Both toolboxes found virtually no difference between neutral and happy expressions, while fearful (compared to neutral and happy) expressions modulated the N170 and EPN but elicited maximum effects after the N170 peak, around 190 ms. Similarities and differences in the spatial and temporal extent of these effects are discussed in comparison to the published classical analysis and the rest of the ERP literature. Circular RNA (circRNA) septin 9 (circSEPT9; hsa_circ_0005320) has been reported to be abnormally up-regulated in glioma. However, the exact role and working mechanism of circSEPT9 in glioma progression are barely known. RNA and protein levels were measured by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot assay, respectively. Cell proliferation was assessed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony formation assay and flow cytometry. Cell apoptosis was evaluated by flow cytometry. Cell motility was analyzed by transwell assays. Cell glycolytic metabolism was analyzed using commercial kits. Dual-luciferase reporter assay, RNA-pull down assay and RNA immunoprecipitation (RIP) assay were conducted to verify the intermolecular interactions. Xenograft mice model was utilized to assess the role of circSEPT9 in vivo. CircSEPT9 was highly expressed in glioma tissues and cell lines. CircSEPT9 interference inhibited the proliferation, migration, invasion and glycolytic metabolism and triggered the apoptosis of glioma cells. MicroRNA-432-5p (miR-432-5p) was a target of circSEPT9, and circSEPT9 silencing-mediated effects in glioma cells were largely alleviated by the addition of anti-miR-432-5p. MiR-432-5p bound to the 3' untranslated region (3'UTR) of LIM and SH3 protein 1 (LASP1), and LASP1 overexpression largely overturned miR-432-5p-induced effects in glioma cells. CircSEPT9 up-regulated LASP1 expression by acting as miR-432-5p sponge. CircSEPT9 silencing suppressed xenograft tumor growth in vivo. CircSEPT9 exerted an oncogenic role to enhance the malignant behaviors of glioma cells by binding to miR-432-5p to induce LASP1 expression.CircSEPT9 exerted an oncogenic role to enhance the malignant behaviors of glioma cells by binding to miR-432-5p to induce LASP1 expression.Mutations in LRRK2 are the most frequent cause of familial Parkinson's disease (PD), with common LRRK2 non-coding variants also acting as risk factors for idiopathic PD. Currently, therapeutic agents targeting LRRK2 are undergoing advanced clinical trials in humans, however, it is important to understand the wider implications of LRRK2 targeted treatments given that LRRK2 is expressed in diverse tissues including the brain, kidney and lungs. This presents challenges to treatment in terms of effects on peripheral organ functioning, thus, protein interactors of LRRK2 could be targeted in lieu to optimize therapeutic effects. Herein an in-silico analysis of LRRK2 direct interactors in brain tissue from various brain regionswas conducted along with a comparative analysis of the LRRK2 interactome in the brain, kidney, and lung tissues. This was carried out based on curated protein-protein interaction (PPI) data from protein interaction databases such as HIPPIE, human gene/protein expression databases and Gene ontology (GO) enrichment analysis using Bingo. Seven targets (MAP2K6, MATK, MAPT, PAK6, SH3GL2, CDC42EP3 and CHGB) were found to be viable objectives for LRRK2 based investigations for PD that would have minimal impact on optimal functioning within peripheral organs. Specifically, MAPT, CHGB, PAK6, and SH3GL2 interacted with LRRK2 in the brain and kidney but not in lung tissue whilst LRRK2-MAP2K6 interacted only in the cerebellum and MATK-LRRK2 interaction was absent in kidney tissues. CDC42EP3 expression levels were low in brain tissues compared to kidney/lung. The results of this computational analysis suggest new avenues for experimental investigations towards LRRK2-targeted therapeutics.Fumonisin B1 (FB1) is the most harmful mycotoxin which prevails in several crops and affects the growth and yield as well. Hence, keeping the alarming consequences of FB1 under consideration, there is still a need to seek other more reliable approaches and scientific knowledge for FB1-induced cell death and a comprehensive understanding of the mechanisms of plant defence strategies. FB1-induced disturbance in sphingolipid metabolism initiates programmed cell death (PCD) through various modes such as the elevated generation of reactive oxygen species, lipid peroxidation, cytochrome c release from the mitochondria, and activation of specific proteases and nucleases causing DNA fragmentation. There is a close interaction between sphingolipids and defence phytohormones in response to FB1 exposure regulating PCD and defence. In this review, the model plant Arabidopsis and various crops have been presented with different levels of susceptibility and resistivity exposed to various concentration of FB1. In addition to this, regulation of PCD and defence mechanisms have been also demonstrated at the physiological, biochemical and molecular levels to help the understanding of the role and function of FB1-inducible molecules and genes and their expressions in plants against pathogen attacks which could provide molecular and biochemical markers for the detection of toxin exposure.When allocating limited vaccines to control an infectious disease, policy makers frequently have goals relating to individual health benefits (e.g., reduced morbidity and mortality) as well as population-level health benefits (e.g., reduced transmission and possible disease eradication). We consider the optimal allocation of a limited supply of a preventive vaccine to control an infectious disease, and four different allocation objectives minimize new infections, deaths, life years lost, or quality-adjusted life years (QALYs) lost due to death. find more We consider an SIR model with n interacting populations, and a single allocation of vaccine at time 0. We approximate the model dynamics to develop simple analytical conditions characterizing the optimal vaccine allocation for each objective. We instantiate the model for an epidemic similar to COVID-19 and consider n=2 population groups one group (individuals under age 65) with high transmission but low mortality and the other group (individuals age 65 or older) with low transmission but high mortality.