453 research outputs found

    Television multiplexing system

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    System with single, standard, wideband line transmits ten or more real time TV video data displays over hard wire to recorders more than 22.5 km from source. Digital logic and integrated circuits ensure high reliability and low maintenance. System is adaptable for video sampling applications

    Estrogen treatment following severe burn injury reduces brain inflammation and apoptotic signaling

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    <p>Abstract</p> <p>Background</p> <p>Patients with severe burn injury experience a rapid elevation in multiple circulating pro-inflammatory cytokines, with the levels correlating with both injury severity and outcome. Accumulations of these cytokines in animal models have been observed in remote organs, however data are lacking regarding early brain cytokine levels following burn injury, and the effects of estradiol on these levels. Using an experimental animal model, we studied the acute effects of a full-thickness third degree burn on brain levels of TNF-α, IL-1β, and IL-6 and the protective effects of acute estrogen treatment on these levels. Additionally, the acute administration of estrogen on regulation of inflammatory and apoptotic events in the brain following severe burn injury were studied through measuring the levels of phospho-ERK, phospho-Akt, active caspase-3, and PARP cleavage in the placebo and estrogen treated groups.</p> <p>Methods</p> <p>In this study, 149 adult Sprague-Dawley male rats received 3rd degree 40% total body surface area (TBSA) burns. Fifteen minutes following burn injury, the animals received a subcutaneous injection of either placebo (n = 72) or 17 beta-estradiol (n = 72). Brains were harvested at 0.5, 1, 2, 4, 6, 8, 12, 18, and 24 hours after injury from the control (n = 5), placebo (n = 8/time point), and estrogen treated animals (n = 8/time point). The brain cytokine levels were measured using the ELISA method. In addition, we assessed the levels of phosphorylated-ERK, phosphorylated-Akt, active caspase-3, and the levels of cleaved PARP at the 24 hour time-point using Western blot analysis.</p> <p>Results</p> <p>In burned rats, 17 beta-estradiol significantly decreased the levels of brain tissue TNF-α (~25%), IL-1β (~60%), and IL-6 (~90%) when compared to the placebo group. In addition, we determined that in the estrogen-treated rats there was an increase in the levels of phospho-ERK (<it>p </it>< 0.01) and Akt (<it>p </it>< 0.05) at the 24 hour time-point, and that 17 beta-estradiol blocked the activation of caspase-3 (<it>p </it>< 0.01) and subsequent cleavage of PARP (<it>p </it>< 0.05).</p> <p>Conclusion</p> <p>Following severe burn injury, estrogens decrease both brain inflammation and the activation of apoptosis, represented by an increase in the levels of phospho-Akt and inhibition of caspase-3 activation and PARP cleavage. Results from these studies will help further our understanding of how estrogens protect the brain following burn injury, and may provide a novel, safe, and effective clinical treatment to combat remote secondary burn injury in the brain and to preserve cognition.</p

    Air entrainment through free-surface cusps

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    In many industrial processes, such as pouring a liquid or coating a rotating cylinder, air bubbles are entrapped inside the liquid. We propose a novel mechanism for this phenomenon, based on the instability of cusp singularities that generically form on free surfaces. The air being drawn into the narrow space inside the cusp destroys its stationary shape when the walls of the cusp come too close. Instead, a sheet emanates from the cusp's tip, through which air is entrained. Our analytical theory of this instability is confirmed by experimental observation and quantitative comparison with numerical simulations of the flow equations

    Estrogen Prevents Oxidative Damage to the Mitochondria in Friedreich's Ataxia Skin Fibroblasts

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    Estrogen and estrogen-related compounds have been shown to have very potent cytoprotective properties in a wide range of disease models, including an in vitro model of Friedreich's ataxia (FRDA). This study describes a potential estrogen receptor (ER)-independent mechanism by which estrogens act to protect human FRDA skin fibroblasts from a BSO-induced oxidative insult resulting from inhibition of de novo glutathione (GSH) synthesis. We demonstrate that phenolic estrogens, independent of any known ER, are able to prevent lipid peroxidation and mitochondrial membrane potential (ΔΨm) collapse, maintain ATP at near control levels, increase oxidative phosphorylation and maintain activity of aconitase. Estrogens did not, however, prevent BSO from depleting GSH or induce an increased expression level of GSH. The cytoprotective effects of estrogen appear to be due to a direct overall reduction in oxidative damage to the mitochondria, enabling the FRDA fibroblast mitochondria to generate sufficient ATP for energy requirements and better survive oxidative stress. These data support the hypothesis that phenol ring containing estrogens are possible candidate drugs for the delay and/or prevention of FRDA symptoms

    Naloxone inhibits immune cell function by suppressing superoxide production through a direct interaction with gp91phox subunit of NADPH oxidase

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    <p>Abstract</p> <p>Background</p> <p>Both (-) and (+)-naloxone attenuate inflammation-mediated neurodegeneration by inhibition of microglial activation through superoxide reduction in an opioid receptor-independent manner. Multiple lines of evidence have documented a pivotal role of overactivated NADPH oxidase (NOX2) in inflammation-mediated neurodegeneration. We hypothesized that NOX2 might be a novel action site of naloxone to mediate its anti-inflammatory actions.</p> <p>Methods</p> <p>Inhibition of NOX-2-derived superoxide by (-) and (+)-naloxone was measured in lipopolysaccharide (LPS)-treated midbrain neuron-glia cultures and phorbol myristate acetate (PMA)-stimulated neutrophil membranes by measuring the superoxide dismutase (SOD)-inhibitable reduction of tetrazolium salt (WST-1) or ferricytochrome c. Further, various ligand (<sup>3</sup>H-naloxone) binding assays were performed in wild type and gp91<it><sup>phox-/- </sup></it>neutrophils and transfected COS-7 and HEK293 cells. The translocation of cytosolic subunit p47<it><sup>phox </sup></it>to plasma membrane was assessed by western blot.</p> <p>Results</p> <p>Both (-) and (+)-naloxone equally inhibited LPS- and PMA-induced superoxide production with an IC50 of 1.96 and 2.52 μM, respectively. Competitive binding of <sup>3</sup>H-naloxone with cold (-) and (+)-naloxone in microglia showed equal potency with an IC50 of 2.73 and 1.57 μM, respectively. <sup>3</sup>H-Naloxone binding was elevated in COS-7 and HEK293 cells transfected with gp91<sup><it>phox</it></sup>; in contrast, reduced <sup>3</sup>H-naloxone binding was found in neutrophils deficient in gp91<sup><it>phox </it></sup>or in the presence of a NOX2 inhibitor. The specificity and an increase in binding capacity of <sup>3</sup>H-naloxone were further demonstrated by 1) an immunoprecipitation study using gp91<sup><it>phox </it></sup>antibody, and 2) activation of NOX2 by PMA. Finally, western blot studies showed that naloxone suppressed translocation of the cytosolic subunit p47<sup><it>phox </it></sup>to the membrane, leading to NOX2 inactivation.</p> <p>Conclusions</p> <p>Strong evidence is provided indicating that NOX2 is a non-opioid novel binding site for naloxone, which is critical in mediating its inhibitory effect on microglia overactivation and superoxide production.</p

    Longer lifespan in male mice treated with a weakly estrogenic agonist, an antioxidant, an α-glucosidase inhibitor or a Nrf2-inducer

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    The National Institute on Aging Interventions Testing Program (ITP) evaluates agents hypothesized to increase healthy lifespan in genetically heterogeneous mice. Each compound is tested in parallel at three sites, and all results are published. We report the effects of lifelong treatment of mice with four agents not previously tested: Protandim, fish oil, ursodeoxycholic acid (UDCA) and metformin – the latter with and without rapamycin, and two drugs previously examined: 17-α-estradiol and nordihydroguaiaretic acid (NDGA), at doses greater and less than used previously. 17-α-estradiol at a threefold higher dose robustly extended both median and maximal lifespan, but still only in males. The male-specific extension of median lifespan by NDGA was replicated at the original dose, and using doses threefold lower and higher. The effects of NDGA were dose dependent and male specific but without an effect on maximal lifespan. Protandim, a mixture of botanical extracts that activate Nrf2, extended median lifespan in males only. Metformin alone, at a dose of 0.1% in the diet, did not significantly extend lifespan. Metformin (0.1%) combined with rapamycin (14 ppm) robustly extended lifespan, suggestive of an added benefit, based on historical comparison with earlier studies of rapamycin given alone. The α-glucosidase inhibitor, acarbose, at a concentration previously tested (1000 ppm), significantly increased median longevity in males and 90th percentile lifespan in both sexes, even when treatment was started at 16 months. Neither fish oil nor UDCA extended lifespan. These results underscore the reproducibility of ITP longevity studies and illustrate the importance of identifying optimal doses in lifespan studies

    Female senior secondary physics students’ engagement in science: a qualitative study of constructive influences

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    Background: Prompted by fewer females compared to males enrolling in physics and advanced mathematics at both secondary and university levels, our research investigated the views and experiences of female students currently studying upper secondary school physics. We interviewed 18 female students about influences they considered important to their own science education, interest in science, and future science-related aspirations. Our purpose was to identify the experiences that these students most strongly associated with the generation and maintenance of their engagement in science, particularly represented in this research by their enrolment in upper secondary physics. Results: The research team used a systematic, iterative process to identify the main themes in the transcribed interview data. We identified the influence each girl reported as the strongest (ranked first). We also combined all influences that the participants had nominated, regardless of their ranking, to further examine all factors participants suggested as influential in their sustained engagement in school science (represented by their decision to study upper secondary physics). Systematic analysis of the interview data confirms that the influences on these females’ choices to study physics at upper secondary originate from a combination of their teachers, their school’s science culture, members of their family, the participants themselves and their peers. Conclusions: The interviews highlighted the idiographic complexities in understanding the wide range of important influences on these students studying physics at upper secondary school and their engagement in science. The unique contribution of this work is giving voice to the participants and reflecting on what these high achieving females have to say about the influential factors in their decisions to pursue science. Supportive teachers and the school science culture play essential roles, and other cultural and/or social factors such as family members and peers are identified as important. References to the culture and expectations of the school, family holidays, and conversations with siblings are support factors that seem to interact and overlap. At the same time, the importance of policy-amenable factors such as competent and caring science teachers, and science-supportive school cultures should be emphasised and encouraged
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