Observation of strong coupling between one atom and a monolithic microresonator

Over the past decade, strong interactions of light and matter at the single-photon level have enabled a wide set of scientific advances in quantum optics and quantum information science. This work has been performed principally within the setting of cavity quantum electrodynamics with diverse physical systems, including single atoms in Fabry-Perot resonators, quantum dots coupled to micropillars and photonic bandgap cavities and Cooper pairs interacting with superconducting resonators. Experiments with single, localized atoms have been at the forefront of these advances with the use of optical resonators in high-finesse Fabry-Perot configurations. As a result of the extreme technical challenges involved in further improving the multilayer dielectric mirror coatings of these resonators and in scaling to large numbers of devices, there has been increased interest in the development of alternative microcavity systems. Here we show strong coupling between individual caesium atoms and the fields of a high-quality toroidal microresonator. From observations of transit events for single atoms falling through the resonator's evanescent field, we determine the coherent coupling rate for interactions near the surface of the resonator. We develop a theoretical model to quantify our observations, demonstrating that strong coupling is achieved, with the rate of coherent coupling exceeding the dissipative rates of the atom and the cavity. Our work opens the way for investigations of optical processes with single atoms and photons in lithographically fabricated microresonators. Applications include the implementation of quantum networks, scalable quantum logic with photons, and quantum information processing on atom chips.     

Increasing adult hippocampal neurogenesis is sufficient to improve pattern separation

Adult hippocampal neurogenesis is a unique form of neural circuit plasticity that results in the generation of new neurons in the dentate gyrus throughout life. Neurons that arise in adults (adult-born neurons) show heightened synaptic plasticity during their maturation and can account for up to ten per cent of the entire granule cell population. Moreover, levels of adult hippocampal neurogenesis are increased by interventions that are associated with beneficial effects on cognition and mood, such as learning, environmental enrichment, exercise and chronic treatment with antidepressants. Together, these properties of adult neurogenesis indicate that this process could be harnessed to improve hippocampal functions. However, despite a substantial number of studies demonstrating that adult-born neurons are necessary for mediating specific cognitive functions, as well as some of the behavioural effects of antidepressants, it is unknown whether an increase in adult hippocampal neurogenesis is sufficient to improve cognition and mood. Here we show that inducible genetic expansion of the population of adult-born neurons through enhancing their survival improves performance in a specific cognitive task in which two similar contexts need to be distinguished. Mice with increased adult hippocampal neurogenesis show normal object recognition, spatial learning, contextual fear conditioning and extinction learning but are more efficient in differentiating between overlapping contextual representations, which is indicative of enhanced pattern separation. Furthermore, stimulation of adult hippocampal neurogenesis, when combined with an intervention such as voluntary exercise, produces a robust increase in exploratory behaviour. However, increasing adult hippocampal neurogenesis alone does not produce a behavioural response like that induced by anxiolytic agents or antidepressants. Together, our findings suggest that strategies that are designed to increase adult hippocampal neurogenesis specifically, by targeting the cell death of adult-born neurons or by other mechanisms, may have therapeutic potential for reversing impairments in pattern separation and dentate gyrus dysfunction such as those seen during normal ageing.     

Streptococcal M1 protein constructs a pathological host fibrinogen network

M1 protein, a major virulence factor of the leading invasive strain of group A Streptococcus, is sufficient to induce toxic-shock-like vascular leakage and tissue injury. These events are triggered by the formation of a complex between M1 and fibrinogen that, unlike M1 or fibrinogen alone, leads to neutrophil activation. Here we provide a structural explanation for the pathological properties of the complex formed between streptococcal M1 and human fibrinogen. A conformationally dynamic coiled-coil dimer of M1 was found to organize four fibrinogen molecules into a specific cross-like pattern. This pattern supported the construction of a supramolecular network that was required for neutrophil activation but was distinct from a fibrin clot. Disruption of this network into other supramolecular assemblies was not tolerated. These results have bearing on the pathophysiology of streptococcal toxic shock.     

Distinct physiological and behavioural functions for parental alleles of imprinted Grb10

Imprinted genes, defined by their preferential expression of a single parental allele, represent a subset of the mammalian genome and often have key roles in embryonic development, but also postnatal functions including energy homeostasis and behaviour. When the two parental alleles are unequally represented within a social group (when there is sex bias in dispersal and/or variance in reproductive success), imprinted genes may evolve to modulate social behaviour, although so far no such instance is known. Predominantly expressed from the maternal allele during embryogenesis, Grb10 encodes an intracellular adaptor protein that can interact with several receptor tyrosine kinases and downstream signalling molecules. Here we demonstrate that within the brain Grb10 is expressed from the paternal allele from fetal life into adulthood and that ablation of this expression engenders increased social dominance specifically among other aspects of social behaviour, a finding supported by the observed increase in allogrooming by paternal Grb10-deficient animals. Grb10 is, therefore, the first example of an imprinted gene that regulates social behaviour. It is also currently alone in exhibiting imprinted expression from each of the parental alleles in a tissue-specific manner, as loss of the peripherally expressed maternal allele leads to significant fetal and placental overgrowth. Thus Grb10 is, so far, a unique imprinted gene, able to influence distinct physiological processes, fetal growth and adult behaviour, owing to actions of the two parental alleles in different tissues.     

Sharply increased mass loss from glaciers and ice caps in the Canadian Arctic Archipelago

Mountain glaciers and ice caps are contributing significantly to present rates of sea level rise and will continue to do so over the next century and beyond. The Canadian Arctic Archipelago, located off the northwestern shore of Greenland, contains one-third of the global volume of land ice outside the ice sheets, but its contribution to sea-level change remains largely unknown. Here we show that the Canadian Arctic Archipelago has recently lost 61?±?7?gigatonnes per year (Gt?yr(-1)) of ice, contributing 0.17?±?0.02 mm?yr(-1) to sea-level rise. Our estimates are of regional mass changes for the ice caps and glaciers of the Canadian Arctic Archipelago referring to the years 2004 to 2009 and are based on three independent approaches: surface mass-budget modelling plus an estimate of ice discharge (SMB+D), repeat satellite laser altimetry (ICESat) and repeat satellite gravimetry (GRACE). All three approaches show consistent and large mass-loss estimates. Between the periods 2004-2006 and 2007-2009, the rate of mass loss sharply increased from 31?±?8?Gt?yr(-1) to 92?±?12?Gt?yr(-1) in direct response to warmer summer temperatures, to which rates of ice loss are highly sensitive (64?±?14?Gt?yr(-1) per 1?K increase). The duration of the study is too short to establish a long-term trend, but for 2007-2009, the increase in the rate of mass loss makes the Canadian Arctic Archipelago the single largest contributor to eustatic sea-level rise outside Greenland and Antarctica.