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The withdrawal of OACs 3 months after successful radiofrequency catheter ablation for patients with AF may be safe and feasible. It needs to be tested by randomized controlled trial.

The present study investigated the effects of food restriction (FR) on memory and the expression of synapsin I in the brain of young mice. The results showed that 20% FR did not retard the body weight gain of mice, while the 60% and 80% FR reduced the mice's body weight. The memory after 24 hr of learning was not changed by FR, whereas long-term memory was improved significantly in 20% FR mice. In addition, 60% and 80% FR did not impair the mice's memory. The transcriptional expression of synapsin I in mice brain was up-regulated by 20% FR, and down-regulated by 60% and 80% FR.

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Pulmonary arterial hypertension (PAH) is a rare and lethal disease characterized by vascular remodeling and vasoconstriction, which is associated with increased intracellular calcium ion (Ca2+) concentration. Platelet-derived growth factor-BB (PDGF-BB) is the most potent mitogen for pulmonary arterial smooth muscle cells (PASMCs) and involved in vascular remodeling during PAH development. PDGF signaling has been proved to participate in maintaining Ca2+ homeostasis of PASMCs, however, the mechanism needs to be further elucidated. Here we illuminate that the expression of PMCA4 was downregulated in PASMCs after PDGF-BB stimulation, which was abolished by MEK/ERK inhibition. Functionally, suppression of PMCA4 attenuated the intracellular Ca2+ ([Ca2+]i) clearance in PASMCs after Ca2+ entry, promoting cell proliferation and elevating cells locomotion through mediating formation of focal adhesion. Additionally, the expression of PMCA4 was decreased in the pulmonary artery of MCT- or hypoxia-induced PAH rats. Moreover, knockdown of PMCA4 could increase the right ventricular systolic pressure and wall thickness of pulmonary artery in rats raised under normal condition. Taken together, our data proved the importance of the PDGF/MEK/ERK/PMCA4 axis in intracellular Ca2+ homeostasis in PASMCs, indicating a functional role of PMCA4 in pulmonary arterial remodeling and PAH development.

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