VIII Encuentro de Docentes e Investigadores en Historia del Diseño, la Arquitectura y la Ciudad

Acta de congresoLa conmemoración de los cien años de la Reforma Universitaria de 1918 se presentó como una ocasión propicia para debatir el rol de la historia, la teoría y la crítica en la formación y en la práctica profesional de diseñadores, arquitectos y urbanistas. En ese marco el VIII Encuentro de Docentes e Investigadores en Historia del Diseño, la Arquitectura y la Ciudad constituyó un espacio de intercambio y reflexión cuya realización ha sido posible gracias a la colaboración entre Facultades de Arquitectura, Urbanismo y Diseño de la Universidad Nacional y la Facultad de Arquitectura de la Universidad Católica de Córdoba, contando además con la activa participación de mayoría de las Facultades, Centros e Institutos de Historia de la Arquitectura del país y la región. Orientado en su convocatoria tanto a docentes como a estudiantes de Arquitectura y Diseño Industrial de todos los niveles de la FAUD-UNC promovió el debate de ideas a partir de experiencias concretas en instancias tales como mesas temáticas de carácter interdisciplinario, que adoptaron la modalidad de presentación de ponencias, entre otras actividades. En el ámbito de VIII Encuentro, desarrollado en la sede Ciudad Universitaria de Córdoba, se desplegaron numerosas posiciones sobre la enseñanza, la investigación y la formación en historia, teoría y crítica del diseño, la arquitectura y la ciudad; sumándose el aporte realizado a través de sus respectivas conferencias de Ana Clarisa Agüero, Bibiana Cicutti, Fernando Aliata y Alberto Petrina. El conjunto de ponencias que se publican en este Repositorio de la UNC son el resultado de dos intensas jornadas de exposiciones, cuyos contenidos han posibilitado actualizar viejos dilemas y promover nuevos debates. El evento recibió el apoyo de las autoridades de la FAUD-UNC, en especial de la Secretaría de Investigación y de la Biblioteca de nuestra casa, como así también de la Facultad de Arquitectura de la UCC; va para todos ellos un especial agradecimiento

Effect of remote ischaemic conditioning on clinical outcomes in patients with acute myocardial infarction (CONDI-2/ERIC-PPCI): a single-blind randomised controlled trial.

BACKGROUND: Remote ischaemic conditioning with transient ischaemia and reperfusion applied to the arm has been shown to reduce myocardial infarct size in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). We investigated whether remote ischaemic conditioning could reduce the incidence of cardiac death and hospitalisation for heart failure at 12 months. METHODS: We did an international investigator-initiated, prospective, single-blind, randomised controlled trial (CONDI-2/ERIC-PPCI) at 33 centres across the UK, Denmark, Spain, and Serbia. Patients (age >18 years) with suspected STEMI and who were eligible for PPCI were randomly allocated (1:1, stratified by centre with a permuted block method) to receive standard treatment (including a sham simulated remote ischaemic conditioning intervention at UK sites only) or remote ischaemic conditioning treatment (intermittent ischaemia and reperfusion applied to the arm through four cycles of 5-min inflation and 5-min deflation of an automated cuff device) before PPCI. Investigators responsible for data collection and outcome assessment were masked to treatment allocation. The primary combined endpoint was cardiac death or hospitalisation for heart failure at 12 months in the intention-to-treat population. This trial is registered with ClinicalTrials.gov (NCT02342522) and is completed. FINDINGS: Between Nov 6, 2013, and March 31, 2018, 5401 patients were randomly allocated to either the control group (n=2701) or the remote ischaemic conditioning group (n=2700). After exclusion of patients upon hospital arrival or loss to follow-up, 2569 patients in the control group and 2546 in the intervention group were included in the intention-to-treat analysis. At 12 months post-PPCI, the Kaplan-Meier-estimated frequencies of cardiac death or hospitalisation for heart failure (the primary endpoint) were 220 (8·6%) patients in the control group and 239 (9·4%) in the remote ischaemic conditioning group (hazard ratio 1·10 [95% CI 0·91-1·32], p=0·32 for intervention versus control). No important unexpected adverse events or side effects of remote ischaemic conditioning were observed. INTERPRETATION: Remote ischaemic conditioning does not improve clinical outcomes (cardiac death or hospitalisation for heart failure) at 12 months in patients with STEMI undergoing PPCI. FUNDING: British Heart Foundation, University College London Hospitals/University College London Biomedical Research Centre, Danish Innovation Foundation, Novo Nordisk Foundation, TrygFonden

Molecular characterization of the gene encoding a new AmpC beta-lactamase in Acinetobacter baylyi

<p><strong>Objectives: </strong>The main objective of the present study was to demonstrate the presence of a beta-lactamase ampC gene in the chromosome of the non-pathogenic bacterium Acinetobacter baylyi ADP1.</p><p><strong>Methods: </strong>beta-Lactam MICs were determined by Etest. The ampC gene was amplified by PCR, with specific oligonucleotides, then cloned into pBGS18 and pAT-RA plasmids and transformed into Escherichia coli TG1 and parental A. baylyi as hosts. The gene was sequenced and analysed. The AmpC protein was expressed, purified by affinity chromatography and the kinetic parameters determined.</p><p><strong>Results: </strong>An ampC gene was amplified from the ADP1 genome. Sequencing of the gene showed typical SVSK and KTG domains and the typical YXN Class C motif. The amplified gene showed significant identity (48.5% to 49.3%) with the AmpC enzymes of Acinetobacter baumannii and AG3 strains, which have recently been renamed ADC-1 to ADC-7. MIC analysis revealed a cephalosporinase profile for the E. coli TG1 clone as well as for the parental A. baylyi strain that overexpressed the ampC gene cloned under the control of an external promoter. Analysis of kinetic parameters of the purified enzyme showed higher catalytic efficiency for cefalotin than for ampicillin.</p><p><strong>Conclusions: </strong>This study represents the first report of an AmpC beta-lactamase in A. baylyi, which was shown by biochemical and microbiological experiments to have a typical cephalosporinase profile. The presence of the respective gene in the chromosome of A. baylyi ADP1 suggested that this ampC gene is the naturally occurring cephalosporinase in this species, as previously reported for other Acinetobacter spp. We tentatively named the enzyme ADC-8.</p&gt

Interspecies spread of CTX-M-32 extended-spectrum beta-lactamase and the role of the insertion sequence IS1 in down-regulating bla CTX-M gene expression

<p><strong>Objectives: </strong>To characterize the extended-spectrum beta-lactamases (ESBLs) as well as their genetic environment in different isolates of Enterobacteriaceae from a patient with repeated urinary tract infections.</p><p><strong>Methods: </strong>Two isolates of Escherichia coli and one Proteus mirabilis, all with ESBL phenotypes, were studied. Conjugation experiments and restriction fragment length polymorphisms (RFLPs) were performed. Cloning of the bla genes was by plasmid restriction and fragments ligation. Antibiotic susceptibility testing was by Etest. The genetic environment was analysed by direct sequencing of the DNA surrounding the bla gene. RT-PCR was performed to study the differences in the bla(CTX-M) gene expression.</p><p><strong>Results: </strong>The bla gene was transferred by conjugation from the three clinical isolates, which by RFLP showed the same plasmid. The bla gene and surrounding sequences were cloned, an approximately 9 kbp AccI fragment was sequenced and the bla(CTX-M-32) gene was identified. The MICs of ceftazidime for transconjugants and transformants bearing the bla(CTX-M-32) gene were lower than those previously reported. Analysis of the DNA surrounding the ESBL gene revealed a new genetic structure with two insertion sequences, IS5 and IS1, located immediately upstream of the bla(CTX-M-32) gene; IS1 was located between the bla gene and IS5, and within the -10 and -35 promoter boxes of the bla(CTX-M-32) gene. Microbiological and biochemical studies revealed lower bla(CTX-M-32) gene expression in bacterial isolates with IS1 between the promoter boxes.</p><p><strong>Conclusions: </strong>Data suggest putative in vivo horizontal bla(CTX-M-32) gene transfer between two different genera of Enterobacteriaceae. A new complex structure, IS5-IS1, was detected upstream of the bla gene and IS1 negatively modulated expression of the bla(CTX-M-32) gene because its location modified the bla promoter region.</p&gt