The map of the 96 cluster regions (48 regions for the left and right hemispheres) and the frequency of sulcal pits from the distribution of the pits in 148 normal subjects.

<p>This is reproduced from our previous study <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0053678#pone.0053678-Im1" target="_blank">[2]</a>. The frequency of sulcal pits is represented as a percentage (number of pits/148×100).</p

Geodesic distance map from sulcal pits as a seed point on the white matter surface.

<p>The areas within 10 mm distance from the sulcal pits are separated from each other.</p

Sulcal pit maps on the different 8 surfaces in the same subject.

<p>The location and existence of the sulcal pits are highly similar across surfaces. All surfaces are inflated for better visualization. The regions marked with black arrows show the variability of the sulcal pit presence.</p

Matrix of all pairwise comparison of sulcal pit map in the same subject.

<p>The effects of different scan session, scanner, and surface extraction tool are evaluated and each case is marked in the cells of the matrix. For the subject scanned 3 times, 6×6 matrix is constructed without rows and columns of AMC_MNI and AMC_FS.</p

Example of intra-subject cortical surface alignment.

<p>Eight white matter surfaces (4 MNI and 4 FS surfaces) are rendered (A) and they are overlapped with a reference volume image (B) after a linear registration with 6 parameters. They are aligned well into a common space, but their local shape of the gray/white matter boundary is slightly different.</p

Schematic illustration of measuring spatial difference between 2 pits from different surfaces.

<p>Sulcal pit <i>a_m</i> on the surface <i>S_A</i> is projected onto the surface <i>S_B</i> with the nearest Euclidean distance (A) and then geodesic distance (<i>G</i>) between projected pit and <i>b_n G</i>(, <i>b_n</i>) is measured (B). <i>t_i</i>, <i>t_j</i>, and <i>t_k</i> are the barycentric coordinates of on the triangle which is composed of vertices <i>i</i>, <i>j</i>, and <i>k</i>. <i>G</i>(, <i>b_n</i>) is computed using an interpolation with distance values of three vertices.</p

Spatial difference (mm) of sulcal pits (<i>M₂</i>) according to effects of scan session, scanner, and surface extraction tool.

<p>Spatial difference (mm) of sulcal pits (<i>M₂</i>) according to effects of scan session, scanner, and surface extraction tool.</p

Similarity of the presence of sulcal pits (<i>M₁</i>) according to effects of scan session, scanner, and surface extraction tool.

<p>Similarity of the presence of sulcal pits (<i>M₁</i>) according to effects of scan session, scanner, and surface extraction tool.</p

Depth and area of sulcal catchment basin measured on matched and unmatched sulcal pits and statistical tests.

<p>Paired <i>t</i>-test <i>P</i> value.</p

Chronic Sleep Deprivation-Induced Proteome Changes in Astrocytes of the Rat Hypothalamus

Sleep deprivation (SD) can influence cognition, memory, and sleep/wake homeostasis and can cause impairments in many physiological processes. Because the homeostatic control of the sleep/wake cycle is closely associated with the hypothalamus, the current study was undertaken to examine proteomic changes occurring in hypothalamic astrocytes following chronic partial SD. After chronic partial SD for 7 days, astrocytes were prepared from rat hypothalamus using a Percoll gradient method, and their proteome profiles were determined by LC–MS/MS. Comparisons of the proteome profiles of hypothalamic astrocytes revealed that chronic partial SD increased (≥1.5-fold) 89 proteins and decreased (≤0.7-fold) 50 proteins; these changes in protein expression were validated by western blot or immunohistochemistry. DAVID and IPA analyses of these proteins suggested that SD may influence gliotransmission and astrocyte activation. PPP2R1A, RTN4, VAMP-2, LGI-1, and SLC17A7 were identified and validated as the main targets of SD in astrocytes. Our results suggest that SD may modulate gliotransmission in the hypothalamus, thereby disturbing sleep/wake homeostasis and increasing susceptibility to neurological disease; however, further studies are required to confirm whether the proteome changes are specific to SD