Malignant brain edema is one of the serious complications of acute ischemic stroke, which is not uncommon after endovascular treatment, and can significantly reduce the benefits of endovascular treatment, leading to poor outcomes and even death of patients. Therefore, early identification and timely treatment are particularly important. This article reviewed the predictive factors, prevention and treatment of malignant brain edema in patients with acute ischemic stroke who received endovascular treatment.

Objective:To develop rapid screening tools for assessing the risk of mild cognitive impairment(MCI)based on neuropsychological scales and cognitive paradigms.Methods:Two baseline datasets from the Beijing Ageing Brain Rejuvenation Initiative(BABRI)cohort were studied: dataset 1 contained 5 593 subjects, with 1 500 cases with MCI and 4 093 cases with normal cognitive function(the control group); dataset 2 consisted of 588 subjects, with 92 cases with MCI and 496 cases with normal cognitive function(the control group). Dataset 1 was used to simplify the Mini-Mental State Examination(MMSE), and the sub-item combination with the strongest MCI discriminative ability was selected to integrate into the cognitive rapid assessment(BABRI-mini MMSE). Dataset 2 with scores of encoding-recognition episodic memory task was used for further MCI discriminant analysis and was adapted into an episodic memory test(BABRI-EMT). We applied the receiver operating characteristic curve(ROC)for those analyses.Results:The control group and the MCI group showed significant differences in multi-domain cognitive ability and episodic memory task performance( P<0.01). Among sub-items of MMSE measured using dataset 1, MMSE12 and MMSE19 had the highest discriminative accuracy for MCI, and the area under the ROC(AUC)was 0.699 and 0.631, respectively.Dataset 2 was used to investigate the discriminative ability of the episodic memory score in combination with the above two MMSE sub-items for MCI, and the AUC value was 0.732, the sensitivity was 0.731, and the specificity was 0.656. Conclusions:The BABRI-mini MMSE and BABRI-EMT are suitable for the large-scale universal screening of MCI risk.

Background and objective FK506, also named tacrolimus, a new macrolide immunosuppressive agent, has been shown to possess anti-proliferation activities in some cancer cells. The aim of this study was to investigate the effect of FK506 on the cell proliferation and migration of lung cancer cell lines and its mechanism. Methods A549 and H1299 cell lines were cultured in vitro. The effect of FK506 on cell viability and DNA synthesis ability of A549 and H1299 were measured by CCK-8 assay and EDU-labeling assay, respectively. Flow cytometry assay was used to detect the cell cycle. The in vitro mi-gration of lung cancer cells was detected by Boyden chamber assay and wound-healing assay after the treatment of FK506. The expression of p27, RB1, CDK4, CDK6 and MMP9 were detected using Western blot. Results FK506 inhibited cell growth and induced cell cycle arrest in G0/G1 phase in A549 and H1299 cells in a dose- and time-dependent manner. Compared to the control groups, the migration of A549 and H1299 cells treated with FK506 were decreased obviously. Moreover, FK506 in-creased the expression of P27 and RB1, and reduced the expression of CDK4, CDK6 and MMP9. Conclusion FK506 inhibit the cell growth and migration of lung cancer cells in vitro. The inhibitive effects may be associated with the up-regulation of p27 expression and inhibition CDK4, CDK6 and MMP9 expression.

BACKGROUND: Angiogenesis is an important process in the development of tumor. PD 0332991, a cell cycle inhibitor, can specifically inhibit CD4/6 phosphorylation and cell cycle progression. In xeongraft mice models, PD 0332991 treated mice had significantly decreased angiogenesis and vascular density compared with the control group, but the mechanism remains unknown. The purpose of this study is to investigate the role and molecular mechanism of PD 0332991 on vascular endothelial cells. METHODS: EA.hy926 cells, a kind of vascular endothelial cell, were used as the research model. The effects of PD 0332991 on the activity and proliferation of EA.hy926 cells were detected by the MTT, EdU assays. Wound-healing assays and transwell assays were used to determine the effects of PD 0332991 on the mobility of EA.hy926. The influence of PD 0332991 on cell cycle and apoptosis of endothelial cells was tested by flow cytometry, and the Western blot was applied to observe the expression of cell cycle related proteins in EA.hy926 cells treated by PD 0332991. RESULTS: PD 0332991 significantly inhibited the proliferation and mobility of EA.hy926 cells, caused cell cycle arrest and apoptosis. At the same time, PD 0332991 inhibited the expression of CDK4/6 and phosphorylation of Rb, and thus inhibited the cell cycle progression of EA.hy926 cells. CONCLUSIONS PD 0332991 can inhibit the proliferation and activity of endothelial cells and induces apoptosis.
Angiogenesis Inhibitors ; pharmacology ; Animals ; Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cell Survival ; drug effects ; Cyclin-Dependent Kinase 4 ; genetics ; metabolism ; Cyclin-Dependent Kinase 6 ; genetics ; metabolism ; Endothelial Cells ; cytology ; drug effects ; metabolism ; Humans ; Lung Neoplasms ; drug therapy ; genetics ; metabolism ; physiopathology ; Mice ; Piperazines ; pharmacology ; Pyridines ; pharmacology