STRUCTURE OF SODIUM ALUMINOSILICATE GLASSES : T1 LUMINESCENCE SPECTROSCOPY

Les spectres optiques des ions Tl+, correspondant à une émission à 350 nm, ont été mesurés dans des verres d'aluminosilicate de sodium. Les spectres mettent en évidence deux contributions dues respectivement à T1+ agissant comme modifieur du réseau ou comme compensateur de charge pour l'aluminium. Quand le rapport Al/Na devient plus grand que 1, le spectre de compensation de charge est seul observé. En dessous de 1, le spectre de modifieur du réseau prend de plus en plus d'importance quand Al/Na décroît. Ceci est bien en accord avec le modèle traditionnel des structures d'aluminosilicate alcalins, où la composition critique pour la disparition des oxygènes non-pontants est donnée par Al/Na = 1.Optical excitation spectra of Tl+ ions, corresponding to emission at 350 nm, have been measured in Na aluminosilicate glasses. The excitation spectra are shown to be superpositions of two primary spectra, which are identified with T1+ acting as network modifiers or as charge compensators for network aluminums. When Al/Na ≥ 1, only the charge compensator spectrum can be observed. As Al/Na decreases below unity, the fraction of the charge compensator spectrum decreases rapidly, and the fraction of the network modifier spectrum increases correspondingly. These results strongly support the traditional model of alkali aluminosilicate structure, in which the critical compositions for (dis)appearance of nonbridging oxygens are given by Al/Na = 1 ; they contradict reports of XPS measurements from which it had been concluded that the critical compositions are given by Al/Na ≈ 0.7. The network modifier spectra do not depend strongly on glass composition, whereas the charge compensator peaks vary significantly with composition. These results are fully consistant with new oxygen is XPS spectra

STRUCTURE OF SODIUM ALUMINOSILICATE GLASSES : X-RAY PHOTOELECTRON SPECTROSCOPY

Plusieurs séries de verre d'aluminosilicate de sodium ont été étudiées par spectroscopie des photoélectrons X (XPS) de l'oxygène. Les spectres sont interprétés sur la base de l'existence de 3 types d'environnement de l'oxygène : des oxygènes pontants symétriques BO1 (Si-O-Si), des oxygènes pontants asymétriques BO2 (Si-O-Al) et des oxygènes non-pontants NBO (Si-O-, Na+) . Les résultats sont compatibles avec la théorie classique qui prédit que la fraction d'oxygène non-pontant tend vers zéro quand le rapport Al/Na croît de 0 à 1, et que le rapport BO2/BO1 croît constamment.X-ray photoelectron spectroscopy (X.P.S) of the oxygen O1S spectra has been measured in several series of sodium alumino silicate glasses. The spectra are interpreted in terms of 3 types of oxygen environment : - a symmetric bridging oxygen - BO1 (Si-O-Si), an assymmetric bridging oxygen - BO2 (Si-O-Al), and a non-bridging oxygen - NBO (Si-O-, Na+). The results are in agreement with the classical theory which predicts that the fraction of non-bridging oxygen atoms fNBO → 0 as Al/Na increases from zero to unity, and the ratio BO2/BO1 steadily increases

Pan-cancer analysis of whole genomes

Cancer is driven by genetic change, and the advent of massively parallel sequencing has enabled systematic documentation of this variation at the whole-genome scale. Here we report the integrative analysis of 2,658 whole-cancer genomes and their matching normal tissues across 38 tumour types from the Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium of the International Cancer Genome Consortium (ICGC) and The Cancer Genome Atlas (TCGA). We describe the generation of the PCAWG resource, facilitated by international data sharing using compute clouds. On average, cancer genomes contained 4-5 driver mutations when combining coding and non-coding genomic elements; however, in around 5% of cases no drivers were identified, suggesting that cancer driver discovery is not yet complete. Chromothripsis, in which many clustered structural variants arise in a single catastrophic event, is frequently an early event in tumour evolution; in acral melanoma, for example, these events precede most somatic point mutations and affect several cancer-associated genes simultaneously. Cancers with abnormal telomere maintenance often originate from tissues with low replicative activity and show several mechanisms of preventing telomere attrition to critical levels. Common and rare germline variants affect patterns of somatic mutation, including point mutations, structural variants and somatic retrotransposition. A collection of papers from the PCAWG Consortium describes non-coding mutations that drive cancer beyond those in the TERT promoter; identifies new signatures of mutational processes that cause base substitutions, small insertions and deletions and structural variation; analyses timings and patterns of tumour evolution; describes the diverse transcriptional consequences of somatic mutation on splicing, expression levels, fusion genes and promoter activity; and evaluates a range of more-specialized features of cancer genomes