To explore the main factors affecting early dental caries among preschool children aged 3–6 years in Xingtai City to formulate effective preventive measures. A cross-sectional study was conducted on 570 preschool children aged 3–6 years in Xingtai City through questionnaire surveys and oral examinations to understand their dental caries situation. Multifactorial logistic regression analysis was used to analyse the main influencing factors for the occurrence of dental caries in preschool children. Univariate analysis showed statistically significant differences in age (χ2 = 2.636, p = 0.008), father's education level (χ2 = 4.207, p < 0.001), mother's education level (χ2 = 4.217, p < 0.001), daily tooth brushing frequency (χ2 = 3.160, p = 0.002), age of starting tooth brushing (χ2 = 8.756, p < 0.001), mouth rinsing after meals (χ2 = 89.401, p < 0.001), Streptococcus mutans positivity (χ2 = 133.503, p < 0.001), non-sweet snack consumption frequency (χ2 = 5.962, p < 0.001), snack flavour preference (χ2 = 116.119, p < 0.001), use of fluoridated toothpaste (χ2 = 75.639, p < 0.001), regular oral examinations (χ2 = 98.711, p < 0.001), sugary drink consumption frequency (χ2 = 10.370, p < 0.001) and sweet food consumption frequency (χ2 = 9.261, p < 0.001) between the caries and non-caries groups. Multifactorial analysis revealed that older age (odds ratio [OR] = 5.342, 95% confidence interval [CI]: 1.434–6.631), later initiation of tooth brushing (OR = 3.244, 95% CI: 2.413–5.424), S. mutans positivity (OR = 5.357, 95% CI: 4.529–8.563), high snack consumption frequency (OR = 3.452, 95% CI: 2.634–5.442), high sugary drink consumption frequency (OR = 4.414, 95% CI: 2.534–6.451) and high sweet food consumption frequency (OR = 4.531, 95% CI: 3.421–6.354) were risk factors for dental caries. Higher father's educational level (OR = 0.724, 95% CI: 0.564–0.891), higher mother's educational level (OR = 0.641, 95% CI: 0.601–0.813), high daily tooth brushing frequency (OR = 0.572, 95% CI: 0.423–0.864), mouth rinsing after meals (OR = 0.743, 95% CI: 0.643–0.813), use of fluoridated toothpaste (OR = 0.657, 95% CI: 0.553–0.931) and regular oral examinations (OR = 0.443, 95% CI: 0.352–0.747) were protective factors against dental caries (all p < 0.05). Multiple factors result in early dental caries in preschool children aged 3–6 years; however, the most influential factors are older age and high snack consumption, as well as high sugary and sweet food/drink consumption.
Acetylcholine causes endothelium-dependent relaxations in the rat aorta. Both muscarinic acetylcholine receptors (mAChRs) and nicotinic acetylcholine receptors (nAChRs) are expressed in endothelial cells. It is generally accepted that mAChRs are responsible for the endothelium-dependent relaxations evoked by acetylcholine. The present study was designed to investigate whether nAChRs can also be involved in such responses evoked by the cholinergic transmitter. Rings with or without endothelium of aortae of spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive rats were suspended in organ chambers for the measurement of isometric tension. In WKY aortae the muscarinic antagonist atropine abolished the relaxations to increasing concentrations of acetylcholine, confirming that mAChRs are responsible mainly for the response under control conditions. In SHR aortae, atropine caused only partial inhibition of the endothelium-dependent relaxations to acetylcholine; the remaining decreases in tension were inhibited by the nicotinic antagonist mecamylamine, which did not significantly affect the response in the absence of atropine in either SHR or WKY preparations. Thus, when mAChRs are inhibited, nAChRs mediate relaxation to the cholinergic transmitter in the SHR but not the WKY aorta. Nicotine, a direct agonist of the nicotinic receptor, induced endothelium-dependent relaxations in both SHR and WKY rats via the activation of α7-nAChRs, but not by mecamylamine-sensitive nicotinic receptors (α3 subtype). The acetylcholine-induced, atropine-insensitive relaxations and those to nicotine both involve the phosphatidylinositol 3-kinase/AKT pathway. The present study demonstrates that the activation of nAChRs can contribute to acetylcholine-induced, endothelium-dependent relaxations in the aortae of hypertensive animals and suggests that these receptors may contribute to the endothelium-dependent regulation of vascular tone.
Abstract Aims Perioperative neurocognitive disorders (PND) are associated with cognitive impairment in the preoperative or postoperative period, and neuroinflammation is thought to be the most important mechanisms especially during the postoperative period. The GABAergic system is easily disrupted by neuroinflammation. This study investigated the impact of the GABAergic system on PND after anesthesia and surgery. Methods An animal model of laparotomy with inhalation anesthesia in 16‐month‐old mice was addressed. Effects of the GABAergic system were assessed using biochemical analysis. Pharmacological blocking of α5GABA A Rs or P38 mitogen‐activated protein kinase (MAPK) were applied to investigate the effects of the GABAergic system. Results After laparotomy, the hippocampus‐dependent memory and long‐term potentiation were impaired, the levels of IL‐6, IL‐1β and TNF‐α up‐regulated in the hippocampus, the concentration of GABA decreased, and the protein levels of the surface α5GABA A Rs up‐regulated. Pharmacological blocking of α5GABA A Rs with L655,708 alleviated laparotomy induced cognitive deficits. Further studies found that the P38 MAPK signaling pathway was involved and pharmacological blocking with SB203,580 alleviated memory dysfunctions. Conclusions Anesthesia and surgery caused neuroinflammation in the hippocampus, which consequently disrupted the GABAergic system, increased the expressions of surface α5GABA A Rs especially through the P38 MAPK signaling pathway, and eventually led to hippocampus‐dependent memory dysfunctions.
Increasing evidence indicates that long non-coding RNAs (lncRNAs) act as important regulatory factors in tumor progression. However, their roles in breast cancer remain largely unknown. In present studies, we identified aberrantly expressed long intergenic non-coding RNA APOC1P1-3 (lincRNA-APOC1P1-3) in breast cancer by microarray, verified it by quantitative real-time PCR, and assessed methylation status in the promoter region by pyrosequencing. We also investigated the biological functions with plasmid transfection and siRNA silencing experiments, and further explored their mechanisms by RNA pull-down and RNA immunoprecipitation to identify binding proteins. We found that 224 lncRNAs were upregulated in breast cancer, whereas 324 were downregulated. The lincRNA-APOC1P1-3 was overexpressed in breast cancer, which was related to tumor size and hypomethylation in its promoter region. We also found that APOC1P1-3 could directly bind to tubulin to decrease α-tubulin acetylation, to inactivate caspase-3, and to inhibit apoptosis. This study demonstrates that overexpression of APOC1P1-3 can inhibit breast cancer apoptosis.
Plants are sensitive to external environmental conditions and the mechanisms of stress tolerance in plants are complex. As one of the most significant epigenetic phenomena, DNA methylation plays a crucial role in plants' adaptation to environmental changes. Recent research has improved our understanding of the relationship between DNA methylation and stress tolerance. Here, we review the mechanism of DNA methylation and discuss recent reports of the dynamics of DNA methylation in plants under abiotic stress conditions, including high salt concentration, drought, and extreme temperatures. The DNA methylation plays important functions during the response to stress in plants, but the differential variations of which were exhibiting in different species. The consistent or the specific mechanisms of DNA methylation need further exploration.
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