Acceleration with Self-Injection for an All-Optical Radiation Source at LNF

We discuss a new compact gamma-ray source aiming at high spectral density, up to two orders of magnitude higher than currently available bremsstrahlung sources, and conceptually similar to Compton Sources based on conventional linear accelerators. This new source exploits electron bunches from laser-driven electron acceleration in the so-called self-injection scheme and uses a counter-propagating laser pulse to obtain X and gamma-ray emission via Thomson/Compton scattering. The proposed experimental configuration inherently provides a unique test-bed for studies of fundamental open issues of electrodynamics. In view of this, a preliminary discussion of recent results on self-injection with the FLAME laser is also given.Comment: 8 pages, 10 figures, 44 references - Channeling 2012 conferenc

Reliability of Mainstream Tablets for 2D Analysis of a Drop Jump Landing

Please refer to the pdf version of the abstract located adjacent to the title

Universal renormalization-group dynamics at the onset of chaos in logistic maps and nonextensive statistical mechanics

We uncover the dynamics at the chaos threshold $\mu_{\infty}$ of the logistic map and find it consists of trajectories made of intertwined power laws that reproduce the entire period-doubling cascade that occurs for $\mu <\mu_{\infty}$. We corroborate this structure analytically via the Feigenbaum renormalization group (RG) transformation and find that the sensitivity to initial conditions has precisely the form of a $q$-exponential, of which we determine the $q$-index and the $q$-generalized Lyapunov coefficient $\lambda _{q}$. Our results are an unequivocal validation of the applicability of the non-extensive generalization of Boltzmann-Gibbs (BG) statistical mechanics to critical points of nonlinear maps.Comment: Revtex, 3 figures. Updated references and some general presentation improvements. To appear published as a Rapid communication of PR

Two-dimensional maps at the edge of chaos: Numerical results for the Henon map

The mixing properties (or sensitivity to initial conditions) of two-dimensional Henon map have been explored numerically at the edge of chaos. Three independent methods, which have been developed and used so far for the one-dimensional maps, have been used to accomplish this task. These methods are (i)measure of the divergence of initially nearby orbits, (ii)analysis of the multifractal spectrum and (iii)computation of nonextensive entropy increase rates. The obtained results strongly agree with those of the one-dimensional cases and constitute the first verification of this scenario in two-dimensional maps. This obviously makes the idea of weak chaos even more robust.Comment: 4 pages, 3 figure

A recent appreciation of the singular dynamics at the edge of chaos

We study the dynamics of iterates at the transition to chaos in the logistic map and find that it is constituted by an infinite family of Mori's $q$-phase transitions. Starting from Feigenbaum's $\sigma$ function for the diameters ratio, we determine the atypical weak sensitivity to initial conditions $\xi _{t}$ associated to each $q$-phase transition and find that it obeys the form suggested by the Tsallis statistics. The specific values of the variable $q$ at which the $q$-phase transitions take place are identified with the specific values for the Tsallis entropic index $q$ in the corresponding $\xi_{t}$. We describe too the bifurcation gap induced by external noise and show that its properties exhibit the characteristic elements of glassy dynamics close to vitrification in supercooled liquids, e.g. two-step relaxation, aging and a relationship between relaxation time and entropy.Comment: Proceedings of: Verhulst 200 on Chaos, Brussels 16-18 September 2004, Springer Verlag, in pres

First πK\pi K atom lifetime and πK\pi K scattering length measurements

The results of a search for hydrogen-like atoms consisting of $\pi^{\mp}K^{\pm}$ mesons are presented. Evidence for $\pi K$ atom production by 24 GeV/c protons from CERN PS interacting with a nickel target has been seen in terms of characteristic $\pi K$ pairs from their breakup in the same target ($178 \pm 49$) and from Coulomb final state interaction ($653 \pm 42$). Using these results the analysis yields a first value for the $\pi K$ atom lifetime of $\tau=(2.5_{-1.8}^{+3.0})$ fs and a first model-independent measurement of the S-wave isospin-odd $\pi K$ scattering length $\left|a_0^-\right|=\frac{1}{3}\left|a_{1/2}-a_{3/2}\right|= \left(0.11_{-0.04}^{+0.09} \right)M_{\pi}^{-1}$ ($a_I$ for isospin $I$).Comment: 14 pages, 8 figure

Metastability, negative specific heat and weak mixing in classical long-range many-rotator system

We perform a molecular dynamical study of the isolated $d=1$ classical Hamiltonian ${\cal H} = {1/2} \sum_{i=1}^N L_i^2 + \sum_{i \ne j} \frac{1-cos(\theta_i-\theta_j)}{r_{ij}^\alpha} ;(\alpha \ge 0)$, known to exhibit a second order phase transition, being disordered for $u \equiv U/N{\tilde N} \ge u_c(\alpha,d)$ and ordered otherwise ($U\equiv$ total energy and ${\tilde N} \equiv \frac{N^{1-\alpha/d}-\alpha/d}{1-\alpha/d}$). We focus on the nonextensive case $\alpha/d \le 1$ and observe that, for $u<u_c$, a basin of attraction exists for the initial conditions for which the system quickly relaxes onto a longstanding metastable state (whose duration presumably diverges with $N$ like ${\tilde N}$) which eventually crosses over to the microcanonical Boltzmann-Gibbs stable state. The temperature associated with the (scaled) average kinetic energy per particle is lower in the metastable state than in the stable one. It is exhibited for the first time that the appropriately scaled maximal Lyapunov exponent $\lambda_{u<u_c}^{max}(metastable) \propto N^{-\kappa_{metastable}} ;(N \to \infty)$, where, for all values of $\alpha/d$, $\kappa_{metastable}$ numerically coincides with {\it one third} of its value for $u>u_c$, hence decreases from 1/9 to zero when $\alpha/d$ increases from zero to unity, remaining zero thereafter. This new and simple {\it connection between anomalies above and below the critical point} reinforces the nonextensive universality scenario.Comment: 9 pages and 4 PS figure

Peroxisome Proliferator-activated Receptors and Hepatic Stellate Cell Activation

The present study examined the roles of peroxisome proliferator-activated receptors (PPAR) in activation of hepatic stellate cells (HSC), a pivotal event in liver fibrogenesis. RNase protection assay detected mRNA for PPARgamma1 but not that for the adipocyte-specific gamma2 isoform in HSC isolated from sham-operated rats, whereas the transcripts for neither isoforms were detectable in HSC from cholestatic liver fibrosis induced by bile duct ligation (BDL). Semi-quantitative reverse transcriptase-polymerase chain reaction confirmed a 70% reduction in PPARgamma mRNA level in HSC from BDL. Nuclear extracts from BDL cells showed an expected diminution of binding to PPAR-responsive element, whereas NF-kappaB and AP-1 binding were increased. Treatment of cultured-activated HSC with ligands for PPARgamma (10 microm 15-deoxy-Delta(12,14)-PGJ(2) (15dPGJ(2)); 0.1 approximately 10 microm BRL49653) inhibited DNA and collagen synthesis without affecting the cell viability. Suppression of HSC collagen by 15dPGJ(2) was abrogated 70% by the concomitant treatment with a PPARgamma antagonist (GW9662). HSC DNA and collagen synthesis were inhibited by WY14643 at the concentrations known to activate both PPARalpha and gamma (>100 microm) but not at those that only activate PPARalpha (<10 microm) or by a synthetic PPARalpha-selective agonist (GW9578). 15dPGJ(2) reduced alpha1(I) procollagen, smooth muscle alpha-actin, and monocyte chemotactic protein-1 mRNA levels while inducing matrix metalloproteinase-3 and CD36. 15dPGJ(2) and BRL49653 inhibited alpha1(I) procollagen promoter activity. Tumor necrosis factor alpha (10 ng/ml) reduced PPARgamma mRNA, and this effect was prevented by the treatment with 15dPGJ(2). These results demonstrate that HSC activation is associated with the reductions in PPARgamma expression and PPAR-responsive element binding in vivo and is reversed by the treatment with PPARgamma ligands in vitro. These findings implicate diminished PPARgamma signaling in molecular mechanisms underlying activation of HSC in liver fibrogenesis and the potential therapeutic value of PPARgamma ligands for liver fibrosis

Investigation of K+K−K^+K^- pairs in the effective mass region near 2mK2m_K

The DIRAC experiment at CERN investigated in the reaction $\rm{p}(24~\rm{GeV}/c) + Ni$ the particle pairs $K^+K^-, \pi^+ \pi^-$ and $p \bar{p}$ with relative momentum $Q$ in the pair system less than 100 MeV/c. Because of background influence studies, DIRAC explored three subsamples of $K^+K^-$ pairs, obtained by subtracting -- using time-of-flight (TOF) technique -- background from initial $Q$ distributions with $K^+K^-$ sample fractions more than 70\%, 50\% and 30\%. The corresponding pair distributions in $Q$ and in its longitudinal projection $Q_L$ were analyzed first in a Coulomb model, which takes into account only Coulomb final state interaction (FSI) and assuming point-like pair production. This Coulomb model analysis leads to a $K^+K^-$ yield increase of about four at $Q_L=0.5$ MeV/c compared to 100 MeV/c. In order to study contributions from strong interaction, a second more sophisticated model was applied, considering besides Coulomb FSI also strong FSI via the resonances $f_0(980)$ and $a_0(980)$ and a variable distance $r^*$ between the produced $K$ mesons. This analysis was based on three different parameter sets for the pair production. For the 70\% subsample and with best parameters, $3680\pm 370$ $K^+K^-$ pairs was found to be compared to $3900\pm 410$ $K^+K^-$ extracted by means of the Coulomb model. Knowing the efficiency of the TOF cut for background suppression, the total number of detected $K^+K^-$ pairs was evaluated to be around $40000\pm 10\%$, which agrees with the result from the 30\% subsample. The $K^+K^-$ pair number in the 50\% subsample differs from the two other values by about three standard deviations, confirming -- as discussed in the paper -- that experimental data in this subsample is less reliable

CDKN1B mutation and copy number variation are associated with tumor aggressiveness in luminal breast cancer

The CDKN1B gene, encoding for the CDK inhibitor p27kip1, is mutated in defined human cancer subtypes, including breast, prostate carcinomas and small intestine neuroendocrine tumors. Lessons learned from small intestine neuroendocrine tumors suggest that CDKN1B mutations could be subclonal, raising the question of whether a deeper sequencing approach could lead to the identification of higher numbers of patients with mutations. Here, we addressed this question and analyzed human cancer biopsies from breast (n = 396), ovarian (n = 110) and head and neck squamous carcinoma (n = 202) patients, using an ultra-deep sequencing approach. Notwithstanding this effort, the mutation rate of CDKN1B remained substantially aligned with values from the literature, showing that essentially only hormone receptor-positive breast cancer displayed CDKN1B mutations in a relevant number of cases (3%). However, the analysis of copy number variation showed that another fraction of luminal breast cancer displayed loss (8%) or gain (6%) of the CDKN1B gene, further reinforcing the idea that the function of p27kip1 is important in this type of tumor. Intriguingly, an enrichment for CDKN1B alterations was found in samples from premenopausal luminal breast cancer patients (n = 227, 4%) and in circulating cell-free DNA from metastatic luminal breast cancer patients (n = 59, 8.5%), suggesting that CDKN1B alterations could correlate with tumor aggressiveness and/or occur later during disease progression. Notably, many of the identified somatic mutations resulted in p27kip1 protein truncation, leading to loss of most of the protein or of its C-terminal domain. Using a gene-editing approach in a luminal breast cancer cell line, MCF-7, we observed that the expression of p27kip1 truncating mutants that lose the C-terminal domains failed to rescue most of the phenotypes induced by CDKN1B gene knockout, indicating that the functions retained by the C-terminal portion are critical for its role as an oncosuppressor, at least in luminal breast cancer. © 2020 The Authors. The Journal of Pathology published by John Wiley &amp; Sons, Ltd. on behalf of The Pathological Society of Great Britain and Ireland