ABSTRACT
BACKGROUND: The corona crisis not only affects professional activities but also teaching and learning at universities. Buzzwords, such as elearning and digitalization suggest the possibility of innovative teaching approaches that are readily available to solve the problems of teaching in the current COVID-19 pandemic. The current conversion to digital teaching is not primarily driven by didactic rationale or institutional strategy but by external circumstances. OBJECTIVE: The aim of the study was to determine the teaching situation at national university ENT clinics and academic teaching hospitals at the start of the virtual corona summer semester in 2020. MATERIAL AND METHODS: A specifically self-designed questionnaire regarding the local situation and conditions as well as nationwide scenarios was sent to all 39 national university ENT clinics and 20 ENT departments at academic teaching hospitals. RESULTS: A total of 31 university hospitals and 10 academic teaching hospitals took part in the survey. There were obvious discrepancies between available resources and effectively available digital teaching and learning contents. Further criticism was expressed regarding the communication with the medical faculty, the digital infrastructure and particularly the frequent lack of collaboration with central support facilities, such as media, didactics and datacenters. CONCLUSION: There are positive examples of successful transformation of classroom teaching to an exclusively virtual summer semester 2020 within the university ENT clinics; however, critical ratings of assistant professors and medical directors regarding the current teaching situation predominated. A time-critical strategic advancement is urgently needed.
Subject(s)
COVID-19 , Universities , Humans , Learning , Pandemics , SARS-CoV-2 , TeachingABSTRACT
Glanzmann thrombasthenia (GT) is a rare autosomal recessive bleeding disorder characterized by quantitative and/or qualitative defects of the platelet glycoprotein (GP) IIb/IIIa complex. Physiologically, the integrin GPIIb/IIIa binds Von Willebrand factor and fibrinogen on activated platelets. GT is caused by genetic alterations in ITGA2B or ITGB3 (genes encoding GPIIb and GPIIIa).This study describes 2 siblings diagnosed with GT type I associated with homozygous point mutations in ITGA2B. All patients presented with typical bleeding disorder including moderate hematomas, petechiae, and mucocutaneous bleedings.Both siblings showed severely reduced platelet aggregation especially after stimulation with collagen and adenosine diphosphate. Absence of platelet GPIIb/GPIIIa complex was determined using flow cytometry. Molecular genetic analysis revealed 2 distinct homozygous point mutations in exon 18 of ITGA2B. Family 1 was identified with c.1878G>C and family 2 with c.1787T>C substitution. While the c.1787T>C mutation causes a single amino acid substitution p.I565T, the c.1878G>C mutation (p.Q595H) is predicted to induce a mRNA splicing anomaly.These mutations were identified as cause of GT type I in the described patients. Patients with GT should be documented in a prospective register to verify the correlation between the severity of bleeding symptoms and the pathogenic mutation. This can have effects on therapeutic decisions.
