Unfolding the Sulcus

Sulci are localized furrows on the surface of soft materials that form by a compression-induced instability. We unfold this instability by breaking its natural scale and translation invariance, and compute a limiting bifurcation diagram for sulcfication showing that it is a scale-free, sub-critical {\em nonlinear} instability. In contrast with classical nucleation, sulcification is {\em continuous}, occurs in purely elastic continua and is structurally stable in the limit of vanishing surface energy. During loading, a sulcus nucleates at a point with an upper critical strain and an essential singularity in the linearized spectrum. On unloading, it quasi-statically shrinks to a point with a lower critical strain, explained by breaking of scale symmetry. At intermediate strains the system is linearly stable but nonlinearly unstable with {\em no} energy barrier. Simple experiments confirm the existence of these two critical strains.Comment: Main text with supporting appendix. Revised to agree with published version. New result in the Supplementary Informatio

Development, characterization, and use of a fetal skin cell bank for tissue engineering in wound healing.

Wound healing in fetal skin is characterized by the absence of scar tissue formation, which is not dependent on the intrauterine environment and amniotic fluid. Fetal cells have the capacity of extraordinary expansion and we describe herein the development of a fetal skin cell bank where from one organ donation (2-4 cm2) it is possible to produce several hundred million fetal skin constructs of 9 x 12 cm2. Fetal cells grow three to four times more rapidly than older skin cells cultured in the same manner and these banked fetal cells are very resistant against physical and oxidative stress when compared to adult skin cells under the same culture conditions. They are up to three times more resistant to UVA radiation and two times more resistant towards hydrogen peroxide treatment. This mechanism may be of major importance for fetal cells when they are delivered to hostile wound environments. For fetal cell delivery to patients, cells were associated with a collagen matrix to form a three-dimensional construct in order to analyze the capacity of these cells for treating various wounds. We have seen that fetal cells can modify the repair response of skin wounds by accelerating the repair process and reducing scarring in severe bums and wounds of various nature in children. Hundreds of thousands of patients could potentially be treated for acute and chronic wounds from one standardized and controlled cell bank

Ultrafast Spin Dynamics in Nickel

The spin dynamics in Ni is studied by an exact diagonalization method on the ultrafast time scale. It is shown that the femtosecond relaxation of the magneto-optical response results from exchange interaction and spin-orbit coupling. Each of the two mechanisms affects the relaxation process differently. We find that the intrinsic spin dynamics occurs during about 10 fs while extrinsic effects such as laser-pulse duration and spectral width can slow down the observed dynamics considerably. Thus, our theory indicates that there is still room to accelerate the spin dynamics in experiments.Comment: 4 pages, Latex, 4 postscript figure

Ultrafast spin dynamics and critical behavior in half-metallic ferromagnet : Sr_2FeMoO_6

Ultrafast spin dynamics in ferromagnetic half-metallic compound Sr_2FeMoO_6 is investigated by pump-probe measurements of magneto-optical Kerr effect. Half-metallic nature of this material gives rise to anomalous thermal insulation between spins and electrons, and allows us to pursue the spin dynamics from a few to several hundred picoseconds after the optical excitation. The optically detected magnetization dynamics clearly shows the crossover from microscopic photoinduced demagnetization to macroscopic critical behavior with universal power law divergence of relaxation time for wide dynamical critical region.Comment: 14 pages, 4 figures. Abstract and Figures 1 & 3 are correcte

A view of Internet Traffic Shifts at {ISP} and {IXPs} during the {COVID}-19 Pandemic

Due to the COVID-19 pandemic, many governments imposed lockdowns that forced hundreds of millions of citizens to stay at home. The implementation of confinement measures increased Internet traffic demands of residential users, in particular, for remote working, entertainment, commerce, and education, which, as a result, caused traffic shifts in the Internet core. In this paper, using data from a diverse set of vantage points (one ISP, three IXPs, and one metropolitan educational network), we examine the effect of these lockdowns on traffic shifts. We find that the traffic volume increased by 15-20% almost within a week – while overall still modest, this constitutes a large increase within this short time period. However, despite this surge, we observe that the Internet infrastructure is able to handle the new volume, as most traffic shifts occur outside of traditional peak hours. When looking directly at the traffic sources, it turns out that, while hypergiants still contribute a significant fraction of traffic, we see (1) a higher increase in traffic of non-hypergiants, and (2) traffic increases in applications that people use when at home, such as Web conferencing, VPN, and gaming. While many networks see increased traffic demands, in particular, those providing services to residential users, academic networks experience major overall decreases. Yet, in these networks, we can observe substantial increases when considering applications associated to remote working and lecturing.EC/H2020/679158/EU/Resolving the Tussle in the Internet: Mapping, Architecture, and Policy Making/ResolutioNe

The use of mantrailing dogs in police and judicial context, future directions, limits and possibilities: A law review

Abtract The extraordinary capabilities of the canine nose are increasingly being used by law enforcement agencies in many countries to solve and reconstruct crimes. As a result, this type of forensic evidence can be and is still being challenged in the courts. So far, only a few publications have addressed the jurisprudence concerning mantrailing. We provide an overview of the jurisprudence in Germany and the USA, as well as insights from France. Relevant databases were searched, and 201 verdicts from Germany and 801 verdicts from the USA were analyzed. As a result, 16 published verdicts on the topic of mantrailing were found for Germany, and 44 verdicts since 2010 were found for the USA. The use of mantrailers and human scent discrimination dogs is employed in the investigative process in all three countries. The results derived from these methods are admissible as evidence in court, albeit not as sole evidence

Neurofascin as a novel target for autoantibody-mediated axonal injury

Axonal injury is considered the major cause of disability in patients with multiple sclerosis (MS), but the underlying effector mechanisms are poorly understood. Starting with a proteomics-based approach, we identified neurofascin-specific autoantibodies in patients with MS. These autoantibodies recognize the native form of the extracellular domains of both neurofascin 186 (NF186), a neuronal protein concentrated in myelinated fibers at nodes of Ranvier, and NF155, the oligodendrocyte-specific isoform of neurofascin. Our in vitro studies with hippocampal slice cultures indicate that neurofascin antibodies inhibit axonal conduction in a complement-dependent manner. To evaluate whether circulating antineurofascin antibodies mediate a pathogenic effect in vivo, we cotransferred these antibodies with myelin oligodendrocyte glycoprotein–specific encephalitogenic T cells to mimic the inflammatory pathology of MS and breach the blood–brain barrier. In this animal model, antibodies to neurofascin selectively targeted nodes of Ranvier, resulting in deposition of complement, axonal injury, and disease exacerbation. Collectively, these results identify a novel mechanism of immune-mediated axonal injury that can contribute to axonal pathology in MS

Ultrastructural changes of the intracellular surfactant pool in a rat model of lung transplantation-related events

<p>Abstract</p> <p>Background</p> <p>Ischemia/reperfusion (I/R) injury, involved in primary graft dysfunction following lung transplantation, leads to inactivation of intra-alveolar surfactant which facilitates injury of the blood-air barrier. The alveolar epithelial type II cells (AE2 cells) synthesize, store and secrete surfactant; thus, an intracellular surfactant pool stored in lamellar bodies (Lb) can be distinguished from the intra-alveolar surfactant pool. The aim of this study was to investigate ultrastructural alterations of the intracellular surfactant pool in a model, mimicking transplantation-related procedures including flush perfusion, cold ischemia and reperfusion combined with mechanical ventilation.</p> <p>Methods</p> <p>Using design-based stereology at the light and electron microscopic level, number, surface area and mean volume of AE2 cells as well as number, size and total volume of Lb were determined in a group subjected to transplantation-related procedures including both I/R injury and mechanical ventilation (I/R group) and a control group.</p> <p>Results</p> <p>After I/R injury, the mean number of Lb per AE2 cell was significantly reduced compared to the control group, accompanied by a significant increase in the luminal surface area per AE2 cell in the I/R group. This increase in the luminal surface area correlated with the decrease in surface area of Lb per AE2. The number-weighted mean volume of Lb in the I/R group showed a tendency to increase.</p> <p>Conclusion</p> <p>We suggest that in this animal model the reduction of the number of Lb per AE2 cell is most likely due to stimulated exocytosis of Lb into the alveolar space. The loss of Lb is partly compensated by an increased size of Lb thus maintaining total volume of Lb per AE2 cell and lung. This mechanism counteracts at least in part the inactivation of the intra-alveolar surfactant.</p