Pre-stroke physical activity is associated with post-stroke physical activity and sedentary behavior in the acute phase.

This study investigated the link between pre-stroke and acute-stage physical activity (PA) and sedentary behavior. Forty individuals with stroke (aged 73.6 ± 8.9 years) were enrolled. Post-stroke activity, including metabolic equivalents (METs), sedentary behavior, light PA, and moderate-to-vigorous PA (MVPA), was measured using a tri-axial accelerometer (ActiGraph wGT3X-BT) over 11 consecutive days starting from the 4th day post-stroke. Pre-stroke PA levels were assessed using the International Physical Activity Questionnaire (IPAQ). We measured skeletal muscle mass index (SMI) and phase angle using a bioelectrical impedance analyzer (Inbody S10) upon admission. Physical therapists assessed the Brunnstrom recovery stage (BRS) within 3 days post-stroke. Total daily activity averaged 1.05 ± 0.05 METs. Throughout the day, 91.2 ± 5.1, 7.6 ± 4.1, and 1.2 ± 1.3% was spent in sedentary behavior, light PA, and MVPA, respectively. Only pre-stroke PA was independently associated with METs (ß = 0.66), sedentary behavior (ß = -0.58), light PA (ß = 0.50), and MVPA (ß = 0.71) after adjusting for age, sex, stroke severity, and activities of daily living. This suggests that pre-stroke PA might play a crucial role in reducing sedentary behavior and promoting PA during the acute phase.

Low-dose nafamostat mesilate ameliorates tissue injury and inhibits 5-hydroxytryptamine synthesis in the rat intestine after methotrexate administration.

We aimed to clarify the effect of nafamostat mesilate (nafamostat) on intestinal mucositis as well as the potentiation of intestinal 5-hydroxytryptamine (5-HT) dynamics induced by methotrexate, an anti-cancer drug, in rats. Rats received intraperitoneal methotrexate at 12.5 mg/kg/day for 4 days. In addition, 1, 3, or 10 mg/kg/day of nafamostat was given subcutaneously for 4 days. Ninety-six hours after the first administration of methotrexate, jejunal tissues were collected for analysis. The results showed that 1 mg/kg, but not 3 or 10 mg/kg, of nafamostat significantly ameliorated the methotrexate-induced body weight loss. Moreover, 1 mg/kg of nafamostat significantly improved methotrexate-induced mucositis, including villus atrophy. Nafamostat (1 mg/kg) significantly inhibited the methotrexate-induced mRNA expression of pro-inflammatory cytokines and cyclooxygenase-2, as well as methotrexate-induced 5-HT content and tryptophan hydroxylase (TPH) activity. In addition, it tended to inhibit the number of anti-TPH antibody-positive cells and significantly inhibited the number of anti-substance P antibody-positive cells. These findings suggest that low-dose nafamostat ameliorates tissue injury and 5-HT and substance P synthesis in methotrexate-induced mucositis. Nafamostat may be a novel therapeutic strategy for the prevention and treatment of mucositis as well as 5-HT- and/or substance P-related adverse effects in cancer chemotherapy.