Koji Yamanaka

A new state transition matrix is described for the nonlinear problem of relative motion on an arbitrary elliptical orbit. A linearization is performed, leading to a set of linear differential equations with time-dependentcoefficients. A new and simpler solution to those equations is represented in a convenient state transition matrix form. This new state transition matrix is valid for arbitrary elliptical orbits of 0≤e<1. The state propagation using the new state transition matrix shows good agr

Dominant mutations in ubiquitously expressed superoxide dismutase (SOD1) cause familial ALS by provoking premature death of adult motor neurons. To test whether mutant damage to cell types beyond motor neurons is required for the onset of motor neuron disease, we generated chimeric mice in which all motor neurons and oligodendrocytes expressed mutant SOD1 at a level sufficient to cause fatal, early-onset motor neuron disease when expressed ubiquitously, but did so in a cellular environment conta

Neuroinflammation, which includes both neuroprotective and neurotoxic reactions by activated glial cells and infiltrated immune cells, is involved in the pathomechanism of amyotrophic lateral sclerosis (ALS). However, the cytokines that regulate the neuroprotective inflammatory response in ALS are not clear. Here, we identify transforming growth factor-β1 (TGF-β1), which is upregulated in astrocytes of murine and human ALS, as a negative regulator of neuroprotective inflammatory response. We dem

Despite significant progress in understanding the molecular and genetic aspects of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease characterized by the progressive loss of motor neurons, the precise and comprehensive pathomechanisms remain largely unknown. In addition to motor neuron involvement, recent studies using cellular and animal models of ALS indicate that there is a complex interplay between motor neurons and neighboring non-neuronal cells, such as astrocytes, in

Abnormal protein accumulation is a pathological hallmark of neurodegenerative diseases, including accumulation of TAR DNA-binding protein 43 (TDP-43) in amyotrophic lateral sclerosis (ALS). Dominant mutations in the TDP-43 gene are causative for familial ALS; however, the relationship between mutant protein biochemical phenotypes and disease course and their significance to disease pathomechanism are not known. Here, we found that longer half-lives of mutant proteins correlated with accelerated

Amyotrophic lateral sclerosis (ALS) is an adult motor neuron disease characterized by premature death of upper and lower motor neurons. Two percent of ALS cases are caused by the dominant mutations in the gene for superoxide dismutase 1 (SOD1) through a gain of toxic property of mutant protein. Genetic and chimeric mice studies using SOD1 models indicate that non-neuronal cells play important roles in neurodegeneration through non-cell autonomous mechanism. We review the contribution of each gli

Abstract Neuroinflammation, which is characterized by activated microglia, astrocytes, infiltrating immune cells and the subsequent production of inflammatory mediators, is linked to a pathological process common to neurodegenerative diseases, such as Alzheimer's disease and amyotrophic lateral sclerosis ( ALS ). Furthermore, increasing evidence suggests that activated glial cells and immune cells surrounding motor neurons also contribute to the non‐cell autonomous neurodegeneration through neur

In soccer, each game lasts a total of 90 min, 45 min for each half. During a game in which defence and offence alternate repeatedly, players, using various ball techniques, perform a variety of actions ranging from some at a low speed to others at full speed. Furthermore, the players are free to move widely throughout the field. In planning training programmes for soccer players, therefore, it is important to study movements in the game in order to establish the type of physical fitness required

Mutations in ALS2, carrying three putative guanine exchange factor (GEF) domains, are causative for a juvenile, autosomal recessive form of amyotrophic lateral sclerosis (ALS), primary lateral sclerosis, and infantile-ascending hereditary spastic paralysis. Endogenous ALS2 is shown here to be enriched in nervous tissue and to be peripherally bound to the cytoplasmic face of endosomal membranes, an association that requires the amino-terminal "RCC1 (regulator of chromatin condensation)-like" GEF

The combined evidence from mice and humans shows that deficiency in ALS2 causes an upper motor neuron disease that in humans closely resembles a severe form of hereditary spastic paralysis, and that is quite distinct from amyotrophic lateral sclerosis.

The present study investigated whether transcranial magnetic stimulation (TMS) to the parietal cortex improves the performance of healthy persons in a spatial working memory (WM) task. The effect of TMS on the frontal cortex was examined by measuring oxygenated hemoglobin (oxy-Hb) with near-infrared spectroscopy. Fifty-two healthy persons received either 100% resting motor threshold TMS at 5 Hz (real TMS) or sham TMS while engaged in a spatial WM task or a control visuospatial attention task. TM

The cytoplasmic aggregation of TAR DNA binding protein-43 (TDP-43), also known as TDP-43 pathology, is the pathological hallmark of amyotrophic lateral sclerosis (ALS). However, the mechanism underlying TDP-43 cytoplasmic mislocalization and subsequent aggregation remains unclear. Here, we show that TDP-43 dimerization/multimerization is impaired in the postmortem brains and spinal cords of patients with sporadic ALS and that N-terminal dimerization-deficient TDP-43 consists of pathological incl

There is compelling evidence that glial-immune interactions contribute to the progression of neurodegenerative diseases. The adaptive immune response has been implicated in disease processes of amyotrophic lateral sclerosis (ALS), but it remains unknown if innate immune signaling also contributes to ALS progression. Here we report that deficiency of the innate immune adaptor TIR domain-containing adaptor inducing interferon-β (TRIF), which is essential for certain Toll-like receptor (TLR) signal