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Ishizu, M.

Publications and source records attributed to Ishizu, M..

2 recordsLinked to original sources

Kinetic modeling of continuous meta-fermentation quantifies metabolic activity in a complex microbial system

One of the serious drawbacks of a complex microbial system is the difficulty in quantifying the metabolic activity of each microorganism. A kinetic model of predominant microbial species was constructed for continuous meta-fermentation in a complex microbial system at several dilution rates (D). The introduction of biomass and lactic acid inhibition terms improved model accuracies at D = 0.05 h-1 and 0.4 h-1, respectively. The coefficient of determination (R2) and root mean square error (RMSE) improved from 0.577 and 5.21 to 0.972 and 0.759, respectively, with the inhibition term at D = 0.05 h-1. The inhibition terms resulted in good R{superscript 2} (0.996) and RMSE (1.27) values at D = 0.4 h-1. By solving the Michaelis-Menten equation in the constructed models, the species flux (SF) was calculated to estimate the metabolic activity (formation and consumption) of each microorganism. At D = 0.05 h-1, Caldibacillus hisashii contributed to lactic acid production at 0.333 g/L/h, whereas Clostridium cochlearium consumed lactic acid at 0.203 g/L/h, suggesting cross-feeding of a metabolite. It is therefore possible to account for consumption that cannot be considered in gene-derived calculations, indicating that this is a promising analytical method for investigating the dynamic behavior of complex microbial systems. Kinetic models for continuous meta-fermentation at several D values were developed. A new metabolic analysis method is proposed to estimate the activity of microbial species in a complex microbial system.

bioinformatics↗

Dormant viral pathways underlie space-induced neural senescence: a neuroprotective strategy for spaceflight and neurological diseases

Long-duration spaceflight is associated with neurological symptoms in astronauts, yet the underlying molecular mechanisms remain unclear. Using human brain organoids cultured aboard the International Space Station, we analyzed three independent spaceflights to demonstrate that exposure to the space environment triggers Space-Induced Neural Senescence (SINS), characterized by chromatin remodeling, mitochondrial dysfunction, and activation of viral-like transcriptional programs in the absence of infection. Multi-omics analyses identified upregulation of endogenous LINE-1 (L1) retroelements, whose activity was markedly enhanced in organoids lacking MECP2, a known L1 repressor implicated in Rett syndrome. The resulting accumulation of cytoplasmic L1 DNA elicited an IL-6-mediated inflammatory and neurotoxic response, which was reversed by reverse transcriptase inhibitors (RTi) such as lamivudine or stavudine. Parallel preclinical experiments in Mecp2-deficient mice confirmed that RTi treatment restored neuronal morphology, synaptogenesis, function, cognition, and survival. These findings reveal that the space environment reactivates dormant genomic retroelements, providing an unexpected mechanistic insight into astronaut neurobiology and identifying a potential therapeutic strategy for both space-induced and terrestrial neurological conditions. Our pioneering study demonstrates the value of space-enabling research in accelerating drug discovery and disease treatment on Earth.

neuroscience↗