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Combined detection of antinuclear antibody (ANA), anti-double-stranded DNA (ds-DNA) antibody and complements C3 and C4 in the diagnosis of systemic lupus erythematosus (SLE) was analyzed. One hundred and ninety-four patients with SLE admitted to Yantaishan Hospital of Yantai from January 2012 to December 2017 were selected as SLE group. A total of 106 patients with non-SLE rheumatic disease were selected as disease control group and 120 healthy subjects as healthy control group. The ANA and anti-ds-DNA antibodies were detected by ELISA and complement C3 and C4 were detected by rate nephelometry. The sensitivity and specificity of these four factors were also analyzed for the diagnosis of SLE. The sensitivity and specificity of ANA in diagnosing SLE were 91.75 and 79.65%, respectively; of anti-ds-DNA antibody were 67.01 and 98.23%, respectively; of complement C3 were 87.11 and 82.74%, respectively; and of complement C4 were 88.66 and 77.43%, respectively. The sensitivity and specificity of ANA and anti-ds-DNA antibody in the diagnosis of SLE were 95.36 and 96.90%, respectively; of C3 and C4 were 92.78 and 79.20%, respectively; and the sensitivity and specificity of the combination of all four indicators were 97.42 and 80.97%, respectively. The combined diagnosis of SLE with ANA, anti-ds-DNA antibody, complement C3 and C4 can play a complementary role in the diagnosis and treatment of SLE patients, and it is of great significance to the diagnosis and treatment planning of SLE patients.

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Disruption of the blood-brain barrier (BBB) can lead to cognitive impairment. Major facilitator superfamily domain-containing protein 2a (Mfsd2a) is a newly discovered protein that is essential for maintaining BBB integrity. However, the role of Mfsd2a in vascular cognitive impairment has not been explored yet. In this study, a rat model of chronic cerebral hypoperfusion (CCH) was established by producing permanent bilateral common carotid artery occlusion (2VO) in rats. We found that after the 2VO procedure, the rats exhibited cognitive impairment, showed increased BBB leakage within the hippocampus, and had reduced expression of the Mfsd2a protein. The overexpression of Mfsd2a in the rat hippocampus reversed these changes. Further investigations using transmission electron microscopy revealed a significantly increased rate of vesicular transcytosis in the BBB of the hippocampus of the CCH rats; the rate reduced after overexpression of Mfsd2a. Moreover, Mfsd2a overexpression did not cause changes in the expression of tight junction-associated proteins and in the ultrastructures of the tight junctions. In conclusion, Mfsd2a attenuated BBB damage and ameliorated cognitive impairment in CCH rats, and its protective effect on the BBB was achieved via inhibition of vesicular transcytosis.