Background Oligodendrocyte precursor cells ( OPC s) regulate neuronal, glial, and vascular systems in diverse ways and display phenotypic heterogeneity beyond their established role as a reservoir for mature oligodendrocytes. However, the detailed phenotypic changes of OPC s after cerebral ischemia remain largely unknown. Here, we aimed to investigate the roles of reactive OPC s in the ischemic brain. Methods and Results The behavior of OPC s was evaluated in a mouse model of ischemic stroke produced by transient middle cerebral artery occlusion in vivo. For in vitro experiments, the phenotypic change of OPC s after oxygen glucose derivation was examined using a primary rat OPC culture. Furthermore, the therapeutic potential of hypoxic OPC s was evaluated in a mouse model of middle cerebral artery occlusion in vivo. Perivascular OPC s in the cerebral cortex were increased alongside poststroke angiogenesis in a mouse model of middle cerebral artery occlusion. In vitro RNA ‐seq analysis revealed that primary cultured OPC s increased the gene expression of numerous pro‐angiogenic factors after oxygen glucose derivation. Hypoxic OPC s secreted a greater amount of pro‐angiogenic factors, such as vascular endothelial growth factor and angiopoietin‐1, compared with normoxic OPC s. Hypoxic OPC ‐derived conditioned media increased the viability and tube formation of endothelial cells. In vivo studies also demonstrated that 5 consecutive daily treatments with hypoxic OPC ‐conditioned media, beginning 2 days after middle cerebral artery occlusion, facilitated poststroke angiogenesis, alleviated infarct volume, and improved functional disabilities. Conclusions Following cerebral ischemia, the phenotype of OPC s in the cerebral cortex shifts from the parenchymal subtype to the perivascular subtype, which can promote angiogenesis. The optimal use of hypoxic OPC s secretome would provide a novel therapeutic option for stroke.

Reduced adenosine triphosphate (ATP) levels in ischemic stroke constitute an upstream contributor to neuronal cell death. We have recently created a small chemical, named Kyoto University Substance 121 (KUS121), which can reduce cellular ATP consumption. In this study, we examined whether KUS121 has neuroprotective effects in rodent cerebral ischemia models. We evaluated cell viability and ATP levels in vitro after oxygen glucose deprivation (OGD) in rat cortical primary neuronal cultures incubated with or without KUS121. We found that KUS121 protected neurons from cell death under OGD by preventing ATP depletion. We also used in vivo ischemic stroke models of transient distal middle cerebral artery occlusion in C57BL/6 and B-17 mice. Administration of KUS121 in these models improved functional deficits and reduced brain infarction volume after transient focal cerebral ischemia in both C57BL/6 and B-17 mice. These results indicate that KUS121 could be a novel type of neuroprotective drug for ischemic stroke.

Here we describe a case of embolic internal carotid artery occlusion even under anticoagulation with dabigatran for chronic atrial fibrillation. Pulmonary vein (PV) thrombus after left upper lung resection was revealed in contrastenhanced CT scan, and suspected as a possible cause of thromboembolism. Potential role of thrombus in the stump of PV to cause embolism to vital organs remains to be elucidated. However, contrast-enhanced CT scan is recommended to detect PV thrombus after left upper lung resection, and anticoagulation therapy is indicated when thrombus is present.

Electrophysiological monitoring might be useful when intraoperative anatomical findings of the hemodynamic structure are inadequate. Moreover, in our case, intraoperative changes in motor evoked potentials indicated the risk to occlude one of posterior SAs, although it is said that posterior circulation of spinal cord has ischemic tolerance.

Objective: We report a rare case of sigmoid sinus dural arteriovenous fistula causing brainstem hemorrhage. Case Presentation: The patient was a 77-year-old woman who presented with right hemiparesis. Computed tomography of the head revealed pontine hemorrhage with marked perifocal edema. Cerebral angiography showed a sigmoid sinus dural arteriovenous fistula with drainage to the superior petrosal sinus connecting to the petrosal and transverse pontine veins. Transvenous embolization was successfully performed, resulting in complete occlusion.Conclusion: Brainstem hemorrhage can result from dural arteriovenous fistula. Careful diagnosis is important to avoid inappropriate treatment and adverse events.