Background: Ischemic stroke is one of the leading causes of human death and disability. Brain edema and peri-infarct astrocyte reactivity are crucial pathological changes, both involving aquaporin-4 (AQP4). Studies revealed that acute inhibition of AQP4 after stroke diminishes brain edema, however, its effect on peri-infarct astrocyte reactivity and the subacute outcome is unclear. And if diffusion-weighted imaging (DWI) could reflect the AQP4 expression patterns is uncertain.Methods: Rats were subjected to middle cerebral artery occlusion (MCAO) and allocated randomly to TGN 020-treated and control groups. One day after stroke, brain swelling and lesion volumes of the rats were checked using T2-weighted imaging (T2-WI). Fourteen days after stroke, the rats successively underwent neurological examination, T2-WI and DWI with standard b-values and ultra-high b-values, apparent diffusion coefficient (ADC) was calculated correspondingly. Finally, the rats’ brains were acquired and used for glial fibrillary acidic protein (GFAP) and AQP4 immunoreactive analysis.Results: At 1 day after stroke, the TGN-020-treated animals exhibited reduced brain swelling and lesion volumes compared with those in the control group. At 14 days after stroke, the TGN-020-treated animals showed fewer neurological function deficits and smaller lesion volumes. In the peri-infarct region, the control group showed evident astrogliosis and AQP4 depolarization, which were reduced significantly in the TGN-020 group. In addition, the ultra-high b-values of ADC (ADCuh) in the peri-infarct region of the TGN-020 group was higher than that of the control group. Furthermore, correlation analysis revealed that peri-infarct AQP4 polarization correlated negatively with astrogliosis extent, and ADCuh correlated positively with AQP4 polarization.Conclusion: We found that acutely inhibiting AQP4 using TGN-020 promoted neurological recovery by diminishing brain edema at the early stage and attenuating peri-infarct astrogliosis and AQP4 depolarization at the subacute stage after stroke. Moreover, ADCuh could reflect the AQP4 polarization.

Objectives: Hemangiopericytomas (HPCs) are rare intracranial tumors. Their differential diagnosis using computed tomography (CT) and magnetic resonance imaging (MRI) is difficult because of similarities in morphologic features with other intracranial tumors and meningiomas. Methods: We retrospectively analyzed the clinical data and CT and MRI findings of 32 patients diagnosed with HPCs via histopathology. We evaluated the location, shape, morphologic patterns, density, and signal intensity of the tumors and classified them into four types. Results: The number of tumors analyzed was 32; 29 were supratentorial and three were infratentorial. Eighteen tumors were lobular, while 14 were oval in shape. Further, 28 tumors had cystic areas, and 16 had signal-void vessels. Among the 20 tumors that had been scanned by MRI; eleven showed isointensity, eight slight hyperintensity, and one slight hypointensity on T1-weighted image. Moreover, 12 showed isointensity, and eight showed slight hyperintensity on T2-weighted image and T2-weighted-fluid-attenuated-inversion recovery. Diffusion-weighted images showed isointensity (9/13) or slight hyperintensity (4/13). Of the 15 tumors scanned by contrast-enhanced MRI, one showed poor enhancement; six, moderate enhancement; and eight, intense enhancement. Only one tumor exhibited the “dural tail” sign. Moreover, calcification was observed in just one tumor on CT imaging (1/22). All tumors (5/5) showed intense enhancement on CT angiography, whereas some exhibited dual blood supply (2/5). Conclusion: We conclude that tumors present outside the brain parenchyma, with isointense to slightly intense regions on MRI scans, oval/lobular shape, well-/ill-defined margins, signal-void vessels, apparent cystic areas, dual blood supply, and intense enhancement on CT or MRI scans, but without calcification or a “dural tail” sign, may be diagnosed as HPCs.