ERC FUNDED PROJECTS

Quantum information science and atom optics are among the most active fields in modern physics. In recent years, many theoretical efforts have been made to combine these two fields. Recent experimental progresses have shown the in-principle possibility to perform scalable quantum information processing (QIP) with linear optics and atomic ensembles. The main purpose of the present project is to use atomic qubits as quantum memory and exploit photonic qubits for information transfer and processing to achieve efficient linear optics QIP. On the one hand, utilizing the interaction between laser pulses and atomic ensembles we will experimentally investigate the potentials of atomic ensembles in the gas phase to build quantum repeaters for long-distance quantum communication, that is, to develop a new technological solution for quantum repeaters making use of the effective qubit-type entanglement of two cold atomic ensembles by a projective measurement of individual photons by spontaneous Raman processes. On this basis, we will further investigate the advantages of cold atoms in an optical trap to enhance the coherence time of atomic qubits beyond the threshold for scalable realization of quantum repeaters. Moreover, building on our long experience in research on multi-photon entanglement, we also plan to perform a number of significant experiments in the field of QIP with particular emphasis on fault-tolerant quantum computation, photon-loss-tolerant quantum computation and cluster-state based quantum simulation. Finally, by combining the techniques developed in the above quantum memory and multi-photon interference experiments, we will further experimentally investigate the possibility to achieve quantum teleportation between photonic and atomic qubits, quantum teleportation between remote atomic qubits and efficient entanglement generation via classical feed-forward. The techniques that will be developed in the present project will lay the basis for future large scale

1 435 000 €

Start date: 2008-07-01, End date: 2013-12-31

Social neuroscientists study the neural mechanisms underlying our capacity to understand our own and other people’s feelings. Despite neuroscientists’ advances in plasticity research and empathy research, little is known about cortical and behavioural plasticity in emotion understanding and empathy. Clearly, in today’s world, acquiring the capacity to effectively enhance empathy and prosocial behaviour is of the utmost importance. In the present project, we will investigate the malleability of empathy via training. We will adopt a multimethod and interdisciplinary approach, combining techniques and paradigms from the fields of neuroscience, (bio-)psychology, and economics. Studies 1-3 will provide a cross-sectional look at structural and functional differences in the brains of individuals scoring high vs. low on empathy, of those with pathological deficits in empathy (psychopaths, alexithymics), and of individuals starting vs. finishing a three-year training program in Carl Rogers’ person-centred therapy, which aims to increase emotional capacity and empathy. Study 4 will examine brain plasticity using real-time fMRI: Participants will learn to self-regulate brain activity through the use of immediate feedback from emotion-related brain areas while practicing certain mental techniques. In Study 5, a small-scale longitudinal study, healthy individuals will receive extensive training by professional instructors in either empathy- or memory-enhancing techniques previously developed in the East and the West. We will measure training-related changes in brain structure and functioning, in hormone levels, and in behaviour. Evidence for emotional brain plasticity in adults and children would not only have important implications for the implementation of scientifically validated, effective training programs for schools and for economic and political organizations, but also for the treatment of the marked social deficits in autistic and psychopathic populations.

1 499 821 €

Start date: 2008-09-01, End date: 2014-08-31

The project aims at unraveling the molecular pathophysiology of recessive ataxias, a heterogeneous set of severely disabling neurodegenerative disorders due to loss of function of proteins involved either in mitochondrial/metabolic pathways or DNA repair. Friedreich ataxia, the most common form, is due to partial loss of function of frataxin, a mitochondrial protein involved in iron-sulfur cluster (ISC) biogenesis. Furthermore, the rare X-linked sideroblastic anemia with cerebellar ataxia is caused by mutation in ABCb7, an ATP-binding cassette transporter of the mitochondrial inner membrane necessary for cytosolic ISC export. ISC are versatile co-factors of proteins involved in electron transport, enzyme catalysis and regulation of gene expression. The synthesis and insertion of ISC into apoproteins involve complex machineries that are still poorly understood in the mammalian cell. The objectives of this proposal are: 1) to elucidate ISC biogenesis and metabolism in the mammalian cell, with an emphasis on the role of frataxin and ABCb7; 2) to better understand the molecular pathways that are involved in neuronal dysfunction due to defects in mitochondrial ISC metabolism. These objectives will be accomplished by a multidisciplinary approach combining molecular and biochemical approaches to study the ISC assembly machineries, bioinformatic and proteomic studies to identify new Fe-S proteins, the development and pathological analysis of animal and cellular models to dissect the molecular mechanisms, and transcriptomic analysis to uncover the common pathways among recessive ataxias. A specific focus of the proposal will be the involvement of DNA damage response pathways in neuronal dysfunction, as several DNA repair enzymes have recently been identified as Fe-S proteins and thus might be directly affected by frataxin and ABCb7 deficiency. This proposal should lead to the identification of different pathways for therapeutic intervention for these devastating disorders.

1 449 924 €

Start date: 2008-07-01, End date: 2013-06-30

I propose to initiate research on a specific group of bacteria, here denominated as the “Dehalococcoides-like Chloroflexi”. This group of bacteria is formed by several cultivated strains of the genus Dehalococcoides and many sequences of uncultivated organisms mostly from marine sediment or subsurface locations. All together form one subphylum of the Chloroflexi. Bacteria of the Dehalococcoides-like Chloroflexi are of particular importance for two independent reasons: first, the subphylum contains all bacteria known to transform under anaerobic conditions toxic and persistent halogenated compounds such as chlorinated dioxins, benzenes, biphenyls, vinyl chloride or brominated biphenylethers; secondly, massive amounts of Dehalococcoides-like Chloroflexi have recently been detected in marine organic-rich deep sediments dominating the populations with up to 80% of the total cell counts. However, many aspects of the physiology of Dehalococcoides species are unclear and almost nothing is known about Chloroflexi in deep sediments. I have worked for many years on the microbiology, biochemistry and genomics of Dehalococcoides species. With the proposed group I plan to focus on the physiological links between Chloroflexi in contaminated aquifers and those in marine sediments. Initially, cultures of marine sediment-Chloroflexi will be established in our lab and compared with pure Dehalococcoides strains. Objectives of our research towards marine Chloroflexi will be the description of the physiology, of the biochemistry of energy conservation and of key genes encoded in the genomes. It is anticipated that the research leads to a substantiated hypothesis on the mode of energy fixation in marine deep-sediments and an initial description of the role of Dehalococcoides-like Chloroflexi in biogeochemical cycles. We also expect to find insights into Chloroflexi evolution and their role in earth history by comparing genomes between Dehalococcoides species and marine Chloroflexi.

1 287 258 €

Start date: 2008-06-01, End date: 2013-12-31