Trabajo en equipo : habilidad social a desarrollar en los ambientes de aprendizaje presencial y virtual de la Universidad

Soraya Julián (biografía): Maestría en Metodología de la Investigación Científica, Maestría en Ciencias de la Educación, Especialidad en Educación en Entorno Virtual, Especialidad en Orientación Educativa Psicopedagógica. Licenciada en Teatro, mención Dirección Teatral; Licenciada en Psicología, Diplomado en Estudios Superiores en Ciencias Pedagógicas con mención en Enseñanza de las Ciencias. Experta en De Bono Thinking. Conferencista College Board de Puerto Rico y América Latina. Tiene cursos de inglés, portugués e italiano. Actualmente trabaja como psicóloga en el Departamento de Bienestar Universitario y como docente de las asignaturas Orientación Universitaria y Metodología de la Investigación Científica, en la Unapec. Escribe cuentos, obras de teatro y poesía, entre otros.En este trabajo la autora nos explica su experiencia docente con las llamadas Habilidad Trabajo en Equipo en unas veintiséis acotaciones. Indica que por lo pronto necesitamos nuevos entornos de aprendizaje, nuevos roles docentes y personales, nuevas competencias para integrar a nuestra forma de vida actual

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Soraya Julián M. (biografía): Maestría en Metodología de la Investigación Científica, Maestría en Ciencias de la Educación, Especialidad en Educación en Entorno Virtual, Especialidad en Orientación Educativa Psicopedagógica. Licenciada en Teatro, mención Dirección Teatral; Licenciada en Psicología, Diplomado en Estudios Superiores en Ciencias Pedagógicas con mención en Enseñanza de las Ciencias. Experta en De Bono Thinking. Conferencista College Board de Puerto Rico y América Latina. Tiene cursos de inglés, portugués e italiano. Actualmente trabaja como psicóloga en el Departamento de Bienestar Universitario y como docente de las asignaturas Orientación Universitaria y Metodología de la Investigación Científica, en la Unapec. Escribe cuentos, obras de teatro y poesía, entre otros

Mutations in TRIM63 cause an autosomal-recessive form of hypertrophic cardiomyopathy

Objective: Up to 50% of patients with hypertrophic cardiomyopathy (HCM) show no disease-causing variants in genetic studies. TRIM63 has been suggested as a candidate gene for the development of cardiomyopathies, although evidence for a causative role in HCM is limited. We sought to investigate the relationship between rare variants in TRIM63 and the development of HCM. Methods: TRIM63 was sequenced by next generation sequencing in 4867 index cases with a clinical diagnosis of HCM and in 3628 probands with other cardiomyopathies. Additionally, 3136 index cases with familial cardiovascular diseases other than cardiomyopathy (mainly channelopathies and aortic diseases) were used as controls. Results: Sixteen index cases with rare homozygous or compound heterozygous variants in TRIM63 (15 HCM and one restrictive cardiomyopathy) were included. No homozygous or compound heterozygous were identified in the control population. Familial evaluation showed that only homozygous and compound heterozygous had signs of disease, whereas all heterozygous family members were healthy. The mean age at diagnosis was 35 years (range 15-69). Fifty per cent of patients had concentric left ventricular hypertrophy (LVH) and 45% were asymptomatic at the moment of the first examination. Significant degrees of late gadolinium enhancement were detected in 80% of affected individuals, and 20% of patients had left ventricular (LV) systolic dysfunction. Fifty per cent had non-sustained ventricular tachycardia. Twenty per cent of patients suffered an adverse cerebrovascular event (20%). Conclusion: TRIM63 appears to be an uncommon cause of HCM inherited in an autosomal-recessive manner and associated with concentric LVH and a high rate of LV dysfunction

COVID-19 outbreaks in a transmission control scenario: challenges posed by social and leisure activities, and for workers in vulnerable conditions, Spain, early summer 2020

Severe acute respiratory syndrome coronavirus 2 community-wide transmission declined in Spain by early May 2020, being replaced by outbreaks and sporadic cases. From mid-June to 2 August, excluding single household outbreaks, 673 outbreaks were notified nationally, 551 active (>6,200 cases) at the time. More than half of these outbreaks and cases coincided with: (i) social (family/friends’ gatherings or leisure venues) and (ii) occupational (mainly involving workers in vulnerable conditions) settings. Control measures were accordingly applied

Clonal chromosomal mosaicism and loss of chromosome Y in elderly men increase vulnerability for SARS-CoV-2

The pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2, COVID-19) had an estimated overall case fatality ratio of 1.38% (pre-vaccination), being 53% higher in males and increasing exponentially with age. Among 9578 individuals diagnosed with COVID-19 in the SCOURGE study, we found 133 cases (1.42%) with detectable clonal mosaicism for chromosome alterations (mCA) and 226 males (5.08%) with acquired loss of chromosome Y (LOY). Individuals with clonal mosaic events (mCA and/or LOY) showed a 54% increase in the risk of COVID-19 lethality. LOY is associated with transcriptomic biomarkers of immune dysfunction, pro-coagulation activity and cardiovascular risk. Interferon-induced genes involved in the initial immune response to SARS-CoV-2 are also down-regulated in LOY. Thus, mCA and LOY underlie at least part of the sex-biased severity and mortality of COVID-19 in aging patients. Given its potential therapeutic and prognostic relevance, evaluation of clonal mosaicism should be implemented as biomarker of COVID-19 severity in elderly people. Among 9578 individuals diagnosed with COVID-19 in the SCOURGE study, individuals with clonal mosaic events (clonal mosaicism for chromosome alterations and/or loss of chromosome Y) showed an increased risk of COVID-19 lethality