Schwarzvilladsen2641

We investigated the effect of Acer tegmentosum Maxim (ATM) on adipocyte differentiation in 3T3-L1 cells and anti-obesity properties in obese rats fed a high-fat diet (HFD). Cellular lipid content in DMI (dexamethasone, 3-isobutyl-1-methylxanthine, and insulin mixture)-treated cells increased, while ATM treatment caused a significant reduction in lipid accumulation in differentiated 3T3-L1 cells. ATM (60 ug/mL) caused inhibition of adipogenesis via down-regulation of the CCAAT/enhancer binding protein β (C/EBPβ) (48%), C/EBPα (66%), and peroxisome proliferator-activated receptor γ (PPARγ) (64%) expressions in 3T3-L1 cells. Moreover, ATM induced a decrease in the expressions of adipocyte-specific genes, such as adipocyte fatty acid-binding protein-2 (aP2), fatty acid synthase (FAS), and lipoprotein lipase (LPL). Protein kinase B (Akt) and glycogen synthase kinase 3β (GSK3β) phosphorylation was also decreased by ATM treatment of 3T3-L1 adipocytes. We investigated the anti-obesity effects of ATM on HFD-induced obese rats. Rats fed with an HFD demonstrated elevations in body weight gain, while the administration of ATM reversed body weight (BW) gains and adipose tissue weights in rats fed an HFD. ATM supplementation caused a decrease in the circulating triglyceride and total cholesterol levels and led to inhibition of lipid accumulation in the adipose tissues in HFD-induced obese rats. Epididymal fat exhibited significantly larger adipocytes in the HFD group than it did in the ATM-treated group. These results demonstrate that ATM administration caused a reduction in adiposity via attenuation in adipose tissue mass and adipocyte size.Plant-derived natural polyphenols exhibit anticancer activity without showing any noticeable toxicities to normal cells. The aim of this study was to investigate the role of p53 on the anticancer effect of polyphenols isolated from Korean Artemisia annua L. (pKAL) in HCT116 human colorectal cancer cells. We confirmed that pKAL induced reactive oxygen species (ROS) production, propidium iodide (PI) uptake, nuclear structure change, and acidic vesicles in a p53-independent manner in p53-null HCT116 cells through fluorescence microscopy analysis of DCF/PI-, DAPI-, and AO-stained cells. The pKAL-induced anticancer effects were found to be significantly higher in p53-wild HCT116 cells than in p53-null by hematoxylin staining, CCK-8 assay, Western blot, and flow cytometric analysis of annexin V/PI-stained cells. In addition, expression of ectopic p53 in p53-null cells was upregulated by pKAL in both the nucleus and cytoplasm, increasing pKAL-induced cell death. Moreover, Western bot analysis revealed that pKAL-induced cell death was associated with upregulation of p53-dependent targets such as p21, Bax and DR5 and cleavage of PARP1 and lamin A/C in p53-wild HCT116 cells, but not in p53-null. Taken together, these results indicate that p53 plays an important role in enhancing the anticancer effects of pKAL by upregulating p53 downstream targets and inducing intracellular cell death processes.When multiple robots are involved in the process of simultaneous localization and mapping (SLAM), a global map should be constructed by merging the local maps built by individual robots, so as to provide a better representation of the environment. Hence, the map-merging methods play a crucial rule in multi-robot systems and determine the performance of multi-robot SLAM. This paper looks into the key problem of map merging for multiple-ground-robot SLAM and reviews the typical map-merging methods for several important types of maps in SLAM applications occupancy grid maps, feature-based maps, and topological maps. These map-merging approaches are classified based on their working mechanism or the type of features they deal with. The concepts and characteristics of these map-merging methods are elaborated in this review. The contents summarized in this paper provide insights and guidance for future multiple-ground-robot SLAM solutions.Neurodegenerative disorders are a family of incurable conditions. Among them, Alzheimer's disease and tauopathies are the most common. Pathological features of these two disorders are synaptic loss, neuronal cell death and increased DNA damage. A key pathological protein for the onset and progression of the conditions is the protein tau, a microtubule-binding protein highly expressed in neurons and encoded by the MAPT (microtubule-associated protein tau) gene. Tau is predominantly a cytosolic protein that interacts with numerous other proteins and molecules. Recent findings, however, have highlighted new and unexpected roles for tau in the nucleus of neuronal cells. This review summarizes the functions of tau in the metabolism of DNA, describing them in the context of the disorders.Parent-implemented language interventions have been used for children with expressive language delays, but no study has yet been carried out using this intervention for low-risk preterm children. The current study examined the effect of a parent-implemented dialogic book reading intervention, determining also whether the intervention differently impacted low-risk preterm and full-term children. Fifty 31-month-old late talkers with their parents participated; 27 late talkers constituted the intervention group, and 23 constituted the control group. Selleck Epacadostat The overall results indicated that more children in the intervention group showed partial or full recovery of their lexical expressive delay and acquired the ability to produce complete sentences relative to the control group. Concerning full-term late talkers, those in the intervention group showed a higher daily growth rate of total words, nouns, function words, and complete sentences, and more children began to produce complete sentences relative to those in the control group. Concerning low-risk preterm late talkers, children in the intervention group increased their ability to produce complete sentences more than those in the control group. We conclude that a parent-focused intervention may be an effective, ecological, and cost-effective program for improving expressive lexical and syntactic skills of full-term and low-risk preterm late talkers, calling for further studies in late talkers with biological vulnerabilities.