Project description:Cellular uptake and cytotoxicity data from neural cells treated with microplastics were compared and contrasted. Transcriptomic data obtained by RNA-seq from astrocytes treated with microplastics was assessed further.
Project description:Ischemia/reperfusion injuries is a known complication to hepatic surgery. Ischemic pre- (IPC) and postconditioning (IPO) protects the liver against ischemia/reperfusion-injuries. Expression profiling were performed on liver biopsies seeking to identify molecular mediators of the protective properties.
Project description:Interventions: capsule endoscopy
Primary outcome(s): Evaluation of the small intestinal injuries induced by chemothelapy
Study Design: Single arm Non-randomized
Project description:Microplastics represent a growing environmental concern for the oceans due to their potential capability to adsorb different classes of pollutants, thus representing a still unexplored source of exposure for aquatic organisms. In this study polystyrene (PS) microplastics were characterized for their capability to adsorb pyrene (PYR) as model compound for polycyclic aromatic hydrocarbons, and transfer this chemical to filter feeding mussels Mytilus galloprovincialis. Gene expression analyses of Mytilus galloprovincialis exposed to polystyrene (PS) microplastics and to polystyrene contaminated with pyrene (PS-PYR) have been performed trough a DNA microarray platform.
Project description:Ischemia/reperfusion injuries is a known complication to hepatic surgery. Ischemic pre- (IPC) and postconditioning (IPO) protects the liver against ischemia/reperfusion-injuries. Expression profiling were performed on liver biopsies seeking to identify molecular mediators of the protective properties. 48 rats were divided into 5 groups; sham (n=8), IRI (n=10), IPC (n=10), IPO (n=10) and IPC+IPO (n=10). All rats except sham rats were subjected to 30 min of total liver ischemia and 30 min of reperfusion before liver biopsies were sampled. In the IPC group, liver ischemia was preceded by 10 min of hepatic ischemia, followed by 10 min of reperfusion. IPO were performed by three cycles of 30 sec of reperfusion and 30 sec of ischemia, applied immediately after the 30 min of total liver ischemia. In the IPC+IPO group the two interventions were combined.
Project description:Hepatic injury is often accompanied by pulmonary inflammation and tissue damage, but the underneath mechanism is not fully elucidated. Here we identify hepatic miR-122 as a culprit of pulmonary inflammation induced by various liver injuries. Analyses of acute and chronic liver injury mouse models confirm that liver dysfunction can cause pulmonary inflammation and tissue damage. Injured livers release large amounts of miR-122 in a microvesicle-independent manner into the circulation compared to normal livers. Circulating miR-122 is then preferentially transported to mouse lungs and taken up by alveolar macrophages, in which it binds toll-like receptor 7 (TLR7) and activates inflammatory responses. Depleting plasma miR-122 largely abolishes liver injury-induced pulmonary inflammation and tissue damage. Furthermore, alveolar macrophage activation by miR-122 is blocked by mutating the TLR7-binding UG-rich sequence on miR-122 or knocking out macrophage TLR7. Our findings reveal a novel causative role of hepatic miR-122 in liver injury-induced pulmonary dysfunction.
Project description:Microplastics (MPs) are considered as one of the main reasons for male and female infertility. However, the reproductive toxicity and its related mechanisms are understood by animal models with acute exposure to MPs at present. In the study, we show the low-dose polystyrene microplastics (PSMPs) exposure results in severely abnormal reproduction in female, but not male in mouse model, exhibiting failed oocyte meiotic maturation. Mechanistically, the PSMPs exposure induces the over-activation of cell metabolism pathways, insufficient HDACs and H4K16 hyperacetylation in oocytes in vivo and in vitro. By addition of HDAC3 inhibitor, the failed oocyte maturation, over-activation of cell metabolism pathways and H4K16 hyperacetylation are recapitulated, and the overexpression of HDAC3 can rescue the defects of meiotic maturation induced by PSMPs. Our observations suggest a direct link of the maturation defects induced by PSMPs to HDAC3 insufficiency. Thus, we propose the potential treatments for therapy of the failed meiotic maturation of oocyte from women highly exposed to MPs by activating or supplying HDAC3.
Project description:There were similarities in the microRNA expression profiles in sheep model and idiopathic pulmonary fibrosis (IPF) suggest that bleomycin induced lung injuries share similar molecular mechanisms associated with the disease IPF
