Characterization, Analysis and Modeling of Complex Flow Networks in Mammalian Organs

Das Studium von Transportmechanismen in komplexen Organismen stellt eine zentrale Herausforderung dar, nicht nur in medizinischen und biologischen Disziplinen, sondern auch zunehmend in der Physik und Netzwerktheorie. Insbesondere sind bionisch inspirierte Designprinzipien zunehmend relevant, da sie zuverlässige Lösungsansätze zu verschiedenen theoretischen und technischen Problemen bieten. Herausstechend sind dabei vaskuläre Netzwerke in Säugetieren, deren Entwicklung auffällig stark auf Selbstorganisation beruhen und die korrekte Verteilung von Sauerstoff, Wasser, Blut oder Ähnlichem erlaubt. Dies wird erreicht durch ein komplexes biochemisches Signalsystem, welches an makroskopische Stimulationen, wie z. B. Reibung und Stress, gekoppelt ist. Die Morphogenese solcher Flussnetzwerke ist allerdings noch anderen Restriktionen unterworfen, da diese räumlich eingebettete Objekte darstellen. Sie sind als solche signifikant beschränkter in ihrer Skalierbarkeitund Dynamik. Diese Dissertation addressiert daher relevante Fragestellungen zur Charakterisierung von Netzwerken und der Morphogenesesimulationen von drei-dimensional eingebetteten Netzwerken Die Schlüsselmechanismen auf die wir uns hier konzentrieren sind Flussfluktuationen, Interaktionen zwischen Paarstrukturen und die Aufnahme von Nährstoffen. Zu Beginn zeigen wir, wie sich konventionelle Ansätze zu Flussfluktuationen als allgemeine Einparametermodelle darstellen lassen. Wir demonstrieren damit den kontinuierlichen Übergang zu zunehmend vernetzten Strukturen und indizieren Topologieabhängigkeiten der Plexus in Anbetracht dieses Übergangs. Darauf aufbauend formulieren wir ein neues Adaptationsmodell für ineinander verwobene Gefäßnetzwerke wie sie auch in der Leber, Bauchspeicheldrüse oder Niere vorkommen. Wir diskutieren anhand dieser Strukturen lokale Wechselwirkungen von dreidimensionalen Netzwerken. Dadurch können wir zeigen, dass repulsiv gekoppelte Netzwerke fluktuationsinduzierte Vernetzungen auflösen und attraktive Kopplungen einen neuen Mechanismus zur Erzeugung eben jener darstellen. Als nächstes verallgemeinern wir die Murray Regel für solch komplexe Wechselwirkungen und Fluktuationen. Die daraus abgeleiteten Relationen nutzen wir zur Regression der Modellparameter und testen diese an den Gefäßnetzwerken der Leber. Weiterhin verallgemeinern wir konventionelle Transportmodelle für die Nährstoffaufnahme in beliebigem Gewebe und testen diese in Morphogenesemodellen gegen die bekannten Ansätze zur Dissipationsminimierung. Hier zeigen sich komplexe Übergänge zwischen vernetzten Strukturen und unkonventionelles Phasenverhalten. Allerdings indizieren die Ergebnisse Widersprüche zu echten Kapillargefäßen und wir vermuten Adaptationsmethoden ohne Gefäßgrößenänderung als wahrscheinlicheren Mechanismus. Im Ausblick schlagen wir auf unseren Ergebnissen aufbauende Folgemodelle vor, welche die Modellierung komplexer Transportprozesse zwischen verschränkten Gefäßnetzwerken zum Ziel haben.:Introduction 1 1.1 Complex networks in biology . . . . . . . . . . . . . . . . . . . . . . . . 1 1.1.1 Flow networks in mammals . . . . . . . . . . . . . . . . . . . . 3 1.1.2 Network morphogenesis . . . . . . . . . . . . . . . . . . . . . . . 5 1.2 State of the art . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 1.2.1 Modelling flow network adaptation . . . . . . . . . . . . . . . . 8 1.2.2 Metrics for biological flow networks . . . . . . . . . . . . . . . . 11 Scaling in spatial networks . . . . . . . . . . . . . . . . . . . . . 12 Redundancy of flow networks . . . . . . . . . . . . . . . . . . . 13 1.3 Problem statement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 1.3.1 Spatial embedding in metabolic costs models . . . . . . . . . . . 16 1.3.2 Characterizing three-dimensional reticulated networks . . . . . . 17 1.3.3 Optimal design for metabolite uptake . . . . . . . . . . . . . . . 20 2 Theory and Methods 23 2.1 Basic principles and mathematics . . . . . . . . . . . . . . . . . . . . 23 2.1.1 Mathematical basics . . . . . . . . . . . . . . . . . . . . . . . . 23 Linear equation systems . . . . . . . . . . . . . . . . . . . . . 23 Dynamical systems and optimization . . . . . . . . . . . . . . 25 Graph theory . . . . . . . . . . . . . . . . . . . . . . . . . . . 27 2.1.2 Basic hydrodynamics . . . . . . . . . . . . . . . . . . . . . . . . 30 Momentum and mass balance . . . . . . . . . . . . . . . . . . . 30 Diffusion-Advection . . . . . . . . . . . . . . . . . . . . . . . . . 31 Flow in a thin channel . . . . . . . . . . . . . . . . . . . . . . . 32 2.1.3 Kirchhoff networks . . . . . . . . . . . . . . . . . . . . . . . . . 33 2.2 Complex transport problems . . . . . . . . . . . . . . . . . . . . . . . . 36 2.2.1 Taylor dispersion . . . . . . . . . . . . . . . . . . . . . . . . . . 36 2.2.2 Flow-driven pruning . . . . . . . . . . . . . . . . . . . . . . . . 38 Metabolic cost functions . . . . . . . . . . . . . . . . . . . . . . 38 Adaptation and topological transitions . . . . . . . . . . . . . . 40 3 Results 43 3.1 On single network adaptation with fluctuating flow patterns . . . . . . 43 3.1.1 Incorporating flow fluctuations: Noisy, uncorrelated sink patterns 44 3.1.2 Fluctuation induced nullity transitions . . . . . . . . . . . . . . 48 3.1.3 Finite size effects and topological saturation limits . . . . . . . 52 3.2 On geometric coupling between intertwined networks . . . . . . . . . . 55 3.2.1 Power law model of interacting multilayer networks . . . . . . . 55 3.2.2 Adaptation dynamics of intertwined vessel systems . . . . . . . 57 x 3.2.3 Repulsive coupling induced nullity breakdown . . . . . . . . . . 59 3.2.4 Attractive coupling induced nullity onset . . . . . . . . . . . . 66 3.3 On generalizing and applying geometric laws to complex transport networks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73 3.3.1 Generalizing Murray’s law for complex flow networks . . . . . . 73 Murray’s law for fluctuating flows . . . . . . . . . . . . . . . . . 74 Murray’s Law for extended metabolic costs models . . . . . . . 77 3.3.2 Interpolating model parameters for intertwined networks . . . . 78 Testing ideal Kirchhoff networks . . . . . . . . . . . . . . . . . . 79 3.3.3 Identifying geometrical fingerprints in the liver lobule . . . . . . 85 3.4 On the optimization of metabolite uptake in complex flow networks . . 91 3.4.1 Metabolite transport in thin channel systems . . . . . . . . . . . 91 On single channel solutions . . . . . . . . . . . . . . . . . . . . 91 On detailed absorption rate models . . . . . . . . . . . . . . . . 93 On linear network solutions . . . . . . . . . . . . . . . . . . . . 96 On the uptake in spanning tree and reticulated networks . . . . 97 3.4.2 Optimizing metabolite uptake in shear-stress driven systems . . 100 Link-wise supply-demand model . . . . . . . . . . . . . . . . . . 101 Volume-wise supply-demand model . . . . . . . . . . . . . . . . 110 4 Discussion and Outlook 119 4.1 Summary of Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119 4.2 Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121 4.3 Outlook . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 124 4.3.1 Metabolite transport in the liver lobule . . . . . . . . . . . . . . 124 Expansion of the Ostrenko model . . . . . . . . . . . . . . . . . 124 Complex multi transport probems in biology . . . . . . . . . . . 127 4.3.2 Absorption rate optimization and microscopic elimination models 128 Appendix A More on coupled intertwined networks 131 A.1 Coupling of Diamond lattices . . . . . . . . . . . . . . . . . . . . . . . 131 A.1.1 Repulsive coupling . . . . . . . . . . . . . . . . . . . . . . . . . 131 A.1.2 Attractive coupling . . . . . . . . . . . . . . . . . . . . . . . . . 133 A.2 Coupling of Laves Graphs . . . . . . . . . . . . . . . . . . . . . . . . . 134 A.2.1 Repulsive coupling . . . . . . . . . . . . . . . . . . . . . . . . . 134 A.2.2 Attractive coupling . . . . . . . . . . . . . . . . . . . . . . . . . 136 B More on metabolite uptake adaptation 139 B.1 Deriving dynamical systems from demand-supply relationships . . . . . 139 B.2 Microscopic uptake models . . . . . . . . . . . . . . . . . . . . . . . . . 142 B.2.1 Detailed uptake estimation in single layer systems . . . . . . . . 142 B.2.2 Detailed uptake estimation in liver sinusoids . . . . . . . . . . . 143 B.3 Metabolite uptake in three-dimensional plexi . . . . . . . . . . . . . . . 145 B.3.1 Link-wise demand adaptation . . . . . . . . . . . . . . . . . . . 145 B.3.2 Volume-wise demand adaptation . . . . . . . . . . . . . . . . . . 150 Bibliography 155Understanding the transport of fluid in complex organisms has proven to be a key challenge not only in the medical and biological sciences, but in physics and network theory as well. This is even more so as biologically-inspired design principles have been increasing in popularity, reliably generating solutions to common theoretical and technical problems. On that note, vascular networks in mammalian organs display a magnificent level of self-organization, allowing them to develop and mature, yet miraculously orchestrate the correct transport of oxygen, water, blood etc. This is achieved by a dedicated biochemical feedback system, which is coupled to macroscopic stimuli, such as mechanical stresses. Another important constraint for the morphogenesis of flow networks is their environment, as these networks are spatially embedded. They are therefore exposed to significant constraints with regards to their scalability and dynamical behavior, which are not yet well understood. This thesis addresses the current challenges of network characterization and morphogenesis modeling for three-dimensional embedded networks. In order to derive proper maturation mechanisms, we propose a set of toy models for the creation of non-planar, entangled and reticulated networks. The key mechanisms we focus on in this thesis are flow fluctuation, coupling of pairing structures and metabolite uptake. We show that in accordance with previous theoretical approaches, fluctuation induced nullity can be formulated as a single parameter problem. We demonstrate that the reticulation transition follows a logarithmic law and find plexi with certain topologies to have limited nullity transitions, rendering such plexi intrinsically wasteful in terms of fluctuation generated reticulation. Moreover, we formulate a new coupling model for entangled adapting networks as an approach for vasculature found in the liver lobules, pancreas, kidneys etc. We discuss a model based on local, distance-dependent interactions between pairs of three-dimensional network skeletons. In doing so we find unprecedented delay and breakdown of the fluctuation induced nullity transition for repulsive interactions. In addition we find a new nullity transition emerging for attractive coupling. Next, we study how flow fluctuations and complex metabolic costs can be incorporated into Murray’s Law. Utilizing this law for interpolation, we are able to derive order of magnitude estimation for the parameters in liver networks, suggesting fluctuation driven adaptation to be the dominant factor. We also conclude that attractive coupling is a reasonable mechanism to account for the maintenance of entangled structures. We test optimal metabolite uptake in Kirchhoff networks by evaluating the impact of solute uptake driven dynamics relative to wall-shear stress driven adaptation. Here, we find that a nullity transition emerges in case of a dominant metabolite uptake machinery. In addition to that, we find re-entrant behavior in case of high absorption rates and discover a complex interaction between shear-stress generation and feedback. Nevertheless, we conclude that metabolite uptake optimization is not likely to occur due to radial adaptation alone. We suggest areas for further studies, which should consider absorption rate variation in order to account for realistic uptake profiles. In our outlook, we suggest a complex morphogenesis model for intertwined networks based on the results of this thesis.:Introduction 1 1.1 Complex networks in biology . . . . . . . . . . . . . . . . . . . . . . . . 1 1.1.1 Flow networks in mammals . . . . . . . . . . . . . . . . . . . . 3 1.1.2 Network morphogenesis . . . . . . . . . . . . . . . . . . . . . . . 5 1.2 State of the art . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8 1.2.1 Modelling flow network adaptation . . . . . . . . . . . . . . . . 8 1.2.2 Metrics for biological flow networks . . . . . . . . . . . . . . . . 11 Scaling in spatial networks . . . . . . . . . . . . . . . . . . . . . 12 Redundancy of flow networks . . . . . . . . . . . . . . . . . . . 13 1.3 Problem statement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 1.3.1 Spatial embedding in metabolic costs models . . . . . . . . . . . 16 1.3.2 Characterizing three-dimensional reticulated networks . . . . . . 17 1.3.3 Optimal design for metabolite uptake . . . . . . . . . . . . . . . 20 2 Theory and Methods 23 2.1 Basic principles and mathematics . . . . . . . . . . . . . . . . . . . . 23 2.1.1 Mathematical basics . . . . . . . . . . . . . . . . . . . . . . . . 23 Linear equation systems . . . . . . . . . . . . . . . . . . . . . 23 Dynamical systems and optimization . . . . . . . . . . . . . . 25 Graph theory . . . . . . . . . . . . . . . . . . . . . . . . . . . 27 2.1.2 Basic hydrodynamics . . . . . . . . . . . . . . . . . . . . . . . . 30 Momentum and mass balance . . . . . . . . . . . . . . . . . . . 30 Diffusion-Advection . . . . . . . . . . . . . . . . . . . . . . . . . 31 Flow in a thin channel . . . . . . . . . . . . . . . . . . . . . . . 32 2.1.3 Kirchhoff networks . . . . . . . . . . . . . . . . . . . . . . . . . 33 2.2 Complex transport problems . . . . . . . . . . . . . . . . . . . . . . . . 36 2.2.1 Taylor dispersion . . . . . . . . . . . . . . . . . . . . . . . . . . 36 2.2.2 Flow-driven pruning . . . . . . . . . . . . . . . . . . . . . . . . 38 Metabolic cost functions . . . . . . . . . . . . . . . . . . . . . . 38 Adaptation and topological transitions . . . . . . . . . . . . . . 40 3 Results 43 3.1 On single network adaptation with fluctuating flow patterns . . . . . . 43 3.1.1 Incorporating flow fluctuations: Noisy, uncorrelated sink patterns 44 3.1.2 Fluctuation induced nullity transitions . . . . . . . . . . . . . . 48 3.1.3 Finite size effects and topological saturation limits . . . . . . . 52 3.2 On geometric coupling between intertwined networks . . . . . . . . . . 55 3.2.1 Power law model of interacting multilayer networks . . . . . . . 55 3.2.2 Adaptation dynamics of intertwined vessel systems . . . . . . . 57 x 3.2.3 Repulsive coupling induced nullity breakdown . . . . . . . . . . 59 3.2.4 Attractive coupling induced nullity onset . . . . . . . . . . . . 66 3.3 On generalizing and applying geometric laws to complex transport networks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73 3.3.1 Generalizing Murray’s law for complex flow networks . . . . . . 73 Murray’s law for fluctuating flows . . . . . . . . . . . . . . . . . 74 Murray’s Law for extended metabolic costs models . . . . . . . 77 3.3.2 Interpolating model parameters for intertwined networks . . . . 78 Testing ideal Kirchhoff networks . . . . . . . . . . . . . . . . . . 79 3.3.3 Identifying geometrical fingerprints in the liver lobule . . . . . . 85 3.4 On the optimization of metabolite uptake in complex flow networks . . 91 3.4.1 Metabolite transport in thin channel systems . . . . . . . . . . . 91 On single channel solutions . . . . . . . . . . . . . . . . . . . . 91 On detailed absorption rate models . . . . . . . . . . . . . . . . 93 On linear network solutions . . . . . . . . . . . . . . . . . . . . 96 On the uptake in spanning tree and reticulated networks . . . . 97 3.4.2 Optimizing metabolite uptake in shear-stress driven systems . . 100 Link-wise supply-demand model . . . . . . . . . . . . . . . . . . 101 Volume-wise supply-demand model . . . . . . . . . . . . . . . . 110 4 Discussion and Outlook 119 4.1 Summary of Results . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119 4.2 Discussion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121 4.3 Outlook . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 124 4.3.1 Metabolite transport in the liver lobule . . . . . . . . . . . . . . 124 Expansion of the Ostrenko model . . . . . . . . . . . . . . . . . 124 Complex multi transport probems in biology . . . . . . . . . . . 127 4.3.2 Absorption rate optimization and microscopic elimination models 128 Appendix A More on coupled intertwined networks 131 A.1 Coupling of Diamond lattices . . . . . . . . . . . . . . . . . . . . . . . 131 A.1.1 Repulsive coupling . . . . . . . . . . . . . . . . . . . . . . . . . 131 A.1.2 Attractive coupling . . . . . . . . . . . . . . . . . . . . . . . . . 133 A.2 Coupling of Laves Graphs . . . . . . . . . . . . . . . . . . . . . . . . . 134 A.2.1 Repulsive coupling . . . . . . . . . . . . . . . . . . . . . . . . . 134 A.2.2 Attractive coupling . . . . . . . . . . . . . . . . . . . . . . . . . 136 B More on metabolite uptake adaptation 139 B.1 Deriving dynamical systems from demand-supply relationships . . . . . 139 B.2 Microscopic uptake models . . . . . . . . . . . . . . . . . . . . . . . . . 142 B.2.1 Detailed uptake estimation in single layer systems . . . . . . . . 142 B.2.2 Detailed uptake estimation in liver sinusoids . . . . . . . . . . . 143 B.3 Metabolite uptake in three-dimensional plexi . . . . . . . . . . . . . . . 145 B.3.1 Link-wise demand adaptation . . . . . . . . . . . . . . . . . . . 145 B.3.2 Volume-wise demand adaptation . . . . . . . . . . . . . . . . . . 150 Bibliography 15

How to Pare a Pair: Topology Control and Pruning in Intertwined Complex Networks

Recent work on self-organized remodeling of vasculature in slime-mold, leaf venation systems and vessel systems in vertebrates has put forward a plethora of potential adaptation mechanisms. All these share the underlying hypothesis of a flow-driven machinery, meant to alter rudimentary vessel networks in order to optimize the system's dissipation, flow uniformity, or more, with different versions of constraints. Nevertheless, the influence of environmental factors on the long-term adaptation dynamics as well as the networks structure and function have not been fully understood. Therefore, interwoven capillary systems such as found in the liver, kidney and pancreas, present a novel challenge and key opportunity regarding the field of coupled distribution networks. We here present an advanced version of the discrete Hu--Cai model, coupling two spatial networks in 3D. We show that spatial coupling of two flow-adapting networks can control the onset of topological complexity in concert with short-term flow fluctuations. We find that both fluctuation-induced and spatial coupling induced topology transitions undergo curve collapse obeying simple functional rescaling. Further, our approach results in an alternative form of Murray's law, which incorporates local vessel interactions and flow interactions. This geometric law allows for the estimation of the model parameters in ideal Kirchhoff networks and respective experimentally acquired network skeletons

Modified Nikaidoh procedure for the correction of complex forms of transposition of the great arteries with ventricular septal defect and left ventricular outflow tract obstruction: mid-term results

OBJECTIVES Different surgical techniques for the treatment of complex transposition of the great arteries (TGA) with ventricular septal defect and left ventricular outflow tract obstruction (LVOTO) have been developed, in particular the Rastelli operation, the réparation à l'étage ventriculaire procedure and the Nikaidoh procedure. The hitherto published results of the Nikaidoh procedure and its modifications compare favourably with those of other techniques; however, experience with the Nikaidoh procedure is still limited. Here, we report our institutions' early and mid-term results with modifications of the Nikaidoh procedure. METHODS Twenty-one patients who underwent a modified Nikaidoh procedure between 2006 and 2012 at our institution, either as aortic root translocation (n = 17) or as en bloc rotation of the arterial trunk (n = 4), were studied retrospectively. RESULTS There were 2 early and 1 mid-term deaths. The follow-up continued for a median of 2.3 years (range 0.3-6.4 years). During the follow-up, the performance of the reconstructed left ventricular outflow tract (LVOT) remained excellent: no reobstruction and no aortic valve regurgitation classified as more than mild were observed. Left ventricular function was well preserved. In 4 patients, a significant reoccurring right ventricular outflow tract obstruction due to conduit failure was observed; so far, two reoperations with conduit replacement have been necessary. The mean right ventricular outflow tract peak gradient was 24 ± 7.2 mmHg at the last follow-up in the remaining patients. No reobstruction of the right ventricular outflow tract occurred in patients with preserved pulmonary valve tissue after en bloc rotation. CONCLUSIONS The aortic translocation procedure is a valuable surgical option for patients with complex (TGA) with ventricular septal defect and LVOTO. The mid-term results document excellent performance of the reconstructed LVOT. Modifications of the Nikaidoh procedure that preserve pulmonary valve tissue may further reduce the need for right ventricular outflow tract reoperatio

Feedback Loops of the Mammalian Circadian Clock Constitute Repressilator

Mammals evolved an endogenous timing system to coordinate their physiology and behaviour to the 24h period of the solar day. While it is well accepted that circadian rhythms are generated by intracellular transcriptional feedback loops, it is still debated which network motifs are necessary and sufficient for generating self-sustained oscillations. Here, we systematically explore a data-based circadian oscillator model with multiple negative and positive feedback loops and identify a series of three subsequent inhibitions known as “repressilator” as a core element of the mammalian circadian oscillator. The central role of the repressilator motif is consistent with time-resolved ChIP- seq experiments of circadian clock transcription factors and loss of rhythmicity in core clock gene knockouts

Interaction-induced delocalization of two particles in a random potential: Scaling properties

The localization length $\xi_2$ for coherent propagation of two interacting particles in a random potential is studied using a novel and efficient numerical method. We find that the enhancement of $\xi_2$ over the one-particle localization length $\xi_1$ satisfies the scaling relation $\xi_2/\xi_1=f(u/\Delta_\xi)$, where $u$ is the interaction strength and $\Delta_{\xi}$ the level spacing of a wire of length $\xi_1$. The scaling function $f$ is linear over the investigated parameter range. This implies that $\xi_2$ increases faster with $u$ than previously predicted. We also study a novel mapping of the problem to a banded-random-matrix model.Comment: 5 pages and two figures in a uuencoded, compressed tar file; uses revtex and psfig.sty (included); substantial revision of a previous version of the paper including newly discovered scaling behavio

Consensus on Wound Antisepsis: Update 2018

Wound antisepsis has undergone a renaissance due to the introduction of highly effective wound-compatible antimicrobial agents and the spread of multidrug-resistant organisms (MDROs). However, a strict indication must be set for the application of these agents. An infected or critically colonized wound must be treated antiseptically. In addition, systemic antibiotic therapy is required in case the infection spreads. If applied preventively, the Wounds-at-Risk Score allows an assessment of the risk for infection and thus appropriateness of the indication. The content of this updated consensus recommendation still largely consists of discussing properties of octenidine dihydrochloride (OCT), polihexanide, and iodophores. The evaluations of hypochlorite, taurolidine, and silver ions have been updated. For critically colonized and infected chronic wounds as well as for burns, polihexanide is classified as the active agent of choice. The combination 0.1% OCT/phenoxyethanol (PE) solution is suitable for acute, contaminated, and traumatic wounds, including MRSA-colonized wounds due to its deep action. For chronic wounds, preparations with 0.05% OCT are preferable. For bite, stab/puncture, and gunshot wounds, polyvinylpyrrolidone (PVP)-iodine is the first choice, while polihexanide and hypochlorite are superior to PVP-iodine for the treatment of contaminated acute and chronic wounds. For the decolonization of wounds colonized or infected with MDROs, the combination of OCT/PE is preferred. For peritoneal rinsing or rinsing of other cavities with a lack of drainage potential as well as the risk of central nervous system exposure, hypochlorite is the superior active agent. Silver-sulfadiazine is classified as dispensable, while dyes, organic mercury compounds, and hydrogen peroxide alone are classified as obsolete. As promising prospects, acetic acid, the combination of negative pressure wound therapy with the instillation of antiseptics (NPWTi), and cold atmospheric plasma are also subjects of this assessment

Einfluss von Baumarten auf Treibhausgasumsätze in verformten Waldböden

Trotz der Beschränkung von Fahrbewegungen auf Rückegassen, kommt es auf 10-20 % der deutschen Waldfläche zu bodenphysikalischen Veränderungen durch die vollmechanisierte Holzernte. Die daraus resultierende verringerte Bodenbelüftung kann CH4-Oxidationsraten verringern sowie N2O-Emissionen erhöhen. Auf drei seit 17 Jahren ungenutzten Rückegassen wurden Treibhausgasumsätze mithilfe monatlich stattfindender Kammermessungen über einen Zeitraum von einem Jahr bestimmt. In unmittelbarer Nachbarschaft wurden Fahrspu-ren in einem Buchenbestand (Fagus sylvatica), Fichtenbestand (Picea abies) und Schwarzer-lenbestand (Alnus glutinosa) untersucht. Schwarzerle wurde aufgrund ihres potentiellen po-sitiven Einflusses auf die Regeneration der Bodenstruktur miteinbezogen. Im Vergleich zur ungestörten Kontrolle wurde im Rückegassenbereich durchweg eine verringerte CH4-Aufnahme beobachtet. Trotz Indizien für eine verbesserte Bodenbelüftung in Form von hö-heren Gasdiffusionskoeffizienten unter Erle, unterschied sich die Methanoxidation nicht von der unter Buche und Fichte. Unterschiede in den N2O-Emissionsraten waren nur im unge-störten Bestand unter Erle ersichtlich, wo deutlich höhere N2O-Emissionen ab Herbst gemes-sen wurden. In den Strukturgestörten Bereichen aller Bestände waren für N2O keine Unter-schiede zwischen den Baumarten ersichtlich. Die Ergebnisse deuten an, dass die Pflanzung von Schwarzerlen auf Fahrspuren zu einer verbesserten Strukturregeneration geführt hat. Positive Auswirkungen des Regenerationseffekts auf die Flüsse klimarelevanter Spurengase wurden möglicherweise durch die Stickstoffakkumulation unter Erle konterkariert. Denkbar wäre eine Inhibition der Methanoxidation durch Ammonium sowie eine Förderung der für die N2O-Bildung verantwortlichen Prozesse Nitrifizierung und Denitrifizierung in Folge einer erhöhten Stickstoffverfügbarkeit

When, Where, and How Nature Matters for Ecosystem Services: Challenges for the Next Generation of Ecosystem Service Models

Many decision-makers are looking to science to clarify how nature supports human well-being. Scientists\u27 responses have typically focused on empirical models of the provision of ecosystem services (ES) and resulting decision-support tools. Although such tools have captured some of the complexities of ES, they can be difficult to adapt to new situations. Globally useful tools that predict the provision of multiple ES under different decision scenarios have proven challenging to develop. Questions from decision-makers and limitations of existing decision-support tools indicate three crucial research frontiers for incorporating cutting-edge ES science into decision-support tools: (1) understanding the complex dynamics of ES in space and time, (2) linking ES provision to human well-being, and (3) determining the potential for technology to substitute for or enhance ES. We explore these frontiers in-depth, explaining why each is important and how existing knowledge at their cutting edges can be incorporated to improve ES decision-making tools