Chemical diplomacy in male tilapia: urinary signal increases sex hormone and decreases aggression

Androgens, namely 11-ketotestosterone (11KT), have a central role in male fish reproductive physiology and are thought to be involved in both aggression and social signalling. Aggressive encounters occur frequently in social species, and fights may cause energy depletion, injury and loss of social status. Signalling for social dominance and fighting ability in an agonistic context can minimize these costs. Here, we test the hypothesis of a 'chemical diplomacy' mechanism through urinary signals that avoids aggression and evokes an androgen response in receiver males of Mozambique tilapia (Oreochromis mossambicus). We show a decoupling between aggression and the androgen response; males fighting their mirror image experience an unresolved interaction and a severe drop in urinary 11KT. However, if concurrently exposed to dominant male urine, aggression drops but urinary 11KT levels remain high. Furthermore, 11KT increases in males exposed to dominant male urine in the absence of a visual stimulus. The use of a urinary signal to lower aggression may be an adaptive mechanism to resolve disputes and avoid the costs of fighting. As dominance is linked to nest building and mating with females, the 11KT response of subordinate males suggests chemical eavesdropping, possibly in preparation for parasitic fertilizations.info:eu-repo/semantics/publishedVersio

Mortality from gastrointestinal congenital anomalies at 264 hospitals in 74 low-income, middle-income, and high-income countries: a multicentre, international, prospective cohort study

Background: Congenital anomalies are the fifth leading cause of mortality in children younger than 5 years globally. Many gastrointestinal congenital anomalies are fatal without timely access to neonatal surgical care, but few studies have been done on these conditions in low-income and middle-income countries (LMICs). We compared outcomes of the seven most common gastrointestinal congenital anomalies in low-income, middle-income, and high-income countries globally, and identified factors associated with mortality. // Methods: We did a multicentre, international prospective cohort study of patients younger than 16 years, presenting to hospital for the first time with oesophageal atresia, congenital diaphragmatic hernia, intestinal atresia, gastroschisis, exomphalos, anorectal malformation, and Hirschsprung's disease. Recruitment was of consecutive patients for a minimum of 1 month between October, 2018, and April, 2019. We collected data on patient demographics, clinical status, interventions, and outcomes using the REDCap platform. Patients were followed up for 30 days after primary intervention, or 30 days after admission if they did not receive an intervention. The primary outcome was all-cause, in-hospital mortality for all conditions combined and each condition individually, stratified by country income status. We did a complete case analysis. // Findings: We included 3849 patients with 3975 study conditions (560 with oesophageal atresia, 448 with congenital diaphragmatic hernia, 681 with intestinal atresia, 453 with gastroschisis, 325 with exomphalos, 991 with anorectal malformation, and 517 with Hirschsprung's disease) from 264 hospitals (89 in high-income countries, 166 in middle-income countries, and nine in low-income countries) in 74 countries. Of the 3849 patients, 2231 (58·0%) were male. Median gestational age at birth was 38 weeks (IQR 36–39) and median bodyweight at presentation was 2·8 kg (2·3–3·3). Mortality among all patients was 37 (39·8%) of 93 in low-income countries, 583 (20·4%) of 2860 in middle-income countries, and 50 (5·6%) of 896 in high-income countries (p<0·0001 between all country income groups). Gastroschisis had the greatest difference in mortality between country income strata (nine [90·0%] of ten in low-income countries, 97 [31·9%] of 304 in middle-income countries, and two [1·4%] of 139 in high-income countries; p≤0·0001 between all country income groups). Factors significantly associated with higher mortality for all patients combined included country income status (low-income vs high-income countries, risk ratio 2·78 [95% CI 1·88–4·11], p<0·0001; middle-income vs high-income countries, 2·11 [1·59–2·79], p<0·0001), sepsis at presentation (1·20 [1·04–1·40], p=0·016), higher American Society of Anesthesiologists (ASA) score at primary intervention (ASA 4–5 vs ASA 1–2, 1·82 [1·40–2·35], p<0·0001; ASA 3 vs ASA 1–2, 1·58, [1·30–1·92], p<0·0001]), surgical safety checklist not used (1·39 [1·02–1·90], p=0·035), and ventilation or parenteral nutrition unavailable when needed (ventilation 1·96, [1·41–2·71], p=0·0001; parenteral nutrition 1·35, [1·05–1·74], p=0·018). Administration of parenteral nutrition (0·61, [0·47–0·79], p=0·0002) and use of a peripherally inserted central catheter (0·65 [0·50–0·86], p=0·0024) or percutaneous central line (0·69 [0·48–1·00], p=0·049) were associated with lower mortality. // Interpretation: Unacceptable differences in mortality exist for gastrointestinal congenital anomalies between low-income, middle-income, and high-income countries. Improving access to quality neonatal surgical care in LMICs will be vital to achieve Sustainable Development Goal 3.2 of ending preventable deaths in neonates and children younger than 5 years by 2030

Emergence and phylodynamics of Citrus tristeza virus in Sicily, Italy

[EN] Citrus tristeza virus (CTV) outbreaks were detected in Sicily island, Italy for the first time in 2002. To gain insight into the evolutionary forces driving the emergence and phylogeography of these CTV populations, we determined and analyzed the nucleotide sequences of the p20 gene from 108 CTV isolates collected from 2002 to 2009. Bayesian phylogenetic analysis revealed that mild and severe CTV isolates belonging to five different clades (lineages) were introduced in Sicily in 2002. Phylogeographic analysis showed that four lineages co-circulated in the main citrus growing area located in Eastern Sicily. However, only one lineage (composed of mild isolates) spread to distant areas of Sicily and was detected after 2007. No correlation was found between genetic variation and citrus host, indicating that citrus cultivars did not exert differential selective pressures on the virus. The genetic variation of CTV was not structured according to geographical location or sampling time, likely due to the multiple introduction events and a complex migration pattern with intense co- and recirculation of different lineages in the same area. The phylogenetic structure, statistical tests of neutrality and comparison of synonymous and nonsynonymous substitution rates suggest that weak negative selection and genetic drift following a rapid expansion may be the main causes of the CTV variability observed today in Sicily. Nonetheless, three adjacent amino acids at the p20 N-terminal region were found to be under positive selection, likely resulting from adaptation events.A.W. and S.F.E. were supported by grant BFU2012-30805 from the Spanish Secretaria de Estado de Investigacion, Desarrollo e Innovacion and by a grant 22371 from the John Templeton Foundation. The opinions expressed in this publication are those of the authors and do not necessarily reflect the views of the John Templeton Foundation. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Davino, S.; Willemsen, A.; Panno. Stefano; Davino, M.; Catara, A.; Elena Fito, SF.; Rubio, L. (2013). Emergence and phylodynamics of Citrus tristeza virus in Sicily, Italy. PLoS ONE. 8:66700-66700. doi:10.1371/journal.pone.0066700S66700667008Domingo, E., & Holland, J. J. (1997). RNA VIRUS MUTATIONS AND FITNESS FOR SURVIVAL. Annual Review of Microbiology, 51(1), 151-178. doi:10.1146/annurev.micro.51.1.151Grenfell, B. T. (2004). Unifying the Epidemiological and Evolutionary Dynamics of Pathogens. Science, 303(5656), 327-332. doi:10.1126/science.1090727Moya, A., Holmes, E. C., & González-Candelas, F. (2004). The population genetics and evolutionary epidemiology of RNA viruses. Nature Reviews Microbiology, 2(4), 279-288. doi:10.1038/nrmicro863Gray, R. R., Tatem, A. J., Lamers, S., Hou, W., Laeyendecker, O., Serwadda, D., … Salemi, M. (2009). Spatial phylodynamics of HIV-1 epidemic emergence in east Africa. AIDS, 23(14), F9-F17. doi:10.1097/qad.0b013e32832faf61Holmes, E. C. (2008). Evolutionary History and Phylogeography of Human Viruses. Annual Review of Microbiology, 62(1), 307-328. doi:10.1146/annurev.micro.62.081307.162912Pybus, O. G., Suchard, M. A., Lemey, P., Bernardin, F. J., Rambaut, A., Crawford, F. W., … Delwart, E. L. (2012). Unifying the spatial epidemiology and molecular evolution of emerging epidemics. Proceedings of the National Academy of Sciences, 109(37), 15066-15071. doi:10.1073/pnas.1206598109Talbi, C., Lemey, P., Suchard, M. A., Abdelatif, E., Elharrak, M., Jalal, N., … Bourhy, H. (2010). Phylodynamics and Human-Mediated Dispersal of a Zoonotic Virus. PLoS Pathogens, 6(10), e1001166. doi:10.1371/journal.ppat.1001166Vijaykrishna, D., Bahl, J., Riley, S., Duan, L., Zhang, J. X., Chen, H., … Guan, Y. (2008). Evolutionary Dynamics and Emergence of Panzootic H5N1 Influenza Viruses. PLoS Pathogens, 4(9), e1000161. doi:10.1371/journal.ppat.1000161Gómez, P., Sempere, R. N., Aranda, M. A., & Elena, S. F. (2012). Phylodynamics of Pepino mosaic virus in Spain. European Journal of Plant Pathology, 134(3), 445-449. doi:10.1007/s10658-012-0019-0Lefeuvre, P., Martin, D. P., Harkins, G., Lemey, P., Gray, A. J. A., Meredith, S., … Heydarnejad, J. (2010). The Spread of Tomato Yellow Leaf Curl Virus from the Middle East to the World. PLoS Pathogens, 6(10), e1001164. doi:10.1371/journal.ppat.1001164TOMITAKA, Y., & OHSHIMA, K. (2006). A phylogeographical study of the Turnip mosaic virus population in East Asia reveals an ‘emergent’ lineage in Japan. Molecular Ecology, 15(14), 4437-4457. doi:10.1111/j.1365-294x.2006.03094.xWu, B., Blanchard-Letort, A., Liu, Y., Zhou, G., Wang, X., & Elena, S. F. (2011). Dynamics of Molecular Evolution and Phylogeography of Barley yellow dwarf virus-PAV. PLoS ONE, 6(2), e16896. doi:10.1371/journal.pone.0016896MORENO, P., AMBRÓS, S., ALBIACH-MARTÍ, M. R., GUERRI, J., & PEÑA, L. (2008). Citrus tristeza virus: a pathogen that changed the course of the citrus industry. Molecular Plant Pathology, 9(2), 251-268. doi:10.1111/j.1364-3703.2007.00455.xTatineni, S., Robertson, C. J., Garnsey, S. M., & Dawson, W. O. (2011). A plant virus evolved by acquiring multiple nonconserved genes to extend its host range. Proceedings of the National Academy of Sciences, 108(42), 17366-17371. doi:10.1073/pnas.1113227108Folimonova, S. Y. (2012). Superinfection Exclusion Is an Active Virus-Controlled Function That Requires a Specific Viral Protein. Journal of Virology, 86(10), 5554-5561. doi:10.1128/jvi.00310-12Bar-Joseph, M., Marcus, R., & Lee, R. F. (1989). The Continuous Challenge of Citrus Tristeza Virus Control. Annual Review of Phytopathology, 27(1), 291-316. doi:10.1146/annurev.py.27.090189.001451Davino, S., Rubio, L., & Davino, M. (2005). Molecular analysis suggests that recent Citrus tristeza virus outbreaks in Italy were originated by at least two independent introductions. European Journal of Plant Pathology, 111(3), 289-293. doi:10.1007/s10658-003-2815-zAlbiach-Marti, M. R., Mawassi, M., Gowda, S., Satyanarayana, T., Hilf, M. E., Shanker, S., … Dawson, W. O. (2000). Sequences of Citrus Tristeza Virus Separated in Time and Space Are Essentially Identical. Journal of Virology, 74(15), 6856-6865. doi:10.1128/jvi.74.15.6856-6865.2000Rubio, L., Ayllon, M. A., Kong, P., Fernandez, A., Polek, M., Guerri, J., … Falk, B. W. (2001). Genetic Variation of Citrus Tristeza Virus Isolates from California and Spain: Evidence for Mixed Infections and Recombination. Journal of Virology, 75(17), 8054-8062. doi:10.1128/jvi.75.17.8054-8062.2001Silva, G., Marques, N., & Nolasco, G. (2011). The evolutionary rate of citrus tristeza virus ranks among the rates of the slowest RNA viruses. Journal of General Virology, 93(2), 419-429. doi:10.1099/vir.0.036574-0Mawassi, M., Mietkiewska, E., Gofman, R., Yang, G., & Bar-Joseph, M. (1996). Unusual Sequence Relationships Between Two Isolates of Citrus Tristeza Virus. Journal of General Virology, 77(9), 2359-2364. doi:10.1099/0022-1317-77-9-2359Vives, M. C., Dawson, W. O., Flores, R., L√≥pez, C., Albiach-Mart√≠, M. R., Rubio, L., … Moreno, P. (1999). The complete genome sequence of the major component of a mild citrus tristeza virus isolate. Journal of General Virology, 80(3), 811-816. doi:10.1099/0022-1317-80-3-811Martín, S., Elena, S. F., Guerri, J., Moreno, P., Sambade, A., Rubio, L., … Vives, M. C. (2009). Contribution of recombination and selection to molecular evolution of Citrus tristeza virus. Journal of General Virology, 90(6), 1527-1538. doi:10.1099/vir.0.008193-0Vives, M. C., Rubio, L., Sambade, A., Mirkov, T. E., Moreno, P., & Guerri, J. (2005). Evidence of multiple recombination events between two RNA sequence variants within a Citrus tristeza virus isolate. Virology, 331(2), 232-237. doi:10.1016/j.virol.2004.10.037D’Urso, F., Sambade, A., Moya, A., Guerri, J., & Moreno, P. (2003). Variation of haplotype distributions of two genomic regions of Citrus tristeza virus populations from eastern Spain. Molecular Ecology, 12(2), 517-526. doi:10.1046/j.1365-294x.2000.01747.xSambade, A., Rubio, L., Garnsey, S. M., Costa, N., Muller, G. W., Peyrou, M., … Moreno, P. (2002). Comparison of viral RNA populations of pathogenically distinct isolates of Citrus tristeza virus : application to monitoring cross-protection. Plant Pathology, 51(3), 257-265. doi:10.1046/j.1365-3059.2002.00720.xReed, J. C., Kasschau, K. D., Prokhnevsky, A. I., Gopinath, K., Pogue, G. P., Carrington, J. C., & Dolja, V. V. (2003). Suppressor of RNA silencing encoded by Beet yellows virus. Virology, 306(2), 203-209. doi:10.1016/s0042-6822(02)00051-xFolimonova, S. Y., Robertson, C. J., Shilts, T., Folimonov, A. S., Hilf, M. E., Garnsey, S. M., & Dawson, W. O. (2009). Infection with Strains of Citrus Tristeza Virus Does Not Exclude Superinfection by Other Strains of the Virus. Journal of Virology, 84(3), 1314-1325. doi:10.1128/jvi.02075-09Kong, P., Rubio, L., Polek, M., & Falk, B. W. (2000). Virus Genes, 21(3), 139-145. doi:10.1023/a:1008198311398Powell, C. A., Pelosi, R. R., Rundell, P. A., & Cohen, M. (2003). Breakdown of Cross-Protection of Grapefruit from Decline-Inducing Isolates of Citrus tristeza virus Following Introduction of the Brown Citrus Aphid. Plant Disease, 87(9), 1116-1118. doi:10.1094/pdis.2003.87.9.1116Roistacher C, Dodds J. (1993) Failure of 100 mild Citrus tristeza virus isolates from california to cross protect against a challenge by severe sweet orange stem pitting isolates. Proc 12th Conf IOCV: 100–107.Ayllón, M. A., Rubio, L., Sentandreu, V., Moya, A., Guerri, J., & Moreno, P. (2006). Variations in Two Gene Sequences of Citrus Tristeza Virus after Host Passage. Virus Genes, 32(2), 119-128. doi:10.1007/s11262-005-6866-4Ayllón, M. A., Rubio, L., Moya, A., Guerri, J., & Moreno, P. (1999). The Haplotype Distribution of Two Genes of Citrus Tristeza Virus Is Altered after Host Change or Aphid Transmission. Virology, 255(1), 32-39. doi:10.1006/viro.1998.9566Sentandreu, V., Castro, J. A., Ayllón, M. A., Rubio, L., Guerri, J., González-Candelas, F., … Moya, A. (2005). Evolutionary analysis of genetic variation observed in citrus tristeza virus (CTV) after host passage. Archives of Virology, 151(5), 875-894. doi:10.1007/s00705-005-0683-xMatos, L. A., Hilf, M. E., Cayetano, X. A., Feliz, A. O., Harper, S. J., & Folimonova, S. Y. (2013). Dramatic Change in Citrus tristeza virus Populations in the Dominican Republic. Plant Disease, 97(3), 339-345. doi:10.1094/pdis-05-12-0421-reDavino, S., Davino, M., Sambade, A., Guardo, M., & Caruso, A. (2003). The First Citrus tristeza virus Outbreak Found in a Relevant Citrus Producing Area of Sicily, Italy. Plant Disease, 87(3), 314-314. doi:10.1094/pdis.2003.87.3.314aRUBIO, L., AYLLONl, M. A., GUERRI, J., PAPPU, H., NIBLETT, C., & MORENO, P. (1996). Differentiation of citrus tristeza closterovirus (CTV) isolates by single-strand conformation polymorphism analysis of the coat protein gene. Annals of Applied Biology, 129(3), 479-489. doi:10.1111/j.1744-7348.1996.tb05770.xLarkin, M. A., Blackshields, G., Brown, N. P., Chenna, R., McGettigan, P. A., McWilliam, H., … Higgins, D. G. (2007). Clustal W and Clustal X version 2.0. Bioinformatics, 23(21), 2947-2948. doi:10.1093/bioinformatics/btm404Tamura, K., Peterson, D., Peterson, N., Stecher, G., Nei, M., & Kumar, S. (2011). MEGA5: Molecular Evolutionary Genetics Analysis Using Maximum Likelihood, Evolutionary Distance, and Maximum Parsimony Methods. Molecular Biology and Evolution, 28(10), 2731-2739. doi:10.1093/molbev/msr121Kosakovsky Pond, S. L., Posada, D., Gravenor, M. B., Woelk, C. H., & Frost, S. D. W. (2006). GARD: a genetic algorithm for recombination detection. Bioinformatics, 22(24), 3096-3098. doi:10.1093/bioinformatics/btl474Martin, D. P., Lemey, P., Lott, M., Moulton, V., Posada, D., & Lefeuvre, P. (2010). RDP3: a flexible and fast computer program for analyzing recombination. Bioinformatics, 26(19), 2462-2463. doi:10.1093/bioinformatics/btq467Librado, P., & Rozas, J. (2009). DnaSP v5: a software for comprehensive analysis of DNA polymorphism data. Bioinformatics, 25(11), 1451-1452. doi:10.1093/bioinformatics/btp187Kimura M. (1985) The neutral theory of molecular evolution. Cambridge Univ Pr.Weir, B. S., & Cockerham, C. C. (1984). Estimating F-Statistics for the Analysis of Population Structure. Evolution, 38(6), 1358. doi:10.2307/2408641Pond, S. L. K., & Frost, S. D. W. (2005). Datamonkey: rapid detection of selective pressure on individual sites of codon alignments. Bioinformatics, 21(10), 2531-2533. doi:10.1093/bioinformatics/bti320Drummond, A. J., & Rambaut, A. (2007). BEAST: Bayesian evolutionary analysis by sampling trees. BMC Evolutionary Biology, 7(1), 214. doi:10.1186/1471-2148-7-214Bielejec, F., Rambaut, A., Suchard, M. A., & Lemey, P. (2011). SPREAD: spatial phylogenetic reconstruction of evolutionary dynamics. Bioinformatics, 27(20), 2910-2912. doi:10.1093/bioinformatics/btr481Stamatakis, A. (2006). RAxML-VI-HPC: maximum likelihood-based phylogenetic analyses with thousands of taxa and mixed models. Bioinformatics, 22(21), 2688-2690. doi:10.1093/bioinformatics/btl446Ott M, Zola J, Stamatakis A, Aluru S. (2007) Large-scale maximum likelihood-based phylogenetic analysis on the IBM BlueGene/L. Proceedings of the 19th ACM/IEEE conference on Supercomputing. Article No. 4.Shimodaira, H., & Hasegawa, M. (1999). Multiple Comparisons of Log-Likelihoods with Applications to Phylogenetic Inference. Molecular Biology and Evolution, 16(8), 1114-1116. doi:10.1093/oxfordjournals.molbev.a026201Soria-Carrasco, V., Talavera, G., Igea, J., & Castresana, J. (2007). The K tree score: quantification of differences in the relative branch length and topology of phylogenetic trees. Bioinformatics, 23(21), 2954-2956. doi:10.1093/bioinformatics/btm466Puigbo, P., Garcia-Vallve, S., & McInerney, J. O. (2007). TOPD/FMTS: a new software to compare phylogenetic trees. Bioinformatics, 23(12), 1556-1558. doi:10.1093/bioinformatics/btm13

Características morfofuncionais do trânsito orofaríngeo na bulimia: revisão de literatura Morphofunctional characteristics of the oropharyngeal tract in bulimia: review of literature

TEMA: deglutição e bulimia. OBJETIVO: apresentar e discutir os achados científicos descritos na literatura quanto às características orofaríngeas relacionadas à deglutição em portadores de bulimia nervosa do tipo purgativa. CONCLUSÃO: a bulimia nervosa acarreta uma série de alterações em estruturas e funções que compõem o trânsito orofaríngeo, como erosão dentária, hipersensibilidade, enfraquecimento e fratura dos dentes, problemas de oclusão, cáries, doenças periodontais, dessensibilização intra-oral, hipogeusia, úlceras, granulomas, queilite angular, hipertrofia das glândulas parótidas, tosse e odinofagia. Existe um predomínio na literatura científica de relatos sobre alterações morfológicas em detrimento das funcionais. Poucos relatos abordaram diretamente a relação entre a bulimia e deglutição, apenas mencionando superficialmente as possibilidades de desencadeamento da disfagia orofaríngea.<br>BACKGROUND: deglutition and bulimia. PURPOSE: to submit and discuss the scientific research concerning oropharyngeal characteristics related to deglutition in patients with purging type bulimia nervosa. CONCLUSIONS: bulimia nervosa entails a series of changes in structures and functions that compose the oropharyngeal tract, such as dental erosion, hypersensitivity, weakness and fracture of the teeth, occlusion problems, caries, periodontal diseases, intraoral desensitization, hypogeusia, ulceration, granulomas, angular cheilitis, enlargement of the parotid glands, coughs and odynophagia. There is a prevalence in the scientific literature of reports about morphologic alterations on the detriment of the functional ones. Few reports discussed the relationship between bulimia and deglutition, superficially mentioning the possibilities for triggering oropharyngeal dysphagia