Fire protection for launch facilities using machine vision fire detection

Fire protection of critical space assets, including launch and fueling facilities and manned flight hardware, demands automatic sensors for continuous monitoring, and in certain high-threat areas, fast-reacting automatic suppression systems. Perhaps the most essential characteristic for these fire detection and suppression systems is high reliability; in other words, fire detectors should alarm only on actual fires and not be falsely activated by extraneous sources. Existing types of fire detectors have been greatly improved in the past decade; however, fundamental limitations of their method of operation leaves open a significant possibility of false alarms and restricts their usefulness. At the Civil Engineering Laboratory at Tyndall Air Force Base in Florida, a new type of fire detector is under development which 'sees' a fire visually, like a human being, and makes a reliable decision based on known visual characteristics of flames. Hardware prototypes of the Machine Vision (MV) Fire Detection System have undergone live fire tests and demonstrated extremely high accuracy in discriminating actual fires from false alarm sources. In fact, this technology promises to virtually eliminate false activations. This detector could be used to monitor fueling facilities, launch towers, clean rooms, and other high-value and high-risk areas. Applications can extend to space station and in-flight shuttle operations as well; fiber optics and remote camera heads enable the system to see around obstructed areas and crew compartments. The capability of the technology to distinguish fires means that fire detection can be provided even during maintenance operations, such as welding

Infrastructure in a Structural Model of Economic Growth

Researchers, commentators, and politicians have devoted steadily more attention to infrastructure in response to claims that inadequate accumulation of public capital has contributed to substandard U.S. economic growth. Despite this, the link between infrastructure and productivity growth remains controversial. In this regard, it is somewhat surprising that infrastructure research has developed in isolation from the large literature on economic growth. We develop a neoclassical growth model that explicitly incorporates infrastructure and is designed to provide a tractable framework within which to analyze the empirical importance of public capital accumulation to productivity growth. We find little support for claims of a dramatic productivity boost from increased infrastructure outlays. In a specification designed to provide an upper bound for the influence of infrastructure, we estimate that raising the rate of infrastructure investment would have had a negligible impact on annual productivity growth between 1971 and 1986.

Social Support an the Impact of Head Injuries on Delinquency in an Urban Sample of Adjudicated Youth: Applications for the Douglas County Department of Corrections

CPACS Urban Research Awards Part of the mission of the College of Public Affairs and Community Service (CPACS) is to conduct research, especially as it relates to concerns of our local and statewide constituencies. CPACS has always had an urban mission, and one way that mission is served is to preform applied research relevant to urban society in general, and the Omaha metropolitan area and other Nebraska urban communities in particular. Beginning in 2014, the CPACS Dean provided funding for the projects with high relevance to current urban issues, with the potential to apply the findings to practice in Nebraska, Iowa, and beyond

The effect of short-term changes in air pollution on respiratory and cardiovascular morbidity in Nicosia, Cyprus.

Presented at the 6th International Conference on Urban Air Quality, Limassol, March, 2007. Short-paper was submitted for peer-review and appears in proceedings of the conference.This study investigates the effect of daily changes in levels of PM10 on the daily volume of respiratory and cardiovascular admissions in Nicosia, Cyprus during 1995-2004. After controlling for long- (year and month) and short-term (day of the week) patterns as well as the effect of weather in Generalized Additive Poisson models, some positive associations were observed with all-cause and cause-specific admissions. Risk of hospitalization increased stepwise across quartiles of days with increasing levels of PM10 by 1.3% (-0.3, 2.8), 4.9% (3.3, 6.6), 5.6% (3.9, 7.3) as compared to days with the lowest concentrations. For every 10μg/m3 increase in daily average PM10 concentration, there was a 1.2% (-0.1%, 2.4%) increase in cardiovascular admissions. With respects to respiratory admissions, an effect was observed only in the warm season with a 1.8% (-0.22, 3.85) increase in admissions per 10μg/m3 increase in PM10. The effect on respiratory admissions seemed to be much stronger in women and, surprisingly, restricted to people of adult age

Chronic Exposure to Fine Particles and Mortality: An Extended Follow-up of the Harvard Six Cities Study from 1974 to 2009

Background: Epidemiologic studies have reported associations between fine particles (aerodynamic diameter ≤ 2.5 µm; PM:2.5) and mortality. However, concerns have been raised regarding the sensitivity of the results to model specifications, lower exposures, and averaging time. Objective: We addressed these issues using 11 additional years of follow-up of the Harvard Six Cities study, incorporating recent lower exposures. Methods: We replicated the previously applied Cox regression, and examined different time lags, the shape of the concentration–response relationship using penalized splines, and changes in the slope of the relation over time. We then conducted Poisson survival analysis with time-varying effects for smoking, sex, and education. Results: Since 2001, average PM:2.5 levels, for all six cities, were < 18 µg/m3. Each increase in PM2.5 (10 µg/m3) was associated with an adjusted increased risk of all-cause mortality (PM2.5 average on previous year) of 14% [95% confidence interval (CI): 7, 22], and with 26% (95% CI: 14, 40) and 37% (95% CI: 7, 75) increases in cardiovascular and lung-cancer mortality (PM2.5 average of three previous years), respectively. The concentration–response relationship was linear down to PM2.5 concentrations of 8 µg/m3. Mortality rate ratios for PM2.5 fluctuated over time, but without clear trends despite a substantial drop in the sulfate fraction. Poisson models produced similar results. Conclusions: These results suggest that further public policy efforts that reduce fine particulate matter air pollution are likely to have continuing public health benefits

Deterministic mathematical models of the cAMP pathway in Saccharomyces cerevisiae

<p>Abstract</p> <p>Background</p> <p>Cyclic adenosine monophosphate (cAMP) has a key signaling role in all eukaryotic organisms. In <it>Saccharomyces cerevisiae</it>, it is the second messenger in the Ras/PKA pathway which regulates nutrient sensing, stress responses, growth, cell cycle progression, morphogenesis, and cell wall biosynthesis. A stochastic model of the pathway has been reported.</p> <p>Results</p> <p>We have created deterministic mathematical models of the PKA module of the pathway, as well as the complete cAMP pathway. First, a simplified conceptual model was created which reproduced the dynamics of changes in cAMP levels in response to glucose addition in wild-type as well as cAMP phosphodiesterase deletion mutants. This model was used to investigate the role of the regulatory Krh proteins that had not been included previously. The Krh-containing conceptual model reproduced very well the experimental evidence supporting the role of Krh as a direct inhibitor of PKA. These results were used to develop the Complete cAMP Model. Upon simulation it illustrated several important features of the yeast cAMP pathway: Pde1p is more important than is Pde2p for controlling the cAMP levels following glucose pulses; the proportion of active PKA is not directly proportional to the cAMP level, allowing PKA to exert negative feedback; negative feedback mechanisms include activating Pde1p and deactivating Ras2 via phosphorylation of Cdc25. The Complete cAMP model is easier to simulate, and although significantly simpler than the existing stochastic one, it recreates cAMP levels and patterns of changes in cAMP levels observed experimentally <it>in vivo </it>in response to glucose addition in wild-type as well as representative mutant strains such as <it>pde1Δ, pde2Δ</it>, <it>cyr1Δ</it>, and others. The complete model is made available in SBML format.</p> <p>Conclusion</p> <p>We suggest that the lower number of reactions and parameters makes these models suitable for integrating them with models of metabolism or of the cell cycle in <it>S. cerevisiae</it>. Similar models could be also useful for studies in the human pathogen <it>Candida albicans </it>as well as other less well-characterized fungal species.</p

Toll-Like Receptor 7 Agonist Therapy with Imidazoquinoline Enhances Cancer Cell Death and Increases Lymphocytic Infiltration and Proinflammatory Cytokine Production in Established Tumors of a Renal Cell Carcinoma Mouse Model

Imidazoquinolines are synthetic toll-like receptor 7 and 8 agonists and potent dendritic cell activators with established anticancer activity. Here we test the hypothesis that imidazoquinoline has in vivo efficacy within established renal cell carcinoma (RCC) tumors. Immunocompetent mice bearing syngeneic RCC xenografts were treated with imidazoquinoline or placebo at two separate time points. Harvested tumors were assayed by TUNEL/caspase-3/Ki67 immunostains to evaluate cell death/apoptosis/proliferation, and CD3/B220/CD45 immunostains to evaluate T-cell lymphocyte/B-cell lymphocyte/pan-leukocyte tumor infiltration. ELISA measurement of tumor and serum levels of proinflammatory cytokines, IL-6 and MCP-1, was performed. A single imidazoquinoline dose significantly decreased RCC tumor growth by 50% and repeat dosing compounded the effect, without observed weight loss or other toxicity. Tumor immunostaining revealed significant increases in cell death and apoptosis without changes in cell proliferation, supporting induction of apoptosis as the primary mechanism of tumor growth suppression. Imidazoquinoline treatment also significantly enhanced peritumoral aggregation and intratumoral infiltration by T-cell lymphocytes, while increasing intratumoral (but not serum) levels of proinflammatory cytokines. In conclusion, imidazoquinoline treatment enhances T-cell lymphocyte infiltration and proinflammatory cytokine production within established mouse RCC tumors, while suppressing tumor growth via induction of cancer cell apoptosis. These findings support a therapeutic role for imidazoquinoline in RCC

Association of Air Pollution with Increased Incidence of Ventricular Tachyarrhythmias Recorded by Implanted Cardioverter Defibrillators

Epidemiologic studies have demonstrated a consistent link between sudden cardiac deaths and particulate air pollution. We used implanted cardioverter defibrillator (ICD) records of ventricular tachyarrhythmias to assess the role of air pollution as a trigger of these potentially life-threatening events. The study cohort consisted of 203 cardiac patients with ICD devices in the Boston metropolitan area who were followed for an average of 3.1 years between 1995 and 2002. Fine particle mass and gaseous air pollution plus temperature and relative humidity were measured on almost all days, and black carbon, sulfate, and particle number on a subset of days. Date, time, and intracardiac electrograms of ICD-detected arrhythmias were downloaded at the patients’ regular follow-up visits (about every 3 months). Ventricular tachyarrhythmias were identified by electrophysiologist review. Risk of ventricular arrhythmias associated with air pollution was estimated with logistic regression, adjusting for season, temperature, relative humidity, day of the week, patient, and a recent prior arrhythmia. We found increased risks of ventricular arrhythmias associated with 2-day mean exposure for all air pollutants considered, although these associations were not statistically significant. We found statistically significant associations between air pollution and ventricular arrhythmias for episodes within 3 days of a previous arrhythmia. The associations of ventricular tachyarrhythmias with fine particle mass, carbon monoxide, nitrogen dioxide, and black carbon suggest a link with motor vehicle pollutants. The associations with sulfate suggest a link with stationary fossil fuel combustion sources