Convergència Democràtica de Catalunya: un partit de gent i nacionalista en l'etapa de fer govern

Convergència Democratica de Catalunya (CDC) és un partit que, des del punteng de vista ideològic, s'ha d'etiquetar com a partit nacionalista, ja que allò que el defineix, tant des d' una òptica interna com des de l'exterior del partit, és el nacionalisme. Els orígens i els fonaments del nacionalisme de CDC cal buscar-los en el nacionalisme personalista de Jordi Pujol i, en general, en el seu pensament polític, l'aplicació del qual s'ha fet en quatre fases acumulatives: la de "fer país", la de "fer política", la de "fer partit" (aquestes tres explicitades pel mateix Jordi Pujol) i la que I'autor anomena "fer govern". I pel que fa al concepte de nació que defensa CDC, s'hi pot percebre la influència de Rovira i Virgili i de Prat de la Riba. CDC i Jordi Pujol no defensen un nacionalisme ideològic, sinó un nacionalisme entès com una ètica i, a més, globalitzador, ès a dir, sense exclusions previes i integrador. Sovint s'ha considerat que CDC més que un partit és un moviment, però I'autor s'inclina per qualificar CDC com un catch-allparty o partit arreplegador o, com el mateix Jordi Pujol diu, un "partit de gent".

Resistência de goiabeiras e araçazeiros a Meloidogyne mayaguensis

O objetivo deste trabalho foi identificar espécies de Myrtaceae resistentes a Meloidogyne mayaguensis. Acessos de araçazeiros e goiabeiras da Coleção de Plantas Frutíferas Nativas e Exóticas da Unesp/FCAV e acessos de araçazeiro de fragmentos de matas nativas do Nordeste do Estado de São Paulo e Triângulo Mineiro foram testados quanto à resistência ao nematódeo. As mudas receberam 4.000 ovos e juvenis de segundo estádio de M. mayaguensis por planta e foram conduzidas em casa de vegetação. Aos 150 dias, os genótipos foram avaliados quanto à resistência ao nematódeo com base no fator de reprodução. Três acessos de Psidium e um de Eugenia foram resistentes a M. mayaguensis.

Setmana internacional de l'accés obert 2011

La UOC participa aquesta edició en la Setmana Internacional de l'Accés obert (Open Access Week), que se celebra arreu del món del 24 al 30 d'octubre de 2011, adoptant el lema "L'accés obert a la UOC". Amb aquest motiu els vicerectors de la UOC ens expliquen la importància dels continguts en accés obert, quina és la política seguida a la UOC, com aquests recursos milloren la visibilitat de la docència i la recerca portades a terme a la UOC...

UOC Open Access Week 2011

La UOC participa aquesta edició en la Setmana Internacional de l'Accés obert (Open Access Week), que se celebra arreu del món del 24 al 30 d'octubre de 2011, adoptant el lema "L'accés obert a la UOC". Amb aquest motiu els vicerectors de la UOC ens expliquen la importància dels continguts en accés obert, quina és la política seguida a la UOC, com aquests recursos milloren la visibilitat de la docència i la recerca portades a terme a la UOC...

Semana internacional del acceso abierto 2011

La UOC participa aquesta edició en la Setmana Internacional de l'Accés obert (Open Access Week), que se celebra arreu del món del 24 al 30 d'octubre de 2011, adoptant el lema "L'accés obert a la UOC". Amb aquest motiu els vicerectors de la UOC ens expliquen la importància dels continguts en accés obert, quina és la política seguida a la UOC, com aquests recursos milloren la visibilitat de la docència i la recerca portades a terme a la UOC...

Job accessibility, employment and job-education mismatch in the metropolitan area of Barcelona

This paper analyses the effect of job accessibility by public and private transport on labour market outcomes in the metropolitan area of Barcelona. Beyond employment, we consider the effect of job accessibility on job-education mismatch, which represents a relevant aspect of job quality. We adopt a recursive system of equations that models car availability, employment and mismatch. Public transport accessibility appears as an exogenous variable in the three equations. Even though it may reflect endogenous residential sorting, falsification proofs suggest that the estimated effect of public transport accessibility is not entirely driven by the endogenous nature of residential decisions.

Onicomicosis distales versus onicomicosis tanto discal como totales. Agentes etiológicos

En el trabajo que se presenta se ha tratado de obtener muestras clínicas de onicomicosis distales única mente, para posteriormente hacerlo de onicomicosis con afectación tanto distal como total, en pacientes de la Clínica de Podología de la Universitat de Barcelona. A partir de estas muestras se procedió a aislar los hongos presentes y determinar las especies fúngicas que los afectan. Finalmente se realizó una comparación de las diferentes especies fúngicas aisladas entre las onicomicosis distales y las totales

A mechanism of carbapenem resistance due to a new insertion element (ISPa133) in Pseudomonas aeruginosa

This study explored the evolutionary mechanism by which the clinical isolate PA110514 yields the imipenemresistant derivative PA116136. Both isolates were examined by PFGE and SDS-PAGE, which led to the identification of a new insertion sequence, ISPa133. This element was shown to have distinct chromosomal locations in each of the original isolates that appeared to explain the differences in imipenem susceptibilty. In strain PA110514, ISPa133 is located 56 nucleotides upstream of the translational start codon, which has no effect on expression of the porin OprD. However, in strain PA116136 ISPa133 it is located in front of nucleotide 696 and, by interrupting the coding region, causes a loss of OprD expression, thus conferring imipenem resistance. In vitro experiments mimicking the natural conditions of selective pressure yielded imipenem-resistant strains in which ISPa133 similarly interrupted oprD. A mechanism is proposed whereby ISPa133 acts as a mobile switch, with its position in oprD depending on the degree of selective pressure exerted by imipenem

A mechanism of carbapenem resistance due to a new insertion element (ISPa133) in Pseudomonas aeruginosa

This study explored the evolutionary mechanism by which the clinical isolate PA110514 yields the imipenemresistant derivative PA116136. Both isolates were examined by PFGE and SDS-PAGE, which led to the identification of a new insertion sequence, ISPa133. This element was shown to have distinct chromosomal locations in each of the original isolates that appeared to explain the differences in imipenem susceptibilty. In strain PA110514, ISPa133 is located 56 nucleotides upstream of the translational start codon, which has no effect on expression of the porin OprD. However, in strain PA116136 ISPa133 it is located in front of nucleotide 696 and, by interrupting the coding region, causes a loss of OprD expression, thus conferring imipenem resistance. In vitro experiments mimicking the natural conditions of selective pressure yielded imipenem-resistant strains in which ISPa133 similarly interrupted oprD. A mechanism is proposed whereby ISPa133 acts as a mobile switch, with its position in oprD depending on the degree of selective pressure exerted by imipenem

A mechanism of carbapenem resistance due to a new insertion element (ISPa133) in Pseudomonas aeruginosa

This study explored the evolutionary mechanism by which the clinical isolate PA110514 yields the imipenemresistant derivative PA116136. Both isolates were examined by PFGE and SDS-PAGE, which led to the identification of a new insertion sequence, ISPa133. This element was shown to have distinct chromosomal locations in each of the original isolates that appeared to explain the differences in imipenem susceptibilty. In strain PA110514, ISPa133 is located 56 nucleotides upstream of the translational start codon, which has no effect on expression of the porin OprD. However, in strain PA116136 ISPa133 it is located in front of nucleotide 696 and, by interrupting the coding region, causes a loss of OprD expression, thus conferring imipenem resistance. In vitro experiments mimicking the natural conditions of selective pressure yielded imipenem-resistant strains in which ISPa133 similarly interrupted oprD. A mechanism is proposed whereby ISPa133 acts as a mobile switch, with its position in oprD depending on the degree of selective pressure exerted by imipenem

A mechanism of carbapenem resistance due to a new insertion element (ISPa133) in Pseudomonas aeruginosa

This study explored the evolutionary mechanism by which the clinical isolate PA110514 yields the imipenemresistant derivative PA116136. Both isolates were examined by PFGE and SDS-PAGE, which led to the identification of a new insertion sequence, ISPa133. This element was shown to have distinct chromosomal locations in each of the original isolates that appeared to explain the differences in imipenem susceptibilty. In strain PA110514, ISPa133 is located 56 nucleotides upstream of the translational start codon, which has no effect on expression of the porin OprD. However, in strain PA116136 ISPa133 it is located in front of nucleotide 696 and, by interrupting the coding region, causes a loss of OprD expression, thus conferring imipenem resistance. In vitro experiments mimicking the natural conditions of selective pressure yielded imipenem-resistant strains in which ISPa133 similarly interrupted oprD. A mechanism is proposed whereby ISPa133 acts as a mobile switch, with its position in oprD depending on the degree of selective pressure exerted by imipenem

A mechanism of carbapenem resistance due to a new insertion element (ISPa133) in Pseudomonas aeruginosa

This study explored the evolutionary mechanism by which the clinical isolate PA110514 yields the imipenemresistant derivative PA116136. Both isolates were examined by PFGE and SDS-PAGE, which led to the identification of a new insertion sequence, ISPa133. This element was shown to have distinct chromosomal locations in each of the original isolates that appeared to explain the differences in imipenem susceptibilty. In strain PA110514, ISPa133 is located 56 nucleotides upstream of the translational start codon, which has no effect on expression of the porin OprD. However, in strain PA116136 ISPa133 it is located in front of nucleotide 696 and, by interrupting the coding region, causes a loss of OprD expression, thus conferring imipenem resistance. In vitro experiments mimicking the natural conditions of selective pressure yielded imipenem-resistant strains in which ISPa133 similarly interrupted oprD. A mechanism is proposed whereby ISPa133 acts as a mobile switch, with its position in oprD depending on the degree of selective pressure exerted by imipenem

A mechanism of carbapenem resistance due to a new insertion element (ISPa133) in Pseudomonas aeruginosa

This study explored the evolutionary mechanism by which the clinical isolate PA110514 yields the imipenemresistant derivative PA116136. Both isolates were examined by PFGE and SDS-PAGE, which led to the identification of a new insertion sequence, ISPa133. This element was shown to have distinct chromosomal locations in each of the original isolates that appeared to explain the differences in imipenem susceptibilty. In strain PA110514, ISPa133 is located 56 nucleotides upstream of the translational start codon, which has no effect on expression of the porin OprD. However, in strain PA116136 ISPa133 it is located in front of nucleotide 696 and, by interrupting the coding region, causes a loss of OprD expression, thus conferring imipenem resistance. In vitro experiments mimicking the natural conditions of selective pressure yielded imipenem-resistant strains in which ISPa133 similarly interrupted oprD. A mechanism is proposed whereby ISPa133 acts as a mobile switch, with its position in oprD depending on the degree of selective pressure exerted by imipenem

A mechanism of carbapenem resistance due to a new insertion element (ISPa133) in Pseudomonas aeruginosa

This study explored the evolutionary mechanism by which the clinical isolate PA110514 yields the imipenemresistant derivative PA116136. Both isolates were examined by PFGE and SDS-PAGE, which led to the identification of a new insertion sequence, ISPa133. This element was shown to have distinct chromosomal locations in each of the original isolates that appeared to explain the differences in imipenem susceptibilty. In strain PA110514, ISPa133 is located 56 nucleotides upstream of the translational start codon, which has no effect on expression of the porin OprD. However, in strain PA116136 ISPa133 it is located in front of nucleotide 696 and, by interrupting the coding region, causes a loss of OprD expression, thus conferring imipenem resistance. In vitro experiments mimicking the natural conditions of selective pressure yielded imipenem-resistant strains in which ISPa133 similarly interrupted oprD. A mechanism is proposed whereby ISPa133 acts as a mobile switch, with its position in oprD depending on the degree of selective pressure exerted by imipenem

A mechanism of carbapenem resistance due to a new insertion element (ISPa133) in Pseudomonas aeruginosa

This study explored the evolutionary mechanism by which the clinical isolate PA110514 yields the imipenemresistant derivative PA116136. Both isolates were examined by PFGE and SDS-PAGE, which led to the identification of a new insertion sequence, ISPa133. This element was shown to have distinct chromosomal locations in each of the original isolates that appeared to explain the differences in imipenem susceptibilty. In strain PA110514, ISPa133 is located 56 nucleotides upstream of the translational start codon, which has no effect on expression of the porin OprD. However, in strain PA116136 ISPa133 it is located in front of nucleotide 696 and, by interrupting the coding region, causes a loss of OprD expression, thus conferring imipenem resistance. In vitro experiments mimicking the natural conditions of selective pressure yielded imipenem-resistant strains in which ISPa133 similarly interrupted oprD. A mechanism is proposed whereby ISPa133 acts as a mobile switch, with its position in oprD depending on the degree of selective pressure exerted by imipenem