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

Early mobilisation in critically ill COVID-19 patients: a subanalysis of the ESICM-initiated UNITE-COVID observational study

Background Early mobilisation (EM) is an intervention that may improve the outcome of critically ill patients. There is limited data on EM in COVID-19 patients and its use during the first pandemic wave. Methods This is a pre-planned subanalysis of the ESICM UNITE-COVID, an international multicenter observational study involving critically ill COVID-19 patients in the ICU between February 15th and May 15th, 2020. We analysed variables associated with the initiation of EM (within 72 h of ICU admission) and explored the impact of EM on mortality, ICU and hospital length of stay, as well as discharge location. Statistical analyses were done using (generalised) linear mixed-effect models and ANOVAs. Results Mobilisation data from 4190 patients from 280 ICUs in 45 countries were analysed. 1114 (26.6%) of these patients received mobilisation within 72 h after ICU admission; 3076 (73.4%) did not. In our analysis of factors associated with EM, mechanical ventilation at admission (OR 0.29; 95% CI 0.25, 0.35; p = 0.001), higher age (OR 0.99; 95% CI 0.98, 1.00; p ≤ 0.001), pre-existing asthma (OR 0.84; 95% CI 0.73, 0.98; p = 0.028), and pre-existing kidney disease (OR 0.84; 95% CI 0.71, 0.99; p = 0.036) were negatively associated with the initiation of EM. EM was associated with a higher chance of being discharged home (OR 1.31; 95% CI 1.08, 1.58; p = 0.007) but was not associated with length of stay in ICU (adj. difference 0.91 days; 95% CI − 0.47, 1.37, p = 0.34) and hospital (adj. difference 1.4 days; 95% CI − 0.62, 2.35, p = 0.24) or mortality (OR 0.88; 95% CI 0.7, 1.09, p = 0.24) when adjusted for covariates. Conclusions Our findings demonstrate that a quarter of COVID-19 patients received EM. There was no association found between EM in COVID-19 patients' ICU and hospital length of stay or mortality. However, EM in COVID-19 patients was associated with increased odds of being discharged home rather than to a care facility. Trial registration ClinicalTrials.gov: NCT04836065 (retrospectively registered April 8th 2021)

TGF-β Prevents Phosphate-Induced Osteogenesis through Inhibition of BMP and Wnt/β-Catenin Pathways

Background: Transforming growth factor-b (TGF-b) is a key cytokine during differentiation of mesenchymal stem cells (MSC) into vascular smooth muscle cells (VSMC). High phosphate induces a phenotypic transformation of vascular smooth muscle cells (VSMC) into osteogenic-like cells. This study was aimed to evaluate signaling pathways involved during VSMC differentiation of MSC in presence or not of high phosphate. Results: Our results showed that TGF-b induced nuclear translocation of Smad3 as well as the expression of vascular smooth muscle markers, such as smooth muscle alpha actin, SM22a, myocardin, and smooth muscle-myosin heavy chain. The addition of high phosphate to MSC promoted nuclear translocation of Smad1/5/8 and the activation of canonical Wnt/bcatenin in addition to an increase in BMP-2 expression, calcium deposition and alkaline phosphatase activity. The administration of TGF-b to MSC treated with high phosphate abolished all these effects by inhibiting canonical Wnt, BMP and TGF-b pathways. A similar outcome was observed in high phosphate-treated cells after the inhibition of canonical Wnt signaling with Dkk-1. Conversely, addition of both Wnt/b-catenin activators CHIR98014 and lithium chloride enhanced the effect of high phosphate on BMP-2, calcium deposition and alkaline phosphatase activity. Conclusions: Full VSMC differentiation induced by TGF-b may not be achieved when extracellular phosphate levels are high. Moreover, TGF-b prevents high phosphate-induced osteogenesis by decreasing the nuclear translocation of Smad 1/5/8 and avoiding the activation of Wnt/b-catenin pathway

Dkk-1 inhibits the high phosphate-induced osteogenic-like characteristics in rat mesenchymal stem cells.

<p>A) Rat mesenchymal cells treated with high phosphate and Dkk-1 were stained for β-catenin immunofluorescence (green) and counterstained with DAPI (blue) to determine β-catenin subcellular localization. Merged images of β-catenin immunofluorescence and DAPI staining are shown. Dkk-1 administration reduced nuclear translocation of β-catenin. Original magnification: 40x. B) BMP-2 mRNA expression in rat mesenchymal stem cells treated with high phosphate and Dkk-1 was determined by RT-PCR (a p<0.001 vs high phosphate treated cells). C) Calcium content and alkaline phosphatase activity (Units/mg protein) in rat mesenchymal stem cells treated with high phosphate and Dkk-1 (a p<0.001 vs high phosphate alone). Image is representative of three experiments.</p

TGF-β administration prevents osteogenic effects induced by high phosphate.

<p>A) High phosphate (P) increased the expression of BMP-2 while TGF-β or the combination of TGF-β plus high phosphate decreased significantly the expression of this osteogenic marker (a p<0.001 vs. all groups). Results are expressed as fold change vs. Control cells. B) High phosphate (P) decreased significantly SM22α and myocardin expression with respect to Control cells (b p<0.01 for SM22α and a p<0.001 for myocardin) and TGF-β group (c p<0.001). The combination of TGF- β and high phosphate (TGF-β + P) decreased the expression of SM22α and Myocardin although less than high phosphate alone (c p <0.001vs. TGF-β group). C) TGF-β alone did not change significantly the alkaline phosphatase activity. This activity increased after high phosphate treatment (a p<0.001 vs. all others groups). The combination of TGF-β and high phosphate for 14 days significantly decreased this activity when compared with high phosphate group. D) Calcium content was significantly increased after high phosphate treatment (a p<0.001 vs other groups). The combination of TGF-β and high phosphate prevented this increase of calcium induced by high phosphate alone.</p

TGF-β induces vascular smooth muscle cells differentiation of mesenchymal stem cells through nuclear translocation of Smad3.

<p>A) Rat mesenchymal cells treated with TGF-β for 14 days were stained for phospho-Smad3 immunofluorescence (red) and counterstained with DAPI (blue) to determine phospho-Smad3 subcellular localization. In TGF-β treated cells, positive phospho-Smad3 immunofluorescence was localized into the nucleus. Original magnification: 40x. B) Vascular smooth muscle actin (VSM-actin, green) was stained and the nuclei were counter-stained with DAPI showing cytoskeleton organization in Control cells and TGF-β treated cells. Original magnification: 20x.C) After 7 and 14 days, TGF-β induced the expression of vascular smooth muscle cells markers such as VSM-actin, SM22α, Myocardin and Myosin heavy chain with respect to control cells (a p<0.001 vs. control cells). Images are representative of three experiments.</p

Wnt/β-catenin pathway activation enhances the high phosphate-induced osteogenic-like characteristics in rat mesenchymal stem cells.

<p>A) Rat mesenchymal cells treated with high phosphate and CHIR98014 (0.4 µM) or lithium chloride (5 mM) were stained for β-catenin immunofluorescence (green) and counterstained with DAPI (blue) to determine β-catenin subcellular localization. Merged images of β-catenin immunofluorescence and DAPI staining are shown. Both Wnt activators (CHIR98014 and lithium chloride) increased nuclear translocation of β-catenin. Original magnification: 40x. B) BMP-2 protein and C) mRNA expression in rat mesenchymal stem cells treated with high phosphate and CHIR98014 or lithium chloride was determined by western blot and RT-PCR respectively (a p < 0.001 vs high phosphate alone). D) Calcium content and E) alkaline phosphatase activity in rat mesenchymal stem cells treated with high phosphate and CHIR98014or lithium chloride (a p<0.001 vs. high phosphate alone). Image is representative of three experiments.</p

High phosphate activates Wnt/β-catenin pathway.

<p>A) Rat mesenchymal cells treated with TGF-β and/or high phosphate were stained for β-catenin immunofluorescence (green) and counterstained with DAPI (blue) to determine β-catenin subcellular localization. Merged images of β-catenin immunofluorescence and DAPI staining are shown. High phosphate induced nuclear translocation of β-catenin while the addition of TGF-β inhibited this translocation. Original magnification: 40x. Image is representative of three experiments. B) Quantification of β-catenin confocal immunofluorescence was performed with Image J software (a p<0.001 vs. all groups). C) With respect to control cells high phosphate decreased the expression of Dkk1 (b p<0.001) and Gsk3β (b p<0.001) while increased the expression of Lrp5 with respect to other groups (d p<0.001). These differences were also significant respect to TGF-β treated groups (c p<0.001 vs. TGF groups). TGF-β alone increased the expression of Dkk1 and Gsk3β (a p<0.001).</p

TGF-β addition inhibits nuclear translocation of Smad 1/5/8 induced by high Phosphate.

<p>A) Rat mesenchymal stem cells treated with high phosphate showed nuclear localization of phospho-Smad1/5/8 (Red) (a p<0.001 vs. all groups). Cells treated with TGF-β (alone or plus high phosphate) were negative for phospho-Smad1/5/8. Merged images of phospho-Smad1/5/8 immunofluorescence and DAPI staining are shown. Original magnification: 40x. Image is representative of three experiments. Colocalization Finder plugging from Image J software was carried out to analyse nuclear localization of Smad 1/5/8 showing a submask with white areas specific to nuclear colocalization with DAPI. Original magnification: 40x. B) Quantification of confocal immunofluorescence was performed with Image J software.</p