Effects of deferoxamine on blood-brain barrier disruption after subarachnoid hemorrhage - Fig 3

<p><b>(A</b>) Occludin immunoreactivity and protein levels in cortex after sham or subarachnoid hemorrhage induction with deferoxamine (DFX) treatment or vehicle at day 3, scale bar = 20μm. Values are mean ± SD; n = 3 for each group, #p<0.01, *p<0.05 vs. SAH+vehicle group at day 3. <b>(B)</b> ZO-1 immunoreactivity and protein levels in cortex after sham or subarachnoid hemorrhage induction with deferoxamine (DFX) treatment or vehicle at day 3, scale bar = 20μm. Values are mean ± SD; n = 3 for each group, #p<0.01 vs. SAH+vehicle group at day 3. <b>(C)</b> Claudin-5 immunoreactivity and protein levels in cortex after sham or subarachnoid hemorrhage induction with deferoxamine (DFX) treatment or vehicle at day 3, scale bar = 20μm. Values are mean ± SD; n = 3 for each group, *p<0.05 vs. SAH+vehicle group at day 3.</p

Double labeling of ferritin with CD31(endothelial marker), SWA (a pericyte marker), GFAP (an astrocyte marker), Iba-1 (a microglia marker) and NeuN (a neuron marker)in the cortex at day 3 after subarachnoid hemorrhage.

Scale bar = 20 μm.</p

Behavior and activity scores.

<p>Behavior and activity scores.</p

Ferritin immunoreactivity, and the ferritin heavy chain (FTH) and light chain (FTL) protein levels in cortex at day 3 after sham or subarachnoid hemorrhage induction with deferoxamine (DFX) treatment or vehicle, scale bar = 20μm.

<p>Values are mean ± SD; n = 3 for each group, #p<0.01 vs. SAH+vehicle group at day 3.</p

Data_Sheet_1_Vigilance or avoidance: How do autistic traits and social anxiety modulate attention to the eyes?.docx

IntroductionSocial anxiety disorder (SAD) and autism spectrum disorder (ASD) are highly overlapping in symptoms and have a high rate of comorbidity, posing challenges in diagnosis and intervention for both disorders. Both disorders are linked to abnormal attention to the eyes, yet how they interactively modulate the attentional process to the eyes remains unclear.MethodsIn this study, we explored how autistic traits and social anxiety in college students separately and together affected different temporal stages of attention to the eyes. Participants were instructed to view virtual faces for 10 s and make an emotional judgment, while their eye movements were recorded.ResultsWe found that social anxiety and autistic traits affected different temporal stages of eye-looking. Social anxiety only affected the first fixation duration on the eyes, while autistic traits were associated with eye avoidance at several time points in the later stage. More importantly, we found an interactive effect of autistic traits and social anxiety on the initial attention to the eyes: Among people scoring high on autistic traits, social anxiety was related to an early avoidance of the eyes as well as attention maintenance once fixated on the eyes.DiscussionOur study suggests the separate and interactive roles of social anxiety and autistic traits in attention to the eyes. It contributes to a deeper understanding of the mechanisms of social attention in both SAD and ASD and highlights the application of psychiatric diagnoses using eye-tracking techniques.</p

Western Blot analysis of autophagic-related protein expression after cerebral I/R injury.

<p>The level of LC3-II and Beclin 1 in ischemic cortex increased significantly from 6 to 24 h after reperfusion, with a maximal induction at 12 h. The expression of active cathepsin-B and LAMP1 in ischemic cortex increased significantly from 6 to 12 h after reperfusion, with a maximal induction at 12 h. Optical density of respective protein bands were analyzed with Sigma Scan Pro 5 and normalized to the loading control (β-actin). *p<0.05 versus sham group.</p

Protective effects of 3-mehtyladenine (3-MA) following cerebral I/R injury.

<p>3-MA (60 µg) solutions were injected icv immediately before reperfusion. (A) The changes of LC3 after the treatment of 3-MA. 3-MA significantly decreased LC3-II levels at 24 h after I/R. Effect of 3-MA on infarct volumes (B) and neurological deficits (C). 3-MA significantly reduced the infarct volume, and ameliorate the neurological symptoms at 24 h after I/R. ^#p<0.05 versus I/R group.</p

Effect of 15-PGJ₂ treatment on LC3 and cathepsin-B immunoreactivity after cerebral I/R injury.

<p>Double staining showed that LC3 punctate labeling and cathepsin-B immunoreactivity increased in neurons compared with sham-operated animals at 12 h after I/R injury. 15-PGJ2 at 50 pg effectively blocked the activation of autophagy as evidence by inhibiting immunoreactivity of LC3 (A) and cathepsin-B (B). Bar = 20 µm.</p

Electron micrographs of morphological changes of cortical neurons after cerebral I/R injury.

<p>(A) N, nucleus; Broad arrows represent autophagosomes; Narrow arrows represent mitochondria. (B) Quantitative analysis of the nubmeber of autophagosomes. Three animals in each group and 10 fields for each animal were examined. *p<0.05 versus sham group.</p

Additional file 1 of The association between ambient air pollution and scarlet fever in Qingdao, China, 2014–2018: a quantitative analysis

Additional file 1: Results of spearman correlation and sensitivity analysis