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The aim of this study was to investigate the abnormities in functional connectivity (FC) within each modular network and between modular networks in patients with systemic lupus erythematosus (SLE). Twelve meaningful modular networks were identified via independent component analysis from 41 patients and 40 volunteers. Parametric tests were used to compare the intra- and intermodular FC between the groups. Partial correlation analysis was used to seek the relationships between abnormal FCs and the clinical data. Compared to the controls, SLE patients showed decreased intramodular FC in the anterior default mode network (aDMN), posterior default mode network (pDMN), ventral attention network (VAN), and sensorimotor network (SMN) and increased intramodular FC in the medial visual network (mVN) and left frontoparietal network. In addition, SLE patients showed decreased intermodular FC between the SMN and the lateral visual network (lVN), between the SMN and the VAN, and between the pDMN and the lVN and exhibited increased intermodular FC between the SMN and the salience network (SAN), between the pDMN and the SAN, and between the aDMN and the VAN. Moreover, we found several correlations among the abnormal FCs and the Mini-Mental State Examination in SLE patients. Mild cognitive impairment is compensated by the hyperconnectivity between the aDMN and the VAN, while severe cognitive impairment tends to be compensated by the hyperconnectivity between the SMN and the SAN. The FC value between the SMN and the SAN and between the aDMN and the VAN may serve as neuroimaging markers for monitoring cognitive progression in SLE patients., (© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Using resting-state functional magnetic resonance imaging and graph theory approaches to investigate the topological characteristics of functional networks and their potential correlations with clinical information in patients with systemic lupus erythematosus (SLE). A total of 41 patients and 35 volunteers were consecutively recruited. Detailed clinical data of all participants were recorded. All participants underwent a resting-state functional magnetic resonance imaging examination. Functional networks were constructed by a Pearson correlation matrix of 116 brain regions. The topological properties were analyzed by graph theory. Parametric tests were used to compare the topological properties between the groups. Partial correlation analysis was used to identify relationships between the abnormal topological properties and the clinical data. The nodal network metrics were abnormal in the SLE patients compared to the controls. Decreased nodal efficiency was identified in the right insula, bilateral putamen, and bilateral Heschl's gyrus in the SLE patients. Decreased degree centrality was also found in the right amygdala and bilateral Heschl's gyrus. In addition, the SLE patients showed decreased network functional connectivity (FC) between several regions, particularly between the basal ganglia and the cerebellum. Moreover, FC values between the right putamen and vermis 6 were positively correlated with Mini-Mental State Examination scores. The nodal efficiency and the degree centrality values in the left Heschl's gyrus were both positively correlated with the course of the disease. The topological structure of the functional network was apparently abnormal in SLE patients. FC values between the right putamen and vermis 6 may serve as a neuroimaging marker for evaluating the progressive cognitive decline in SLE patients. Decreased synergy between the basal ganglia region and the cerebellum in the extrapyramidal system may be one cause of cognitive dysfunction in SLE patients.

We previously reported that inhibition of Rho-kinase (ROCK) by hydroxyl fasudil improves cognitive deficit and neuronal damage in rats with chronic cerebral ischemia (Huang et al., Cell Mol Neurobiol 28:757-768, 2008). In this study, fasudil mesylate (FM) was investigated for its neuroprotective potential in rats with ischemia following middle cerebral artery occlusion (MCAO) and reperfusion. The effect of fasudil mesylate was also studied in rat brain cortical and hippocampal slices treated with oxygen-glucose deprivation (OGD) injury. Gross anatomy showed that cerebral infarct size, measured with 2,3,5-triphenyltetrazolium chloride (TTC) staining, was significantly smaller in the FM-treated than in the non-FM-treated ischemic rats. In the brain regions vulnerable to ischemia of ischemic rats, fasudil mesylate was also found to significantly restore the enzyme protein expression level of endothelial nitric oxide synthase (eNOS), which was decreased in ischemia. However, it remarkably reduced the protein synthesis of inducible nitric oxide synthase (iNOS) that was induced by ischemia and reperfusion. In rat brain slices treated with OGD injury, fasudil mesylate increased the neuronal cell viability by 40% for cortex and by 61% for hippocampus, respectively. Finally, in the presence of OGD and fasudil mesylate, superoxide dismutase (SOD) activity was increased by 50% for cortex and by 58% for hippocampus, compared to OGD only group. In conclusion, our in vivo study showed that fasudil mesylate not only decreased neurological deficit but also reduced cerebral infarct size, possibly and at least partially by augmenting eNOS protein expression and inhibiting iNOS protein expression after ischemia-reperfusion.