313 Probability of significant coronary artery disease in Southern France: A need for distinctive predictive models

Como podrá establecerse en el desarrollo de esta investigación, la búsqueda de derroteros para la solución a este grave problema de “falta de vivienda”, ha determinado que los estados se preocupen por integrar a sus cartas magnas los derechos de las personas a contar con el apoyo de ellos para la satisfacción de su necesidad de contar con una vivienda, y a los organismos internacionales así mismo a interesarse por apoyar a los estados, en el estudio de la problemática y a dispensar recursos humanos y económicos para coadyuvar en la solución sobre todo, en beneficio de los sectores económicamente menos favorecidos. Por otro lado hay que entender que el problema de la vivienda es estructural y por lo tanto debe ser enfrentado desde los aspectos, teóricos, poblacionales, de desarrollo urbano, diseño, tecnología, factores económicos, sociales, políticos y culturales y sobre todo del aprovechamiento los recursos adaptándolos a la realidad existente en un mundo tan velozmente cambiante por la globalización. Además hay que destacar la importancia que para los países, conlleva el establecimiento de políticas de vivienda con tecnologías apropiadas, sobre todo en la Vivienda de Interés Social, que de manera integral y pragmática determinen acciones novedosas y dinámicas, que sostenidas en el tiempo y el espacio se conviertan en Objetivo Nacional Permanente, que permita elevar el bienestar y el mejoramiento de las condiciones de vida de los pueblos.1. Antecedentes 2.Aspectos Normativos Institucionales 3.Situación de la Vivienda en el Ecuador durante los períodos censales 4. Política de Vivienda 5.Propuesta 6.Conclusiones y Recomendacione

COVID-19 Vaccination Limits Systemic Danger Signals in SARS-CoV-2 Infected Patients

Vaccination with an mRNA COVID-19 vaccine determines not only a consistent reduction in the risk of SARS-CoV-2 infection but also contributes to disease attenuation in infected people. Of note, hyperinflammation and damage-associated molecular patterns (DAMPs) have been clearly associated with severe illness and poor prognosis in COVID-19 patients. In this report, we revealed a significant reduction in the levels of IL-1ß and DAMPs molecules, as S100A8 and High Mobility Group Protein B1 (HMGB1), in vaccinated patients as compared to non-vaccinated ones. COVID-19 vaccination indeed prevents severe clinical manifestations in patients and limits the release of systemic danger signals in SARS-CoV-2 infected people

IL1β Promotes TMPRSS2 Expression and SARS-CoV-2 Cell Entry Through the p38 MAPK-GATA2 Axis

: After the outburst of the SARS-CoV-2 pandemic, a worldwide research effort has led to the uncovering of many aspects of the COVID-19, among which we can count the outstanding role played by inflammatory cytokine milieu in the disease progression. Despite that, molecular mechanisms that regulate SARS-CoV-2 pathogenesis are still almost unidentified. In this study, we investigated whether the pro-inflammatory milieu of the host affects the susceptibility of SARS-CoV-2 infection by modulating ACE2 and TMPRSS2 expression. Our results indicated that the host inflammatory milieu favors SARS-CoV-2 infection by directly increasing TMPRSS2 expression. We unveiled the molecular mechanism that regulates this process and that can be therapeutically advantageously targeted

Constitutive activation of MAPK cascade in Acute Quadriplegic Myopathy

Acute quadriplegic myopathy (AQM; also called "critical illness myopathy") shows acute muscle wasting and weakness and is experienced by some patients with severe systemic illness, often associated with administration of corticosteroids and/or neuroblocking agents. Key aspects of AQM include muscle atrophy and myofilament loss. Although these features are shared with neurogenic atrophy, myogenic atrophy in AQM appears mechanistically distinct from neurogenic atrophy. Using muscle biopsies from AQM, neurogenic atrophy, and normal controls, we show that both myogenic and neurogenic atrophy share induction of myofiber-specific ubiquitin/proteosome pathways (eg, atrogin-1). However, AQM patient muscle showed a specific strong induction of transforming growth factor (TGF)-beta/MAPK pathways. Atrophic AQM myofibers showed coexpression of TGF-beta receptors, p38 MAPK, c-jun, and c-myc, including phosphorylated active forms, and these same fibers showed apoptotic features. Our data suggest a model of AQM pathogenesis in which stress stimuli (sepsis, corticosteroids, pH imbalance, osmotic imbalance) converge on the TGF-beta pathway in myofibers. The acute stimulation of the TGF-beta/MAPK pathway, coupled with the inactivity-induced atrogin-1/proteosome pathway, leads to the acute muscle loss seen in AQM patients