Trapping atoms on a transparent permanent-magnet atom chip

We describe experiments on trapping of atoms in microscopic magneto-optical traps on an optically transparent permanent-magnet atom chip. The chip is made of magnetically hard ferrite-garnet material deposited on a dielectric substrate. The confining magnetic fields are produced by miniature magnetized patterns recorded in the film by magneto-optical techniques. We trap Rb atoms on these structures by applying three crossed pairs of counter-propagating laser beams in the conventional magneto-optical trapping (MOT) geometry. We demonstrate the flexibility of the concept in creation and in-situ modification of the trapping geometries through several experiments.Comment: Modifications: A) Reference I. Barb et al., Eur. Phys. JD, 35, 75 (2005) added. B)Sentence rewritten: We routinely capture more than 10^6 atoms in a micro-MOT on a magnetized pattern. C) The magnetic field strengths are now given in Teslas. D) The second sentence in the fourth paragraph has been rewritten in order to more clearly describe the geometry and purpose of the compensation coils.E) In the seventh paragraph we have rewritten the sentence about the creation of the external magnetic field for the magnetic-domain patterning. F) In the ninth paragraph, we clarify the way to shift the trap center. G) Caption of Fig. 4 changed. H) We have modified paragraph 12 to improve the description on the guiding of the trap center along a toroidal pattern. I) The last two sentences of the manuscript have been rewritte

Surface ruptures on cross-faults in the 24 November 1987 Superstition Hills, California, earthquake sequence

Left-lateral slip occurred on individual surface breaks along northeast-trending faults associated with the 24 November 1987 earthquake sequence in the Superstition Hills, Imperial Valley, California. This sequence included the M_s = 6.2 event on a left-lateral, northeast-trending “cross-fault” between the Superstition Hills fault (SHF) and Brawley seismic zone, which was spatially associated with the left-lateral surface breaks. Six distinct subparallel cross-faults broke at the surface, with rupture lengths ranging from about Formula to 10 km and maximum displacements ranging from 30 to 130 mm. About half a day after the M_s = 6.2 event, an M_s = 6.6 earthquake nucleated near the intersection of the cross-faults with the SHF, and rupture propagated southeast along the SHF. Whereas right-lateral slip on the SHF occurred dominantly on a single trace in a narrow zone, the cross-fault surface slip was distributed over several stands across a 10-km-wide zone. Also, whereas afterslip accounted for a large proportion of total slip on the SHF, there is no evidence for afterslip on the cross-faults. We present documentation of these surface ruptures. A simple mechanical model of faulting illustrates how the foreshock sequence may have triggered the main rupture. Displacement on other cross-faults could trigger an event on the southern San Andreas fault by a similar mechanism in the future

The Wnt Co-Receptor Lrp6 Is Required for Normal Mouse Mammary Gland Development

Canonical Wnt signals are transduced through a Frizzled receptor and either the LRP5 or LRP6 co-receptor; such signals play central roles during development and in disease. We have previously shown that Lrp5 is required for ductal stem cell activity and that loss of Lrp5 delays normal mammary development and Wnt1-induced tumorigenesis. Here we show that canonical Wnt signals through the Lrp6 co-receptor are also required for normal mouse mammary gland development. Loss of Lrp6 compromises Wnt/β-catenin signaling and interferes with mammary placode, fat pad, and branching development during embryogenesis. Heterozygosity for an inactivating mutation in Lrp6 is associated with a reduced number of terminal end buds and branches during postnatal development. While Lrp6 is expressed in both the basal and luminal mammary epithelium during embryogenesis, Lrp6 expression later becomes restricted to cells residing in the basal epithelial layer. Interestingly, these cells also express mammary stem cell markers. In humans, increased Lrp6 expression is associated with basal-like breast cancer. Taken together, our results suggest both overlapping and specific functions for Lrp5 and Lrp6 in the mammary gland

Determination of the Bending Rigidity of Graphene via Electrostatic Actuation of Buckled Membranes

The small mass and atomic-scale thickness of graphene membranes make them highly suitable for nanoelectromechanical devices such as e.g. mass sensors, high frequency resonators or memory elements. Although only atomically thick, many of the mechanical properties of graphene membranes can be described by classical continuum mechanics. An important parameter for predicting the performance and linearity of graphene nanoelectromechanical devices as well as for describing ripple formation and other properties such as electron scattering mechanisms, is the bending rigidity, {\kappa}. In spite of the importance of this parameter it has so far only been estimated indirectly for monolayer graphene from the phonon spectrum of graphite, estimated from AFM measurements or predicted from ab initio calculations or bond-order potential models. Here, we employ a new approach to the experimental determination of {\kappa} by exploiting the snap-through instability in pre-buckled graphene membranes. We demonstrate the reproducible fabrication of convex buckled graphene membranes by controlling the thermal stress during the fabrication procedure and show the abrupt switching from convex to concave geometry that occurs when electrostatic pressure is applied via an underlying gate electrode. The bending rigidity of bilayer graphene membranes under ambient conditions was determined to be $35.5^{+20}_{-15}$ eV. Monolayers have significantly lower {\kappa} than bilayers

Epigenetic alterations in skin homing CD4+CLA+ T cells of atopic dermatitis patients

T cells expressing the cutaneous lymphocyte antigen (CLA) mediate pathogenic inflammation in atopic dermatitis (AD). The molecular alterations contributing to their dysregulation remain unclear. With the aim to elucidate putative altered pathways in AD we profiled DNA methylation levels and miRNA expression in sorted T cell populations (CD4+, CD4+CD45RA+ naïve, CD4+CLA+, and CD8+) from adult AD patients and healthy controls (HC). Skin homing CD4+CLA+ T cells from AD patients showed significant differences in DNA methylation in 40 genes compared to HC (p < 0.05). Reduced DNA methylation levels in the upstream region of the interleukin-13 gene (IL13) in CD4+CLA+ T cells from AD patients correlated with increased IL13 mRNA expression in these cells. Sixteen miRNAs showed differential expression in CD4+CLA+ T cells from AD patients targeting genes in 202 biological processes (p < 0.05). An integrated network analysis of miRNAs and CpG sites identified two communities of strongly interconnected regulatory elements with strong antagonistic behaviours that recapitulated the differences between AD patients and HC. Functional analysis of the genes linked to these communities revealed their association with key cytokine signaling pathways, MAP kinase signaling and protein ubiquitination. Our findings support that epigenetic mechanisms play a role in the pathogenesis of AD by affecting inflammatory signaling molecules in skin homing CD4+CLA+ T cells and uncover putative molecules participating in AD pathways. © 2020, The Author(s).Peer reviewe