Phase diagram for a Bose-Einstein condensate moving in an optical lattice

The stability of superfluid currents in a system of ultracold bosons was studied using a moving optical lattice. Superfluid currents in a very weak lattice become unstable when their momentum exceeds 0.5 recoil momentum. Superfluidity vanishes already for zero momentum as the lattice deep reaches the Mott insulator(MI) phase transition. We study the phase diagram for the disappearance of superfluidity as a function of momentum and lattice depth between these two limits. Our phase boundary extrapolates to the critical lattice depth for the superfluid-to-MI transition with 2% precision. When a one-dimensional gas was loaded into a moving optical lattice a sudden broadening of the transition between stable and unstable phases was observed.Comment: 4 figure

Imaging the Mott Insulator Shells using Atomic Clock Shifts

Microwave spectroscopy was used to probe the superfluid-Mott Insulator transition of a Bose-Einstein condensate in a 3D optical lattice. Using density dependent transition frequency shifts we were able to spectroscopically distinguish sites with different occupation numbers, and to directly image sites with occupation number n=1 to n=5 revealing the shell structure of the Mott Insulator phase. We use this spectroscopy to determine the onsite interaction and lifetime for individual shells

AC-induced superfluidity

We argue that a system of ultracold bosonic atoms in a tilted optical lattice can become superfluid in response to resonant AC forcing. Among others, this allows one to prepare a Bose-Einstein condensate in a state associated with a negative effective mass. Our reasoning is backed by both exact numerical simulations for systems consisting of few particles, and by a theoretical approach based on Floquet-Fock states.Comment: Accepted for publication in Europhysics letters, 6 pages, 4 figures, Changes in v2: reference 7 replaced by a more recent on

Calpain restrains the stem cells compartment in breast cancer

CAPNS1 is essential for the stability and function of ubiquitous CAPN1 and CAPN2. Calpain modulates by proteolytic cleavage many cellular substrates and its activity is often deregulated in cancer cells, therefore calpain inhibition has been proposed as a therapeutical strategy for a number of malignancies. Here we show that CAPNS1 depletion is coupled to impairment of MCF7 and MCF10AT cell lines growth on plate and defective architecture of mammary acini derived from MCF10A cells. In soft agar CAPNS1 depletion leads to cell growth increase in MCF7, and decrease in MCF10AT cells. In both MCF7 and MCF10AT, CAPNS1 depletion leads to the enlargement of the stem cell compartment, as demonstrated by mammosphere formation assays and evaluation of stem cell markers by means of FACS and western blot analysis. Accordingly, activation of calpain by thapsigargin treatment leads to a decrease in the stem cell reservoir. The expansion of the cancer stem cell population in CAPNS1 depleted cells is coupled to a defective shift from symmetric to asymmetric division during mammosphere growth coupled to a decrease in NUMB protein level

Raman Spectroscopy of Mott insulator states in optical lattices

We propose and analyse a Raman spectroscopy technique for probing the properties of quantum degenerate bosons in the ground band of an optical lattice. Our formalism describes excitations to higher vibrational bands and is valid for deep lattices where a tight-binding approach can be applied to the describe the initial state of the system. In sufficiently deep lattices, localized states in higher vibrational bands play an important role in the system response, and shifts in resonant frequency of excitation are sensitive to the number of particles per site. We present numerical results of this formalism applied to the case of a uniform lattice deep in the Mott insulator regime.Comment: 10 pages, 3 figure

Impact of imaging protocol on left ventricular ejection fraction using gated-SPECT myocardial perfusion imaging

10noopenopenMarcassa, C; Giubbini, R.; Acampa, W.; Cittanti, C.; Djepaxhija, O.; Gimelli, A.; Kokomani, A.; Medolago, G.; Milan, E.; Sciagrà, R.Marcassa, C; Giubbini, Raffaele; Acampa, W.; Cittanti, C.; Djepaxhija, O.; Gimelli, A.; Kokomani, A.; Medolago, Giuseppe; Milan, E.; Sciagrà, R

Subtractive CRISPR screen identifies the ATG16L1/vacuolar ATPase axis as required for non-canonical LC3 lipidation

Although commonly associated with autophagosomes, LC3 can also be recruited to membranes by covalent lipidation in a variety of non-canonical contexts. These include responses to ionophores such as the M2 proton channel of influenza A virus. We report a subtractive CRISPR screen that identifies factors required for non-canonical LC3 lipidation. As well as the enzyme complexes directly responsible for LC3 lipidation in all contexts, we show the RALGAP complex is important for M2-induced, but not ionophore drug-induced, LC3 lipidation. In contrast, ATG4D is responsible for LC3 recycling in M2-induced and basal LC3 lipidation. Identification of a vacuolar ATPase subunit in the screen suggests a common mechanism for non-canonical LC3 recruitment. Influenza-induced and ionophore drug-induced LC3 lipidation lead to association of the vacuolar ATPase and ATG16L1 and can be antagonized by Salmonella SopF. LC3 recruitment to erroneously neutral compartments may therefore represent a response to damage caused by diverse invasive pathogens

Measurement of the electric dipole moments for transitions to rubidium Rydberg states via Autler-Townes splitting

We present the direct measurements of electric-dipole moments for $5P_{3/2}\to nD_{5/2}$ transitions with $20<n<48$ for Rubidium atoms. The measurements were performed in an ultracold sample via observation of the Autler-Townes splitting in a three-level ladder scheme, commonly used for 2-photon excitation of Rydberg states. To the best of our knowledge, this is the first systematic measurement of the electric dipole moments for transitions from low excited states of rubidium to Rydberg states. Due to its simplicity and versatility, this method can be easily extended to other transitions and other atomic species with little constraints. Good agreement of the experimental results with theory proves the reliability of the measurement method.Comment: 12 pages, 6 figures; figure 6 replaced with correct versio

Dual role of USP 30 in controlling basal pexophagy and mitophagy

USP 30 is an integral protein of the outer mitochondrial membrane that counteracts PINK 1 and Parkin‐dependent mitophagy following acute mitochondrial depolarisation. Here, we use two distinct mitophagy reporter systems to reveal tonic suppression by USP 30, of a PINK 1‐dependent component of basal mitophagy in cells lacking detectable Parkin. We propose that USP 30 acts upstream of PINK 1 through modulation of PINK 1‐substrate availability and thereby determines the potential for mitophagy initiation. We further show that a fraction of endogenous USP 30 is independently targeted to peroxisomes where it regulates basal pexophagy in a PINK 1‐ and Parkin‐independent manner. Thus, we reveal a critical role of USP 30 in the clearance of the two major sources of ROS in mammalian cells and in the regulation of both a PINK 1‐dependent and a PINK 1‐independent selective autophagy pathway