When Did It Begin? Catholic and Public School Classroom Commonalities

Catholic educational historians note that although preserving Catholic identity has been a constant in the mission of Catholic schools, their curriculum and instructional practices evolved in ways that were similar to public schools, thus enabling Catholic parents to select schools that were both faith based and modern. Since there is an absence of information about when and how this change in Catholic education began, this article documents its origin in the 1940s when Catholic educators joined a public school reform movement called Life Adjustment Education. Once begun, there was no turning back, and Catholic educators participated in the major reforms of the next two decades, discipline-centered curriculum reform and humanistic education. Two case studies are presented to illustrate what reform-based Catholic schools were like in the 1970s, followed by a brief analysis of Catholic school participation in the contemporary common core state standards movement. Points communs entre les classes des écoles catholiques et des écoles publiques : Une perspective historique Les historiens de l\u27enseignement catholique ont remarqué que si la préservation de leur identité catholique représente un trait constant de la mission des écoles catholiques, leurs programmes et pratiques pédagogiques ont évolué de la même manière que dans les écoles publiques, ce qui permet aux parents catholiques de choisir des écoles à la fois confessionnelles et modernes. Étant donné le manque d\u27information sur le moment et le lieu où ces changements ont commencé dans l\u27enseignement catholique, cet article cite des documents qui situent son origine dans les années 1940, lorsque les enseignants catholiques se sont associés à un mouvement de réforme des écoles publiques appelé enseignement adapté à la vie. Une fois ce mouvement amorcé, aucun retour en arrière n\u27a été possible et les enseignants catholiques ont pris part aux principales réformes des vingt ans suivants : réforme de l\u27enseignement basé sur la discipline et éducation humaniste. L\u27essai qui suit présente deux études de cas illustrant la manière dont se présentaient les écoles catholiques inspirées par la réforme dans les années 1970, suivies d\u27une brève analyse de la participation des écoles catholiques dans le mouvement actuel en faveur du « Common Core State Standards » (Socle de normes communes établies par État). Mots-clés: Identité catholique, mission, enseignement adapté à la vie, réforme de l\u27enseignement Semejanzas en las aulas de las escuelas católicas y públicas: una perspectiva histórica Los historiadores de la educación católica han constatado que a pesar de que la preservación de la identidad católica ha sido una misión constante de las escuelas católicas, su currículo y sus prácticas educativas se han desarrollado de manera muy similar a las de las escuelas públicas, lo que ha permitido que los padres católicos pudieran elegir escuelas que fueran a la vez religiosas y modernas. Debido a la ausencia de información sobre cuándo y cómo empezó este cambio en la educación católica, este artículo documenta su origen en los años 40, momento en que los educadores católicos se unieron al movimiento de reforma educativa llamado educación adaptada a la vida. En cuanto empezó este esfuerzo, no hubo marcha atrás. Los educadores católicos participaron en las profundas reformas de las siguientes dos décadas: reforma del currículo centrado en las disciplinas y educación humanística. El siguiente ensayo presenta dos estudios de caso que ilustran cómo eran las escuelas católicas basadas en la reforma en los años 70, y finalmente expone un breve análisis de la participación de la escuela católica en el movimiento contemporáneo de los estándares estatales comunes. Palabras clave: Identidad católica, misión, educación adaptada a la vida, reforma educativ

Global patterns of care in advanced stage mycosis fungoides/Sezary syndrome: a multicenter retrospective follow-up study from the Cutaneous Lymphoma International Consortium

ABSTRACT Background Advanced-stage mycosis fungoides (MF)/Sezary syndrome (SS) patients are weighted by an unfavorable prognosis and share an unmet clinical need of effective treatments. International guidelines are available detailing treatment options for the different stages but without recommending treatments in any particular order due to lack of comparative trials. The aims of this second CLIC study were to retrospectively analyze the pattern of care worldwide for advanced-stage MF/SS patients, the distribution of treatments according to geographical areas (USA versus non-USA), and whether the heterogeneity of approaches has potential impact on survival. Patients and methods This study included 853 patients from 21 specialist centers (14 European, 4 USA, 1 each Australian, Brazilian, and Japanese). Results Heterogeneity of treatment approaches was found, with up to 24 different modalities or combinations used as first-line and 36% of patients receiving four or more treatments. Stage IIB disease was most frequently treated by total-skin-electron-beam radiotherapy, bexarotene and gemcitabine; erythrodermic and SS patients by extracorporeal photochemotherapy, and stage IVA2 by polychemotherapy. Significant differences were found between USA and non-USA centers, with bexarotene, photopheresis and histone deacetylase inhibitors most frequently prescribed for first-line treatment in USA while phototherapy, interferon, chlorambucil and gemcitabine in non-USA centers. These differences did not significantly impact on survival. However, when considering death and therapy change as competing risk events and the impact of first treatment line on both events, both monochemotherapy (SHR = 2.07) and polychemotherapy (SHR = 1.69) showed elevated relative risks. Conclusion This large multicenter retrospective study shows that there exist a large treatment heterogeneity in advanced MF/SS and differences between USA and non-USA centers but these were not related to survival, while our data reveal that chemotherapy as first treatment is associated with a higher risk of death and/or change of therapy and thus other therapeutic options should be preferable as first treatment approach

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Common, low-frequency, rare, and ultra-rare coding variants contribute to COVID-19 severity

The combined impact of common and rare exonic variants in COVID-19 host genetics is currently insufficiently understood. Here, common and rare variants from whole-exome sequencing data of about 4000 SARS-CoV-2-positive individuals were used to define an interpretable machine-learning model for predicting COVID-19 severity. First, variants were converted into separate sets of Boolean features, depending on the absence or the presence of variants in each gene. An ensemble of LASSO logistic regression models was used to identify the most informative Boolean features with respect to the genetic bases of severity. The Boolean features selected by these logistic models were combined into an Integrated PolyGenic Score that offers a synthetic and interpretable index for describing the contribution of host genetics in COVID-19 severity, as demonstrated through testing in several independent cohorts. Selected features belong to ultra-rare, rare, low-frequency, and common variants, including those in linkage disequilibrium with known GWAS loci. Noteworthily, around one quarter of the selected genes are sex-specific. Pathway analysis of the selected genes associated with COVID-19 severity reflected the multi-organ nature of the disease. The proposed model might provide useful information for developing diagnostics and therapeutics, while also being able to guide bedside disease management. © 2021, The Author(s)

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

A first update on mapping the human genetic architecture of COVID-19

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