Optofluidic microreactors are promising prospects for photocatalytic reactions. However, because the flow type in conventional designs is typically laminar, the mass transport mainly relies on diffusion, and thus the rate of mass transport is limited. Accordingly, poor mass transport reduces the photocatalytic reaction rate. To alleviate the limitation of mass transport, in this work, we proposed a novel optofluidic microreactor with TiO2-coated fiberglasses immersed in the microreaction chamber. Such a design enables enhanced mass transport by shortening the transport length and inducing the perturbation to liquid flow so as to improve the performance. We demonstrated the feasibility of the optofluidic microreactor with the TiO2-coated fiberglass by the photocatalytic water treatment of methylene blue under UV irradiation. Results showed that the proposed optofluidic microreactor yielded much higher degradation efficiency than did the conventional optofluidic microreactor as a result of enhanced mass transport. The microreactor with the TiO2-coated fiberglass showed a 2-3-fold improvement in the reaction rate constant as opposed to conventional ones. The maximal increment of the degradation efficiency can reach more than 40%.
Background Neuroinflammation is one of the most important processes in secondary injury after traumatic brain injury (TBI). Triggering receptor expressed on myeloid cells 2 (TREM2) has been proven to exert neuroprotective effects in neurodegenerative diseases and stroke by modulating neuroinflammation, and promoting phagocytosis and cell survival. However, the role of TREM2 in TBI has not yet been elucidated. In this study, we are the first to use COG1410, an agonist of TREM2, to assess the effects of TREM2 activation in a murine TBI model. Methods Adult male wild-type (WT) C57BL/6 mice and adult male TREM2 KO mice were subjected to different treatments. TBI was established by the controlled cortical impact (CCI) method. COG1410 was delivered 1 h after CCI via tail vein injection. Western blot analysis, immunofluorescence, laser speckle contrast imaging (LSCI), neurological behaviour tests, brain electrophysiological monitoring, Evans blue assays, magnetic resonance imaging (MRI), and brain water content measurement were performed in this study. Results The expression of endogenous TREM2 peaked at 3 d after CCI, and it was mainly expressed on microglia and neurons. We found that COG1410 improved neurological functions within 3 d, as well as neurological functions and brain electrophysiological activity at 2 weeks after CCI. COG1410 exerted neuroprotective effects by inhibiting neutrophil infiltration and microglial activation, and suppressing neuroinflammation after CCI. In addition, COG1410 treatment alleviated blood brain barrier (BBB) disruption and brain oedema; furthermore, COG1410 promoted cerebral blood flow (CBF) recovery at traumatic injury sites after CCI. In addition, COG1410 suppressed neural apoptosis at 3 d after CCI. TREM2 activation upregulated p-Akt, p-CREB, BDNF, and Bcl-2 and suppressed TNF-α, IL-1β, Bax, and cleaved caspase-3 at 3 d after CCI. Moreover, TREM2 knockout abolished the effects of COG1410 on vascular phenotypes and microglial states. Finally, the neuroprotective effects of COG1410 were suppressed by TREM2 depletion. Conclusions Altogether, we are the first to demonstrate that TREM2 activation by COG1410 alleviated neural damage through activation of Akt/CREB/BDNF signalling axis in microglia after CCI. Finally, COG1410 treatment improved neurological behaviour and brain electrophysiological activity after CCI. Graphical Abstract
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