A modularity based spectral method for simultaneous community and anti-community detection

In a graph or complex network, communities and anti-communities are node sets whose modularity attains extremely large values, positive and negative, respectively. We consider the simultaneous detection of communities and anti-communities, by looking at spectral methods based on various matrix-based definitions of the modularity of a vertex set. Invariant subspaces associated to extreme eigenvalues of these matrices provide indications on the presence of both kinds of modular structure in the network. The localization of the relevant invariant subspaces can be estimated by looking at particular matrix angles based on Frobenius inner products

Additional file 2: of TRPA1 channels promote astrocytic Ca2+ hyperactivity and synaptic dysfunction mediated by oligomeric forms of amyloid-β peptide

Characterization of Fluo-4-loaded cells in the stratum radiatum of mouse coronal slice. (a) Confocal image of Fluo-4-loaded (cyan) and SR101-labeled (magenta) cells in the CA1 stratum radiatum. Merged image showing the proportion of loaded astrocytes (white), confirming that most of the loaded cells are astrocytes. One hour before slicing, animals were iv injected with SR101 as described previously [51]. Vessels are only labeled with SR101 (white arrow). (b) Z-stack projections of confocal images of a patched astrocyte loaded with Fluo-4 (cyan) and SR101 (magenta). Merged image showing the Fluo-4 diffusion in the whole astrocytic territory. (c) Example of a passive whole-cell current recorded in a stratum radiatum astrocyte. Cell was held at −70 mV and 10 mV hyper- and depolarizing voltage steps of 80 ms duration were applied (−110 to +80 mV). (TIFF 1907 kb

Additional file 7: of TRPA1 channels promote astrocytic Ca2+ hyperactivity and synaptic dysfunction mediated by oligomeric forms of amyloid-β peptide

TRPA1 channels expression is located in thick GFAP-positive processes and in adjacent thin processes lacking GFAP staining. 3D–recontsruct of astrocytic processes objectivized by GFAP staining (magenta) showing that TRPA1 channels (green) expression went over in contiguous processes excluding GFAP staining. Scale bar: 50 nm. (ZIP 1736 kb

CRF2 signaling reorganizes cell-matrix contacts.

<p>(A) Phaloidin-TRITC fluorescence is analyzed by confocal microscopy at the basal pole of HT-29 CRF2-GFP cells following Ucn3 treatment. Scale bar, 5 µm. (B) ERK-P^Tyr204/ERK total ratio quantified from immunoblot in HT-29 cells treated with Ucn3 (0 to 60 min) (Upper panel). Effects of Src (PP2: 10 µM, 1 hr) or MEK (U0126: 10 µM, 1 hr) inhibitors on Ucn3 induced ERK-P^Tyr204 (Lower panel). (C) Ucn3-mediated phosphorylation of FAK- P^Ser910 in HT-29. Quantifications were performed from immunoblots and normalized to actin (upper panel). Effects of Src (PP2, 10 µM, 1 hr) and ERK (U0126, 10 µM, 1 hr) inhibitors on Ucn3 induced FAK-P^Ser910 (Lower panel). (D) Confocal analysis of vinculin distribution at the basal pole of HT-29 following Ucn3 treatment. Scale bar, 20 µm. (E) Quantification of the patch number by size at 30 min of Ucn3 treatment.</p

Patient's clinicopathological findings.

<p>Patient's clinicopathological findings.</p

CRF2-mediated dissociation of AJ leads to nuclear shuttling of p120ctn and Kaiso.

<p>(A) Confocal analysis of p120ctn location in HT-29 cells pretreated with cycloheximide before Ucn3 treatment. Scale bar, 10 µm. (B) Immunoblot analysis of p120ctn and Kaiso protein expression in nuclear extracts from HT-29 cells treated or not with Ucn3 (expression was normalized to histones). (C) Effects of Src and MEK inhibitors (PP2 and U0126: 10 µM, 1 hr) on p120ctn and Kaiso protein expression in nuclear extracts from HT-29 treated or not with Ucn3. Expression was normalized to histones. (D) Confocal analysis of cellular distribution of Kaiso in HT-29 cells. Nuclei were stained with Topro3. Cells negative for nuclei labeling of Kaiso were circumscribed by a white dotted line. Scale bar, 60 µm.</p

Oligonucleotide sequences of primers used for qPCR and RT-PCR.

<p>GAPDH, glyceraldehydes-3-phosphate dehydrogenase; MMP, matrixmetalloproteinase; PGK, phosphoglycerate kinase; HPRT, human phosphoribosyltransferase.</p

CRF2 and ligand expression are increased in high grade and poorly differentiated human CRC.

<p>(A) Histograms representing CRF2α, Ucn2 and Ucn3 transcript expression normalized to the housekeeping gene PGK (phosphoglycerate kinase) in human normal tissues or CRC (low and high grades). (B) Representative CRF2 immunohistochemistry performed on CRC tissues from low to high grade. Scale bar, 50 µm. (C) Histograms representing CRF2 protein expression quantified from immunohistochemistry. Each sample is represented as dark bars +/− SD (left) and the mean value of each group +/− SD (right). High grade is statistically different from normal at *, p<0.05.</p

CRF2 signaling disrupts AJ.

<p>(A) Immunoblot analysis of Src-P^Tyr418 and Src total expression in HT-29 cells following the time course of Ucn3 treatment. (B) Confocal analysis of E-cadherin distribution in HT-29 cells pretreated with cycloheximide before Ucn3 treatment. Scale bar, 15 µm. (C) Effect of PP2 (10 µM, 1 hr) on E-cadherin distribution in HT-29 cells treated or not with Ucn3, analyzed by epifluorescence microscopy. Scale bar, 20 µM. (D) Effect of CRF2 antagonist (A2b, 8 nM, 24 hrs) on E-cadherin expression in SW620 cells. Quantification was performed from immunoblots and normalized to actin. (E) E-cadherin distribution in SW620 cells pretreated or not with A2b and further treated or not with Ucn3. Analyzed were performed by epifluorescence microscopy. Scale bar, 10 µM.</p

CRF2 signaling alters cell adhesion in favor to cell migration and invasion.

<p>(A) HT-29 were treated or not with Ucn3 (100 nM) 30 min before adhesion and then plated on either COIV or LN-332. Cell-ECM adhesion was evaluated at 60 min with the use of a Cell Titer Aqueous MTT reagent kit. Values are normalized to the adhesion without Ucn3. Data represent the mean +/− SEN of 4 separate experiments. Effect of Ucn3 on HT-29 cells transmigration after 72 hrs was determined using a transwell assay (B) and on HT-29 cell invasion after 48 hrs by a matrigel assay (C). In both assays cells were visualized by phase contrast microscopy and counted. A phase contrast image has been joined. A circle has indicated some migrating cells and some invaded cells have been indicated by a white arrow. Data (n>3) are given as mean +/− SEM. (D) Effects of Ucn3 on HT-29 cell viability. (E) Regulation of MMP3 and MMP7 mRNA expression analyzed by RT-PCR in HT-29 cells treated with Ucn3 100 nM. (F) Immunoblot analysis of MMP3 and MMP7 protein expression in HT-29 cells following the time course of Ucn3 treatment. (G) Zymogram of gelatinolytic activities in supernatant of HT-29 cells treated or not with Ucn3 (100 nM) during 24 and 48 hrs.</p