Enhancing patient self-management after a first stroke: An application of the wearable devices and the health management platform.

BACKGROUND: Post-stroke disability restricts a patient's physical activity, affects the patient's quality of life, and leads to higher medical costs. Therefore, it is essential to promote patients' continuous exercise during this period of recovery. OBJECTIVE: This study aimed to verify the effectiveness of applying a health management platform combined with wearable devices to enhance stroke patients' self-management of recovery and to allow comparisons with active care intervention management. METHOD: This quasi-experimental study aimed at examining those participants who had sustained a stroke for the first time. A 90-day experiment was implemented with the intervention of monitoring and active care from the researchers who also interviewed the selected participants at the end of the study. A total of 26 participants were examined (14 in the experimental group and 12 in the control group). RESULT: The participants in the experimental group made significant progress between the pre- and post-tests. Firstly, their six-minute walking distance improved by 89.5 m (p < 0.001). Secondly, their sit-to-stand transfers in 60 s improved 2.85 times (p = 0.017), and their Berg balance test improved by 6.36 points (p = 0.003). Finally, the Partners in Health scale (PIH) scores also improved. According to the data collected in the interviews, the researchers' intervention improved the patients' self-management ability. CONCLUSION: The short-term physical performance in the experimental group after the intervention was better than that in the control group. In clinical practice, it is suggested that continuous interaction between medical staff and patients be sustained while applying wearable devices to promote the patient's self-management ability.

Elevated activation of CaMKIIα in the CPEB3-knockout hippocampus impairs a specific form of NMDAR-dependent synaptic depotentiation.

Cytoplasmic polyadenylation element binding protein 3 (CPEB3) is a sequence-specific RNA-binding protein that confines the strength of glutamatergic synapses by translationally downregulating the expression of multiple plasticity-related proteins (PRPs), including the N-methyl-D-aspartate receptor (NMDAR) and the postsynaptic density protein 95 (PSD95). CPEB3 knockout (KO) mice exhibit hippocampus-dependent abnormalities related not only to long-term spatial memory but also to the short-term acquisition and extinction of contextual fear memory. In this study, we identified a specific form of NMDAR-dependent synaptic depotentiation (DPT) that is impaired in the adult CPEB3 KO hippocampus. In parallel, cultured KO neurons also exhibited delayed morphological and biochemical responses under NMDA-induced chemical long-term depression (c-LTD). The c-LTD defects in the KO neurons include elevated activation of calcium/calmodulin-dependent protein kinase II alpha subunit (CaMKIIα), increased Ser831 phosphorylation of GluA1 and slow degradation of PSD95 and GluA1. Because transient pharmacological suppression of CaMKIIα activity during the DPT-initiating phase successfully reversed the LTP in the KO hippocampus, DPT and c-LTD in the two different systems shared common molecular defects due to the absence of CPEB3. Together, our results suggest that CPEB3 deficiency imbalances NMDAR-activated CaMKIIα signaling, which consequently fails to depress synaptic strength under certain stimulation conditions.