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The patients with CM in VPA and placebo groups were compared.
This means that there was a statistically significant decrease in MaxVAS levels and pain frequencies in VPA given group.
In VPA pre-treated groups, the densities of brown granules obviously reduced under the observation with a microscope at 400× magnification.
Only PF parameter was significantly reduced in VPA group when compared to placebo group at the end of the first and third months (P = 0.000, for both).
The patients in VPA and placebo groups suffered from headache for the range of 6 240 and 6 120 months, respectively.
In CM patients, the decreases in MaxVAS, GnVAS and PF parameters were more in VPA treated patients (P = 0.006, P = 0.03, and P = 0.000, respectively).
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Furthermore, 5hmC levels were also increased in VPA-induced Neuro2a cells.
Next, we investigated the effects on neuronal differentiation in VPA-induced Neuro2a cells following transfection of these three plasmids.
In addition, we found that TBI-associated disruption of hippocampal MAP2 immunoreactivity, an indicator of dendritic damage, was also reduced in VPA-treated animals.
Figure 7E shows that the cumulative area of TBI-associated hippocampal MAP2 disruption/section was significantly reduced in VPA-treated rats compared to that measured in vehicle-treated controls (Student's t-test p = 0.049).
We used RTQ-PCR to confirm expression of Pou5f1 and Nanog at the 8-cell to morula stage and to show that expression was moderately enhanced in VPA-treated morula-stage embryos (Fig. 1C).
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