Based on these data, CatL might play an important role in the development of proteinuria. Furthermore, identifying the functions of CatL may contribute to a better understanding of the pathogenesis of childhood-onset NS. We hypothesize that high levels of CatL can lead to cytoskeletal instability of podocytes, resulting in proteinuria in childhood-onset NS. The role of extracellular vesicles is widely studied. As well as other organs, placenta produces extracellular vesicles during both, normal and pathological pregnancies. During pregnancy, placental/fetal free DNA circulates in maternal blood.  https://www.selleckchem.com/products/Thiazovivin.html  Concentrations of free placental DNA are much higher when pregnancy complications of various etiologies occur. Such a complication could be preeclampsia. In our previous animal model, administration of pure DNA isolated from fetus did not induce any prenatal complications. Here we hypothesize that in real life during preeclampsia or other pregnancy complications, placental DNA might be transported by extracellular vesicles to maternal cells. Also, our preliminary data prove that placental DNA is present in circulating exosomes in maternal blood. Therefore, a lipid bilayer of extracellular vesicles could protect DNA from degradation by enzymes. Extracellular vesicles tend to merge with other cells, therefore, following expression of fetal genes from placental extracellular vesicles in maternal cells could lead to an immune response already observed in pregnancy complications. Future studies should be mainly focused on verification of our hypothesis and evaluate the potential of placental/fetal extracellular vesicles and their gene transfer in preeclampsia or other pregnancy complications. Sepsis is a grievous health concern with limited understanding of its precise etiology. Although studies on sepsis have implicated the Warburg effect (mitigation of mitochondrial oxidative phosphorylation, as evident from aerobic glycolysis), we propose that an evolutionary perspective might further unravel its etiology. The endosymbiotic theory suggests that evolution of a eukaryotic cell is a consequence of the fruitful association between an archaea (Asgard) and an alphaproteobacterium (Rickettsia). We hypothesize that, during pathological conditions like sepsis, such endosymbiotic homeostasis between the two systems is perturbed. We underscore the fact (supported by in silico homology analyses) that during sepsis, the Asgard component of a cell is promoted to trigger aerobic glycolysis as well as the innate immune response (spearheaded by the TLR pathway), while suppressing the Rickettsia counterpart, thereby promoting the Warburg effect. It might be this discord between the two endosymbiotic partners (Asgard and Rickettsia-derived cellular components) that promotes sepsis. Although coexposure to pharmaceuticals and microplastics (MPs) may frequently occur, the synergistic impact of MPs and antidepressants on marine species still remains poorly understood. In this study, the immunotoxicities of polystyrene MPs (diameters 500 nm and 30 μm) and sertraline (Ser), alone and in combination, were investigated in a bivalve mollusk Tegillarca granosa. Results showed that both MPs and Ser significantly suppressed the immune responses of T. granosa. In addition, though the toxic effect of Ser was not affected by microscale MPs, an evident synergistic immuno-toxic effect was observed between Ser and nanoscale MPs, which indicates a size-dependent interaction between the two. To further ascertain the underlying toxication mechanisms, the intracellular content of reactive oxygen species, apoptosis status, ATP content, pyruvate kinase activity, plasma cortisol level, and in vivo concentrations of neurotransmitters and cytochrome P450 1A1 were analysed. A transcriptomic analysis was also performed to reveal global molecular alterations following Ser and/or MPs exposure. The obtained results indicated that the presence of nanoscale MPs may enhance the immunotoxicity of Ser by (i) inducing apoptosis of haemocytes and, hence, reducing the THC; (ii) constraining the energy availability for phagocytosis; and (iii) hampering the detoxification of Ser. Metal oxide nanoparticles (NPs), and among them metal oxides Quantum Dots (QDs), exhibit a multifactorial toxicity combining metal leaching, oxidative stress and possibly direct deleterious interactions, the relative contribution of each varying according to the NP composition and surface chemistry. Their wide use in public and industrial domains requires a good understanding and even a good control of their toxicity. To address this question, we engineered ZnO QDs with different surface chemistries, expecting that they would exhibit different photo-induced reactivities and possibly different levels of interaction with biological materials. No photo-induced toxicity could be detected on whole bacterial cell toxicity assays, indicating that ROS-dependent damages, albeit real, are hidden behind a stronger source of toxicity, which was comforted by the fact that the different ZnO QDs displayed the same level of cell toxicity. However, using in vitro DNA damage assays based on quantitative PCR, significant photo-induced reactivity could be measured precisely, showing that different NPs exhibiting similar inhibitory effects on whole bacteria could differ dramatically in terms of ROS-generated damages on biomolecules. We propose that direct interactions between NPs and bacterial cell surfaces prime over any kind of intracellular damages to explain the ZnO QDs toxicity on whole bacterial cells. Seed dormancy and germination in rice (Oryza sativa L.) are complex and important agronomic traits that involve a number of physiological processes and energy. A mutant named h470 selected from a60Co-radiated indica cultivar N22 population had weakened dormancy that was insensitive to Gibberellin (GA) and Abscisic acid (ABA). The levels of GA4 and ABA were higher in h470 than in wild-type (WT) plants. The gene controlling seed dormancy in h470 was cloned by mut-map and transgenesis and confirmed to encode an ADP-glucose transporter protein. A 1 bp deletion in Os02g0202400 (OsBT1) caused the weaker seed dormancy in h470. Metabolomics analyses showed that most sugar components were higher in h470 seeds than the wild type. The mutation in h470 affected glycometabolism.