Working memory components modulation of attentional disengagement from evaluative distractor.

It is important for people to disengage attention from a distraction, which can help them complete the task at hand as quickly as possible. Recent studies have shown that people's attention stays longer on reward-distractors than on loss-distractors, and a delay in attentional disengagement is noted when reward-distractors are present. However, few studies have examined whether attentional disengagement from an evaluative distractor relies upon working memory (WM) components. In the present study, we used an attentional disengagement paradigm in which reward- or loss-distractors were presented at a central location and the target was presented at a peripheral location, in combination with different WM tasks. The results from Experiment 1 showed that participants were slower to disengage their attention from a central reward-distractor than a loss-distractor regardless of cognitive load when the phonological loop component of WM was involved. The results from Experiment 2 revealed that people had difficulty in shifting their attention away from a reward-distractor in comparison to a loss-distractor when spatial WM was low, whereas no such difference was observed when spatial WM was high. We conclude that WM components differently modulate attentional disengagement from evaluative distractors. That is, the processing of evaluative (reward and loss) distractors may rely on the same cognitive resources as the spatial WM component, but not the phonological loop component.

Metformin alleviates junctional epithelium senescence via the AMPK/SIRT1/autophagy pathway in periodontitis induced by hyperglycemia.

The junctional epithelium (JE) serves a crucial protective role in the periodontium. High glucose-related aging results in accelerated barrier dysfunction of the gingival epithelium, which may be associated with diabetic periodontitis. Metformin, an oral hypoglycemic therapeutic, has been proposed as a anti-aging agent. This study aimed to clarify the effect of metformin on diabetic periodontitis and explore its mechanism in ameliorating senescence of JE during hyperglycemia. The db/db mice was used as a diabetic model mice and alterations in the periodontium were observed by hematoxylin-eosin staining and immunohistochemistry. An ameloblast-like cell line (ALC) was cultured with high glucose to induce senescence. Cellular senescence and oxidative stress were evaluated by SA-ß-gal staining and Intracellular reactive oxygen species (ROS) levels. Senescence biomarkers, P21 and P53, and autophagy markers, LC3-II/LC3-I, were measured by western blotting and quantitative real-time PCR. To construct a stable SIRT1 (Sirtuin 1) overexpression cell line, we transfected ALCs with lentiviral vectors overexpressing the mouse SIRT1 gene. Cellular senescence was increased in the JE of db/db mice and the periodontium was destroyed, which could be alleviated by metformin. Moreover, oxidative stress and cellular senescence in a high glucose environment were reduced by metformin in in-vitro assays. The autophagy inhibitor 3-MA and SIRT1 inhibitor EX-527 could dampen the effects of metformin. Overexpression of SIRT1 resulted in increased autophagy and decreased oxidative stress and cellular senescence. Meanwhile, AMPK (AMP-activated protein kinase) inhibition reversed the anti-senescence effects of metformin. Overall, these results suggest that metformin alleviates periodontal damage in db/db mice and cellular senescence in ALCs under high glucose conditions via the AMPK/SIRT1/autophagy pathway.

TGF-ß1/Smad3 Signaling Is Required to Alleviate Fluoride-Induced Enamel Hypomineralization.

Excessive fluoride intake during enamel development can affect enamel mineralization, leading to dental fluorosis. However, its potential mechanisms remain largely unexplored. In the present study, we aimed to investigate the impact of fluoride on the expressions of RUNX2 and ALPL during mineralization and the effect of TGF-ß1 administration on fluoride treatment. A dental fluorosis model of newborn mice and an ameloblast cell line ALC were both used in the present study. The mice of the NaF group, including the mothers and newborns, were fed with water containing 150 ppm NaF after delivery to induce dental fluorosis. The mandibular incisors and molars showed significant abrasion in the NaF group. Immunostaining, qRT-PCR, and Western blotting analysis indicated that exposure to fluoride markedly down-regulated RUNX2 and ALPL in mouse ameloblasts and ALCs. Besides, fluoride treatment significantly decreased the mineralization level detected by ALP staining. Furthermore, exogenous TGF-ß1 up-regulated RUNX2 and ALPL and promoted mineralization, while the addition of SIS3 could block such TGF-ß1-induced up-regulation. In TGF-ß1 conditional knockout mice, the immunostaining of RUNX2 and ALPL was weaker compared with wild-type mice. Exposure to fluoride inhibited the expressions of TGF-ß1 and Smad3. Co-treatment of TGF-ß1 and fluoride up-regulated RUNX2 and ALPL compared with the fluoride alone treatment, promoting mineralization. Collectively, our data indicated that TGF-ß1/Smad3 signaling pathway was necessary for the regulatory effects of fluoride on RUNX2 and ALPL, and the fluoride-induced suppression of ameloblast mineralization was mitigated by activating TGF-ß1/Smad3 signaling pathway.

The influence of perceptual load on gaze-induced attentional orienting: The modulation of expectation.

Humans tend to focus on others' gaze. Previous studies have shown that the gaze direction of others can induce corresponding attentional orienting. However, gaze cues have typically been presented alone in these studies. It is unclear how gaze cues induce observers' attention in complicated contexts with additional perceptual information. Therefore, the present study investigated gaze-induced attentional orienting at different levels of perceptual load. Results indicated that the attentional effect of the dynamic gaze cue (i.e., GCE: gaze cue effect) emerged under low perceptual load and disappeared under high perceptual load. The absence of GCE could not attribute to perceptual capacity exhaustion. Moreover, the influence of perceptual load on gaze-induced attentional orienting was modulated by individuals' expectation. Specifically, the GCE occurred under high perceptual load when the gaze cue was predictive (with individuals' expectation). These findings provide new evidence on the mode of gaze-induced attentional orienting under different perceptual load conditions.

Focused attention: its key role in gaze and arrow cues for determining where attention is directed.

Others' gaze direction and traffic arrow signal lights play significant roles in guiding observers' attention in daily life. Previous studies have shown that gaze and arrow cues can direct attention to the cued location. However, it is ambiguous where gaze and arrow cues guide attention: the cued location or a broader cued region. Therefore, the present study adopted a primary cue-target task and manipulated possible target locations to explore this issue. The results revealed that due to the different physical characteristics of non-predictive gaze and arrow cues, physically unfocused-pointing gaze cues guided attention to a broader cued region, whereas focused-pointing arrow cues guided attention to the exact cued location. Furthermore, gaze cues could also direct attention to the exact cued location when observers' attention was focused in a top-down manner (with highly predictive probability). These findings suggest that where gaze and arrow cues direct attention depends on whether observers' attention is focused by the cues, either in a bottom-up or top-down manner. Accordingly, a preliminary framework called the "Focused-Diffused Attentional Orienting Model" is proposed to explain how gaze and arrow cues direct humans' attention. The present study enhances our understanding of human attentional orienting systems from a behavioral perspective.