460 research outputs found
Abstracts of oral and poster presentations given at the Ascochyta 2012 Workshop, Córdoba, Spain, 22–26 April 2012
The third International Ascochyta Workshop was held in Córdoba, Spain 22 - 26 April 2012. This meeting was attended by 70 participants, and 33 oral presentations, 17 posters and 4 invited speeches were presented dealing with Ascochyta blights of the cool season food legumes (peas, lentils, chickpeas and faba beans). In addition, a special session was held on “Food legumes Research in North Africa”. Abstracts of the oral presentations and the posters of the congress are presented in this issue
Genetic Diversity in Rosa as Revealed by RAPDs
We aim to study the variability within genus Rosa. To accomplish this we have analyzed a plant material collection (109 accessions) including all sections but one, as well as many intermediate forms and hybrids. We also aim to study the consistency of the groups considered within section Caninae (‘caninae’, ‘rubiginosa’ and ‘tomentosa’) as well as of the subgenus Hulthemia. A dendrogram was constructed based on RAPDs data. The variability found in the dendrogram was discussed according to sectional status and geographic origin. Our results indicate that there is no clear distinction between Caninae groups when many intermediate forms are considered. Besides, the subgenus Hulthemia seems to merit just a sectional status as proposed by other authors for other subgenus. The heterogeneity found in the dendrogram with respect to sectional status suggests the lack of clear reproductive barriers as is common with long lived woody perennial plants. Sect. Cassiorhodon may be considered as the Type of the genus since it shows the widest geographical distribution, the widest crossing ability within the Genus and it appears in most groups of the dendrogram suggesting to be the most representative Section
Internet et les cartes géographiques : création d\u27un répertoire thématique sur le web en vue d\u27enrichir le site existant
Systemic antibiotic prophylaxis to reduce early implant failure: a systematic review and meta-analysis
Systemic antibiotics are routinely prescribed in implant procedures, but the lack of consensus causes large differences between clinicians regarding antibiotic prophylaxis regimens. The objectives of this systematic review are to assess the need to prescribe antibiotics to prevent early implant failure and find the most appropriate antibiotic prophylaxis regimen. The electronic search was conducted in PubMed/MEDLINE, Scielo and Cochrane Central Trials Database for randomized clinical trials of at least 3 months of follow-up. Eleven studies were included in the qualitative analysis. Antibiotics were found to statistically significantly reduce early implant failures (RR = 0.30, 95% CI: 0.19-0.47, p < 0.00001; heterogeneity I2 = 0%, p = 0.54). No differences were seen between preoperative or both pre- and postoperative antibiotic regimens (RR = 0.57, 95% CI: 0.21-1.55, p = 0.27; heterogeneity I2 = 0%, p = 0.37). A single preoperative antibiotic prophylaxis dose was found to be enough to significantly reduce early implant failures compared to no antibiotic (RR = 0.34, 95% CI: 0.21-0.53, p < 0.00001; heterogeneity I2 = 0%, p = 0.61). In conclusion, in healthy patients a single antibiotic prophylaxis dose is indicated to prevent early implant failure
Simulating the Influence of Conjugative-Plasmid Kinetic Values on the Multilevel Dynamics of Antimicrobial Resistance in a Membrane Computing Model
[EN] Bacterial plasmids harboring antibiotic resistance genes are critical in the spread of antibiotic resistance. It is known that plasmids differ in their kinetic values, i.e., conjugation rate, segregation rate by copy number incompatibility with related plasmids, and rate of stochastic loss during replication. They also differ in cost to the cell in terms of reducing fitness and in the frequency of compensatory mutations compensating plasmid cost. However, we do not know how variation in these values influences the success of a plasmid and its resistance genes in complex ecosystems, such as the microbiota. Genes are in plasmids, plasmids are in cells, and cells are in bacterial populations and microbiotas, which are inside hosts, and hosts are in human communities at the hospital or the community under various levels of cross-colonization and antibiotic exposure. Differences in plasmid kinetics might have consequences on the global spread of antibiotic resistance. New membrane computing methods help to predict these consequences. In our simulation, conjugation frequency of at least 10(-3) influences the dominance of a strain with a resistance plasmid. Coexistence of different antibiotic resistances occurs if host strains can maintain two copies of similar plasmids. Plasmid loss rates of 10(-4) or 10(-5) or plasmid fitness costs of >= 0.06 favor plasmids located in the most abundant species. The beneficial effect of compensatory mutations for plasmid fitness cost is proportional to this cost at high mutation frequencies (10(-3) to 10(-5)). The results of this computational model clearly show how changes in plasmid kinetics can modify the entire population ecology of antibiotic resistance in the hospital setting.F. Baquero, M. Campos, and T. M. Coque were supported by EU Joint Programming Initiative JPIAMR2016-AC16/00043 (JPIonAMR-Third call on Transmission, ST131TS project), the Health Institute Carlos III of Spain (grants PI15-00818 and PI18-01942 and CIBER [CIBER in Epidemiology and Public Health, CIBERESP; CB06/02/0053]), and the Regional Government of Madrid (InGEMICS-C; S2017/BMD-3691), all of them cofinanced by the European Development Regional Fund (ERDF) "A Way to Achieve Europe." A. San Millan was supported by the European Research Council under the European Union's Horizon 2020 Research and Innovation Program (ERC grant agreement number 757440-PLASREVOLUTION)Campos Frances, M.; San Millan, A.; Sempere Luna, JM.; Lanza, VF.; Coque, TM.; Llorens, C.; Baquero, F. (2020). Simulating the Influence of Conjugative-Plasmid Kinetic Values on the Multilevel Dynamics of Antimicrobial Resistance in a Membrane Computing Model. Antimicrobial Agents and Chemotherapy. 64(8):1-19. https://doi.org/10.1128/AAC.00593-20S119648De Gelder, L., Ponciano, J. M., Joyce, P., & Top, E. M. (2007). Stability of a promiscuous plasmid in different hosts: no guarantee for a long-term relationship. Microbiology, 153(2), 452-463. doi:10.1099/mic.0.2006/001784-0Norman, A., Hansen, L. H., & Sørensen, S. J. (2009). Conjugative plasmids: vessels of the communal gene pool. Philosophical Transactions of the Royal Society B: Biological Sciences, 364(1527), 2275-2289. doi:10.1098/rstb.2009.0037Andam, C. P., Fournier, G. P., & Gogarten, J. P. (2011). Multilevel populations and the evolution of antibiotic resistance through horizontal gene transfer. FEMS Microbiology Reviews, 35(5), 756-767. doi:10.1111/j.1574-6976.2011.00274.xBaquero, F., Tedim, A. P., & Coque, T. M. (2013). Antibiotic resistance shaping multi-level population biology of bacteria. Frontiers in Microbiology, 4. doi:10.3389/fmicb.2013.00015Wein, T., Hülter, N. F., Mizrahi, I., & Dagan, T. (2019). Emergence of plasmid stability under non-selective conditions maintains antibiotic resistance. Nature Communications, 10(1). doi:10.1038/s41467-019-10600-7Yano, H., Shintani, M., Tomita, M., Suzuki, H., & Oshima, T. (2019). Reconsidering plasmid maintenance factors for computational plasmid design. Computational and Structural Biotechnology Journal, 17, 70-81. doi:10.1016/j.csbj.2018.12.001Gumpert, H., Kubicek-Sutherland, J. Z., Porse, A., Karami, N., Munck, C., Linkevicius, M., … Sommer, M. O. A. (2017). Transfer and Persistence of a Multi-Drug Resistance Plasmid in situ of the Infant Gut Microbiota in the Absence of Antibiotic Treatment. Frontiers in Microbiology, 8. doi:10.3389/fmicb.2017.01852Durão, P., Balbontín, R., & Gordo, I. (2018). Evolutionary Mechanisms Shaping the Maintenance of Antibiotic Resistance. Trends in Microbiology, 26(8), 677-691. doi:10.1016/j.tim.2018.01.005Campos, M., Llorens, C., Sempere, J. M., Futami, R., Rodriguez, I., Carrasco, P., … Baquero, F. (2015). A membrane computing simulator of trans-hierarchical antibiotic resistance evolution dynamics in nested ecological compartments (ARES). Biology Direct, 10(1). doi:10.1186/s13062-015-0070-9Campos, M., Capilla, R., Naya, F., Futami, R., Coque, T., Moya, A., … Baquero, F. (2019). Simulating Multilevel Dynamics of Antimicrobial Resistance in a Membrane Computing Model. mBio, 10(1), e02460-18. doi:10.1128/mbio.02460-1813. Baquero F, Campos M, Llorens C, Sempere JM. 2018. A model of antibiotic resistance evolution dynamics through P systems with active membranes and communication rules, p 33–44. In Graciani C, Agustín Riscos-Núñez A, Păun Gh, Rozenberg G, Salomaa A (ed), Enjoying natural computing. Springer, Cham, Switzerland.Leclerc, Q. J., Lindsay, J. A., & Knight, G. M. (2019). Mathematical modelling to study the horizontal transfer of antimicrobial resistance genes in bacteria: current state of the field and recommendations. Journal of The Royal Society Interface, 16(157), 20190260. doi:10.1098/rsif.2019.0260Blanquart, F. (2019). Evolutionary epidemiology models to predict the dynamics of antibiotic resistance. Evolutionary Applications, 12(3), 365-383. doi:10.1111/eva.1275316. Rozenberg G, Salomaa A, Păun G (ed). 2010. The Oxford handbook of membrane computing. Oxford University Press, Oxford, England.17. Păun G. 2002. Membrane computing. An introduction. Springer-Verlag, Heidelberg, Germany.Novais, A., Cantón, R., Moreira, R., Peixe, L., Baquero, F., & Coque, T. M. (2006). Emergence and Dissemination of Enterobacteriaceae Isolates Producing CTX-M-1-Like Enzymes in Spain Are Associated with IncFII (CTX-M-15) and Broad-Host-Range (CTX-M-1, -3, and -32) Plasmids. Antimicrobial Agents and Chemotherapy, 51(2), 796-799. doi:10.1128/aac.01070-06Mathers, A. J., Peirano, G., & Pitout, J. D. D. (2015). The Role of Epidemic Resistance Plasmids and International High-Risk Clones in the Spread of Multidrug-Resistant Enterobacteriaceae. Clinical Microbiology Reviews, 28(3), 565-591. doi:10.1128/cmr.00116-1420. Poirel L, Madec JY, Lupo A, Schink AK, Kieffer N, Nordmann P, Schwarz S. 2018. Antimicrobial resistance in Escherichia coli, p 289–316. In Schwarz S, Cavaco LM, Shen J (ed), Antimicrobial resistance in bacteria from livestock and companion animals. ASM Press, Washington, DC.Livermore, D. M., & Hawkey, P. M. (2005). CTX-M: changing the face of ESBLs in the UK. Journal of Antimicrobial Chemotherapy, 56(3), 451-454. doi:10.1093/jac/dki23923. European Centre for Disease Prevention and Control. 2015. Antimicrobial resistance surveillance in Europe 2015. Annual report of the European Antimicrobial Resistance Surveillance Network (EARS-Net). European Centre for Disease Prevention and Control, Stockholm, Sweden.Bush, K., & Fisher, J. F. (2011). Epidemiological Expansion, Structural Studies, and Clinical Challenges of New β-Lactamases from Gram-Negative Bacteria. Annual Review of Microbiology, 65(1), 455-478. doi:10.1146/annurev-micro-090110-102911Bush, K. (2018). Past and Present Perspectives on β-Lactamases. Antimicrobial Agents and Chemotherapy, 62(10). doi:10.1128/aac.01076-18Hawser, S. P., Bouchillon, S. K., Hoban, D. J., Badal, R. E., Cantón, R., & Baquero, F. (2010). Incidence and Antimicrobial Susceptibility of Escherichia coli and Klebsiella pneumoniae with Extended-Spectrum β-Lactamases in Community- and Hospital-Associated Intra-Abdominal Infections in Europe: Results of the 2008 Study for Monitoring Antimicrobial Resistance Trends (SMART). Antimicrobial Agents and Chemotherapy, 54(7), 3043-3046. doi:10.1128/aac.00265-10Simonsen, L., Gordon, D. M., Stewart, F. M., & Levin, B. R. (1990). Estimating the rate of plasmid transfer: an end-point method. Journal of General Microbiology, 136(11), 2319-2325. doi:10.1099/00221287-136-11-2319Levin, B. R., Stewart, F. M., & Rice, V. A. (1979). The kinetics of conjugative plasmid transmission: Fit of a simple mass action model. Plasmid, 2(2), 247-260. doi:10.1016/0147-619x(79)90043-xTurner, P. E., Williams, E. S. C. P., Okeke, C., Cooper, V. S., Duffy, S., & Wertz, J. E. (2014). Antibiotic resistance correlates with transmission in plasmid evolution. Evolution, 68(12), 3368-3380. doi:10.1111/evo.12537Porse, A., Schønning, K., Munck, C., & Sommer, M. O. A. (2016). Survival and Evolution of a Large Multidrug Resistance Plasmid in New Clinical Bacterial Hosts. Molecular Biology and Evolution, 33(11), 2860-2873. doi:10.1093/molbev/msw163Smillie, C., Garcillán-Barcia, M. P., Francia, M. V., Rocha, E. P. C., & de la Cruz, F. (2010). Mobility of Plasmids. Microbiology and Molecular Biology Reviews, 74(3), 434-452. doi:10.1128/mmbr.00020-1038. Taylor DE, Gibreel A, Tracz DM, Lawley TD. 2004. Antibiotic resistance plasmids, p 473–492. In Funnell BE, Phillips GJ (ed), Plasmid biology. American Society of Microbiology, Washington, DC.Million-Weaver, S., & Camps, M. (2014). Mechanisms of plasmid segregation: Have multicopy plasmids been overlooked? Plasmid, 75, 27-36. doi:10.1016/j.plasmid.2014.07.002Lau, B. T. C., Malkus, P., & Paulsson, J. (2013). New quantitative methods for measuring plasmid loss rates reveal unexpected stability. Plasmid, 70(3), 353-361. doi:10.1016/j.plasmid.2013.07.007Vogwill, T., & MacLean, R. C. (2014). The genetic basis of the fitness costs of antimicrobial resistance: a meta-analysis approach. Evolutionary Applications, 8(3), 284-295. doi:10.1111/eva.12202Andersson, D. I., & Levin, B. R. (1999). The biological cost of antibiotic resistance. Current Opinion in Microbiology, 2(5), 489-493. doi:10.1016/s1369-5274(99)00005-3Andersson, D. I., & Hughes, D. (2010). Antibiotic resistance and its cost: is it possible to reverse resistance? Nature Reviews Microbiology, 8(4), 260-271. doi:10.1038/nrmicro2319Loftie-Eaton, W., Bashford, K., Quinn, H., Dong, K., Millstein, J., Hunter, S., … Top, E. M. (2017). Compensatory mutations improve general permissiveness to antibiotic resistance plasmids. Nature Ecology & Evolution, 1(9), 1354-1363. doi:10.1038/s41559-017-0243-2Zwanzig, M., Harrison, E., Brockhurst, M. A., Hall, J. P. J., Berendonk, T. U., & Berger, U. (2019). Mobile Compensatory Mutations Promote Plasmid Survival. mSystems, 4(1). doi:10.1128/msystems.00186-18Yang, Q. E., MacLean, C., Papkou, A., Pritchard, M., Powell, L., Thomas, D., … Walsh, T. R. (2020). Compensatory mutations modulate the competitiveness and dynamics of plasmid-mediated colistin resistance in Escherichia coli clones. The ISME Journal, 14(3), 861-865. doi:10.1038/s41396-019-0578-6Gama, J. A., Zilhão, R., & Dionisio, F. (2018). Impact of plasmid interactions with the chromosome and other plasmids on the spread of antibiotic resistance. Plasmid, 99, 82-88. doi:10.1016/j.plasmid.2018.09.009Harrison, E., Dytham, C., Hall, J. P. J., Guymer, D., Spiers, A. J., Paterson, S., & Brockhurst, M. A. (2016). Rapid compensatory evolution promotes the survival of conjugative plasmids. Mobile Genetic Elements, 6(3), e1179074. doi:10.1080/2159256x.2016.1179074Hall, J. P. J., Brockhurst, M. A., Dytham, C., & Harrison, E. (2017). The evolution of plasmid stability: Are infectious transmission and compensatory evolution competing evolutionary trajectories? Plasmid, 91, 90-95. doi:10.1016/j.plasmid.2017.04.00354. Shintani M, Suzuki H. 2019. Plasmids and their hosts, p 109–133. In Nishida H, Oshima T (ed), DNA traffic in the environment. Springer, Singapore.Komp Lindgren, P., Karlsson, A., & Hughes, D. (2003). Mutation Rate and Evolution of Fluoroquinolone Resistance in Escherichia coli Isolates from Patients with Urinary Tract Infections. Antimicrobial Agents and Chemotherapy, 47(10), 3222-3232. doi:10.1128/aac.47.10.3222-3232.2003Krone, S. M., Lu, R., Fox, R., Suzuki, H., & Top, E. M. (2007). Modelling the spatial dynamics of plasmid transfer and persistence. Microbiology, 153(8), 2803-2816. doi:10.1099/mic.0.2006/004531-0Baquero, F., Coque, T. M., & de la Cruz, F. (2011). Ecology and Evolution as Targets: the Need for Novel Eco-Evo Drugs and Strategies To Fight Antibiotic Resistance. Antimicrobial Agents and Chemotherapy, 55(8), 3649-3660. doi:10.1128/aac.00013-11Buckner, M. M. C., Ciusa, M. L., & Piddock, L. J. V. (2018). Strategies to combat antimicrobial resistance: anti-plasmid and plasmid curing. FEMS Microbiology Reviews, 42(6), 781-804. doi:10.1093/femsre/fuy031Bush, K. (2008). Extended-spectrum β-lactamases in North America, 1987–2006. Clinical Microbiology and Infection, 14, 134-143. doi:10.1111/j.1469-0691.2007.01848.xJacoby, G. A., & Han, P. (1996). Detection of extended-spectrum beta-lactamases in clinical isolates of Klebsiella pneumoniae and Escherichia coli. Journal of clinical microbiology, 34(4), 908-911. doi:10.1128/jcm.34.4.908-911.1996Valverde, A., Coque, T. M., Sanchez-Moreno, M. P., Rollan, A., Baquero, F., & Canton, R. (2004). Dramatic Increase in Prevalence of Fecal Carriage of Extended-Spectrum -Lactamase-Producing Enterobacteriaceae during Nonoutbreak Situations in Spain. Journal of Clinical Microbiology, 42(10), 4769-4775. doi:10.1128/jcm.42.10.4769-4775.2004Hernández, J. R., Martínez-Martínez, L., Cantón, R., Coque, T. M., & Pascual, A. (2005). Nationwide Study of Escherichia coli and Klebsiella pneumoniae Producing Extended-Spectrum β-Lactamases in Spain. Antimicrobial Agents and Chemotherapy, 49(5), 2122-2125. doi:10.1128/aac.49.5.2122-2125.2005PEREZ, F., ENDIMIANI, A., HUJER, K., & BONOMO, R. (2007). The continuing challenge of ESBLs. Current Opinion in Pharmacology, 7(5), 459-469. doi:10.1016/j.coph.2007.08.003Hernández-García, M., Pérez-Viso, B., Navarro-San Francisco, C., Baquero, F., Morosini, M. I., Ruiz-Garbajosa, P., & Cantón, R. (2019). Intestinal co-colonization with different carbapenemase-producing Enterobacterales isolates is not a rare event in an OXA-48 endemic area. EClinicalMedicine, 15, 72-79. doi:10.1016/j.eclinm.2019.09.005Jensen, R. B., & Gerdes, K. (1995). Programmed cell death in bacteria: proteic plasmid stabilization systems. Molecular Microbiology, 17(2), 205-210. doi:10.1111/j.1365-2958.1995.mmi_17020205.xStalder, T., Cornwell, B., Lacroix, J., Kohler, B., Dixon, S., Yano, H., … Top, E. M. (2020). Evolving Populations in Biofilms Contain More Persistent Plasmids. Molecular Biology and Evolution, 37(6), 1563-1576. doi:10.1093/molbev/msaa024McNally, A., Oren, Y., Kelly, D., Pascoe, B., Dunn, S., Sreecharan, T., … Corander, J. (2016). Combined Analysis of Variation in Core, Accessory and Regulatory Genome Regions Provides a Super-Resolution View into the Evolution of Bacterial Populations. PLOS Genetics, 12(9), e1006280. doi:10.1371/journal.pgen.1006280Baquero, M.-R., Galán, J. C., del Carmen Turrientes, M., Cantón, R., Coque, T. M., Martínez, J. L., & Baquero, F. (2005). Increased Mutation Frequencies in Escherichia coli Isolates Harboring Extended-Spectrum β-Lactamases. Antimicrobial Agents and Chemotherapy, 49(11), 4754-4756. doi:10.1128/aac.49.11.4754-4756.2005Baquero, F. (2004). From pieces to patterns: evolutionary engineering in bacterial pathogens. Nature Reviews Microbiology, 2(6), 510-518. doi:10.1038/nrmicro909Andersson, D. I., Balaban, N. Q., Baquero, F., Courvalin, P., Glaser, P., Gophna, U., … Tønjum, T. (2020). Antibiotic resistance: turning evolutionary principles into clinical reality. 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La integración y sus convenios internacionales en América Latina
Hablar hoy de globalización conlleva consigo a relacionar la temática de la integración y sus convenios internacionales, los cuales van tipificándose de acuerdo a las regiones, los bloques y los países donde más requieren de desarrollo y necesidad de asociatividad. En tal sentido, el objetivo del presente paper es hacer un constructo teórico y bibliográfico en forma breve de los convenios de integración más importantes en América Latina, en donde se presenta una compilación de la historia y la explicación de los principales convenios fruto de la integración en Latinoamérica. En la parte metodológica, el tipo y método de estudio fue la recopilación documental, la síntesis y la compilación, por último, la investigación da cuenta de que estos esquemas de integración son mecanismos de choque a poblaciones, que requieren de ajustes en diversas facetas económicas, normativas, tecnológicas, ambientales e industriales, sin embargo, los gobiernos tendrán que realizar ajustes en sus normas, en sus infraestructuras, en sus trámites, y prepararse al interior de su administración para dichos procesos de integración. De la misma manera, quedo claro que el tema de la integración debe ser inherente a los pueblos Latinoamericanos, a fin de consolidar y fortalecer sus democracias como garantías de cambios profundos, en procura de una mejor calidad de vida para la región.Globalization today is closelylinked to topics regarding integration and international agreements, which, in turn, are categorized according to the regions, blocs and countries needing
the most development and association. In this sense, this paper aims at providing a theoretical construct and a literature review of the most important integration agreements in Latin
America. A historic compilation and a brief explanation of the main agreements are set forth.
The methodology used was a document review, synthesis, and compilation. Finally, it is established that these integration schemes are urgent measures to be adopted by the countries
or regions that require adjustments in different areas: Economy, Regulation, Technology,
Environment, and/or Industry. However, governments need to modify their regulations, infrastructure, and procedures -especially their administrative procedures- in order to prepare
for these integration processes. To conclude, integration must be an inherent topic for the
Latin American countries so as to consolidate and strengthen democratic regimes and grant
deep changes to improve the quality of life for people in the region
Four haplotype blocks linked to Ascochyta blight disease resistance in chickpea under Mediterranean conditions
Ascochyta blight, caused by the fungal pathogen Ascochyta blight, caused by the fungal pathogen Ascochyta rabiei, is a devastating biotic stress that poses a significant threat to chickpea cultivation worldwide. To combat this disease, breeding programs have focused on developing cultivars with resistance to Ascochyta blight. However, a comprehensive understanding of the underlying plant defense mechanism is still lacking. To identify genomic regions associated with resistance, a recombinant inbred line (RIL) population was created by crossing ILC3279 (kabuli, resistant) and WR315 (desi, susceptible), which was then phenotyped and sequenced using a tuneable genotyping-by-sequencing (tGBS) protocol to obtain single nucleotide polymorphisms (SNPs). We further validated the association of genomic regions with Ascochyta blight resistance in a second recombinant inbred line\population derived from the cross between JG62 (desi, susceptible) and ILC72 (kabuli, resistant). Our analysis identified four genomic regions associated with Ascochyta blight resistance in chromosomes 2 and 4, among which a region spanning from 3.52 to 8.20 Mb in chromosome 4 was the most robust candidate for resistance, being associated with resistance in both years and populations. A total of 30 genes from the identified regions were selected as robust candidates, and LOC101507066, which encodes a leucine-rich repeat receptor-like protein kinase, was the most robust candidate gene, as it plays critical roles in plant stress responses and immunity. Our findings have potential to accelerate marker-assisted genetic improvement and facilitate the development of integrated strategies for crop protection
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