Controllable optical phase shift over one radian from a single isolated atom

Fundamental optics such as lenses and prisms work by applying phase shifts to incoming light via the refractive index. In these macroscopic devices, many particles each contribute a miniscule phase shift, working together to impose a total phase shift of many radians. In principle, even a single isolated particle can apply a radian-level phase shift, but observing this phenomenon has proven challenging. We have used a single trapped atomic ion to induce and measure a large optical phase shift of $1.3 \pm 0.1$ radians in light scattered by the atom. Spatial interferometry between the scattered light and unscattered illumination light enables us to isolate the phase shift in the scattered component. The phase shift achieves the maximum value allowed by atomic theory over the accessible range of laser frequencies, validating the microscopic model that underpins the macroscopic phenomenon of the refractive index. Single-atom phase shifts of this magnitude open up new quantum information protocols, including long-range quantum phase-shift-keying cryptography [1,2] and quantum nondemolition measurement [3,4].Comment: submitte

In-situ bandaged Josephson junctions for superconducting quantum processors

Shadow evaporation is commonly used to micro-fabricate the key element of superconducting qubits—the Josephson junction. However, in conventional two-angle deposition circuit topology, unwanted stray Josephson junctions are created which contribute to dielectric loss. So far, this could be avoided by shorting the stray junctions with a so-called bandage layer deposited in an additional lithography step, which may further contaminate the chip surface. Here, we present an improved shadow evaporation technique allowing one to fabricate sub-micrometer-sized Josephson junctions together with bandage layers in a single lithography step. We also show that junction aging is significantly reduced when junction electrodes are passivated in an oxygen atmosphere directly after deposition

Oscillations in the Lateral Pressure of Lipid Monolayers Induced by Nonlinear Chemical Dynamics of the Second Messengers MARCKS and Protein Kinase C

AbstractThe binding of the MARCKS peptide to the lipid monolayer containing PIP2 increases the lateral pressure of the monolayer. The unbinding dynamics modulated by protein kinase C leads to oscillations in lateral pressure of lipid monolayers. These periodic dynamics can be attributed to changes in the crystalline lipid domain size. We have developed a mathematical model to explain these observations based on the changes in the physical structure of the monolayer by the translocation of MARCKS peptide. The model indicates that changes in lipid domain size drives these oscillations. The model is extended to an open system that sustains chemical oscillations

A new human adipocyte model with PTEN haploinsufficiency

Few human cell strains are suitable and readily available as in vitro adipocyte models. We used resected lipoma tissue from a patient with germline phosphatase and tensin homolog (PTEN) haploinsufficiency to establish a preadipocyte cell strain termed LipPD1 and aimed to characterize cellular functions and signalling pathway alterations in comparison to the established adipocyte model Simpson-Golabi-Behmel-Syndrome (SGBS) and to primary stromal-vascular fraction cells. We found that both cellular life span and the capacity for adipocyte differentiation as well as adipocyte-specific functions were preserved in LipPD1 and comparable to SGBS adipocytes. Basal and growth factor-stimulated activation of the PI3 K/AKT signalling pathway was increased in LipPD1 preadipocytes, corresponding to reduced PTEN levels in comparison to SGBS cells. Altogether, LipPD1 cells are a novel primary cell model with a defined genetic lesion suitable for the study of adipocyte biology. © 2020, © 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group

Augenveränderungen im All: Aktuelles zu Klinik, Pathogenese und Prävention [Eye changes in space : New insights into clinical aspects, pathogenesis and prevention]

Hintergrund Mehr denn je rückt die Erforschung der Veränderungen am Auge, die durch den Aufenthalt im All verursacht werden, ins Zentrum des Interesses der internationalen und nationalen Weltraumagenturen NASA (National Aeronautics and Space Administration), ESA (European Space Agency) und DLR (Deutsches Zentrum für Luft- und Raumfahrt). Neben weltraumstrahlungbedingten Katarakten können erhebliche Augenveränderungen, zusammengefasst unter dem „space flight-associated neuro-ocular syndrome“ (SANS) auftreten. Ziele der Arbeit Diese Übersicht soll den aktuellen Forschungsstand und künftige Bestrebungen auf dem Gebiet der Erforschung der Augenveränderungen bei SANS wiedergeben und die Relevanz für die terrestrische ophthalmologische Forschung aufzeigen. Material und Methoden Es erfolgt eine Analyse der bestehenden Publikationen zu dem Thema in PubMed sowie von Berichten bezüglich des Risikos von SANS, veröffentlicht von der NASA der USA. Ergebnisse Die Ursachen für die Entstehung der Augenveränderungen im All sind nicht geklärt. Faktoren wie die Erhöhung des intrakraniellen Drucks, Flüssigkeitsverschiebungen, Hyperkapnie und genetische Einflüsse sind Gegenstand intensiver Forschungsbemühungen. Ein terrestrisches Modell zur Induktion des Papillenödems konnte etabliert werden (Bettruhestudien mit −6° Kopftieflagerung als Weltraumanalogon). Gegenmaßnahmen zur Entwicklung der Augenveränderungen, wie beispielsweise intermittierend künstliche Schwerkraft, sind Gegenstand der aktuellen Studien. Schlussfolgerung Die Erforschung von SANS im Rahmen von Bettruhestudien wird in Zukunft sowohl für die Weltraumforschung als auch für die terrestrische Forschung weitere wichtige Erkenntnisse liefern. Klinische Forschungsprojekte können aus der Weltraumforschung abgeleitet werden

Cell membrane softening in human breast and cervical cancer cells

Biomechanical properties are key to many cellular functions such as cell division and cell motility and thus are crucial in the development and understanding of several diseases, for instance cancer. The mechanics of the cellular cytoskeleton have been extensively characterized in cells and artificial systems. The rigidity of the plasma membrane, with the exception of red blood cells, is unknown and membrane rigidity measurements only exist for vesicles composed of a few synthetic lipids. In this study, thermal fluctuations of giant plasma membrane vesicles (GPMVs) directly derived from the plasma membranes of primary breast and cervical cells, as well as breast cell lines, are analyzed. Cell blebs or GPMVs were studied via thermal membrane fluctuations and mass spectrometry. It will be shown that cancer cell membranes are significantly softer than their non-malignant counterparts. This can be attributed to a loss of fluid raft forming lipids in malignant cells. These results indicate that the reduction of membrane rigidity promotes aggressive blebbing motion in invasive cancer cells

Activity and components of the granulocyte colony‐stimulating factor pathway in hidradenitis suppurativa*

Background Hidradenitis suppurativa (HS) is a chronic inflammatory disease, characterized by painful, purulent and destructive skin alterations in intertriginous areas. Objectives We investigated the expression and role in HS of granulocyte colony-stimulating factor (G-CSF), the regulator of neutrophil biology, as clinical signs of a neutrophilic granulocyte-driven inflammation are distinctive in the disease. Methods Skin and blood samples obtained from different cohorts of patients with HS and control individuals were assessed by RNA sequencing, quantitative polymerase chain reaction on reverse transcribed mRNA, and/or enzyme-linked immunosorbent assay. Mechanistic studies using keratinocytes, dermal fibroblasts, immune cell populations and skin biopsies were performed. Results G-CSF was abundant in HS skin, particularly in inflamed nodules and abscesses. Its levels even exceeded those found in other inflammatory skin diseases. Interleukin (IL)-1 and IL-17, respectively, induced G-CSF production by fibroblasts and keratinocytes. These effects were enhanced by tumour necrosis factor (TNF)-alpha and IL-36. Accordingly, fibroblasts separated from HS lesions expressed G-CSF, and IL-1 receptor antagonist reduced G-CSF levels in explanted HS skin. G-CSF blood levels positively correlated with severity of HS. Elevated lesional G-CSF receptor levels were linked to upregulation of molecules that contribute to prolonged activation of neutrophils by components of bacteria and damaged host cells [formyl peptide receptor 1 (FPR1), FPR2 and free fatty acid receptor 2 (FFAR2)], neutrophil survival [TNF receptor superfamily member 10C (TNFRSF10C/TRAIL-R3) and TNF receptor superfamily member 6B], kinases (tyrosine-protein kinase HCK and hexokinase 3), and skin destruction [MMP25 (matrix metalloproteinase 25) and ADAM8 (disintegrin and metalloproteinase domain-containing protein 8)]. G-CSF elevated the expression of FPR1, FFAR2, and TNFRSF10C/TRAIL-R3 in neutrophils and synergized with bacterial components to induce skin-destructive enzymes. Conclusions The G-CSF pathway engages both tissue and immune cells, is strongly activated in HS lesions, and offers the opportunity to target the neutrophil-driven inflammation

Age-related changes in global motion coherence: conflicting haemodynamic and perceptual responses

Our aim was to use both behavioural and neuroimaging data to identify indicators of perceptual decline in motion processing. We employed a global motion coherence task and functional Near Infrared Spectroscopy (fNIRS). Healthy adults (n = 72, 18-85) were recruited into the following groups: young (n = 28, mean age = 28), middle-aged (n = 22, mean age = 50), and older adults (n = 23, mean age = 70). Participants were assessed on their motion coherence thresholds at 3 different speeds using a psychophysical design. As expected, we report age group differences in motion processing as demonstrated by higher motion coherence thresholds in older adults. Crucially, we add correlational data showing that global motion perception declines linearly as a function of age. The associated fNIRS recordings provide a clear physiological correlate of global motion perception. The crux of this study lies in the robust linear correlation between age and haemodynamic response for both measures of oxygenation. We hypothesise that there is an increase in neural recruitment, necessitating an increase in metabolic need and blood flow, which presents as a higher oxygenated haemoglobin response. We report age-related changes in motion perception with poorer behavioural performance (high motion coherence thresholds) associated with an increased haemodynamic response