Biomechanical Analysis of Body Movement During Skiing Over Bumps

Maintenance of balance of the skier's body is one of the most important and basic techniques in skiing on slopes of various conditions. However, skiers, especially beginners are likely to lose their balance on an uneven terrain with dips and swells. In order to keep his balance during skiing on an uneven terrain, it seems to be important for a skier to avoid receiving impulse from the snow surface. Some investigations have been conducted about maintenance of balance of body during skiing over artificially constructed bumps by means of electromyography (Miyashita and Sakurai, 1979), electrogoniometry (Iizuka and Miyashita, 1979) and cinematography (Miyashita and Sakurai, 1979, Iizuka and Miyashita, 1979, Sodeyama et al., 1979 and Ikegami et al. 1985). However, there is no research to try to measure force or acceleration acting on the skier's body during running over bumps. Therefore the purpose of this study is to measure force acting on skier's body by analyzing the movement of skier's body mechanically as well as kinematically, and to find out essential motions to maintain the balance of skier's body against rapid change of force acting from snow surface while skiing over bumps on a straight downhill run

Connectivity-based parcellation of the thalamus explains specific cognitive and behavioural symptoms in patients with bilateral thalamic infarct

A novel approach based on diffusion tractography was used here to characterise the cortico-thalamic connectivity in two patients, both presenting with an isolated bilateral infarct in the thalamus, but exhibiting partially different cognitive and behavioural profiles. Both patients (G.P. and R.F.) had a pervasive deficit in episodic memory, but only one of them (R.F.) suffered also from a dysexecutive syndrome. Both patients had an MRI scan at 3T, including a T1-weighted volume. Their lesions were manually segmented. T1-volumes were normalised to standard space, and the same transformations were applied to the lesion masks. Nineteen healthy controls underwent a diffusion-tensor imaging (DTI) scan. Their DTI data were normalised to standard space and averaged. An atlas of Brodmann areas was used to parcellate the prefrontal cortex. Probabilistic tractography was used to assess the probability of connection between each voxel of the thalamus and a set of prefrontal areas. The resulting map of corticothalamic connections was superimposed onto the patients' lesion masks, to assess whether the location of the thalamic lesions in R.F. (but not in G. P.) implied connections with prefrontal areas involved in dysexecutive syndromes. In G.P., the lesion fell within areas of the thalamus poorly connected with prefrontal areas, showing only a modest probability of connection with the anterior cingulate cortex (ACC). Conversely, R.F.'s lesion fell within thalamic areas extensively connected with the ACC bilaterally, with the right dorsolateral prefrontal cortex, and with the left supplementary motor area. Despite a similar, bilateral involvement of the thalamus, the use of connectivity-based segmentation clarified that R.F.'s lesions only were located within nuclei highly connected with the prefrontal cortical areas, thus explaining the patient's frontal syndrome. This study confirms that DTI tractography is a useful tool to examine in vivo the effect of focal lesions on interconnectivity brain patterns

Electronic Structure Calculation by First Principles for Strongly Correlated Electron Systems

Recent trends of ab initio studies and progress in methodologies for electronic structure calculations of strongly correlated electron systems are discussed. The interest for developing efficient methods is motivated by recent discoveries and characterizations of strongly correlated electron materials and by requirements for understanding mechanisms of intriguing phenomena beyond a single-particle picture. A three-stage scheme is developed as renormalized multi-scale solvers (RMS) utilizing the hierarchical electronic structure in the energy space. It provides us with an ab initio downfolding of the global band structure into low-energy effective models followed by low-energy solvers for the models. The RMS method is illustrated with examples of several materials. In particular, we overview cases such as dynamics of semiconductors, transition metals and its compounds including iron-based superconductors and perovskite oxides, as well as organic conductors of kappa-ET type.Comment: 44 pages including 38 figures, to appear in J. Phys. Soc. Jpn. as an invited review pape

Methamphetamine induces Shati/Nat8L expression in the mouse nucleus accumbens via CREB- and dopamine D1 receptor-dependent mechanism

Shati/Nat8L significantly increased in the nucleus accumbens (NAc) of mice after repeated methamphetamine (METH) treatment. We reported that Shati/Nat8L overexpression in mouse NAc attenuated METH-induced hyperlocomotion, locomotor sensitization, and conditioned place preference. We recently found that Shati/Nat8L overexpression in NAc regulates the dopaminergic neuronal system via the activation of group II mGluRs by elevated Nacetylaspartylglutamate following N-acetylaspartate increase due to the overexpression. These findings suggest that Shati/Nat8L suppresses METH-induced responses. However, the mechanism by which METH increases the Shati/Nat8L mRNA expression in NAc is unclear. To investigate the regulatory mechanism of Shati/Nat8L mRNA expression, we performed a mouse Shati/Nat8L luciferase assay using PC12 cells. Next, we investigated the response of METH to Shati/Nat8L expression and CREB activity using mouse brain slices of NAc, METH administration to mice, and western blotting for CREB activity of specific dopamine receptor signals in vivo and ex vivo. We found that METH activates CREB binding to the Shati/Nat8L promoter to induce the Shati/Nat8L mRNA expression. Furthermore, the dopamine D1 receptor antagonist SCH23390, but not the dopamine D2 receptor antagonist sulpiride, inhibited the upregulation of Shati/Nat8L and CREB activities in the mouse NAc slices. Thus, the administration of the dopamine D1 receptor agonist SKF38393 increased the Shati/Nat8L mRNA expression in mouse NAc. These results showed that the Shati/ Nat8L mRNA was increased by METH-induced CREB pathway via dopamine D1 receptor signaling in mouse NAc. These findings may contribute to development of a clinical tool for METH addiction

Anti-Hu antibodies activate enteric and sensory neurons.

IgG of type 1 anti-neuronal nuclear antibody (ANNA-1, anti-Hu) specificity is a serological marker of paraneoplastic neurological autoimmunity (including enteric/autonomic) usually related to small-cell lung carcinoma. We show here that IgG isolated from such sera and also affinity-purified anti-HuD label enteric neurons and cause an immediate spike discharge in enteric and visceral sensory neurons. Both labelling and activation of enteric neurons was prevented by preincubation with the HuD antigen. Activation of enteric neurons was inhibited by the nicotinic receptor antagonists hexamethonium and dihydro-β-erythroidine and reduced by the P2X antagonist pyridoxal phosphate-6-azo (benzene-2,4-disulfonic acid (PPADS) but not by the 5-HT3 antagonist tropisetron or the N-type Ca-channel blocker ω-Conotoxin GVIA. Ca(++) imaging experiments confirmed activation of enteric neurons but not enteric glia. These findings demonstrate a direct excitatory action of ANNA-1, in particular anti-HuD, on visceral sensory and enteric neurons, which involves nicotinic and P2X receptors. The results provide evidence for a novel link between nerve activation and symptom generation in patients with antibody-mediated gut dysfunction

Isoaspartylation appears to trigger small cell lung cancer-associated autoimmunity against neuronal protein ELAVL4

Autoantibodies against SCLC-associated neuronal antigen ELAVL4 (HuD) have been linked to smaller tumors and improved survival, but the antigenic epitope and mechanism of autoimmunity have never been solved. We report that recombinant human ELAVL4 protein incubated under physiological conditions acquires isoaspartylation, a type of immunogenic protein damage. Specifically, the N-terminal region of ELAVL4, previously implicated in SCLC-associated autoimmunity, undergoes isoaspartylation in vitro, is recognized by sera from anti-ELAVL4 positive SCLC patients and is highly immunogenic in subcutaneously injected mice and in vitro stimulated human lymphocytes. Our data suggest that isoaspartylated ELAVL4 is the trigger for the SCLC-associated anti-ELAVL4 autoimmune response

Association of a polymorphism of the transforming growth factor-ß1 gene with cerebral amyloid angiopathy

Background: A recent study showed that transforming growth factor-ß1 (TGF-ß1) induces amyloid-ß deposition in cerebral blood vessels and meninges of a transgenic mouse model of Alzheimer's disease (AD), and that TGF-ß1 mRNA levels are correlated with cerebral amyloid angiopathy (CAA) in human AD brains. A T/C polymorphism at codon 10 in exon 1 of the TGF-ß1 gene has been reported to be associated with the serum TGF-ß1 concentration. We investigated whether the TGF-ß1 polymorphism is associated with the risk of CAA. Methods: The association between the severity of CAA and the T/C polymorphism at codon 10 in exon 1 of the TGF-ß1 was investigated in 167 elderly Japanese autopsy cases, including 73 patients with AD. The apolipoprotein E (APOE) genotype was also determined. Results: The genotypes (TT/ TC/ CC) were associated with the severity of CAA significantly in all patients (p = 0.0026), in non-AD patients (p = 0.011), and APOE non-ε4 carriers (p = 0.0099), but not in AD patients or APOE ε4 carriers. The number of the T alleles positively correlated with the severity of CAA in all patients (p = 0.0011), non-AD patients (p = 0.0026), and APOE non-ε4 carriers (p = 0.0028), but not in AD patients or APOE ε4 carriers. The polymorphism was not significantly associated with AD. Conclusions: Our results suggest that the polymorphism in TGF-ß1 is associated with the severity of CAA, especially in non-AD patients and APOE non-ε4 carriers