25 research outputs found

    On Eigenvalues of Random Complexes

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    We consider higher-dimensional generalizations of the normalized Laplacian and the adjacency matrix of graphs and study their eigenvalues for the Linial-Meshulam model Xk(n,p)X^k(n,p) of random kk-dimensional simplicial complexes on nn vertices. We show that for p=Ω(logn/n)p=\Omega(\log n/n), the eigenvalues of these matrices are a.a.s. concentrated around two values. The main tool, which goes back to the work of Garland, are arguments that relate the eigenvalues of these matrices to those of graphs that arise as links of (k2)(k-2)-dimensional faces. Garland's result concerns the Laplacian; we develop an analogous result for the adjacency matrix. The same arguments apply to other models of random complexes which allow for dependencies between the choices of kk-dimensional simplices. In the second part of the paper, we apply this to the question of possible higher-dimensional analogues of the discrete Cheeger inequality, which in the classical case of graphs relates the eigenvalues of a graph and its edge expansion. It is very natural to ask whether this generalizes to higher dimensions and, in particular, whether the higher-dimensional Laplacian spectra capture the notion of coboundary expansion - a generalization of edge expansion that arose in recent work of Linial and Meshulam and of Gromov. We show that this most straightforward version of a higher-dimensional discrete Cheeger inequality fails, in quite a strong way: For every k2k\geq 2 and nNn\in \mathbb{N}, there is a kk-dimensional complex YnkY^k_n on nn vertices that has strong spectral expansion properties (all nontrivial eigenvalues of the normalised kk-dimensional Laplacian lie in the interval [1O(1/n),1+O(1/n)][1-O(1/\sqrt{n}),1+O(1/\sqrt{n})]) but whose coboundary expansion is bounded from above by O(logn/n)O(\log n/n) and so tends to zero as nn\rightarrow \infty; moreover, YnkY^k_n can be taken to have vanishing integer homology in dimension less than kk.Comment: Extended full version of an extended abstract that appeared at SoCG 2012, to appear in Israel Journal of Mathematic

    Human epicardial cell-conditioned medium contains HGF/IgG complexes that phosphorylate RYK and protect against vascular injury

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    Complejo universitario en Madrid. Convocatoria Abril. Plan 1996. Proyecto fin de carrera. Universidad Politécnica de Madrid. Escuela Técnica Superior de Arquitectur

    Internalized FGF-2-Loaded Nanoparticles Increase Nuclear ERK1/2 Content and Result in Lung Cancer Cell Death

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    Innovative cancer treatments, which improve adjuvant therapy and reduce adverse events, are desperately needed. Nanoparticles provide controlled intracellular biomolecule delivery in the absence of activating external cell surface receptors. Prior reports suggest that intracrine signaling, following overexpression of basic fibroblast growth factor (FGF-2) after viral transduction, has a toxic effect on diseased cells. Herein, the research goals were to (1) encapsulate recombinant FGF-2 within stable, alginate-based nanoparticles (ABNs) for non-specific cellular uptake, and (2) determine the effects of ABN-mediated intracellular delivery of FGF-2 on cancer cell proliferation/survival. In culture, human alveolar adenocarcinoma basal epithelial cell line (A549s) and immortalized human bronchial epithelial cell line (HBE1s) internalized ABNs through non-selective endocytosis. Compared to A549s exposed to empty (i.e., blank) ABNs, the intracellular delivery of FGF-2 via ABNs significantly increased the levels of lactate dehydrogenase, indicating that FGF-2-ABN treatment decreased the transformed cell integrity. Noticeably, the nontransformed cells were not significantly affected by FGF-2-loaded ABN treatment. Furthermore, FGF-2-loaded ABNs significantly increased nuclear levels of activated-extracellular signal-regulated kinase ½ (ERK1/2) in A549s but had no significant effect on HBE1 nuclear ERK1/2 expression. Our novel intracellular delivery method of FGF-2 via nanoparticles resulted in increased cancer cell death via increased nuclear ERK1/2 activation
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