Linezolid is an oxazolidinone antibacterial drug, and its therapeutic drug monitoring and individualized treatment have been challenged since its approval. With the in-depth clinical research of linezolid, we have changed our attitude toward its therapeutic drug monitoring and our view of individualized treatment. On the basis of summarizing the existing clinical studies, and based on the practical experience of each expert in their respective professional fields, we have formed this expert consensus. Our team of specialists is a multidisciplinary team that includes pharmacotherapists, clinical pharmacology specialists, critical care medicine specialists, respiratory specialists, infectious disease specialists, emergency medicine specialists and more. We are committed to the safe and effective use of linezolid in patients in need, and the promotion of its therapeutic drug monitoring.

Objectives: To explore the protection and the mechanism of dexmedetomidine on the oxygen–glucose deprivation (OGD) insults in rat C6 glioma cells. Methods: Cells were subjected to OGD then assessed by viability studies. After dexmedetomidine treatment, p-AKT, hypoxia-inducible factor (HIF)-1α, vascular endothelial growth factor (VEGF) and RTP801 expression were measured. Key findings: Three hours of OGD decreased cell viability to 48.8%, which was reversed to 67.4% by 1 µm dexmedetomidine. Hoechst 33342 and propidium iodide double stains showed that the protection of dexmedetomidine was mainly by an anti-apoptosis effect, which was also strengthened by decreasing caspase-3 expression. Dexmedetomidine protection was mainly blocked by the I2 imidazoline receptor antagonist idazoxan and BU 224, but not by the α1-adrenoceptor antagonist prazosin, the α2-adrenoceptor antagonist yohimbine and RX 821002, or the I1 imidazoline receptor antagonist efaroxan. On the other hand, dexmedetomidine enhanced AKT phosphorylation. Furthermore, the protection of dexmedetomidine was blocked by the PI3K/AKT inhibitor wortmannin. The proteins of HIF-1α, VEGF and RTP801 were significantly increased by dexmedetomidine treatment. Conclusions: Dexmedetomidine activated the I2 imidazoline receptor-PI3K/AKT pathway, and up-regulated HIF-1α, VEGF and RTP801 expression to protect against OGD-induced injury in rat C6 cells.

Complex febrile seizures (FSs) lead to a high risk of intractable temporal lobe epilepsy during adulthood, yet the pathological process of complex FSs is largely unknown. Here, we demonstrate that activated microglia extensively associated with glutamatergic neuronal soma displace surrounding GABAergic presynapses in complex FSs. Patch-clamp electrophysiology establishes that the microglial displacement of GABAergic presynapses abrogates a complex-FS-induced increase in GABAergic neurotransmission and neuronal excitability, whereas GABA exerts an excitatory action in this immature stage. Pharmacological inhibition of microglial displacement of GABAergic presynapses or selective ablation of microglia in CD11bDTR mice promotes the generation of complex FSs. Blocking or deleting the P2Y12 receptor (P2Y12R) reduces microglial displacement of GABAergic presynapses and shortens the latency of complex FSs. Together, microglial displacement of GABAergic presynapses, regulated by P2Y12R, reduces neuronal excitability to mitigate the generation of complex FSs. Microglial displacement is a protective event during the pathological process of complex FSs.

Adropin is expressed in the CNS and plays a crucial role in the development of stroke. However, little is currently known about the effects of adropin on the blood‐brain barrier (BBB) function after intracerebral hemorrhage (ICH). In this study, the role of adropin in collagenase‐induced ICH was investigated in mice. At 1‐h post‐ICH, mice were administered with recombinant human adropin by intranasal. Brain water +content, BBB permeability, and neurological function were measured at different time intervals. Proteins were quantified using western blot analysis, and the localizations of adropin and Notch1 were visualized via immunofluorescence staining. It is shown that adropin reduced brain water content and improved neurological functions. Adropin preserved the functionality of BBB by increasing N‐cadherin expression and reducing extravasation of albumin. Moreover, in vivo knockdown of Notch1 and Hes1 both abolished the protective effects of adropin. Taken together, our data demonstrate that adropin constitutes a potential treatment value for ICH by preserving BBB and improving functional outcomes through the Notch1 signaling pathway. image