Carbon quantum dots (CQDs) doping semiconductors can boost solar-to-hydrogen conversion and the photodegradation in VIS-NIR light, therefore attract great attention, but the perspective of CQDs role is seldom explored. Here, a biomass-CQDs was assembled with BiOCl (CQDs/BiOCl), then served as the visible-photodegradation model for a mechanistic investigation. Furthermore, CQDs/BiOCl removed 90% bisphenol A (BPA) within 2 h under visible light. It was attributed to the C-localized state (CLS) produced by CQDs, which transfers forceless photo-electrons (e-) to generate holes (h+) in the CQDs/BiOCl valence band (VB) under visible light, the h+ mainly involved in the BPA degradation process. Then, the electrochemical experiments and theoretical calculations further proved that the efficiencies of charge separation (ηCS) and injection (ηCI) were proved by CQDs. Meanwhile, the possible BPA degradation pathways were accordingly proposed, and the ecotoxicity evaluation of the intermediates was also conducted by ECOSAR. The transformation pathways of BPA were divided into five orientations, and the toxicity of intermediates was decreased for Fish (LC50, ChV), Daphnid (LC50, ChV), Algae (EC50, ChV) except for P10 and P12. As the result, this study confirmed the feasibility of bio-CQDs/BiOCl preparation and it could be a photocatalyst to remove and detoxify BPA under visible light. The purpose of this study was to explore the effects of a short-term high-calorie diet and the regulation mechanism of Raphanus sativus L. seeds (RSL seeds) on the intestinal motility of young rats. We fed 20 Specific Pathogen Free (SPF) 4-week-old male Sprague-Dawley (SD) rats special high-calorie diet for 3 days and then randomized them to a high-calorie diet group (HCG, 10 rats) and an RSL seeds treatment group (TG, 10 rats). https://www.selleckchem.com/products/fl118.html Ten rats of the same age served as the control group (CG). HCG and TG rats continued to be fed high-calorie feed. All of the rats were weighed every 2 days. After 3 days of treatment, the effects of RSL seeds on the regulation of intestinal motility in rats consuming a high-calorie diet were examined. After 3 days of consuming a high-calorie diet, body weight was significantly lower in the HCG group than in the control group, and body weight of the HCG group increased slowly with time. Serum substance P (SP) and ghrelin levels were significantly lower, while the nitric oxide (NOs may improve the intestinal motility by regulating the secretion of gastrointestinal motility hormones and the expression of intestinal motility-related proteins, such as Cx43 and BDNF.In the current study, we conducted two experiments to investigate the impact of concurrent, action-induced auditory feedback on gait patterns, gaze behavior and outcome performance in long jumping. In Experiment 1, we examined the effects of present vs. absent auditory feedback on gait, gaze and performance outcome measures. Results revealed a significant interaction effect between condition (present vs. absent auditory feedback) and phase (acceleration vs. zeroing-in phase) on participants' step lengths indicating that the absence (rather than the presence) of auditory feedback led to facilitatory effects in terms of a more prototypical gait pattern (i.e., shorter steps in the acceleration phase and longer steps in the zeroing-in phase). Similarly, the absent auditory feedback led to a higher gaze stability in terms of less switches between areas of interest (AOIs). However, there was no effect on jumped distance. In Experiment 2, we scrutinized the influence of concurrent vs. delayed auditory feedback on all three performance parameters. In contrast to concurrent feedback, delayed auditory feedback negatively affected all three measures participants showed (i) dysfunctional deviations from their prototypical gait pattern (i.e., shorter steps across both phases of the run-up), (ii) less stable, maladaptive gaze patterns (i.e., more switches between AOIs) and (iii) poorer jumping performance (i.e., shorter jumped distances). Together, the two experiments provide clear evidence for the impact of concurrent, action-induced auditory feedback on the coordination of complex, rhythmical motor tasks such as the long jump. The apolipoprotein A-I mimetic peptide D-4F, among its anti-atherosclerotic effects, improves vasodilation through mechanisms not fully elucidated yet. Low-density lipoprotein (LDL) receptor null (LDLr ) mice were fed Western diet with or without D-4F. We then measured atherosclerotic lesion formation, endothelial nitric oxide synthase (eNOS) phosphorylation and its association with heat shock protein 90 (HSP90), nitric oxide (NO) and superoxide anion (O ) production, and tetrahydrobiopterin (BH4) and GTP-cyclohydrolase 1 (GCH-1) concentration in the aorta. Human umbilical vein endothelial cells (HUVECs) and aortas were treated with oxidized LDL (oxLDL) with or without D-4F; subsequently, BH4 and GCH-1 concentration, NO and O production, eNOS association with HSP90, and endothelium-dependent vasodilation were measured. Unexpectedly, eNOS phosphorylation, eNOS-HSP90 association, and O production were increased, whereas BH4 and GCH-1 concentration and NO production were reduced in atheroscleropression and decreasing eNOS phosphorylation and eNOS-HSP90 association. Our findings elucidate a novel mechanism by which hypercholesterolemia induces atherosclerosis and D-4F inhibits it, providing a potential therapeutic approach.Long non-coding RNAs (lncRNAs) are essential drivers or suppressors in human hepatocellular carcinoma (HCC) by participating in controlling transcription, translation, mRNA stability, and protein degradation protein-protein interaction. TM4SF1-AS1 is recently identified as a tumor-promoting factor in lung cancer. Nevertheless, its function in HCC and related molecular mechanisms remain unknown. Here, our data indicated that either hypoxia or hypoxia-inducible factor (HIF) prolyl hydroxylase inhibitor (DMOG) induced the upregulation of TM4SF1-AS1 in HCC cells. HIF-1α knockdown rather than HIF-2α silencing remarkably abrogated hypoxia-upregulated TM4SF1-AS1 expression. Furthermore, we confirmed the elevated expression of TM4SF1-AS1 in HCC tissue samples and cell lines. The silencing of TM4SF1-AS1 prominently inhibited the proliferative, migratory, and invasive abilities of HCC cells. TM4SF1-AS1 depletion significantly blocked hypoxia-enhanced Hep3B cell proliferation and mobility. Interfering TM4SF1-AS1 remarkably reduced TM4SF1 mRNA and protein levels in HCC cells.