Kotaro Takeda

Abstract The reflexive excitation of the sympathetic nervous system in response to psychological stress leads to elevated blood pressure, a condition that persists even after the stress has been alleviated. This sustained increase in blood pressure, which may contribute to the pathophysiology of hypertension, could be linked to neural plasticity in sympathetic nervous activity. Given the critical role of astrocytes in various forms of neural plasticity, we investigated their involvement in maintaining elevated blood pressure during the post-stress phase. Specifically, we examined the effects of arundic acid, an astrocytic inhibitor, on blood pressure and heart rate responses to air-jet stress. First, we confirmed that the inhibitory effect of arundic acid is specific to astrocytes. Using c-Fos immunohistology, we then observed that psychological stress activates neurons in cardiovascular brain regions, and that this stress-induced neuronal activation was suppressed by arundic acid pre-treatment in rats. By evaluating astrocytic process thickness, we also confirmed that astrocytes in the cardiovascular brain regions were activated by stress, and this activation was blocked by arundic acid pre-treatment. Next, we conducted blood pressure measurements on unanesthetized, unrestrained rats. Air-jet stress elevated blood pressure, which remained high for a significant period during the post-stress phase. However, pre-treatment with arundic acid, which inhibited astrocytic activation, suppressed stress-induced blood pressure elevation both during and after stress. In contrast, arundic acid had no significant impact on heart rate. These findings suggest that both neurons and astrocytes play integral roles in stress-induced blood pressure elevation and its persistence after stress, offering new insights into the pathophysiological mechanisms underlying hypertension.

Introduction Qualitative information in the form of written reflection reports is vital for evaluating students’ progress in education. As a pilot study, we used text mining, which analyzes qualitative information with quantitative features, to investigate how rehabilitation students’ goals change during their first year at university. Methods We recruited 109 first-year students (66 physical therapy and 43 occupational therapy students) enrolled in a university rehabilitation course. These students completed an open-ended questionnaire about their learning goals at the time of admission and at 6 and 12 months after admission to the university. Text mining was used to objectively interpret the descriptive text data from all three-time points to extract frequently occurring nouns at once. Then, hierarchical cluster analysis was performed to generate clusters. The number of students who mentioned at least one noun in each cluster was counted and the percentages of students in each cluster were compared for the three periods using Cochran’s Q test. Results The 31 nouns that appeared 10 or more times in the 427 sentences were classified into three clusters: “Socializing,” “Practical Training,” and “Classroom Learning.” The percentage of students in all three clusters showed significant differences across the time periods (p < 0.001 for “Socializing”; p < 0.01 for “Practical Training” and “Classroom Learning”). Conclusion These findings suggest that the students’ learning goals changed during their first year of education. This objective analytical method will enable researchers to examine transitional trends in students’ reflections and capture their psychological changes, making it a useful tool in educational research.

Severe hypoxia induces seizures, which reduces ventilation and worsens the ictal state. It is a health threat to patients, particularly those with underlying hypoxic respiratory pathologies, which may be conducive to a sudden unexpected death in epilepsy (SUDEP). Recent studies provide evidence that brain microglia are involved with both respiratory and ictal processes. Here, we investigated the hypothesis that microglia could interact with hypoxia-induced seizures. To this end, we recorded electroencephalogram (EEG) and acute ventilatory responses to hypoxia (5% O₂ in N₂) in conscious, spontaneously breathing adult mice. We compared control vehicle pre-treated animals with those pre-treated with minocycline, an inhibitory modulator of microglial activation. First, we histologically confirmed that hypoxia activates microglia and that pre-treatment with minocycline blocks hypoxia-induced microglial activation. Then, we analyzed the effects of minocycline pre-treatment on ventilatory responses to hypoxia by plethysmography. Minocycline alone failed to affect respiratory variables in room air or the initial respiratory augmentation in hypoxia. The comparative results showed that hypoxia caused seizures, which were accompanied by the late phase ventilatory suppression in all but one minocycline pre-treated mouse. Compared to the vehicle pre-treated, the minocycline pre-treated mice showed a delayed occurrence of seizures. Further, minocycline pre-treated mice tended to resist post-ictal respiratory arrest. These results suggest that microglia are conducive to seizure activity in severe hypoxia. Thus, inhibition of microglial activation may help suppress or prevent hypoxia-induced ictal episodes.