362 research outputs found

    A mini-phoswich scintillator as a possible stop detector for the NUMEN project

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    AbstractIn the framework of the NUMEN project, aimed at the investigation of the nuclear matrix elements connected to the neutrinoless double beta decay by means of the Double Charge Exchange nuclear reactions (Cappuzzello et al., 2015), a high granularity stop detector for heavy ions is needed. It has to allow the identification of ions up to Z≈10 while maintaining a total energy resolution around 2%. As the use of silicon detectors is not possible, due to their poor radiation hardness, scintillators are being investigated as possible candidates. In this paper we show a promising result obtained using a plastic+inorganic phoswich scintillator readout by means of a Silicon Photo Multiplier

    Microscopic cluster model for the description of new experimental results on the C 13 (O 18, O 16) C 15 two-neutron transfer at 84 MeV incident energy

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    The C13(O18,O16)C15 reaction is studied at 84 MeV incident energy. Excitation energy spectra and absolute cross-section angular distributions for the strongest transitions are measured with good energy and angular resolutions. Strong selectivity for two-neutron configurations in the states of the residual nucleus is found. The measured cross-section angular distributions are analyzed by exact finite-range coupled reaction channel calculations. The two-particle wave functions are extracted using the extreme cluster and the independent coordinate scheme with shell-model derived coupling strengths. A new approach also is introduced, the microscopic cluster, in which the spectroscopic amplitudes in the center-of-mass reference frame are derived from shell-model calculations using the Moshinsky transformation brackets. This new model is able to describe well the experimental cross section and to highlight cluster configurations in the involved wave functions

    Efficacy of mesenchymal stem cells depends on administration route in a murine model of acid inhalation ARD8

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    INTRODUCTION. Acute respiratory distress syndrome (ARDS) is still associated with high mortality, as only few effective therapies are available. Mesenchymal stem cells (MSCs) showed beneficial effects in various experimental ARDS model, by fine balancing inflammation with increased ability of eliminating the noxa without additional injury. Data on the effects of MSCs in acid inhalation-induced ARDS still lack. OBJECTIVES. Aim of this study was to test the therapeutic effects of MSCs, administered by intravenous (iv) and intraperitoneal (ip) route, in a murine model of ARDS induced by acid inhalation. METHODS. Intubated and ventilated mice received 1.5 mL/kg HCl (0.1M) into the right bronchus and were immediately extubated. One hour after acid instillation, MSCs were injected ip or iv (106 cells in 200 μl solution for both routes). Mice treated by iv or ip PBS (200μl) served as controls. Twenty-four hours after MSCs administration mice were sacrificed and arterial blood gases (FiO2 = 0.21) and bronchoalveolar lavage (BAL) were analyzed to assess lung injury. RESULTS. Survival at 24 hours was 95% for MSCs ip and 85% for iv; no mice died in the PBS groups. Mice treated with MSCs ip showed significantly (p=0.013) higher partial pressure of oxygen in arterial blood (Figure 1) associated with reduction in number of neutrophils recovered in BAL (p=0.055), compared to PBS ip group (Figure 2). In contrast, mice that received MSCs intravenously did not show any beneficial effects in terms of oxygenation and neutrophils recruitment in the alveolar space, if compared to PBS iv group. CONCLUSIONS. MSCs injected intraperitoneally 1 h after onset of acid-induced experimental ARDS determine a significant improvement in oxygenation at 24 h, possibly by dampening recruitment of activated neutrophils in the alveolar space. On the other hand, MSCs iv do not seem to attenuate acid-induced ARDS, maybe because acid environment in lung parenchyma destroy a significant amount of MSCs as they pass through lung vascular tree

    Mesenchymal Stromal Cell-Derived PTX3 Promotes Wound Healing via Fibrin Remodeling

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    Although mesenchymal stromal cells (MSCs) can promote wound healing in different clinical settings, the underlying mechanism of MSC-mediated tissue repair has yet to be determined. Because a nonredundant role of pentraxin 3 (PTX3) in tissue repair and remodeling has been recently described, here we sought to determine whether MSC-derived PTX3 might play a role in wound healing. Using a murine model of skin repair, we found that Ptx3-deficient (Ptx3−/−) MSCs delayed wound closure and reduced granulation tissue formation compared with wt MSCs. At day 2, confocal microscopy revealed a dramatic reduction in green fluorescent protein (GFP)-expressing Ptx3−/− MSCs recruited to the wound, where they appeared to be not only poorly organized in bundles but also scattered in the extracellular matrix. These findings were further confirmed by quantitative biochemical analysis of GFP content in wound extracts. Furthermore, Ptx3−/− MSC-treated skins displayed increased levels of fibrin and lower levels of D-dimer, suggesting delayed fibrin-rich matrix remodeling compared with control skins. Consistently, both pericellular fibrinolysis and migration through fibrin were found to be severely affected in Ptx3−/− MSCs. Overall, our findings identify an essential role of MSC-derived PTX3 in wound repair underscoring the beneficial potential of MSC-based therapy in the management of intractable wounds

    Two-step transfer mechanisms in the charge-exchange reaction 40Ca(18O, 18F) 40K at 275 MeV

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    The nuclear collision O18+Ca40 at 275 MeV is theoretically studied in the elastic, inelastic, one-nucleon transfer, and charge-exchange channels. The elastic scattering channel is treated within the optical model framework with the help of semimicroscopic double folding potentials, which are constructed by using the realistic nuclear matter densities obtained within the Hartree-Fock-Bogoliubov method, while the distorted wave Born approximation method is adopted to calculate differential cross sections for the other channels. The charge exchange nuclear reaction Ca40(O18, F18)K40 is analyzed by assuming the two-step transfer mechanisms, namely by considering a succession of proton-neutron pickup-stripping processes. Large-scale shell-model calculations are employed to compute the spectroscopic amplitudes, needed in our approach. When compared to the available experimental angular distributions, the obtained results show that the two-step transfer mechanisms play a relevant role in the description of the Ca40(O18, F18)K40 reaction and need to be accounted for in any accurate analysis of the measured cross section

    Ex vivo acidic preconditioning enhances bone marrow ckit+ cell therapeutic potential via increased CXCR4 expression.

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    Aims The chemokine receptor CXCR4 modulates endothelial progenitor cell migration, homing, and differentiation, and plays a key role in cardiovascular regeneration. Here we examined the effect of ex vivo acidic preconditioning (AP) on CXCR4 expression and on the regenerative potential of mouse bone marrow (BM) ckit(+) cells. Methods and results Acidic preconditioning was achieved by exposing BM ckit(+) cells to hypercarbic acidosis (pH 7.0) for 24 h; control cells were kept at pH 7.4. Acidic preconditioning enhanced CXCR4 and stromal cell-derived factor 1 (SDF-1) mRNA levels, as well as CXCR4 phosphorylation. Acidic preconditioning ability to modulate CXCR4 expression depended on cytosolic calcium [Ca(2+)](i) mobilization and on nitric oxide (NO), as determined by [Ca(2+)](i) buffering with BAPTA, and by treatment with the NO donor (DETA/NO) and the NO synthase inhibitor (L-NAME). Further, AP increased SDF-1-driven chemotaxis, transendothelial migration, and differentiation toward the endothelial lineage in vitro. In a mouse model of hindlimb ischaemia, control and AP ckit(+) cells were transplanted into the ischaemic muscle; AP cells accelerated blood flow recovery, increased capillary, and arteriole number as well as the number of regenerating muscle fibres vs. control. These effects were abolished by treating AP cells with L-NAME. Conclusion Acidic preconditioning represents a novel strategy to enhance BM ckit(+) cell therapeutic potential via NO-dependent increase in CXCR4 expression

    Identification of circulating placental mRNA in maternal blood of pregnancies affected with fetal congenital heart diseases at the second trimester of pregnancy: implications for early molecular screening

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    OBJECTIVE: To investigate whether a significantly aberrant expression of circulating placental mRNA genes related with cardiogenesis can be detected at the second trimester of pregnancy. METHODS: The study was performed in two stages. First stage (development model group): match of 14 placental tissues at delivery of fetuses with congenital heart disease versus 20 controls. Second stage (validation model group): mRNA amplification of abnormal expressed genes in maternal blood samples from 26 women bearing a fetus with a congenital heart disease matched with 28 controls. RESULTS: We identified four functional categories of genes possibly involved in abnormal heart development: cardiac morphogenesis: tenascin, thioredoxin, salvador homolog 1 protein; extracellular matrix (ECM) and valvular tissue biosynthesis; placental-associated plasma protein, collagen, type I, alpha 2, fibulin-1, heparanase, procollagen-proline, 2-oxoglutarate 4-dioxygenase, alpha polypeptide II, Jumonji, AT rich interactive domain 1B RBP2-like; normal contractile activity: actinin, alpha 4, fascin homolog 1, actin-bundling protein; and congestive heart failure. CONCLUSION: Altered placental genetic expression was found at term delivery in affected fetuses. The aberration was also confirmed in maternal blood at the second trimester of women bearing a fetus with congenital heart disease. Sensitivity for the most aberrant genes ranged between 42% and 95% at a false positive rate (FPR) of 10%
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