Challenges for medical educators: results of a survey among members of the German Association for Medical Education

BACKGROUND Despite the increasing interest in medical education in the German-speaking countries, there is currently no information available on the challenges which medical educators face. To address this problem, we carried out a web-based survey among the members of the Association for Medical Education (Gesellschaft für medizinische Ausbildung, GMA). METHODS A comprehensive survey was carried out on the need for further qualifications, expertise and the general conditions of medical educators in Germany. As part of this study, the educators were asked to list the three main challenges which they faced and which required urgent improvement. The results were analysed by means of qualitative content analysis. RESULTS The questionnaire was completed by 147 of the 373 members on the GMA mailing list (response rate: 39%). The educators named a total of 346 challenges and emphasised the following areas: limited academic recognition for engagement in teaching (53.5% of educators), insufficient institutional (31.5%) and financial support (28.4%), a curriculum in need of reform (22.8%), insufficient time for teaching assignments (18,9%), inadequate teacher competence in teaching methods (18.1%), restricted faculty development programmes (18.1%), limited networking within the institution (11.0%), lack of teaching staff (10.2%), varying preconditions of students (8.7%), insufficient recognition and promotion of medical educational research (5.5%), extensive assessment requirements (4.7%), and the lack of role models within medical education (3.2%). CONCLUSION The medical educators found the biggest challenges which they faced to be limited academic recognition and insufficient institutional and financial support. Consequently, improvements should be implemented to address these issues.

Rat lungs show a biphasic formation of new alveoli during postnatal development

Roughly 90% of the gas-exchange surface is formed by alveolarization of the lungs. To the best of our knowledge, the formation of new alveoli has been followed in rats only by means of morphological description or interpretation of semiquantitative data until now. Therefore, we estimated the number of alveoli in rat lungs between postnatal days 4 and 60 by unambiguously counting the alveolar openings. We observed a bulk formation of new alveoli between days 4 and 21 (17.4 times increase from 0.8 to 14.3 millions) and a second phase of continued alveolarization between days 21 and 60 (1.3 times increase to 19.3 million). The (number weighted) mean volume of the alveoli decreases during the phase of bulk alveolarization from ∼593,000 μm(3) at day 4 to ∼141,000 μm(3) at day 21, but increases again to ∼298,000 μm(3) at day 60. We conclude that the "bulk alveolarization" correlates with the mechanism of classical alveolarization (alveolarization before the microvascular maturation is completed) and that the "continued alveolarization" follows three proposed mechanisms of late alveolarization (alveolarization after microvascular maturation). The biphasic pattern is more evident for the increase in alveolar number than for the formation of new alveolar septa (estimated as the length of the free septal edge). Furthermore, a striking negative correlation between the estimated alveolar size and published data on retention of nanoparticles was detected.

A Drosophila XPD model links cell cycle coordination with neuro-development and suggests links to cancer

XPD functions in transcription, DNA repair and in cell cycle control. Mutations in human XPD (also known as ERCC2) mainly cause three clinical phenotypes: xeroderma pigmentosum (XP), Cockayne syndrome (XP/CS) and trichothiodystrophy (TTD), and only XP patients have a high predisposition to developing cancer. Hence, we developed a fly model to obtain novel insights into the defects caused by individual hypomorphic alleles identified in human XP-D patients. This model revealed that the mutations that displayed the greatest in vivo UV sensitivity in Drosophila did not correlate with those that led to tumor formation in humans. Immunoprecipitations followed by targeted quantitative MS/MS analysis showed how different xpd mutations affected the formation or stability of different transcription factor IIH (TFIIH) subcomplexes. The XP mutants most clearly linked to high cancer risk, Xpd R683W and R601L, showed a reduced interaction with the core TFIIH and also an abnormal interaction with the Cdk-activating kinase (CAK) complex. Interestingly, these two XP alleles additionally displayed high levels of chromatin loss and free centrosomes during the rapid nuclear division phase of the Drosophila embryo. Finally, the xpd mutations showing defects in the coordination of cell cycle timing during the Drosophila embryonic divisions correlated with those human mutations that cause the neurodevelopmental abnormalities and developmental growth defects observed in XP/CS and TTD patients.