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Background The WHO ordinal severity scale has been used to predict mortality and guide trials in COVID-19. However, it has its limitations. Objective The present study aims to compare three classificatory and predictive models: the WHO ordinal severity scale, the model based on inflammation grades, and the hybrid model. Design Retrospective cohort study with patient data collected and followed up from March 1, 2020, to May 1, 2021, from the nationwide SEMI-COVID-19 Registry. The primary study outcome was in-hospital mortality. As this was a hospital-based study, the patients included corresponded to categories 3 to 7 of the WHO ordinal scale. Categories 6 and 7 were grouped in the same category. Key Results A total of 17,225 patients were included in the study. Patients classified as high risk in each of the WHO categories according to the degree of inflammation were as follows: 63.8% vs. 79.9% vs. 90.2% vs. 95.1% (p

Uncontrolled inflammation following COVID-19 infection is an important characteristic of the most seriously ill patients. The present study aims to describe the clusters of inflammation in COVID-19 and to analyze their prognostic role. This is a retrospective observational study including 15,691 patients with a high degree of inflammation. They were included in the Spanish SEMI-COVID-19 registry from March 1, 2020 to May 1, 2021. The primary outcome was in-hospital mortality. Hierarchical cluster analysis identified 7 clusters. C1 is characterized by lymphopenia, C2 by elevated ferritin, and C3 by elevated LDH. C4 is characterized by lymphopenia plus elevated CRP and LDH and frequently also ferritin. C5 is defined by elevated CRP, and C6 by elevated ferritin and D-dimer, and frequently also elevated CRP and LDH. Finally, C7 is characterized by an elevated D-dimer. The clusters with the highest in-hospital mortality were C4, C6, and C7 (17.4% vs. 18% vs. 15.6% vs. 36.8% vs. 17.5% vs. 39.3% vs. 26.4%). Inflammation clusters were found as independent factors for in-hospital mortality. In detail and, having cluster C1 as reference, the model revealed a worse prognosis for all other clusters: C2 (OR = 1.30, p = 0.001), C3 (OR = 1.14, p = 0.178), C4 (OR = 2.28, p < 0.001), C5 (OR = 1.07, p = 0.479), C6 (OR = 2.29, p < 0.001), and C7 (OR = 1.28, p = 0.001). We identified 7 groups based on the presence of lymphopenia, elevated CRP, LDH, ferritin, and D-dimer at the time of hospital admission for COVID-19. Clusters C4 (lymphopenia + LDH + CRP), C6 (ferritin + D-dimer), and C7 (D-dimer) had the worst prognosis in terms of in-hospital mortality.

Background Old age is one of the most important risk factors for severe COVID-19. Few studies have analyzed changes in the clinical characteristics and prognosis of COVID-19 among older adults before the availability of vaccines. This work analyzes differences in clinical features and mortality in unvaccinated very old adults during the first and successive COVID-19 waves in Spain. Methods This nationwide, multicenter, retrospective cohort study analyzes unvaccinated patients ≥ 80 years hospitalized for COVID-19 in 150 Spanish hospitals (SEMI-COVID-19 Registry). Patients were classified according to whether they were admitted in the first wave (March 1-June 30, 2020) or successive waves (July 1-December 31, 2020). The endpoint was all-cause in-hospital mortality, expressed as the case fatality rate (CFR). Results Of the 21,461 patients hospitalized with COVID-19, 5,953 (27.7%) were ≥ 80 years (mean age [IQR]: 85.6 [82.3–89.2] years). Of them, 4,545 (76.3%) were admitted during the first wave and 1,408 (23.7%) during successive waves. Patients hospitalized in successive waves were older, had a greater Charlson Comorbidity Index and dependency, less cough and fever, and met fewer severity criteria at admission (qSOFA index, PO2/FiO2 ratio, inflammatory parameters). Significant differences were observed in treatments used in the first (greater use of antimalarials, lopinavir, and macrolides) and successive waves (greater use of corticosteroids, tocilizumab and remdesivir). In-hospital complications, especially acute respiratory distress syndrome and pneumonia, were less frequent in patients hospitalized in successive waves, except for heart failure. The CFR was significantly higher in the first wave (44.1% vs. 33.3%; -10.8%; p p Conclusions Mortality declined significantly between the first and successive waves in very old unvaccinated patients hospitalized with COVID-19 in Spain. This decline could be explained by a greater availability of hospital resources and more effective treatments as the pandemic progressed, although other factors such as changes in SARS-CoV-2 virulence cannot be ruled out.

Background Advanced age is a well-known risk factor for poor prognosis in COVID-19. However, few studies have specifically focused on very old inpatients with COVID-19. This study aims to describe the clinical characteristics of very old inpatients with COVID-19 and identify risk factors for in-hospital mortality at admission. Methods We conducted a nationwide, multicenter, retrospective, observational study in patients ≥ 80 years hospitalized with COVID-19 in 150 Spanish hospitals (SEMI-COVID-19) Registry (March 1–May 29, 2020). The primary outcome was in-hospital mortality. A uni- and multivariate logistic regression was performed to assess predictors of mortality at admission. Results A total of 2772 consecutive patients (49.4% men, median age 86.3 years) were analyzed. Rates of atherosclerotic cardiovascular disease, diabetes mellitus, dementia, and Barthel Index < 60 were 30.8%, 25.6%, 30.5%, and 21.0%, respectively. The overall case-fatality rate was 46.9% (n: 1301) and increased with age (80–84 years: 41.6%; 85–90 years: 47.3%; 90–94 years: 52.7%; ≥95 years: 54.2%). After analysis, male sex and moderate-to-severe dependence were independently associated with in-hospital mortality; comorbidities were not predictive. At admission, independent risk factors for death were: oxygen saturation < 90%; temperature ≥ 37.8°C; quick sequential organ failure assessment (qSOFA) score ≥ 2; and unilateral–bilateral infiltrates on chest x-rays. Some analytical findings were independent risk factors for death, including estimated glomerular filtration rate < 45 mL/min/1.73 m2; lactate dehydrogenase ≥ 500 U/L; C-reactive protein ≥ 80 mg/L; neutrophils ≥ 7.5 × 103/μL; lymphocytes < 0.8 × 103/μL; and monocytes < 0.5 × 103/μL. Conclusions This first large, multicenter cohort of very old inpatients with COVID-19 shows that age, male sex, and poor preadmission functional status—not comorbidities—are independently associated with in-hospital mortality. Severe COVID-19 at admission is related to poor prognosis.

Additional file 1. List of the SEMI-COVID-19 Network members.

(1) Background: This work aims to analyze clinical outcomes according to ethnic groups in patients hospitalized for COVID-19 in Spain. (2) Methods: This nationwide, retrospective, multicenter, observational study analyzed hospitalized patients with confirmed COVID-19 in 150 Spanish hospitals (SEMI-COVID-19 Registry) from 1 March 2020 to 31 December 2021. Clinical outcomes were assessed according to ethnicity (Latin Americans, Sub-Saharan Africans, Asians, North Africans, Europeans). The outcomes were in-hospital mortality (IHM), intensive care unit (ICU) admission, and the use of invasive mechanical ventilation (IMV). Associations between ethnic groups and clinical outcomes adjusted for patient characteristics and baseline Charlson Comorbidity Index values and wave were evaluated using logistic regression. (3) Results: Of 23,953 patients (median age 69.5 years, 42.9% women), 7.0% were Latin American, 1.2% were North African, 0.5% were Asian, 0.5% were Sub-Saharan African, and 89.7% were European. Ethnic minority patients were significantly younger than European patients (median (IQR) age 49.1 (40.5–58.9) to 57.1 (44.1–67.1) vs. 71.5 (59.5–81.4) years, p < 0.001). The unadjusted IHM was higher in European (21.6%) versus North African (11.4%), Asian (10.9%), Latin American (7.1%), and Sub-Saharan African (3.2%) patients. After further adjustment, the IHM was lower in Sub-Saharan African (OR 0.28 (0.10–0.79), p = 0.017) versus European patients, while ICU admission rates were higher in Latin American and North African versus European patients (OR (95%CI) 1.37 (1.17–1.60), p < 0.001) and (OR (95%CI) 1.74 (1.26–2.41), p < 0.001). Moreover, Latin American patients were 39% more likely than European patients to use IMV (OR (95%CI) 1.43 (1.21–1.71), p < 0.001). (4) Conclusion: The adjusted IHM was similar in all groups except for Sub-Saharan Africans, who had lower IHM. Latin American patients were admitted to the ICU and required IMV more often.

Background: The WHO ordinal severity scale has been used to predict mortality and guide trials in COVID-19. However, it has its limitations. Objective The present study aims to compare three classificatory and predictive models: the WHO ordinal severity scale, the model based on inflammation grades, and the hybrid model. Design Retrospective cohort study with patient data collected and followed up from March 1, 2020, to May 1, 2021, from the nationwide SEMI-COVID-19 Registry. The primary study outcome was in-hospital mortality. As this was a hospital-based study, the patients included corresponded to categories 3 to 7 of the WHO ordinal scale. Categories 6 and 7 were grouped in the same category. Key Results A total of 17,225 patients were included in the study. Patients classified as high risk in each of the WHO categories according to the degree of inflammation were as follows: 63.8% vs. 79.9% vs. 90.2% vs. 95.1% (p

Objective To describe the impact of different doses of corticosteroids on the evolution of patients with COVID-19 pneumonia, based on the potential benefit of the non-genomic mechanism of these drugs at higher doses. Methods Observational study using data collected from the SEMI-COVID-19 Registry. We evaluated the epidemiological, radiological and analytical scenario between patients treated with megadoses therapy of corticosteroids vs low-dose of corticosteroids and the development of complications. The primary endpoint was all-cause in-hospital mortality according to use of corticosteroids megadoses. Results Of a total of 14,921 patients, corticosteroids were used in 5,262 (35.3%). Of them, 2,216 (46%) specifically received megadoses. Age was a factor that differed between those who received megadoses therapy versus those who did not in a significant manner (69 years [IQR 59–79] vs 73 years [IQR 61–83]; p < .001). Radiological and analytical findings showed a higher use of megadoses therapy among patients with an interstitial infiltrate and elevated inflammatory markers associated with COVID-19. In the univariate study it appears that steroid use is associated with increased mortality (OR 2.07 95% CI 1.91–2.24 p < .001) and megadose use with increased survival (OR 0.84 95% CI 0.75–0.96, p 0.011), but when adjusting for possible confounding factors, it is observed that the use of megadoses is also associated with higher mortality (OR 1.54, 95% CI 1.32–1.80; p < .001). There is no difference between megadoses and low-dose (p .298). Although, there are differences in the use of megadoses versus low-dose in terms of complications, mainly infectious, with fewer pneumonias and sepsis in the megadoses group (OR 0.82 95% CI 0.71–0.95; p < .001 and OR 0.80 95% CI 0.65–0.97; p < .001) respectively. Conclusion There is no difference in mortality with megadoses versus low-dose, but there is a lower incidence of infectious complications with glucocorticoid megadoses.

Objectives: We aimed to develop and validate a prediction model, based on clinical history and examination findings on initial diagnosis of coronavirus disease 2019 (COVID-19), to identify patients at risk of critical outcomes. Methods: We used data from the SEMI-COVID-19 Registry, a cohort of consecutive patients hospitalized for COVID-19 from 132 centres in Spain (23rd March to 21st May 2020). For the development cohort, tertiary referral hospitals were selected, while the validation cohort included smaller hospitals. The primary outcome was a composite of in-hospital death, mechanical ventilation, or admission to intensive care unit. Clinical signs and symptoms, demographics, and medical history ascertained at presentation were screened using least absolute shrinkage and selection operator, and logistic regression was used to construct the predictive model. Results: There were 10 433 patients, 7850 in the development cohort (primary outcome 25.1%, 1967/7850) and 2583 in the validation cohort (outcome 27.0%, 698/2583). The PRIORITY model included: age, dependency, cardiovascular disease, chronic kidney disease, dyspnoea, tachypnoea, confusion, systolic blood pressure, and SpO2 ≤93% or oxygen requirement. The model showed high discrimination for critical illness in both the development (C-statistic 0.823; 95% confidence interval (CI) 0.813, 0.834) and validation (C-statistic 0.794; 95%CI 0.775, 0.813) cohorts. A freely available web-based calculator was developed based on this model (https://www.evidencio.com/models/show/2344). Conclusions: The PRIORITY model, based on easily obtained clinical information, had good discrimination and generalizability for identifying COVID-19 patients at risk of critical outcomes., No funding was received for this work.

Background The effects of cardiometabolic drugs on the prognosis of diabetic patients with COVID-19, especially very old patients, are not well known. This work was aimed to analyze the association between preadmission cardiometabolic therapy (antidiabetic, antiaggregant, antihypertensive, and lipid-lowering drugs) and in-hospital mortality among patients ≥80 years with type 2 diabetes mellitus (T2DM) hospitalized for COVID-19. Method We conducted a nationwide, multicenter, observational study in patients ≥80 years with T2DM hospitalized for COVID-19 between March 1 and May 29, 2020. The primary outcome measure was in-hospital mortality. A multivariate logistic regression analysis was performed to assess the association between preadmission cardiometabolic therapy and in-hospital mortality. Results Of the 2 763 patients ≥80 years old hospitalized due to COVID-19, 790 (28.6%) had T2DM. Of these patients, 385 (48.7%) died during admission. On the multivariate analysis, the use of dipeptidyl peptidase-4 inhibitors (adjusted odds ratio [AOR] 0.502, 95% confidence interval [CI]: 0.309–0.815, p = .005) and angiotensin receptor blockers (AOR 0.454, 95% CI: 0.274–0.759, p = .003) were independent protectors against in-hospital mortality, whereas the use of acetylsalicylic acid was associated with higher in-hospital mortality (AOR 1.761, 95% CI: 1.092–2.842, p = .020). Other antidiabetic drugs, angiotensin-converting enzyme inhibitors, and statins showed neutral association with in-hospital mortality. Conclusions We found important differences between cardiometabolic drugs and in-hospital mortality in older patients with T2DM hospitalized for COVID-19. Preadmission treatment with dipeptidyl peptidase-4 inhibitors and angiotensin receptor blockers could reduce in-hospital mortality; other antidiabetic drugs, angiotensin-converting enzyme inhibitors, and statins seem to have a neutral effect; and acetylsalicylic acid could be associated with excess mortality.

[Purpose]: The aim of the present work is the molecular diagnosis of three patients with deafness and retinal degeneration. [Methods]: Three patients from two unrelated families were initially analyzed with custom gene panels for Usher genes, non-syndromic hearing loss, or inherited syndromic retinopathies and further investigated by means of clinical or whole exome sequencing. [Results]: The study allowed us to detect likely pathogenic variants in PEX6, a gene typically involved in peroxisomal biogenesis disorders (PBDs). Beside deaf–blindness, both families showed additional features: Siblings from Family 1 showed enamel alteration and abnormal peroxisome. In addition, the brother had mild neurodevelopmental delay and nephrolithiasis. The case II:1 from Family 2 showed intellectual disability, enamel alteration, and dysmorphism. [Conclusions]: We have reported three new cases with pathogenic variants in PEX6 presenting with milder forms of the Zellweger spectrum disorders (ZSD). The three cases showed distinct clinical features. Thus, expanding the phenotypic spectrum of PBDs and ascertaining exome sequencing is an effective strategy for an accurate diagnosis of clinically overlapping and genetically heterogeneous disorders such as deafness–blindness association., This work was financially supported by grants of the Institute of Health Carlos III (ISCIII /FEDER), (Ref.: PI13/00638 PI16/00415, PI16/00539 and CIBER-ER 06/07/0036; Biobank FJD (RD09/0076/00101),); Fundación ONCE (Ref.: 2015/0398) ONCE & Fundaluce, Sponsored Chair IIS-FJD, UAM of Genomics Medicine. CNAG's 2013 call “300 exomes to elucidate rare diseases.” Institutional Development Fund at CAG from The Children’s Hospital of Philadelphia. CFG, ISN and MCP are recipients of fellowshipsfrom the ISCIII (Ref.: IFI14/00021; Sara Borrell CD13–00085 and Miguel Servet CPII17_00006 respectively). Carmen Ayuso (CAyuso@fjd.es) and José M. Millán (millan_jos@gva.es) are co-corresponding authors of this work

El síndrome de Usher (USH) es una enfermedad hereditaria autosómica recesiva, caracterizada por la asociación de hipoacusia neurosensorial, retinosis pigmentaria y, en ocasiones, alteración de la función vestibular. Clínicamente, el USH se puede clasificar en tres tipos (USH1, USH2 y USH3), principalmente en base a la gravedad y progresión de la hipoacusia y presencia o no de disfunción vestibular. El USH es heterogéneo tanto a nivel clínico como genético y, hasta la fecha, se han descrito 11 genes implicados en la enfermedad. El USH2 es la forma más común y tres son los genes responsables conocidos: USH2A (72 exones), GPR98 (90 exones) y DFNB31 (12 exones). USH2A es responsable de más del 70% de los casos USH2, teniendo una menor implicación los otros dos genes. Hasta esta tesis, no se había realizado un análisis exhaustivo de estos tres genes en pacientes españoles con síndrome de Usher. Por ello, uno de los objetivos fue el análisis molecular de los tres genes USH2 en una cohorte inicial de 88 pacientes con síndrome de Usher. El estudio consintió en el análisis de los exones, más las regiones intrónicas flanqueantes, mediante amplificación por PCR y secuenciación directa por Sanger. El estudio no se limitó a la detección de mutaciones puntuales, las variantes detectadas fueron analizadas con varios programas bioinformáticos para predecir su posible patogenicidad y, cuando fue necesario, se realizaron estudios funcionales para comprobar los efectos predichos. Además también se realizaron análisis de CGH-array (comparative genome hibrydization array) para detectar posibles grandes inserciones/deleciones, que no identifican los típicos análisis por PCR. El estudio se inició con USH2A,y en los pacientes en los que no se encontraron mutaciones en este gen, se continuó con el análisis de GPR98 y DFNB31. Treinta y siete (23 nuevas) mutaciones diferentes se detectaron en USH2A y 7 (5 nuevas) en GPR98. No se detectaron mutaciones en DFNB31. Las mutaciones detectadas fueron de naturaleza muy diversa (cambios de aminoácido, isocodificantes, codones de parada prematuro directos, pequeñas deleciones e inserciones) y en la mayoría de casos las mutaciones fueron privadas, demostrando la elevada heterogeneidad alélica de esta enfermedad. Además, se identificaron dos grandes deleciones gracias al uso de la técnica de CGH-array. En el desarrollo de este estudio se describió por primera vez en el USH, la presencia de una mutación intrónica profunda en el gen USH2A que produce la activación de un pseudoexon. Esta variante fue detectada en 4 pacientes españoles, completando y mejorando de esta forma el diagnóstico molecular del USH. Esta parte del estudio nos permitió estimar la prevalencia de los genes USH2 en población española. USH2A está implicado en un 76% de los casos USH2, seguido de GPR98 con un 5,2%. DFNB31 tiene una menor implicación en nuestra población. CLRN1,es el único gen responsable del USH3 conocido. Sin embargo, se ha publicado que este gen también puede estar implicado en pacientes con USH1 o USH2. El análisis de este gen en una cohorte de 17 pacientes con USH nos ha permitido identificar 2 nuevas mutaciones y confirmar la baja implicación de este gen en pacientes españoles. Debido a la elevada heterogeneidad genética y alélica del USH y al gran tamaño de algunos de los genes implicados, el diagnóstico del USH mediante las técnicas de secuenciación tradicionales resulta una tarea muy laboriosa. En los últimos años, las técnicas de secuenciación de nueva generación se han desarrollado considerablemente y son muchas sus posibles aplicaciones. Nosotros hemos elegido el método de captura de regiones (Nimblegen, Roche) seguido de secuenciación masiva mediante la plataforma GS Junior (454, Roche) para el estudio de los genes Usher y su posible aplicación al diagnóstico. Un total de 19 genes fueron incluidos en el diseño (genes Usher, candidatos y otros implicados en sordera). De media, se obtuvieron cerca de 53Mb de secuencias, con un on target del 52%. La profundidad de cobertura obtenida fue de 77X, superando los 40X necesarios. Para evaluar la sensibilidad y fiabilidad de la técnica, en una primera fase se estudiaron 47 pacientes que tenían analizados previamente algunos de los genes Usher. Esta primera cohorte de pacientes nos permitió establecer los criterios adecuados para los sucesivos filtros que se aplicaron a las variantes obtenidas. Esto se automatizó mediante el diseño de un propio programa bioinformático, llamado GSdot. Solo un 2% de las variaciones conocidas no fueron detectadas por NGS debido principalmente a la presencia de regiones con homopolímeros, problemas de alineamiento o una baja cobertura. También nos permitió detectar mutaciones adicionales en 12 de los 47 pacientes, bien porque las mutaciones no se habían detectado por Sanger o el gen implicado no se había estudiado. Una vez comprobada la validez de la técnica, se estudiaron 13 nuevos pacientes con USH, pero sin ningún gen analizado anteriormente. Se detectaron las dos mutaciones en 10 de los 13 casos y en otros dos pacientes se detectó una variante clasificada como UV3. Además, se estudiaron 11 pacientes con sordera no sindrómica, lo que permitió identificar 3 mutaciones en 3 de ellos. En varios pacientes solo se identificó una mutación, y aunque alguno de ellos pueda ser simplemente portador de una mutación en los genes Usher y las mutaciones responsables estén en otro gen, la mayoría de ellos deben tener una segunda mutación, posiblemente en regiones no analizadas con esta técnica (por ejemplo: regiones intrónicas). En otros pacientes, no se pudo detectar ninguna mutación. En estos casos, el estudio del exoma entero ayudará a encontrar el gen implicado. Aunque es necesario mejorar la técnica, los resultados obtenidos son muy prometedores para una futura traslación al diagnóstico. Esta estrategia facilitará el diagnóstico del USH de pacientes que no presentan mutaciones en los genes principalmente implicados o de aquellos casos que presentan mutaciones en genes típicamente responsables de otro subtipo clínico. Usher syndrome is a genetic disorder combining sensorineural hearing loss (HL) and retinitis pigmentosa (RP). Some patients will also exhibit vestibular areflexia (VA). The majority of patients with Usher syndrome usually fall into one of three clinical categories. Of these, Usher syndrome type I (USH1) is the most severe form, consisting of profound hearing loss and vestibular dysfunction from birth. Moreover, onset of RP occurs earlier in USH1 than in Usher syndrome type II (USH2), which produces less severe congenital hearing loss and does not impair normal vestibular function. In most populations, USH1 accounts for approximately one-third of USH patients whereas two- thirds are classified as USH2. Usher syndrome type III (USH3) is a less common form except in such populations as Finns and Ashkenazi Jews. In this USH3 type, hearing loss is progressive and leads to variable vestibular dysfunction and onset of RP. It is important to use all accessible genetic tools to identify and characterize molecular origin in order to improve the knowledge of the physiopathological mechanisms causing Usher Syndrome. This clinical heterogeneity is accompanied by high genetic heterogeneity. To date a minimum of eleven genes responsible for the disease are known. Five USH1 genes have been extensively studied: MYO7A (USH1B), CDH23 (USH1D), PCDH15 (USH1F), USH1C (USH1C) and USH1G (USH1G), with MYO7A being the most prevalent. A sixth gene, CIB2 (USH1J), has been very recently reported in a single family. Among the three identified USH2 genes, USH2A (USH2A), GPR98 (USH2C) and DFNB31 (USH2D), USH2A has been shown to be responsible for 70-80% of the USH2. Until recently, CLRN1 (USH3A) was the only gene known responsible for USH3 In this context, we have performed an exhaustive molecular analysis of the three causative USH2 genes (USH2A, GPR98 and DFNB31). The study was not limited to the search of point mutations; CGH-array analysis, computational predictions and functional studies were carried out when necessary. Thanks to this work, we determined that in Spain, USH2A and GPR98 are responsible for 94.8% and 5.2% of USH2 mutated cases, respectively. DFNB31 plays a minor role in the Spanish population. USH3 is thought to be a minor type of USH in our population. Mutations in CLRN1 were initially responsible for USH3, but mutations in this gene have also been reported in patients with clinical features similar to USH1 or USH2. In this work, we have reported the results of the molecular analysis of CLRN1 in a cohort of patients and the low involvement of this gene in our population. We have then designed a targeted exome of the Usher genes to be sequenced using the GS Junior system (Roche 454). The aim of the study was to test the feasibility of this new technics for a possible transfer to diagnostic facilities. Quality criteria and variant prioritization were set up on a control cohort (previously studied in one of the USH gene). The study has then been extended on a patient cohort. Our results indicate that NGS Usher-exome can be used in molecular diagnostics but improvement of the reliability of the sequencing technology, bioinformatics tools and dedicated databases is essential.

Resumen tomado de la publicación Investigación en la que se analizan los intercambios verbales registrados a lo largo de doce sesiones de apoyo a dos grupos de alumnos con necesidades educativas especiales. Los resultados muestran una estructura de participación particularmente didáctica y vinculada entre maestra y alumno. Más de una tercera parte de las interacciones configuraban secuencias encadenadas de iniciación, respuesta, ayuda y respuesta, dirigidas a que un mismo alumno verbalizara y posteriormente reelaborará su representación interna de la tarea, hasta definir un significado suficientemente compartido con la profesora. Las ayudas se centraron principalmente en corregir las respuestas erróneas o dar instrucciones, aunque también se detectaron un elevado número de acciones que otorgaban una mayor participación al alumno, encaminadas a evaluar, evocar, precisar, sintetizar o justificar ideas, etc. Cuando se trataba de una respuesta incompleta, las maestras reaccionaron principalmente demandando más precisión a través de preguntas. Cuando los alumnos no respondían, la ayuda más frecuente se centró en recuperar conocimientos previos relevantes. Las maestras con más experiencia registraron casi el doble de interacciones, provocaron menos aportaciones erróneas y ofrecieron ayudas más eficaces para conseguir que los propios estudiantes las reelaboraran. Madrid Madrid (Comunidad Autónoma). Servicio de Formación del Profesorado. CRIF Las Acacias; Calle General Ricardos, 179; 28025 Madrid; Tel. +34915250893; Fax +34914660991; SRPPIDE@madrid.org ESP

Resumen basado en el de la publicación Se presenta una investigación comparativa entre profesores expertos y principiantes de educación especial. Se grabaron 12 sesiones de apoyo a alumnos con necesidades educativos especiales fuera del aula ordinaria. Se describen las principales características de la interacción verbal profesor-alumno en el aula de apoyo. Se obtuvieron 22 categorías específicas de mediación verbal, en función de la participación que se demandaba al alumno. Las maestras con más experiencia registraron casi el doble de interacciones en el mismo tiempo, corrigieron menos las aportaciones de los alumnos y ofrecieron más ayudas, explícitamente dirigidas a que éstos las modificaran o reelaboraran. Madrid Biblioteca de Educación del Ministerio de Educación, Cultura y Deporte; Calle San Agustín, 5 - 3 Planta; 28014 Madrid; Tel. +34917748000; biblioteca@mecd.es ESP