MOSAiC drift expedition from October 2019 to July 2020: sea ice conditions from space and comparison with previous years

We combine satellite data products to provide a first and general overview of the physical sea ice conditions along the drift of the international Multidisciplinary drifting Observatory for the Study of Arctic Climate (MOSAiC) expedition and a comparison with previous years (2005–2006 to 2018–2019). We find that the MOSAiC drift was around 20 % faster than the climatological mean drift, as a consequence of large-scale low-pressure anomalies prevailing around the Barents–Kara–Laptev sea region between January and March. In winter (October–April), satellite observations show that the sea ice in the vicinity of the Central Observatory (CO; 50 km radius) was rather thin compared to the previous years along the same trajectory. Unlike ice thickness, satellite-derived sea ice concentration, lead frequency and snow thickness during winter months were close to the long-term mean with little variability. With the onset of spring and decreasing distance to the Fram Strait, variability in ice concentration and lead activity increased. In addition, the frequency and strength of deformation events (divergence, convergence and shear) were higher during summer than during winter. Overall, we find that sea ice conditions observed within 5 km distance of the CO are representative for the wider (50 and 100 km) surroundings. An exception is the ice thickness; here we find that sea ice within 50 km radius of the CO was thinner than sea ice within a 100 km radius by a small but consistent factor (4 %) for successive monthly averages. Moreover, satellite acquisitions indicate that the formation of large melt ponds began earlier on the MOSAiC floe than on neighbouring floes

Essential role of sympathetic endothelin A receptors for adverse cardiac remodeling

In preclinical studies, endothelin receptor A (ETA) antagonists (ETAi) attenuated the progression of heart failure (HF). However, clinical HF trials failed to demonstrate beneficial effects of ETAi. These conflicting data may be explained by the possibility that established HF drugs such as adrenergic receptor blockers interfered with the mechanism of ETAi action in clinical trials. Here we report that mice lacking ETA only in sympathetic neurons (SN-KO) showed less adverse structural remodeling and cardiac dysfunction in response to pathological pressure overload induced by transverse aortic constriction (TAC). In contrast, mice lacking ETA only in cardiomyocytes (CM-KO) were not protected. TAC led to a disturbed sympathetic nerve function as measured by cardiac norepinephrine (NE) tissue levels and [(124)I]-metaiodobenzylguanidine-PET, which was prevented in SN-KO. In a rat model of HF, ETAi improved cardiac and sympathetic nerve function. In cocultures of cardiomyocytes (CMs) and sympathetic neurons (SNs), endothelin-1 (ET1) led to a massive NE release and exaggerated CM hypertrophy compared with CM monocultures. ETA-deficient CMs gained a hypertrophic response through wild-type SNs, but ETA-deficient SNs failed to mediate exaggerated CM hypertrophy. Furthermore, ET1 mediated its effects indirectly via NE in CM-SN cocultures through adrenergic receptors and histone deacetylases, resulting in activation of the prohypertrophic transcription factor myocyte enhancer factor 2. In conclusion, sympathetic ETA amplifies ET1 effects on CMs through adrenergic signaling pathways. Thus, antiadrenergic therapies may blunt potentially beneficial effects of ETAi. Taken together, this may indicate that patients with β blocker intolerance or disturbed sympathetic nerve function could be evaluated for a potential benefit from ETAi

Ca M

CaMKII was suggested to mediate ischemic myocardial injury and adverse cardiac remodeling. Here, we investigated the roles of different CaMKII isoforms and splice variants in ischemia/reperfusion (I/R) injury by the use of new genetic CaMKII mouse models. Although CaMKIIδC was upregulated 1 day after I/R injury, cardiac damage 1 day after I/R was neither affected in CaMKIIδ-deficient mice, CaMKIIδ-deficient mice in which the splice variants CaMKIIδB and C were re-expressed, nor in cardiomyocyte-specific CaMKIIδ/γ double knockout mice (DKO). In contrast, 5 weeks after I/R, DKO mice were protected against extensive scar formation and cardiac dysfunction, which was associated with reduced leukocyte infiltration and attenuated expression of members of the chemokine (C-C motif) ligand family, in particular CCL3 (macrophage inflammatory protein-1α, MIP-1α). Intriguingly, CaMKII was sufficient and required to induce CCL3 expression in isolated cardiomyocytes, indicating a cardiomyocyte autonomous effect. We propose that CaMKII-dependent chemoattractant signaling explains the effects on post-I/R remodeling. Taken together, we demonstrate that CaMKII is not critically involved in acute I/R-induced damage but in the process of post-infarct remodeling and inflammatory processes