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Universities around the world are increasingly digitalising all of their operations, with the current COVID-19 pandemic speeding up otherwise steady developments. This article focuses on the political economy of higher education (HE) digitalisation and suggests a new research programme. I foreground three principal arguments, which are empirically, theoretically, and politically crucial for HE scholars. First, most literature is examining the impacts of digitalisation on the HE sector and its subjects alone. I argue that current changes in digitalising HE cannot be studied in isolation from broader changes in the global economy. Specifically, HE digitalisation is embedded in the expansion of the digital economy, which is marked by new forms of value extraction and rentiership. Second, the emerging research on the intersection of marketisation and digitalisation in HE seems to follow the theories of marketisation qua production and commodification. I argue that we need theories with better explanatory power in analysing the current digitalisation dynamics. I propose to move from commodification to assetisation, and from prices to rents. Finally, universities are digitalising in the time when the practice is superseding policy, and there is no regulation beyond the question of data privacy. However, digital data property is already a reality, governed by 'terms of use', and protected by the intellectual property rights regime. The current pandemic has led to 'emergency pedagogy', which has intensified overall digitalisation in the sector and is bypassing concerns of data value redistribution. I argue that we urgently need public scrutiny and political action to address issues of value extraction and redistribution in HE., (© The Author(s) 2020.)

Cardiac ventricular myofibroblast motility, proliferation, and contraction contribute to post-myocardial infarct wound healing, infarct scar formation, and remodeling of the ventricle remote to the site of infarction. The Na+-Ca2+ exchanger (NCX1) is involved in altered calcium handling in cardiac myocytes during cardiac remodeling associated with heart failure, however, its role in cardiac myofibroblast cell function is unexplored. In this study we investigated the involvement of NCX1 as well as the role of non-selective-cation channels (NSCC) in cardiac myofibroblast cell function in vitro. Immunofluorescence and Western blots revealed that P1 cells upregulate alpha-smooth muscle actin (alphaSMA) and embryonic smooth muscle myosin heavy chain (SMemb) expression. NCX1 mRNA and proteins as well as Ca(v)1.2a protein are also expressed in P1 myofibroblasts. Myofibroblast motility in the presence of 50 ng/ml PDGF-BB was blocked with AG1296. Myofibroblast motility, contraction, and proliferation were sensitive to KB-R7943, a specific NCX1 reverse-mode inhibitor. In contrast, only proliferation and contraction, but not motility were sensitive to nifedipine, while gadolinium (NSCC blocker) was only associated with decreased motility. ML-7 treatment was associated with inhibition of the chemotactic response and contraction. Thus cardiac myofibroblast chemotaxis, contraction, and proliferation were sensitive to different pharmacologic treatments suggesting that regulation of transplasmalemmal calcium movements may be important in growth factor receptor-mediated processes. NCX1 may represent an important moiety in suppression of myofibroblast functions.