A Microstructural View of Burrowing with RoboClam

RoboClam is a burrowing technology inspired by Ensis directus, the Atlantic razor clam. Atlantic razor clams should only be strong enough to dig a few centimeters into the soil, yet they burrow to over 70 cm. The animal uses a clever trick to achieve this: by contracting its body, it agitates and locally fluidizes the soil, reducing the drag and energetic cost of burrowing. RoboClam technology, which is based on the digging mechanics of razor clams, may be valuable for subsea applications that could benefit from efficient burrowing, such as anchoring, mine detonation, and cable laying. We directly visualize the movement of soil grains during the contraction of RoboClam, using a novel index-matching technique along with particle tracking. We show that the size of the failure zone around contracting RoboClam, can be theoretically predicted from the substrate and pore fluid properties, provided that the timescale of contraction is sufficiently large. We also show that the nonaffine motions of the grains are a small fraction of the motion within the fluidized zone, affirming the relevance of a continuum model for this system, even though the grain size is comparable to the size of RoboClam

Tetrahalidocuprates(II)-structure and EPR spectroscopy. Part 1: Tetrabromidocuprates(II)

Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG geförderten) Allianz- bzw. Nationallizenz frei zugänglich.This publication is with permission of the rights owner freely accessible due to an Alliance licence and a national licence (funded by the DFG, German Research Foundation) respectively.Tetrahalidocuprates(II) show a high degree of structural flexibility. We present the results of crystallographic and electron paramagnetic resonance (EPR) spectroscopic analyses of four new tetrabromidocuprate(II) compounds and compare the results with previously reported data. The cations in the new compounds are the sterically demanding benzyltriphenylphosphonium, methyltriphenylphosphonium, tetraphenylphosphonium, and hexadecyltrimethylammonium ions; they were used to achieve a reasonable separation of the paramagnetic Cu(II) ions for EPR spectroscopy. X-Ray crystallography shows that in all four complexes the [CuBr4]2− units have a distorted tetrahedral coordination geometry which is in agreement with DFT calculations. The EPR hyperfine structure was not resolved. This is due to the exchange broadening resulting from still incomplete separation of the paramagnetic Cu(II) centres. Nevertheless, the principal values of the electron Zeemann tensor (gand g⊥) of the complexes could be determined. A correlation of structural (X-ray) parameters with the spin density at the copper centres (DFT) is well reflected in the EPR spectra of the bromidocuprates. This enables the correlation of X-ray and EPR parameters to predict the structure of tetrabromidocuprates in physical states other than the crystalline state. As a result, we provide a method to structurally characterize [CuBr4]2− in, for example, ionic liquids or in solution, which has important implications for e.g. catalysis or materials science

Einfluss des Gαq-Proteins auf die myokardiale Infarktgröße der knochenmarktransplantierten Gαq-Knockout-Maus im Ischämie/Reperfusionsmodell

Influence of the Gαq-protein on myocardial infarct size of the bone marrow-engrafted Gαq-knockout-mouse in a ischemia/reperfusion-model Platelets play a key role in the pathogenesis of an acute myocardial infarction. Thrombus formation, which is mediated by the activation of platelets, results in the occlusion of the coronary artery. On the other hand, agglutinated platelets in the small myocardial vessels impair the myocardial microcirculation. Due to their pro-inflammatory effects, platelets also contribute to the pathogenesis of ischemia/reperfusion injury. The myocardium of Gαq-deficient mice showed a reduced susceptibility to ischemia and reperfusion compared to that of wild-type mice (HEUER, in preparation). Activation of platelets lacking the Gαq-protein is markedly impaired, resulting not only in an increased haemophilia but also in a decreased thrombophilia of Gαq-deficient mice. A bone marrow transplantation was performed to investigate whether the impaired platelet-activation is responsible for the reduced susceptibility of Gαq-deficient mice to ischemia/reperfusion injury. Wild-type mice were lethally irradiated to facilitate the engraftment of bone marrow cells of Gαq-deficient mice and vice versa. A reconstitution phase of at least 90 days for both groups guaranteed, that blood of wild-type mice contained normal levels of Gαq-deleted platelets, while blood of Gαq- deficient mice contained only wild-type platelets. Afterwards, according to the study of HEUER (in preparation), myocardial ischemia was artificially induced by surgically ligating the left coronary artery for 30 minutes and was followed by a reperfusion phase of 24 hours. Heart function of both groups was examined by echocardiography before and after surgery. After euthanasia the size of infarction-area to area at risk (I/AAR) and infarction-area to left ventricle (I/LV) in the stained hearts was determined by planimetry. As a result neither the cardioechography (relative difference of fractional shortening prae and post op: 17, 1 % ± 2,9 % (SEM) versus 10,8 % ± 4,0 % (SEM)) nor the infarct-sizes (I/AAR: 18,2 % ± 4,2 % (SEM) versus 10,0 % ± 3,7 % (SEM); I/LV: 9,5 % ± 2,7 % (SEM) versus 5,6 % ± 2,2 % (SEM)) showed any significant differences between the two groups. In conclusion it could be assumed, that the impaired platelet-activation is not the only reason for the different susceptibility of wild-type and Gαq-deficient mice to ischemia/reperfusion injury; in fact, the reduced susceptibility of Gαq-deficient mice seems to be a result of both - their impaired platelet-activation and unknown protecting effects based on the absence of the Gαq-protein in other cells such as cardiomyocytes.In der Pathogenese des akuten Myokardinfarkts spielen die Thrombozyten eine wichtige Rolle. Die Thrombusbildung, die durch Aktivierung dieser Zellen in Gang gesetzt wird, resultiert in einer Okklusion der Koronararterie. Abgeschwemmte Thrombozytenemboli sind in der Lage, die Mikrozirkulation des Myokards zu beeinträchtigen. Aufgrund ihrer pro-inflammatorischen Wirkung fördern die Thrombozyten außerdem die Ausprägung des Ischämie/Reperfusionsschadens. Vorhergehende Untersuchungen von HEUER (in Vorbereitung) zeigten, dass das Myokard von Gαq-Knockout-Mäusen auf eine Ischämie und Reperfusion weniger empfindlich reagiert als das der Wildtyp-Mäuse. Die Aktivierung von Thrombozyten, denen das Gαq-Protein fehlt, ist hochgradig gestört; das führt nicht nur zu einer verstärkten Hämophilie, sondern auch zu einer reduzierten Thrombophilie der Gαq-Knockout-Tiere. Um herauszufinden, ob diese Störung der Thrombozyten-Aktivierung der Grund für die unterschiedliche Reaktion auf eine Ischämie/Reperfusion von Gαq-Knockout- und Wildtyp-Mäusen ist, wurde eine Knochenmarktransplantation durchgeführt. Dazu wurden Wildtyp-Mäuse letal bestrahlt, um die Transplantation von Knochenmarkzellen der Gαq-Knockout-Mäuse zu ermöglichen, während Gαq-Knockout-Mäuse auf diese Weise Blutzellen von Wildtyp-Tieren erhielten. Nach einer mindestens 90-tägigen Erholungsphase zur Gewährleistung einer vollständigen Rekonstitution wurden die Tiere dieser beiden Versuchsgruppen, entsprechend der Studie von HEUER (in Vorbereitung), einer 30-minütigen myokardialen Ischämie mit anschließender 24-stündiger Reperfusionsphase ausgesetzt. Sonographische Messungen prä und post operationem sollten Aufschluss über die Herzleistung geben. Am entnommenen, gefärbten Herzen wurde planimetrisch die Infarktgröße im Verhältnis zur area at risk (I/AAR) und zum linken Ventrikel (I/LV) ermittelt. Weder die Ergebnisse der Echokardiographie (relative Differenz des fractional shortening prä und post OP: 17,1 % ± 2,9 % (SEM), versus 10,8 % ± 4,0 % (SEM)) noch die gemessenen Infarktgrößen (I/AAR: 18,2 % ± 4,2 % (SEM) versus 10,0 % ± 3,7 % (SEM); I/LV: 9,5 % ± 2,7 % (SEM) versus 5,6 % ± 2,2 % (SEM)) unterscheiden sich signifikant zwischen den beiden Versuchsgruppen. Aus diesem Grund ist anzunehmen, dass für die verminderte Sensibilität der Gαq-Knockout-Mäuse gegenüber einer myokardialen Ischämie/Reperfusion nicht allein die gestörte Thrombozyten-Aktivierung verantwortlich ist; vielmehr scheinen zusätzlich weitere molekularbiologische Effekte, die beispielsweise das Fehlen der Gαq-Untereinheit im Kardiomyozyten bewirken könnte, einen gewissen Schutz vor den Pathomechanismen der Ischämie/Reperfusion darzustellen

Gene expression analysis using single molecule detection

Recent developments of single molecule detection techniques and in particular the introduction of fluorescence correlation spectroscopy (FCS) led to a number of important applications in biological research. We present a unique approach for the gene expression analysis using dual‐color cross‐correlation. The expression assay is based on gene‐specific hybridization of two dye‐labeled DNA probes to a selected target gene. The counting of the dual‐labeled molecules within the solution allows the quantification of the expressed gene copies in absolute numbers. As detection and analysis by FCS can be performed at the level of single molecules, there is no need for any type of amplification. We describe the gene expression assay and present data demonstrating the capacity of this novel technology. In order to prove the gene specificity, we performed experiments with gene‐depleted total cDNA. The biological application was demonstrated by quantifying selected high, medium and low abundant genes in cDNA prepared from HL‐60 cell

C4-dicarboxylates and L-aspartate utilization by Escherichia coli K-12 in the mouse intestine : L-aspartate as a major substrate for fumarate respiration and as a nitrogen source

C4-dicarboxylates, such as fumarate, l-malate and l-aspartate represent substrates for anaerobic growth of Escherichia coli by fumarate respiration. Here, we determined whether C4-dicarboxylate metabolism, as well as fumarate respiration, contribute to colonization of the mammalian intestinal tract. Metabolite profiling revealed that the murine small intestine contained high and low levels of l-aspartate and l-malate respectively, whereas fumarate was nearly absent. Under laboratory conditions, addition of C4-dicarboxylate at concentrations corresponding to the levels of the C4-dicarboxylates in the small intestine (2.6 mmol kg−1 dry weight) induced the dcuBp-lacZ reporter gene (67% of maximal) in a DcuS-DcuR-dependent manner. In addition to its role as a precursor for fumarate respiration, l-aspartate was able to supply all the nitrogen required for anaerobically growing E. coli. DcuS-DcuR-dependent genes were transcribed in the murine intestine, and mutants with defective anaerobic C4-dicarboxylate metabolism (dcuSR, frdA, dcuB, dcuA and aspA genes) were impaired for colonizing the murine gut. We conclude that l-aspartate plays an important role in providing fumarate for fumarate respiration and supplying nitrogen for E. coli in the mouse intestine

Myocyte Enhancer Factor 2A (MEF2A) Defines Oxytocin-Induced Morphological Effects and Regulates Mitochondrial Function in Neurons

The neuropeptide oxytocin (OT) is a well-described modulator of socio-emotional traits, such as anxiety, stress, social behavior, and pair bonding. However, when dysregulated, it is associated with adverse psychiatric traits, such as various aspects of autism spectrum disorder (ASD). In this study, we identify the transcription factor myocyte enhancer factor 2A (MEF2A) as the common link between OT and cellular changes symptomatic for ASD, encompassing neuronal morphology, connectivity, and mitochondrial function. We provide evidence for MEF2A as the decisive factor defining the cellular response to OT: while OT induces neurite retraction in MEF2A expressing neurons, OT causes neurite outgrowth in absence of MEF2A. A CRISPR-Cas-mediated knockout of MEF2A and retransfection of an active version or permanently inactive mutant, respectively, validated our findings. We also identified the phosphatase calcineurin as the main upstream regulator of OT-induced MEF2A signaling. Further, MEF2A signaling dampens mitochondrial functioning in neurons, as MEF2A knockout cells show increased maximal cellular respiration, spare respiratory capacity, and total cellular ATP. In summary, we reveal a central role for OT-induced MEF2A activity as major regulator of cellular morphology as well as neuronal connectivity and mitochondrial functioning, with broad implications for a potential treatment of disorders based on morphological alterations or mitochondrial dysfunction

Analyzing body dissatisfaction and gender dysphoria in the context of minority stress among transgender adolescents

Background Gender dysphoria among transgender adolescents has predominantly been examined in relation to body dissatisfaction. While in adult transgender samples, body dissatisfaction is higher than in cisgender controls, this has so far rarely been investigated for adolescents. In the context of a cisnormative society, the impact of influences from the social environment on body dissatisfaction and gender dysphoria has been neglected in research. Therefore, this study aimed to (1) provide a detailed analysis of body dissatisfaction among young transgender people and (2) investigate whether body dissatisfaction and gender dysphoria are associated with experiences of minority stress such as trans hostility and poor peer relations (PPR). Methods The paper presents a cross-sectional study among a sample of transgender adolescents, presenting at a specialized outpatient counseling clinic (N = 99; age M = 15.36, SD = 1.85). First, body dissatisfaction (assessed by the Body-Image-Scale; BIS), was explored and compared to data from a population-based control group of cisgender peers (N = 527; age M = 14.43, SD = 0.97). Second, within a clinic-referred transgender subsample (n = 74), associations between body dissatisfaction and gender dysphoria (measured by Utrecht Gender Dysphoria Scale; UGDS), PPR (measured by the Youth-Self-Report; YSR-R), and trans hostile experiences (assessed in clinical interview) were examined by correlations, t-tests and multivariate regression. Results Transgender adolescents reported more body dissatisfaction than cisgender peers. The dissatisfaction with sex characteristics, non-hormonal reactive body regions and the total score for body dissatisfaction were positively related with gender dysphoria. The majority had experienced trans hostility in the present and/or past (54.1%) and PPR (63.5%). More body dissatisfaction was correlated with more PPR regarding visible body parts i.e., hair, overall appearance and muscles, whilst PPR and gender dysphoria were not associated. Transgender adolescents who experienced trans hostility showed higher gender dysphoria and PPR, but not more body dissatisfaction. In multiple regression, trans hostility predicted gender dysphoria, whilst age and PPR predicted body dissatisfaction. Discussion Experiences of minority-stress differentially interact with body dissatisfaction and gender dysphoria among transgender adolescents. Social correlates of body dissatisfaction and gender dysphoria must be considered when working with young transgender people

AERoS: Assurance of Emergent Behaviour in Autonomous Robotic Swarms

The behaviours of a swarm are not explicitly engineered. Instead, they are an emergent consequence of the interactions of individual agents with each other and their environment. This emergent functionality poses a challenge to safety assurance. The main contribution of this paper is a process for the safety assurance of emergent behaviour in autonomous robotic swarms called AERoS, following the guidance on the Assurance of Machine Learning for use in Autonomous Systems (AMLAS). We explore our proposed process using a case study centred on a robot swarm operating a public cloakroom.Comment: 12 pages, 11 figure