Background: The occurrence of acute ischemic stroke in cancer patients is not unusual. In clinical practice, acute ischemic stroke with cancer usually cannot be diagnosed promptly due to lack of specific markers. But for cancer patients, advanced prevention, accurate diagnosis and proper treatment of acute ischemic stroke are very important. The aim of the present study was to investigate the clinical and neuroimaging features of acute ischemic stroke in patients with cancer. Methods: We conducted a retrospective review of all cancer-associated acute ischemic stroke patients (n = 46) admitted to the Affiliated Hospital of Academy of Military Medical Sciences between October 2011 and March 2015. A group of non-cancer acute ischemic stroke patients (n = 50) at the same period were selected randomly as control. The clinical and neuroimaging data were collected and compared between the 2 groups. Results: Patients with cancer-associated stroke (CS) had a lower body mass index (23.26 ± 3.70 vs. 24.88 ± 2.83, p = 0.021) compared to non-cancer stroke (NC) patients. A lower proportion of CS patients suffered from hypertension (45.7 vs. 68.0%, p = 0.039) and hyperlipidemia (10.9 vs. 72.0%, p = 0.000) than the NC group. A higher proportion of CS patients had deep vein catheter (24.0 vs. 0%) before the onset of stoke than that of the NC group. Levels of hemoglobin, albumin and triglyceride were lower in CS groups compared with that of the NC group (p < 0.05). The prothrombin time, international normalized ratio, D-dimer and fibrinogen levels were significantly higher in the CS group than in the NC group (p < 0.05). As to the neuroimaging patterns, disperse lesions (OR 7.01; 95% CI 1.17-42.12; p < 0.05) was independently associated with CS. Conclusions: Cancer-associated ischemic stroke was different form conventional ischemic stroke in the aspect of clinical and neuroimaging manifestation. This phenomenon might be because of the embolic etiology of CS. These features together could become a clue to CS.

Background and Purpose: This study aimed to analyze the association between hyperattenuated lesions (HALs) and postoperative intracranial hemorrhage (IH) and predict perioperative IH through quantitative analysis of HALs in acute ischemic stroke (AIS) with anterior large vessel occlusion (LVO) after endovascular therapy (ET).Materials and Methods: This retrospective, propensity-matched study enrolled AIS who received ET from a single-center registry study between August 2017 and May 2020. The enrolled patients were divided into two groups: IH and non-IH, by follow-up postoperative CT. The occurrences of HALs on immediate CT after ET were also recorded. The association between IH and HALs after propensity score matching (PSM) was determined by binary logistic regression models. The receiver operating characteristic (ROC) curve was used to determine the predictive value of the highest CT Hounsfield units (HU) value on immediate CT.Results: Initially, 1,418 patients who underwent digital subtraction angiography were reviewed and 114 AIS patients with immediate postoperative CT and follow-up CT after ET were enrolled. Forty-nine out of the 114 patients developed IH after therapy. After PSM analysis, patients with IH were more likely to have HALs on immediate CT (Odds Ratio, OR 11.9, P = 0.002, and 95% CI: 2.485–57.284). For 80 patients with HALs, ROC analysis of the highest CT value in the HALs territory showed that the cut-off value was 97 HU, the sensitivity was 70.21%, and the specificity was 81.82%.Conclusions: Patients with HALs after ET are more likely to have perioperative IH. The highest CT value in the HALs area might be used to predict IH.

Background Sepsis‐associated encephalopathy (SAE) is a serious complication of sepsis which results from neuroinflammation and could lead to cognitive dysfunction. Ubiquitin‐specific peptidase 8 (USP8) is involved in cognitive dysfunction. This study investigated the mechanism by which USP8 plays a role in cognitive dysfunction of SAE mice. Methods The SAE models were established by performing cecal ligation and puncture in the mice. Subsequently, a series of tests and procedures were conducted to assess the cognitive dysfunction and pathological impairment of mice, including the Morris water maze test, Y‐maze test, open field test, tail suspension test, fear conditioning test, and haematoxylin–eosin staining. The levels of USP8 and Yin Yang 1 (YY1) in brain tissues of mice were detected. In order to determine the effects of USP8 or YY1 on cognitive function, SAE mice were injected with an adenovirus‐packaged vector that had overexpressed levels of USP8 or YY1 short hairpin RNA. The binding of USP8 to YY1 and the ubiquitination level of YY1 were analyzed using immunoprecipitation and ubiquitination experiments. Lastly, chromatin immunoprecipitation was carried out to analyze enrichment of YY1 on the USP8 promoter. Results In SAE models, USP8 and YY1 were downregulated and cognitive functions were impaired. USP8 overexpression upregulated YY1 and attenuated the brain histopathological damage and cognitive dysfunction in SAE mice. USP8 upregulated YY1 protein level through deubiquitination, while YY1 was enriched on the USP8 promoter and activated USP8 transcription. The effects of USP8 overexpression on SAE mice was reversed secondary to YY1 silencing. Conclusion USP8 upregulated YY1 protein level through deubiquitination and YY1 activated USP8 transcription, and USP8‐YY1 feedback loop attenuated cognitive dysfunction in SAE mice, which could potentially serve as a novel theoretical foundation for the management of SAE.