Re-thinking the Fiscal and Monetary Political Economy of the Green State

Proponents of the Green State repudiate the historical antipathy to the state from many in the green movement and endorse the pragmatic usage of state capacity and legitimacy to realise environmental protection. This article offers a sympathetic critique of the Green State’s fiscal and monetary institutional design in order to refine the concept further. It will investigate an under-theorised contradiction in the political economy of the Green State; centring upon the operationalisation of an interventionist state, moving beyond economic growth, and deference to the ceteris paribus conventions of state financing. It is argued that the three cannot co-exist harmoniously, given the ramifications of moving beyond growth for the fiscal capacity of the state. Therefore, there is a need to go further than even Eckersley does in re-politicising and challenging capitalist conventions. Specifically, Eckersley’s own critical constructivist approach is invoked to interrogate the capitalist conventions that constitute the constraints surrounding state financing, such as the depoliticised production of money and the viability of debt relations

Heterozygous ANKRD17 loss-of-function variants cause a syndrome with intellectual disability, speech delay, and dysmorphism

ANKRD17 is an ankyrin repeat-containing protein thought to play a role in cell cycle progression, whose ortholog in Drosophila functions in the Hippo pathway as a co-factor of Yorkie. Here, we delineate a neurodevelopmental disorder caused by de novo heterozygous ANKRD17 variants. The mutational spectrum of this cohort of 34 individuals from 32 families is highly suggestive of haploinsufficiency as the underlying mechanism of disease, with 21 truncating or essential splice site variants, 9 missense variants, 1 in-frame insertion-deletion, and 1 microdeletion (1.16 Mb). Consequently, our data indicate that loss of ANKRD17 is likely the main cause of phenotypes previously associated with large multi-gene chromosomal aberrations of the 4q13.3 region. Protein modeling suggests that most of the missense variants disrupt the stability of the ankyrin repeats through alteration of core structural residues. The major phenotypic characteristic of our cohort is a variable degree of developmental delay/intellectual disability, particularly affecting speech, while additional features include growth failure, feeding difficulties, non-specific MRI abnormalities, epilepsy and/or abnormal EEG, predisposition to recurrent infections (mostly bacterial), ophthalmological abnormalities, gait/balance disturbance, and joint hypermobility. Moreover, many individuals shared similar dysmorphic facial features. Analysis of single-cell RNA-seq data from the developing human telencephalon indicated ANKRD17 expression at multiple stages of neurogenesis, adding further evidence to the assertion that damaging ANKRD17 variants cause a neurodevelopmental disorder.Neurolog

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