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Objective: This study was to investigate the potential protective effects of curcumin in cerebral ischemia-reperfusion (CIR) and its regulation of miR-7. Methods: Rats were occluded by middle cerebral artery occlusion (MCAO) for 1.5 h and reperfused for 2 h to establish a local CIR model. After 24 hours of model establishment, MCAO rats were given curcumin for 3 days by intragastric administration. PC12 cells were cultured for 6 h in oxygen-glucose deprivation medium and then reoxygenated for 24 h to establish an oxygenglucose deprivation/reoxygenation (OGD/R) model. The OGD/R model cells were treated with curcumin for 48 h. Results: Curcumin inhibited the decrease of miR-7-5p expression and an increase of RelA p65 expression induced by CIR and ODG/R. RelA p65 was a target of miR-7-5p. MiR-7-5p antagonists were able to counteract the effect of curcumin on the expression of RelA p65 in ischemic brain tissue of MCAO rats and OGD/R model cells. Curcumin improved OGD/R-induced inhibition of cell activity, necrosis and apoptosis. Curcumin significantly reduced the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, reactive oxygen species (ROS) and malondialdehyde (MDA) and increased the activity of superoxide dismutases (SOD) and catalase (CAT) in OGD/R-induced cells. Curcumin may inhibit OGD/R-induced cell damage by regulating miR-7-5p. Curcumin improved cerebral infarction, nerve damage and cognitive dysfunction in rats with CIR, which may be related to the regulation of miR-7-5p/RelA p65 axis. Conclusion: Curcumin exerts cerebral protection by attenuating cell necrosis and apoptosis, inflammatory response and oxidative stress following CIR, which may be related to its regulation of the miR-7/RELA p65 axis.

BackgroundChronic diseases are long-term, recurring and prolonged, requiring frequent travel to and from the hospital, community, and home settings to access different levels of care. Hospital-to-home transition is challenging travel for elderly patients with chronic diseases. Unhealthy care transition practices may be associated with an increased risk of adverse outcomes and readmission rates. The safety and quality of care transitions have gained global attention, and healthcare providers have a responsibility to help older adults make a smooth, safe, and healthy transition.ObjectiveThis study aims to provide a more comprehensive understanding of what may shape health transitions in older adults from multiple perspectives, including older chronic patients, caregivers, and healthcare providers.MethodsSix databases were searched during January 2022, including Pubmed, web of science, Cochrane, Embase, CINAHL (EBSCO), and PsycINFO (Ovid). The qualitative meta-synthesis was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) recommendations. The quality of included studies was appraised using the Critical Appraisal Skills Programme (CASP) qualitative research appraisal tool. A narrative synthesis was conducted informed by Meleis's Theory of Transition.ResultsSeventeen studies identified individual and community-focused facilitators and inhibitors mapped to three themes, older adult resilience, relationships and connections, and uninterrupted care transfer supply chain.ConclusionThis study identified potential transition facilitators and inhibitors for incoming older adults transitioning from hospital to home, and these findings may inform the development of interventions to target resilience in adapting to a new home environment, and human relations and connections for building partnerships, as well as an uninterrupted supply chain of care transfer at hospital-home delivery.Systematic review registrationwww.crd.york.ac.uk/prospero/, identifier: CRD42022350478.

Cell-based therapy is a promising clinic strategy to address many unmet medical needs. However, engineering cells faces some inevitable challenges, such as limited sources of cells, cell epigenetic alterations, and short shelf life during in vitro culture. Here, the worm-like nanocell mimics are fabricated to engineer effectively the tumor cells in vivo through the synergistic combination of nongenetic membrane surface engineering and inside encapsulation using in situ cell membrane fusion. The specific targeting and deformability of nanocell mimics play a vital role in membrane fusion mechanisms. The engineered primary tumor cells improved the tumor penetration of therapeutic cargoes via extracellular vesicles, while the engineered circulating tumor cells (CTCs) can capture the homologous cells to form the CTC clusters in the bloodstream and eliminate the CTC clusters in the lung, thus achieving excellent antitumor and antimetastasis efficacy. Above all, we find an intriguing phenomenon, in situ cell membrane fusion by the worm-like nanocell mimics, and our finding of in situ cell membrane fusion inspired us to engineer tumor cells in vivo. The present study would be a particularly meaningful strategy to directly engineer cells in vivo for cell-based therapy.