[1] MPI-ESM is a new version of the global Earth system model developed at the Max Planck Institute for Meteorology. This paper describes the ocean state and circulation as well as basic aspects of variability in simulations contributing to the fifth phase of the Coupled Model Intercomparison Project (CMIP5). The performance of the ocean/ sea-ice model MPIOM, coupled to a new version of the atmosphere model ECHAM6 and modules for land surface and ocean biogeochemistry, is assessed for two model versions with different grid resolution in the ocean. The low-resolution configuration has a nominal resolution of 1.5, whereas the higher resolution version features a quasiuniform, eddy-permitting global resolution of 0.4. The paper focuses on important oceanic features, such as surface temperature and salinity, water mass distribution, large-scale circulation, and heat and freshwater transports. In general, these integral quantities are simulated well in comparison with observational estimates, and improvements in comparison with the predecessor system are documented; for example, for tropical variability and sea ice representation. Introducing an eddy-permitting grid configuration in the ocean leads to improvements, in particular, in the representation of interior water mass properties in the Atlantic and in the representation of important ocean currents, such as the Agulhas and Equatorial current systems. In general, however, there are more similarities than differences between the two grid configurations, and several shortcomings, known from earlier versions of the coupled model, prevail.

Calcifications in the basal ganglia are a common incidental finding and are sometimes inherited as an autosomal dominant trait (idiopathic basal ganglia calcification (IBGC)). Recently, mutations in the PDGFRB gene coding for the platelet-derived growth factor receptor β (PDGF-Rβ) were linked to IBGC. Here we identify six families of different ancestry with nonsense and missense mutations in the gene encoding PDGF-B, the main ligand for PDGF-Rβ. We also show that mice carrying hypomorphic Pdgfb alleles develop brain calcifications that show age-related expansion. The occurrence of these calcium depositions depends on the loss of endothelial PDGF-B and correlates with the degree of pericyte and blood-brain barrier deficiency. Thus, our data present a clear link between Pdgfb mutations and brain calcifications in mice, as well as between PDGFB mutations and IBGC in humans.

This first comprehensive MDSGene review is devoted to the 3 autosomal recessive Parkinson's disease forms: PARK-Parkin, PARK-PINK1, and PARK-DJ1. It followed MDSGene's standardized data extraction protocol and screened a total of 3652 citations and is based on fully curated phenotypic and genotypic data on >1100 patients with recessively inherited PD because of 221 different disease-causing mutations in Parkin, PINK1, or DJ1. All these data are also available in an easily searchable online database (www.mdsgene.org), which also provides descriptive summary statistics on phenotypic and genetic data. Despite the high degree of missingness of phenotypic features and unsystematic reporting of genotype data in the original literature, the present review recapitulates many of the previously described findings including early onset (median age at onset of ∼30 years for carriers of at least 2 mutations in any of the 3 genes) of an overall clinically typical form of PD with excellent treatment response, dystonia and dyskinesia being relatively common and cognitive decline relatively uncommon. However, when comparing actual data with common expert knowledge in previously published reviews, we detected several discrepancies. We conclude that systematic reporting of phenotypes is a pressing need in light of increasingly available molecular genetic testing and the emergence of first gene-specific therapies entering clinical trials. © 2018 International Parkinson and Movement Disorder Society.

In the mid-1990s, the subpolar gyre of the North Atlantic underwent a remarkable rapid warming, with sea surface temperatures increasing by around 18C in just 2 yr. This rapid warming followed a prolonged positive phase of the North Atlantic Oscillation (NAO) but also coincided with an unusually negative NAO index in the winter of 1995/96. By comparing ocean analyses and carefully designed model experiments, it is shown that this rapid warming can be understood as a delayed response to the prolonged positive phase of the NAO and not simply an instantaneous response to the negative NAO index of 1995/96. Furthermore, it is inferred that the warming was partly caused by a surge and subsequent decline in the meridional overturning circulation and northward heat transport of the Atlantic Ocean. These results provide persuasive evidence of significant oceanic memory on multiannual time scales and are therefore encouraging for the prospects of developing skillful predictions.