MicroArray analysis of cortical sample from supragranular vs subgranular layers at different time-points.

<p>MicroArray analysis of cortical sample from supragranular vs subgranular layers at different time-points.</p

Peak enhancement in control (A, C) and pilocarpine-treated animals (B, D).

<p>Compared to controls, in rats during SE, sub-granular layers showed a decreased contrast medium peak concentration (D, blue dots), indicating a relative ischemic core, whereas supra-granular layers were characterized by hyperemia (D, red dots). Overlay rTTP maps on source images showing a generalized increase in blood flow rate in pilocarpine-treated (B) versus control brain (A). These alterations in the cerebral cortex of pilocarpine-treated rats present a specific spatial distribution (supra- (red arrow) versus sub-granular layers (blue arrow)).</p

EM images in control animals and 2 h and 24 h after SE in both supergranular (A, A′, A″) and subgranular levels (B, B′, B″).

<p>Subgranular layers are characterized of profound tissue damage 2 h after SE (B′) whereas supergranular layers at this time point appear to be normal except for the perivascular edema (A′). Twenty-four h after SE pathological evidences are detectable in both areas (A″′, B″′).</p

Agrin expression in control (A) and pilocarpine-treated (B) animals.

<p>Increased agrin expression in the endothelial cells is evident in both superficial and deeper layers 2 h after SE-onset. This increase was more evident in the supergranular than in the subgranular layers. Localization of GFAP-like immunoreactivity revealed a selective increase in astrocytic GFAP expression in the less acutely damaged superficial layers (square).</p

Vascular casts revealed structural alterations in brain vessels 2 h after SE-onset.

<p>In the superficial, hyperperfused zone, veins were increased in diameter (B, E) whereas in the hypoperfused, edematous subgranular region, veins appeared collapsed (C, F).</p

Cancer cell culture.

<p>The figure shows the untreated cells (a) and MNs-treated cells (b-d) observed after 24 h. Prussian Blue evidences the iron depots. Enlargement: a>50 µm, b>10 µm, c>10 µm and d>10 µm.</p

MR Images of representative animals.

<p>A) MRI Upper line: animal treated with MNs injection; images acquired before MNs injection (a), 24 h (b), one week (c) and two weeks (d) after MNs injection. Second line: animal treated with MNs injection with AMF; images acquired before MNs injection (e), 24 h (f), one week (g) and two weeks (h) after MNs injection. Magnetosomes are injected in tumor mass and MRI allows the detection of injection sites (white stars). B) animal treated with AMF; images acquired before 24 h (i), one week (l) and two weeks (m) after treatment. Control animal not treated with MNs and AMF; images acquired after two weeks (n).</p

TEM of MNs.

<p>Panel a shows the organization of MNs in chains in the bacteria (scale bar, 500 nm). Panels b-c show that the typical conformation of chains is maintained after isolation of MNs. Scale bars: b>200 nm, c>100 nm. Panel d, X-ray microanalysis shows the iron content of the MNs.</p

Thermal properties of MNs in alternate magnetic field.

<p>Variation of temperature of samples containing: (a) 6.7 mg of MNs lyophilized and (b) MNs diluted in distilled water at concentration of: 3 mg/ml, 2 mg/ml, 1 mg/ml, 0.5 mg/ml exposed to an AMF of 187 kHz (23kA/m) as a function of time, measured by infrared camera.</p

TEM shows the internalization of chains of MNs in HT-29 cancer cells.

<p>The chains that have penetrated in the cells are composed by 6-10 units of MNs and are positioned near the nucleus (Panel a). In Panel b, MNs are visible at cell membrane (arrows) or in the Golgi complex. Panel c shows the localization of the MNs in cytoplasmic vacuoles at high enlargement (Scale bars, a 2 µm, b 1 µm, c 120 nm, d 10 µm). Panel d shows a representative SEM image of HT-29 cancer cell (0.2 mg/ml MNs 12 h); no appreciable alterations of the surface are visible when compared to controls.</p