops [1–4]. This ubiquitous fungal pathogen is present often as latent infection. Latency is generally defined as the period between infection and the appearance AZD9291 of visible symptoms and can in the case of B. cinerea be long and variable [5–8]. Consequently, an apparently healthy fruit can deteriorate suddenly due to the development of this latent infection [9, 10]. Many synthetic fungicides are used as the principal mean of controlling

this important postharvest disease [11]. However, the growing public concern over the health and environmental hazards associated with fungicide use in orchards, the development of fungicide resistant strains of B. cinerea [12], and the deregistration of some of the most effective fungicides [13], have generated a great interest in the development of alternative methods to control the postharvest disease caused by this fungal pathogen. To prevent the indiscriminate use of fungicides, a sensitive and reliable method to early determination of the fungus in fruit tissues becomes crucial. The ability to detect latent infections in fruit

tissues should prove useful not only for early disease management but also for identifying infected fruit in postharvest. In addition, the quantification of the pathogen is necessary for the application of alternative methods of control, such as biological control using antagonist microorganisms because the success Ureohydrolase AR-13324 datasheet of this method depend of the ratio antagonist/pathogen [14]. The detection of fungus in fruit includes classical methods such as isolation on selective media, which is useful but subject to limitations [15] due to many pathogens can be masked by overgrowth of faster growing fungi. Other methods, such as quantitative real-time polymerase chain reaction (Q-PCR), or reverse transcription

polymerase chain reaction (RT-PCR) represent new tools for the detection of the pathogens by determination of their DNA/RNA [16–25]. Unfortunately these methods are expensive and not easy to perform routinely, because they require highly qualified personnel and need sophisticated instrumentation [26, 27]. In addition, to methods mentioned previously, some direct enzyme-linked immunosorbent assays (ELISAs) using microtiter plates have been developed for the detection of B. cinerea in pear steam, grape juice, and plants [28–32], but at present has not been reported any validated method based in an indirect competitive immunoassay for detection and quantification of the mentioned fungus in tissues of fruits. The aim of this study was the development and corroboration of a sensitive and specific ELISA for B.

2, red circles and Additional File 5, Table S5) Of these 82 stat

2, red circles and Additional File 5, Table S5). Of these 82 statistically significant altered transcripts, only 4 were commonly altered with the same magnitude by a deletion of vjbR or wildtype cells treated with C12-HSL (Fig. 2). At the exponential growth phase, administration of C12-HSL exerted an equal effect on gene expression, up and down-regulating

19 and find more 23 genes (respectively, Fig. 2). On the contrary, at the stationary phase all 48 genes were up-regulated, a dramatically different profile than the down-regulation observed for the majority of differently expressed genes in C12-HSL treated wildtype cells (Fig. 2). Collectively, this data supports that C12-HSL is capable of influencing gene expression independent of VjbR. There is evidence that C12-HSL may interact with a second LuxR homologue, BlxR [18]. Induction of blxR expression in response to C12-HSL was highly variable by microarray analysis; however, qRT-PCR revealed that blxR was up-regulated 99.5-fold in bacteria lacking HSP inhibitor drugs vjbR treated with C12-HSL, compared to 27.5-fold in wildtype cells that were administered C12-HSL at the stationary growth phase. One possible explanation for this observation is that VjbR inhibits the induction of blxR by binding the AHL substrate and therefore

lowering the cellular concentration of available C12-HSL for blxR induction, but has not been demonstrated. Interestingly, 58% of the gene transcripts found to be altered in an recent study of the function of ΔblxR were also found to be altered by the addition of C12-HSL in the ΔvjbR background, and increased to 88% if we lowered the threshold from our 1.5-fold cutoff (Additional File 5, Table S5) [15]. A second study that similarly examined the transcript and proteomic alterations due to a deletion in babR corresponded with 6 genes identified in our study: with 2 genes found to be unique to the addition of C12-HSL in the ΔvjbR background (BMEI0231 and I1638, Additional File 5, Table S5), and 4 genes additionally altered by the deletion of vjbR or addition

of C12-HSL in the wildtype background (BMEI0451, I0712, I1196 and II0358, Additional File 3, Table S3) [23]. Although Cyclin-dependent kinase 3 many of these genes were not statistically significant in our analyses, this is a strikingly high correlation since the same conditions were not examined (ΔblxR vs. wt compared to ΔvjbR vs. ΔvjbR + C12-HSL), as well as the use of differing microarray platforms and analyses procedures. This connection may suggest that the genes altered by the presence of C12-HSL in the absence of VjbR may be due to C12-HSL activation of BlxR. Conclusions The goal of this work was to provide an elementary understanding in the role of the putative QS components in the virulence and survival of B. melitensis.

Anti-tumor effect of CIK plus L-OHP in the human drug-resistant g

Anti-tumor effect of CIK plus L-OHP in the human drug-resistant gastric cancer cellular peritoneal transplantation model Tumor weight and abdominal circumference were measured 21 days postinoculation (i.e., 7 days after intraperitoneal administration). The mice were sacrificed, and the number of ascites was calculated. The criterion for being cured was 60-day survival after inoculation with tumor cells. Pathomorphological observations in the human drug-resistant gastric cancer cellular peritoneal transplantation model after the treatment of L-OHP and CIK cells Tissue

sections were acquired 24 h after final injection in each group, and macroscopic observation was used to detect changes of P005091 chemical structure peritoneal transplantation nodules. The transplantation nodules in the omentum majus of each mouse were selected and divided into two sections, which were then used for routine pathological sectioning and transmission

electron microscope examination. Statistical analyses All data are expressed as mean ± SD, and buy CAL-101 analyses were carried out using SPSS 12.0 software (SPSS Inc, Chicago, IL). One-way analyses of variance (ANOVA), homogeneity tests for variance and Student’s t-tests were used for comparisons of means. A p-value less than 0.05 was considered statistically significant. Results Cell biological characteristics of OCUM-2MD3/L-OHP cells Morphological observations of drug-resistant cells As is shown in Fig.1A and 1B, the two cell types in suspension appeared round under an inverted phase contrast microscope. Following cell adhesion, cells appeared spindle-shaped, were arranged in a single layer of different sizes, and showed no significant difference in cell morphology. The microvilli on the surface of parental cells were quite abundant under a transmission electron

microscope, and the morphology of organelles in the cytoplasm was normal. The nuclei of the cells appeared abnormally large and were irregularly shaped. Moreover, euchromatin was abundant, heterochromatin was limited, and the nucleolus was large and clearly visible (Fig. 1C). There was no significant difference in morphology of drug-resistant cells compared with OCUM-2MD3 cells. (Fig. 1D). Figure 1 A. OCUM-2MD3 cell (Phase contrast microscope × 400); B. OCUM-2MD3/L-OHP L-NAME HCl cell (Phase contrast microscope × 400); C. OCUM-2MD3 cell (TEM × 5000); D. OCUM-2MD3/L-OHP cell (TEM × 5000). Growth curve and population doubling time of drug-resistant cells As shown in Fig. 2, proliferation speed of drug-resistant cells was slower than that of parental cells. The population doubling time of drug-resistant cells was 27.0 ± 2.04 h by cell counts, which extended for approximately 3 h (P < 0.05). Figure 2 Cell-growth curve of OCUM-2MD3/L-OHP. Cell cycle distribution and apoptosis of drug-resistant cells As shown in Table 1, Fig. 3 and Fig.

It has also been shown that spermine can reduce the inflammatory

It has also been shown that spermine can reduce the inflammatory response by post-transcriptional inhibition of the production of pro-inflammatory cytokines, including TNFα, IL6, MIP-1α, and MIP-1β [19], and even though IL-8 was not included in this study, it is possible that it is regulated by spermine as well. Thus, in the interaction of wild type H. pylori with AGS cells, spermine levels may be elevated in the AGS cells, leading to a dampening of the chemokine/cytokine pro-inflammatory response. These possibilities await selleck screening library further in depth analyses. We performed pair-wise comparison of transcriptome on

the human adenocarcinoma CA4P manufacturer gastric cell line AGS after infection with 26695 wild type, its isogenic rocF- knockout mutant, and a rocF- complemented (rocF+) H. pylori strain, with uninfected AGS cells as a control. The first observation with the microarray analysis was an overall increase in the number of genes that participate in several signaling pathways previously investigated with H. pylori infection, notably with NFKB and AP-1 activation and mitogen-activated protein

kinase (especially ERKs, JNKs, SAPKs) [20], along with JUN-mediated signaling. From this activation cascade, the induction of IL-8 marked the greatest difference between the rocF- mutant H. pylori versus either the WT or the rocF + complemented strain. Our results show

a significant increase of mRNA and protein levels of IL-8 in AGS cells infected with the rocF- mutant strain, suggesting that WT bacteria may be able to control the inflammatory infiltration of immune cells by controlling the production of IL-8, which is a potent chemotactic factor for inflammatory cells, especially neutrophils [21–24]. While many H. pylori factors have been suggested to stimulate IL-8 expression, including peptidoglycan, LPS, CagA, VacA, PicB, IceA, urease (and even ammonia) [25–28], less is known about bacterial factors involved in suppression of cytokine production, especially in epithelial cells. Mechanisms for immune 17-DMAG (Alvespimycin) HCl evasion by H. pylori have been demonstrated, including the presence of a less potent LPS and cholesterol glycosylation [29]; however, fewer studies dealt with reduced host cytokine production as an immune suppressive mechanism, including effects on IL-12 [30–32]. While an increased amount of cytokines can result in histologically more intense gastritis [33], the limitation of this cytokine induction could be an advantage to the bacteria so that it can stay under the radar of the immune system. However, due to the complexity of the H.

Previously, Sedgwick et al [1] reported that the Ada regulon cou

Previously, Sedgwick et al. [1] reported that the Ada regulon could be induced

CA3 during stationary phase and could protect against active alkylators produced by nitrosation of amino acids in non-growing cells. Therefore, an increase in expression of the adaptive response genes, in parallel with expression of the genes producing active alkylators during the stationary phase prevents alkylation damage to DNA and subsequent mutagenesis. Transcriptome and proteome profiles of the ada mutant strain in response to MMS The transcriptional and translational responses of the ada mutant strain to alkylation stress were vastly different from those observed in W3110 strain (Figure 2). In the ada mutant strain, the expression levels of many more genes were significantly changed at 0.5 h after MMS treatment; 932 genes were up-regulated, which was about seven-fold more than that observed in the wild-type strain. Also, 12 genes of known function were down-regulated (Figure 2). The responses of the ada mutant to alkylating agents revealed several common themes, including the activation of genes involved in the transport of ions, sugars and amino acids and in detoxification processes (Figure 4).

This result indicates that the ada mutant cells induce various genes related to influx or efflux of solutes as a means of preventing and repairing alkylation damage. However, unlike the wild-type cells, in which these genes were up-regulated at 3.9 h after MMS treatment, the CX-5461 in vivo expression of transport genes was down-regulated in the ada mutant cells after the initial alkylation

stress was compensated. Based on these results, it can be assumed that the transport system substitutes for the adaptive response system in the ada mutant strain to coordinate the instant activation of the cellular repair systems after MMS treatment. More details are described below. Figure 4 Schematic diagram of up-regulated genes in the MMS-treated E. coli ada mutant strain. The two-component system related to drug or antibiotic resistance and the operons of genes related to respiration and transport are shown. The genes up-regulated more than 2-fold by 0.5 h MMS treatment, based Ribonucleotide reductase on the corresponding untreated control in the ada mutant strain, are indicated in black bold type. Proteome analysis showed variations in the production levels of 21 protein spots; the spot intensities of 18 proteins increased while 3 proteins decreased (Figure 3, Additional file 1: Table S1). Consistent with the transcriptome data, the intensities of proteins involved in metabolism and transport were increased. Proteins that showed significantly increased spot intensities in MMS-treated ada mutant cells at 0.

In this study we administered tylosin at therapeutic doses to hea

In this study we administered tylosin at therapeutic doses to healthy dogs with a pre-existing jejunal fistula and analyzed changes in bacterial communities before, during, and 14 days after cessation of tylosin by 16S rRNA gene pyrosequencing. Our results indicate a previously uncharacterized high species richness in the canine jejunum. Tylosin had a profound effect on the microbial selleck kinase inhibitor composition in the small intestine of dogs. Furthermore, tylosin had also a pervasive effect on specific bacterial taxa, which failed to recover within 14 days. However, these changes were not associated with any short-term clinical signs of gastrointestinal disease in healthy dogs.

Our results illustrate the complexity of

the intestinal microbiota and the challenges associated with evaluating the effect of antibiotic administration on the various bacterial groups and their potential interactions. The results also suggest that the proposed mode of action of an antibiotic on different bacterial genera does not necessarily match the in vivo effects, as several bacterial groups that are considered to be sensitive to tylosin increased in their proportions. Results Animals All dogs tolerated the course of antibiotics well and no obvious side effects (e.g., clinical signs of gastrointestinal disease such as diarrhea) were ABT-263 concentration noted during the study period. The body weights or body condition scores of the dogs did not change during the study. Characterization of the canine small intestinal microbiota A total of 44,069 pyrosequencing GBA3 tags were evaluated across all 15 samples (mean ± SD: 3188 ± 1091 sequencing tags per sample). All dogs showed highly diverse microbial communities within their small intestine. Table 1 lists the mean number of obtained and maximum predicted OTUs and richness estimators at strain (1% dissimilarity), species (3%), and genus (5%) level [19]. At day 0 and at 3% dissimilarity, which is commonly used to describe the species level [19], a range of 25-453 OTUs (mean: 218 OTUs) was observed,

indicating strong inter-individual differences in microbial diversity in the canine jejunum. The Chao 1 and Ace richness estimators were used to estimate the total number of OTUs in the canine jejunum. On day 0 and at 3% dissimilarity, the Chao 1 estimated between 32 and 707 OTUs (mean: 342 OTUs) per sample, and the Ace estimated between 32 and 721 OTUs (mean: 332 OTUs) per sample. To estimate the maximum number of OTUs at various dissimilarities, a Richards equation was fit to the obtained rarefaction curves [20]. Table 1 shows the mean number of maximum predicted OTUs in the canine jejunum: on day 0 (begin of the study) and at 3% dissimilarity (species level), the maximum predicted number of OTUs ranged from 32 to 666 (mean: 293 OTUs). At 1% dissimilarity (strain level), a mean of 950 OTUs (range: 183 to 1,789) was predicted.

For example,

selective thymidylate kinase inhibitors have

For example,

selective thymidylate kinase inhibitors have been developed and showed potent inhibitory effect in vivo against methicillin-resistant Staphylococcus aureus and vancomycin-resistant Enterococcus[22, 23]. Toxicity or side effect of these thymidylate kinase inhibitors to humans remains to be seen. Mycoplasmas, in general, depend on exogenous supply of precursors for their nucleotide biosynthesis because they lack the de novo synthesis of purine and pyrimidine bases. Nucleosides and deoxynucleosides are efficiently taken up and phosphorylated to their respective nucleotides by deoxynucleoside kinases such as thymidine kinase (TK) and deoxyadenosine kinase. Nucleobases are salvaged through hypoxanthine guanine phosphoribosyltransferase (HPRT), adenine phosphoribosyltransferase R406 (APRT) and uracil phosphoribosyltransferase (UPRT) systems [24–32]. P5091 research buy Of a total of 17 enzymes in nucleotide biosynthesis identified in the Mpn genome, 15 are essential. Enzymes mentioned above, TK, HPRT, APRT and UPRT are essential for Mpn survival while thymidylate synthase (TS), an enzyme catalyses the reductive synthesis of thymidylate from uridylate, is not since thyA mutant Mpn strain that lacks TS is viable [31, 33, 34]. In this study, 30 FDA-approved nucleoside and nucleobase analogs that

are anticancer or antiviral drugs were screened for inhibitory effects on Mpn growth. Seven analogs showed potent inhibitory effects on Mpn growth at clinically achievable plasma concentrations.

Among Nutlin-3 them, 6-thioguanine (6-GT) inhibited Mpn growth with a MIC (minimum inhibitory concentration required to cause 90% of growth inhibition) value of 0.20 μg ml-1. To investigate the mechanism of action of these drugs, we studied the effects of these analogs on uptake and metabolism of natural nucleoside and nucleobases by using tritium labelled natural substrates. Furthermore Mpn hypoxanthine guanine phosphoribosyl transferase (HPRT) was cloned and expressed, and the recombinant enzyme was purified and characterized using tritium labelled hypoxanthine and guanine as substrates, and 6-thiuoguanine and other purine analogs as inhibitors. The role of thymidine kinase in the inhibitory effect of trifluorothymidine against Mpn growth was also investigated. Results Inhibition of Mpn growth by nucleoside and nucleobase analogs Some nucleoside analogs have been reported to inhibit Mycoplasma growth [30, 35]. Recently a nucleoside and nucleobase analog library consisting of FDA-approved prodrugs used in anticancer and antiviral therapy was used to screen human enzymes in nucleotide metabolism, and new interactions were found [36], which promoted the use of these analogs in screening for inhibitory effects on Mpn growth.

, Carlsbad, CA, USA) and Oligo(dT) primer Primer sequences, gene

, Carlsbad, CA, USA) and Oligo(dT) primer. Primer sequences, generated using GenBank searches with BLASTN, were used to generate PCR products using Taq DNA polymerase (TaKaRa Ex Taq™ Takara Bio Inc., Kyoto, Japan) and an iCycler thermocycler (Bio-Rad Laboratories, Inc., Hercules, CA, USA). Pilot studies were performed to determine the optimal annealing temperature and to confirm a linear correlation between the number of PCR cycles and the densitometric intensity of amplicons. Samples were analyzed for genomic

DNA contamination by PCR analysis of total RNA. PCR products were size-separated by electrophoresis on 2% agarose gel, NCT-501 mw visualized by ethidium bromide staining under UV light, and analyzed by scanning densitometry. Results were expressed as density of transgelin 2 in relation to β-actin, an internal control, expression within the same sample. Western blotting Western blot detection of transgelin 2 and the internal control β-actin, was performed using standard protocols. In detail, lung tissue specimens from all subjects

were homogenized to obtain protein extracts. The protein lysate was added to one-third volume of the SDS preparation buffer (NuPAGE 4× LDS Sample Buffer, Invitrogen Corp.). These protein samples (50 μg) were separated by 12.5% SDS-polyacrylamide gel electrophoresis. The proteins were then transferred electrophoretically to nitrocellulose membranes, which were incubated with a GM6001 solubility dmso mouse anti-transgelin 2 monoclonal antibody (Santa Cruz Biotechnology Inc., Santa Cruz, CA, USA). After secondary antibody application, immunodetection was performed by enhanced chemiluminescence on X-ray films (Fuji films). The mouse

anti-actin antibody (MAB 1501, Chemicon, Temecula, CA, USA) was used to normalize transgelin before 2 expression. Films were scanned and the protein lanes were quantified using Photoshop CS2 image analysis software (Adobe Systems Inc., San Jose, CA, USA). Results Characteristics of the three nanomaterials The size and shape of nanoparticles were summarized in Figure  1 (1-1). Our characterizations indicated that SiO2 nanoparticles exhibited a crystal structure with an average size of 20.2 nm (Figure  1 (1-1A)), that Fe3O4 nanoparticles had a sphere shape with an average size of 40 nm (Figure  1 (1-1B)), and that CNTs were rope-shaped with lengths <5 μm and diameters of approximately 8 nm (Figure  1 (1-1C)). Each chemical composition was quantitatively analyzed using a Raman spectroscopic technique and showed a purity >99.0% for all three nanomaterials. Pathological observations of the lung Histopathological evaluation of lung tissues revealed that pulmonary exposures to nanoparticles in rats produced persistent and progressive lung inflammatory responses.

Eur Respir J 2013 doi:10 1183/09031936 00149212 erj01492–2012;

Eur Respir J 2013. doi:10.1183/09031936.00149212. erj01492–2012; published ahead of print 29. Dawson D: Potential pathogens among strains of mycobacteria isolated from house-dusts. Med J Aust 1971, 1:679–681.PubMed 30. Reznikov M, Leggo JH, Dawson DJ: Investigation by seroagglutination of strains of the Mycobacterium Alisertib in vivo intracellulare-M. scrofulaceum group from house dusts and sputum in Southeastern Queensland. Am Rev Respir Dis 1971, 104:951–953.PubMed 31. Tuffley RJ, Hollbeche D: Isolation of the mycobacterium avium-M. intracellulare-M. scrofulaceum

complex from tank water in Queensland, Australia. Appl Environ Microbiol 1980, 39:48–53.PubMed 32. McSwiggan DA, Collins CH: The isolation of M. kansasii and M. xenopi from water systems. Tubercle 1974, 55:291–297.PubMedCrossRef 33. September S, Brozel V, Venter S: Diversity of nontuberculoid mycobacterium species in biofilms of urban and semiurban drinking water

distribution systems. Appl Environ Microbiol 2004, 70:7571–7573.PubMedCrossRef 34. Van Ingen J, Boeree M, Dekhuijzen P, Van Soolingen D: Environmental sources of rapid growing nontuberculous mycobacteria causing disease in humans. Clin Micro Inf 2009, 15:888–892.CrossRef 35. Huang W-C, Chiou C-S, Chen J-H, Shen G-H: Molecular epidemiology of Mycobacterium abscessus in a subtropcal chronic ventilatory setting. J Med Micro 2010, 59:1203–1211.CrossRef 36. Pedley SBJ, Rees G, Dufour A, Cotruvo J: Pathogenic Mycobacteria in Water. London: IWA Publishing; 2004. 37. Feazel L, Baumgartner L, Peterson K, Frank D, Harris J, Pace N: Opportunistic Urease pathogens enriched in showerhead biofilms. PNAS 2009, 106:16393–16399.PubMedCrossRef Authors’ contributions

RT designed the study, coordinated the collection of samples, participated in the processing of water samples, collated and analysed the data, and wrote the manuscript. RC coordinated, received and processed the water samples (including subculturing and sequencing), collated the results and reviewed the manuscript. CT processed water samples, performed sequencing and collated results.CC contributed to the study design, provided institutional support and reviewed the manuscript. FH intellectually contributed to the study design and methodology and the writing of the manuscript. MH intellectually contributed to the study design and methodology, liaised with Brisbane Water, and contributed to the writing of the manuscript. All authors read and approved the final manuscript.”
“Background Legionella pneumophila is the major cause of sporadic cases and outbreaks of legionellosis (91.5%), with sero-group 1 being the predominant serotype (84.

​wjes ​org/​supplements/​7/​S1 References 1 Country Profiles: 2

​wjes.​org/​supplements/​7/​S1. References 1. Country Profiles: 2009: Top 20 Countries in ALL FIELDS, 1999- August 31, 2009 Avaible at: http://​sciencewatch.​com/​dr/​cou/​pdf/​09decALL.​pdf. Avaible at: . 2. Heldwein FL, Hartmann AA, Kalil AN, Neves BVD, Ratti GSB, Beber MC Jr, et al.: Cited Brazilian papers in general surgery between 1970 and

2009. Clinics 2010,65(5):521–529.PubMedCrossRef 3. Waiselfisz JJ: Captisol order Map of Violence 2011. The young people of Brazil. Brasília: Ministry of Justice 2009. 4. Reichenheim ME, Souza ER, Moraes CL, Jorge MHPM, Silva CMFP, Minaya MCS: Violence and injuries in Brazil: the effect, progress made, and challenges ahead. Lancet 2011, 377:1962–1975.PubMedCrossRef 5. Paim J, Travassos C, Almeida C, Bahia L, Macinko J: The Brazilian health system: history, advances, and challenges. Lancet 2011, 377:1778–1797.PubMedCrossRef 6. Victora GC, Barreto ML, Leal MC, Monteiro CA, Schmidt MI, Paim J, et al.: Health conditions and health-policy innovations in Brazil: the way forward. Lancet 2011, 377:2042–2053.PubMedCrossRef 7. Almeida-Filho A: Higher education and health care in Brazil. Lancet 2011, 377:1898–1900.PubMedCrossRef 8. Birolini D: Trauma: social and medical challenge. J Am Coll Surg 2008,207(1):1–6.PubMedCrossRef 9. Green SM: Trauma surgery: discipline in crisis. Ann Emerg Med 2009, 53:198–207.PubMedCrossRef 10. The Committee to Development the Reorganized Specialty of Trauma, Surgical Critical

Care, and Emergency Surgery: Acute Care Surgery: Trauma, Critical care, and Emergency Surgery. J Trauma 2005, 58:614–616.CrossRef 11. ISI Web of knowledge database Available

Selleckchem RXDX-101 at: http://​apps.​isiknowledge.​com. Available at: . 12. Ministry of Health Department of Science and Technology, Ministry of Science, Technology and Strategic Inputs: Decentralization in the context of promoting health research. Rev. Saúde Pública 2011,45(3):626–630. 13. Marques F: Advances and challenges. Fapesp 2011, 185:26–33. 14. Berwanger O, Riberio RA, Finkelsztejn A, Watanabe M, Suzumura EA, Duncan BB, et al.: The quality of reporting DNA ligase of trial abstracts is suboptimal: Survey of major general medical journals. Journal of Clinical Epidemiology 2009, 62:387–392.PubMedCrossRef 15. Ciesla DJ, Moore EE, Moore JB, Johnson JL, Cothren CC, Burch JM: The Academic Trauma Center Is a Model for the Future Trauma and Acute Care Surgeon. J.Trauma 2005,58(4):657–662.PubMedCrossRef 16. Schimidt MI, Duncan BB, Silva GA, Menezes AN, Monteiro AC, Barreto SM, et al.: Chronic non-communicable diseases in Brazil: burden and current challenges. Lancet 2011, 377:1949–1961.CrossRef 17. Mello Jorge M, Koizumi M: Traffic accidents in Brazil: an atlas of their distribution. In São Paulo. ABRAMET; 2007. 18. Krug EG, Dahlberg LL, Mercy JA, Zwi AB, Lozano R: World report on violence and health. Geneva: World Health Organization; 2002. 19. WHO: Age-standardized mortality rates by cause (per 100 000 population). Geneva: World Health Organization; 2008. 20.