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Background: Progression of nontarget lesions (NTLs) after percutaneous coronary intervention (PCI) has been reported. However, it remains unknown whether progression of NTLs was causally related to stenting. This study was undertaken to test the hypothesis that stent implantation triggers acute phase response and systemic inflammation which may be associated with progression of NTLs. Methods: Thirty New Zealand rabbits receiving endothelial denudation and atherogenic diet were randomly divided into stenting, sham, and control groups. Angiography and intravascular ultrasonography were performed in the stenting and sham groups, and stent implantation performed only in the stenting group. Histopathologic study was conducted and serum levels of APPs (acute phase proteins) measured in all rabbits. Proteomics analysis was performed to screen the potential proteins related to NTLs progression after stent implantation. The serum levels of APPs and inflammatory cytokines were measured in 147 patients undergoing coronary angiography or PCI. Results: Plaque burden in the NTLs was significantly increased 12 weeks after stent implantation in the stenting group versus sham group. Serum levels of APPs and their protein expression in NTLs were significantly increased and responsible for stenting-triggered inflammation. In patients receiving PCI, serum levels of SAA-1 (serum amyloid A protein 1), CRP (C-reactive protein), TNF (tumor necrosis factor)-α, and IL (interleukin)-6 were substantially elevated up to 1 month post-PCI. Conclusions: In a rabbit model of atherosclerosis, stent implantation triggered acute phase response and systemic inflammation, which was associated with increased plaque burden and pathological features of unstable plaque in NTLs. The potential mechanism involved vessel injury-triggered acute phase response manifested as increased serum levels of SAA-1, CRP, and LBP (lipopolysaccharide-binding protein) and their protein expression in NTLs. These findings provided a new insight into the relation between stent implantation and progression of NTLs, and further studies are warranted to clarify the detailed mechanism and clinical significance of these preliminary results. Registration: URL: http://www.chictr.org.cn ; Unique identifier: ChiCTR1900026393. Graphic Abstract: A graphic abstract is available for this article.

Many businesses and organisations have found that the application of Knowledge Management (KM)has enabled them to improve their performance and enhance their development. It has been emphasised in various studies related to KM that the most central activity in managing knowledge is to ensure that knowledge is transferred between different parties. The practice of Knowledge Transfer (KT) is extremely valuable in the healthcare sector, and this especially applies to hospitals and nursing teams. Hence, the ability to transfer knowledge in the nursing workforce has a critical impact on the development of the healthcare system, particularly newborn health care in the New-born Intensive Care Unit (NICU). Therefore, the aim of this paper is to identify and understand the key concepts involved in Social Networks and Knowledge Transfer Mechanisms in a new-born Intensive Care Unit (NICU) in order to develop a knowledge transfer framework for NICUs in future research.

Background: Visceral adipose tissue derived serine protease inhibitor (vaspin), a secretory adipokine, was reported to play a protective role in insulin resistance. Recent studies have demonstrated that serum vaspin levels are downregulated in patients with coronary artery disease (CAD) and that vaspin has a protective effect on myocardial ischaemia/reperfusion injury (IRI) and atherosclerosis. However, whether vaspin exerts specific effects on pathological cardiac hypertrophy remains unknown.Methods: Pathologic cardiac hypertrophy was induced in male C57BL/6J wild type (WT) and vaspin knockout (vaspin ko) mice. Buparlisib (PI3K inhibitor, 50 mg/kg), rapamycin (mTOR inhibitor, 20 mg/kg), or A 769662 (AMPK agonist, 30 mg/kg) wer e pre and co administered to vaspin ko mice daily for a period of 15 days. Induction of pathological cardiac hypertrophy was performed by the subcutaneous administration of isoproterenol (ISO) (5 mg/kg) into mice from the 7th to the 15th day. Cardiac hype rtrophy, fibrosis, and cardiac function were examined in these mice. Critical characteristics of senescence (senescence associated β galactosidase activity and expression of cyclin dependent kinase inhibitors) were examined in the cardiac hypertrophy modelResults: We provide the first evidence that the serum level of vaspin decreased during pathological cardiac hypertrophy; further, knocking out of vaspin resulted in markedly exaggerated cardiac h ypertrophy and fibrosis, and increased cardiomyocyte senesc senescence in mice treated with ISO. Conversely, the administration of exogenous ence in mice treated with ISO. Conversely, the administration of exogenous recombinant human vaspin in vitro protected myocardial cells against hypertrophy recombinant human vaspin in vitro protected myocardial cells against hypertrophy and senescence caused by ISO. and senescence caused by ISO. MechanisticallyMechanistically, PI3K, PI3K--AKTAKT--mTOR mTOR pathwaypathway--dependent activation of autophadependent activation of autophagic flux was involved in the protective gic flux was involved in the protective effects of vaspin toward cardiac hypertrophy.effects of vaspin toward cardiac hypertrophy.Conclusion: Our results showed for the first time that vaspin functions as a critical Our results showed for the first time that vaspin functions as a critical regulator that alleviates pathological cardiac hypertrophy by regulating regulator that alleviates pathological cardiac hypertrophy by regulating autophagyautophagy--ddependent myocardial senescence, which provides potential preventive and ependent myocardial senescence, which provides potential preventive and therapeutic targets for pathological cardiac hypertrophy.therapeutic targets for pathological cardiac hypertrophy.

Visceral adipose tissue-derived serine protease inhibitor (vaspin), as a secretory adipokine, was reported to exert a protective role on insulin resistance. Recent studies showed that serum vaspin level was downregulated in patients with coronary artery disease. However, whether vaspin exerted specific effects on myocardial injury remains unknown. In this study, we determined to explore the role of vaspin overexpression in myocardial ischaemia/reperfusion (I/R) injury and the underlying mechanisms. Our results showed that the systemic delivery of adeno-associated virus-vaspin to mice reduced myocardial infarct size and apoptosis, and improved cardiac function after reperfusion, accompanied with upregulated autophagic flux and restored lysosomal function in the ischaemic heart. Blockage of the autophagic flux with choroquine mitigated the protection of vaspin on myocardial I/R injury. Moreover, we testified that administration of exogenous recombinant human vaspin on cultured cardiomyocytes suppressed hypoxia/reoxygenation-induced apoptosis, through the AMPK-mTOR-upregulated autophagic flux. Overall, we verified that vaspin functions as an adipokine which can alleviate I/R injury in the heart by suppressing myocardial apoptosis through AMPK-mTOR-dependent activation of autophagic flux, and then provided a potential breakthrough in the treatment of myocardial I/R injury and other ischaemic diseases.

Background Stress‐induced cell premature senescence participates in a variety of tissue and organ remodeling by secreting such proteins as proinflammatory cytokines, chemokines, and growth factors. However, the role of cardiomyocyte senescence in heart remodeling after acute myocardial infarction has not been thoroughly elucidated to date. Therefore, we sought to clarify the impact of premature myocardial senescence on postinfarction heart function. Methods and Results Senescence markers, including p16 INK 4a , p21 CIP 1/ WAF 1 , and SA ‐β‐gal staining, were analyzed in several heart disease models by immunostaining. Both postinfarction mouse hearts and ischemic human myocardium demonstrated increased senescence markers. Additionally, senescence‐related secretory phenotype was activated after acute myocardial infarction, which upregulated senescence‐related secretory phenotype factors, including CCN family member 1 ( CCN 1), interleukin‐1α, tumor necrosis factor α, and monocyte chemoattractant protein‐1. In vivo, a tail vein injection of AAV 9‐ Gata4 ‐sh RNA significantly attenuated senescence‐related secretory phenotype secretion and aggravated postinfarction heart dysfunction. Furthermore, among activated senescence‐related secretory phenotype factors, CCN 1 administration reduced myofibroblast viability in vitro and rescued the deleterious effect of AAV 9‐ Gata4 ‐sh RNA in vivo. Conclusions Myocardial premature senescence was observed in the ischemic hearts and improved postinfarction heart function, partly through the GATA‐binding factor 4‐ CCN 1 pathway.