ABSTRACT
Objective:To investigate the effectiveness and safety of endovascular therapy for acute progressive stroke caused by large vessel occlusion (LVO).Methods:Patients with progressive stroke caused by LVO admitted to the Department of Neurology, Yueyang Central Hospital from January 2019 to February 2022 were retrospective included. Patients with an Alberta Stroke Program Early CT Score (ASPECTS) or posterior circulation ASPECTS (pc-ASPECTS) ≥6 after progression were selected for endovascular therapy, including mechanical thromboectomy, thrombus aspiration, balloon angioplasty, stenting, or a combination of the above methods. Patients in the time window (anterior circulation within 12 h and posterior circulation within 24 h) and outside the time window (anterior circulation >12 h, posterior circulation >24 h) as well as those in the anterior and posterior circulation were compared.Results:A total of 20 patients with progressive stroke caused by LVO received endovascular treatment were included. There were 17 males and 3 females, aged 59.45±12.06 years. Three patients (15%) developed asymptomatic intracranial hemorrhage, and 12 (60%) had a good outcome 3 months after procedure. There were no statistically significant differences in the rate of successful vascular recanalization, incidence of intracranial hemorrhage, and the rate of poor outcomes between patients within and outside the time window and between the patients with anterior and posterior circulation.Conclusion:Endovascular therapy may be safe and effective for patients with progressive stroke caused by LVO with ASPECTS or pc-ASPECTS scores ≥6.
ABSTRACT
OBJECTIVE To investigate the risk factors for hypokalemia caused by amphotericin B liposome， and to provide reference for clinical use of drugs. METHODS A retrospective analysis was used to collect the information of patients who used amphotericin B liposome during the hospitalization in First Affiliated Hospital of Hainan Medical College from January 2012 to December 2021. The details of use information about amphotericin B liposome and the potassium supplementation were collected. The patients were divided into hypokalemia group and normal group according to the occurrence of hypokalemia. Univariate and multi-variate Logistic regression analyses were used to analyze the risk factors for hypokalemia induced by amphotericin B liposome. RESULTS Of the 121 patients included in this analysis， 60 patients were in hypokalemia group， 61 patients were in normal group. The following parameters of the hypokalemic group were significantly higher or longer than those of the normal group， such as the maintenance dose， cumulative dose and maximum daily dose （in patients with severe hypokalemia） of amphotericin B liposome， treatment days， the maintained days of hypokalemia， daily dose of potassium supplement （in patients with moderate or severe hypokalemia）， the duration of potassium supplement （in patients with moderate hypokalemia）. Results of single factor analysis showed that the cumulative dose of amphotericin B liposome ≥200 mg and the duration of treatment ≥5 days were independent risk factors of hypokalemia caused by this drug （P＜0.05）. Multi-variate analysis results showed that the presence of basic hypokalemia， body weight ＜50 kg， cumulative dose of amphotericin B liposome ≥200 mg and the duration of treatment ≥5 days were the independent risk factors for hypokalemia caused by amphotericin B liposome （P＜0.05）. CONCLUSIONS The incidence of hypokalemia caused by amphotericin B liposome is high， the independent risk factors for hypokalemia include cumulative dose ≥200 mg， treatment days ≥5 days， the presence of basic hypokalemia and body weight ＜ 50 kg. It is suggested that serum potassium should be elevated to normal level before amphotericin B liposome treatment， and the level of serum potassium should be monitored during medication to reduce the occurrence of hypokalemia.
ABSTRACT
Nonalcoholic fatty liver disease (NAFLD) is closely related to glycolipid metabolism and liver inflammation. And there is no effective drug approved for its clinical therapy. In this study, we focused on mangiferin (Man) and explored its effects and mechanisms on NAFLD treatment based on the regulation of glycolipid metabolism and anti-inflammatory in vivo and in vitro. The results exhibited that Man can significantly attenuate liver injury, insulin resistance, and glucose tolerance in high-fat diet- (HFD-) induced NAFLD mice and significantly reduce fat accumulation and inflammation in hepatic tissue of NAFLD mice. The transcriptome level RNA-seq analysis showed that the significantly different expression genes between the Man treatment group and the HFD-induced NAFLD model group were mainly related to regulation of energy, metabolism, and inflammation in liver tissue. Furthermore, western blots, real-time PCR, and immunohistochemistry experiments confirmed that Man significantly activated the AMPK signal pathway and inhibited NLRP3 inflammasome activation and pyroptosis in NAFLD mice. In in vitro cell experiments, we further confirmed that Man can promote glucose consumption and reduce intracellular triglyceride (TG) accumulation induced by free fatty acids in HepG2 cells and further that it can be blocked by AMPK-specific inhibitors. Western blot results showed that Man upregulated p-AMPKα levels and exhibited a significant AMPK activation effect, which was blocked by compound C. At the same time, Man downregulated the expression of NLRP3 inflammasome-related proteins and inhibited the activation of NLRP3 inflammasome, alleviating cell pyroptosis and inflammation effects. These results indicate that Man anti-NAFLD activity is mediated through its regulation of glucolipid metabolism by AMPK activation and its anti-inflammatory effects by NLRP3 inflammasome inhibition. Our study indicates that Man is a promising prodrug for the therapy of NAFLD patients.
