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Objectives: Frailty and hypertension often coexist in older adults, which may lead to fall risks. This study aimed to examine the relationship between frailty status, hypertension, and fall risk. Methods: In this cross-sectional study, a total of 401 older adults were conveniently recruited from communities in Wuxi, China, between September 2022 and November 2022. The fall risk self-assessment checklist from the Stopping Elderly Accidents, Deaths & Injuries (STEADI) Toolkit was used to evaluate their fall risks. The FRAIL scale questionnaire was used to assess frailty status. Participants’ demographic information and comorbidities were collected. Multivariate logistic regression, generalized additive model, and smooth curve fitting were used to analyze the association between frailty, hypertension, and fall risk. Results: Frailty had a strong association with increased prevalence of fall risk among the participants (OR 8.52, 95% CI 3.21–22.57; P

PurposeTo evaluate a noval bilateral asymmetric single-rivet occluder with reserved interatrial septal puncture area for treating patent foramen ovale (PFO).Materials and methodsThe study established a pig model of patent foramen ovale (PFO) by puncturing the oval fossa and then performing high-pressure balloon dilation. A specially designed bilateral asymmetric occluder for the reserved interatrial septal puncture area was then. used to close the PFO through catheter-based intervention. The pigs were kept for 3 months before undergoing a second catheter-based intervention, involving interatrial septal puncture using a newly developed occluder in the reserved interatrial septal puncture area. During 6 months, the experimental pigs underwent assessment using digital subtraction angiography (DSA), echocardiography, and histological evaluation.ResultsA patent foramen ovale (PFO) model was successfully established in 6 pigs using the puncture atrial septum high-pressure balloon dilation method. The diameter of the unclosed PFO was measured (3.56 ± 0.25 mm). Using the newly developed occluder device, all 6 pigs with unclosed PFO underwent successful catheter-based closure surgeries, with intraoperative and postoperative transesophageal echocardiography showing excellent device positioning and complete closure without residual shunting. After 3 months of implantation, the catheter-based interatrial septal puncture was performed through the reserved interatrial septal puncture area, and all procedures were successful. Immediately following euthanasia, a histological examination revealed intact and undamaged occluder devices with visible puncture holes in the reserved interatrial septal puncture area. No fracture of the nitinol wire was observed, and the surface of the occluder device showed coverage of endothelial and connective tissues. Utilizing a bilateral asymmetric single-rivet occluder device implanted through the reserved interatrial septal puncture area has proven effective in closing PFO. After implantation, the occluder device allows subsequent interatrial septal puncture procedures through the reserved area.ConclusionThe novel occluder device demonstrated excellent closure performance, biocompatibility, and puncturability in the experiment. This indicates the feasibility of conducting further catheter-based interventions on the interatrial septum.

Background: Myocardial fibrosis is a key pathological process after myocardial infarction, which leads to poor outcomes in patients at the end stage. Effective treatments for improving prognosis of myocardial fibrosis are needed to be further developed. Methyl ferulic acid (MFA), a biologically active monomer extracted and purified from the Chinese herbal medicine, is reported as an attenuator in many diseases. In this study, we aim to reveal the role it plays in myocardial fibrosis after myocardial infarction and its possible mechanism.Results: Firstly, we found that MFA attenuated the expression of fibrosis-related proteins and the ability of migration and proliferation in TGF-β1–induced human cardiac fibroblasts (HCFs). Then, myocardial fibrosis after myocardial infarction models on mouse was built to reveal the in vivo affection of MFA. After 28 days of treatments, fibrosis areas, cardiac function, and expression of fibrosis-related proteins were all improved in the MFA-treated group than the myocardial infarction group. Finally, to elucidate the mechanism of phenomenon we observed, we found that MFA attenuated HCF differentiation after myocardial infarction by suppressing the migration and proliferation in HCFs, which was by suppressing the pRB-E2F1/CCNE2 and the RhoA/ROCK2 pathway.Conclusion: Our findings showed that MFA attenuated the expression of fibrosis-related proteins, and the ability of migration and proliferation in HCFs improved the cardiac function of myocardial infarction mice; meanwhile, the mechanism of that was by suppressing the pRB-E2F1/CCNE2 and the RhoA/ROCK2 pathway.

Septic cardiomyopathy is a common complication of severe sepsis, which is one of the leading causes of death in intensive care units. Therefore, finding an effective therapy target is urgent. Neferine is an alkaloid extracted from the green embryos of mature seeds of Nelumbo nucifera Gaertn., which has been reported to exhibit various biological activities and pharmacological properties. This study aims to explore the protective effects of neferine against lipopolysaccharide (LPS)-induced myocardial dysfunction and its mechanisms. The LPS-induced cardiac dysfunction mouse model was employed to investigate the protective effects of neferine. In this study, we demonstrated that neferine remarkably improved cardiac function and survival rate and ameliorated morphological damage to heart tissue in LPS-induced mice. Neferine also improved cell viability and mitochondrial function and reduced cell apoptosis and the production of reactive oxygen species in LPS-treated H9c2 cells. In addition, neferine significantly upregulated Bcl-2 expression and suppressed cleaved caspase 3 activity in LPS-induced mouse heart tissue and H9c2 cells. Furthermore, neferine also upregulated the phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/AKT/mTOR) signaling pathway in vivo and in vitro. Conversely, LY294002 (a PI3K inhibitor) reversed the protective effect of neferine in LPS-induced H9c2 cells. Our findings thus demonstrate that neferine ameliorates LPS-induced cardiac dysfunction by activating the PI3K/AKT/mTOR signaling pathway and presents a promising therapeutic agent for the treatment of LPS-induced cardiac dysfunction.