A macroscopic quantum state analysed particle by particle

Explaining how microscopic entities collectively produce macroscopic phenomena is a fundamental goal of many-body physics. Theory predicts that large-scale entanglement is responsible for exotic macroscopic phenomena, but observation of entangled particles in naturally occurring systems is extremely challenging. Synthetic quantum systems made of atoms in optical lattices have been con- structed with the goal of observing macroscopic quantum phenomena with single-atom resolution. Serious challenges remain in producing and detecting long-range quantum correlations in these systems, however. Here we exploit the strengths of photonic technology, including high coherence and efficient single-particle detection, to study the predicted large-scale entanglement underlying the macroscopic quantum phenomenon of polarization squeezing. We generate a polarization-squeezed beam, extract photon pairs at random, and make a tomographic reconstruction of their joint quantum state. We present experimental evidence showing that all photons arriving within the squeezing coherence time are entangled, that entanglement monogamy dilutes entanglement with increasing photon density and that, counterintuitively, increased squeezing can reduce bipartite entanglement. The results provide direct evidence for entanglement of macroscopic numbers of particles and introduce micro-analysis to the study of macroscopic quantum phenomena

Learning styles: Assessing our student needs

The research of learning styles and their importance in education has been investigated for several decades. Educators and researchers know that all children can learn, and know that all students learn in different ways. Recent research has substantiated and validated much of what we knew about learning. These investigations have also produced new information about how the effects of sociological, environmental, emotional, physiological, and cognitive preferences affect the achievement of individual students (Dunn, Beaudry and Klanas, 1989)

Structural basis of complement membrane attack complex formation

In response to complement activation, the membrane attack complex (MAC) assembles from fluid-phase proteins to form pores in lipid bilayers. MAC directly lyses pathogens by a ‘multi-hit’ mechanism; however, sublytic MAC pores on host cells activate signalling pathways. Previous studies have described the structures of individual MAC components and subcomplexes; however, the molecular details of its assembly and mechanism of action remain unresolved. Here we report the electron cryo-microscopy structure of human MAC at subnanometre resolution. Structural analyses define the stoichiometry of the complete pore and identify a network of interaction interfaces that determine its assembly mechanism. MAC adopts a ‘split-washer’ configuration, in contrast to the predicted closed ring observed for perforin and cholesterol-dependent cytolysins. Assembly precursors partially penetrate the lipid bilayer, resulting in an irregular β-barrel pore. Our results demonstrate how differences in symmetric and asymmetric components of the MAC underpin a molecular basis for pore formation and suggest a mechanism of action that extends beyond membrane penetration

Reversal of aging-induced increases in aortic stiffness by targeting cytoskeletal protein-protein interfaces

BACKGROUND: The proximal aorta normally functions as a critical shock absorber that protects small downstream vessels from damage by pressure and flow pulsatility generated by the heart during systole. This shock absorber function is impaired with age because of aortic stiffening. METHODS AND RESULTS: We examined the contribution of common genetic variation to aortic stiffness in humans by interrogating results from the AortaGen Consortium genome‐wide association study of carotid‐femoral pulse wave velocity. Common genetic variation in the N‐WASP (WASL) locus is associated with carotid‐femoral pulse wave velocity (rs600420, P=0.0051). Thus, we tested the hypothesis that decoy proteins designed to disrupt the interaction of cytoskeletal proteins such as N‐WASP with its binding partners in the vascular smooth muscle cytoskeleton could decrease ex vivo stiffness of aortas from a mouse model of aging. A synthetic decoy peptide construct of N‐WASP significantly reduced activated stiffness in ex vivo aortas of aged mice. Two other cytoskeletal constructs targeted to VASP and talin‐vinculin interfaces similarly decreased aging‐induced ex vivo active stiffness by on‐target specific actions. Furthermore, packaging these decoy peptides into microbubbles enables the peptides to be ultrasound‐targeted to the wall of the proximal aorta to attenuate ex vivo active stiffness. CONCLUSIONS: We conclude that decoy peptides targeted to vascular smooth muscle cytoskeletal protein‐protein interfaces and microbubble packaged can decrease aortic stiffness ex vivo. Our results provide proof of concept at the ex vivo level that decoy peptides targeted to cytoskeletal protein‐protein interfaces may lead to substantive dynamic modulation of aortic stiffness.Published versio