Aims: Nonvalvular atrial fibrillation often occurs in combination with carotid atherosclerosis, but less is known about it in combination with cerebral artery stenosis. This study investigated the characteristics of cerebral infarction in patients with nonvalvular atrial fibrillation with or without cerebral artery stenosis. 13.3%) were higher in the stenosis group (n 107) than in the non-stenosis group (n 65) (P 0.01). In the stenosis group, there were different types of cerebral infarction lesions, including multiple infarction (multifocal type), massive infarction, watershed infarction, and lacunar infarction; in the non-stenosis group, the 60.0% lesions were multiple infarction (multifocal type), a significantly higher proportion than the stenosis group (26.2%, P 0.05). NIHSS score was an independent risk factor for worse prognosis at follow-up (OR (95%CI) 1.251-1.674, P 0.001). Methods Conclusions:Advanced age, hypertension, and stroke/TIA were increased in patients with cerebral infarction with nonvalvular atrial fibrillation combined with cerebral artery stenosis.bral infarction patients with atrial fibrillation are higher than that of cerebral infarction patients without atrial fibrillation 3) . Understanding the risk factors for cerebral infarction in patients with NVAF relies on the reasonable assessment of the risk of complicated cerebral infarction. These risks can then guide strategies for the prevention of thromboembolism. Clinicians can use the CHA2DS2-VASc score as a way of Introduction Nonvalvular atrial fibrillation (NVAF) is the most common type of atrial fibrillation and an independent risk factor for cerebral infarction; about 20% of the cases of cerebral infarction are cardiogenic cerebral infarction and, of these, nearly 50% are caused by NVAF 1, 2)

Primary familial brain calcification (PFBC) is a rare neurodegenerative disorder with four causative genes (SLC20A2, PDGFRB, PDGFB, and XPR1) that have been identified. Here, we aim to describe the mutational spectrum of four causative genes in a series of 226 unrelated Chinese PFBC patients. Mutations in four causative genes were detected in 16.8% (38/226) of PFBC patients. SLC20A2 mutations accounted for 14.2% (32/226) of all patients. Mutations in the other three genes were relatively rare, accounting for 0.9% (2/226) of all patients, respectively. Clinically, 44.8% of genetically confirmed patients (probands and relatives) were considered symptomatic. The most frequent symptoms were chronic headache, followed by movement disorders and vertigo. Moreover, the total calcification score was significantly higher in the symptomatic group compared to the asymptomatic group. Functionally, we observed impaired phosphate transport induced by seven novel missense mutations in SLC20A2 and two novel mutations in XPR1. The mutation p.D164Y in XPR1 might result in low protein expression through an enhanced proteasome pathway. In conclusion, our study further confirms that mutations in SLC20A2 are the major cause of PFBC and provides additional evidence for the crucial roles of phosphate transport impairment in the pathogenies of PFBC.

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MRI is suitable to evaluate tumor extent with high accuracy, and it can offer more objective information for the diagnosis and staging of UCC. Compared with clinical examinations based on FIGO, MRI illustrated relatively high accuracy in evaluating UCC staging, and is worthwhile to be recommended in future clinical practice.