50 years training high-quality professionals: The plans of study at the School of Architecture, University of the Bío-Bío (1969-2014)

This article presents the evolution of the Architecture degree program at the University of the Bío-Bío (UBB) from its creation to the present, through the eight plans of study that have marked the training of the different cohorts that have graduated from this school. The methodology involved the exploration of the existing documentation in archives, from the founding ideology up until today. The agreements that defined the graduate profile and that identify the architects trained at UBB, and the creation of the plans of study and the curriculum diagrams were also examined. The career paths of some of the teachers who brought to life these teaching processes in the classroom were analyzed in accordance with the national and local events of that time. Precisely when this school celebrates 50 years of training professional architects of great national prestige, this tour of its pedagogical models reaffirms its well-deserved third place ranking in architectural degrees in the country and revalidates its international accreditation by the Royal Institute of British Architects (RIBA) since 1991.El artículo presenta la trayectoria de la carrera de Arquitectura de la UBB, desde su creación a la actualidad, a través de los ocho planes de estudio que marcaron la formación de las distintas cohortes profesionales que egresaron de esta escuela. La metología exploró la documentación existente en archivos desde su ideario fundacional a la fecha, también revisó los acuerdos que definieron el perfil de egreso y que identifican al arquitecto UBB, la construcción de los planes de estudio, de las mallas curriculares, y analizó la trayectoria de algunos de los profesores que materializaron en las aulas esos procesos de enseñanza en correspondencia con los acontecimientos nacionales y locales de esa época. Justamente, cuando esta Escuela cumple 50 años formando profesionales arquitectos de gran prestigio nacional, este recorrido por sus modelos pedagógicos reafirma el merecido tercer lugar que le fuera concedido entre las carreras de arquitectura en el país y revalida la acreditación internacional otorgada por el Royal Institute of British Architects (RIBA) desde el año 1991.O artigo apresenta a trajetória do curso de Arquitetura da UBB desde sua criação até a atualidade através dos oitos planos de estudo que marcaram a formação de distintos grupos professionais egressos desta escola. A metodologia explorou a documentação existente em arquivos desde sua ideologia fundadora à atualidade, também revisou os acordos que definiram o perfil de egresso e que identificam o arquiteto UBB, a construção dos planos de estudo, das grades curriculares, e analizou a trajetória de alguns dos professores que materializaram em classe esses processos de ensino em correspondência com os acontecimentos nacionais e locais da época. Justamente, quando esta Escola completa 50 anos de trajetória formando profissionais arquitetos de grande perstigio nacional, esta incursão por seus modelos pedagógicos reafirma o merecido terceiro lugar que lhe foi concedido entre os cursos de arquitetura do país e revalida a acreditação internacional outorgada pela Royal Institute of British Architects (RIBA) desde 1991

The mTOR inhibitor Rapamycin protects from premature cellular senescence early after experimental kidney transplantation

Interstitial fibrosis and tubular atrophy, a major cause of kidney allograft dysfunction, has been linked to premature cellular senescence. The mTOR inhibitor Rapamycin protects from senescence in experimental models, but its antiproliferative properties have raised concern early after transplantation particularly at higher doses. Its effect on senescence has not been studied in kidney transplantation, yet. Rapamycin was applied to a rat kidney transplantation model (3 mg/kg bodyweight loading dose, 1.5 mg/kg bodyweight daily dose) for 7 days. Low Rapamycin trough levels (2.1-6.8 ng/mL) prevented the accumulation of p16(INK4a) positive cells in tubules, interstitium, and glomerula. Expression of the cytokines MCP-1, IL-1 beta, and TNF-alpha, defining the proinflammatory senescence-associated secretory phenotype, was abrogated. Infiltration with monocytes/macrophages and CD8(+) T-lymphocytes was reduced and tubular function was preserved by Rapamycin. Inhibition of mTOR was not associated with impaired structural recovery, higher glucose levels, or weight loss. mTOR inhibition with low-dose Rapamycin in the immediate posttransplant period protected from premature cellular senescence without negative effects on structural and functional recovery from preservation/reperfusion damage, glucose homeostasis, and growth in a rat kidney transplantation model. Reduced senescence might maintain the renal regenerative capacity rendering resilience to future injuries resulting in protection from interstitial fibrosis and tubular atrophy

The use of interstitial echo-guided diode laser 980-nm for deep vascular anomalies in pediatric patients: a preliminary study

A wide range of therapeutic options is available to treat vascular anomalies, arising from the systemic therapies to surgery or using lasers. The purpose of this preliminary study is to assess the effectiveness of treatment of vascular anomalies anywhere in the body, along with the use of interstitial echo-guided 980 nm diode laser. The analysis occurs through accurate angio magnetic resonance imaging (MRI) pre- and post-treatment measurements. We enrolled all the patients (16) affected on vascular malformations everywhere in the body, treated from January to August 2012. We obtained excellent results in 6 patients (37.5%) with mean mass reduction of 85%, good in 9 patients (56%) with mean mass reduction of 65% and unsatisfactory in 1 patient (6%). In pediatric patients, low-flow vascular malformations resistant to progressive sclerotherapy or in critical anatomical sites, benefit of echo guided interstitial 980-nm diode laser

Toscana Virus in Spain

Toscana virus (TOSV, Phlebovirus, family Bunyaviridae) infection is one of the most prevalent arboviruses in Spain. Within the objectives of a multidisciplinary network, a study on the epidemiology of TOSV was conducted in Granada, in southern Spain. The overall seroprevalence rate was 24.9%, significantly increasing with age. TOSV was detected in 3 of 103 sandfly pools by viral culture or reverse transcription–polymerase chain reaction from a region of the L gene. Nucleotide sequence homology was 99%–100% in TOSV from vectors and patients and 80%–81% compared to the Italian strain ISS Phl.3. Sequencing of the N gene of TOSV isolates from patients and vectors indicated 87%–88% and 100% homology at the nucleotide and amino acid levels, respectively, compared to the Italian strain. These findings demonstrate the circulation of at least 2 different lineages of TOSV in the Mediterranean basin, the Italian lineage and the Spanish lineage.Grant sponsor was Red EVITAR, Fondo de Investigaciones Sanitarias, Spanish Ministry of Health, grant no. G03/059. Ximena Collao has a research grant from Valparaiso University (MECESUP project, Chile). The study of vectors, i.e., capture of phlebotomines and taxonomic classification, was supported by the Junta de Andalucía, research grant CVI 176. Dr Sanbonmatsu-Gámez is a microbiologist on a fellowship from the EVITAR network (Fondo de Investigaciones Sanitarias, Spanish Ministry of Health; grant no. G03/059). Her research interest focuses on viral infectious diseases, especially arthropodborne viral diseases

Scn1a gene reactivation after symptom onset rescues pathological phenotypes in a mouse model of Dravet syndrome

Dravet syndrome is a severe epileptic encephalopathy caused primarily by haploinsufficiency of the SCN1A gene. Repetitive seizures can lead to endurable and untreatable neurological deficits. Whether this severe pathology is reversible after symptom onset remains unknown. To address this question, we generated a Scn1a conditional knock-in mouse model (Scn1a Stop/+) in which Scn1a expression can be re-activated on-demand during the mouse lifetime. Scn1a gene disruption leads to the development of seizures, often associated with sudden unexpected death in epilepsy (SUDEP) and behavioral alterations including hyperactivity, social interaction deficits and cognitive impairment starting from the second/third week of age. However, we showed that Scn1a gene re-activation when symptoms were already manifested (P30) led to a complete rescue of both spontaneous and thermic inducible seizures, marked amelioration of behavioral abnormalities and normalization of hippocampal fast-spiking interneuron firing. We also identified dramatic gene expression alterations, including those associated with astrogliosis in Dravet syndrome mice, that, accordingly, were rescued by Scn1a gene expression normalization at P30. Interestingly, regaining of Nav1.1 physiological level rescued seizures also in adult Dravet syndrome mice (P90) after months of repetitive attacks. Overall, these findings represent a solid proof-of-concept highlighting that disease phenotype reversibility can be achieved when Scn1a gene activity is efficiently reconstituted in brain cells

Bunyaviruses and the Type I Interferon System

The family Bunyaviridae contains more than 350 viruses that are distributed throughout the world. Most members of the family are transmitted by arthopods, and several cause disease in man, domesticated animals and crop plants. Despite being recognized as an emerging threat, details of the virulence mechanisms employed by bunyaviruses are scant. In this article we summarise the information currently available on how these viruses are able to establish infection when confronted with a powerful antiviral interferon system

dCas9-Based Scn1a Gene Activation Restores Inhibitory Interneuron Excitability and Attenuates Seizures in Dravet Syndrome Mice

Dravet syndrome (DS) is a severe epileptic encephalopathy caused mainly by heterozygous loss-of-function mutations of the SCN1A gene, indicating haploinsufficiency as the pathogenic mechanism. Here we tested whether catalytically dead Cas9 (dCas9)-mediated Scn1a gene activation can rescue Scn1a haploinsufficiency in a mouse DS model and restore physiological levels of its gene product, the Nav1.1 voltage-gated sodium channel. We screened single guide RNAs (sgRNAs) for their ability to stimulate Scn1a transcription in association with the dCas9 activation system. We identified a specific sgRNA that increases Scn1a gene expression levels in cell lines and primary neurons with high specificity. Nav1.1 protein levels were augmented, as was the ability of wild-type immature GABAergic interneurons to fire action potentials. A similar enhancement of Scn1a transcription was achieved in mature DS interneurons, rescuing their ability to fire. To test the therapeutic potential of this approach, we delivered the Scn1a-dCas9 activation system to DS pups using adeno-associated viruses. Parvalbumin interneurons recovered their firing ability, and febrile seizures were significantly attenuated. Our results pave the way for exploiting dCas9-based gene activation as an effective and targeted approach to DS and other disorders resulting from altered gene dosage

Roberto Goycoolea I.

Toda su historia desde 1948 - 1995