The European Union funded NEOShield project: a global approach to near-Earth object impact threat mitigation

Although discussions are underway within the Action Team 14 of the United Nations COPUOS, there is currently no concerted international plan addressing the impact threat from near-Earth objects (NEOs) and how to organize, prepare and implement mitigation measures. We report on a new international project to address impact hazard mitigation issues, being the subject of a proposal submitted to the European Commission in response to the 2011 FP7 Call “Prevention of impacts from near-Earth objects on our planet”. Our consortium consists of 13 research institutes, universities, and industrial partners from 6 countries and includes leading US and Russian space organizations. The primary aim of the project, NEOShield, is to investigate in detail the three most promising mitigation techniques: the kinetic impactor, blast deflection, and the gravity tractor, and devise feasible demonstration missions. Furthermore, we will investigate options for an international strategy for implementation when an actual impact threat arises. The NEOShield project was formally accepted by the European Commission on 17 November 2011 and funded with a total of 5.8 million Euros for a period of 3.5 years. The kick-off meeting took place at the DLR Institute of Planetary Research, Berlin, in January 2012. In this paper we present a brief overview of the planned scope of the project

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field

A global approach to near-Earth object impact threat mitigation

There is currently no concerted international plan addressing the impact threat and how to organize, prepare and implement mitigation measures. We report on a new international project to address impact hazard mitigation issues, being the subject of a proposal to the European Commission in response to the 2011 FP7 Call “Prevention of impacts from near-Earth objects on our planet”. Our consortium consists of 13 research institutes, universities, and industrial partners and includes leading US and Russian space organizations. The primary aim of the project, NEOShield, is to investigate in detail the three most promising mitigation techniques: the kinetic impactor, blast deflection, and the gravity tractor, and devise feasible demonstration missions. Furthermore, we will investigate options for an international strategy for implementation when an actual impact threat arises. The European Commission’s funding contribution for the successful project in this Call will be a maximum of 4 million Euro. Final confirmation of funding is preceded by a phase of negotiation between the Consortium and the European Commission. At the time of writing the proposal assessment exercise has been completed and the NEOShield proposal has far exceeded all thresholds for acceptance into the negotiation phase. We anticipate a project duration of some 3.5 years with a kick-off meeting at the end of 2011. In this paper we present a brief overview of the planned scope of the project

How many watts: a data driven approach to aggregated residential air-conditioning load forecasting

by Clement Lork, Batchu Rajasekhar, Chau Yuen and Naran M. Pindoriy

Depolymerization of aryltellurinic anhydrides with sodium hydroxide. Synthesis and structure of the hydrated sodium aryltellurinates [Na(H2O)4](RTeO2) (R = 4-MeOC6H4, 8-Me2NC10H6)

Depolymerization of the aryltellurinic anhydrides [(RTe)2O3]n (9, R = 4-MeOC6H4; 6, R = 8-Me2NC10H6) with aqueous NaOH afforded the hydrated sodium aryltellurinates [Na(H2O)4](4-MeOC6H4TeO2) (10) and [Na(H2O)4](8-Me2NC10H6TeO2)·H2O (11·H2O) as highly crystalline materials

An adaptive data driven approach to single unit residential air-conditioning prediction and forecasting using regression trees

by Clement Lork, Yuren Zhou, Rajasekhar Batchu, Chau Yuen and Naran M. Pindoriy

Enterovirus 2Apro targets MDA5 and MAVS in infected cells

Contains fulltext : 137931.pdf (publisher's version ) (Open Access)RIG-I-like receptors (RLRs) MDA5 and RIG-I are key players in the innate antiviral response. Upon recognition of viral RNA, they interact with MAVS, eventually inducing type I interferon production. The interferon induction pathway is commonly targeted by viruses. How enteroviruses suppress interferon production is incompletely understood. MDA5 has been suggested to undergo caspase- and proteasome-mediated degradation during poliovirus infection. Additionally, MAVS is reported to be cleaved during infection with coxsackievirus B3 (CVB3) by the CVB3 proteinase 3C(pro), whereas MAVS cleavage by enterovirus 71 has been attributed to 2A(pro). As yet, a detailed examination of the RLR pathway as a whole during any enterovirus infection is lacking. We performed a comprehensive analysis of crucial factors of the RLR pathway, including MDA5, RIG-I, LGP2, MAVS, TBK1, and IRF3, during infection of CVB3, a human enterovirus B (HEV-B) species member. We show that CVB3 inhibits the RLR pathway upstream of TBK1 activation, as demonstrated by limited phosphorylation of TBK1 and a lack of IRF3 phosphorylation. Furthermore, we show that MDA5, MAVS, and RIG-I all undergo proteolytic degradation in CVB3-infected cells through a caspase- and proteasome-independent manner. We convincingly show that MDA5 and MAVS cleavages are both mediated by CVB3 2A(pro), while RIG-I is cleaved by 3C(pro). Moreover, we show that proteinases 2A(pro) and 3C(pro) of poliovirus (HEV-C) and enterovirus 71 (HEV-A) exert the same functions. This study identifies a critical role of 2A(pro) by cleaving MDA5 and MAVS and shows that enteroviruses use a common strategy to counteract the interferon response in infected cells. IMPORTANCE: Human enteroviruses (HEVs) are important pathogens that cause a variety of diseases in humans, including poliomyelitis, hand, foot, and mouth disease, viral meningitis, cardiomyopathy, and more. Like many other viruses, enteroviruses target the host immune pathways to gain replication advantage. The MDA5/MAVS pathway is responsible for recognizing enterovirus infections in the host cell and leads to expression of type I interferons (IFN-I), crucial antiviral signaling molecules. Here we show that three species of HEVs all employ the viral proteinase 2A (2A(pro)) to proteolytically target MDA5 and MAVS, leading to an efficient blockade upstream of IFN-I transcription. These observations suggest that MDA5/MAVS antagonization is an evolutionarily conserved and beneficial mechanism of enteroviruses. Understanding the molecular mechanisms of enterovirus immune evasion strategies will help to develop countermeasures to control infections with these viruses in the future