Real Time Mission Planning

The different advantageous embodiments provide a system comprising a number of computers, a graphical user interface, first program code stored on the computer, and second program code stored on the computer. The graphical user interface is executed by a computer in the number of computers. The computer is configured to run the first program code to define a mission using a number of mission elements. The computer is configured to run the second program code to generate instructions for a number of assets to execute the mission and monitor the number of assets during execution of the mission

Real Time Mission Planning

The different advantageous embodiments provide a system comprising a number of computers, a graphical user interface, first program code stored on the computer, and second program code stored on the computer. The graphical user interface is executed by a computer in the number of computers. The computer is configured to run the first program code to define a mission using a number of mission elements. The computer is configured to run the second program code to generate instructions for a number of assets to execute the mission and monitor the number of assets during execution of the mission

Convocation

https://dc.ewu.edu/music_performances/1707/thumbnail.jp

Population genomics and structure of the critically endangered Mariana Crow (Corvus kubaryi)

Funding: UK Biotechnology and Biological Sciences Research Council (BBSRC) David Phillips Fellowship (BB/G023913/2) (C.R.).The Mariana Crow, or Åga (Corvus kubaryi), is a critically endangered species (IUCN - International Union for Conservation of Nature), endemic to the islands of Guam and Rota in the Mariana Archipelago. It is locally extinct on Guam, and numbers have declined dramatically on Rota to a historical low of less than 55 breeding pairs throughout the island in 2013. Because of its extirpation on Guam and population decline on Rota, it is of critical importance to assess the genetic variation among individuals to assist ongoing recovery efforts. We conducted a population genomics analysis comparing the Guam and Rota populations and studied the genetic structure of Rota individuals population. We used blood samples from five birds from Guam and 78 birds from Rota. We identified 145,552 candidate single nucleotide variants (SNVs) from a genome sequence of an individual from Rota and selected a subset of these to develop an oligonucleotide in-solution capture assay. The Guam and Rota populations were genetically differentiated from each other. Crow populations sampled broadly across their range on Rota showed significant genetic structuring – a surprising result given the small size of this island and the good flight capabilities of the species. Knowledge of its genetic structure will help improve management policies strategies to help with its recovery.Publisher PDFPeer reviewe

Attenuation of Na/K-ATPase Mediated Oxidant Amplification with pNaKtide Ameliorates Experimental Uremic Cardiomyopathy

We have previously reported that the sodium potassium adenosine triphosphatase (Na/K-ATPase) can effect the amplification of reactive oxygen species. In this study, we examined whether attenuation of oxidant stress by antagonism of Na/K-ATPase oxidant amplification might ameliorate experimental uremic cardiomyopathy induced by partial nephrectomy (PNx). PNx induced the development of cardiac morphological and biochemical changes consistent with human uremic cardiomyopathy. Both inhibition of Na/K-ATPase oxidant amplification with pNaKtide and induction of heme oxygenase-1 (HO-1) with cobalt protoporphyrin (CoPP) markedly attenuated the development of phenotypical features of uremic cardiomyopathy. In a reversal study, administration of pNaKtide after the induction of uremic cardiomyopathy reversed many of the phenotypical features. Attenuation of Na/K-ATPase oxidant amplification may be a potential strategy for clinical therapy of this disorder

Exploiting Large Neuroimaging Datasets to Create Connectome-Constrained Approaches for more Robust, Efficient, and Adaptable Artificial Intelligence

Despite the progress in deep learning networks, efficient learning at the edge (enabling adaptable, low-complexity machine learning solutions) remains a critical need for defense and commercial applications. We envision a pipeline to utilize large neuroimaging datasets, including maps of the brain which capture neuron and synapse connectivity, to improve machine learning approaches. We have pursued different approaches within this pipeline structure. First, as a demonstration of data-driven discovery, the team has developed a technique for discovery of repeated subcircuits, or motifs. These were incorporated into a neural architecture search approach to evolve network architectures. Second, we have conducted analysis of the heading direction circuit in the fruit fly, which performs fusion of visual and angular velocity features, to explore augmenting existing computational models with new insight. Our team discovered a novel pattern of connectivity, implemented a new model, and demonstrated sensor fusion on a robotic platform. Third, the team analyzed circuitry for memory formation in the fruit fly connectome, enabling the design of a novel generative replay approach. Finally, the team has begun analysis of connectivity in mammalian cortex to explore potential improvements to transformer networks. These constraints increased network robustness on the most challenging examples in the CIFAR-10-C computer vision robustness benchmark task, while reducing learnable attention parameters by over an order of magnitude. Taken together, these results demonstrate multiple potential approaches to utilize insight from neural systems for developing robust and efficient machine learning techniques.Comment: 11 pages, 4 figure

G9a regulates group 2 innate lymphoid cell development by repressing the group 3 innate lymphoid cell program.

Innate lymphoid cells (ILCs) are emerging as important regulators of homeostatic and disease-associated immune processes. Despite recent advances in defining the molecular pathways that control development and function of ILCs, the epigenetic mechanisms that regulate ILC biology are unknown. Here, we identify a role for the lysine methyltransferase G9a in regulating ILC2 development and function. Mice with a hematopoietic cell-specific deletion of G9a (Vav.G9a(-/-) mice) have a severe reduction in ILC2s in peripheral sites, associated with impaired development of immature ILC2s in the bone marrow. Accordingly, Vav.G9a(-/-) mice are resistant to the development of allergic lung inflammation. G9a-dependent dimethylation of histone 3 lysine 9 (H3K9me2) is a repressive histone mark that is associated with gene silencing. Genome-wide expression analysis demonstrated that the absence of G9a led to increased expression of ILC3-associated genes in developing ILC2 populations. Further, we found high levels of G9a-dependent H3K9me2 at ILC3-specific genetic loci, demonstrating that G9a-mediated repression of ILC3-associated genes is critical for the optimal development of ILC2s. Together, these results provide the first identification of an epigenetic regulatory mechanism in ILC development and function

TNPO2 variants associate with human developmental delays, neurologic deficits, and dysmorphic features and alter TNPO2 activity in Drosophila

Transportin-2 (TNPO2) mediates multiple pathways including non-classical nucleocytoplasmic shuttling of >60 cargoes, such as developmental and neuronal proteins. We identified 15 individuals carrying de novo coding variants in TNPO2 who presented with global developmental delay (GDD), dysmorphic features, ophthalmologic abnormalities, and neurological features. To assess the nature of these variants, functional studies were performed in Drosophila. We found that fly dTnpo (orthologous to TNPO2) is expressed in a subset of neurons. dTnpo is critical for neuronal maintenance and function as downregulating dTnpo in mature neurons using RNAi disrupts neuronal activity and survival. Altering the activity and expression of dTnpo using mutant alleles or RNAi causes developmental defects, including eye and wing deformities and lethality. These effects are dosage dependent as more severe phenotypes are associated with stronger dTnpo loss. Interestingly, similar phenotypes are observed with dTnpo upregulation and ectopic expression of TNPO2, showing that loss and gain of Transportin activity causes developmental defects. Further, proband-associated variants can cause more or less severe developmental abnormalities compared to wild-type TNPO2 when ectopically expressed. The impact of the variants tested seems to correlate with their position within the protein. Specifically, those that fall within the RAN binding domain cause more severe toxicity and those in the acidic loop are less toxic. Variants within the cargo binding domain show tissue-dependent effects. In summary, dTnpo is an essential gene in flies during development and in neurons. Further, proband-associated de novo variants within TNPO2 disrupt the function of the encoded protein. Hence, TNPO2 variants are causative for neurodevelopmental abnormalities

The neuropeptide NMU amplifies ILC2-driven allergic lung inflammation

Type 2 innate lymphoid cells (ILC2s) both contribute to mucosal homeostasis and initiate pathologic inflammation in allergic asthma. However, the signals that direct ILC2s to promote homeostasis versus inflammation are unclear. To identify such molecular cues, we profiled mouse lung-resident ILCs using single-cell RNA sequencing at steady state and after in vivo stimulation with the alarmin cytokines IL-25 and IL-33. ILC2s were transcriptionally heterogeneous after activation, with subpopulations distinguished by expression of proliferative, homeostatic and effector genes. The neuropeptide receptor Nmur1 was preferentially expressed by ILC2s at steady state and after IL-25 stimulation. Neuromedin U (NMU), the ligand of NMUR1, activated ILC2s in vitro, and in vivo co-administration of NMU with IL-25 strongly amplified allergic inflammation. Loss of NMU-NMUR1 signalling reduced ILC2 frequency and effector function, and altered transcriptional programs following allergen challenge in vivo. Thus, NMUR1 signalling promotes inflammatory ILC2 responses, highlighting the importance of neuro-immune crosstalk in allergic inflammation at mucosal surfaces