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This study investigates the career consequences of the COVID-19 pandemic among both clinical and non-clinical academics in a University Medical Center (UMC), utilizing the literature on career shocks and the Job Demands-Resources theory. The study is based on a survey conducted in May 2021 among early- and mid-career academics working within a university medical center (n = 250), as well as insights from in-depth interviews with mid-career academics (n = 38) between September 2021 and February 2022. The results illustrate that COVID-19 functioned as a career shock for the majority of academics in the medical context as it forced them to reflect on their career investments. The data illustrate the underlying interplay of resources and demands that determines career consequences and how this subsequently leads to a heterogeneity of career experiences. Another finding of the study is that the categorization of job characteristics as either resources or demands can vary in a changing work environment. Partly due to this shift, the career consequences of COVID-19 have fluctuated over time. The practical implications of this chapter highlight the importance of taking a long-term perspective on the career consequences of career shocks, as well as the importance of a tailored approach.

Attention to shaping the direction of one’s career according to personal needs and preferences is growing. However, there is limited understanding how contextual antecedents affect career authenticity. Moreover, little is known about whether antecedents of career authenticity operate in the same way for men compared to women and if the impact of these antecedents differs per position. In this study, we contribute to these gaps in the literature by analysing the role of five antecedents of career authenticity in the academic context. Our analysis is based on a cross-sectional survey collected among a sample of 398 academics working in The Netherlands. It shows that justice in promotion practices is the most important contextual antecedent in explaining career authenticity in academia. After analysing the data using multi-group Structural Equation Modelling (SEM), we found that some antecedents relate differently to career authenticity for men compared to women. Our data also showed how most antecedents operate differently per academic rank. These insights show that higher education institutes can boost their academics’ career authenticity but should tailor such actions to academics of different genders and in different positions.

Het aantal zorgnetwerken dat de kwaliteit van medisch-specialistische zorg moet verbeteren, neemt in rap tempo toe. Een evaluatie van tien jaar BeterKeten in de regio Rijnmond leert hoe hieraan sturing wordt gegeven.

Background: Alkaline phosphatase (AP) is a ubiquitously expressed enzyme which can neutralize endotoxin as well as adenosine triphosphate (ATP), an endogenous danger signal released during brain injury. In this study we assessed a potential therapeutic role for AP in inhibiting neuroinflammation using three complementary approaches. Methods: Mice were immunized to induce experimental autoimmune encephalomyelitis (EAE) and treated with AP for seven days during different phases of disease. In addition, serological assays to determine AP activity, endotoxin levels and endotoxin-reactive antibodies were performed in a cohort of multiple sclerosis (MS) patients and controls. Finally, the expression of AP and related enzymes CD39 and CD73 was investigated in brain tissue from MS patients and control subjects. Results: AP administration during the priming phase, but not during later stages, of EAE significantly reduced neurological signs. This was accompanied by reduced proliferation of splenocytes to the immunogen, myelin oligodendrocyte glycoprotein peptide. In MS patients, AP activity and isoenzyme distribution were similar to controls. Although endotoxin-reactive IgM was reduced in primary-progressive MS patients, plasma endotoxin levels were not different between groups. Finally, unlike AP and CD Conclusions: Our findings demonstrate that: 1) pre-symptomatic AP treatment reduces neurological signs of EAE; 2) MS patients do not have altered circulating levels of AP or endotoxin; and 3) the expression of the AP-like enzyme CD39 is increased on microglia in white matter lesions of MS patients.

Immediately after sampling, leukocyte counts in native cerebrospinal fluid (CSF) start to decrease rapidly. As the time lapse between CSF collection to analysis is not routinely registered, the clinical significance of decreasing cell counts in native CSF is not known. Earlier data suggest that addition of serum-containing medium to CSF directly after sampling prevents this rapid decrease in leukocyte counts and, thus, may improve the accuracy of CSF cell counting and cell characterization. Here, we prospectively examined the effect of storage time after lumbar puncture on counts of leukocytes and their major subsets in both native CSF and after immediate addition of serum-containing medium, measured by flow cytometry and microscopy. We collected CSF samples of 69 patients in tubes with and tubes without serum-containing medium and determined counts of leukocytes and subsets at 30 minutes, 1 hour, and 5 hours after sampling. Compared to cell counts at 30 minutes, no significant decrease in cell number was observed in CSF with serum-containing medium 1 and 5 hours after sampling, except for the granulocytes at 1 hour. In native CSF, approximately 50% of leukocytes and all their subsets were lost after 1 hour, both in flow cytometric and microscopic counting. In 6/7 (86%) samples with mild pleocytosis (5-15 x 10(6) leukocytes/l), native CSF at 1 hour was incorrectly diagnosed as normocellular. In conclusion, addition of serum-containing medium to CSF directly after sampling prevents cell loss and allows longer preservation of CSF cells prior to analysis, both for microscopic and flow cytometric enumeration. We suggest that this protocol results in more accurate CSF cell counts and may prevent incorrect conclusions based on underestimated CSF cell counts.