5 research outputs found

    Einstein-Podolsky-Rosen experiment with two Bose-Einstein condensates

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    In 1935, Einstein, Podolsky, and Rosen (EPR) conceived a Gedankenexperiment in which two particles are entangled through interactions, spatially separated, and measured. Under the classical assumption of local realism, they showed that the measurement correlations predicted by quantum mechanics for this scenario lead to a violation of the Heisenberg uncertainty principle. This contradiction, later denominated EPR paradox, revealed that the completeness of quantum mechanics is not compatible with the local realist description of nature that characterises classical physics. Although the EPR paradox has been observed between systems consisting of few particles, this has not yet been achieved between larger systems: The entanglement of macroscopic objects has already been demonstrated, but the measured correlations were not strong enough to demonstrate the EPR paradox. However, the presence of entanglement of the EPR type in many-particle systems has been shown by measuring correlations within single systems. In this thesis I describe an EPR experiment with two spatially separated massive many-particle systems: In close analogy to the original Gedankenexperiment, we entangle about 1400 atoms in a two-component Rubidium-87 Bose-Einstein condensate (BEC) via tunable collisional interactions and coherently split them into two separate condensates. Our splitting technique preserves the overlap and coherence between the components in each of the split BECs, allowing us to individually manipulate them. The entanglement inherited from the initial system results in measurement correlations between the two BECs that are strong enough to show the EPR paradox. Our work shows that the conflict between quantum mechanics and local realism does not disappear when the size of the involved systems is increased to ∼103 {\sim 10^3} atoms. In addition to this, EPR entanglement - in conjunction with the spatial separation and individual addressability of the two systems demonstrated in our experiment - is a valuable resource for quantum metrology and quantum information processing with many-particle systems

    Einstein-Podolsky-Rosen experiment with two Bose-Einstein condensates

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    In 1935, Einstein, Podolsky and Rosen (EPR) conceived a Gedankenexperiment which became a cornerstone of quantum technology and still challenges our understanding of reality and locality today. While the experiment has been realized with small quantum systems, a demonstration of the EPR paradox with spatially separated, massive many-particle systems has so far remained elusive. We observe the EPR paradox in an experiment with two spatially separated Bose-Einstein condensates containing about 700 Rubidium atoms each. EPR entanglement in conjunction with individual manipulation of the two condensates on the quantum level, as demonstrated here, constitutes an important resource for quantum metrology and information processing with many-particle systems. Our results show that the conflict between quantum mechanics and local realism does not disappear as the system size is increased to over a thousand massive particles.Comment: 9 pages, 5 figure

    Fundamental limit of phase coherence in two-component Bose-Einstein condensates

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    We experimentally and theoretically study phase coherence in two-component Bose-Einstein condensates of 87Rb^{87}{\rm Rb} atoms on an atom chip. Using Ramsey interferometry we measure the temporal decay of coherence between the ∣F=1,mF=−1⟩|F=1,m_{F}=-1\rangle and ∣F=2,mF=+1⟩|F=2,m_{F}=+1\rangle hyperfine ground states. We observe that the coherence is limited by random collisional phase shifts due to the stochastic nature of atom loss. The mechanism is confirmed quantitatively by a quantum trajectory method based on a master equation which takes into account collisional interactions, atom number fluctuations, and losses in the system. This decoherence process can be slowed down by reducing the density of the condensate. Our findings are relevant for experiments on quantum metrology and many-particle entanglement with Bose-Einstein condensates and the development of chip-based atomic clocks

    Time course and mechanisms of motoneuron death in a type II spinal muscular atrophy mouse model

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    Spinal muscular atrophy (SMA) is an autosomal recessive neuromuscular disease leading to motor impairment, muscle atrophy and premature death caused by motoneuron degeneration. It is caused by the deletion/mutation of the telomeric survival motoneuron gene (SMN1), whereas the number of copies of the centromeric gene SMN2, which produces reduced levels of functional protein, is inversely proportional to the severity of disease (from severe to mild). However, the causes of selective motoneuron death still remain elusive. To clarify the time course and the mechanisms of motoneuron (MN) death, we investigated the SMNdelta7 murine model of SMA II (the intermediate SMA form), in which motor dysfunction leads to death at P13. We collected brains and spinal cords from SMA II and wild type embryos/pups at E19, P4, P9 and P13 for neuron counts and immunohistochemistry. Newborns underwent a battery of motor tasks and were assessed daily for body weight and survival. In ChAT-immunoreacted and Nissl-stained spinal sections, stereological counts reported a dramatic reduction in the number of lower (cervical) MNs (almost 40% at P13) in the SMA II mice; in particular MNs innervating proximal muscles seemed the most affected. In addition, we noticed an increased ChAT expression through time, making ChAT-MN count less reliable than Nissl-ones. Moreover, even though most studies mainly report death of lower motoneurons, stereological counts in the motor cortex revealed a specific decrease of layer V cortical pyramidal neurons in SMA II mice compared to WT. Also the corpus callosum thickness appeared halved in the P9 SMA II mice. Finally, immunohistochemistry against cleaved Caspase-3 and LC-3 suggested an involvement of the apoptotic and autophagic modes of cell death, respectively. Therefore, at least in the animal model, SMA affects both upper and lower motoneurons, and SMN1 role in neuronal development and survival should be further investigated. Targeting apoptotic and autophagic pathways can delay the disease progression, as we are currently showing in other studies

    Spinal muscular atrophy pathogenic mutations impair the axonogenic properties of axonal-survival of motor neuron

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    The axonal survival of motor neuron (a-SMN) protein is a truncated isoform of SMN1, the spinal muscular atrophy (SMA) disease gene. a-SMN is selectively localized in axons and endowed with remarkable axonogenic properties. At present, the role of a-SMN in SMA is unknown. As a first step to verify a link between a-SMN and SMA, we investigated by means of over-expression experiments in neuroblastoma-spinal cord hybrid cell line (NSC34) whether SMA pathogenic mutations located in the N-terminal part of the protein affected a-SMN function. We demonstrated here that either SMN1 missense mutations or small intragenic re-arrangements located in the Tudor domain consistently altered the a-SMN capability of inducing axonal elongation in vitro. Mutated human a-SMN proteins determined in almost all NSC34 motor neurons the growth of short axons with prominent morphologic abnormalities. Our data indicate that the Tudor domain is critical in dictating a-SMN function possibly because it is an association domain for proteins involved in axon growth. They also indicate that Tudor domain mutations are functionally relevant not only for FL-SMN but also for a-SMN, raising the possibility that also a-SMN loss of function may contribute to the pathogenic steps leading to SMA
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