Transmission electron microscopic images.

<p>(A) normal brain cell in control (B) apoptotic cell in S4 brain. Ultrastructural changes include mitochondrial swelling, disintegrating mitochondrial cristae (black arrow), nucleus membrane shrinkage (red arrow) and chromatin margination (yellow arrow) by ultrahistological analysis. The scale bar represents 5μm.</p

Effects of sevoflurane anesthesia on early and late caspase3 activation in the mouse hippocampus.

<p>(A) The activated caspase3 was increased in S2, S3 and S4 groups at 24 hours post-anesthesia compared to control group. (B) The activated caspase3 was increased in S3 and S4 groups at 2 weeks post- anesthesia compared to control group. Data are presented as mean ± SD. (*<i>P</i> < 0.05, **<i>P</i> < 0.01).</p

Transmission electron microscopic images.

<p>(A) normal brain cell in control (B) apoptotic cell in S4 brain. Ultrastructural changes include mitochondrial swelling, disintegrating mitochondrial cristae (black arrow), nucleus membrane shrinkage (red arrow) and chromatin margination (yellow arrow) by ultrahistological analysis. The scale bar represents 5μm.</p

Sevoflurane anesthesia induced mice spatial cognitive changes.

<p>(A) The mice in S1, S2 and S3 groups exhibited significantly shorter escape latency than that in the control group. No significant difference was noted between S4 group and the control group except that on the second day of MWM test S4 had longer escape latency. (B) Platform crossings were increased in S1, S2 and S3 groups but not in S4 group as compared to control group (*: <i>P</i> < 0.05, **: <i>P</i> < 0.01; ^#: p<0.05, S4 VS S0)</p

Effects of sevoflurane anesthesia on early and late ERK1/2 activation in the mouse hippocampus.

<p>(A) Activated ERK1/2 was increased in all sevoflurane-treated groups compared to control group at 24 hours post-anesthesia (<i>P</i> < 0.01). (B) Activated ERK1/2 was increased in S2, S3 and S4 groups at 2 weeks post-anesthesia. Data are presented as mean ± SD.(*<i>P</i> < 0.05, **<i>P</i> < 0.01).</p

Schematic time-line of the experimental design.

<p>Schematic time-line of the experimental design.</p

Overview of the measurements and their meaning in brain functional network.

<p>Overview of brain functional network parameters and their meanings.</p

Surface rendering of the distribution of altered nodes at a connection density of 22%.

<p><b>Colored bars indicate differences in network properties between the NC and AD groups.</b> Blue indicates regions showing an increase in the AD group but not the NCs. Yellow indicates regions showing a decrease in the AD group but not the NCs. In the AD group, the regions showing significant increases in C_p, L_p and E_local are widely distributed across the brain, especially in default mode network regions such as the ACC, PCC, MPFC, HIP and IPL; regions in the temporal lobe such as the STGp/MTGp; and regions in the subcortical structure such as the THA, INS and PUT. The regions showing significant E_global decreases in AD are distributed primarily in the bilateral MTG and motor areas such as the SMA_R and PreCG_R.</p

Statistical tests on the small-world properties of the networks for all the groups after the permutation test.

<p>D_P, the P value of the difference between the normal control and AD group.</p><p>P_P, the permutation P value of the difference between the normal control and AD group.</p><p>Statistical tests on the small-world properties of the networks for all the groups of the permutation test.</p

Demographic, clinical and neuropsychological data.

a<p>Chi-square was used for gender comparisons.</p>b<p>Two samples two sides <i>t</i>-test was used for age and neuropsychological tests comparisons between AD and NC.</p>c<p>One-way ANOVA was performed for age and neuropsychological tests comparisons.</p>d<p>Two samples two sides <i>t</i>-test was used for age and neuropsychological tests comparisons between ApoE− and ApoE+ in AD group.</p><p>MMSE, Mini-Mental State Examination, DRS, Dementia Rating Scale.</p><p>Gray background means the detail statistical of the subject divided by using ApoE genotype.</p><p>Demographic, clinical and neuropsychological data in normal control patients (NCs) and Alzheimer's disease patients (AD).</p