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1.
Nature ; 629(8012): 561-566, 2024 May.
Artículo en Inglés | MEDLINE | ID: mdl-38658761

RESUMEN

Entanglement and its propagation are central to understanding many physical properties of quantum systems1-3. Notably, within closed quantum many-body systems, entanglement is believed to yield emergent thermodynamic behaviour4-7. However, a universal understanding remains challenging owing to the non-integrability and computational intractability of most large-scale quantum systems. Quantum hardware platforms provide a means to study the formation and scaling of entanglement in interacting many-body systems8-14. Here we use a controllable 4 × 4 array of superconducting qubits to emulate a 2D hard-core Bose-Hubbard (HCBH) lattice. We generate superposition states by simultaneously driving all lattice sites and extract correlation lengths and entanglement entropy across its many-body energy spectrum. We observe volume-law entanglement scaling for states at the centre of the spectrum and a crossover to the onset of area-law scaling near its edges.

2.
Expert Rev Hematol ; 11(4): 315-324, 2018 04.
Artículo en Inglés | MEDLINE | ID: mdl-29516749

RESUMEN

INTRODUCTION: The outlook for patients with myeloproliferative neoplasms, particularly myelofibrosis, has improved in recent years, with greater understanding of the pathogenesis and the subsequent development of a plethora of new agents. Areas covered: This article will discuss some of the advances in the field in recent years and explore in greater detail some of the most advanced emerging agents as well as those with greatest potential. An extensive literature review has been performed to identify recent clinical trials and any relevant pre-clinical work. Expert commentary: Important discoveries regarding molecular pathogenesis have led to advances in diagnostic algorithms, prognosis and ultimately also treatment strategies. However, the therapeutic armamentarium for MPN is still largely inadequate to cope with significant challenges including normalization of life span, reduction of cardiovascular complications, prevention of hematological progression and improved quality of life. Sadly, no currently available drugs have shown clear evidence of disease-modifying activity and results of early phase I and II clinical trials have been quite disappointing to date, with toxicities sometimes limiting and a lack of meaningful biological surrogate end points.


Asunto(s)
Neoplasias Hematológicas/tratamiento farmacológico , Janus Quinasa 2/antagonistas & inhibidores , Mielofibrosis Primaria/tratamiento farmacológico , Inhibidores de Proteínas Quinasas/uso terapéutico , Neoplasias Hematológicas/genética , Neoplasias Hematológicas/metabolismo , Neoplasias Hematológicas/patología , Humanos , Janus Quinasa 2/genética , Janus Quinasa 2/metabolismo , Mielofibrosis Primaria/metabolismo , Mielofibrosis Primaria/patología
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