The administration of CD34-positive cells after stroke has been shown to have a beneficial effect on functional recovery by accelerating angiogenesis and neurogenesis in rodent models. Granulocyte colony-stimulating factor (G-CSF) is known to mobilize CD34-positive cells from bone marrow and has displayed neuroprotective properties after transient ischemic stress. This led us to investigate the effects of G-CSF administration after stroke in mouse. We utilized permanent ligation of the M1 distal portion of the left middle cerebral artery to develop a reproducible focal cerebral ischemia model in CB-17 mice. Animals treated with G-CSF displayed cortical atrophy and impaired behavioral function compared with controls. The negative effect of G-CSF on outcome was associated with G-CSF induction of an exaggerated inflammatory response, based on infiltration of the peri-infarction area with CD11b-positive and F4/80-positive cells. Although clinical trials with G-CSF have been started for the treatment of myocardial and limb ischemia, our results indicate that caution should be exercised in applying these results to cerebral ischemia.

Objective This study aimed to investigate the effect of sequential bilateral low‐frequency repetitive transcranial magnetic stimulation (rTMS) over dorsolateral prefrontal cortex (DLPFC) on patients with primary insomnia (PI). Methods A total of 32 eligible right‐handed participants diagnosed by PI according to International classification of sleep disorders (ICD‐3) were recruited into this study. Participants received 10 daily sessions of sequential bilateral 1 Hz rTMS over DLPFC. Before and after the whole procedure of rTMS, patients were assessed by Pittsburgh Sleep Quality Index (PSQI) for the severity of sleep disturbance. Meanwhile, serum concentration of brain‐derived neurotrophic factor (BDNF) and gamma‐aminobutyric acid (GABA) in patients was measured by ELISA and UPLC, respectively. Moreover, the amplitude of MEPs reflecting the right cortical excitability was examined. Finally, Pearson correlation analysis was performed to evaluate the correlation among the change of these variables. Results After rTMS treatment, the PSQI score was markedly decreased as compared to pre‐rTMS; the concentrations of serum BDNF and GABA were significantly higher; the amplitude of MEPs was markedly reduced. Pearson correlation analysis revealed that the change of PSQI score was negatively associated with the alteration of serum BDNF level and serum GABA level, and positively associated with the change of MEPs amplitude; the change of MEPs amplitude was negatively associated with fold change in the serum BDNF level and the serum GABA level; the increase in serum GABA level was positively associated with the serum BDNF level. Conclusions A sequential bilateral low‐frequency rTMS over DLPFC significantly improves primary insomnia probably by increasing the level of BDNF and GABA in the brain and reducing cortical excitability.

Aspirin down regulates transferrin receptor 1 (TfR1) and up regulates ferroportin 1 (Fpn1) and ferritin expression in BV-2 microglial cells treated without lipopolysaccharides (LPS), as well as down regulates hepcidin and interleukin 6 (IL-6) in cells treated with LPS. However, the relevant mechanisms are unknown. Here, we investigate the effects of aspirin on expression of hepcidin and iron regulatory protein 1 (IRP1), phosphorylation of Janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3) and P65 (nuclear factor-κB), and the production of nitric oxide (NO) in BV-2 microglial cells treated with and without LPS. We demonstrated that aspirin inhibited hepcidin mRNA as well as NO production in cells treated with LPS, but not in cells without LPS, suppresses IL-6, JAK2, STAT3, and P65 (nuclear factor-κB) phosphorylation and has no effect on IRP1 in cells treated with or without LPS. These findings provide evidence that aspirin down regulates hepcidin by inhibiting IL6/JAK2/STAT3 and P65 (nuclear factor-κB) pathways in the cells under inflammatory conditions, and imply that an aspirin-induced reduction in TfR1 and an increase in ferritin are not associated with IRP1 and NO.

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