Αντιστροφή φύλου του διακοσμητικού ψαριού μονομάχος (Betta splendens, Regan 1910)

<p>C2 phage bound to amyloid aggregates in 50 µm-thick brain tissue sections of temporal cortex from AD patients (A–D) and from cognitively normally aging (NA) elderly subjects (E). Each panel shows, from the left: the reactivity of phage (green); the reactivity of BAM 90.1, an anti-Aβ1–42 monoclonal antibody (red); the merge between red and green channels. A, C and E: scale bar represents 150 µm; B and D: scale bar represents 10 µm.</p

Co-immunoprecipitation of CcOX1 and Aβ42 from mitochondrial protein extracts from IMR-32 cells.

<p>Aβ42 was co-incubated with mitochondrial protein lysate from IMR-32 cells, then Aβ42 and CcOX1 were immunoprecipitated using goat anti-CcOX1 antibodies or non-related goat-anti-EGF antibodies, followed by western blotting for Aβ42 and CcOX1. BAM90.1, a mouse monoclonal anti-Aβ42 antibody, and rabbit anti-Aβ42 antibodies were used to detect Aβ42. Goat polyclonal anti-CcOX1 antibodies were used to detect CcOX1.</p

Western blot analysis of recombinant C2 phage expressing the fragment of CcOX1.

<p>10¹¹ phage particles diluted in loading buffer were resolved on 4–12% NuPAGE Bis-Tris gel (Invitrogen) at 200 V for 45 min at room temperature and immunoblotted for detection with anti-pIII antibody. Wild-type M13 phage was used as a control. Migration of the molecular mass standards as well as pIII and pIII–CcOX1 fusion protein are indicated by arrowheads.</p

Screening of a human brain cDNA library expressed on M13 phage.

<p>A. Amino acid sequence of the insert of the positive phage clone designated C2. B. BLASTP analysis results. Amino acid sequence of the insert of C2 is identical to a fragment of CcOX1. C. Complete amino acid sequence of CcOX1. Residues of the insert of C2 are in bold. D. Analysis of interaction of Aβ1–42/Aβ 1–40 with C2 phage bearing the fragment of CcOX 1. Phage concentration used was 10¹¹ per ml, and 100 µl were added to each well. M13 phage and a non-related peptide (NRP) were used as negative controls. OD at 405 was registered. Data are means of three independent experiments.</p

CcOX1 fragment-bearing phage bound to amyloid deposits in AD brain.

<p>C2 phage bound to amyloid aggregates in 50 µm-thick brain tissue sections of temporal cortex from AD patients (A–D) and from cognitively normally aging (NA) elderly subjects (E). Each panel shows, from the left: the reactivity of phage (green); the reactivity of BAM 90.1, an anti-Aβ1–42 monoclonal antibody (red); the merge between red and green channels. A, C and E: scale bar represents 150 µm; B and D: scale bar represents 10 µm.</p

Levels of MUFAs and mead acid (nmol/g) in temporal cortex of control subjects and subjects with AD.

<p>Abbreviations: CI, confidence interval. P values for differences between means were computed by linear regression analysis for each fatty acid after adjustment for age, gender, and post mortem interval.</p

Molecular Dynamics complex of Aβ1–42 (blue) and CcOX1p (gold).

<p>Upper panel: nine pairs of carbons (spheres) interacting through van der Waals forces forming hydrophobic contacts between both peptides are showed. Insets show the hydrogen-bond (green dots) between E11-Y54 (left); the salt bridge (red dots) of H13 and H14 with D51 (left) and the salt bridge between E22-H61 (right).</p

Levels of MUFAs and mead acid (nmol/g) in mid-frontal cortex of control subjects and subjects with AD.

<p>Abbreviations: CI, confidence interval. P values for differences between means were computed by linear regression analysis for each fatty acid after adjustment for age, gender, and post mortem interval.</p

Levels of nervonic acid-containing lipids in the brain of subjects with AD and control subjects.

<p>Levels of ceramide d18:1/24:1 (Panel A), sphingomyelin d18:1/24:1 (Panel B), hexosylceramide d18:1/24:1 (Panel C) in mid-frontal cortex from control subjects (N = 17, open squares) and AD patients (N = 37, closed circles). Two-tailed Welch's <i>t-</i>test.</p

Untargeted lipidomic analyses.

<p>Representative mirror-display images and differential LC/MS analysis of lipids from a subject with AD and a control subject. The component detected as being qualitatively different between the two samples (Panel A, arrow), was subsequently identified as nervonic acid, using LC/MS² (Panel B). Quantitative measures of nervonic acid in mid-frontal cortex (Panel C), temporal cortex (Panel D) and cerebellum (Panel E) from control subjects (open squares) and AD patients (closed circles). Two-tailed Welch's <i>t-</i>test.</p