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Carriers for Nucleic Acid Delivery to the Brain
Published in Carla Vitorino, Andreia Jorge, Alberto Pais, Nanoparticles for Brain Drug Delivery, 2021
Intracranial injection into the cerebral parenchyma or cerebrospinal fluid (CSF) initially avoids systemic circulation and brings therapeutics close to the target side. Therapeutics injected into the CSF face the much less restrictive single-layer barrier of epithelial cells with gap-junctions between the CSF and the brain tissue [84]. However, the much smaller barrier surface compared to the BBB, constant turnover of CSF into the blood and limited diffusion within the brain parenchyma limit intracranial approaches [85, 86]. Still, the antisense oligonucleotide Nusinersen (Spinraza) gained FDA approval in 2016 for the treatment of spinal muscular atrophy and is administered by intrathecal injection into the CSF for the delivery of a therapeutic gene to neural stem cells [87]. Intraventricularly administered cationic liposomes and organically modified silica nanoparticles were used to successfully deliver siRNA [88] and pDNA [89] to neuronal cells in vivo. Luciferase encoding pDNA encapsulated in liposomes showed luciferase activity throughout the brain after injection in the cisterna magna of rats, but not after direct injection into the parenchyma [90]. Injection of luciferase expressing mRNA incorporated in polyplex nanomicelles into the cisterna magna of mice resulted in protein expression in the CSF for almost a week [91]. Biodegradable arginine ester of PAMAM dendrimers were used to deliver siRNA in the post-ischaemic brain by injection into the cortex of rats [92]. Tf-decorated siRNA-containing liposomes showed extensive local distribution and gene silencing after stereotactic administration into the striatum [93]. Silencing of the transcription factor c-Jun by RNA interference significantly decreased both cell death following glutamate-induced excitotoxic damage in primary neuronal cultures and neuronal death and inflammation following kainic acid-mediated lesions in the mouse hippocampus [94, 95]. Continuous injections of siRNA against toxic Huntingtin protein into the brain parenchyma were performed with osmotic pumps [96] and convection-enhanced delivery [97].
Reduction of fouling of gravity-driven membrane by combined treatment of persulphate/nanoscale zero-valent iron/ultraviolet and dynamic dual coagulant flocs layer
Published in Environmental Technology, 2023
Fuwang Zhao, Zhiwei Zhou, Peng Du, Xing Li, Qingxuan Lu
After the experiment, the used UF membranes were analysed by CLSM (Figure 5). Bacteria were clearly observed on the membrane following treatment of HA and HA-SA, but not for the membrane used with HA-BSA and HA-BSA-SA. This was attributed to the fact that BAS adhered to the UF membrane to block the pores, which also exacerbates membrane fouling. In HA-BSA treatment, BSA aggregated more effectively to adhere to the UF membrane pre-layered by flocs, while SA in HA-SA were typically small particles with a wider MW distribution. SA removal by PS/nZVI/UV was relatively low and a considerable quantity of SA diffused to the membrane cisterna. Flocs hardly cause SA agglomeration so that SA with small particle sizes was distributed on the UF membrane. However, pore blockage by SA was not complete and the membrane flux remained high. In HA-BSA-SA treatment, a floc layer was observed on the UF membrane that, according to CLSM, consisted of bacteria and protein. The flocs layer containing EPS adhered to the membrane, resulting in exacerbated membrane fouling. Compared with HA-SA, BSA in HA-BSA-SA exhibited a smaller particle size, indicating that the presence of SA hinders BSA agglomeration caused by flocs, resulting in severe membrane fouling in the treatment of HA-BSA-SA. As shown by CLSM, the particle size and distribution range of SA were smaller in HA-BSA-SA than in the treated HA-SA. This is possibly because BSA was the major component causing membrane fouling in HA-BSA-SA.