Signatures of the superfluid to Mott insulator transition in equilibrium and in dynamical ramps

We investigate the equilibrium and dynamical properties of the Bose-Hubbard model and the related particle-hole symmetric spin-1 model in the vicinity of the superfluid to Mott insulator quantum phase transition. We employ the following methods: exact-diagonalization, mean field (Gutzwiller), cluster mean-field, and mean-field plus Gaussian fluctuations. In the first part of the paper we benchmark the four methods by analyzing the equilibrium problem and give numerical estimates for observables such as the density of double occupancies and their correlation function. In the second part, we study parametric ramps from the superfluid to the Mott insulator and map out the crossover from the regime of fast ramps, which is dominated by local physics, to the regime of slow ramps with a characteristic universal power law scaling, which is dominated by long wavelength excitations. We calculate values of several relevant physical observables, characteristic time scales, and an optimal protocol needed for observing universal scaling.Comment: 23 pages, 13 figure

Transition from Cassie to Wenzel state in patterned soft elastomer sliding contacts

In this paper, we presented an experimental and theoretical analysis of the formation of the contact between a smooth elastomer lens and an elastomer substrate micropatterned with hexagonal arrays of cylindrical pillars. We show using a JKR model coupled with a full description of the deformation of the substrate between the pillars that the transition between the top to the full contact is obtain when the normal load is increased above a well predicted threshold. We have also shown that above the onset of full contact, the evolution of the area of full contact was obeying a simple scaling.Comment: 4 pages, 6 figures. Submitte

Loss of the interferon-γ-inducible regulatory immunity-related GTPase (IRG), Irgm1, causes activation of effector IRG proteins on lysosomes, damaging lysosomal function and predicting the dramatic susceptibility of Irgm1-deficient mice to infection

The interferon-γ (IFN-γ)-inducible immunity-related GTPase (IRG), Irgm1, plays an essential role in restraining activation of the IRG pathogen resistance system. However, the loss of Irgm1 in mice also causes a dramatic but unexplained susceptibility phenotype upon infection with a variety of pathogens, including many not normally controlled by the IRG system. This phenotype is associated with lymphopenia, hemopoietic collapse, and death of the mouse.Deutscher Akademischer Austausch Dienst (DAAD); International Graduate School in Development Health and Disease (IGS-DHD); Deutsche For-schungsgemeinschaft (SFBs 635, 670, 680); Max-Planck-Gesellschaft (Max Planck Fellowship)

Cytogenetic identification of four generations of crossbred buffaloes maintained in a conservation program in the Marajó island/Brazil.

Os búfalos domésticos são divididos em dois grupos: os búfalos de rio, com número diploide 2n= 50 e os búfalos de pântano, 2n= 48. O cruzamento F1 entre estes resultam em animais com 2n= 49, que são viáveis e férteis. No Brasil os búfalos do tipo Baio e da raça Carabao são mantidos em um programa de conservação genética que visa manter esses grupos separados, conservando seu patrimônio genético in situ e ex situ. O objetivo deste estudo foi avaliar citogeneticamente búfalos da raça Carabao, tipo Baio e suas crusas F1, F2, F3 e F4 mantidos em um programa de conservação genética. As metáfases foram obtidas a partir de cultura de linfócitos de 50 animais da raça Carabao, 45 do tipo Baio e 10 descendentes de uma fêmea mestiça. Os animais do tipo Baio apresentaram 2n= 50, os da raça Carabao 2n= 48. Para os descendentes foram observados 2n= 48 e 2n= 49, com variações morfológicas no primeiro par. O número diplóides 2n= 49 confirma a presença de animais cruzados no programa de conservação. Assim, a exclusão destes animais e seus descendentes é altamente recomendada dos rebanhos originais a fim de manter os genótipos separados para cada grupo genético

Pathogen-selective killing by guanylate-binding proteins as a molecular mechanism leading to inflammasome signaling.

Inflammasomes are cytosolic signaling complexes capable of sensing microbial ligands to trigger inflammation and cell death responses. Here, we show that guanylate-binding proteins (GBPs) mediate pathogen-selective inflammasome activation. We show that mouse GBP1 and GBP3 are specifically required for inflammasome activation during infection with the cytosolic bacterium Francisella novicida. We show that the selectivity of mouse GBP1 and GBP3 derives from a region within the N-terminal domain containing charged and hydrophobic amino acids, which binds to and facilitates direct killing of F. novicida and Neisseria meningitidis, but not other bacteria or mammalian cells. This pathogen-selective recognition by this region of mouse GBP1 and GBP3 leads to pathogen membrane rupture and release of intracellular content for inflammasome sensing. Our results imply that GBPs discriminate between pathogens, confer activation of innate immunity, and provide a host-inspired roadmap for the design of synthetic antimicrobial peptides that may be of use against emerging and re-emerging pathogens

Immunity against Moraxella catarrhalis requires guanylate-binding proteins and caspase-11-NLRP3 inflammasomes.

Moraxella catarrhalis is an important human respiratory pathogen and a major causative agent of otitis media and chronic obstructive pulmonary disease. Toll-like receptors contribute to, but cannot fully account for, the complexity of the immune response seen in M. catarrhalis infection. Using primary mouse bone marrow-derived macrophages to examine the host response to M. catarrhalis infection, our global transcriptomic and targeted cytokine analyses revealed activation of immune signalling pathways by both membrane-bound and cytosolic pattern-recognition receptors. We show that M. catarrhalis and its outer membrane vesicles or lipooligosaccharide (LOS) can activate the cytosolic innate immune sensor caspase-4/11, gasdermin-D-dependent pyroptosis, and the NLRP3 inflammasome in human and mouse macrophages. This pathway is initiated by type I interferon signalling and guanylate-binding proteins (GBPs). We also show that inflammasomes and GBPs, particularly GBP2, are required for the host defence against M. catarrhalis in mice. Overall, our results reveal an essential role for the interferon-inflammasome axis in cytosolic recognition and immunity against M. catarrhalis, providing new molecular targets that may be used to mitigate pathological inflammation triggered by this pathogen

Guanylate binding proteins promote caspase-11-dependent pyroptosis in response to cytoplasmic LPS

A major component of the cell envelope of Gram-negative bacteria is LPS, also known as endotoxin. LPS produced during bacterial infections triggers inflammation, which can lead to septic shock and death. Our immune system can recognize LPS both outside and inside of cells. The recognition of extracellular and vacuolar LPS by LPS binding proteins is well described, but little is known about the recognition of cytoplasmic LPS. Here, we show that cytoplasmic LPS derived from the intracellular bacterial pathogen Legionella activated a proinflammatory immune response. We further identified host guanylate binding proteins as critical mediators of immunity triggered by cytoplasmic LPS. These findings are likely to advance our understanding of how cells can sense intracellular LPS

Tack energy and switchable adhesion of liquid crystal elastomers

The mechanical properties of liquid crystal elastomers (LCEs) make them suitable candidates for pressure-sensitive adhesives (PSAs). Using the nematic dumbbell constitutive model, and the block model of PSAs, we study their tack energy and the debonding process as could be measured experimentally in the probe-tack test. To investigate their performance as switchable PSAs we compare the tack energy for the director aligned parallel, and perpendicular to the substrate normal, and for the isotropic state. We find that the tack energy is larger in the parallel alignment than the isotropic case by over a factor of two. The tack energy for the perpendicular alignment can be 50% less than the isotropic case. We propose a mechanism for reversibly switchable adhesion based on the reversibility of the isotropic to nematic transition. Finally we consider the influence of several material parameters that could be used to tune the stress-strain response

A Giant Arc in a ROSAT Detected Cluster of Galaxies

We report the serendipitous discovery of a giant grvitational arc in the Abell Supplementary cluster S295 during optical follow-up observations of clusters detected in the ROSAT All-Sky Survey. The cluster has a redshift z=0.3007 and a velocity dispersion of about 900 km/sec. This is the first giant arc newly found in a ROSAT Survey cluster, indicating the potential advantage of searching for giant arcs in X-ray selected clusters