On the contribution of the horizontal sea-bed displacements into the tsunami generation process

The main reason for the generation of tsunamis is the deformation of the bottom of the ocean caused by an underwater earthquake. Usually, only the vertical bottom motion is taken into account while the horizontal co-seismic displacements are neglected in the absence of landslides. In the present study we propose a methodology based on the well-known Okada solution to reconstruct in more details all components of the bottom coseismic displacements. Then, the sea-bed motion is coupled with a three-dimensional weakly nonlinear water wave solver which allows us to simulate a tsunami wave generation. We pay special attention to the evolution of kinetic and potential energies of the resulting wave while the contribution of the horizontal displacements into wave energy balance is also quantified. Such contribution of horizontal displacements to the tsunami generation has not been discussed before, and it is different from the existing approaches. The methods proposed in this study are illustrated on the July 17, 2006 Java tsunami and some more recent events.Comment: 30 pages; 14 figures. Accepted to Ocean Modelling. Other authors papers can be downloaded at http://www.lama.univ-savoie.fr/~dutykh

Hydrodynamic modeling of tsunamis from the Currituck landslide

This paper is not subject to U.S. copyright. The definitive version was published in Marine Geology 264 (2009): 41-52, doi:10.1016/j.margeo.2008.09.005.Tsunami generation from the Currituck landslide offshore North Carolina and propagation of waves toward the U.S. coastline are modeled based on recent geotechnical analysis of slide movement. A long and intermediate wave modeling package (COULWAVE) based on the non-linear Boussinesq equations are used to simulate the tsunami. This model includes procedures to incorporate bottom friction, wave breaking, and overland flow during runup. Potential tsunamis generated from the Currituck landslide are analyzed using four approaches: (1) tsunami wave history is calculated from several different scenarios indicated by geotechnical stability and mobility analyses; (2) a sensitivity analysis is conducted to determine the effects of both landslide failure duration during generation and bottom friction along the continental shelf during propagation; (3) wave history is calculated over a regional area to determine the propagation of energy oblique to the slide axis; and (4) a high-resolution 1D model is developed to accurately model wave breaking and the combined influence of nonlinearity and dispersion during nearshore propagation and runup. The primary source parameter that affects tsunami severity for this case study is landslide volume, with failure duration having a secondary influence. Bottom friction during propagation across the continental shelf has a strong influence on the attenuation of the tsunami during propagation. The high-resolution 1D model also indicates that the tsunami undergoes nonlinear fission prior to wave breaking, generating independent, short-period waves. Wave breaking occurs approximately 40–50 km offshore where a tsunami bore is formed that persists during runup. These analyses illustrate the complex nature of landslide tsunamis, necessitating the use of detailed landslide stability/mobility models and higher-order hydrodynamic models to determine their hazard.Research conducted by Lynett for this paper was partially supported by grants from the National Science Foundation (CBET- 0427014, CMMI-0619083)

Mass spectrometry of short peptides reveals common features of metazoan peptidergic neurons

The evolutionary origins of neurons remain unknown. Although recent genome data of extant early-branching animals have shown that neural genes existed in the common ancestor of animals, the physiological and genetic properties of neurons in the early evolutionary phase are still unclear. Here, we performed a mass spectrometry-based comprehensive survey of short peptides from early-branching lineages Cnidaria, Porifera and Ctenophora. We identified a number of mature ctenophore neuropeptides that are expressed in neurons associated with sensory, muscular and digestive systems. The ctenophore peptides are stored in vesicles in cell bodies and neurites, suggesting volume transmission similar to that of cnidarian and bilaterian peptidergic systems. A comparison of genetic characteristics revealed that the peptide-expressing cells of Cnidaria and Ctenophora express the vast majority of genes that have pivotal roles in maturation, secretion and degradation of neuropeptides in Bilateria. Functional analysis of neuropeptides and prediction of receptors with machine learning demonstrated peptide regulation of a wide range of target effector cells, including cells of muscular systems. The striking parallels between the peptidergic neuronal properties of Cnidaria and Bilateria and those of Ctenophora, the most basal neuron-bearing animals, suggest a common evolutionary origin of metazoan peptidergic nervous systems

Drag reduction in turbulent channel flow using bidirectional wavy Lorentz force

Turbulent control and drag reduction in a channel flow via a bidirectional traveling wave induced by spanwise oscillating Lorentz force have been investigated in the paper. The results based on the direct numerical simulation (DNS) indicate that the bidirectional wavy Lorentz force with appropriate control parameters can result in a regular decline of near-wall streaks and vortex structures with respect to the flow direction, leading to the effective suppression of turbulence generation and significant reduction in skin-friction drag. In addition, experiments are carried out in a water tunnel via electro-magnetic (EM) actuators designed to produce the bidirectional traveling wave excitation as described in calculations. As a result, the actual substantial drag reduction is realized successfully in these experiments

Changes in Glial Cell Line-derived Neurotrophic Factor Expression in the Rostral and Caudal Stumps of the Transected Adult Rat Spinal Cord

Limited information is available regarding the role of endogenous Glial cell line-derived neurotrophic factor (GDNF) in the spinal cord following transection injury. The present study investigated the possible role of GDNF in injured spinal cords following transection injury (T9–T10) in adult rats. The locomotor function recovery of animals by the BBB (Basso, Beattie, Bresnahan) scale score showed that hindlimb support and stepping function increased gradually from 7 days post operation (dpo) to 21 dpo. However, the locomotion function in the hindlimbs decreased effectively in GDNF-antibody treated rats. GDNF immunoreactivty in neurons in the ventral horn of the rostral stump was stained strongly at 3 and 7 dpo, and in the caudal stump at 14 dpo, while immunostaining in astrocytes was also seen at all time-points after transection injury. Western blot showed that the level of GDNF protein underwent a rapid decrease at 7 dpo in both stumps, and was followed by a partial recovery at a later time-point, when compared with the sham-operated group. GDNF mRNA-positive signals were detected in neurons of the ventral horn, especially in lamina IX. No regenerative fibers from corticospinal tract can be seen in the caudal segment near the injury site using BDA tracing technique. No somatosensory evoked potentials (SEP) could be recorded throughout the experimental period as well. These findings suggested that intrinsic GDNF in the spinal cord could play an essential role in neuroplasticity. The mechanism may be that GDNF is involved in the regulation of local circuitry in transected spinal cords of adult rats

Restriction of trophic factors and nutrients induces PARKIN expression

Parkinson’s disease (PD) is the most frequent neurodegenerative movement disorder and manifests at old age. While many details of its pathogenesis remain to be elucidated, in particular the protein and mitochondrial quality control during stress responses have been implicated in monogenic PD variants. Especially the mitochondrial kinase PINK1 and the ubiquitin ligase PARKIN are known to cooperate in autophagy after mitochondrial damage. As autophagy is also induced by loss of trophic signaling and PINK1 gene expression is modulated after deprivation of cytokines, we analyzed to what extent trophic signals and starvation stress regulate PINK1 and PARKIN expression. Time course experiments with serum deprivation and nutrient starvation of human SH-SY5Y neuroblastoma cells and primary mouse neurons demonstrated phasic induction of PINK1 transcript up to twofold and PARKIN transcript levels up to sixfold. The corresponding threefold starvation induction of PARKIN protein was limited by its translocation to lysosomes. Analysis of primary mouse cells from PINK1-knockout mice indicated that PARKIN induction and lysosomal translocation occurred independent of PINK1. Suppression of the PI3K-Akt-mTOR signaling by pharmacological agents modulated PARKIN expression accordingly. In conclusion, this expression survey demonstrates that PARKIN and PINK1 are coregulated during starvation and suggest a role of both PD genes in response to trophic signals and starvation stress

Gene Expression Profiles in Parkinson Disease Prefrontal Cortex Implicate FOXO1 and Genes under Its Transcriptional Regulation

Parkinson disease (PD) is a complex neurodegenerative disorder with largely unknown genetic mechanisms. While the degeneration of dopaminergic neurons in PD mainly takes place in the substantia nigra pars compacta (SN) region, other brain areas, including the prefrontal cortex, develop Lewy bodies, the neuropathological hallmark of PD. We generated and analyzed expression data from the prefrontal cortex Brodmann Area 9 (BA9) of 27 PD and 26 control samples using the 44K One-Color Agilent 60-mer Whole Human Genome Microarray. All samples were male, without significant Alzheimer disease pathology and with extensive pathological annotation available. 507 of the 39,122 analyzed expression probes were different between PD and control samples at false discovery rate (FDR) of 5%. One of the genes with significantly increased expression in PD was the forkhead box O1 (FOXO1) transcription factor. Notably, genes carrying the FoxO1 binding site were significantly enriched in the FDR–significant group of genes (177 genes covered by 189 probes), suggesting a role for FoxO1 upstream of the observed expression changes. Single-nucleotide polymorphisms (SNPs) selected from a recent meta-analysis of PD genome-wide association studies (GWAS) were successfully genotyped in 50 out of the 53 microarray brains, allowing a targeted expression–SNP (eSNP) analysis for 52 SNPs associated with PD affection at genome-wide significance and the 189 probes from FoxO1 regulated genes. A significant association was observed between a SNP in the cyclin G associated kinase (GAK) gene and a probe in the spermine oxidase (SMOX) gene. Further examination of the FOXO1 region in a meta-analysis of six available GWAS showed two SNPs significantly associated with age at onset of PD. These results implicate FOXO1 as a PD–relevant gene and warrant further functional analyses of its transcriptional regulatory mechanisms