Time-resolved collapse and revival of the Kondo state near a quantum phase transition

One of the most successful paradigms of many-body physics is the concept of quasiparticles: excitations in strongly interacting matter behaving like weakly interacting particles in free space. Quasiparticles in metals are very robust objects. Yet, when a system's ground state undergoes a qualitative change at a quantum critical point (QCP), the quasiparticles may disintegrate and give way to an exotic quantum-fluid state of matter. The nature of this breakdown is intensely debated, because the emergent quantum fluid dominates the material properties up to high temperature and might even be related to the occurence of superconductivity in some compounds. Here we trace the dynamics of heavy-fermion quasiparticles in CeCu$_{6-x}$Au$_{x}$ and monitor their evolution towards the QCP in time-resolved experiments, supported by many-body calculations. A terahertz pulse disrupts the many-body heavy-fermion state. Under emission of a delayed, phase-coherent terahertz reflex the heavy-fermion state recovers, with a coherence time 100 times longer than typically associated with correlated metals. The quasiparticle weight collapses towards the QCP, yet its formation temperature remains constant -- phenomena believed to be mutually exclusive. Coexistence in the same experiment calls for revisions in our view on quantum criticality.Comment: Published version, including data on CeCu6, CeCu5.9Au0.1, and CeCu5Au1 and extended Supplementary Information. 7 pages, 4 figures, Supplementary Information: 5 pages, 3 figure

Iron Behaving Badly: Inappropriate Iron Chelation as a Major Contributor to the Aetiology of Vascular and Other Progressive Inflammatory and Degenerative Diseases

The production of peroxide and superoxide is an inevitable consequence of aerobic metabolism, and while these particular "reactive oxygen species" (ROSs) can exhibit a number of biological effects, they are not of themselves excessively reactive and thus they are not especially damaging at physiological concentrations. However, their reactions with poorly liganded iron species can lead to the catalytic production of the very reactive and dangerous hydroxyl radical, which is exceptionally damaging, and a major cause of chronic inflammation. We review the considerable and wide-ranging evidence for the involvement of this combination of (su)peroxide and poorly liganded iron in a large number of physiological and indeed pathological processes and inflammatory disorders, especially those involving the progressive degradation of cellular and organismal performance. These diseases share a great many similarities and thus might be considered to have a common cause (i.e. iron-catalysed free radical and especially hydroxyl radical generation). The studies reviewed include those focused on a series of cardiovascular, metabolic and neurological diseases, where iron can be found at the sites of plaques and lesions, as well as studies showing the significance of iron to aging and longevity. The effective chelation of iron by natural or synthetic ligands is thus of major physiological (and potentially therapeutic) importance. As systems properties, we need to recognise that physiological observables have multiple molecular causes, and studying them in isolation leads to inconsistent patterns of apparent causality when it is the simultaneous combination of multiple factors that is responsible. This explains, for instance, the decidedly mixed effects of antioxidants that have been observed, etc...Comment: 159 pages, including 9 Figs and 2184 reference

Rats exposed to cocaine during late gestation and early postnatal life show deficits in hippocampal pyramidal and granule cells in later life

In humans, the offspring of maternal cocaine misusers are known to have subtle cognitive and motor impairments in later life. It was therefore hypothesized that such exposure in animals would also affect the morphological structure of the brain. This possibility was investigated by exposing rats to cocaine between embryonic day 15 and postnatal day 6. Samples of the cocaine-exposed and control rats were killed for examination at 22 and 150 postnatal days of age. Stereological procedures (the Cavalieri principle together with the physical disector method) were utilized to estimate the total number of pyramidal and granule cells in defined regions of the hippocampal formation. At 22 days of age, the control offspring had about 373 000 pyramidal cells whereas the cocaine-treated animals only had about 310 000 cells in the CA1 + CA2 + CA3 region. By 150 days of age the values were about 396 000 and 348 000, respectively. The differences between age-matched groups were statistically significant. There were about 626 000 and 687 000 dentate gyrus granule cells in the 22-day-old control and cocaine-treated groups, respectively. By postnatal day 150 the control rats had about 832 000 granule cells whilst the cocaine-treated rats had about 693 000. There was a significant main effect of age as well as group–age interaction in this measure. These results show that even moderate exposure to cocaine during the late gestation and early postnatal period in rats is a potent teratogen and can markedly influence the development of neurons in the hippocampal formation

Targeting iron metabolism in drug discovery and delivery

Iron fulfils a central role in many essential biochemical processes in human physiology; thus, proper processing of iron is crucial. Although iron metabolism is subject to relatively strict physiological control, numerous disorders, such as cancer and neurodegenerative diseases, have recently been linked to deregulated iron homeostasis. Consequently, iron metabolism constitutes a promising and largely unexploited therapeutic target for the development of new pharmacological treatments for these diseases. Several iron metabolism-targeted therapies are already under clinical evaluation for haematological disorders, and these and newly developed therapeutic agents are likely to have substantial benefit in the clinical management of iron metabolism-associated diseases, for which few efficacious treatments are currently available