Angiographic demonstration of a cutoff sign as an unfavorable prognostic indicator for patients with acute ischemic stroke undergoing mechanical thrombectomy.

OBJECTIVES: The aim was to investigate whether the angiographic demonstration of a cutoff sign on the initial angiogram could predict recanalization and prognosis in acute ischemic stroke patients treated by endovascular thrombectomy. METHODS: The angiographic and clinical data of patients who underwent endovascular treatment from October 2018 to April 2023 were retrospectively reviewed. The pretreatment angiographic appearance of the thrombus's proximal part was assessed and classified as either the cutoff sign (+) or (-). Patients' baseline characteristics and angiographic and clinical outcomes between the two groups were analyzed using propensity score matching. Then, the two commonly used techniques, stent retrieval and contact aspiration, were compared in terms of successful reperfusion and clinical outcome in patients with the cutoff sign. RESULTS: The cutoff sign was observed in 77 (36.2%) of 213 patients. Patients with the cutoff sign were younger and were less likely to have involvement of the anterior circulation. Compared with the cutoff sign (-) group, the cutoff sign (+) group had a significantly longer procedure time (103 versus 80 min, P =0.002) and a lower percentage of 3-month good functional outcomes (18.2% versus 36%, P =0.006). After propensity score matching, the procedure time (100 versus 75 min, P =0.002) and the 3-month good outcome (19.2% versus 41.4%, P =0.004) remained significantly different. No significant differences were observed in the radiological (OR 0.758, 95% CI 0.157 to 3.658; P =0.730) and clinical (OR 0.747, 95% CI 0.147 to 3.787; P =0.725) outcomes between the two techniques. CONCLUSIONS: The cutoff sign might be an unfavorable prognostic indicator in patients undergoing mechanical thrombectomy, and the efficacy of mechanical thrombectomy techniques does not differ in patients positive for the cutoff sign.

Clinical Value of Long Non-Coding RNA HOTAIR in Carotid Artery Stenosis and Its Role in Vascular Smooth Muscle Cell Proliferation.

This study investigated the clinical role of HOTAIR in patients with carotid artery stenosis (CAS) and its mechanism in vascular smooth muscle cells (VSMCs). Patients with CAS were collected. The expression of HOTAIR was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The clinical importance of HOTAIR was revealed by the receiver operating characteristic curve. Overexpression and knockdown of HOTAIR were achieved by transfecting pCDNA3.1-HOTAIR plasmid and si-HOTAIR respectively. CCK-8 assay or Transwell assay were used to analyze the changes in cell viability or migration after transfection treatments. Double luciferase reporter gene assay confirmed the targeted relationship between HOTAIR and miR-148b-3p. The levels of miR-148b-3p in VSMCs and patients were detected by qRT-PCR. Pearson analysis was used to analyze the relationship between HOTAIR and miR-148b-3p in patients with CAS. The expression of HOTAIR in patients with CAS was significantly higher than that in healthy individuals. HOTAIR appeared to discriminate CAS patients from healthy people. The overexpression of HOTAIR increased the viability and migration of VSMCs. Silenced HOTAIR restricted the abnormal viability and migration of VSMCs. A double luciferase reporter revealed a region of complementary binding between HOTAIR and miR-148b-3p. The expression of miR-148b-3p in VSMCs was regulated by the levels of HOTAIR. Reduction of miR-148b-3p expression was substantiated in CAS patients. Pearson analysis exhibited that the expression of HOTAIR was negatively relative to the levels of miR-148b-3p. The long noncoding RNA HOTAIR might be a diagnostic biomarker for CAS patients, and it was involved in the activity of vascular smooth muscle cells.

Macrophage migration inhibitory factor (MIF) acetylation protects neurons from ischemic injury.

Ischemia-induced neuronal death leads to serious lifelong neurological deficits in ischemic stroke patients. Histone deacetylase 6 (HDAC6) is a promising target for neuroprotection in many neurological disorders, including ischemic stroke. However, the mechanism by which HDAC6 inhibition protects neurons after ischemic stroke remains unclear. Here, we discovered that genetic ablation or pharmacological inhibition of HDAC6 reduced brain injury after ischemic stroke by increasing macrophage migration inhibitory factor (MIF) acetylation. Mass spectrum analysis and biochemical results revealed that HDAC6 inhibitor or aspirin treatment promoted MIF acetylation on the K78 residue. MIF K78 acetylation suppressed the interaction between MIF and AIF, which impaired MIF translocation to the nucleus in ischemic cortical neurons. Moreover, neuronal DNA fragmentation and neuronal death were impaired in the cortex after ischemia in MIF K78Q mutant mice. Our results indicate that the neuroprotective effect of HDAC6 inhibition and aspirin treatment results from MIF K78 acetylation; thus, MIF K78 acetylation may be a therapeutic target for ischemic stroke and other neurological diseases.

Hypereosinophilic syndrome with central nervous system involvement: Two case reports and literature review.

OBJECTIVE: To report two cases of hypereosinophilic syndrome (HES) with central nervous system involvement and explore its possible pathogenesis. METHODS: We have analysed the clinical data and relevant features of two patients who presented themselves to The Affiliated Hospital of Xuzhou Medical University between 2012 and 2015. We have reviewed the relevant literature, elaborated the possible pathogenesis, and discussed the treatment options. RESULTS: Both patients had consistently high levels of absolute eosinophil count which led to multiple cerebral infarcts in the arterial border zone and small-vessel disease. Blood tests were taken several times during their course of disease showing elevated eosinophils. Both patients underwent head computed tomography (CT), magnetic resonance imaging, and magnetic resonance angiography, which indicated small-vessel disease and watershed infarction. Glucocorticoids, improvement cycle, and neuro-nutrition treatments resulted in a significant improvement of their clinical state. CONCLUSION: HES can involve central nervous system by causing small-vessel disease and watershed infarction, which can be its presenting features. Repeated blood tests should be done to rule out HES in central nervous system lesion.