Exploring 4D Quantum Hall Physics with a 2D Topological Charge Pump

The discovery of topological states of matter has profoundly augmented our understanding of phase transitions in physical systems. Instead of local order parameters, topological phases are described by global topological invariants and are therefore robust against perturbations. A prominent example thereof is the two-dimensional integer quantum Hall effect. It is characterized by the first Chern number which manifests in the quantized Hall response induced by an external electric field. Generalizing the quantum Hall effect to four-dimensional systems leads to the appearance of a novel non-linear Hall response that is quantized as well, but described by a 4D topological invariant - the second Chern number. Here, we report on the first observation of a bulk response with intrinsic 4D topology and the measurement of the associated second Chern number. By implementing a 2D topological charge pump with ultracold bosonic atoms in an angled optical superlattice, we realize a dynamical version of the 4D integer quantum Hall effect. Using a small atom cloud as a local probe, we fully characterize the non-linear response of the system by in-situ imaging and site-resolved band mapping. Our findings pave the way to experimentally probe higher-dimensional quantum Hall systems, where new topological phases with exotic excitations are predicted

Allometric scaling of metabolic rate from molecules and mitochondria to cells and mammals

The fact that metabolic rate scales as the three-quarter power of body mass (M) in unicellular, as well as multicellular, organisms suggests that the same principles of biological design operate at multiple levels of organization. We use the framework of a general model of fractal-like distribution networks together with data on energy transformation in mammals to analyze and predict allometric scaling of aerobic metabolism over a remarkable 27 orders of magnitude in mass encompassing four levels of organization: individual organisms, single cells, intact mitochondria, and enzyme molecules. We show that, whereas rates of cellular metabolism in vivo scale as M(−1/4), rates for cells in culture converge to a single predicted value for all mammals regardless of size. Furthermore, a single three-quarter power allometric scaling law characterizes the basal metabolic rates of isolated mammalian cells, mitochondria, and molecules of the respiratory complex; this overlaps with and is indistinguishable from the scaling relationship for unicellular organisms. This observation suggests that aerobic energy transformation at all levels of biological organization is limited by the transport of materials through hierarchical fractal-like networks with the properties specified by the model. We show how the mass of the smallest mammal can be calculated (≈1 g), and the observed numbers and densities of mitochondria and respiratory complexes in mammalian cells can be understood. Extending theoretical and empirical analyses of scaling to suborganismal levels potentially has important implications for cellular structure and function as well as for the metabolic basis of aging

Identification of genomic loci associated with resting heart rate and shared genetic predictors with all-cause mortality

Resting heart rate is a heritable trait correlated with life span. Little is known about the genetic contribution to resting heart rate and its relationship with mortality. We performed a genome-wide association discovery and replication analysis starting with 19.9 million genetic variants and studying up to 265,046 individuals to identify 64 loci associated with resting heart rate (P <5 x 10(-8)); 46 of these were novel. We then used the genetic variants identified to study the association between resting heart rate and all-cause mortality. We observed that a genetically predicted resting heart rate increase of 5 beats per minute was associated with a 20% increase in mortality risk (hazard ratio 1.20, 95% confidence interval 1.11-1.28, P = 8.20 x 10(-7)) translating to a reduction in life expectancy of 2.9 years for males and 2.6 years for females. Our findings provide evidence for shared genetic predictors of resting heart rate and all-cause mortality