Resource sharing leads to the emergence of division of labour

Division of labour occurs in a broad range of organisms. Yet, how division of labour can emerge in the absence of pre-existing interindividual differences is poorly understood. Using a simple but realistic model, we show that in a group of initially identical individuals, division of labour emerges spontaneously if returning foragers share part of their resources with other group members. In the absence of resource sharing, individuals follow an activity schedule of alternating between foraging and other tasks. If non-foraging individuals are fed by other individuals, their alternating activity schedule becomes interrupted, leading to task specialisation and the emergence of division of labour. Furthermore, nutritional differences between individuals reinforce division of labour. Such differences can be caused by increased metabolic rates during foraging or by dominance interactions during resource sharing. Our model proposes a plausible mechanism for the self-organised emergence of division of labour in animal groups of initially identical individuals. This mechanism could also play a role for the emergence of division of labour during the major evolutionary transitions to eusociality and multicellularity

Clinical-pathological features and gene profile in colorectal cancer

El cáncer colorectal es el tercer cáncer más frecuente en hombres y el segundo más frecuente en mujeres, con una incidencia mundial aproximada de 1.2 millones de casos nuevos por año. El objetivo primario es estudiar la relación existente entre las características clínico-histológicas de individuos con cáncer colorectal y el estado mutacional de los codones 12 y 13 del gen KRAS (7 mutaciones validadas), con el fin de hallar un marcador histopatológico para los tumores mutados. El objetivo secundario es determinar cuantos pacientes tienen mutaciones adicionales en los codones 15 y 61 del gen KRAS y 600 del gen BRAF que podrían modificar el fenotipo tumoral. Fueron seleccionados 60 individuos con cáncer colorrectal (30 wild-type y 30 con mutaciones validadas en los codones 12 y 13 del gen KRAS). Se amplificaron y secuenciaron del gen KRAS los exones 2 y 3, y del gen BRAF el exón 15. La información recolectada se examinó mediante un análisis descriptivo, análisis univariado y/ó análisis multivariado según correspondiese. En conclusión, no se encontró relación entre las características clínico-histológicas de los tumores de individuos con diagnostico de cáncer colorectal y el estado mutacional de los codones 12 y 13 del gen KRAS. No hallamos un marcador histopatológico para los tumores mutados resulta interesante considerar el estudio del codón 600 del gen BRAF.Colorectal cancer is the third most frequent cancer in men and the second most frequent in women, with a worldwide incidence of approximately 1.2 million new cases per year. Our primary objective was to study the relationship between clinical and histological features of individuals with colorectal cancer and the mutational status of codons 12 and 13 of the KRAS gene (7 validated mutations), in order to find a histopathological marker to mutated tumors. The secondary objective was to determine how many patients had additional mutations in codons 15 and 61 of the KRAS gene, and codon 600 of the BRAF gene, which could modify the tumor phenotype. Sixty individuals with colorectal cancer (30 wild-type subjects and 30 with validated mutations in codons 12 and 13 of the KRAS gene) were selected. Exons 2 and 3 of the KRAS gene, and exon 15 of the BRAF gene were amplified and sequenced. The data collected were reviewed by a descriptive, univariate and/or multivariate analysis, as appropriate. In conclusion, no relation was found between clinical and histological features of individuals with colorectal cancer and their mutational status for codons 12 and 13 of the KRAS gene. This suggests that those easily available data do not allow predicting the response to anti-EGFR therapy. In patients with advanced colorectal adenocarcinomas and KRAS wild-type status, further study of codon 600 of the BRAF gene could be required.Fil: Perazzo, Florencia. Centro de Educación Médica e Investigaciones Clínicas; ArgentinaFil: Piaggio, Fernando. Centro de Educación Médica e Investigaciones Clínicas; ArgentinaFil: Krupitzki, Hugo Bernardo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Centro de Educación Médica e Investigaciones Clínicas; ArgentinaFil: Garcia, Alejandro Javier. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Centro de Educación Médica e Investigaciones Clínicas; ArgentinaFil: Avagnina, Alejandra. Centro de Educación Médica e Investigaciones Clínicas; ArgentinaFil: Elsner, Boris. Centro de Educación Médica e Investigaciones Clínicas; ArgentinaFil: Denninghoff, Valeria Cecilia. Centro de Educación Médica e Investigaciones Clínicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentin

Variable Number Tandem Repeats in the promoter region of prostacyclin synthase gene in choline deficient rats.

Weanling Sprague-Dawley rats were fed on a choline-deficient diet with hydrogenated vegetable oil and corn oil as lipids develop acute renal failure. Pathogenesis of the latter is controversial and an ischemic mechanism has been proposed. Arachidonic acid derivatives are involved in the regulation of vascular tonus. Vasospasm could be due to an increase in tromboxane A2-mediated vasoconstriction or to a decrease in prostacyclin-induced vasodilatation. Enzymes involved in the synthesis of both compounds are tromboxane A2- and prostacyclin-synthase respectively. The aim of this study was to identify the variable number tandem repeats (VNTR) in the promoter region of prostacyclin synthase gene and verify if there exists a relationship between the occurrence of VNTR in those choline-deficient rats which die because of acute renal failure and those which do not. We verified the presence of the VNTR in the prostacyclin synthase rat gene, but we did not find any difference in the molecular weight of the alleles between experimental and control rats. Renal reparation of the acute kidney injury due to choline deficiency in some rats is not related with differences in VNTR in the promoter region of the prostacyclin synthase gene. Weanling Sprague-Dawley rats fed a choline-deficient diet with hydrogenated vegetable oil and corn oil as lipids develop acute renal failure. Its pathogenesis is controversial. The ischemic mechanism has been proposed. Derivatives from arachidonic acid are involved in the regulation of vascular tone. Vasospasm could be due to an increase in vasoconstriction mediated by tromboxane A2 or a decrease in vasodilatation by prostacyclin. Enzymes involved in the synthesis of them are tromboxane A2 and prostacyclin synthase respectively. The aim of this study is to identify the variable number tandem repeats (VNTR) in the promoter region of prostacyclin synthase gene and verify if there exists a relationship between the VNTR and those rats which dye as a consequence of acute renal failure due to choline deficiency and those which do not die. The VNTR presence was detected by molecular methods. We verified the presence of the VNTR in the prostacyclin synthase rat gene. We did not find difference in the molecular weight of the alleles between experimental and control rats. Renal reparation of the acute kidney injury due to choline deficiency in Sprague-Dawley rats is not related with differences in prostacyclin synthase VNTR, in the promoter region of this gene.Fil: Denninghoff, Valeria Cecilia. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Patología. Centro de Patología Experimental; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; ArgentinaFil: Ossani, Georgina Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Patología. Centro de Patología Experimental; ArgentinaFil: Uceda, Ana Margarita. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Patología. Centro de Patología Experimental; ArgentinaFil: Avagnina Iribarren, Maria Alejandra. Centro de Educaciones Médicas e Investigación Clínica "Norberto Quirno"; ArgentinaFil: Elsner, Boris. Centro de Educaciones Médicas e Investigación Clínica "Norberto Quirno"; ArgentinaFil: Monserrat, Alberto Juan. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Patología. Centro de Patología Experimental; Argentin

Hantavirus pulmonary syndrome in Southern Argentina

Fil: Resa, Amanda J. Hospital de Area El Bolsón; Argentina.Fil: Barclay, Carlos M. Sanatorio San Carlos; Argentina.Fil: Calanni, Liliana. Hospital Provincial de Neuquén; Argentina.Fil: Samengo, Luis. Hospital Zonal Bariloche; Argentina.Fil: Lazaro, María Ester. Hospital Zonal Bariloche; Argentina.Fil: Martinez, Lucia. Hospital Zonal Bariloche; Argentina.Fil: Padula, Paula. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina.Fil: Pini, Noemi. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Virales Humanas; Argentina,Fil: Lasala, María Beatriz. Universidad de Buenos Aires. Hospital de Clínicas José de San Martín; Argentina.Fil: Elsner, Boris. Universidad de Buenos Aires. Hospital de Clínicas José de San Martín; Argentina.Fil: Enria, Delia. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Virales Humanas; Argentina,Fil: Resa, Amanda J. Hospital de Area El Bolsón; Argentina.Fil: Barclay, Carlos M. Sanatorio San Carlos; Argentina.Fil: Calanni, Liliana. Hospital Provincial de Neuquén; Argentina.Fil: Samengo, Luis. Hospital Zonal Bariloche; Argentina.Fil: Lazaro, María Ester. Hospital Zonal Bariloche; Argentina.Fil: Martinez, Lucia. Hospital Zonal Bariloche; Argentina.Fil: Padula, Paula. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina.Fil: Pini, Noemi. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Virales Humanas Dr. Julio Maiztegui; Argentina.Fil: Lasala, María Beatriz. Universidad de Buenos Aires. Hospital de Clínicas José de San Martín; Argentina.Fil: Elsner, Boris. Universidad de Buenos Aires. Hospital de Clínicas José de San Martín; Argentina.Fil: Enria, Delia. Instituto Nacional de Enfermedades Virales Humanas Dr. Julio Maiztegui; Argentina.El virus Andes fue identificado en 1995 como el agente etiológico del Síndrome Pulmonar por Hantavirus (SPH) en la región surandina argentina. En este trabajo describimos la presentación clínica de 25 casos de SPH confirmados adquiridos en la zona entre 1993 y septiembre de 1999. La edad media fue de 34 años (rango 11-70) y el 72% eran varones. Las características clínicas fueron similares a las referidas para el virus Sin Nombre (VSN), con algunas diferencias: se presentó inyección conjuntival en 10 casos (42%), rubicundez facial en 8 (33%), fauces congestivas en 7 (29%) y petequias en 3 casos (12%). El laboratorio mostró urea plasmática elevada en 83% de los casos (media 0.77 g/l; rango 0.31-2.01) y en el 56% la creatininemia superó 20 mg/l (media 26.8 mg/l; rango: 9.6-110); en 12/12 pacientes el sedimento urinario fue patológico con proteinuria, hematuria y cilindros granulosos. Las transaminasas, elevadas en el 90% de los casos, superaron 5-10 veces su valor normal en el 50% de los pacientes. La creatinfosfoquinasa estuvo elevada en 11/14 casos. Dos pacientes requirieron hemodiálisis. Se observó miocarditis mononuclear en dos casos, un hallazgo no descripto para VSN. La letalidad fue del 44% y diez pacientes fallecieron dentro de los primeros 10 días de enfermedad. Durante el brote de SPH por virus Andes en 1996 hubo evidencias epidemiológicas y moleculares de transmisión interpersonal no demostrada hasta entonces para otros miembros del género hantavirus. Estos datos muestran algunas diferencias clínicas del SPH por virus Andes con mayor frecuencia de compromiso renal que el descripto para el VSN

Presmooth geometries

This thesis explores the geometric principles underlying many of the known Trichotomy Theorems. The main aims are to unify the field construction in non-linear o-minimal structures and generalizations of Zariski Geometries as well as to pave the road for completely new results in this direction. In the first part of this thesis we introduce a new axiomatic framework in which all the relevant structures can be studied uniformly and show that these axioms are preserved under elementary extensions. A particular focus is placed on the study of a smoothness condition which generalizes the presmoothness condition for Zariski Geometries. We also modify Zilber's notion of universal specializations to obtain a suitable notion of infinitesimals. In addition, families of curves and the combinatorial geometry of one-dimensional structures are studied to prove a weak trichotomy theorem based on very weak one-basedness. It is then shown that under suitable additional conditions groups and group actions can be constructed in canonical ways. This construction is based on a notion of ``geometric calculus'' and can be seen in close analogy with ordinary differentiation. If all conditions are met, a definable distributive action of one one-dimensional type-definable group on another are obtained. The main result of this thesis is that both o-minimal structures and generalizations of Zariski Geometries fit into this geometric framework and that the latter always satisfy the conditions required in the group constructions. We also exhibit known methods that allow us to extract fields from this. In addition to unifying the treatment of o-minimal structures and Zariski Geometries, this also gives a direct proof of the Trichotomy Theorem for "type-definable" Zariski Geometries as used, for example, in Hrushovski's proof of the relative Mordell-Lang conjecture.This thesis is not currently available in OR

Linfadenitis necrotizante de Kikuchi-Fujimoto: presentación de dos casos

Área de Salud, Economía y Socieda