Scattering hypervolume for ultracold bosons from weak to strong interactions

The elastic scattering properties of three bosons at low energy enter the many-body description of ultracold Bose gases via the three-body scattering hypervolume $D$. We study this quantity for identical bosons that interact via a pairwise finite-range potential. Our calculations cover the regime from strongly repulsive potentials towards attractive potentials supporting multiple two-body bound states and are consistent with the few existing predictions for $D$. We present the first numerical confirmation of the universal predictions for $D$ in the strongly interacting regime, where Efimov physics dominates, for a local nonzero-range potential. Our findings highlight how $D$ is influenced by three-body quasibound states with strong $d$-wave or $g$-wave characteristics in the weakly interacting regime.Comment: 13 pages, 8 figure

P. FARNÉS SCHERER, Construir y adaptar las Iglesias. Orientaciones y sugerencias prácticas sobre el espacio celebrativo, según el espíritu del Concilio Vaticano II, Ed. Regina, Barcelona 1989, 272 pp., 13 x 19,5. [RECENSIÓN]

We study the growth of two- and three-body correlations in an ultracold Bose gas quenched to unitarity. This is encoded in the dynamics of the two- and three-body contacts analyzed in this work. Via a set of relations connecting many-body correlations dynamics with few-body models, signatures of the Efimov effect are mapped out as a function of evolution time at unitarity over a range of atomic densities $n$. For the thermal resonantly interacting Bose gas, we find that atom-bunching leads to an enhanced growth of few-body correlations. These atom-bunching effects also highlight the interplay between few-body correlations that occurs before genuine many-body effects enter on Fermi timescales

Electrospray Mass Spectrometric Detection of Products and Short-Lived Intermediates in Aqueous Aerosol Microdroplets Exposed to a Reactive Gas

The intermediates ISO_3^- (m/z = 207) and IS2O3- (m/z = 239) generated in aqueous (NaI/Na_2S2O_3) microdroplets traversing dilute O_3 gas plumes are detected via online electrospray mass spectrometry within ∼1 ms, and their stabilities gauged by collisionally induced dissociation. The simultaneous detection of anionic reactants and the S_2O_6^(2-), HSO_4^-, IO_3^-, and I_3^- products as a function of experimental conditions provides evidence of genuinely interfacial reaction kinetics. Although O_3(aq) reacts about 3 times faster with I- than with S_2O_3^(2-) in bulk solution, only S_2O_3^(2-) is significantly depleted in the interfacial layers of [I^-]/[S_2O_3^(2-)] = 10 microdroplets below [O_3(g)] ∼ 50 ppm

Estrogen-dependent dynamic profile of eNOS-DNA associations in prostate cancer

In previous work we have documented the nuclear translocation of endothelial NOS (eNOS) and its participation in combinatorial complexes with Estrogen Receptor Beta (ERβ) and Hypoxia Inducible Factors (HIFs) that determine localized chromatin remodeling in response to estrogen (E2) and hypoxia stimuli, resulting in transcriptional regulation of genes associated with adverse prognosis in prostate cancer (PCa). To explore the role of nuclear eNOS in the acquisition of aggressive phenotype in PCa, we performed ChIP-Sequencing on chromatin-associated eNOS from cells from a primary tumor with poor outcome and from metastatic LNCaP cells. We found that: 1. the eNOS-bound regions (peaks) are widely distributed across the genome encompassing multiple transcription factors binding sites, including Estrogen Response Elements. 2. E2 increased the number of peaks, indicating hormone-dependent eNOS re-localization. 3. Peak distribution was similar with/without E2 with ≈ 55% of them in extragenic DNA regions and an intriguing involvement of the 5′ domain of several miRs deregulated in PCa. Numerous potentially novel eNOS-targeted genes have been identified suggesting that eNOS participates in the regulation of large gene sets. The parallel finding of downregulation of a cluster of miRs, including miR-34a, in PCa cells associated with poor outcome led us to unveil a molecular link between eNOS and SIRT1, an epigenetic regulator of aging and tumorigenicity, negatively regulated by miR-34a and in turn activating eNOS. E2 potentiates miR-34a downregulation thus enhancing SIRT1 expression, depicting a novel eNOS/SIRT1 interplay fine-tuned by E2-activated ER signaling, and suggesting that eNOS may play an important role in aggressive PCa

Caspase-2 is upregulated after sciatic nerve transection and its inhibition protects dorsal root ganglion neurons from Apoptosis after serum withdrawal

Sciatic nerve (SN) transection-induced apoptosis of dorsal root ganglion neurons (DRGN) is one factor determining the efficacy of peripheral axonal regeneration and the return of sensation. Here, we tested the hypothesis that caspase-2(CASP2) orchestrates apoptosis of axotomised DRGN both in vivo and in vitro by disrupting the local neurotrophic supply to DRGN. We observed significantly elevated levels of cleaved CASP2 (C-CASP2), compared to cleaved caspase-3 (C-CASP3), within TUNEL+DRGN and DRG glia (satellite and Schwann cells) after SN transection. A serum withdrawal cell culture model, which induced 40% apoptotic death in DRGN and 60% in glia, was used to model DRGN loss after neurotrophic factor withdrawal. Elevated C-CASP2 and TUNEL were observed in both DRGN and DRG glia, with C-CASP2 localisation shifting from the cytosol to the nucleus, a required step for induction of direct CASP2-mediated apoptosis. Furthermore, siRNAmediated downregulation of CASP2 protected 50% of DRGN from apoptosis after serum withdrawal, while downregulation of CASP3 had no effect on DRGN or DRG glia survival. We conclude that CASP2 orchestrates the death of SN-axotomised DRGN directly and also indirectly through loss of DRG glia and their local neurotrophic factor support. Accordingly, inhibiting CASP2 expression is a potential therapy for improving both the SN regeneration response and peripheral sensory recovery

Collapse and revival of the monopole mode of a degenerate Bose gas in an isotropic harmonic trap

We study the monopole (breathing) mode of a finite temperature Bose-Einstein condensate in an isotropic harmonic trap recently developed by Lobser et al. [Nat. Phys. 11, 1009 (2015)]. We observe a nonexponential collapse of the amplitude of the condensate oscillation followed by a partial revival. This behavior is identified as being due to beating between two eigenmodes of the system, corresponding to in-phase and out-of-phase oscillations of the condensed and noncondensed fractions of the gas. We perform finite temperature simulations of the system dynamics using the Zaremba-Nikuni-Griffin methodology [J. Low Temp. Phys. 116, 277 (1999)], and find good agreement with the data, thus confirming the two mode description