Purpose: This study systematically reviewed and synthesized the evidence on the effectiveness of mobile health (mHealth) interventions in improving medication adherence among patients with cardiovascular disease. Methods: This systematic review included randomized controlled trials that evaluated the effects of mHealth interventions on medication adherence among patients with cardiovascular disease. PubMed, the Cochrane Library, CINAHL, and Embase were searched for peer-reviewed studies and grey literature published in English between January 1, 2013, and July 31, 2025. The Cochrane Risk of Bias 2 (RoB 2) tool was used to assess the risk of bias in the included studies. R software ver. 4.5.2 was used to perform the meta-analysis. Results: Fifty-two studies were included in the systematic review, of which 20 were included in the meta-analysis. The pooled analysis demonstrated a significant improvement in medication adherence among patients with cardiovascular disease receiving mHealth interventions, with a moderate to large effect size (Hedges’ g=0.72; 95% confidence interval, 0.20–1.25; p<.001), despite substantial heterogeneity (I2=97%). However, a considerable proportion of the included studies were assessed as having a high risk of bias, which may limit the internal validity of the findings. Subgroup analyses indicated that the effects of mHealth interventions on medication adherence did not differ significantly according to intervention type, duration, or outcome measurement tools. Conclusion mHealth interventions appear to be effective in improving medication adherence among patients with cardiovascular disease. However, these findings should be interpreted with caution because of the high risk of bias and substantial heterogeneity among the included studies. Future research should explore the use of emerging technologies, such as artificial intelligence and virtual reality, to address medication non-adherence (PROSPERO registration number: CRD42023450502).

Background: We analyzed the status of organ distribution in pediatric deceased donor liver transplantation (DDLT) in Korea. Additionally, we estimated how many pediatric patients could have avoided living donor liver transplantation (LDLT) or survived if new criteria for splittable deceased donors were adopted. Based on the findings, we advocate expanding policy to promote the universal adoption of split liver transplantation (SLT). Methods: Using the Korean Network for Organ Sharing database, we identified patients who underwent DDLT between January 2000 and December 2020. We considered “po-tential splittable donors” those with a donor-to-recipient weight ratio of ≥1.0 who met the existing SLT criteria (age 10–40 years; weight ≥50 kg). By comparing the numbersof pediatric LDLT recipients and potential splittable donors annually, we estimated how many patients might have avoided LDLT if the left lateral section of each splittable liver had been allocated to a child. Additionally, we compared the number of deaths on the DDLT waiting list with the number of potential splittable donors to estimate possibly preventable deaths. Results: Overall, we identified 640 potential splittable donors. Over the 20-year period, 1,210 pediatric patients (<19 years old) received LDLT. If potentially splittable livers had been split, this number could have been nearly halved. Furthermore, 127 patients died while on the DDLT waiting list. Using SLT with potential splittable donors, these deaths might have been prevented. Conclusions SLT could reduce avoidable deaths among pediatric patients while decreasing the economic and social burden of LDLT, without compromising survival for adult DDLT recipients.

Amyloid precursor protein binding protein-1 (APP-BP1) binds to the carboxyl terminus of amyloid precursor protein and serves as a bipartite activation enzyme for the ubiquitin-like protein, NEDD8. Previously, it has been reported that APP-BP1 rescues the cell cycle S-M checkpoint defect in Ts41 hamster cells, that this rescue is dependent on the interaction of APP-BP1 with hUba3. The exogenous expression of APP-BP1 in neurons has been reported to cause DNA synthesis and apoptosis via a signaling pathway that is dependent on APP-BP1 binding to APP. These results suggest that APP-BP1 overexpression contributes to neurodegeneration. In the present study, we explored whether APP-BP1 expression was altered in the brains of Tg2576 mice, which is an animal model of Alzheimer's disease. APP-BP1 was found to be up-regulated in the hippocampus and cortex of 12 month-old Tg2576 mice compared to age-matched wild-type mice. In addition, APP-BP1 knockdown by siRNA treatment reduced cullin-1 neddylation in fetal neural stem cells, suggesting that APP-BP1 plays a role in cell cycle progression in the cells. Collectively, these results suggest that increased expression of APP-BP1, which has a role in cell cycle progression in neuronal cells, contributes to the pathogenesis of Alzheimer's disease.
Alzheimer Disease ; Amyloid ; Animals ; Apoptosis ; Brain ; Cell Cycle ; Cricetinae ; DNA ; Hippocampus ; Mice ; Models, Animal ; Neural Stem Cells ; Neurons ; Protein Binding ; RNA, Small Interfering