480 research outputs found

    Constructing Narcoterrorism as Danger: Afghanistan and the Politics of Security and Representation

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    Afghanistan has become a country synonymous with danger. Discourses of narcotics, terrorism, and narcoterrorism have come to define the country and the current conflict. However, despite the prevalence of these dangers globally, they are seldom treated as political representations. This project theorizes danger as a political representation by deconstructing and problematizing contemporary discourses of (narco)terrorism in Afghanistan. Despite the globalisation of these two discourses of danger, (narco)terrorism remains largely under-theorised, with the focus placed on how to overcome this problem rather than critically analysing it as a representation. The argument being made here is that (narco)terrorism is not some ‘new’ existential danger, but rather reflects the hegemonic and counterhegemonic use of danger to establish authority over the collective identity. Using the case study of Afghanistan, this project critically analyses representations of danger emerging from the Afghan government and the Taliban. While many studies have looked at terrorism and narcotics as security concerns, there has not been a critical analysis of these two dangers as a political representation in the Afghan context. Therefore, this study will be of great benefit to scholars and practitioners of security as it presents a unique look on how identity is shaped through representations of danger in Afghanistan. Through applying Critical Discourse Analysis to contemporary representations in Afghanistan, this study provides new insight into the aims and objectives of both the Government of the Islamic Republic of Afghanistan and the Taliban

    The EMC of satellite power systems and DoD C-E systems

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    The solar power satellite (SPS) technical parameters that are needed to accurately assess the electromagnetic compatibility (EMC) between SPS systems and DoD communications-electronics (C-E) systems are identified and assessed. The type of electromagnetic interactions that could degrade the performance of C-E systems are described and the major military installations in the southwestern portions of CONUS where specially sensitive C-E systems are being used for combat training and evaluation are identified. Classes of C-E systems that are generally in the vicinity of these military installations are considered. The Technical parameters that govern the degree of compatibility of the SPS with these C-E systems, and some technical requirements that are necessary to ensure short-term and long-term EMC are identified

    Thermal fluctuations on the freeze-out surface of heavy-ion collisions and their impact on particle correlations

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    Particle momentum distributions originating from a quark-gluon plasma asproduced in high-energy nuclear collisions can be influenced by thermalfluctuations in fluid dynamic fields. We study this effect by generalizing thecommonly used kinetic freeze-out prescription by allowing for smallfluctuations around an average in fluid velocity, chemical potentials andtemperature. This leads to the appearance of specific two-body momentumcorrelations. Combining a blast-wave parametrization of the kinetic freeze-outsurface with the thermal correlation functions of an ideal resonance gas, weperform an exploratory study of angular net-charge correlations induced bythermal fluctuations around vanishing chemical potential. We note a diffusionof the near-side peak around Δy=Δϕ=0\Delta y=\Delta\phi=0 induced by variances ofdifferent chemical potentials, which could be investigated experimentally.<br

    Sites of Biosynthesis of Outer and Inner Membrane Proteins of Neurospora crassa Mitochondria

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    Outer and inner membranes of Neurospora crassa mitochondria were separated by the combined swelling, shrinking, sonication procedure. Membranes were characterized by electron microscopy and by marker enzyme activities. A red carotenoid pigment was found to be concentrated in the outer membrane. The inner mitochondrial membrane was resolved into about 20 protein bands on polyacrylamide gel electrophoresis, whereas the outer membrane shows essentially one single protein band. Only negligible incorporation of radioactive amino acids occurs into outer membrane when isolated mitochondria are synthesizing polypeptide chains. In agreement with this observation labeling of outer membrane protein is almost entirely blocked, when whole Neurospora cells are incubated with radioactive amino acids in the presence of cycloheximide, an inhibitor of cytoplasmic protein synthesis. Finally, the essential electrophoretic protein band from outer membrane does not become labeled when mitochondria are incubated with radioactive amino acids either in vitro or in vivo in the presence of cycloheximide. It is concluded that the vast majority, if not all, of the outer membrane protein is synthesized by the cytoplasmic system and that polypeptide chains formed by the mitochondrial ribosomes are integrated into the inner mitochondrial membrane

    Processing quantum information with relativistic motion of atoms

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    We show that particle detectors, such as two-level atoms, in noninertial motion (or in gravitational fields) could be used to build quantum gates for the processing of quantum information. Concretely, we show that through suitably chosen noninertial trajectories of the detectors the interaction Hamiltonian's time dependence can be modulated to yield arbitrary rotations in the Bloch sphere due to relativistic quantum effects

    Connexins in cancer: bridging the gap to the clinic

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    Gap junctions comprise arrays of intercellular channels formed by connexin proteins and provide for the direct communication between adjacent cells. This type of intercellular communication permits the coordination of cellular activities and plays key roles in the control of cell growth and differentiation and in the maintenance of tissue homoeostasis. After more than 50 years, deciphering the links among connexins, gap junctions and cancer, researchers are now beginning to translate this knowledge to the clinic. The emergence of new strategies for connexin targeting, combined with an improved understanding of the molecular bases underlying the dysregulation of connexins during cancer development, offers novel opportunities for clinical applications. However, different connexin isoforms have diverse channel-dependent and -independent functions that are tissue and stage specific. This can elicit both pro- and anti-tumorigenic effects that engender significant challenges in the path towards personalised medicine. Here, we review the current understanding of the role of connexins and gap junctions in cancer, with particular focus on the recent progress made in determining their prognostic and therapeutic potential

    Cx43 and Associated Cell Signaling Pathways Regulate Tunneling Nanotubes in Breast Cancer Cells

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    Altres ajuts: A. acknowledges funding from Fundación Científica Asociación Española Contra el Cáncer (IDEAS SEMILLA AECC 2020/IDEAS20033PUIG) and Instituto de Salud Carlos III co-financed by the European Regional Development Fund (ERDF) . The APC was funded by Instituto de Salud Carlos III co-financed by the European Regional Development Fund (ERDF). H.G is funded by the European Regional Development Fund (ERDF) through the Operational Program for Competitiveness Factors (COMPETE; under the projects PAC "NETDIAMOND" POCI-01-0145-FEDER-016385; HealthyAging2020 CENTRO-01-0145-FEDER-000012-N2323; POCI-01-0145-FEDER-007440, CENTRO-01-0145-FEDER-032179, CENTRO-01-0145-FEDER-032414, POCI-01-0145-FEDER-022122, FCTUID/NEU/04539/2013, UID/NEU/04539/2019, UIDB/04539/2020 and UIDP/04539/2020.Connexin 43 (Cx43) forms gap junctions that mediate the direct intercellular diffusion of ions and small molecules between adjacent cells. Cx43 displays both pro- and anti-tumorigenic properties, but the mechanisms underlying these characteristics are not fully understood. Tunneling nanotubes (TNTs) are long and thin membrane projections that connect cells, facilitating the exchange of not only small molecules, but also larger proteins, organelles, bacteria, and viruses. Typically, TNTs exhibit increased formation under conditions of cellular stress and are more prominent in cancer cells, where they are generally thought to be pro-metastatic and to provide growth and survival advantages. Cx43 has been described in TNTs, where it is thought to regulate small molecule diffusion through gap junctions. Here, we developed a high-fidelity CRISPR/Cas9 system to knockout (KO) Cx43. We found that the loss of Cx43 expression was associated with significantly reduced TNT length and number in breast cancer cell lines. Notably, secreted factors present in conditioned medium stimulated TNTs more potently when derived from Cx43-expressing cells than from KO cells. Moreover, TNT formation was significantly induced by the inhibition of several key cancer signaling pathways that both regulate Cx43 and are regulated by Cx43, including RhoA kinase (ROCK), protein kinase A (PKA), focal adhesion kinase (FAK), and p38. Intriguingly, the drug-induced stimulation of TNTs was more potent in Cx43 KO cells than in wild-type (WT) cells. In conclusion, this work describes a novel non-canonical role for Cx43 in regulating TNTs, identifies key cancer signaling pathways that regulate TNTs in this setting, and provides mechanistic insight into a pro-tumorigenic role of Cx43 in cancer

    Targeting of chondrocyte plasticity via connexin43 modulation attenuates cellular senescence and fosters a pro-regenerative environment in osteoarthritis

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    Osteoarthritis (OA), a chronic disease characterized by articular cartilage degeneration, is a leading cause of disability and pain worldwide. In OA, chondrocytes in cartilage undergo phenotypic changes and senescence, restricting cartilage regeneration and favouring disease progression. Similar to other wound-healing disorders, chondrocytes from OA patients show a chronic increase in the gap junction channel protein connexin43 (Cx43), which regulates signal transduction through the exchange of elements or recruitment/release of signalling factors. Although immature or stem-like cells are present in cartilage from OA patients, their origin and role in disease progression are unknown. In this study, we found that Cx43 acts as a positive regulator of chondrocyte-mesenchymal transition. Overactive Cx43 largely maintains the immature phenotype by increasing nuclear translocation of Twist-1 and tissue remodelling and proinflammatory agents, such as MMPs and IL-1β, which in turn cause cellular senescence through upregulation of p53, p16INK4a and NF-κB, contributing to the senescence-associated secretory phenotype (SASP). Downregulation of either Cx43 by CRISPR/Cas9 or Cx43-mediated gap junctional intercellular communication (GJIC) by carbenoxolone treatment triggered rediferentiation of osteoarthritic chondrocytes into a more differentiated state, associated with decreased synthesis of MMPs and proinflammatory factors, and reduced senescence. We have identified causal Cx43- sensitive circuit in chondrocytes that regulates dedifferentiation, redifferentiation and senescence. We propose that chondrocytes undergo chondrocyte-mesenchymal transition where increased Cx43-mediated GJIC during OA facilitates Twist-1 nuclear translocation as a novel mechanism involved in OA progression. These findings support the use of Cx43 as an appropriate therapeutic target to halt OA progression and to promote cartilage regeneration.This work was supported in part through funding from the Spanish Society for Rheumatology (SER; FER 2013) and Spanish Foundation for Research on Bone and Mineral Metabolism (FEIOMM), grant PRECIPITA-2015-000139 from the FECYT-Ministry of Economy and Competitiveness (to M.D.M.), grant PI16/00035 from the Health Institute ‘Carlos III’ (ISCIII, Spain), the European Regional Development Fund, ‘A way of making Europe’ from the European Union (to M.D.M.) and a grant from Xunta de Galicia IN607B 2017/21 (to M.D.M.) and pre-doctoral fellowship to M.V.-E. T.A. acknowledges support from Instituto de Salud Carlos III grants PI16/00772 and CPII16/00042, co-financed by the European Regional Development Fund (ERDF)S
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