RESUMO
Nanoplastics (NPs) present a hidden risk to organisms and the environment via migration and enrichment. Detecting NPs remains challenging because of their small size, low ambient concentrations, and environmental variability. There is an urgency to exploit detection approaches that are more compatible with real-world environments. Herein, this study provides a surface-enhanced Raman spectroscopy (SERS) technique for the in situ reductive generation of silver nanoparticles (Ag NPs), which is based on photoaging-induced modifications in NPs. The feasibility of generating Ag NPs on the surface of NPs was derived by exploring the photoaging mechanism, which was then utilized to SERS detection. The approach was applied successfully for the detection of polystyrene (PS), polyvinyl chloride (PVC), and polyethylene terephthalate (PET) NPs with excellent sensitivity (e.g., as low as 1 × 10-6 mg/mL for PVC NPs, and an enhancement factor (EF) of up to 2.42 × 105 for small size PS NPs) and quantitative analytical capability (R2 > 0.95579). The method was successful in detecting NPs (PS NPs) in lake water. In addition, satisfactory recoveries (93.54-105.70 %, RSD < 12.5 %) were obtained by spiking tap water as well as lake water, indicating the applicability of the method to the actual environment. Therefore, the proposed approach offers more perspectives for testing real environmental NPs.
RESUMO
Alzheimer's disease (AD) is the most common neurodegenerative disorder, characterized by progressive cognitive decline and the accumulation of amyloid-beta plaques, tau tangles, and neuroinflammation in the brain. Postoperative cognitive dysfunction (POCD) is a prevalent and debilitating condition characterized by cognitive decline following neuroinflammation and oxidative stress induced by procedures. POCD and AD are two conditions that share similarities in the underlying mechanisms and pathophysiology. Compared to normal aging individuals, individuals with POCD are at a higher risk for developing AD. Emerging evidence suggests that astrocytes, the most abundant glial cells in the central nervous system, play a critical role in the pathogenesis of these conditions. Comprehensive functions of astrocyte in AD has been extensively explored, but very little is known about POCD may experience late-onset AD pathogenesis. Herein, in this context, we mainly explore the multifaceted roles of astrocytes in the context of POCD, highlighting their involvement in neuroinflammation, neurotransmitter regulation, synaptic plasticity and neurotrophic support, and discuss how POCD may augment the onset of AD. Additionally, we discuss potential therapeutic strategies targeting astrocytes to mitigate or prevent POCD, which hold promise for improving the quality of life for patients undergoing surgeries and against AD in the future.
Assuntos
Doença de Alzheimer , Disfunção Cognitiva , Complicações Cognitivas Pós-Operatórias , Humanos , Astrócitos/patologia , Complicações Cognitivas Pós-Operatórias/patologia , Doenças Neuroinflamatórias , Qualidade de Vida , Doença de Alzheimer/tratamento farmacológico , Disfunção Cognitiva/etiologia , Disfunção Cognitiva/patologia , Peptídeos beta-AmiloidesRESUMO
Traumatic brain injury (TBI), a significant contributor to mortality and morbidity worldwide, is a devastating condition characterized by initial mechanical damage followed by subsequent biochemical processes, including neuroinflammation. Astrocytes, the predominant glial cells in the central nervous system, play a vital role in maintaining brain homeostasis and supporting neuronal function. Nevertheless, in response to TBI, astrocytes undergo substantial phenotypic alternations and actively contribute to the neuroinflammatory response. This article explores the multifaceted involvement of astrocytes in neuroinflammation subsequent to TBI, with a particular emphasis on their activation, release of inflammatory mediators, modulation of the blood-brain barrier, and interactions with other immune cells. A comprehensive understanding the dynamic interplay between astrocytes and neuroinflammation in the condition of TBI can provide valuable insights into the development of innovative therapeutic approaches aimed at mitigating secondary damage and fostering neuroregeneration.