ABSTRACT
Although cyberbullying is an emerging public health problem, it is unclear how the COVID-19 pandemic affects cyberbullying. This systematic review and meta-analysis aimed to examine the effect of the COVID-19 pandemic on cyberbullying, to estimate the global cyberbullying prevalence and to explore factors related to cyberbullying during the COVID-19 pandemic. We searched the Medline, Embase, PubMed, Scopus, Eric, PsycINFO, Web of Science, Cochrane Library, Wanfang, Chinese CNKI, and EBSCO databases to identify relevant empirical studies published between 2019 and 2022. A total of 36 studies were included. Quality assessment, meta-analyses, and subgroup analyses were conducted. The pooled prevalences were 16% for overall cyberbullying, 18% for victimization and 11% for perpetration during the COVID-19 pandemic, which were lower than before the COVID-19 pandemic. The pooled prevalence of postpandemic cyberbullying perpetration is lower in children than in adults. In addition, both virus- and lockdown-related stressors were the main factors contributing to cyberbullying. The COVID-19 crisis may reduce cyberbullying, and the pooled prevalence of cyberbullying during the pandemic in adults is higher than in children and adolescents. In addition, the transient-enduring factor model of postpandemic cyberbullying built in this review could help identify people at high risk of cyberbullying during public health emergencies.
Subject(s)
Bullying , COVID-19 , Cyberbullying , Humans , PandemicsABSTRACT
Recent studies have proposed three lymphatic drainage systems in the brain, that is, the glymphatic system, the intramural periarterial drainage pathway, and meningeal lymphatic vessels, whose roles in various neurological diseases have been widely explored. The glymphatic system is a fluid drainage and waste clearance pathway that utilizes perivascular space and aquaporin-4 protein located in the astrocyte endfeet to provide a space for exchange of cerebrospinal fluid and interstitial fluid. The intramural periarterial drainage pathway drives the flow of interstitial fluid through the capillary basement membrane and the arterial tunica media. Meningeal lymphatic vessels within the dura mater are involved in the removal of cerebral macromolecules and immune responses. After ischemic stroke, impairment of these systems could lead to cerebral edema, accumulation of toxic factors, and activation of neuroinflammation, while restoration of their normal functions can improve neurological outcomes. In this review, we summarize the basic concepts of these drainage systems, including drainage routes, physiological functions, regulatory mechanisms, and detection technologies. We also focus on the roles of lymphatic drainage systems in brain injury after ischemic stroke, as well as recent advances in therapeutic strategies targeting these drainage systems. These findings provide information for potential novel strategies for treatment of stroke.
ABSTRACT
Interstitial fluid (ISF) from brain drains along the basement membranes of capillaries and arteries as Intramural Periarterial Drainage (IPAD); failure of IPAD results in cerebral amyloid angiopathy (CAA). In this study, we test the hypothesis that IPAD fails after subarachnoid haemorrhage (SAH). The rat SAH model was established using endovascular perforation method. Fluorescence dyes with various molecular weights were injected into cisterna magna of rats, and the pattern of IPAD after SAH was detected using immunofluorescence staining, two-photon fluorescent microscope, transmission electron microscope and magnetic resonance imaging tracking techniques. Our results showed that fluorescence dyes entered the brain along a periarterial compartment and were cleared from brain along the basement membranes of the capillaries, with different patterns based on individual molecular weights. After SAH, there was significant impairment in the IPAD system: marked expansion of perivascular spaces, and ISF clearance rate was significantly decreased, associated with the apoptosis of endothelial cells, activation of astrocytes, over-expression of matrix metalloproteinase 9 and loss of collagen type IV. In conclusion, experimental SAH leads to a failure of IPAD, clinically significant for long term complications such as CAA, following SAH.