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This finding adds strength to the prevailing notion that glutamatergic excess plays a critical role in shaping the poor outcome trajectory in psychosis
Model overfitting and the impact of type I error should not be discarded
Studies have explored its potential involvement in nitric oxide (NO) signaling, growth factor modulation (including VEGF, FGF2, and EGF receptor pathways), and FAK-paxillin pathway activation
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Are absent from most reconstitution guides
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