Summary
Background
The short‐term effect of ambient air pollution on atopic dermatitis (AD), along with its effect modifiers, has not been fully addressed.
Objectives
To examine the short‐term associations between air pollution and AD, and to identify effect modifications by age and season.
Methods
We used the generalized additive model to evaluate the short‐term effect of ambient air pollution on daily hospital visits for AD, adjusting for potential confounders. Subgroup analyses were performed to identify potential effect modifications by season and age (< 18 years and ≥ 18 years).
Results
A total of 29 972 hospital visits for AD were recorded in Guangzhou, China, from 19 January 2013 to 31 December 2017. Among them, 72·8% were visits by children and 51·4% occurred in the cool season. Acute and delayed effects on AD hospital visits were significant for all air pollutants. Stronger effects were seen in the cool season (approximately 1·7–3·0 times higher than effects in the warm season). Stronger effects were also observed in children (approximately 1·3–1·8 times higher than effects in adults). Sensitivity analyses indicated the results were robust.
Conclusions
Air pollution might be an important trigger for AD in subtropical Guangzhou, China. Children are more vulnerable than adults, and the effects are stronger in the cool season.
The dyshomeostasis of transition metal ions, accumulation of amyloid-β (Aβ) senile plaques and neuroinflammatory response found in the brain of patients with Alzheimer's disease (AD) have been suggested to be involved in AD pathogenesis. Novel compounds capable of targeting metal-Aβ species and neuroinflammation would be valuable. AD-35 is such a patented small-molecule compound derived from innovative modification of the chemical structure of donepezil. This compound could moderately inhibit acetylcholinesterase and metal-induced Aβ aggregation in vitro and showed disassembly of Aβ aggregates. The effects of AD-35 on cognitive impairments and neuroinflammatory changes caused by intracerebroventricular injection of Aβ25-35 were studied in rats. Compared to sham group, Aβ25-35 injection significantly led to learning and memory deficits, astrocyte activation, and pro-inflammatory cytokines releases (TNF-α and IL-1β). Further studies indicated that the phosphorylation of extracellular signal-regulated kinase was involved in astrocyte activation and pro-inflammatory cytokines production. Oral administration of AD-35 could markedly attenuate Aβ25-35 injection-induced astrocyte activation, pro-inflammatory cytokines TNF-α and IL-1β release, and memory deficits. On the contrary, donepezil only showed inhibition of IL-1β production, but failed to block astrocyte activation and TNF-α production. These results showed that AD-35 would be a novel multi-mechanism drug for the prevention and/or treatment of AD.
Using Sprague-Dawley rats and rat
PC12 cells treated with sodium
fluoride (NaF), we investigated the effects of SIK2-CRTC1 signaling
on the neurobehavioral toxicity induced by fluoride. The in
vivo results demonstrated that NaF treatment induced anxiety-
and depression-like behaviors in juvenile rats, resulting in histological
and ultrastructural abnormalities in the rat hippocampus and medial
prefrontal cortex. Moreover, NaF exposure induced neuronal loss and
excessive apoptosis. We also found that NaF elevated the expression
of SIK2 and reduced the expression of CRTC1, brain-derived neurotrophic
factor (BDNF), and VGF. The in vitro results showed
that NaF suppressed cell viability, induced SIK2-CRTC1 signaling dysfunction,
and caused excessive apoptosis in PC12 cells. Notably, targeted knockout
of SIK2 with SIK2-siRNA or blocking of SIK2-CRTC1 signaling with 7,8-dihydroxyflavone
(7,8-DHF) (as well as venlafaxine) can reduce apoptosis and increase
cell viability in vitro. These findings suggest that
neuronal death resulting from abnormal SIK2-CRTC1 signaling contributes
to neurobehavioral toxicity induced by fluoride.
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