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1.
Nature ; 590(7846): 401-404, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33597757

RESUMO

Coherent control of quantum dynamics is key to a multitude of fundamental studies and applications1. In the visible or longer-wavelength domains, near-resonant light fields have become the primary tool with which to control electron dynamics2. Recently, coherent control in the extreme-ultraviolet range was demonstrated3, with a few-attosecond temporal resolution of the phase control. At hard-X-ray energies (above 5-10 kiloelectronvolts), Mössbauer nuclei feature narrow nuclear resonances due to their recoilless absorption and emission of light, and spectroscopy of these resonances is widely used to study the magnetic, structural and dynamical properties of matter4,5. It has been shown that the power and scope of Mössbauer spectroscopy can be greatly improved using various control techniques6-16. However, coherent control of atomic nuclei using suitably shaped near-resonant X-ray fields remains an open challenge. Here we demonstrate such control, and use the tunable phase between two X-ray pulses to switch the nuclear exciton dynamics between coherent enhanced excitation and coherent enhanced emission. We present a method of shaping single pulses delivered by state-of-the-art X-ray facilities into tunable double pulses, and demonstrate a temporal stability of the phase control on the few-zeptosecond timescale. Our results unlock coherent optical control for nuclei, and pave the way for nuclear Ramsey spectroscopy17 and spin-echo-like techniques, which should not only advance nuclear quantum optics18, but also help to realize X-ray clocks and frequency standards19. In the long term, we envision time-resolved studies of nuclear out-of-equilibrium dynamics, which is a long-standing challenge in Mössbauer science20.

2.
Phys Rev Lett ; 123(15): 153902, 2019 Oct 11.
Artigo em Inglês | MEDLINE | ID: mdl-31702302

RESUMO

We introduce an analytical phase-reconstruction principle that retrieves atomic scale motion via time-domain interferometry. The approach is based on a resonant interaction with high-frequency light and does not require temporal resolution on the time scale of the resonance period. It is thus applicable to hard x rays and γ rays for measurements of extremely small spatial displacements or relative-frequency changes. Here, it is applied to retrieve the temporal phase of a 14.4 keV emission line of an ^{57}Fe sample, which corresponds to a spatial translation of this sample. The small wavelength of this transition (λ=0.86 Å) allows for determining the motion of the emitter on sub-Ångström length and nanosecond timescales.

3.
J Neurochem ; 92(5): 1091-103, 2005 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-15715660

RESUMO

An early biochemical change in the Parkinsonian substantia nigra (SN) is reduction in total glutathione (GSH + GSSG) levels in affected dopaminergic neurons prior to depletion in mitochondrial complex I activity, dopamine loss, and cell death. We have demonstrated using dopaminergic PC12 cell lines genetically engineered to inducibly down-regulate glutathione synthesis that total glutathione depletion in these cells results in selective complex I inhibition via a reversible thiol oxidation event. Here, we demonstrate that inhibition of complex I may occur either by direct nitric oxide (NO) but not peroxinitrite-mediated inhibition of complex I or through H2O2-mediated inhibition of the tricarboxylic acid (TCA) cycle enzyme alpha-ketoglutarate dehydrogenase (KGDH) which supplies NADH as substrate to the complex; activity of both enzymes are reduced in PD. While glutathione depletion causes a reduction in spare KGDH enzymatic capacity, it produces a complete collapse of complex I reserves and significant effects on mitochondrial function. Our data suggest that NO is likely the primary agent involved in preferential complex I inhibition following acute glutathione depletion in dopaminergic cells. This may have major implications in terms of understanding mechanisms of dopamine cell death associated with PD especially as they relate to complex I inhibition.


Assuntos
Dopamina/metabolismo , Complexo I de Transporte de Elétrons/metabolismo , Glutationa/metabolismo , Óxido Nítrico/metabolismo , Doença de Parkinson/metabolismo , Difosfato de Adenosina/metabolismo , Trifosfato de Adenosina/metabolismo , Aldeídos/metabolismo , Animais , Antibacterianos/farmacologia , Western Blotting/métodos , Diferenciação Celular/efeitos dos fármacos , Citrato (si)-Sintase/metabolismo , Relação Dose-Resposta a Droga , Doxiciclina/farmacologia , Peróxido de Hidrogênio/metabolismo , Complexo Cetoglutarato Desidrogenase/metabolismo , Mitocôndrias/metabolismo , Complexos Multienzimáticos/metabolismo , Oxigênio/metabolismo , Células PC12/efeitos dos fármacos , Ratos , Transdução de Sinais/fisiologia
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