ObjectiveTo explore the difference of anesthesia recovery and postoperative conscious state between remimazolam toluenesulfonic acid and propofol after induction and maintenance of general anesthesia.Methods104 patients undergoing elective tracheal intubation general anesthesia in our hospital were randomly divided into 2 groups: Remimazolam Toluenesulfonic acid group (Group R) and Propofol group (Group P). MOAA/S score, the modified Aldrete score, recovery index, time point, a state of consciousness, interpretative vital signs and adverse events were monitored at different time.ResultsCompared with the Group P, the extubation time and orientation recovery time of the Group R were significantly shorter. When the operation time was less than 1 hour, the MOAA/S score of the Group R was shorter than that of Group P at 5 min and 15 min after the operation. To compare with the Group P, the score of MOAA/S in the Group R increased at 5 min, 20 min and 30 min after the operation. When the operation time was less than or equal to 1 h, the modified Aldrete score in the Group R was slightly higher than that in the Group P at 30 min after extubation. There was no injection pain in the the Group R, and the incidence of hypotension was lower than that of propofol.ConclusionCompared with Propofol, when the operation time of general anesthesia is more than 1 hour, recovery time of Remimazolam Toluenesulfonic acid is shorter, with more complete and higher‐quality recovery.

Alzheimer's disease (AD) is a degenerative brain disease with complex clinical manifestations and pathogeneses such as abnormal deposition of beta-amyloid protein and inflammation caused by the excessive activation of microglia. CXC motif chemokine receptor type 4 (CXCR4) is a type of G protein-coupled receptor that binds to CXC motif ligand 12 (CXCL12) to activate downstream signaling pathways, such as the Janus kinase/signal transducer and activator of transcription and the renin-angiotensin system (Ras)/RAF proto-oncogene serine (Raf)/mitogen-activated protein kinase/extracellular-regulated protein kinase; most of these signaling pathways are involved in inflammatory responses. CXCR4 is highly expressed in the microglia and astrocytes; this might be one of the important causes of inflammation caused by microglia and astrocytes. In this review, we summarize the mechanism and therapeutics of AD, the structures of CXCR4 and the CXCL12 ligand, and the mechanisms of CXCR4/CXCL12 that are involved in the occurrence and development of AD.The possible treatment of AD through microglia and astrocytes is also discussed, with the aim of providing a new method for the treatment of AD.

Background: Hypoxic-ischemic encephalopathy (HIE) could induce exacerbated changes and unpredictable efects in brain cells, and the mechanism remains unclear.Methods: HIE model was established in neonatal rats, Zea-Longa score and TTC staining were used to observe the neurobehavior and brain infarct volume in rats subjected to cerebral hypoxia-ischemia (HI). Primary cortical neurons were then cultured in vitro to establish an oxygen and glucose deprivation model. To determine the role of synaptosomal-associated protein-25 (SNAP25) in HIE, PC12 cells were cultured and efective siRNA fragments were screened, and SNAP25 was transfected into primary neurons. Then, quantitative real-time polymerase chain reaction was used to detect the mRNA expression level and immunofluorescence staining was used to observe the morphological changes of neurons before and after the injury. Finally, the abundance values of SNAP25 and its associated genes were iltered using the NCBI and GeneMANIA, respectively. Results: HI leads to a decrease in neuronal number and an increase in SNAP25 expression. Whereas, the interference of SNAP25 caused marked decrease in neuronal number and the length of neurite. Moreover, the expression levels of CREB and SYP were signiicantly decreased after interference of SNAP25. Conclusion:SNAP25 exhibited several neuroprotective efects to neuronal protection in neonatal cerebral HI by regulating CREB and SYP. others promote neuronal death (Papadopoulos MC, et al., 2000). In addition, HIE is often difficult to diagnose in real time because of convulsions and other non-speciic encephalopathy, and is the most common reason of perinatal asphyxia (Zhang Y, et al., 2016). HIE can also lead to severe brain damage and is a common cause of neurological handicaps in adulthood (Kojima T, et al., 2013). Currently, there is no efective clinical treatments to mitigate HI-induced brain injury, due to the lack of understanding of the neural networks associated with HIinduced neurodegeneration and its mechanisms (Liu S, Article history:

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