658 research outputs found

    Development of a Reusable, Low-Shock Clamp Band Separation System for Small Spacecraft Release Applications

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    In small spacecraft, the proximity of sensitive components to release systems has led to the need for lowshock spacecraft release systems. Marmon band systems are often desirable for their flight history, structural capability, and reliability. Until recently, only pyrotechnically released clamp bands were readily available. The clamp band system described in ths paper reduces shock in two ways: it eliminates shock typically associated with pyrotechnic release devices as well as utilizing a release device that reduces the shock associated with the rapid release of the preload strain energy. Patented Fast Acting Shockless Separation Nut (FASSN) technology is utilized to convert strain energy stored in the system into rotational energy of a flywheel. Early FASSN devices were designed for discrete point applications and were somewhat large and massive. Additional development of the FASSN device has reduced the size and weight to enable the use of the technology in a medium sized (12 to 24 inch diameter) clamp band system. This paper describes the overall design, performance, and initial test results for the FASSN-based, non-pyrotechnic, low-shock clamp band release system

    Development of Shape Memory Alloy (SMA) Actuated Mechanisms for Spacecraft Release Applications

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    Current methods of deploying spacecraft payloads typically employ explosive-type separation devices which do not address shock concerns and are not resettable without disassembly from the spacecraft or significant refurbishment of parts. Other separation mechanisms exist which eliminate explosives, but also do not offer reduced shock or the advantages of insitu resettability. Several new, shape-memory alloy (SMA) actuated release mechanisms have been developed for satellite release applications for loads of 500 lbf and greater. These mechanisms all offer fast, non-pyro releases and are completely testable and reusable while mounted on the spacecraft. The Qwknut and the Low-Force Nut (LFN) are suitable for release applications up to 3000 lbf, while the Fast-Acting, Shockless Separation Nut (FASSN) is suitable for higher load releases above 5000 lbf. FASSNs have been successfully prototyped for release applications of 80,000 lbf. Shawn H. Smith Applications for SMA mechanisms include satellite hold-down and release from the launch vehicle, hold-down and release of solar panels, and hold-down and release of cover panels and satellite appendages

    Ballistic protective properties of material representative of English civil war buff-coats and clothing

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    One type of clothing system used in the English Civil War, more common amongst cavalrymen than infantrymen, was the linen shirt, wool waistcoat and buff-coat. Ballistic testing was conducted to estimate the velocity at which 50% of 12-bore lead spherical projectiles (V50) would be expected to perforate this clothing system when mounted on gelatine (a tissue simulant used in wound ballistic studies). An estimated six-shot V50 for the clothing system was calculated as 102 m/s. The distance at which the projectile would have decelerated from the muzzle of the weapon to this velocity in free flight was triple the recognised effective range of weapons of the era suggesting that the clothing system would provide limited protection for the wearer. The estimated V50 was also compared with recorded bounce-and-roll data; this suggested that the clothing system could provide some protection to the wearer from ricochets. Finally, potential wounding behind the clothing system was investigated; the results compared favourably with seventeenth century medical writings

    Maternal Inheritance: Longevity Programs Nourish Progeny via Yolk

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    Epigenetic effects can be mediated by changes in chromatin state that are transmitted from parent to child via gametes, but support is gathering for maternal yolk, which is deposited into ooctyes, as an extranuclear epigenetic factor that can contribute to phenotypic plasticity across generations in Caenorhabditis elegans

    Aberrant Activation of p38 MAP Kinase-Dependent Innate Immune Responses Is Toxic to Caenorhabditis elegans

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    Inappropriate activation of innate immune responses in intestinal epithelial cells underlies the pathophysiology of inflammatory disorders of the intestine. Here we examine the physiological effects of immune hyperactivation in the intestine of the nematode Caenorhabditis elegans. We previously identified an immunostimulatory xenobiotic that protects C. elegans from bacterial infection by inducing immune effector expression via the conserved p38 MAP kinase pathway, but was toxic to nematodes developing in the absence of pathogen. To investigate a possible connection between the toxicity and immunostimulatory properties of this xenobiotic, we conducted a forward genetic screen for C. elegans mutants that are resistant to the deleterious effects of the compound, and identified five toxicity suppressors. These strains contained hypomorphic mutations in each of the known components of the p38 MAP kinase cassette (tir-1, nsy-1, sek-1, and pmk-1), demonstrating that hyperstimulation of the p38 MAPK pathway is toxic to animals. To explore mechanisms of immune pathway regulation in C. elegans, we conducted another genetic screen for dominant activators of the p38 MAPK pathway, and identified a single allele that had a gain-of-function (gf) mutation in nsy-1, the MAP kinase kinase kinase that acts upstream of p38 MAPK pmk-1. The nsy-1(gf) allele caused hyperinduction of p38 MAPK PMK-1-dependent immune effectors, had greater levels of phosphorylated p38 MAPK, and was more resistant to killing by the bacterial pathogen Pseudomonas aeruginosa compared to wild-type controls. In addition, the nsy-1(gf) mutation was toxic to developing animals. Together, these data suggest that the activity of the MAPKKK NSY-1 is tightly regulated as part of a physiological mechanism to control p38 MAPK-mediated innate immune hyperactivation, and ensure cellular homeostasis in C. elegans

    The phosphatase laforin crosses evolutionary boundaries and links carbohydrate metabolism to neuronal disease

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    Lafora disease (LD) is a progressive myoclonic epilepsy resulting in severe neurodegeneration followed by death. A hallmark of LD is the accumulation of insoluble polyglucosans called Lafora bodies (LBs). LD is caused by mutations in the gene encoding the phosphatase laforin, which reportedly exists solely in vertebrates. We utilized a bioinformatics screen to identify laforin orthologues in five protists. These protists evolved from a progenitor red alga and synthesize an insoluble carbohydrate whose composition closely resembles LBs. Furthermore, we show that the kingdom Plantae, which lacks laforin, possesses a protein with laforin-like properties called starch excess 4 (SEX4). Mutations in the Arabidopsis thaliana SEX4 gene results in a starch excess phenotype reminiscent of LD. We demonstrate that Homo sapiens laforin complements the sex4 phenotype and propose that laforin and SEX4 are functional equivalents. Finally, we show that laforins and SEX4 dephosphorylate a complex carbohydrate and form the only family of phosphatases with this activity. These results provide a molecular explanation for the etiology of LD

    Opposing action of the FLR-2 glycoprotein hormone and DRL-1/FLR-4 MAP kinases balance p38-mediated growth and lipid homeostasis in C. elegans

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    AAUnim: Pallseainsetecgonrafitremdtheavteallolhpemadeinntgalleavenldsanruertreiptiroensaenl tseidgcnoarlrsebctelyfo: re committing crucial resources to growth and reproduction; however, the pathways that perceive and respond to these inputs remain poorly understood. Here, we demonstrate that DRL-1 and FLR-4, which share similarity with mammalian mitogen-activated protein kinases, maintain lipid homeostasis in the C. elegans intestine. DRL-1 and FLR-4 function in a protein complex at the plasma membrane to promote development, as mutations in drl-1 or flr-4 confer slow growth, small body size, and impaired lipid homeostasis. To identify factors that oppose DRL-1/FLR-4, we performed a forward genetic screen for suppressors of the drl-1 mutant phenotypes and identified mutations in flr-2 and fshr-1, which encode the orthologues of follicle stimulating hormone and its putative G protein-coupled receptor, respectively. In the absence of DRL-1/FLR-4, neuronal FLR-2 acts through intestinal FSHR-1 and protein kinase A signaling to restrict growth. Furthermore, we show that opposing signaling through DRL-1 and FLR-2 coordinates TIR-1 oligomerization, which modulates downstream p38/ PMK-1 activity, lipid homeostasis, and development. Finally, we identify a surprising noncanonical role for the developmental transcription factor PHA-4/FOXA in the intestine where it restricts growth in response to impaired DRL-1 signaling. Our work uncovers a complex multi-tissue signaling network that converges on p38 signaling to maintain homeostasis during development

    Kombucha Tea-associated microbes remodel host metabolic pathways to suppress lipid accumulation

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    The popularity of the ancient, probiotic-rich beverage Kombucha Tea (KT) has surged in part due to its purported health benefits, which include protection against metabolic diseases; however, these claims have not been rigorously tested and the mechanisms underlying host response to the probiotics in KT are unknown. Here, we establish a reproducible method to maintain C. elegans on a diet exclusively consisting of Kombucha Tea-associated microbes (KTM), which mirrors the microbial community found in the fermenting culture. KT microbes robustly colonize the gut of KTM-fed animals and confer normal development and fecundity. Intriguingly, animals consuming KTMs display a marked reduction in total lipid stores and lipid droplet size. We find that the reduced fat accumulation phenotype is not due to impaired nutrient absorption, but rather it is sustained by a programed metabolic response in the intestine of the host. KTM consumption triggers widespread transcriptional changes within core lipid metabolism pathways, including upregulation of a suite of lysosomal lipase genes that are induced during lipophagy. The elevated lysosomal lipase activity, coupled with a decrease in lipid droplet biogenesis, is partially required for the reduction in host lipid content. We propose that KTM consumption stimulates a fasting-like response in the C. elegans intestine by rewiring transcriptional programs to promote lipid utilization. Our results provide mechanistic insight into how the probiotics in Kombucha Tea reshape host metabolism and how this popular beverage may impact human metabolism
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