Interaction of surface erosion and sequential thrust progression: implications on exhumation processes

This paper investigates the evolution of thrust wedges with concomitant surface erosion, and its bearing on the exhumation processes in orogenic belts. We performed sandbox experiments, simulating syn-orogenic erosion on forelandward sloping surfaces (~4°). Experiments show that the erosion process has a significant control on the progression of frontal thrusts. In case of no-erosion condition, wedges with high basal friction develop frontal thrusts with strongly increasing spacing. In contrast, for the same basal friction the thrusts show uniform spacing as the wedge development involves concomitant surface erosion. On the other hand, the erosion promotes reactivation of hinterland thrusts in wedges with low basal friction. We show that erosion-assisted thrust reactivation is the principal mechanism for exhumation of deeper level materials in orogens. Efficiency of this mechanism is largely controlled by basal friction. The exhumation of deeper level materials is limited, and occurs within a narrow, sub-vertical zone in the extreme hinterland when the basal friction is high (μb = 0.46). In contrast, the process is quite effective in wedges with low basal friction (μb =0.36), resulting in exhumation along gently dipping foreland-vergent thrusts as well as along thrusts, subsequently rotated into steep attitude. The zone of exhumation also shifts in the foreland direction in the course of horizontal movement. Consequently, deeper level materials cover a large area of the elevated part of the wedge

Krüppel-like factor 6 regulates transforming growth factor-β gene expression during human respiratory syncytial virus infection

<p>Abstract</p> <p>Background</p> <p>Human respiratory syncytial virus (RSV) infection is associated with airway remodeling and subsequent asthma development. Transforming growth factor-beta (TGF) plays a crucial role in asthma development. The mechanism regulating TGF gene expression during RSV infection is not known. Kruppel-like factor family of transcription factors are critical regulators of cellular/tissue homeostasis. Previous studies have shown that Kruppel-like factor 6 (KLF6) could function as a trans-activator of TGF gene; however, whether KLF members play a role during infection is unknown. In the current study we have evaluated the role of KLF6 during TGF expression in RSV infected cells.</p> <p>Findings</p> <p>Silencing KLF6 expression by shRNA led to drastic inhibition in TGF production during RSV infection, as assessed by ELISA analysis of medium supernatants. RT-PCR analysis revealed loss of TGF expression in KLF6 silenced cells. Chromatin-immunoprecipitation assay conducted with RSV infected cells showed binding of KLF6 protein to the TGF promoter during RSV infection. We further observed reduced RSV infectivity in KLF6 silenced cells and in cells incubated with TGF neutralizing antibody. In contrast, enhanced RSV infection was noted in cells incubated with purified TGF.</p> <p>Conclusion</p> <p>We have identified KLF6 as a key transcription factor required for trans-activation of TGF gene during RSV infection. Moreover, TGF production is required for efficient RSV infection and thus, KLF6 is also required for efficient RSV infection by virtue of KLF6 dependent TGF production during infection.</p

Autophagy, TGF-β, and SMAD-2/3 Signaling Regulates Interferon-β Response in Respiratory Syncytial Virus Infected Macrophages

Human respiratory syncytial virus (RSV) is a lung tropic virus causing severe airway diseases including bronchiolitis and pneumonia among infants, children and immuno-compromised individuals. RSV triggers transforming growth factor-beta(TGF-beta) production from lung epithelial cells and TGF-beta facilitates RSV infection of these cells. However, it is still unknown whether RSV infected myeloid cells like macrophages produce TGF-beta and the role of TGF-beta if any during RSV infection of these cells. Our study revealed that RSV infected macrophages produce TGF-beta and as a consequence these cells activate TGF-beta dependent SMAD-2/3 signaling pathway. Further mechanistic studies illustrated a role of autophagy in triggering TGF-beta production from RSV infected macrophages. In an effort to elucidate the role of TGF-beta and SMAD-2/3 signaling during RSV infection, we surprisingly unfolded the requirement of TGF-beta---SMAD2/3 signaling in conferring optimal innate immune antiviral response during RSV infection of macrophages. Type-I interferon (e.g. interferon-beta or IFN-beta) is a critical host factor regulating innate immune antiviral response during RSV infection. Our study revealed that loss of TGF-beta---SMAD2/3 signaling pathway in RSV infected macrophages led to diminished expression and production of IFN-beta. Inhibiting autophagy in RSV infected macrophages also resulted in reduced production of IFN-beta. Thus, our studies have unfolded the requirement of autophagy---TGF-beta---SMAD2/3 signaling network for optimal innate immune antiviral response during RSV infection of macrophages

Siliciclastic–carbonate mixing modes in the river-mouth bar palaeogeography of the Upper Cretaceous Garudamangalam Sandstone (Ariyalur, India)

AbstractMixed siliciclastic–carbonate rocks constitute the Upper Cretaceous Garuda-mangalam Sandstone Formation, Ariyalur (India), and offer an opportunity to look into the broad spectrum of mixing of compositionally and genetically different components. The palaeogeographic reconstruction indicates that deposition in the nearshore zone differed strongly in energy and active processes operatives due to the presence of a shore-parallel river-mouth bar. The western wing of the Mississippi bird-foot delta is considered to be a present-day analogon. Facies analysis in combination with petrography clearly shows the variability in palaeoenvironmental characteristics, both biogenic and non-biogenic. It also indicates diagenetic uptake of carbonate that filled empty spaces and actively replaced original components. Chemical staining followed by limited application of cathodoluminescence and energy dispersive X-ray analysis (EDAX) hint at intricacies in mixing arising from the compositional variations in the carbonate components. A model of siliciclastic–carbonate sediment mixing, including both the depositional and diagenetic developments, is presented; it is aimed at generating a better overview of, and a deeper insight into, the physical and chemical mechanisms involved

Retinoic acid inducible gene I Activates innate antiviral response against human parainfluenza virus type 3

Human parainfluenza virus type 3 (HPIV3) is a respiratory paramyxovirus that infects lung epithelial cells to cause high morbidity among infants and children. To date, no effective vaccine or antiviral therapy exists for HPIV3 and therefore, it is important to study innate immune antiviral response induced by this virus in infected cells. Type-I interferons (IFN, interferon-α/β) and tumor necrosis factor-α (TNFα activated by NFκB) are potent antiviral cytokines that play an important role during innate immune antiviral response. A wide-spectrum of viruses utilizes pattern recognition receptors (PRRs) like toll-like receptors (TLRs) and RLH (RIG like helicases) receptors such as RIGI (retinoic acid inducible gene -I) and Mda5 to induce innate antiviral response. Previously it was shown that both TNFα and IFNβ are produced from HPIV3 infected cells. However, the mechanism by which infected cells activated innate response following HPIV3 infection was not known. In the current study, we demonstrated that RIGI serves as a PRR in HPIV3 infected cells to induce innate antiviral response by expressing IFNβ (via activation of interferon regulatory factor-3 or IRF3) and TNFα (via activation of NF-κB)

Channel flow, tectonic overpressure, and exhumation of high-pressure rocks in the greater himalayas

The Himalayas are the archetype of continental collision, where a number of long-standing fundamental problems persist in the Greater Himalayan Sequence (GHS): (1) contemporaneous reverse and normal faulting, (2) inversion of metamorphic grade, (3) origin of high-(HP) and ultrahigh-pressure (UHP) rocks, (4) mode of ductile extrusion and exhumation of HP and UHP rocks close to the GHS hanging wall, (5) flow kinematics in the subduction channel, and (6) tectonic overpressure, here defined as TOP&thinsp; Combining double low line Pĝ•PL where P is total (dynamic) pressure and PL is lithostatic pressure. In this study we couple Himalayan geodynamics to numerical simulations to show how one single model, upward-Tapering channel (UTC) flow, can be used to find a unified explanation for the evidence. The UTC simulates a flat-ramp geometry of the main underthrust faults, as proposed for many sections across the Himalayan continental subduction. Based on the current knowledge of the Himalayan subduction channel geometry and geological/geophysical data, the simulations predict that a UTC can be responsible for high TOP ( &gt; 2). TOP increases exponentially with a decrease in UTC mouth width, and with an increase in underthrusting velocity and channel viscosity. The highest overpressure occurs at depths &lt; ĝ'60&thinsp;km, which, combined with the flow configuration in the UTC, forces HP and UHP rocks to exhume along the channel's hanging wall, as in the Himalayas. By matching the computed velocities and pressures wi

Phospholipid Scramblase 1 Potentiates The Antiviral Activity of Interferon

Phospholipid scramblase 1 (PLSCR1) is an interferon (IFN)- and growth factor-inducible, calcium-binding protein that either inserts into the plasma membrane or binds DNA in the nucleus depending on its state of palmyitoylation. In certain hematopoietic cells, PLSCR1 is required for normal maturation and terminal differentiation from progenitor cells as regulated by select growth factors, where it promotes recruitment and activation of Src kinases. PLSCR1 is a substrate of Src (and Abl) kinases, and transcription of the PLSCR1 gene is regulated by the same growth factor receptor pathways in which PLSCR1 potentiates afferent signaling. The marked transcriptional upregulation of PLSCR1 by IFNs led us to explore whether PLSCR1 plays an analogous role in cellular responses to IFN, with specific focus on antiviral activities. Accordingly, human cells in which PLSCR1 expression was decreased with short interfering RNA were rendered relatively insensitive to the antiviral activity of IFNs, resulting in higher titers of vesicular stomatitis virus (VSV) and encephalomyocarditis virus. Similarly, VSV replicated to higher titers in mouse PLSCR1−/− embryonic fibroblasts than in identical cells transduced to express PLSCR1. PLSCR1 inhibited accumulation of primary VSV transcripts, similar to the effects of IFN against VSV. The antiviral effect of PLSCR1 correlated with increased expression of a subset of IFN-stimulated genes (ISGs), including ISG15, ISG54, p56, and guanylate binding proteins. Our results suggest that PLSCR1, which is itself an ISG-encoded protein, provides a mechanism for amplifying and enhancing the IFN response through increased expression of a select subset of potent antiviral genes

Sedimentation patterns during the Precambrian : a unique record?

Although the similarities between depositional processes and products as well as the analogous controls on basin-filling and evolution appear to have enjoyed great uniformity throughout the sedimentary rock record, a noticeable distinction exists in the rates and intensities of a broad range of geological processes in the Precambrian epoch. This paper searches for distinctiveness in the Precambrian sedimentary record, both siliciclastic and carbonate, through an extensive, though not exhaustive, review of the relevant literature augmented by new observations. While differences in Precambrian deltaic, aeolian, glacial and possibly also lacustrine deposits and settings appear to have been small, their large-scale development was controlled largely by a combination of temporal and geodynamic influences, essentially of global compass. In this regard the onset of the supercontinent cycle and major perturbations in palaeo-atmospheric composition appear to have been significant. Marine environments provide a poor platform for PrecambrianePhanerozoic comparisons of sedimentation patterns, as those from the former period are preserved almost exclusively in epeiric settings, an environment essentially lacking on modern Earth. For the shallow marine carbonates, biological mediation of chemical sediment deposition changed radically from dominance by microbial biota in the Precambrian to a combination of metazons, protozoans and algae for the skeletal carbonates of the Phanerozoic. Despite it being widely recognized that Precambrian channel systems were braided in all environments (deltaic, tidal, alluvial, fluvial) as a consequence of the lack of vegetation and poor development of soils, the fluvial setting has some enigmatic aspects. Amongst these is evidence for ponding of muddy detritus in apparently sandstone bed-load dominated braided systems, with effects on local palaeoslopes which have resulted in unusual palaeohydraulic parameters for Precambrian fluvial systems. This is perhaps a field of research which holds greater promise when investigating sedimentation patterns prior to the Phanerozoic.SS acknowledges field grants from the CSIR, Government of India and the INSA-DFG for providing a fellowship to work with WA in Munich on molar tooth structure. PGE thanks both the University of Pretoria and the National Research Foundation of South Africa for funding.http://www.elsevier.com/locate/marpetgeonf201

Structure and lithology of the Japan Trench subduction plate boundary fault

The 2011 Mw9.0 Tohoku-oki earthquake ruptured to the trench with maximum coseismic slip located on the shallow portion of the plate boundary fault. To investigate the conditions and physical processes that promoted slip to the trench, Integrated Ocean Drilling Program Expedition 343/343T sailed 1 year after the earthquake and drilled into the plate boundary ∼7 km landward of the trench, in the region of maximum slip. Core analyses show that the plate boundary décollement is localized onto an interval of smectite-rich, pelagic clay. Subsidiary structures are present in both the upper and lower plates, which define a fault zone ∼5–15m thick. Fault rocks recovered from within the clay-rich interval contain a pervasive scaly fabric defined by anastomosing, polished, and lineated surfaces with two predominant orientations. The scaly fabric is crosscut in several places by discrete contacts across which the scaly fabric is truncated and rotated, or different rocks are juxtaposed. These contacts are inferred to be faults. The plate boundary décollement therefore contains structures resulting from both distributed and localized deformation. We infer that the formation of both of these types of structures is controlled by the frictional properties of the clay: the distributed scaly fabric formed at low strain rates associated with velocity-strengthening frictional behavior, and the localized faults formed at high strain rates characterized by velocity-weakening behavior. The presence of multiple discrete faults resulting from seismic slip within the décollement suggests that rupture to the trench may be characteristic of this margin