Enhancement of Local Pairing Correlations in Periodically Driven Mott Insulators

We investigate a model for a Mott insulator in presence of a time-periodic modulated interaction and a coupling to a thermal reservoir. The combination of drive and dissipation leads to non-equilibrium steady states with a large number of doublon excitations, well above the maximum thermal-equilibrium value. We interpret this effect as an enhancement of local pairing correlations, providing analytical arguments based on a Floquet Hamiltonian. Remarkably, this Hamiltonian shows a tendency to develop long-range staggered superconducting correlations. This suggests the possibility of realizing the elusive eta-pairing phase in driven-dissipative Mott Insulators.Comment: 6+5 page

SETBP1 induces transcription of a network of development genes by acting as an epigenetic hub

SETBP1 variants occur as somatic mutations in several hematological malignancies such as atypical chronic myeloid leukemia and as de novo germline mutations in the Schinzel-Giedion syndrome. Here we show that SETBP1 binds to gDNA in AT-rich promoter regions, causing activation of gene expression through recruitment of a HCF1/KMT2A/PHF8 epigenetic complex. Deletion of two AT-hooks abrogates the binding of SETBP1 to gDNA and impairs target gene upregulation. Genes controlled by SETBP1 such as MECOM are significantly upregulated in leukemias containing SETBP1 mutations. Gene ontology analysis of deregulated SETBP1 target genes indicates that they are also key controllers of visceral organ development and brain morphogenesis. In line with these findings, in utero brain electroporation of mutated SETBP1 causes impairment of mouse neurogenesis with a profound delay in neuronal migration. In summary, this work unveils a SETBP1 function that directly affects gene transcription and clarifies the mechanism operating in myeloid malignancies and in the Schinzel- Giedion syndrome caused by SETBP1 mutations.Peer reviewe

La politica nella Unione Europea all'Orizzonte 2009: gruppi e partiti in azione

In June 2009, about 350 millions European citizens have been asked to cast their vote for the new European Parliament. The European Parliament is no longer a merely consultative assembly, but the co-legislator of the European Union in a wide array of policy areas: the European citizens were thus offered the opportunity to shape the course of action of the European Union for the next five years. Once more, however, the participation of the European people(s) failed to reach a satisfactory level and the “democratic deficit” argument regained momentum. This result appears to be in sharp contrast with the expectations enshrined in the Treaty of Lisbon, declaring that the Union “shall be founded on representative democracy”, with the direct representation of the EU citizens in the European Parliament and a linkage role explicitly assigned to the EU transnational parties. This paper, relying on an ample documentary evidence concerning European institutions and parties and on a questionnaire targeting the Italian elected representatives in the Sixth EP, seeks to depict the current state of “representative democracy” in the EU. It focuses, specifically, on the “European” elements of the EU elections: the definition of common electoral rules among the Member States, the presentation of clear and distinct manifestos by the Euro-parties and the consolidation of autonomous party organizations in Brussels. Finally, the effects of the entry into force of the Lisbon Treaty on the political and institutional architecture of the EU are also briefly evaluated

Transient Dynamics of d-Wave Superconductors after a Sudden Excitation

Motivated by recent ultrafast pump-probe experiments on high-temperature superconductors, we discuss the transient dynamics of a d-wave BCS model after a quantum quench of the interaction parameter. We find that the existence of gap nodes, with the associated nodal quasiparticles, introduces a decay channel which makes the dynamics much faster than in the conventional s-wave model. For every value of the quench parameter, the superconducting gap rapidly converges to a stationary value smaller than the one at equilibrium. Using a sudden approximation for the gap dynamics, we find an analytical expression for the reduction of spectral weight close to the nodes, which is in qualitative agreement with recent experiments. © 2015 American Physical Society

Resonant thermalization of periodically driven strongly correlated electrons

We study the dynamics of the Fermi-Hubbard model driven by a time-periodic modulation of the interaction within nonequilibrium Dynamical Mean-Field Theory. For moderate interaction, we find clear evidence of thermalization to a genuine infinite-temperature state with no residual oscillations. Quite differently, in the strongly correlated regime, we find a quasi-stationary extremely long-lived state with oscillations synchronized with the drive (Floquet prethermalization). Remarkably, the nature of this state dramatically changes upon tuning the drive frequency. In particular, we show the existence of a critical frequency at which the system rapidly thermalizes despite the large interaction. We characterize this resonant thermalization and provide an analytical understanding in terms of a break down of the periodic Schrieffer-Wolff transformation

Notch transactivates Rheb to maintain the multipotency of TSC-null cells

Differentiation abnormalities are a hallmark of tuberous sclerosis complex (TSC) manifestations; however, the genesis of these abnormalities remains unclear. Here we report on mechanisms controlling the multi-lineage, early neuronal progenitor and neural stem-like cell characteristics of lymphangioleiomyomatosis (LAM) and angiomyolipoma cells. These mechanisms include the activation of a previously unreported Rheb-Notch-Rheb regulatory loop, in which the cyclic binding of Notch1 to the Notch-responsive elements (NREs) on the Rheb promoter is a key event. This binding induces the transactivation of Rheb. The identified NRE2 and NRE3 on the Rheb promoter are important to Notch-dependent promoter activity. Notch cooperates with Rheb to block cell differentiation via similar mechanisms in mouse models of TSC. Cell-specific loss of Tsc1 within nestin-expressing cells in adult mice leads to the formation of kidney cysts, renal intraepithelial neoplasia, and invasive papillary renal carcinoma

Recurrent ETNK1 mutations in atypical chronic myeloid leukemia

Despite the recent identification of recurrent SETBP1 mutations in atypical chronic myeloid leukemia (aCML), a complete description of the somatic lesions responsible for the onset of this disorder is still lacking. To find additional somatic abnormalities in aCML, we performed whole-exome sequencing on 15 aCML cases. In 2 cases (13.3%), we identified somatic missense mutations in the ETNK1 gene. Targeted resequencing on 515 hematological clonal disorders revealed the presence of ETNK1 variants in 6 (8.8%) of 68 aCML and 2 (2.6%) of 77 chronic myelomonocytic leukemia samples. These mutations clustered in a small region of the kinase domain, encoding for H243Y and N244S (1/8 H243Y; 7/8 N244S). They were all heterozygous and present in the dominant clone. The intracellular phosphoethanolamine/phosphocholine ratio was, on average, 5.2-fold lower in ETNK1-mutated samples ( P < .05). Similar results were obtained using myeloid TF1 cells transduced with ETNK1 wild type, ETNK1-N244S, and ETNK1-H243Y, where the intracellular phosphoethanolamine/phosphocholine ratio was significantly lower in ETNK1-N244S (0.76 \ub1 0.07) and ETNK1-H243Y (0.37 \ub1 0.02) than in ETNK1-WT (1.37 \ub1 0.32; P = .01 and P = .0008, respectively), suggesting that ETNK1 mutations may inhibit the catalytic activity of the enzyme. In summary, our study shows for the first time the evidence of recurrent somatic ETNK1 mutations in the context of myeloproliferative/myelodysplastic disorders