Tomohiro Araki

Roger P Simon9
Clara K Schindler8
Jing-Quan Lan7
Waro Taki7
9Roger P Simon
8Clara K Schindler
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Programmed cell death pathways have been implicated in the mechanism by which neurons die following brief and prolonged seizures, but the significance of proapoptotic Bcl-2 family proteins in the process remains poorly defined. Expression of the death agonist Bcl-2-interacting mediator of cell death (Bim) is under the control of the forkhead in(More)
Bcl-2 family gene products are critical to the integration of cell death stimuli that target the mitochondrion. Proapoptotic BAD (Bcl-2-associated death protein) has been shown to dissociate from its sequestered site with the molecular chaperone protein 14-3-3 and displace proapoptotic BAX (Bcl-2-associated X protein) from antiapoptotic BCL-Xl. BAX(More)
Death-associated protein (DAP) kinase is calcium-regulated and known to function downstream of death receptors, prompting us to examine its role in the mechanism of seizure-induced neuronal death. Brief seizures were focally evoked in rats, eliciting neuronal death within the CA3 subfield of the hippocampus, and to a lesser extent, cortex. Western blotting(More)
The consequences of activation of tumour necrosis factor receptor 1 (TNFR1) during neuronal injury remain controversial. The apoptosis signal-regulating kinase 1 (ASK1), a mitogen-activated protein kinase kinase kinase, can mediate cell death downstream of TNFR1. Presently, we examined the formation of the TNFR1 signalling cascade and response of ASK1(More)
The caspase family of cell death proteases has been implicated in the mechanism of neuronal death following seizures. We investigated the expression and processing of caspases 6 and 7, putative executioner caspases. Brief limbic seizures were evoked by intraamygdala kainic acid to elicit unilateral death of target hippocampal CA3 neurons in the rat.(More)
Research into the molecular mechanisms of epileptic brain injury is hampered by the resistance of key mouse strains to seizure-induced neuronal death evoked by systemically administered excitotoxins such as kainic acid. Because C57BL/6 mice are extensively employed as the genetic background for transgenic/knockout modeling in cell death research but are(More)
Although mice are amenable to gene knockout, they have not been exploited in the setting of seizure-induced neurodegeneration due to the resistance to injury of key mouse strains. We refined and developed models of seizure-induced neuronal death in the C57BL/6 and BALB/c strains by focally evoking seizures using intra-amygdala kainic acid. Seizures in adult(More)
In this paper, we propose <i>On-mouse projector</i>, an interface that combines a mouse and a mobile projector. This system satisfies both portability and large information space and enables stable operation. The mobile projector is placed on the mouse and projects images on a surface in front of the mouse. The projected image presents a part of large(More)
Simultaneous spinal and intracranial chronic subdural hematoma (CSDH) is a rare entity. A 67-year-old man visited our hospital due to headache after diving into a river 2 weeks before. Non-enhanced computed tomography (CT) and magnetic resonance imaging (MRI) revealed bilateral intracranial CSDH. The bilateral CSDH was evacuated and his symptoms improved.(More)
PURPOSE Arterial spin-labeling (ASL) perfusion MRI, a noninvasive method of assessing cerebral blood flow, is becoming a diagnostic tool of epilepsy. This study was undertaken to evaluate the diagnostic validity of ASL in patients with status epilepticus (SE) in a periictal state. METHOD Twenty cases with SE were studied. Patients were imaged at a 3T MRI(More)