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Autism spectrum disorder (ASD) is a group of developmental diseases characterized by social dysfunction and repetitive stereotype behaviors. Besides genetic mutations, environmental factors play important roles in the development of ASD. Valproic acid (VPA) is widely used for modeling environmental factor induced ASD in rodents. However, traditional VPA modeling is low-in-efficiency and the phenotypes often vary among different batches of experiments. To optimize this ASD-modeling method, we tested “two-hit” hypothesis by single or double exposure of VPA and poly:IC at the critical time points of embryonic and postnatal stage. The autistic-like behaviors of mice treated with two-hit schemes (embryonic VPA plus postnatal poly:IC, embryonic poly:IC plus postnatal VPA, embryonic VPA plus poly: IC, or postnatal VPA plus poly:IC) were compared with mice treated with traditional VPA protocol. The results showed that all single-hit and two-hit schemes produced core ASD phenotypes as VPA single treatment did. Only one group, namely, mice double-hit by VPA and poly:IC simultaneously at E12.5 showed severe impairment of social preference, social interaction and ultrasonic communication, as well as significant increase of grooming activity and anxiety-like behaviors, in comparation with mice treated with the traditional VPA protocol. These data demonstrated that embryonic two-hit of VPA and poly:IC is more efficient in producing ASD phenotypes in mice than the single-hit of VPA, indicating this two-hit scheme could be utilized for modeling environmental factors induced ASD.

Abstract Background A laser doppler flowmetry (LDF) test can reflect the pulp vitality caused by the change in pulp blood flow (PBF). This study aimed to investigate the PBF of the permanent maxillary incisors using LDF and to calculate the clinical reference range and coincidence rate for pulp vitality using PBF as an indicator. Methods School-age children (7–12 years) were recruited randomly. A total of 455 children (216 female and 239 male) were included in this study. An additional 395 children (7–12 years) who attended the department due to anterior tooth trauma from October 2015 to February 2018 were included to assess the clinical occurrence rate. The PBF was measured using LDF equipment and an LDF probe. Results The clinical reference range of PBF values for the permanent maxillary incisors (teeth 11, 12, 21, and 22) in children were from 7 to 14 perfusion units (PU), 11 (6.016; 11.900 PU), 12 (6.677; 14.129 PU), 21 (6.043;11.899 PU), and 22 (6.668; 14.174 PU). There was a statistically significant correlation between PBF and children’s age (p

IntroductionStreptococcus mutans is the most prevalent biofilm-forming pathogen in dental caries, while Candida albicans is often detected in the presence of S. mutans.MethodsWe aimed to evaluate the anti-caries effect of stevioside in medium trypticase soy broth (TSB) with or without sucrose supplementation compared with the same sweetness sucrose and xylitol in a dual-species model of S. mutans and C. albicans, based on planktonic growth, crystal violet assay, acid production, biofilm structural imaging, confocal laser scanning microscopy, and RNA sequencing.ResultsOur results showed that compared with sucrose, stevioside significantly inhibited planktonic growth and acid production, changed the structure of the mixed biofilm, and reduced the viability of biofilm and the production of extracellular polysaccharides in dual-species biofilm. Through RNA-seq, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway impact analysis showed that stevioside decreased sucrose metabolism and increased galactose and intracellular polysaccharide metabolism in S. mutans, and decreased genes related to GPI-modified proteins and secreted aspartyl proteinase (SAP) family in C. albicans. In contrast to xylitol, stevioside also inhibited the transformation of fungal morphology of C. albicans, which did not form mycelia and thus had reduced pathogenicity. Stevioside revealed a superior suppression of dual-species biofilm formation compared to sucrose and a similar anti-caries effect with xylitol. However, sucrose supplementation diminished the suppression of stevioside on S. mutans and C. albicans.ConclusionsOur study is the first to confirm that stevioside has anticariogenic effects on S. mutans and C. albicans in a dual-species biofilm. As a substitute for sucrose, it may help reduce the risk of developing dental caries.

InstructionThe purpose of this study was to evaluate the three-year success rate of the treatment for early childhood caries (ECC) under general anesthesia in different periods (2011 and 2018).MethodsChildren (

Abstract Background Nicotine is an important risk factor and the main toxic component associated with periodontitis. However, the mechanism of nicotine induced periodontitis is not clear. To investigated the mechanism through which nicotine regulates autophagy of human periodontal ligament cells (hPDLCs) through the alpha7 nicotinic acetylcholine receptor (α7 nAChR) and how autophagy further regulates the release of IL-1β and IL-8 secretion in hPDLCs. Methods HPDLCs were obtained from root of extracted teeth and pre-incubated in alpha-bungarotoxin (α-BTX) or 3-Methyladenine (3-MA), followed by culturing in nicotine. We used a variety of experimental detection techniques including western blotting, immunofluorescence, enzyme-linked immunosorbent assay (ELISA), transmission electron microscopy (TEM) and RT-qPCR to assess the expression of the LC3 protein, autolysosome, and release of IL-1β and IL-8 from hPDLCs. Results Western blots, immunofluorescence and TEM results found that the nicotine significantly increased the autophagy expression in hPDLCs that was time and concentration dependent and reversed by α-BTX treatment (p < 0.05). RT-qPCR and ELISA results revealed a noticeable rise in the release of inflammatory factors IL-1β and IL-8 from hPDLCs in response to nicotine. RT-qPCR and ELISA results showed that nicotine can significantly up-regulate the release of inflammatory factors IL-1β and IL-8 in hPDLCs, and this effect can be inhibited by 3-MA (p < 0.05). Conclusions Nicotine regulated autophagy of hPDLCs through α7 nAChR and in turn the regulation of the release of inflammatory factors 1L-1β and 1L-8 by hPDLCs.

Autophagy is a widespread biological process that controls cellular growth, survival, development, and death. Circadian rhythm is a recurring reaction of living organisms and behaviors to variations in surrounding brightness and obscurity. Most of the fundamental physiological processes in mammals, such as the sleep-wake pattern and the rhythm of nutrition and energy metabolism, are governed by circadian rhythms. Research has indicated that autophagy exhibits a specific circadian pattern in both normal and abnormal conditions. Autophagy can modulate circadian rhythms by breaking down proteins that regulate the circadian clock. The potential regulatory connection between the two has been a popular subject of clinical and fundamental research. Understanding the interaction between circadian rhythm and autophagy could potentially lead to the development of novel approaches for disease treatment in the future. The present analysis presented a summary of the molecular processes implicated in the interplay between autophagy and circadian rhythm, as well as the pathological importance of the disrupted regulatory association between these two phenomena. [ABSTRACT FROM AUTHOR]

Background and Objectives: Periodontitis is the top reason for tooth loss, and smoking significantly increases severe periodontitis risk. Defective autophagy has been reported to play a vital role in periodontitis. This study aimed to elucidate the relationship between autophagy and inflammation factors production in nicotine-treated periodontal ligament stem cells (PDLSCs) and the underlying mechanism. Methods: In this study, transmission electron microscopy, immunofluorescence, and the mCherry-GFP- LC3 plasmid were used to study autophagy flux. The gene levels of inflammation factors and long noncoding RNA nuclear paraspeckle assembly transcript 1 (lncRNA NEAT1) were detected by quantitative real-time PCR (qRT-PCR). Western blot was performed to assess the protein levels of autophagic markers and α7 nicotinic acetylcholine receptor (α7nAChR). Results: We found that nicotine impaired autophagosome-lysosome fusion and lysosome functions to block autophagy flux, contributing to inflammatory factors production in nicotine-treated PDLSCs. Moreover, nicotine upregulated NEAT1 by activating α7nAChR. NEAT1 decreased autophagy flux by downregulating syntaxin 17 (STX17). Conclusion: Our data indicate that NEAT1-decreased autophagy flux is pivotal for inflammation factors production in nicotine-treated PDLSCs. [ABSTRACT FROM AUTHOR]