Search

Background The acute inhibition of glymphatic after stroke has been shown to aggravate post-stroke inflammation and apoptosis; however, the related mechanisms remain ambiguous. This study aimed to assess the specific mechanism of inflammation and apoptosis after cerebral ischemia-reperfusion (I/R) injury by improving glymphatic dysfunction. Materials and Methods Ischemic stroke was induced using the mice middle cerebral artery occlusion (MCAO) model. The C57/BL6 mice were randomly divided into three groups as follows: sham operation, Ischemia-reperfusion (I/R) 48 hours, and N-(1,3,4-thiadiazol-2-yl) pyridine-3-carboxamide dihydrochloride (TGN-020) + I/R 48 hours treatment. Neurological examination, TTC, fluorescence tracer, western blot, and immunofluorescence staining were performed in all mice in sequence. The glymphatic function in the cortex surrounding cerebral infarction was determined using tracer, glial fibrillary acid protein (GFAP), aquaporin-4 (AQP4) co-staining, and beta-amyloid precursor protein (APP) staining, differential genes were detected using RNA-seq. Iba-1, IL-1β, TNF-α, cleaved caspase 3, and tunel staining were used to verify inflammation and apoptosis after TGN-020 treatment. Results Compared with I/R group, the degree of neurological deficit was alleviated in TGN-020 group. TGN-020 alleviated glymphatic dysfunction by improving astrocyte proliferation and reducing tracer accumulation in the peri-infarct area. RNA-seq showed that the differentially expressed genes were mainly involved in the activation of astrocytes and microglia, and involved in the ERK pathway. RNA-seq was verified by western blot and immunofluorescence. Conclusions The inflammation of astrocytes and microglia after cerebral ischemia-reperfusion (I/R) is closely related to the glymphatic system. The improvement of glymphatic function may play a neuroprotective role after cerebral I/R by inhibiting inflammation through ERK pathway.

Background: In-stent restenosis (ISR) remains a serious clinical problem that affects the efficacy of endovascular treatment. Inflammation and platelet activation play an important role in the development of ISR after cerebrovascular bare-metal stenting. The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR), which are the indicators of inflammation, have been associated with stent restenosis, while low serum albumin (ALB) level has been associated with the adverse outcomes of cardiovascular diseases. We therefore explored the associations among preprocedural NLR, ALB level, and PLR with ISR after cerebrovascular bare-metal stenting and then investigated the value of preprocedural NLR, ALB level, and PLR for the development of ISR. Methods: In this study, we enrolled 223 patients who underwent cerebrovascular bare-metal stenting (both intracranial and extracranial) and retrospectively analyzed their clinical, hematological, and angiographic data. Radiographic evaluations were performed at 6 and 12 months after the procedure. Results: ISR was defined as ≥ 50% stenosis of the treated lesion. Patients were divided into two groups based on the occurrence of ISR. ISR occurred in 89 (39.91%) of the 223 included patients. Increased pre-procedural NLR (p < 0.001) and PLR (p < 0.001) and decreased pre-procedural ALB level (p < 0.001) were significantly associated with ISR. Conclusions: High pre-procedural NLR and PLR, and low pre-procedural ALB level may be used as predictors of ISR after cerebrovascular bare-metal stenting. Trial Registration: retrospective registration.

With the development of 5G wireless technology and Internet of Things, electromagnetic interference (EMI) and heat generation in electronic devices and interconnects are becoming increasingly ubiquitous due to the proliferation of wearable electronics. It raises great concerns that EMI and elevated heat degrade device performance and also cause detrimental effects on human health. The soft and deformable materials that are capable of simultaneously shielding EMI and dissipating heat effectively are thus in high demand. Herein, a flexible composite material exhibiting substantial increases of electrical/thermal conductivities and EMI shielding effectiveness (SE) under compression was developed by introducing three-dimensional (3D) liquid metal (LM) network into an elastomer foam. The electrical conductivity, thermal conductivity, and EMI SE of the 3D LM/elastomer foam increase more than 14, 8.3, and 1.8 times, respectively, when compressed to a strain of 60% due to the compress-induced improvement in percolation of the LM. Moreover, neither microstructure damage nor performance degradation was observed in the foam during 10,000 compress-release cycles under 50% strain. Furthermore, we have demonstrated the proof-of-concept applications of the 3D LM/elastomer foam used as soft EMI shields and heat spreaders in wearable electronics.