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Background: This meta-analysis aimed to evaluate the efficacy of carotid endarterectomy (CE) compared with carotid angioplasty (CA) in preventing stroke. Whether the use of CE is more efficient in preventing stroke than CA is a matter of debate.Methods: Data were gathered from randomized controlled trials to evaluate the effect of CE compared with CA on the risk of stroke. Electronic searches in PubMed, Embase, and the Cochrane Library were performed to identify studies till November 2014. Only randomized controlled trials performed on patients who received either CE or CA for stroke prevention were included.Results: Nine relevant trials (n = 7163) that met the inclusion criteria were identified. In a pooled analysis, CE resulted in 35 % reduction in relative risk (RR) for short-term stroke [RR, 0.65; 95 % confidence interval (CI): 0.47-0.89; P = 0.007)] and 22 % reduction in RR for long-term stroke (RR, 0.78; 95 % CI: 0.66-0.93; P = 0.006) relative to CA. However, CE also increased the risk of 30-day myocardial infarction by 114 % compared with CA (RR, 2.14; 95 % CI: 1.30-3.53; P = 0.003). Sensitivity analyses suggested that CE might influence the risk of 30-day major vascular events and 1-year major vascular events compared with CA.Conclusions: CE could reduce the risk of stroke (whether short term or long term), but resulted in a relative increase in the risk of myocardial infarction. This study might guide appropriate judgments about treatment approach. It also provided evidence to justify general guidelines for patients with carotid artery stenosis. [ABSTRACT FROM AUTHOR]

Inhibition of amyloid β (Aβ)-induced mitochondrial damage is considered crucial for reducing the pathological damage in Alzheimer's disease (AD). We evaluated the effect of neural stem cell-conditioned medium (NSC-CDM) on Aβ25-35-induced damage in SH-SY5Y cells. An in vitro model of AD was established by treating SH-SY5Y cells with 40 µM Aβ25-35 for 24 h. SH-SY5Y cells were divided into control, Aβ25-35 (40 µM), Aβ25-35 (40 µM) + NSC-CDM, and Aβ25-35 (40 µM) + neural stem cell-complete medium (NSC-CPM) groups. Cell viability was detected by CCK-8 assay. Apoptosis, reactive oxygen species (ROS) production, and mitochondrial membrane potential (MMP) were detected by flow cytometry. Malondialdehyde content was detected by ELISA assay. Western blot analysis was used to detect cytochrome c release and apoptosis-related proteins. Transmission electron microscopy was used to observe mitochondrial morphology. Cell viability significantly decreased and apoptosis significantly increased in SH-SY5Y cells treated with Aβ25-35, and both effects were rescued by NSC-CDM. In addition, NSC-CDM reduced ROS production and significantly inhibited the reduction of MMP caused by Aβ25-35. Furthermore, NSC-CDM ameliorated Aβ25-35-induced reduction in Bcl-2 expression levels and increased the expression levels of cytochrome c, caspase-9, caspase-3, and Bax. Moreover, Aβ25-35 induced the destruction of mitochondrial ultrastructure and this effect was reversed by NSC-CDM. Collectively, our findings demonstrated the protective effect of NCS-CDM against Aβ25-35-induced SH-SY5Y cell damage and clarified the mechanism of action of Aβ25-35 in terms of mitochondrial maintenance and mitochondria-associated apoptosis signaling pathways, thus providing a theoretical basis for the development of novel anti-AD treatments.

On behalf of the coauthors and with much regret, I must retract our publication entitled "Neural stem cell conditioned medium alleviates Aβ25-35 damage to SH-SY5Y cells through the PCMT1/MST1 pathway" published on European Journal of Histochemistry 2020;64(s2):3135 for the following reasons: In Figure 1A, the data of 20 μM Aβ25-35 for different time were confused with the data of 30 μM Aβ25-35 for different time. In Figure 2, the differential expression of PCMT1 is poor in repeatability. The authors need to revise the experimental design and steps to verify it again, re-do the experiment and conduct a more in-depth study. Dr. Congcong Sun Department of Neurology Qilu Hospital Cheeloo College of Medicine Shandong University China.

Alzheimer's disease (AD) is a progressive, neurodegenerative disease. Accumulating evidence suggests that protein isoaspartate methyltransferase 1 (PCMT1) is highly expressed in brain tissue (substantia nigra, blue plaque, paraventricular nucleus). In this study, we investigated the effect of neural stem cell conditioned medium alleviates Aβ25-35 damage to SH-SY5Y cells by PCMT1/MST1 pathway. Results demonstrated that Aβ25-35 significantly decreased the cell viability in time and dose dependent manner. However, Neural stem cell-complete medium (NSC-CPM) or NSC-CDM had inhibitory effect on toxicity when fibrillation of Aβ25-35 occurred in their presence and NSC-CDM had a better inhibitor result. An increase of the PCMT1 expression levels was found in Aβ25-35 + NSC-CDM group. sh-PCMT1 significantly reduced the PCMT1, the cell viability and inhibited the protective effect; induced apoptosis and increased the expression of p-MST1. Overexpression of PCMT1 group reversed the effect of Aβ25-35 inhibited the cell viability and Aβ25-35 induced the apoptosis. In conclusion, NSC-CDM corrects the damage of Aβ25-35 to cells by increasing PCMT1, reducing MST phosphorylation.