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El presente artículo realiza un acercamiento a la estructura educativa ecuatoriana y su capacidad de respuesta frente a una crisis social o sanitaria. A través de la revisión de documentos oficiales, normativa, investigaciones, estudios de caso y datos históricos, se abordan algunas aristas que permitirán comprender cómo está cimentado el actual modelo educativo, donde prima la modalidad presencial y los cambios a los que se somete en una emergencia. Pone especial interés en la teleducación, el uso del internet y los medios tradicionales -radio y televisión- como alternativas de formación escolarizada en tiempos de la COVID-19. A su vez, testimonios del estudiantado, plataformas educativas, recursos audiovisuales y propuestas desde lo privado, servirán para reflexionar sobre algunos efectos puntuales de la pandemia y visibilizar realidades donde la vida y la salud se anteponen a otros derechos.

Airway remodeling (AR) with chronic inflammation, are key features in asthma pathogenesis. AR characterized by structural changes in the bronchial wall is associated with a specific asthma phenotype with poor clinical outcomes, impaired lung function and reduced treatment response. Most studies focus on the role of inflammation, while understanding the mechanisms driving AR is crucial for developing disease-modifying therapeutic strategies. This review paper summarizes current knowledge on the mechanisms underlying AR, diagnostic tools, and therapeutic approaches. Mechanisms explored include the role of the resident cells and the inflammatory cascade in AR. Diagnostic methods such as bronchial biopsy, lung function testing, imaging, and possible biomarkers are described. The effectiveness on AR of different treatments of asthma including corticosteroids, leukotriene modifiers, bronchodilators, macrolides, biologics, and bronchial thermoplasty is discussed, as well as other possible therapeutic options. AR poses a significant challenge in asthma management, contributing to disease severity and treatment resistance. Current therapeutic approaches target mostly airway inflammation rather than smooth muscle cell dysfunction and showed limited benefits on AR. Future research should focus more on investigating the mechanisms involved in AR to identify novel therapeutic targets and to develop new effective treatments able to prevent irreversible structural changes and improve long-term asthma outcomes., (Copyright © 2024 SEPAR. Published by Elsevier España, S.L.U. All rights reserved.)

Introduction: Lupus nephritis (LN) is a disease marked by autoantibodies against complement components. Autoantibodies against negative complement regulator factor H (anti-FH) are prevalent in aHUS, are associated with deletion of factor H-related protein 1 (FHR1) gene, and have overt functional consequences. They are also observed in C3 glomerulopathies. The frequency and relevance of anti-FH in LN are poorly studied., Aim: The aim of our investigation was to screen for the presence of anti-FH and FHR1 gene deletion in a cohort of LN patients and to evaluate their association with LN activity., Method: ELISA test and Western blot for detection of anti-FH and FHR1 deletion were used, respectively. Patients' clinical and laboratory parameters regarding anti-FH role were processed by statistical analysis., Results: Anti-FH were found at low level in a small number of LN patients - 11.7% (7/60) and were not associated with deletion of FHR1. Anti-FH did not correlate with ANA titers, anti-dsDNA, C3/C4 hypocomplementemia, eGFR, proteinuria, or active urinary sediment in LN patients. A weak correlation was found between anti-FH and anti-C3 levels. Anti-FH were linked with endocapillary proliferation and histological activity index. Four anti-FH positive patients had severe to moderate LN as per the BILAG renal score., Conclusions: Anti-FH autoantibodies are an accessory finding in LN and are more likely to manifest during the active phase of the disease. Due to their low frequency and plasma levels, they do not seem suitable for routine laboratory investigation in patients with LN., (Copyright © 2024 The Authors. Published by Elsevier España, S.L.U. All rights reserved.)