Nonlocal Games and Quantum Permutation Groups

We present a strong connection between quantum information and quantum permutation groups. Specifically, we define a notion of quantum isomorphisms of graphs based on quantum automorphisms from the theory of quantum groups, and then show that this is equivalent to the previously defined notion of quantum isomorphism corresponding to perfect quantum strategies to the isomorphism game. Moreover, we show that two connected graphs $X$ and $Y$ are quantum isomorphic if and only if there exists $x \in V(X)$ and $y \in V(Y)$ that are in the same orbit of the quantum automorphism group of the disjoint union of $X$ and $Y$. This connection links quantum groups to the more concrete notion of nonlocal games and physically observable quantum behaviours. We exploit this link by using ideas and results from quantum information in order to prove new results about quantum automorphism groups, and about quantum permutation groups more generally. In particular, we show that asymptotically almost surely all graphs have trivial quantum automorphism group. Furthermore, we use examples of quantum isomorphic graphs from previous work to construct an infinite family of graphs which are quantum vertex transitive but fail to be vertex transitive, answering a question from the quantum group literature. Our main tool for proving these results is the introduction of orbits and orbitals (orbits on ordered pairs) of quantum permutation groups. We show that the orbitals of a quantum permutation group form a coherent configuration/algebra, a notion from the field of algebraic graph theory. We then prove that the elements of this quantum orbital algebra are exactly the matrices that commute with the magic unitary defining the quantum group. We furthermore show that quantum isomorphic graphs admit an isomorphism of their quantum orbital algebras which maps the adjacency matrix of one graph to that of the other.Comment: 39 page

Ruolo del miR-221 nella tumorigenesi epatica

MicroRNAs are short non-coding RNA molecules, involved in post-transcriptional gene expression regulation. Their aberrant expression is involved in several pathological conditions, including cancer. MicroRNA-221 was frequently found overexpressed in human neoplasms. This study focused on biological and molecular function of miR-221 in hepatocellular carcinoma (HCC). By analyzing miR-221 expression in 70 clinical samples from normal liver, cirrhosis and hepatocellular carcinoma we found miR-221 overexpression in 80% of cancer samples, compared to non-neoplastic tissues, suggesting that this microRNA played an important role in HCC development. Previous molecular studies identified some miR-221 target genes, that were involved in cell cycle inhibition and apoptosis. To further understand miR-221 molecular role in hepatocellular carcinoma development, gene expression profile of miR-221-transfected-SNU-398 cells (derived from human liver cancer) was analyzed through microarray assay and Sylamer algorithm. Results revealed that several down-regulated genes included sequence homology for miR-221 sequence in their 3’UTR, allowing us to identify new potential miR-221 target genes. Pathways analysis performed on the genes identified by this approach revealed that miR-221 affected cell proliferation and apoptosis. Furthermore some miR-221 target genes from Sylamer results were investigated: RB1, WEE1 (cell cycle inhibitors), APAF1 (pro-apoptotic gene), ANXA1, CTCF (transcriptional repressor) were validated as miR-221 target genes, confirming the efficacy of Sylamer analysis and the ability of microRNA to promote HCC tumorigenesis by affecting these pathways. To more directly demonstrate miR-221 oncogenic role, we created a transgenic mouse model of liver miR-221 overexpression. We proved the efficacy of this model by measuring miR-221 hepatic levels and protein expression of some miR-221 target genes (CDKN1B/p27, CDKN1C/p57, BMF), compared to wild type mice. We found that transgenic mice were prone to HCC development, since hepatic nodules were detectable in 50% of 9-12 months-old male animals. Treatment with DENA carcinogen allowed to speed tumor development and we found several liver tumors in 3 months-DENA-treated transgenic animals, while DENA-treated wild type mice developed hepatic cancer 2 months later. Tumors showed high miR-221 levels and low target proteins expression, meaning the microRNA was still present and active in cancer cells. Finally we demonstrated that anti-miR-221 injection in transgenic mice was able to reduce number and size of tumor nodules. tumorigenesis. In vivo studies allowed to demonstrate an important role of miR-221 in HCC development and growth and provided evidence of efficacy of anti-miR-221 oligonucleotide in HCC treatment

Polar-Graded Multiferroic SrMnO3 Thin Films

Engineering defects and strains in oxides provides a promising route for the quest of thin film materials with coexisting ferroic orders, multiferroics, with efficient magnetoelectric coupling at room temperature. Precise control of the strain gradient would enable custom tailoring of the multiferroic properties but presently remains challenging. Here we explore the existence of a polar-graded state in epitaxially strained antiferromagnetic SrMnO3 thin films, whose polar nature was predicted theoretically and recently demonstrated experimentally. By means of aberration-corrected scanning transmission electron microscopy we map the polar rotation of the ferroelectric polarization with atomic resolution, both far from and near the domain walls, and find flexoelectricity resulting from vertical strain gradients. The origin of this particular strain state is a gradual distribution of oxygen vacancies across the film thickness, according to electron energy loss spectroscopy. Herein we present a chemistry-mediated route to induce polar rotations in oxygen-deficient multiferroic films, resulting in flexoelectric polar rotations and with potentially enhanced piezoelectricity

miR-221 affects multiple cancer pathways by modulating the level of hundreds messenger RNAs.

microRNA miR-221 is frequently over-expressed in a variety of human neoplasms. Aim of this study was to identify new miR-221 gene targets to improve our understanding on the molecular tumor-promoting mechanisms affected by miR-221. Gene expression profiling of miR-221-transfected-SNU-398 cells was analyzed by the Sylamer algorithm to verify the enrichment of miR-221 targets among down-modulated genes. This analysis revealed that enforced expression of miR-221 in SNU-398 cells caused the down-regulation of 602 mRNAs carrying sequences homologous to miR-221 seed sequence within their 3'UTRs. Pathways analysis performed on these genes revealed their prominent involvement in cell proliferation and apoptosis. Activation of E2F, MYC, NFkB, and β-catenin pathways was experimentally proven. Some of the new miR-221 target genes, including RB1, WEE1 (cell cycle inhibitors), APAF1 (pro-apoptotic), ANXA1, CTCF (transcriptional repressor), were individually validated as miR-221 targets in SNU-398, HepG2, and HEK293 cell lines. By identifying a large set of miR-221 gene targets, this study improves our knowledge about miR-221 molecular mechanisms involved in tumorigenesis. The modulation of mRNA level of 602 genes confirms the ability of miR-221 to promote cancer by affecting multiple oncogenic pathways

MicroRNAs involvement in fludarabine refractory chronic lymphocytic leukemia

<p>Abstract</p> <p>Background</p> <p>Fludarabine, is one of the most active single agents in the treatment of chronic lymphocytic leukemia (CLL). Over time, however, virtually all CLL patients become fludarabine-refractory. To elucidate whether microRNAs are involved in the development of fludarabine resistance, we analyzed the expression of 723 human miRNAs before and 5-days after fludarabine mono-therapy in 17 CLL patients which were classified as responder or refractory to fludarabine treatment based on NCI criteria.</p> <p>Results</p> <p>By comparing the expression profiles of these two groups of patients, we identified a microRNA signature able to distinguish refractory from sensitive CLLs. The expression of some microRNAs was also able to predict fludarabine resistance of 12 independent CLL patients. Among the identified microRNAs, miR-148a, miR-222 and miR-21 exhibited a significantly higher expression in non-responder patients either before and after fludarabine treatment. After performing messenger RNA expression profile of the same patients, the activation of p53-responsive genes was detected in fludarabine responsive cases only, therefore suggesting a possible mechanism linked to microRNA deregulation in non-responder patients. Importantly, inhibition of miR-21 and miR-222 by anti-miRNA oligonucleotides induced a significant increase in caspase activity in fludarabine-treated p53-mutant MEG-01 cells, suggesting that miR-21 and miR-222 up-regulation may be involved in the establishment of fludarabine resistance.</p> <p>Conclusions</p> <p>This is the first report that reveals the existence of a microRNA profile that differentiate refractory and sensitive CLLs, either before and after fludarabine mono-therapy. A p53 dysfunctional pathway emerged in refractory CLLs and could contribute in explaining the observed miRNA profile. Moreover, this work indicates that specific microRNAs can be used to predict fludarabine resistance and may potentially be used as therapeutic targets, therefore establishing an important starting point for future studies.</p

Occipital atrophy signature in prodromal Lewy bodies disease

Introduction: Dementia with Lewy bodies (DLB) is typically characterized by parietal, temporal, and occipital atrophy, but less is known about the newly defined prodromal phases. The objective of this study was to evaluate structural brain alterations in prodromal DLB (p-DLB) as compared to healthy controls (HC) and full-blown dementia (DLB-DEM). Methods: The study included 42 DLB patients (n = 20 p-DLB; n = 22 DLB-DEM) and 27 HC with a standardized neurological assessment and 3-tesla magnetic resonance imaging. Voxel-wise analyses on gray-matter and cortical thickness were implemented to evaluate differences between p-DLB, DLB-DEM, and HC. Results: p-DLB and DLB-DEM exhibited reduced occipital and posterior parieto-temporal volume and thickness, extending from prodromal to dementia stages. Occipital atrophy was more sensitive than insular atrophy in differentiating p-DLB and HC. Occipital atrophy correlated to frontotemporal structural damage increasing from p-DLB to DLB-DEM. Discussion: Occipital and posterior-temporal structural alterations are an early signature of the DLB continuum and correlate with a long-distance pattern of atrophy

Salinity in Autumn-Winter Season and Fruit Quality of Tomato Landraces

Tomato landraces, originated by adaptive responses to local habitats, are considered a valuable resource for many traits of agronomic interest, including fruit nutritional quality. Primary and secondary metabolites are essential determinants of fruit organoleptic quality, and some of them, such as carotenoids and phenolics, have been associated with beneficial proprieties for human health. Landraces' fruit taste and flavour are often preferred by consumers compared to the commercial varieties' ones. In an autumn-winter greenhouse hydroponic experiment, the response of three Southern-Italy tomato landraces (Ciettaicale, Linosa and Corleone) and one commercial cultivar (UC-82B) to different concentrations of sodium chloride (0 mM, 60 mM or 120 mM NaCl) were evaluated. At harvest, no losses in marketable yield were noticed in any of the tested genotypes. However, under salt stress, fresh fruit yield as well as fruit calcium concentration were higher affected in the commercial cultivar than in the landraces. Furthermore, UC-82B showed a trend of decreasing lycopene and total antioxidant capacity with increasing salt concentration, whereas no changes in these parameters were observed in the landraces under 60 mM NaCl. Landraces under 120 mM NaCl accumulated more fructose and glucose in the fruits, while salt did not affect hexoses levels in UC-82B. Ultra-performance liquid chromatography-tandem mass spectrometry analysis revealed differential accumulation of glycoalkaloids, phenolic acids, flavonoids and their derivatives in the fruits of all genotypes under stress. Overall, the investigated Italian landraces showed a different behaviour compared to the commercial variety UC-82B under moderate salinity stress, showing a tolerable compromise between yield and quality attributes. Our results point to the feasible use of tomato landraces as a target to select interesting genetic traits to improve fruit quality under stress conditions

Serum NFL as a predictor of disease progression in dementia with Lewy bodies

AbstractBackgroundCSF and plasma neurofilament light chain (NfL) levels have been consistently proposed as reliable markers of neurodegeneration able to discriminate between Parkinson's disease (PD) and atypical parkinsonisms. Increased Serum NfL might predict worse motor and cognitive progression in PD patients at single subject level.Methodplasma NfL was assessed in a longitudinal study including 93 patients with Parkinson's disease and 27 patients with DLB who underwent an extensive motor and cognitive assessment and after 2 years of follow‐up. The study evaluated the correlation between NfL plasma levels and motor, non‐motor symptoms, cognitive and behavioral abnormalities in the two cohorts, as well as benignant/malignant phenotypes and motor/cognitive progression in PD after 2 years of follow‐up.ResultSerum NfL correlated with age and age at onset in the cohort. In DLB, NfL correlated with disease duration, hyposmia and neuropsychiatric symptoms, but not with motor function assessed by UPDRS‐III. We found no significant associations between NfL and disease progression in DLB patients. In PD, higher NfL levels correlated with hyposmia (p=0.01), total UPDRS‐II and UPDRS‐III scores (0.001), gait speed (0.04) and several disability milestones, including mild cognitive impairment (0.001), symptomatic dysautonomia (0.001), loss of independency in activities of daily living (p=0.01) and instrumental daily living (p=0.001). At two years of follow‐up, NfL was the best marker in multivariate regression analyses for both motor and cognitive progression beyond malignant/benignant phenotypes.ConclusionElevated serum NfL levels are associated with fast progression in PD patients and could thus represent target of interventions in specific subpopulation of patients