Svanedreyer5750

Zirconia nanoparticles (NPs) have been widely used in biomedicine, which will likely lead to their interactions with endothelial cells (ECs). However, the toxicity of zirconia NPs to ECs is less investigated and the toxicological data are not consistent. Furthermore, no previous study, to the best of our knowledge, investigated the influence of zirconia NPs on lipid metabolism. This study investigated lipid profiles in human umbilical vein ECs (HUVECs) exposed to zirconia NPs with or without the presence of free fatty acids (FFAs). Incubation with FFA changed the hydrodynamic size, zeta potential, and surface profiles of zirconia NPs, indicating the surface coating effects. Exposure of HUVECs to various concentrations of zirconia NPs with or without the presence of FFA did not significantly decrease cellular viability, but FFA decreased zirconium elemental levels in NP-exposed cells. Oil Red O staining showed that FFA or zirconia NPs and FFA, but not zirconia NPs alone, significantly increased lipid accumulation in HUVECs. Consistently, lipidomic data suggested that exposure to FFA or zirconia NPs and FFA up-regulated most lipid classes in HUVECs. learn more As the mechanisms for increased lipid accumulation, exposure to FFA or zirconia NPs and FFA up-regulated endoplasmic reticulum (ER) stress axis IRE1α-XBP-1, leading to increased FASN and ACSL3, proteins involved in lipid metabolism. Combined, our results demonstrated that zirconia NPs were noncytotoxic and showed minimal impact on ER stress-mediated lipid metabolism in HUVECs under both normal and FFA-challenged conditions, which indicated the relatively high biocompatibility of zirconia NPs to ECs.

Microalgae are a promising alternative source to meet the increasing global demand for protein. The insoluble microalgae protein fraction that makes up over half of the protein composition of the biomass has shown potential to serve as a functional emulsifier after acidic hydrolysis. However, creaming was observed due to the flocculation of emulsion droplets, suggesting a preferable use in concentrated emulsions.

In this study, we examined the emulsifying behavior of the untreated insoluble microalgae protein fraction and two of its hydrolysates obtained in 0.5 mol L

HCl for 4 h at 65 °C (Hydrolysates 65) or 85 °C (Hydrolysates 85), at a concentration of 3% (w/w), and elevated levels of oil (50-70%). The results showed an increase in droplet size and apparent viscosity with increasing oil content in the emulsions. The emulsions made with Hydrolysates 85 had the smallest droplet size and the highest apparent viscosity. The gravitational separation was hindered when oil content was increased. The Hydrolysates 85 stabilized emulsions had a gel-like structure and were stable against coalescence or creaming during a 7 day storage test.

The results suggest that the thermal acid-treated fraction Hydrolysates 85 may, in particular, be a good emulsifier to formulate concentrated emulsion-based foods with oil content over 50%, such as mayonnaise, salad dressings, or dips. © 2020 The Authors. Journal of The Science of Food and Agriculture published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

The results suggest that the thermal acid-treated fraction Hydrolysates 85 may, in particular, be a good emulsifier to formulate concentrated emulsion-based foods with oil content over 50%, such as mayonnaise, salad dressings, or dips. © 2020 The Authors. Journal of The Science of Food and Agriculture published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.Meiotic chromosome pairing between homoeologous chromosomes was reported in many nascent allopolyploids. Homoeologous pairing is gradually eliminated and replaced by exclusive homologous pairing in well-established allopolyploids, an evolutionary process referred to as the diploidization of allopolyploids. A fundamental question of the diploidization of allopolyploids is whether and to what extent the DNA sequence variation among homoeologous chromosomes contribute to the establishment of exclusive homologous chromosome pairing. We developed aneuploid tetraploid maize lines that contain three copies of chromosome 10 derived from inbred lines B73 and H99. We were able to identify the parental origin of each copy of chromosome 10 in the materials using oligonucleotide-based haplotype-specific chromosome painting. We demonstrate that the two identical copies of chromosome 10 from H99 pair preferentially over chromosome 10 from B73 in different stages of prophase I and metaphase I during meiosis. Thus, homologous chromosome pairing is favored to partners with the most similar DNA sequences and can be discriminated based on cryptic sequence variation. We propose that innate preference of homologous chromosome pairing exists in nascent allopolyploids and serves as the first layer that would eventually block all homoeologous chromosome pairing in allopolyploids.Fibrosis is a common pathological change characterized by the excessive accumulation of fibrous connective tissue. Once uncontrolled, this pathological progress can lead to irreversible damage to the structure and function of organs, which is a serious threat to human health and life. Actually, the disability and death of patients caused by many chronic diseases have a closed relationship with fibrosis. The CCN protein family, including six members, is a small group of matrix proteins exhibiting structurally similar features. In the past 20 years, different biological functions of CCN proteins have been identified in various diseases. Of note, it has been recently shown that they are implicated in the key pathological process of fibrosis. In this review, we summarize the current status of knowledge regarding the role of CCN proteins involved in the pathogenesis of fibrosis diseases in detail. Furthermore, we highlight some of the underlying interaction mechanisms of CCN protein acting in fibrosis that helps to develop new drugs and determine appropriate clinical strategies for fibrotic diseases.The Fanconi anaemia protein FANCD2 suppresses PPARƔ to maintain haematopoietic stem cell's (HSC) function; however, the underlying mechanism is not known. Here we show that FANCD2 acts in concert with the Notch target HES1 to suppress inflammation-induced PPARƔ in HSC maintenance. Loss of HES1 exacerbates FANCD2-KO HSC defects. However, deletion of HES1 does not cause more severe inflammation-mediated HSC defects in FANCD2-KO mice, indicating that both FANCD2 and HES1 are required for limiting detrimental effects of inflammation on HSCs. Further analysis shows that both FANCD2 and HES1 are required for transcriptional repression of inflammation-activated PPARg promoter. Inflammation orchestrates an overlapping transcriptional programme in HSPCs deficient for FANCD2 and HES1, featuring upregulation of genes in fatty acid oxidation (FAO) and oxidative phosphorylation. Loss of FANCD2 or HES1 augments both basal and inflammation-primed FAO. Targeted inhibition of PPARƔ or the mitochondrial carnitine palmitoyltransferase-1 (CPT1) reduces FAO and ameliorates HSC defects in inflammation-primed HSPCs deleted for FANCD2 or HES1 or both.