Universal patterns in sound amplitudes of songs and music genres

We report a statistical analysis over more than eight thousand songs. Specifically, we investigate the probability distribution of the normalized sound amplitudes. Our findings seems to suggest a universal form of distribution which presents a good agreement with a one-parameter stretched Gaussian. We also argue that this parameter can give information on music complexity, and consequently it goes towards classifying songs as well as music genres. Additionally, we present statistical evidences that correlation aspects of the songs are directly related with the non-Gaussian nature of their sound amplitude distributions.Comment: Accepted for publication as a Brief Report in Physical Review

Shimanto geosyncline and Kuroshio paleoland

The late Mesozoic to early Neogene geosyncline in the Outer zone of Southwest Japan has been studied in detail in the Kii Peninsula by the Research Group for the Shimanto Geosyncline. The existence of the Kuroshio Paleoland to the south of the geosyncline was inferred by various sedimentologic evidences. The Shimanto belt in the Kii Peninsula is divided from north to south into three zones of Cretaceous, Eocene and Oligocene to lower Miocene. In these belts thick geosynclinal sediments were accumulated showing coarsening upward. The southward migration of the basin occurred in Cretaceous/Eocene, Eocene/Oligocene, and in early Miocene. In the present paper the reconstruction of paleogeography of the Shimanto geosyncline was attempted and the Kuroshio Paleoland was discussed in relation to the geohistory of the Philippine Sea. In spite of the detailed geologic survey in the Kii Peninsula there is no evidence of large exotic blocks nor tectonic mélanges, and this does not support the plate tectonic model ofthe Pacific-type orogeny for the Shimanto belt.ArticleJournal of Physics of the Earth. 26(suppl):357-366 (1978)journal articl

PCNA Ubiquitination Is Important, But Not Essential for Translesion DNA Synthesis in Mammalian Cells

Translesion DNA synthesis (TLS) is a DNA damage tolerance mechanism in which specialized low-fidelity DNA polymerases bypass replication-blocking lesions, and it is usually associated with mutagenesis. In Saccharomyces cerevisiae a key event in TLS is the monoubiquitination of PCNA, which enables recruitment of the specialized polymerases to the damaged site through their ubiquitin-binding domain. In mammals, however, there is a debate on the requirement for ubiquitinated PCNA (PCNA-Ub) in TLS. We show that UV-induced Rpa foci, indicative of single-stranded DNA (ssDNA) regions caused by UV, accumulate faster and disappear more slowly in Pcna(K164R/K164R) cells, which are resistant to PCNA ubiquitination, compared to Pcna(+/+) cells, consistent with a TLS defect. Direct analysis of TLS in these cells, using gapped plasmids with site-specific lesions, showed that TLS is strongly reduced across UV lesions and the cisplatin-induced intrastrand GG crosslink. A similar effect was obtained in cells lacking Rad18, the E3 ubiquitin ligase which monoubiquitinates PCNA. Consistently, cells lacking Usp1, the enzyme that de-ubiquitinates PCNA exhibited increased TLS across a UV lesion and the cisplatin adduct. In contrast, cells lacking the Rad5-homologs Shprh and Hltf, which polyubiquitinate PCNA, exhibited normal TLS. Knocking down the expression of the TLS genes Rev3L, PolH, or Rev1 in Pcna(K164R/K164R) mouse embryo fibroblasts caused each an increased sensitivity to UV radiation, indicating the existence of TLS pathways that are independent of PCNA-Ub. Taken together these results indicate that PCNA-Ub is required for maximal TLS. However, TLS polymerases can be recruited to damaged DNA also in the absence of PCNA-Ub, and perform TLS, albeit at a significantly lower efficiency and altered mutagenic specificity

A neomorphic cancer cell-specific role of MAGE-A4 in trans-lesion synthesis

Trans-lesion synthesis (TLS) is an important DNA-damage tolerance mechanism that permits ongoing DNA synthesis in cells harbouring damaged genomes. The E3 ubiquitin ligase RAD18 activates TLS by promoting recruitment of Y-family DNA polymerases to sites of DNA-damage-induced replication fork stalling. Here we identify the cancer/testes antigen melanoma antigen-A4 (MAGE-A4) as a tumour cell-specific RAD18-binding partner and an activator of TLS. MAGE-A4 depletion from MAGE-A4-expressing cancer cells destabilizes RAD18. Conversely, ectopic expression of MAGE-A4 (in cell lines lacking endogenous MAGE-A4) promotes RAD18 stability. DNA-damage-induced mono-ubiquitination of the RAD18 substrate PCNA is attenuated by MAGE-A4 silencing. MAGE-A4-depleted cells fail to resume DNA synthesis normally following ultraviolet irradiation and accumulate γH2AX, thereby recapitulating major hallmarks of TLS deficiency. Taken together, these results demonstrate a mechanism by which reprogramming of ubiquitin signalling in cancer cells can influence DNA damage tolerance and probably contribute to an altered genomic landscape