132 research outputs found

    Thoracoscopic Left Atrial Appendage Excision Plus Ablation for Atrial Fibrillation to Prevent Stroke

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    Atrial fibrillation (AF) patients with a previous stroke are often at a high risk of recurrent stroke and bleeding. Anticoagulation therapy in such patients is a challenging dilemma. Thoracoscopic left atrial appendage excision (LAAE) plus AF ablation is an interventional approach offered to some AF patients. We hypothesized that this approach may be suitable as a secondary stroke prevention strategy for these high-risk patients. Between January 2013 and December 2016, a total of 44 patients (26 male; mean age 65.0 ± 9.1 years) with nonvalvular AF and a previous stroke or systemic thromboembolic event were enrolled. The patients underwent thoracoscopic LAAE plus AF ablation by experienced operators and were followed up for 2 years (at 1, 3, 6, 9, and 12 months postoperatively and every 6 months thereafter). Thromboembolic and major bleeding events were recorded. Cerebral computed tomography or magnetic resonance imaging and 7-day Holter monitoring were performed annually. Mean CHA2DS2-VASc and HAS-BLED scores were 4.2 ± 1.2 and 3.3 ± 0.7, respectively. All patients discontinued oral anticoagulation therapy after the surgical intervention. One patient suffered a periprocedural transient ischemic attack, and another was diagnosed with a new ischemic stroke at 491 days after surgery. The annual rate of total thromboembolism was 2.05%. No deaths or major bleeding events were observed postoperatively. The rate of successful AF ablation with no AF recurrence was 76.3%. Transthoracoscopic LAAE plus AF ablation may be a promising approach for this high-risk population. Thromboembolism event in this secondary prevention cohort was low, even without oral anticoagulation treatment

    An egg holders-inspired structure design for large-volume-change anodes with long cycle life

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    Abstract(#br)Silicon has been considered as a potential alternative of anodes for advanced lithium ion battery as it possesses high capacity and abundance. However, it encounters excessive volume expansion and inferior electoral conductivity, which imposes restrictions on its further development. In order to address these two problems, yolk-shell structure is employed, in which there is a suitable void for the expansion with a shell to protect the core and promote the conductivity. Here, by the inspiration from the egg holders and inverse-opal structure, an egg-stacking-like Si/C composite (ES) anode with spherical air holes was fabricated to gather the yolk-shell particles in a 3D carbon network with abundant channels allowing electrolyte to enter the material, which can facilitate the cycling performance. The half-cell battery assembled with these anodes presents high capacity and good rate performance, with a capacity reduction of only 2–7% per current density. And the cycling performance of ES anode is also praiseworthy that it delivers a high reversible discharge capacity of 2175 mAh g −1 after 300 cycles at 0.5 A g −1 . This kind of structure design is expected to be applicative for most of large-volume-change anodes

    Family-based whole-exome sequencing identifies novel loss-of-function mutations of FBN1 for Marfan syndrome

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    Background Marfan syndrome (MFS) is an inherited connective tissue disorder affecting the ocular, skeletal and cardiovascular systems. Previous studies of MFS have demonstrated the association between genetic defects and clinical manifestations. Our purpose was to investigate the role of novel genetic variants in determining MFS clinical phenotypes. Methods We sequenced the whole exome of 19 individuals derived from three Han Chinese families. The sequencing data were analyzed by a standard pipeline. Variants were further filtered against the public database and an in-house database. Then, we performed pedigree analysis under different inheritance patterns according to American College of Medical Genetics guidelines. Results were confirmed by Sanger sequencing. Results Two novel loss-of-function indels (c.5027_5028insTGTCCTCC, p.D1677Vfs*8; c.5856delG, p.S1953Lfs*27) and one nonsense variant (c.8034C>A, p.Y2678*) of FBN1 were identified in Family 1, Family 2 and Family 3, respectively. All affected members carried pathogenic mutations, whereas other unaffected family members or control individuals did not. These different kinds of loss of function (LOF) variants of FBN1 were located in the cbEGF region and a conserved domain across species and were not reported previously. Conclusions Our study extended and strengthened the vital role of FBN1 LOF mutations in the pathogenesis of MFS with an autosomal dominant inheritance pattern. We confirm that genetic testing by next-generation sequencing of blood DNA can be fundamental in helping clinicians conduct mutation-based pre- and postnatal screening, genetic diagnosis and clinical management for MFS
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