Ordovician klippen structures of the Sierra de Umango: New insights on Tectonic evolution of the Western Sierras Pampeanas, Argentina

The basement rock of the Pampean flat-slab (Sierras Pampeanas) in the Central Andes was uplifted and rotated in the Cenozoic era. The Western Sierras Pampeanas are characterised by meta-igneous rocks of Grenvillian Mesoproterozoic age and metasedimentary units metamorphosed in the Ordovician period. These rocks, known as the northern Cuyania composite terrane, were derived from Laurentia and accreted toward Western Gondwana during the Early Paleozoic. The Sierra de Umango is the westernmost range of the Western Sierras Pampeanas.This range is bounded by the Devonian sedimentary rocks of the Precordillera on the western side and Tertiary rocks from the Sierra de Maz and Sierra del Espinal on the eastern side and contains igneous and sedimentary rocks outcroppings from the Famatina System on the far eastern side. The Sierra de Umango evolved during a period of polyphase tectonic activity, including an Ordovician collisional event, a Devonian compressional deformation, Late Paleozoic and Mesozoic extensional faulting and sedimentation (Paganzo and Ischigualasto basins) and compressional deformation of the Andean foreland during the Cenozoic. A Nappe System and an important shear zone, La Puntilla-La Falda Shear Zone (PFSZ), characterise the Ordovician collisional event, which was related to the accretion of Cuyania Terrane to the proto-Andean margin of Gondwana. Three continuous deformational phases are recognised for this event: the D1 phase is distinguished by relics of 51 preserved as internal foliation within interkinematic staurolite por-phyroblasts and likely represents the progressive metamorphic stage; the D2 phase exhibits P-T conditions close to the metamorphic peak that were recorded in an 52 transposition or a mylonitic foliation and determine the main structure of Umango; and the D3 phase is described as a set of tight to recumbent folds with S3 axial plane foliation, often related to thrust faults, indicating the retrogressive metamorphic stage. The Nappe System shows a top-to-the S/SW sense direction of movement, and the PFSZ served as a right lateral ramp in the exhumation process. This structural pattern is indicative of an oblique collision, with the Cuyania Terrane subducting under the proto-Andean margin of Gondwana in the NE direction. This continental subduction and exhumation lasted at least 30 million years, nearly the entire Ordovician period, and produced metamorphic conditions of upper amphibolite-to-granulite facies in medium- to high-pressure regimes. At least two later events deformed the earlier structures: D4 and D5 deformational phases. The D4 deformational phase corresponds to upright folding, with wavelengths of approximately 10 km and a general N-S orientation. These folds modified the S2 surface in an approximately cylindrical manner and are associated with exposed, discrete shear zones in the Silurian Guandacolinos Granite. The cylindrical pattern and subhorizontal axis of the D4 folds indicates that the S2 surface was originally flat-lying. The D4 folds are responsible for preserving the basement unit Juchi Orthogneiss synformal klippen. This deformation corresponds to the Chanica Tectonic during the interval between the Devonian and Carboniferous periods. The D5 deformational phase comprehends cuspate-lobate shaped open plunging folds with E W high-angle axes (D5 folds) and sub-vertical spaced cleavage. The D5 folds and related spaced cleavage deformed the previous structures and could be associated with uplifting during the Andean Cycle. (C) 2012 Elsevier Ltd. All rights reserved.

Galaxy interactions I. Major and minor mergers

Aims. We study galaxy pair samples selected from the Sloan Digital Sky Survey (SDSS-DR7) and we perform an analysis of minor and major mergers with the aim of investigating the dependence of galaxy properties on interactions. Methods. We build a galaxy pair catalog requiring r(p) < 25 kpc h(-1) and Delta V < 350 km s(-1) within redshift z < 0.1. By visual inspection of SDSS images we remove false identifications and we classify the interactions into three categories: pairs undergoing merging, M; pairs with evident tidal features, T; and non disturbed, N. We also divide the pair sample into minor and major interactions according to the luminosity ratio of the galaxy members. We study star formation activity through colors, the 4000 angstrom break, and star formation rates. Results. We find that similar to 10% of the pairs are classified as M. These systems show an excess of young stellar populations as inferred from the D-n(4000) spectral index, colors, and star formation rates of the member galaxies, an effect which we argue is directly related to the ongoing merging process. We find similar to 30% of the pairs exhibiting tidal features (T pairs) with member galaxies showing evidence of old stellar populations. This can be associated either to the disruptive effect of some tidal interactions, or to the longer time-scale of morphological disturbance with respect to the bursts of the tidal induced star formation. Regardless of the color distribution, we find a prominent blue peak in the strongest mergers, while pairs with tidal signs under a minor merger show a strong red peak. Therefore, our results show that galaxy interactions are important in driving the evolution of galaxy bimodality. By adding stellar masses and star formation rates of the two members of the pairs, we explore the global efficiency of star formation of the pairs as a whole. We find that, at a given total stellar mass, major mergers are significantly more efficient (a factor approximate to 2) in forming new stars, with respect to both minor mergers or a control sample of non-interacting galaxies. We conclude that the characteristics of the interactions and the ratio of luminosity galaxy pair members involved in a merger are important parameters in setting galaxy properties.

Kinin-B2 Receptor Mediated Neuroprotection after NMDA Excitotoxicity Is Reversed in the Presence of Kinin-B1 Receptor Agonists

Background: Kinins, with bradykinin and des-Arg(9)-bradykinin being the most important ones, are pro-inflammatory peptides released after tissue injury including stroke. Although the actions of bradykinin are in general well characterized; it remains controversial whether the effects of bradykinin are beneficial or not. Kinin-B2 receptor activation participates in various physiological processes including hypotension, neurotransmission and neuronal differentiation. The bradykinin metabolite des-Arg(9)-bradykinin as well as Lys-des-Arg(9)-bradykinin activates the kinin-B1 receptor known to be expressed under inflammatory conditions. We have investigated the effects of kinin-B1 and B2 receptor activation on N-methyl-Daspartate (NMDA)-induced excitotoxicity measured as decreased capacity to produce synaptically evoked population spikes in the CA1 area of rat hippocampal slices. Principal Findings: Bradykinin at 10 nM and 1 mu M concentrations triggered a neuroprotective cascade via kinin-B2 receptor activation which conferred protection against NMDA-induced excitotoxicity. Recovery of population spikes induced by 10 nM bradykinin was completely abolished when the peptide was co-applied with the selective kinin-B2 receptor antagonist HOE-140. Kinin-B2 receptor activation promoted survival of hippocampal neurons via phosphatidylinositol 3-kinase, while MEK/MAPK signaling was not involved in protection against NMDA-evoked excitotoxic effects. However, 100 nM Lys-des-Arg(9)-bradykinin, a potent kinin-B1 receptor agonist, reversed bradykinin-induced population spike recovery. The inhibition of population spikes recovery was reversed by PD98059,showing that MEK/MAPK was involved in the induction of apoptosis mediated by the B1 receptor. Conclusions: Bradykinin exerted protection against NMDA-induced excitotoxicity which is reversed in the presence of a kinin-B1 receptor agonist. As bradykinin is converted to the kinin-B1 receptor metabolite des-Arg(9)-bradykinin by carboxypeptidases, present in different areas including in brain, our results provide a mechanism for the neuroprotective effect in vitro despite of the deleterious effect observed in vivo.