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In vivo studies suggested it to be resulting from oscillations of inhibition and excitatory thalamic and corticothalamic neurons, which in turn, initiate Grand Mal epilepsy [80]
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The results indicated that the proportion of mature DCs (CD80 + CD86 + ) in the TDLNs of mice treated with NP4 (82.8%) was approximately 1.46 times higher than that in the mice treated with NP2 (56.7%) (Fig
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In contrast, the VPA-exposed group showed substantial pathological alterations, including mitochondrial pathologies featuring cristae disorganization and membrane rupture with alternating swelling and shrinkage (Fig
Leaf samples of 0.3 g were ground with 3 mL ice-cold 25 mM HEPES buffer (pH 7.8) containing 0.2 mM EDTA and 2% PVP
