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Yonekura, S.

Publications and source records attributed to Yonekura, S..

2 recordsLinked to original sources

A neuromodulatory model for determining the effect of emotion-respiration-cognition coupling on the time-to-respond

Respiration and emotional stimuli modulate cognitive ability and the reaction time to generate bodily movement. To understand mechanisms for emotion-respiration-cognition coupling, first, we considered a schematic feed-forward neural network, in which neurons was biased by respiratory-relevant sensory input and the activation function of a neuron was modulated by a neuromodulator, such as norepinephrine (NE). Furthermore, we assumed that the neural model received a stimulus input and generated a response action upon the activity of the output neuron exceeding a certain threshold. Time-to-respond (TTR) was equivalently modulated by the intensity of the input bias and the neuromodulator strength for small action execution threshold; however, it was dominantly modulated by only the neuromodulator for high threshold. Second, we implemented a comprehensive model comprising a cardio-respiration relevant neuromechanical-gas system, a respiratory central pattern generator (CPG), NE dynamics to modulate neurocognitive dynamics, and a locus coeruleus (LC) circuit, which was the primary nucleus for controlling NE. The LC neurons received pCO2 or synaptic current from an inspiratory neurons, which resulted in shortened TTR by a stimulus input during inhalation. By contrast, upon receiving pulmonary stretch information, the TTR was shortened by a stimulus input during exhalation. In humans, TTR is shortened when a fear-related stimulus is presented during inhalation, and likewise, TTR is weakly-shortened when surprise-related stimulus is presented during exhalation. Hence, we conclude that emotional stimuli in humans may switch the gating strategies of information and the inflow to LC to change the attention or behavior strategy.

neuroscience↗

Myogenetic oligodeoxynucleotide (myoDN) recovers the differentiation of skeletal muscle myoblasts deteriorated by diabetes mellitus

Sarcopenic obesity is a complication of decreased muscle mass and strength associated with obesity, and sarcopenia associated with diabetes mellitus (DM) is a serious risk factor that may result in mortality. Deteriorated differentiation of muscle precursor cells, called myoblasts, in DM patients is considered to be one of the causes of muscle atrophy. We recently developed myogenetic oligodeoxynucleotides (myoDNs), which are 18-base single-strand DNAs that promote myoblast differentiation by targeting nucleolin. Herein, we report the applicability of a myoDN, iSN04, to myoblasts isolated from patients with type 1 and type 2 DM. Myogenesis of DM myoblasts was exacerbated concordantly with a delayed shift of myogenic transcription and induction of interleukins. Analogous phenotypes were reproduced in healthy myoblasts cultured with excessive glucose or palmitic acid, mimicking hyperglycemia or hyperlipidemia. iSN04 treatment recovered the deteriorated differentiation of plural DM myoblasts by downregulating myostatin and interleukin-8. iSN04 also ameliorated the impaired myogenic differentiation induced by glucose or palmitic acid. These results demonstrate that myoDNs can directly facilitate myoblast differentiation in DM patients, making them novel candidates for nucleic acid drugs to treat sarcopenic obesity.

cell biology↗