Autonomous Close Formation Flight Control with Fixed Wing and Quadrotor Test Beds

Autonomous formation flight is a key approach for reducing energy cost and managing traffic in future high density airspace. The use of Unmanned Aerial Vehicles (UAVs) has allowed low-budget and low-risk validation of autonomous formation flight concepts. This paper discusses the implementation and flight testing of nonlinear dynamic inversion (NLDI) controllers for close formation flight (CFF) using two distinct UAV platforms: a set of fixed wing aircraft named “Phastball” and a set of quadrotors named “NEO.” Experimental results show that autonomous CFF with approximately 5-wingspan separation is achievable with a pair of low-cost unmanned Phastball research aircraft. Simulations of the quadrotor flight also validate the design of the NLDI controller for the NEO quadrotors

Simian hemorrhagic fever virus infection of rhesus macaques as a model of viral hemorrhagic fever: Clinical characterization and risk factors for severe disease

AbstractSimian Hemorrhagic Fever Virus (SHFV) has caused sporadic outbreaks of hemorrhagic fevers in macaques at primate research facilities. SHFV is a BSL-2 pathogen that has not been linked to human disease; as such, investigation of SHFV pathogenesis in non-human primates (NHPs) could serve as a model for hemorrhagic fever viruses such as Ebola, Marburg, and Lassa viruses. Here we describe the pathogenesis of SHFV in rhesus macaques inoculated with doses ranging from 50PFU to 500,000PFU. Disease severity was independent of dose with an overall mortality rate of 64% with signs of hemorrhagic fever and multiple organ system involvement. Analyses comparing survivors and non-survivors were performed to identify factors associated with survival revealing differences in the kinetics of viremia, immunosuppression, and regulation of hemostasis. Notable similarities between the pathogenesis of SHFV in NHPs and hemorrhagic fever viruses in humans suggest that SHFV may serve as a suitable model of BSL-4 pathogens

Sequential action of FRUITFULL as modulator of the activity of the floral regulators SVP and SOC1

[EN] The role in flowering time of the MADS-box transcription factor FRUITFULL (FUL) has been proposed in many works. FUL has been connected to several flowering pathways as a target of the photoperiod, ambient temperature, and age pathways and it is has been shown to promote flowering in a partially redundant manner with SUPPRESSOR OF OVEREXPRESSION OF CONSTANS 1 (SOC1). However, the position of FUL in these genetic networks, as well as the functional output of FUL activity during floral transition, remains unclear. In this work, a genetic approach has been undertaken to understand better the functional hierarchies involving FUL and other MADS-box factors with well established roles as floral integrators such as SOC1, SHORT VEGETATIVE PHASE (SVP) or FLOWERING LOCUS C (FLC). Our results suggest a prominent role of FUL in promoting reproductive transition when photoinductive signalling is suppressed by short-day conditions or by high levels of FLC expression, as in non-vernalized winter ecotypes. A model is proposed where the sequential formation of FUL–SVP and FUL–SOC1 heterodimers may mediate the vegetative and meristem identity transitions, counteracting the repressive effect of FLC and SVP on flowering.We thank Francisco Madueno and Jose Antonio Jarillo for critical reading of the manuscript and their helpful comments and suggestions. Our work was supported by grants BIO2009-09920 from the Spanish Ministerio de Ciencia e Innovacion and BIO2012-32902 from the Spanish Ministerio de Economia y Competitividad to CF. VB was supported by a doctoral fellowship of the Generalitat Valenciana.Balanzá Pérez, V.; Martinez-Fernandez, I.; Ferrandiz Maestre, C. (2014). Sequential action of FRUITFULL as modulator of the activity of the floral regulators SVP and SOC1. Journal of Experimental Botany. 65(4):1193-1203. https://doi.org/10.1093/jxb/ert482S1193120365

A prenylated dsRNA sensor protects against severe COVID-19

Inherited genetic factors can influence the severity of COVID-19, but the molecular explanation underpinning a genetic association is often unclear. Intracellular antiviral defenses can inhibit the replication of viruses and reduce disease severity. To better understand the antiviral defenses relevant to COVID-19, we used interferon-stimulated gene (ISG) expression screening to reveal that OAS1, through RNase L, potently inhibits SARS-CoV-2. We show that a common splice-acceptor SNP (Rs10774671) governs whether people express prenylated OAS1 isoforms that are membrane-associated and sense specific regions of SARS-CoV-2 RNAs, or only express cytosolic, nonprenylated OAS1 that does not efficiently detect SARS-CoV-2. Importantly, in hospitalized patients, expression of prenylated OAS1 was associated with protection from severe COVID-19, suggesting this antiviral defense is a major component of a protective antiviral response