Apparent multiple Delta m^2_32 in muon anti-neutrino and muon neutrino survival oscillations from non-standard interaction matter effect

Neutrinos propagating through matter may participate in forward coherent neutral-current-like scattering arising from non-standard interactions as well as from the Mikheyev-Smirnov-Wolfenstein matter potential $V_e$. We show that at fixed long baselines through matter of constant density, the non-standard interaction potential $\epsilon_{\mu\tau} V_e$ can contribute an additional term to the oscillation phase whose sign differs for \anumu versus \numu propagation in matter. Its presence can cause different apparent $\Delta m^2$ to be erroneously inferred on the basis of oscillations in vacuum, with values lying above (for \anumu) or below (for \numu) the actual $\Delta m^2_{32}$ for the case where $\epsilon_{\mu\tau}$ is predominantly real-valued and of sign opposite to $\Delta m_{32}^2$. An NSI scenario invoking only $\Re(\epsilon_{\mu\tau})$ is shown to be capable of accounting for a disparity recently reported between oscillation survival for \anumu and \numu fluxes measured at $735~\mathrm{km}$ by the MINOS experiment. Implications for mantle traversal by atmospheric neutrinos are examined. The NSI matter potential with non-maximal mixing could evade conventional atmospheric neutrino analyses which do not distinguish \numu from \anumu on an event-by-event basis.Comment: 7 pages, 5 figures. Accepted for publication in Physical Review

Genetic changes of MLH1 and MSH2 genes could explain constant findings on microsatellite instability in intracranial meningioma

Postreplicative mismatch repair safeguards the stability of our genome. The defects in its functioning will give rise to microsatellite instability. In this study, 50 meningiomas were investigated for microsatellite instability. Two major mismatch repair genes, MLH1 and MSH2, were analyzed using microsatellite markers D1S1611 and BAT26 amplified by polymerase chain reaction and visualized by gel electrophoresis on high-resolution gels. Furthermore, genes DVL3 (D3S1262), AXIN1 (D16S3399), and CDH1 (D16S752) were also investigated for microsatellite instability. Our study revealed constant presence of microsatellite instability in meningioma patients when compared to their autologous blood DNA. Altogether 38% of meningiomas showed microsatellite instability at one microsatellite locus, 16% on two, and 13.3% on three loci. The percent of detected microsatellite instability for MSH2 gene was 14%, and for MLH1, it was 26%, for DVL3 22.9%, for AXIN1 17.8%, and for CDH1 8.3%. Since markers also allowed for the detection of loss of heterozygosity, gross deletions of MLH1 gene were found in 24% of meningiomas. Genetic changes between MLH1 and MSH2 were significantly positively correlated (p = 0.032). We also noted a positive correlation between genetic changes of MSH2 and DVL3 genes (p = 0.034). No significant associations were observed when MLH1 or MSH2 was tested against specific histopathological meningioma subtype or World Health Organization grade. However, genetic changes in DVL3 were strongly associated with anaplastic histology of meningioma (χ2 = 9.14; p = 0.01). Our study contributes to better understanding of the genetic profile of human intracranial meningiomas and suggests that meningiomas harbor defective cellular DNA mismatch repair mechanisms

Brain metastases from lung cancer show increased expression of DVL1, DVL3 and beta-catenin and down-regulation of E-cadherin

The susceptibility of brain to secondary formation from lung cancer primaries is a well-known phenomenon. In contrast, the molecular basis for invasion and metastasis to the brain is largely unknown. In the present study, 31 brain metastases that originated from primary lung carcinomas were analyzed regarding over expression of Dishevelled-1 (DVL1), Dishevelled-3 (DVL3), E-cadherin (CDH1) and beta-catenin (CTNNB1). Protein expressions and localizations were analyzed by immunohistochemistry. Genetic alterations of E-cadherin were tested by polymerase chain reaction (PCR)/loss of heterozygosity (LOH). Heteroduplex was used to investigate mutations in beta-catenin. DVL1 and DVL3 showed over expression in brain metastasis in 87.1% and 90.3% of samples respectively. Nuclear staining was observed in 54.8% of cases for DVL1 and 53.3% for DVL3. The main effector of the Wnt signaling, beta-catenin, was up-regulated in 56%, and transferred to the nucleus in 36% of metastases. When DVL1 and DVL3 were up-regulated the number of cases with nuclear beta-catenin significantly increased (p=0.0001). Down-regulation of E-cadherin was observed in 80% of samples. Genetic analysis showed 36% of samples with LOH of the CDH1. In comparison to other lung cancer pathologies, the diagnoses adenocarcinoma and small cell lung cancer (SCLC) were significantly associated to CDH1 LOH (p=0.001). Microsatellite instability was detected in one metastasis from adenocarcinoma. Exon 3 of beta-catenin was not targeted. Altered expression of Dishevelled-1, Dishevelled-3, E-cadherin and beta-catenin were present in brain metastases which indicates that Wnt signaling is important and may contribute to better understanding of genetic profile conditioning lung cancer metastasis to the brain

La réconciliation germano-tchèque : sprint après la course de fond

abstract : Through the question of the price of freedom, a question directly related to the reparations to be paid to East European victims of Nazism and, thus, to the end of a bipolar world, a long-coming, difficult process is described: German-Czech reconciliation, the "ugly duckling" of Germany's relations with central Europe. Whereas Germany's relations with its central European neighbors took a hopeful turn after 1989, no new start could be made in relations with the Czech Republic before both parties accepted to openly face a tragic past, covered up on both sides. The consequences had to be drawn in material as well as moral terms.À travers la question du prix de la liberté, question directement liée au dédommagement des victimes est-européennes du nazisme et par là même à la fin d'un monde bipolaire, l'auteur s'attache à nous décrire un processus de réconciliation aussi tardif que difficile : le processus de réconciliation germano-tchèque, qui a fait longtemps office de « vilain petit canard » (pour reprendre les termes de l'auteur) des relations entre l'Allemagne et l'Europe centrale. Alors que la question des relations de l'Allemagne avec ses voisins centre-européens se posait dans des termes nouveaux après 1989, offrant une chance pour un nouveau départ, dans le cas des relations germano-tchèques, celui-ci ne put avoir effectivement lieu que lorsque les deux parties acceptèrent d'affronter ouvertement un passé tragique, occulté de part et d'autre, et d'en tirer les conséquences qui s'imposaient en termes aussi bien matériels que moraux.Kafka Tomas, Perron Catherine. La réconciliation germano-tchèque : sprint après la course de fond. In: Revue d'études comparatives Est-Ouest, vol. 31, 2000, n°1. l'Allemagne et l'Europe centrale à l'heure de la réconciliation, sous la direction de Anne Bazin et Catherine Perron. pp. 97-108

Genetic changes observed in a case of adult pilocytic astrocytoma revealed by array CGH analysis

BACKGROUND A palette of copy number changes in a case of adult pilocytic astrocytoma analyzed by Array Comparative Genomic Hybridization (aCGH) is presented. Pilocytic astrocytomas are specific gliomas that are benign and biologically distinct and the molecular mechanisms responsible for their development remain unexplained. The aCGH was performed using SurePrint G3 Human CGH microarrays 4 × 180 K (Agilent Technologies). To ascertain whether some of the aberrations were of constitutive nature, we also analyzed the blood sample from the same patient. ----- RESULTS The result of aCGH analysis demonstrated differences in the tumor tissue when compared to normal control on the array and also to autologous DNA from patient's blood. The total number of aberrations found in our case was 41 including 37 deletions and 4 amplifications. Whole chromosomal gains and losses were not observed. Collectively, our results showed three deletions and one amplification at 1p, two deletions at 2q, two deletions at 4q, two deletion at 5q, two deletions at 7p and two deletions at 7q; there were also three deletions at 8q, one deletion at 9p, one deletion at 10p, three deletions and one amplification at 10q. Chromosome 11 showed two deletions at 11p, while there was one deletion at 12p and one at 12q. Four deletions at 14q; two deletions at 15q, one amplification at 17q and one deletion at 17q; one deletion at 18p, two deletions at 22q and finally one deletion at Xp and one deletion and one amplification at Xq. Among the signaling pathways, olfactory transduction, Fc gamma R-mediated phagocytosis and p53 signaling pathway showed significant enrichment ascertained by gene ontology (GO) analysis using the DAVID software. ----- CONCLUSIONS Our aCGH analysis is bringing subtle genomic alterations thus broadening genetic spectrum of adult pilocytic astrocytoma in order to offer new molecular biomarkers that will help in diagnostics and therapeutic decision-making

Expression Levels and Localizations of DVL3 and sFRP3 in Glioblastoma

The expression patterns of critical molecular components of Wnt signaling, sFRP3 and DVL3, were investigated in glioblastoma, the most aggressive form of primary brain tumors, with the aim to offer potential biomarkers. The protein expression levels and localizations in tumor tissue were revealed by immunohistochemistry and evaluated by the semiquantitative method and immunoreactivity score. Majority of glioblastomas had moderate expression levels for both DVL3 (52.4%) and sFRP3 (52.3%). Strong expression levels were observed in 23.1% and 36.0% of samples, respectively. DVL3 was localized in cytoplasm in 97% of glioblastomas, of which 44% coexpressed the protein in the nucleus. sFRP3 subcellular distribution showed that it was localized in the cytoplasm in 94% of cases. Colocalization in the cytoplasm and nucleus was observed in 50% of samples. Wilcox test indicated that the domination of the strong signal is in connection with simultaneous localization of DVL3 protein in the cytoplasm and the nucleus. Patients with strong expression of DVL3 will significantly more often have the protein in the nucleus (P=6.33×10−5). No significant correlation between the two proteins was established, nor were their signal strengths correlated with epidemiological parameters. Our study contributes to better understanding of glioblastoma molecular profile

Enabling Efficient Discovery of and Access to Spatial Data Services

Spatial data represent valuable information and a basis for decision making processes in society. The number of specialisms that use spatial data for such purposes is increasing. Increasing is also the number of services enabling to search, access, process, analyse or visualise spatial data. Standardisation activities of the Open Geospatial Consortium (OGC) support standardised sharing of services through the Web. However, many services declared as OGC compliant do not respond or they are not available. The paper introduces an innovative solution for efficient discovery of and access to spatial data services compliant with OGC specifications. The research was performed in the context of the EnviroGRIDS geoportal. Several thousands of harvested services were quality checked and the summary of the testing including the identified problems are presented

Wnt signaling transcription factors TCF-1 and LEF-1 are upregulated in malignant astrocytic brain tumors

Since the discovery of the TCF/LEF family of transcription factors, their functions have been under intensive investigation in the area of cancer biology. The work presented in this paper focused on the changes in TCF-1 and LEF-1 expression levels in a set of astrocytic brain tumors. Protein expression was detected using immunohistochemistry and then evaluated by Ellipse software (ViDiTo, Slovakia). Statistical evaluations were performed with the SPSS statistical package, version 14.0 (SPSS Inc., Chicago, IL, USA). Strong TCF-1 and LEF-1 expression was observed in 51.6% and 71% of glioblastoma samples. Statistical analysis confirmed significant differences in protein expression levels associated to 3 important values, weak expression of TCF-1, weak expression of LEF-1 and strong expression of LEF-1. Analysis of variances performed on the total sample also indicated significant differences in the values of TCF-1 weak (F=2.804; p=0.045), LEF-1 weak (F=4.255; p=0.008) and LEF-1 strong (F=5.498; p=0.002) with regard to malignancy grade. Thus, glioblastomas were characterized by –in relative terms- the lowest values for weak expression of TCF-1 and LEF-1, combined with the highest values of LEF-1 strong expression. The F-ratios for two variables (LEF-1 strong and LEF-1 weak) indicated that differences between astrocytomas (II, III) and glioblastomas were statistically significant (p<0.02). Discriminant function analysis further showed that strong LEF-1 expression alone could discriminate between astrocytomas (II, III) and glioblastomas. Elevated TCF-1 and LEF-1 expression is characteristic of malignant gliomas. LEF-1, in particular, may serve as a potential marker for malignant transformation