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Previous studies on working memory processing characteristics of anxious people have focused more on effects of trait than state anxiety, especially the processing characteristics of working memory under emotional faces. Learning anxiety not only affects teenagers' learning but also their life and overall personality development. This is the first study to examine adolescents with learning anxiety and explore effects of different negative emotional faces on working memory. Adolescents with learning anxiety (n = 30) and typically developing (n = 30) adolescents completed the emotional 2-back task with both facial emotion and gender as target stimulus. When facial emotion was the target stimulus, the two groups were asked to remember facial emotions (anger, sadness, and neutral). When facial gender was the target and facial emotion was the background stimulus, the two groups remembered the facial gender. Working memory performance in the learning anxiety group was worse than in the typically developing group. When facial emotion was the target stimulus, angry and sad faces significantly interfered with working memory performance in the learning anxiety group. When facial gender was the target stimulus and facial emotion was the background stimulus, the interference effect of negative emotion was greater and the accuracy was lower in the learning anxiety group. Therefore, different from the biased effect of trait anxiety on negative emotions, negative emotions (anger and sadness) interfere with the working memory of adolescents in the learning anxiety group. This interference exists regardless of whether negative emotions are the target or background. This result suggests recommendations for educational practices. That is, the interference from negative emotions on students should be avoided, especially those with learning anxiety. [ABSTRACT FROM AUTHOR]

The Zhaoanzhuang-type iron depositsoccur in the ultrabasic unit of the late Archaean greenstone belt. They are late magmatic apatite-titanomagnetite deposits, superimposed and enriched by hydrothermal solutions after their formation. Later they have also been subjected to regional metamorphism. These deposits are extremely complex in mineralogy, containing 87 kinds of mìnerals characteristic of ultrabasic-alkali complexes. Mineralization of iron, titanium and phosphorus took place mainly during the magmatic stage, while that of uranium and thorium during the pneumatolytic-hydrothermal stage. [ABSTRACT FROM AUTHOR]

Background: The activation of NOD-like receptor protein 3 (NLRP3) inflammasome-dependent pyroptosis has been shown to play a vital role in the pathology of manganese (Mn)-induced neurotoxicity. Sodium para-aminosalicylic acid (PAS-Na) has a positive effect on the treatment of manganism. However, the mechanism is still unclear. We hypothesized that PAS-Na might act through NLRP3.Methods: The microglial cell line BV2 and male Sprague-Dawley rats were used to investigate the impacts of PAS-Na on Mn-induced NLRP3 inflammasome-dependent pyroptosis. The related protein of the NF-κB pathway and NLRP3-inflammasome-dependent pyroptosis was detected by western blot. The reactive oxygen species and mitochondrial membrane potential were detected by immunofluorescence staining and flow cytometry. The activation of microglia and the gasdermin D (GSDMD) were detected by immunofluorescence staining.Results: Our results showed that Mn treatment induced oxidative stress and activated the NF-κB pathway by increasing the phosphorylation of p65 and IkB-α in BV2 cells and in the basal ganglia of rats. PAS-Na could alleviate Mn-induced oxidative stress damage by inhibiting ROS generation, increasing mitochondrial membrane potential and ATP levels, thereby reducing the phosphorylation of p65 and IkB-α. Besides, Mn treatment could activate the NLRP3 pathway and promote the secretion of IL-18 and IL-1β, mediating pyroptosis in BV2 cells and in the basal ganglia and hippocampus of rats. But an inhibitor of NF-κb (JSH-23) treatment could significantly reduce LDH release, the expression of NLRP3 and Cleaved CASP1 protein and IL-1β and IL-18 mRNA level in BV2 cells. Interestingly, the effect of PAS-Na treatment in Mn-treated BV2 cells is similar to those of JSH-23. Besides, immunofluorescence results showed that PAS-Na reduced the increase number of activated microglia, which stained positively for GSDMD.Conclusion: PAS-Na antagonized Mn-induced NLRP3 inflammasome dependent pyroptosis through inhibiting NF-κB pathway activation and oxidative stress. [ABSTRACT FROM AUTHOR]