Continuous observations of the surface energy budget and meteorology over the Arctic sea ice during MOSAiC.

The Multidisciplinary drifting Observatory for the Study of Arctic Climate (MOSAiC) was a yearlong expedition supported by the icebreaker R/V Polarstern, following the Transpolar Drift from October 2019 to October 2020. The campaign documented an annual cycle of physical, biological, and chemical processes impacting the atmosphere-ice-ocean system. Of central importance were measurements of the thermodynamic and dynamic evolution of the sea ice. A multi-agency international team led by the University of Colorado/CIRES and NOAA-PSL observed meteorology and surface-atmosphere energy exchanges, including radiation; turbulent momentum flux; turbulent latent and sensible heat flux; and snow conductive flux. There were four stations on the ice, a 10 m micrometeorological tower paired with a 23/30 m mast and radiation station and three autonomous Atmospheric Surface Flux Stations. Collectively, the four stations acquired ~928 days of data. This manuscript documents the acquisition and post-processing of those measurements and provides a guide for researchers to access and use the data products.

Role of soluble guanylyl cyclase in renal afferent and efferent arterioles.

Renal arteriolar tone depends considerably on the dilatory action of nitric oxide (NO) via activation of soluble guanylyl cyclase (sGC) and cGMP action. NO deficiency and hypoxia/reoxygenation are important pathophysiological factors in the development of acute kidney injury. It was hypothesized that the NO-sGC-cGMP system functions differently in renal afferent arterioles (AA) compared with efferent arterioles (EA) and that the sGC activator cinaciguat differentially dilates these arterioles. Experiments were performed in isolated, perfused mouse glomerular arterioles. Hypoxia (0.1% oxygen) was achieved by using a hypoxia chamber. Phosphodiesterase 5 (PDE5) and sGC subunits were considerably expressed on the mRNA level in AA. PDE5 inhibition with sildenafil, which blocks cGMP degradation, diminished the responses to ANG II bolus application in AA, but not significantly in EA. Vasodilation induced by sildenafil in ANG II-preconstricted vessels was stronger in EA than AA. Cinaciguat, an NO- and heme-independent sGC activator, dilated EA more strongly than AA after NG-nitro-l-arginine methyl ester (l-NAME; NO synthase inhibitor) treatment and preconstriction with ANG II. Cinaciguat-induced dilatation of l-NAME-pretreated and ANG II-preconstricted arterioles was similar to controls without l-NAME treatment. Cinaciguat also induced dilatation in iodinated contrast medium treated AA. Furthermore, it dilated EA, but not AA, after hypoxia/reoxygenation. The results reveal an important role of the NO-sGC-cGMP system for renal dilatation and that EA have a more potent sGC activated dilatory system. Furthermore, AA seem to be more sensitive to hypoxia/reoxygenation than EA under these experimental conditions.

[Contrast medium-induced acute kidney injury-Consensus paper of the working group "Heart and Kidney" of the German Cardiac Society and the German Society of Nephrology]. / Kontrastmittelinduzierte akute Nierenschädigung ­ Konsensuspapier der Arbeitsgemeinschaft "Herz ­ Niere" der Deutschen Gesellschaft für Kardiologie ­ Herz- und Kreislaufforschung e. V. und der Deutschen Gesellschaft für Nephrologie e. V.

This consensus paper summarizes the expert consensus and recommendations of the working group "Heart and Kidney" of the German Cardiac Society (DGK) and the German Society of Nephrology (DGfN) on contrast medium-induced acute kidney injury. Potentially nephrotoxic contrast agents containing iodine are frequently used in interventional medicine and for computer tomography diagnostics. Acute kidney injury occurs in approximately 8-17% of patients exposed to contrast media. The risk factors and underlying pathophysiology are discussed and recommendations for the prophylaxis and treatment of contrast medium-induced acute nephropathy are presented.

The effects of microstructure, Nb content and secondary Ruddlesden-Popper phase on thermoelectric properties in perovskite CaMn1-x Nb x O3 (x = 0-0.10) thin films.

CaMn1-x Nb x O3 (x = 0, 0.5, 0.6, 0.7 and 0.10) thin films have been grown by a two-step sputtering/annealing method. First, rock-salt-structured (Ca,Mn1-x ,Nb x )O thin films were deposited on 11̄00 sapphire using reactive RF magnetron co-sputtering from elemental targets of Ca, Mn and Nb. The CaMn1-x Nb x O3 films were then obtained by thermally induced phase transformation from rock-salt-structured (Ca,Mn1-x Nb x )O to orthorhombic during post-deposition annealing at 700 °C for 3 h in oxygen flow. The X-ray diffraction patterns of pure CaMnO3 showed mixed orientation, while Nb-containing films were epitaxially grown in [101] out of-plane-direction. Scanning transmission electron microscopy showed a Ruddlesden-Popper (R-P) secondary phase in the films, which results in reduction of the electrical and thermal conductivity of CaMn1-x Nb x O3. The electrical resistivity and Seebeck coefficient of the pure CaMnO3 film were measured to 2.7 Ω cm and -270 µV K-1 at room temperature, respectively. The electrical resistivity and Seebeck coefficient were reduced by alloying with Nb and was measured to 0.09 Ω cm and -145 µV K-1 for x = 0.05. Yielding a power factor of 21.5 µW K-2 m-1 near room temperature, nearly eight times higher than for pure CaMnO3 (2.8 µW K-2 m-1). The power factors for alloyed samples are low compared to other studies on phase-pure material. This is due to high electrical resistivity originating from the secondary R-P phase. The thermal conductivity of the CaMn1-x Nb x O3 films is low for all samples and is the lowest for x = 0.07 and 0.10, determined to 1.6 W m-1 K-1. The low thermal conductivity is attributed to grain boundary scattering and the secondary R-P phase.

Ti n+1C n MXenes with fully saturated and thermally stable Cl terminations.

MXenes are a rapidly growing family of 2D materials that exhibit a highly versatile structure and composition, allowing for significant tuning of the materials properties. These properties are, however, ultimately limited by the surface terminations, which are typically a mixture of species, including F and O that are inherent to the MXene processing. Other and robust terminations are lacking. Here, we apply high-resolution scanning transmission electron microscopy (STEM), corresponding image simulations and first-principles calculations to investigate the surface terminations on MXenes synthesized from MAX phases through Lewis acidic melts. The results show that atomic Cl terminates the synthesized MXenes, with mere residual presence of other termination species. Furthermore, in situ STEM-electron energy loss spectroscopy (EELS) heating experiments show that the Cl terminations are stable up to 750 °C. Thus, we present an attractive new termination that widely expands the MXenes' functionalization space and enables new applications.

Self-structuring in Zr1-xAlxN films as a function of composition and growth temperature.

Nanostructure formation via surface-diffusion-mediated segregation of ZrN and AlN in Zr1-xAlxN films during high mobility growth conditions is investigated for 0 ≤ × ≤ 1. The large immiscibility combined with interfacial surface and strain energy balance resulted in a hard nanolabyrinthine lamellar structure with well-defined (semi) coherent c-ZrN and w-AlN domains of sub-nm to ~4 nm in 0.2 ≤ × ≤ 0.4 films, as controlled by atom mobility. For high AlN contents (x > 0.49) Al-rich ZrN domains attain wurtzite structure within fine equiaxed nanocomposite wurtzite lattice. Slow diffusion in wurtzite films points towards crystal structure dependent driving force for decomposition. The findings of unlikelihood of iso-structural decomposition in c-Zr1-xAlxN, and stability of w-Zr1-xAlxN (in large × films) is complemented with first principles calculations.

A dual role of miR-22 in rhabdomyolysis-induced acute kidney injury.

AIM: In acute kidney injury (AKI), regions of the kidney are hypoxic. However, for reasons yet unknown, adaptation to hypoxia through hypoxia-inducible factor (HIF) is limited. Here, we studied miR-22, a potential HIF repressor, in normal kidneys, as well as in rhabdomyolysis-induced AKI, a condition where miR-22 is up-regulated. METHODS: AKI in mice was provoked by IM injection of glycerol. Tissue homogenates were processed to determine the levels of candidate RNAs and proteins, as well as global gene expression profiles. Reporter assays quantified in vitro miR-22 activity and its modulation by mimic or inhibitor molecules, under normoxia or hypoxia (1% O2 ) respectively. In vivo, anti-miR-22 molecules were applied to normal mice or prior to induction of AKI. Renal outcome was assessed by measuring plasma creatinine, plasma urea and the levels of the injury markers Kim-1 and Ngal. RESULTS: Renal miR-22 is inducible by hypoxia and represses hypoxia-inducible factor (HIF). Specific inhibition of miR-22 regulates 1913 gene transcripts in kidneys controls and 3386 in AKI, many of which are involved in development or carcinogenesis. Specific inhibition of miR-22 up-regulates tissue protective HIF target genes, yet renal function and injury markers are unchanged or worsened. CONCLUSIONS: miR-22 is a HIF repressor constitutively expressed in the adult kidney and up-regulated in AKI. Specific inhibition of miR-22 is efficient in vivo and profoundly affects renal gene expression in health and disease, including up-regulation of HIF. However, the net effect on rhabdomyolysis-induced AKI outcome is neutral or even negative.

Evaluation of lung and chest wall mechanics during anaesthesia using the PEEP-step method.

BACKGROUND: Postoperative pulmonary complications are common. Between patients there are differences in lung and chest wall mechanics. Individualised mechanical ventilation based on measurement of transpulmonary pressures would be a step forward. A previously described method evaluates lung and chest wall mechanics from a change of ΔPEEP and calculation of change in end-expiratory lung volume (ΔEELV). The aim of the present study was to validate this PEEP-step method (PSM) during general anaesthesia by comparing it with the conventional method using oesophageal pressure (PES) measurements. METHODS: In 24 lung healthy subjects (BMI 18.5-32), three different sizes of PEEP steps were performed during general anaesthesia and ΔEELVs were calculated. Transpulmonary driving pressure (ΔPL) for a tidal volume equal to each ΔEELV was measured using PES measurements and compared to ΔPEEP with limits of agreement and intraclass correlation coefficients (ICC). ΔPL calculated with both methods was compared with a Bland-Altman plot. RESULTS: Mean differences between ΔPEEP and ΔPL were <0.15 cm H2O, 95% limits of agreements -2.1 to 2.0 cm H2O, ICC 0.6-0.83. Mean differences between ΔPL calculated by both methods were <0.2 cm H2O. Ratio of lung elastance and respiratory system elastance was 0.5-0.95. CONCLUSIONS: The large variation in mechanical properties among the lung healthy patients stresses the need for individualised ventilator settings based on measurements of lung and chest wall mechanics. The agreement between ΔPLs measured by the two methods during general anaesthesia suggests the use of the non-invasive PSM in this patient population. CLINICAL TRIAL REGISTRATION: NCT 02830516.

Deletion of Uncoupling Protein-2 reduces renal mitochondrial leak respiration, intrarenal hypoxia and proteinuria in a mouse model of type 1 diabetes.

AIM: Uncoupling protein-2 (UCP-2) can induce mitochondrial uncoupling in the diabetic kidney. Although mitochondrial uncoupling reduces oxidative stress originating from the mitochondria and can be regarded as a protective mechanism, the increased oxygen consumption occurring secondarily to increased mitochondria uncoupling, that is leak respiration, may contribute to kidney tissue hypoxia. Using UCP-2-/- mice, we tested the hypothesis that UCP-2-mediated leak respiration is important for the development of diabetes-induced intrarenal hypoxia and proteinuria. METHODS: Kidney function, in vivo oxygen metabolism, urinary protein leakage and mitochondrial function were determined in wild-type and UCP-2-/- mice during normoglycaemia and 2 weeks after diabetes induction. RESULTS: Diabetic wild-type mice displayed mitochondrial leak respiration, pronounced intrarenal hypoxia, proteinuria and increased urinary KIM-1 excretion. However, diabetic UCP-2-/- mice did not develop increased mitochondrial leak respiration and presented with normal intrarenal oxygen levels, urinary protein and KIM-1 excretion. CONCLUSION: Although functioning as an antioxidant system, mitochondria uncoupling is always in co-occurrence with increased oxygen consumption, that is leak respiration; a potentially detrimental side effect as it can result in kidney tissue hypoxia; an acknowledged unifying pathway to nephropathy. Indeed, this study demonstrates a novel mechanism in which UCP-2-mediated mitochondrial leak respiration is necessary for the development of diabetes-induced intrarenal tissue hypoxia and proteinuria.