Burning Rate of Liquid Fuel on Carpet (Porous Media)

Research paper published in the journal Fire Technology 2004The occurrence of a liquid fuel burning on carpet has been involved in many incendiary and accidental fires. While the research on a liquid fuel fire on carpet is still limited, much work on porous media has been performed using sand or glass beads soaked with liquid fuel. In this study, a heat and mass transfer theory was first developed to analyze the burning process of liquid on carpet, and then several small-scale tests were performed to validate the theory. This analysis is valid for pool fires intermediate in size (5-20 cm. in diameter). The experimental apparatus consisted of a circular pan (105mm) and a load cell. Varying amounts of fuels (heptane, kerosene and methanol) were spilled onto the carpet, which was allowed to burn in a quiescent environment. It was found that due to the different controlling mechanisms, the liquid burning rate could be less or more than that of a similarly spilled free-burning pool fire. For the worst-case scenario in fires, the maximum enhancement of the burning rate due to the porous media is predictable through the physical properties of the fuel. This analysis is valid for both combustion and evaporation. Several similar results in the scientific literature are analyzed to further describe the trend. This work explains the role of carpet in liquid pool fires and also helps to explain special risks related to the presence of carpet involved in arsons and will be useful in reconstruction of the early development of an incendiary or accidental fire

MicroRNA-940 suppresses prostate cancer migration and invasion by regulating MIEN1.

BACKGROUND: MicroRNAs (miRNAs) are crucial molecules that regulate gene expression and hence pathways that are key to prostate cancer progression. These non-coding RNAs are highly deregulated in prostate cancer thus facilitating progression of the disease. Among the many genes that have gained importance in this disease, Migration and invasion enhancer 1 (MIEN1), a novel gene located next to HER2/neu in the 17q12 amplicon of the human chromosome, has been shown to enhance prostate cancer cell migration and invasion, two key processes in cancer progression. MIEN1 is differentially expressed between normal and cancer cells and tissues. Understanding the regulation of MIEN1 by microRNA may enable development of better targeting strategies. METHODS: The miRNAs that could target MIEN1 were predicted by in silico algorithms and microarray analysis. The validation for miRNA expression was performed by qPCR and northern blotting in cells and by in situ hybridization in tissues. MIEN1 and levels of other molecules upon miRNA regulation was determined by Western blotting, qPCR, and immunofluorescence. The functional effects of miRNA on cells were determined by wound healing cell migration, Boyden chamber cell invasion, clonal and colony formation assays. For knockdown or overexpression of the miRNA or overexpression of MIEN1 3'UTR, cells were transfected with the oligomiRs and plasmids, respectively. RESULTS: A novel miRNA, hsa-miR-940 (miR-940), identified and validated to be highly expressed in immortalized normal cells compared to cancer cells, is a regulator of MIEN1. Analysis of human prostate tumors and their matched normal tissues confirmed that miR-940 is highly expressed in the normal tissues compared to its low to negligible expression in the tumors. While MIEN1 is a direct target of miR-940, miR-940 alters MIEN1 RNA, in a quantity as well as cell dependent context, along with altering its downstream effectors. The miR-940 inhibited migratory and invasive potential of cells, attenuated their anchorage-independent growth ability, and increased E-cadherin expression, implicating its role in mesenchymal-to-epithelial transition (MET). CONCLUSIONS: These results, for the first time, implicate miR-940, a regulator of MIEN1, as a promising novel diagnostic and prognostic tool for prostate cancer

AmFm and lithium gap stars: Stellar evolution models with mass loss

A thorough study of the effects of mass loss on internal and surface abundances of A and F stars is carried out in order to constrain mass loss rates for these stars, as well as further elucidate some of the processes which compete with atomic diffusion. Self-consistent stellar evolution models of 1.3 to 2.5 M_sun stars including atomic diffusion and radiative accelerations for all species within the OPAL opacity database were computed with mass loss and compared to observations as well as previous calculations with turbulent mixing. Models with unseparated mass loss rates between 5 x 10^-14 and 10^-13 M_sun/yr reproduce observations for many cluster AmFm stars as well as Sirius A and o Leonis. These models also explain cool Fm stars, but not the Hyades lithium gap. Like turbulent mixing, these mass loss rates reduce surface abundance anomalies; however, their effects are very different with respect to internal abundances. For most of the main sequence lifetime of an A or F star, surface abundances in the presence of such mass loss depend on separation which takes place between log(Delta M/M_star)= -6 and -5. The current observational constraints do not allow us to conclude that mass loss is to be preferred over turbulent mixing (induced by rotation or otherwise) in order to explain the AmFm phenomenon. Internal concentration variations which could be detectable through asteroseismic tests should provide further information. If atomic diffusion coupled with mass loss are to explain the Hyades Li gap, the wind would need to be separated.Comment: 27 pages, 25 figures, accepted for publication in A&

Systemwide Evaluation of Avian Predation on Juvenile Salmonids from the Columbia River Based on Recoveries of Passive Integrated Transponder Tags

We recovered passive integrated transponder (PIT) tags from nine piscivorous waterbird colonies in the Columbia River basin to evaluate avian predation on Endangered Species Act (ESA)-listed salmonid Oncorhynchus spp. populations during 2007–2010. Avian predation rates were calculated based on the percentage of PIT-tagged juvenile salmonids that were detected as passing hydroelectric dams and subsequently were consumed and deposited by birds on their nesting colonies. Caspian terns Hydroprogne caspia (hereafter, “terns”) and double-crested cormorants Phalacrocorax auritus (hereafter, “cormorants”) nesting on East Sand Island in the Columbia River estuary consumed the highest proportions of available PIT-tagged salmonids, with minimum predation rates ranging from 2.5% for Willamette River spring Chinook salmon O. tshawytscha to 16.0% for Snake River steelhead O. mykiss. Estimated predation rates by terns, cormorants, gulls of two species (California gull Larus californicus and ring-billed gull L. delawarensis), and American white pelicans Pelecanus erythrorhynchos nesting near the confluence of the Snake and Columbia rivers were also substantial; minimum predation rates ranged from 1.4% for Snake River fall Chinook salmon to 13.2% for upper Columbia River steelhead. Predation on ESA-listed salmonids by gulls and American white pelicans were minor (<2.0% per ESA-listed salmonid population) relative to predation by terns and cormorants. Cumulative impacts were greater for Snake River and upper Columbia River salmonids than for salmonids originating closer to the estuary because upriver salmonids must migrate past more bird colonies to reach the ocean. Predation rates adjusted for colony size (per capita rates) were significantly higher for terns and cormorants nesting at inland colonies (upstream of Bonneville Dam) than for those nesting in the estuary, suggesting that inland colonies have a greater reliance on salmonids as a food source. Management actions to increase salmonid survival by reducing avian predation in the estuary could be offset if birds that disperse from the estuary relocate to inland nesting sites on or near the Columbia River.This is the publisher’s final pdf. The article is copyrighted by the American Fisheries Society and published by Taylor & Francis. It can be found at: http://www.tandfonline.com/toc/utaf20/curren

LSST: from Science Drivers to Reference Design and Anticipated Data Products

(Abridged) We describe here the most ambitious survey currently planned in the optical, the Large Synoptic Survey Telescope (LSST). A vast array of science will be enabled by a single wide-deep-fast sky survey, and LSST will have unique survey capability in the faint time domain. The LSST design is driven by four main science themes: probing dark energy and dark matter, taking an inventory of the Solar System, exploring the transient optical sky, and mapping the Milky Way. LSST will be a wide-field ground-based system sited at Cerro Pach\'{o}n in northern Chile. The telescope will have an 8.4 m (6.5 m effective) primary mirror, a 9.6 deg$^2$ field of view, and a 3.2 Gigapixel camera. The standard observing sequence will consist of pairs of 15-second exposures in a given field, with two such visits in each pointing in a given night. With these repeats, the LSST system is capable of imaging about 10,000 square degrees of sky in a single filter in three nights. The typical 5$\sigma$ point-source depth in a single visit in $r$ will be $\sim 24.5$ (AB). The project is in the construction phase and will begin regular survey operations by 2022. The survey area will be contained within 30,000 deg$^2$ with $\delta<+34.5^\circ$, and will be imaged multiple times in six bands, $ugrizy$, covering the wavelength range 320--1050 nm. About 90\% of the observing time will be devoted to a deep-wide-fast survey mode which will uniformly observe a 18,000 deg$^2$ region about 800 times (summed over all six bands) during the anticipated 10 years of operations, and yield a coadded map to $r\sim27.5$. The remaining 10\% of the observing time will be allocated to projects such as a Very Deep and Fast time domain survey. The goal is to make LSST data products, including a relational database of about 32 trillion observations of 40 billion objects, available to the public and scientists around the world.Comment: 57 pages, 32 color figures, version with high-resolution figures available from https://www.lsst.org/overvie

Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis

Increased immunogenicity of surviving tumor cells enables cooperation between liposomal doxorubicin and IL-18

<p>Abstract</p> <p>Background</p> <p>Liposomal doxorubicin (Doxil) is a cytotoxic chemotherapy drug with a favorable hematologic toxicity profile. Its active drug, doxorubicin, has interesting immunomodulatory properties. Here, the effects of Doxil on surviving tumor cell immunophenotype were investigated.</p> <p>Methods</p> <p>Using ID8 murine ovarian cancer cells, the immunomodulatory effects of Doxil were studied by measuring its impact on ovarian cancer cell expression of MHC class-I and Fas, and susceptibility to immune attack <it>in vitro</it>. To evaluate the ability of Doxil to cooperate with cancer immunotherapy, the interaction between Doxil and Interleukin 18 (IL-18), a pleiotropic immunostimulatory cytokine, was investigated <it>in vivo </it>in mice bearing ID8-Vegf tumors.</p> <p>Results</p> <p>While Doxil killed ID8 tumor cells in a dose-dependent manner, tumor cells escaping Doxil-induced apoptosis upregulated surface expression of MHC-I and Fas, and were sensitized to CTL killing and Fas-mediated death <it>in vitro</it>. We therefore tested the hypothesis that the combination of immunotherapy with Doxil provides positive interactions. Combination IL-18 and Doxil significantly suppressed tumor growth compared with either monotherapy <it>in vivo </it>and uniquely resulted in complete tumor regression and long term antitumor protection in a significant proportion of mice.</p> <p>Conclusion</p> <p>These data demonstrate that Doxil favorably changes the immunophenotype of a large fraction of the tumor that escapes direct killing thus creating an opportunity to expand tumor killing by immunotherapy, which can be capitalized through addition of IL-18 <it>in vivo</it>.</p

A meta-analysis of gene expression signatures of blood pressure and hypertension.

Genome-wide association studies (GWAS) have uncovered numerous genetic variants (SNPs) that are associated with blood pressure (BP). Genetic variants may lead to BP changes by acting on intermediate molecular phenotypes such as coded protein sequence or gene expression, which in turn affect BP variability. Therefore, characterizing genes whose expression is associated with BP may reveal cellular processes involved in BP regulation and uncover how transcripts mediate genetic and environmental effects on BP variability. A meta-analysis of results from six studies of global gene expression profiles of BP and hypertension in whole blood was performed in 7017 individuals who were not receiving antihypertensive drug treatment. We identified 34 genes that were differentially expressed in relation to BP (Bonferroni-corrected p<0.05). Among these genes, FOS and PTGS2 have been previously reported to be involved in BP-related processes; the others are novel. The top BP signature genes in aggregate explain 5%-9% of inter-individual variance in BP. Of note, rs3184504 in SH2B3, which was also reported in GWAS to be associated with BP, was found to be a trans regulator of the expression of 6 of the transcripts we found to be associated with BP (FOS, MYADM, PP1R15A, TAGAP, S100A10, and FGBP2). Gene set enrichment analysis suggested that the BP-related global gene expression changes include genes involved in inflammatory response and apoptosis pathways. Our study provides new insights into molecular mechanisms underlying BP regulation, and suggests novel transcriptomic markers for the treatment and prevention of hypertension

A meta-analysis of gene expression signatures of blood pressure and hypertension

Genome-wide association studies (GWAS) have uncovered numerous genetic variants (SNPs) that are associated with blood pressure (BP). Genetic variants may lead to BP changes by acting on intermediate molecular phenotypes such as coded protein sequence or gene expression, which in turn affect BP variability. Therefore, characterizing genes whose expression is associated with BP may reveal cellular processes involved in BP regulation and uncover how transcripts mediate genetic and environmental effects on BP variability. A meta-analysis of results from six studies of global gene expression profiles of BP and hypertension in whole blood was performed in 7017 individuals who were not receiving antihypertensive drug treatment. We identified 34 genes that were differentially expressed in relation to BP (Bonferroni-corrected p<0.05). Among these genes, FOS and PTGS2 have been previously reported to be involved in BP-related processes; the others are novel. The top BP signature genes in aggregate explain 5%-9% of inter-individual variance in BP. Of note, rs3184504 in SH2B3, which was also reported in GWAS to be associated with BP, was found to be a trans regulator of the expression of 6 of the transcripts we found to be associated with BP (FOS, MYADM, PP1R15A, TAGAP, S100A10, and FGBP2). Gene set enrichment analysis suggested that the BP-related global gene expression changes include genes involved in inflammatory response and apoptosis pathways. Our study provides new insights into molecular mechanisms underlying BP regulation, and suggests novel transcriptomic markers for the treatment and prevention of hypertension