Extended Bose-Hubbard model with dipolar excitons.

The Hubbard model constitutes one of the most celebrated theoretical frameworks of condensed-matter physics. It describes strongly correlated phases of interacting quantum particles confined in lattice potentials1,2. For bosons, the Hubbard Hamiltonian has been deeply scrutinized for short-range on-site interactions3-6. However, accessing longer-range couplings has remained elusive experimentally7. This marks the frontier towards the extended Bose-Hubbard Hamiltonian, which enables insulating ordered phases at fractional lattice fillings8-12. Here we implement this Hamiltonian by confining semiconductor dipolar excitons in an artificial two-dimensional square lattice. Strong dipolar repulsions between nearest-neighbour lattice sites then stabilize an insulating state at half filling. This characteristic feature of the extended Bose-Hubbard model exhibits the signatures theoretically expected for a chequerboard spatial order. Our work thus highlights that dipolar excitons enable controlled implementations of boson-like arrays with strong off-site interactions, in lattices with programmable geometries and more than 100 sites.

Postprandial activation of coagulant factor VII by long-chain dietary fatty acids.

Factor VII coagulant activity (FVIIc) is associated with an increased risk of fatal ischaemic heart disease (IHD). Several reports have suggested that dietary fat intake or hypertriglyceridaemia are associated with elevated levels of FVII. This study demonstrates that an intake of long-chain fatty acids sufficient to induce postprandial lipaemia in healthy subjects leads to a substantial elevation in both FVIIc and the concentration of FVII circulating in the activated form. Such an increase in FVIIc could not be induced by medium-chain triglycerides. These results suggest that the consumption of a sufficient amount of long-chain triglycerides to induce postprandial lipaemia induces the activation of FVII.

Activation of myocardial angiogenesis and upregulation of fibroblast growth factor-2 in transmyocardial-revascularization-treated mice.

OBJECTIVE: To evaluate the growth factor responses associated with myocardial angiogenesis. DESIGN: Mice were treated with transmyocardial revascularization (TMR) and evaluated for angiogenic and growth factor responses. METHODS: TMR was performed via thoractomy with a 27 g needle. At 2, 5, and 7 days post-treatment, hearts were removed from the TMR treated and control groups, then assayed for angiogenesis, fibroblast growth factor (FGF)-2 expression and vascular endothelial cell growth factor (VEGF) expression. RESULTS: TMR caused an angiogenic reaction in the myocardial blood vessels at 7 days post-TMR treatment. Elevated FGF-2 corresponded with increased TMR related angiogenesis. VEGF levels only increased in hearts that were prewounded then TMR treated. CONCLUSIONS: The data show that TMR stimulates myocardial angiogenesis. The angiogenic reaction is mediated by FGF-2 which increased in most experimental treatment groups. The VEGF response was more specific, requiring prewounding then TMR treatment for a VEGF increase.

Engineering p-wave interactions in ultracold atoms using nanoplasmonic traps.

Engineering strong p-wave interactions between fermions is one of the challenges in modern quantum physics. Such interactions are responsible for a plethora of fascinating quantum phenomena, such as topological quantum liquids and exotic superconductors. Here we propose a method to generate these fermionic interactions by combining recent developments in nanoplasmonics with progress in realizing laser-induced gauge fields. Nanoplasmonics allows for strong confinement, leading to a geometric resonance in the atom-atom scattering. In combination with the laser coupling of the atomic states, this is shown to result in the desired interaction. We illustrate how this scheme can be used for the stabilization of strongly correlated fractional quantum Hall states in ultracold fermionic gases.

[The allergy syndrome in childhood. Immunologic principles--risk factors--prevention]. / Das Atopiesyndrom im Kindesalter. Immunologische Grundlagen-Prädiktion-Prävention.

The time of manifestation, severity and clinical course of atopic diseases are primarily determined by genetic factors. However, a number of environmental influences, like exposure to allergens and adjuvant trigger factors are modulating the clinical course. The risk for atopic disease can be predicted from cord blood IgE levels and the atopic family history of first degree relatives. Since no predictor is of sufficient sensitivity and specificity, there is a need for further predictors of atopy. Different prevention strategies, i.e. effect of early infant diet and maternal food avoidance during pregnancy or lactation are discussed.