A mathematical model for apical growth, septation, and branching of mycelial microorganisms is presented. The model consists of two parts: the deterministic part of the model is based on fundamental cellular and physical mechanisms; it represents the kinetics for growth of hyphal tips and septation of apical as well as intercalary compartments. In regard to random occurrences of hyphal growth and branching, the stochastic part deals with branching processes, tip growth directions, and outgrowth orientations of branches. The model can explain the morphological development of mycelia up to the formation of pellets. The results, as predicted by the model, correspond very closely to those observed in experiments. In addition, some unmeasured states can be ascertained, such as the distribution functions of hyphal length (biomass) and tips along pellet radii.
Magnolol, an orally available compound from Magnolia officinalis used widely in traditional herbal medicine against a variety of neuronal diseases, possesses potent antioxidant properties and protects the brain against oxidative damage. The aim of the work is to examine the protective mechanisms of magnolol on human neuroblastoma SH-SY5Y cells against apoptosis induced by the neurotoxin acrolein, which can cause neurodegenerative disorders by inducing oxidative stress. By investigating the effect of magnolol on neural cell damage induced by the neurotoxin acrolein, we found that magnolol pretreatment significantly attenuated acrolein-induced oxidative stress through inhibiting reactive oxygen species accumulation caused by intracellular glutathione depletion and nicotinamide adenine dinucleotide phosphate oxidase activation. We next examined the signaling cascade(s) involved in magnolol-mediated antiapoptotic effects. The results showed that acrolein induced SH-SY5Y cell apoptosis by activating mitochondria/caspase and MEK/ERK signaling pathways. Our findings provide the first evidence that magnolol protects SH-SY5Y cells against acrolein-induced oxidative stress and prolongs SH-SY5Y cell survival through regulating JNK/mitochondria/caspase, PI3K/MEK/ERK, and PI3K/Akt/FoxO1 signaling pathways.
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