Table_1_Advanced cueing of auditory stimulus to the head induces body sway in the direction opposite to the stimulus site during quiet stance in male participants.XLSX

Under certain conditions, a tactile stimulus to the head induces the movement of the head away from the stimulus, and this is thought to be caused by a defense mechanism. In this study, we tested our hypothesis that predicting the stimulus site of the head in a quiet stance activates the defense mechanism, causing a body to sway to keep the head away from the stimulus. Fourteen healthy male participants aged 31.2 ± 6.8 years participated in this study. A visual cue predicting the forthcoming stimulus site (forehead, left side of the head, right side of the head, or back of the head) was given. Four seconds after this cue, an auditory or electrical tactile stimulus was given at the site predicted by the cue. The cue predicting the tactile stimulus site of the head did not induce a body sway. The cue predicting the auditory stimulus to the back of the head induced a forward body sway, and the cue predicting the stimulus to the forehead induced a backward body sway. The cue predicting the auditory stimulus to the left side of the head induced a rightward body sway, and the cue predicting the stimulus to the right side of the head induced a leftward body sway. These findings support our hypothesis that predicting the auditory stimulus site of the head induces a body sway in a quiet stance to keep the head away from the stimulus. The right gastrocnemius muscle contributes to the control of the body sway in the anterior–posterior axis related to this defense mechanism.</p

Probucol attenuates hyperoxia-induced lung injury in mice

<div><p>Hyperoxic lung injury is pathologically characterized by alveolar edema, interlobular septal edema, hyaline membrane disease, lung inflammation, and alveolar hemorrhage. Although the precise mechanism by which hyperoxia causes lung injury is not well defined, oxidative stress, epithelial cell death, and proinflammatory cytokines are thought to be involved. Probucol—a commercially available drug for treating hypercholesterolemia—has been suggested to have antioxidant and antiapoptotic effects. This study aimed to assess whether probucol could attenuate hyperoxic lung injury in mice. Mice were exposed to 95% O₂ for 72 h, with or without pre-treatment with 130 μg/kg probucol intratracheally. Probucol treatment significantly decreased both the number of inflammatory cells in the bronchoalveolar lavage fluid and the degree of lung injury in hyperoxia-exposed mice. Probucol treatment reduced the number of cells positive for 8-hydroxyl-2′-deoxyguanosine or terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and suppressed NF-κB activation, Bax expression, and caspase-9 activation in lung tissues from hyperoxia-exposed mice. These results suggest that probucol can reduce oxidative DNA damage, apoptotic cell death, and inflammation in lung tissues. Intratracheal administration of probucol may be a novel treatment for lung diseases induced by oxidative stress, such as hyperoxic lung injury and acute respiratory distress syndrome.</p></div

Additional file 2: Table S2. of The predictive prognostic factors for polymyositis/dermatomyositis-associated interstitial lung disease

Comparison of demographic data among each PM/DM subtype in PM/DM-ILD patients. (PDF 102 kb