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Too much glutamate left in the synapse could cause excess activation of the glutamate receptors
Greater stability is usually achieved by bridging modalities through shared biological representations, such as pathway activity scores, gene modules, latent factors, or calibrated model outputs, which also makes partial-data contribution feasible [450, 452, 455, 456]
However, the same authors found that the carrier N59.1 and N459.3 strains and the invasive strain MC58 did not affect the barrier function of the Calu3 ALI monolayer (Dave et al., 2023)
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