A high-resolution map of direct and indirect connectivity of erosion risk areas to surface waters in Switzerland: A risk assessment tool for planning and policy-making

Off-site effects of soil erosion are becoming increasingly important, particularly the pollution of surface waters. In order to develop environmentally efficient and cost effective mitigation options it is essential to identify areas that bear both a high erosion risk and high connectivity to surface waters. This paper introduces a simple risk assessment tool that allows the delineation of potential critical source areas (CSA) of sediment input into surface waters concerning the agricultural areas of Switzerland. The basis are the erosion risk map with a 2 m resolution (ERM2) and the drainage network, which is extended by drained roads, farm tracks, and slope depressions. The probability of hydrological and sedimentological connectivity is assessed by combining soil erosion risk and extended drainage network with flow distance calculation. A GIS-environment with multiple-flow accumulation algorithms is used for routing runoff generation and flow pathways. The result is a high resolution connectivity map of the agricultural area of Switzerland (888,050 ha). Fifty-five percent of the computed agricultural area is potentially connected with surface waters, 45% is not connected. Surprisingly, the larger part of 34% (62% of the connected area) is indirectly connected with surface waters through drained roads, and only 21% are directly connected. The reason is the topographic complexity and patchiness of the landscape due to a dense road and drainage network. A total of 24% of the connected area and 13% of the computed agricultural area, respectively, are rated with a high connectivity probability. On these CSA an adapted land use is recommended, supported by vegetated buffer strips preventing sediment load. Even areas that are far away from open water bodies can be indirectly connected and need to be included in planning of mitigation measures. Thus, the connectivity map presented is an important decision-making tool for policy-makers and extension services. The map is published on the web and thus available for application.

Toward Cove-Edged Low Band Gap Graphene Nanoribbons

Graphene nanoribbons (GNRs), defined as nanometer-wide strips of graphene, have attracted increasing attention as promising candidates for next-generation semiconductors. Here, we demonstrate a bottom-up strategy toward novel low band gap GNRs (E-g = 1.70 eV) with a well-defined cove-type periphery both in solution and on a solid substrate surface with chrysene as the key monomer. Corresponding cyclized chrysene-based oligornerS consisting of the dimer and tetramer are obtained via an Ullmann Coupling followed by oxidative intramolecular cyclodehydrogenation in solution, and much higher GNR homologues via on-surface synthesis. These oligomers adopt nonplanar structures due to the isteric repulsion between the two C-H bonds at the inner cove position. Characterizations by single crystal X-ray analysis, UV-vis absorption spectroscopy, NMR spectroscopy, and scanning tunneling microscopy (STM) are described. The interpretation is assisted by density functional theory (DFT) calculations.

Post-operative monitoring of free muscle transfers by Laser Doppler Imaging: A prospective study.

PURPOSE Despite different existing methods, monitoring of free muscle transfer is still challenging. In the current study we evaluated our clinical setting regarding monitoring of such tissues, using a recent microcirculation-imaging camera (EasyLDI) as an additional tool for detection of perfusion incompetency. PATIENTS AND METHODS This study was performed on seven patients with soft tissue defect, who underwent reconstruction with free gracilis muscle. Beside standard monitoring protocol (clinical assessment, temperature strips, and surface Doppler), hourly EasyLDI monitoring was performed for 48 hours. Thereby a baseline value (raised flap but connected to its vascular bundle) and an ischaemia perfusion value (completely resected flap) were measured at the same point. RESULTS The mean age of the patients, mean baseline value, ischaemia value perfusion were 48.00 ± 13.42 years, 49.31 ± 17.33 arbitrary perfusion units (APU), 9.87 ± 4.22 APU, respectively. The LDI measured values in six free muscle transfers were compatible with hourly standard monitoring protocol, and normalized LDI values significantly increased during time (P < 0.001, r = 0.412). One of the flaps required a return to theatre 17 hours after the operation, where an unsalvageable flap loss was detected. All normalized LDI values of this flap were under the ischaemia perfusion level and the trend was significantly descending during time (P < 0.001, r = -0.870). CONCLUSION Due to the capability of early detection of perfusion incompetency, LDI may be recommended as an additional post-operative monitoring device for free muscle flaps, for early detection of suspected failing flaps and for validation of other methods.

Dysfunction of respiratory muscles in critically ill patients on the intensive care unit.

Muscular weakness and muscle wasting may often be observed in critically ill patients on intensive care units (ICUs) and may present as failure to wean from mechanical ventilation. Importantly, mounting data demonstrate that mechanical ventilation itself may induce progressive dysfunction of the main respiratory muscle, i.e. the diaphragm. The respective condition was termed 'ventilator-induced diaphragmatic dysfunction' (VIDD) and should be distinguished from peripheral muscular weakness as observed in 'ICU-acquired weakness (ICU-AW)'. Interestingly, VIDD and ICU-AW may often be observed in critically ill patients with, e.g. severe sepsis or septic shock, and recent data demonstrate that the pathophysiology of these conditions may overlap. VIDD may mainly be characterized on a histopathological level as disuse muscular atrophy, and data demonstrate increased proteolysis and decreased protein synthesis as important underlying pathomechanisms. However, atrophy alone does not explain the observed loss of muscular force. When, e.g. isolated muscle strips are examined and force is normalized for cross-sectional fibre area, the loss is disproportionally larger than would be expected by atrophy alone. Nevertheless, although the exact molecular pathways for the induction of proteolytic systems remain incompletely understood, data now suggest that VIDD may also be triggered by mechanisms including decreased diaphragmatic blood flow or increased oxidative stress. Here we provide a concise review on the available literature on respiratory muscle weakness and VIDD in the critically ill. Potential underlying pathomechanisms will be discussed before the background of current diagnostic options. Furthermore, we will elucidate and speculate on potential novel future therapeutic avenues.