Effects of genetic and agronomic factors on grain composition in oats

The effects of genetic variability and agronomic practises on the chemical compounds of the grain were evaluated in a set of oat cultivars (16 naked and four husked) grown in different experiments in the years 2004–2008. In the first experiment, carried out for two years, β-glucan and Total Dietary Fibre (TDF) from eight oat cultivars, grown under three different levels of nitrogen fertilization and two seed doses, were considered. The second experiment, involving 12 cultivars for two years, explored the variation of β-glucan solubility and further characterized six cultivars for the content of TDF and arabinoxylans. In both experiments, genotype was found to exert the largest effect on the grain composition; nitrogen levels and seed doses had positive significant effects on protein and β-glucan contents, but did not affect fibre content. Among the naked cultivars, Irina, Abel, Luna, Hendon and Expression showed a good ability to accumulate the examined grain compounds. However, in general, the highest contents of protein and β-glucan were found in the groats of husked cultivars, suggesting that specific breeding programs are a crucial step to identify the suitable naked oat genotypes to produce foods of high nutritional value

Comparison of silver nanoparticles confined in nanoporous silica prepared by chemical synthesis and by ultra-short pulsed laser ablation in liquid

Hexagonally ordered mesoporous silica materials MCM-41 and SBA-15 have been synthesized and loaded with Ag nanoparticles, utilizing both chemical synthesis and ultra-short pulsed laser ablation in liquid. In laser ablation, a silver target, immersed in aqueous suspension of ordered mesoporous silica SBA-15, was irradiated by ultra-short laser pulses to generate silver nanoparticles. For comparison samples of similar silver contents were prepared either by incorporating silver into the SBA-15 during a hydrothermal synthesis or by introducing silver in MCM-41 by template ion-exchange. Samples were characterized by XRD, N2 physisorption, TEM and UV-vis spectroscopy. All preparations contained significant amount of 5-50 nm size silver agglomerates on the outer surface of the silica particles. The laser ablation process did not cause significant destruction of the SBA-15 structure and metallic silver (Ag0) nanoparticles were mainly generated. It is demonstrated that by laser ablation in aqueous silica suspension smaller and more uniform metallic silver particles can be produced and loaded on the surface of the silica support than by synthesis procedures. Catalytic properties of the samples have been tested in the total oxidation of toluene. Because of its favorable Ag dispersity the Ag/SBA-15 catalyst, generated by the laser ablation method, had better catalytic stability and, relative to its Ag load, higher activity than the conventional Ag/SBA-15 preparations

Two-dimensional lattice-fluid model with water-like anomalies

We investigate a lattice-fluid model defined on a two-dimensional triangular lattice, with the aim of reproducing qualitatively some anomalous properties of water. Model molecules are of the "Mercedes Benz" type, i.e., they possess a D3 (equilateral triangle) symmetry, with three bonding arms. Bond formation depends both on orientation and local density. We work out phase diagrams, response functions, and stability limits for the liquid phase, making use of a generalized first order approximation on a triangle cluster, whose accuracy is verified, in some cases, by Monte Carlo simulations. The phase diagram displays one ordered (solid) phase which is less dense than the liquid one. At fixed pressure the liquid phase response functions show the typical anomalous behavior observed in liquid water, while, in the supercooled region, a reentrant spinodal is observed.Comment: 9 pages, 1 table, 7 figure

Intake of fruits and vegetables and polymorphisms in DNA repair genes in bladder cancer

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The η′g∗g∗\eta^\prime g^* g^* vertex with arbitrary gluon virtualities in the perturbative QCD hard scattering approach

We study the $\eta^\prime g^* g^*$ vertex for arbitrary gluon virtualities in the time-like and space-like regions, using the perturbative QCD hard scattering approach and an input wave-function of the $\eta^\prime$-meson consistent with the measured $\eta^\prime \gamma^* \gamma$ transition form factor. The contribution of the gluonic content of the $\eta^\prime$-meson is taken into account, enhancing the form factor over the entire virtuality considered. However, data on the electromagnetic transition form factor of the $\eta^\prime$-meson is not sufficient to quantify the gluonic enhancement. We also study the effect of the transverse momenta of the partons in the $\eta^\prime$-meson on the $\eta^\prime g^* g^*$ vertex, using the modified hard scattering approach based on Sudakov formalism. Analytic expressions for the $\eta^\prime g^* g^*$ vertex are presented in limiting kinematic regions and parametrizations are given satisfying the QCD anomaly, for real gluons, and perturbative QCD behavior for large gluon virtualities, in both the time-like and space-like regions. Our results have implications for the inclusive decay $B \to \eta^\prime X$ and exclusive decays, such as $B \to \eta^\prime (K,K^*)$, and in hadronic production processes $N + N (\bar N) \to \eta^\prime X$.Comment: 23 pages, 19 figures (requires revtex4, amssymb, epsf); several typos corrected, this version now identical to the one accepted for publication in Phys. Rev.

Neuroblastoma-secreted exosomes carrying miR‐375 promote osteogenic differentiation of bone-marrow mesenchymal stromal cells

Bone marrow (BM) is the major target organ for neuroblastoma (NB) metastasis and its involvement is associated with poor outcome. Yet, the mechanism by which NB cells invade BM is largely unknown. Tumour microenvironment represents a key element in tumour progression and mesenchymal stromal cells (MSCs) have been recognized as a fundamental part of the associated tumour stroma. Here, we show that BM-MSCs isolated from NB patients with BM involvement exhibit a greater osteogenic potential than MSCs from non-infiltrated BM. We show that BM metastasis-derived NB-cell lines secrete higher levels of exosomal miR-375, which promotes osteogenic differentiation in MSCs. Of note, clinical data demonstrate that high level of miR-375 correlates with BM metastasis in NB patients. Our findings suggest, indeed, a potential role for exosomal miR-375 in determining a favourable microenvironment in BM to promote metastatic progression. MiR-375 may, thus, represent a novel biomarker and a potential target for NB patients with BM involvement

Interaction between SNAI2 and MYOD enhances oncogenesis and suppresses differentiation in Fusion Negative Rhabdomyosarcoma

Rhabdomyosarcoma (RMS) is an aggressive pediatric malignancy of the muscle, that includes Fusion Positive (FP)-RMS harboring PAX3/7-FOXO1 and Fusion Negative (FN)-RMS commonly with RAS pathway mutations. RMS express myogenic master transcription factors MYOD and MYOG yet are unable to terminally differentiate. Here, we report that SNAI2 is highly expressed in FN-RMS, is oncogenic, blocks myogenic differentiation, and promotes growth. MYOD activates SNAI2 transcription via super enhancers with striped 3D contact architecture. Genome wide chromatin binding analysis demonstrates that SNAI2 preferentially binds enhancer elements and competes with MYOD at a subset of myogenic enhancers required for terminal differentiation. SNAI2 also suppresses expression of a muscle differentiation program modulated by MYOG, MEF2, and CDKN1A. Further, RAS/MEK-signaling modulates SNAI2 levels and binding to chromatin, suggesting that the differentiation blockade by oncogenic RAS is mediated in part by SNAI2. Thus, an interplay between SNAI2, MYOD, and RAS prevents myogenic differentiation and promotes tumorigenesis

Interaction between SNAI2 and MYOD enhances oncogenesis and suppresses differentiation in Fusion Negative Rhabdomyosarcoma

Rhabdomyosarcoma (RMS) is an aggressive pediatric malignancy of the muscle, that includes Fusion Positive (FP)-RMS harboring PAX3/7-FOXO1 and Fusion Negative (FN)-RMS commonly with RAS pathway mutations. RMS express myogenic master transcription factors MYOD and MYOG yet are unable to terminally differentiate. Here, we report that SNAI2 is highly expressed in FN-RMS, is oncogenic, blocks myogenic differentiation, and promotes growth. MYOD activates SNAI2 transcription via super enhancers with striped 3D contact architecture. Genome wide chromatin binding analysis demonstrates that SNAI2 preferentially binds enhancer elements and competes with MYOD at a subset of myogenic enhancers required for terminal differentiation. SNAI2 also suppresses expression of a muscle differentiation program modulated by MYOG, MEF2, and CDKN1A. Further, RAS/MEK-signaling modulates SNAI2 levels and binding to chromatin, suggesting that the differentiation blockade by oncogenic RAS is mediated in part by SNAI2. Thus, an interplay between SNAI2, MYOD, and RAS prevents myogenic differentiation and promotes tumorigenesis. Rhabdomyosarcomas are tumours blocked in myogenic differentiation, which despite the expression of master muscle regulatory factors, including MYOD, are unable to differentiate. Here, the authors show that SNAI2 is upregulated by MYOD through super enhancers, binds to MYOD target enhancers, and arrests differentiation

MYOD-SKP2 axis boosts tumorigenesis in fusion negative rhabdomyosarcoma by preventing differentiation through p57Kip2^{Kip2} targeting

Rhabdomyosarcomas (RMS) are pediatric mesenchymal-derived malignancies encompassing PAX3/7-FOXO1 Fusion Positive (FP)-RMS, and Fusion Negative (FN)-RMS with frequent RAS pathway mutations. RMS express the master myogenic transcription factor MYOD that, whilst essential for survival, cannot support differentiation. Here we discover SKP2, an oncogenic E3-ubiquitin ligase, as a critical pro-tumorigenic driver in FN-RMS. We show that SKP2 is overexpressed in RMS through the binding of MYOD to an intronic enhancer. SKP2 in FN-RMS promotes cell cycle progression and prevents differentiation by directly targeting p27$^{Kip1}$ and p57$^{Kip2}$, respectively. SKP2 depletion unlocks a partly MYOD-dependent myogenic transcriptional program and strongly affects stemness and tumorigenic features and prevents in vivo tumor growth. These effects are mirrored by the investigational NEDDylation inhibitor MLN4924. Results demonstrate a crucial crosstalk between transcriptional and post-translational mechanisms through the MYOD-SKP2 axis that contributes to tumorigenesis in FN-RMS. Finally, NEDDylation inhibition is identified as a potential therapeutic vulnerability in FN-RMS