Acute myocardial infarction (MI) is a major cause of death worldwide. This study utilized collagen-targeted phase change material (PCM) nanoparticles (NPs) to co-encapsulate HO-1 and explored the efficacy of composite PCM NPs on cardiomyocyte progression and development of MI. In this study, we enrolled 32 acute MI patients and 32 healthy participants, and ELISA assay was used to assess the content of creatine kinase isoenzyme (CK-MB). Mice with MI received tail vein administration of HO-1-loaded PCM NPs, followed by RT-qPCR detection of expressions of hypoxia-reoxygenation related genes (SpA, SpB, SpC, Occludin, KGF, and CK18). Patients with acute MI had a higher level of CK-MB. Treatment with HO-1-loaded collagen-targeted PCM NPs decreased expressions of SpA, SpB, SpC, Occludin, KGF, and CK18, facilitating repair of damaged tissues. Of note, NPs loaded with siRNA HO-1 up-regulated the expression of these genes. Collagen-targeted PCM NPs carrying HO-1 effectively promoted the repair of myocardial cells and relieved MI through down-regulation of hypoxia-reoxygenation related genes, which may enhance prevention and treatment for acute MI.

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BackgroundFamilial hypercholesterolemia (FH), an autosomal dominant genetic disorder, is underdiagnosed and undertreated. The majority of FH cases are caused by low density lipoprotein receptor (LDL-R) gene mutations. The C308Y mutation in LDL-R results in approximately 70% loss of LDL-R activity, leading to the elevation of low density lipoprotein-cholesterol (LDL-C) and an increased risk of premature coronary heart disease (CHD). The aim of this study was to identify FH cases by cascade screening in family members and relatives of a 37-year old male with premature CHD and hypercholesterolemia.MethodsClinical exam, blood lipid profiling and genomic DNA sequencing of all exons of LDL-R were performed for the proband and his 14 family members and relatives. FH diagnosis was carried out using the Dutch Lipid Clinic Network (DLCN) criteria.ResultsLipid profiling showed that 9 individuals, including the proband, had hypercholesterolemia. All these 9 subjects had a G > A substitution at nucleotide 986 in exon 7 resulting in the C308Y mutation as determined by DNA sequencing, and all those carrying the mutation were diagnosed as having definite FH under the DLCN criteria. However, most (7/9) did not have suggestive clinical manifestations of CHD.ConclusionsThe C308Y mutation was discovered in multiple family members and relatives for the first time in mainland China. Cascade screening is key for the confirmatory diagnosis of FH. Our hypothesis that the C308Y is a common variant in the population of Southern China origin warrants further validation by screening for the C308Y mutation in a large population.

Purpose To evaluate the effi cacy and ancenity of interventional technique combined with surgical treatment for children congenital heart disease. Methods Coil embolisation to occlude aortopulmonary collateral vessels was attempted in 4 patients with PDA congenital heart disease. The underlying disease were pulmonary atresia with ventricular septal defect in 2 patients. Coil embolisation was performed before corrective surgery. There were 5 spring coils were used to embolise 3 vessels in 2 children received corrective surgery immediately after the procedure. Results 19 vessels were embolised successfully. Among them occlusion was complete in 15 (79 %) and partial in 4 (21 %). During the corrective surgery, the systemic pressure was kept stable easily. After surgery, 2 children recovered and were discharged uneventfully. Conclusion The results demonstrate that coil embolisation to occlude PDA could reduce the diffi culty of extracorporeal circulation during surgery and simplify the corrective surgery procedure. ABSTRACT WITHDRAWN ABSTRACT WITHDRAWN