Abelian hypercomplex structures on central extensions of H-type Lie algebras

It is the aim of this work to give a characterization of the two-step nilpotent Lie algebras carrying abelian hypercomplex structures. In the special case of trivial extensions of irreducible H-type Lie algebras this characterization is given in terms of the dimension of the commutator subalgebra. As a consequence, we obtain the corresponding theorem for arbitrary H-type Lie algebras, extending a result in Barberis and Dotti, J. Math. Oxford (2) 47 (1996) 389-404.Fil: Barberis, Maria Laura Rita. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Centro de Investigación y Estudios de Matemática. Universidad Nacional de Córdoba. Centro de Investigación y Estudios de Matemática; Argentin

Abelian Hermitian geometry

We study the structure of Lie groups admitting left invariant abelian complex structures in terms of commutative associative algebras. If, in addition, the Lie group is equipped with a left invariant Hermitian structure, it turns out that such a Hermitian structure is K\"ahler if and only if the Lie group is the direct product of several copies of the real hyperbolic plane by a euclidean factor. Moreover, we show that if a left invariant Hermitian metric on a Lie group with an abelian complex structure has flat first canonical connection, then the Lie group is abelian.Comment: 14 page

Morphological variation of the leaves of Aechmea distichantha Lem. plants from contrasting habitats of a Chaco forest: a trade-off between leaf area and mechanical support

Several authors have reported phenotypic plasticity for bromeliad plants growing in contrasting habitats. Morphological and physiological differences of leaves seem to be an adaptation to water and light use, but there is also a compromise between carbon gain and the costs of sustaining static and dynamic loads. We hypothesized that plastic responses to habitat at the leaf level represent a trade-off between the photosynthetic area for capturing light and mechanical support. In this study, we measured morphological and architectural variables of central and basal leaves of Aechmea distichantha plants from the understory and forest edge, as well as anatomical variables of plants from each habitat. Understory plants had longer leaves, larger blade areas and greater length/width ratios than forest-edge plants. Blades of understory plants were less erect, less succulent, had thicker fiber tissue surrounding the vascular bundles and a higher curvature index than blades of forest-edge plants. Thus, understory plants increased their flexural stiffness by modifying their tissue structure as well as the shape of their leaves. On the other hand, blades of forest-edge plants had higher stomatal density and higher trichome density on their adaxial sides than understory plants. These patterns could be adaptations for higher gas exchange and to reduce vulnerability to photoinhibition in sun plants when compared to shade plants. Finally, most of the morphological and architectural variables were significantly different between positions. These results support our view that there is a trade-off at the leaf level between photosynthetic leaf area (for light capture and water use) and mechanical support

La organización Cauces

La organización Cauces conduce actualmente, en su rama estudiantil, tres de los nueve Centros de Estudiantes de la Universidad Nacional de Mar del Plata (UNMdP) además de ocupar la presidencia de la Federación Universitaria Marplatense (FUM) desde su normalización en 2011. También cuenta con graduados y docentes ocupando distintos roles de importancia en el cogobierno y la gestión de nuestra casa de estudios. Ha tenido un papel preponderante en la historia de distintas facultades y de la universidad, impulsando y participando de la reforma del estatuto, propiciando reformas en el ingreso, planes de estudios, regímenes de enseñanza, curricularizando la extensión mediante las practicas comunitarias, ampliando las políticas de bienestar, entre otras. Por ello, resulta imprescindible que un libro sobre la historia de la UNMdP cuente con un apartado sobre la organización que hace varios años cuenta con el mayor peso político en el claustro estudiantil, y que ha desempeñado un rol protagónico en los distintos procesos de discusión y cambio que ha atravesado nuestra universidad en dicho período. Este artículo pretende analizar la historia de la organización Cauces, desde su surgimiento a mediados de los años noventa en el seno la Facultad de Ciencias Económicas y Sociales (FCEyS) hasta la actualidad, identificando las distintas etapas de su desarrollo, momentos bisagra, principales procesos y transformaciones impulsadas en la Universidad. Finalmente, esperamos ofrecer una perspectiva complementaria al análisis histórico que viene desarrollando la universidad, incorporando la dimensión subjetiva al estudio de los distintos procesos de cambio que ha experimentado nuestra casa. Este enfoque, supone como condición necesaria para una precisa reflexión del pasado, la reconstrucción de los hechos históricos y el análisis de los principales actores involucrados en los mismos

A selective role for phosphatidylinositol 3,4,5-trisphosphate in the Gi-dependent activation of platelet Rap1B.

The small GTP-binding protein Rap1B is activated in human platelets upon stimulation of a G(i)-dependent signaling pathway. In this work, we found that inhibition of platelet adenylyl cyclase by dideoxyadenosine or SQ22536 did not cause activation of Rap1B and did not restore Rap1B activation in platelets stimulated by cross-linking of Fcgamma receptor IIA (FcgammaRIIA) in the presence of ADP scavengers. Moreover, elevation of the intracellular cAMP concentration did not impair the G(i)-dependent activation of Rap1B. Two unrelated inhibitors of phosphatidylinositol 3-kinase (PI3K), wortmannin and LY294002, totally prevented Rap1B activation in platelets stimulated by cross-linking of FcgammaRIIA, by stimulation of the P2Y(12) receptor for ADP, or by epinephrine. However, in platelets from PI3Kgamma-deficient mice, both ADP and epinephrine were still able to normally stimulate Rap1B activation through a PI3K-dependent mechanism, suggesting the involvement of a different isoform of the enzyme. Moreover, the lack of PI3Kgamma did not prevent the ability of epinephrine to potentiate platelet aggregation through a G(i)-dependent pathway. The inhibitory effect of wortmannin on Rap1B activation was overcome by addition of phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P(3)), but not PtdIns(3,4)P(2), although both lipids were found to support phosphorylation of Akt. Moreover, PtdIns(3,4,5)P(3) was able to relieve the inhibitory effect of apyrase on FcgammaRIIA-mediated platelet aggregation. We conclude that stimulation of a G(i)-dependent signaling pathway causes activation of the small GTPase Rap1B through the action of the PI3K product PtdIns(3,4,5)P(3), but not PtdIns(3,4)P(2), and that this process may contribute to potentiation of platelet aggregation

Distinct Roles of the Adaptor Protein Shc and Focal Adhesion Kinase in Integrin Signaling to ERK

It has been proposed that integrins activate ERK through the adaptor protein Shc independently of focal adhesion kinase (FAK) or through FAK acting on multiple target effectors, including Shc. We show that disruption of the actin cytoskeleton by cytochalasin D causes a complete inhibition of FAK but does not inhibit Shc signaling and activation of ERK. We have then generated primary fibroblasts carrying a targeted deletion of the segment of beta(1) subunit cytoplasmic domain required for activation of FAK. Analysis of these cells indicates that FAK is not necessary for efficient tyrosine phosphorylation of Shc, association of Shc with Grb2, and activation of ERK in response to matrix adhesion. In addition, integrin-mediated activation of FAK does not appear to be required for signaling to ERK following growth factor stimulation. To examine if FAK could contribute to the activation of ERK in a cell type-specific manner through the Rap1/B-Raf pathway, we have used Swiss-3T3 cells, which in contrast to primary fibroblasts express B-Raf. Dominant negative studies indicate that Shc mediates the early phase and peak, whereas FAK, p130(CAS), Crk, and Rap1 contribute to the late phase of integrin-dependent activation of ERK in these cells. In addition, introduction of B-Raf enhances and sustains integrin-mediated activation of ERK in wild-type primary fibroblasts but not in those carrying the targeted deletion of the beta(1) cytoplasmic domain. Thus, the Shc and FAK pathways are activated independently and function in a parallel fashion. Although not necessary for signaling to ERK in primary fibroblasts, FAK may enhance and prolong integrin-mediated activation of ERK through p130(CAS), Crk, and Rap1 in cells expressing B-Raf

CC-chemokine ligand 16 induces a novel maturation program in human immature monocyte-derived dendritic cells

Dendritic cells (DCs) are indispensable for initiation of primary T cell responses and a host's defense against infection. Many proinflammatory stimuli induce DCs to mature (mDCs), but little is known about the ability of chemokines to modulate their maturation. In the present study, we report that CCL16 is a potent maturation factor for monocyte-derived DCs (MoDCs) through differential use of its four receptors and an indirect regulator of Th cell differentiation. MoDCs induced to mature by CCL16 are characterized by increased expression of CD80 and CD86, MHC class II molecules, and ex novo expression of CD83 and CCR7. They produce many chemokines to attract monocytes and T cells and are also strong stimulators in activating allogeneic T cells to skew toward Th1 differentiation. Interestingly, they are still able to take up Ag and express chemokine receptors usually bound by inflammatory ligands and can be induced to migrate to different sites where they capture Ags. Our findings indicate that induction of MoDC maturation is an important property of CCL16 and suggest that chemokines may not only organize the migration of MoDCs, but also directly regulate their ability to prime T cell responses