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

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

Temporal and sequential changes of glial cells and cytokine expression during neuronal degeneration after transient global ischemia in rats

<p>Abstract</p> <p>Background</p> <p>How glial cells and cytokines are associated with the progression of delayed neuronal death induced by transient global ischemia is still unclear. To further clarify this point, we studied morphological changes in glial cells (microglial cells and astrocytes), and cytokine protein levels, during the progression of neuronal cell loss in CA1 (Cornu Ammonis 1) of the hippocampus after transient global ischemia.</p> <p>Methods</p> <p>Morphological changes in glial cells were studied immuno-histochemically. Nine cytokines (IL-1α, IL-1β, IL-2, IL-4, IL-6, IL-10, GM-CSF, IFN-γ and TNF-α) were simultaneously measured by a multiplexed bead-based immunoassay from 6 h to day21 after transient four vessel occlusion (4VO) in rats.</p> <p>Results</p> <p>During the process of neuronal loss, we observed four distinct phases: (1) lag phase day0-2 (no NeuN+ cell loss observed), (2) exponential phase day2-7 (NeuN+ cells reduced in number exponentially), (3) deceleration phase day7-14 (reduction rate of NeuN+ cells became low), (4) stationary phase day14 onward (NeuN+ cell loss progressed no longer). In the lag phase, activated glial cells were observed in the entire hippocampus but later were gradually restricted to CA1. Cytokine protein levels in the lag and exponential phases were lower than in the deceleration and stationary phases. IL-1α, IL-1β, IL-4, IL-6 and IFN-γ in 4VO were significantly higher in all four phases than in sham. Compared with sham level, GM-CSF was significantly high in the deceleration phase. TNF-α was significantly high in both the deceleration and stationary phases.</p> <p>Conclusion</p> <p>Ischemic stress in 4VO activated glial cells in areas beyond CA1 in the lag phase. Pyramidal neurons were injured in CA1 from the end of the lag phase and then neuronal cells reduced in CA1 in the exponential phase. After neuronal death began, the influence of dead cells on glial cells and cytokine expression gradually became stronger than the influence by ischemic stress. Therefore, from the deceleration phase, changes in glial cells and cytokine production were likely caused by dead cells. Cytokine interaction in the microenvironment may determine the functions of IL-1α, IL-1β, IL-4, IL-6 and IFN-γ in all four phases. The function of GM-CSF and TNF-α in the deceleration phase may be neurotrophic.</p

Gerstmann-Straussler-Scheinker disease in an Alsatian family: clinical and genetic studies

The clinical progression of Gerstmann-Straussler-Scheinker disease in a family of Alsatian origin is reported. The age of onset and the duration of evolution were variable. The clinical picture became more complex over the generations: in the first generations, isolated dementia and in later generations a triad of pyramidal, pseudobulbar syndromes and dementia associated with spinal cord and cerebellar features. Prion gene analysis showed that four surviving patients carry double missense changes at codons 117 and 129, identical to those found in one case at necropsy and 10 other healthy members of the family. The missense changes were not found in 100 controls. No member of the family had modification of condons 102, 178, or 200. The lod score suggests linkage between the missense change at codon 117 and Gerstmann- Straussler-Scheinker disease in this family