1,225 research outputs found

    Detecting Spam Publishers By Serving Honeypot Ads

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    Click fraud, wherein bots or other unauthorized users click on ads to falsely inflate click-through rates, is a major problem in the online ad industry. This disclosure describes a type of ad, known as a honeypot ad, that is not particularly attractive to humans, but for bots is indistinguishable from a genuine ad. Publishers who employ bots to fraudulently inflate click-through rates, or to misrepresent the popularity of their app or website, are detected when the number of clicks on such honeypot ads are substantially larger than the number of clicks on genuine ads

    Taphonomic and Depositional Analysis of Megaflora of the Cretaceous Hell Creek Formation near Marmarth, North Dakota

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    The Hell Creek formation of western North Dakota and eastern Montana contains a large variety of plant, pollen, and vertebrate fossils. A high quality plant fossil site near Marmarth, North Dakota was studied to obtain megafloral fossils characteristic of the unit. Plant fossils from the unit were obtained, photographed, and identified so as to obtain a more thorough knowledge of the depositional environment and climate of the region during the Cretaceous period. Fossils identified indicate a forested, deltaic environment rich in water and sediment influx. Introduction The Hell Creek formation of Western North Dakota and Eastern Montana has long been considered one of the richest Cretaceous vertebrate fossil sources in the globe. During the Cretaceous period, a large inland sea covered much of what is now the central United States. This large waterway deposited a wide variety of lithologic facies, ranging from ash beds to coarse, cross-bedded sandstones. Many of the facies within the Hell Creek contain fossils of large vertebrate species, such as the Tyrannosaurus rex and Triceratops. While these sensational finds have given the Hell Creek its fame, much more can be learned from the plant and pollen fossils also preserved. The Hell Creek formation and the overlying tertiary For

    The Southern 2MASS AGN Survey: spectroscopic follow-up with 6dF

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    The Two Micron All-Sky Survey (2MASS) has provided a uniform photometric catalog to search for previously unknown red AGN and QSOs. We have extended the search to the southern equatorial sky by obtaining spectra for 1182 AGN candidates using the 6dF multifibre spectrograph on the UK Schmidt Telescope. These were scheduled as auxiliary targets for the 6dF Galaxy Redshift Survey. The candidates were selected using a single color cut of J - Ks > 2 to Ks ~ 15.5 and a galactic latitude of |b|>30 deg. 432 spectra were of sufficient quality to enable a reliable classification. 116 sources (or ~27%) were securely classified as type 1 AGN, 20 as probable type 1s, and 57 as probable type 2 AGN. Most of them span the redshift range 0.05<z<0.5 and only 8 (or ~6%) were previously identified as AGN or QSOs. Our selection leads to a significantly higher AGN identification rate amongst local galaxies (>20%) than in any previous galaxy survey. A small fraction of the type 1 AGN could have their optical colors reddened by optically thin dust with A_V<2 mag relative to optically selected QSOs. A handful show evidence for excess far-IR emission. The equivalent width (EW) and color distributions of the type 1 and 2 AGN are consistent with AGN unified models. In particular, the EW of the [OIII] emission line weakly correlates with optical--near-IR color in each class of AGN, suggesting anisotropic obscuration of the AGN continuum. Overall, the optical properties of the 2MASS red AGN are not dramatically different from those of optically-selected QSOs. Our near-IR selection appears to detect the most near-IR luminous QSOs in the local universe to z~0.6 and provides incentive to extend the search to deeper near-IR surveys.Comment: 57 pages, 12 figures, 4 tables, to appear in vol.27/4 of Publications of the Astronomical Society of Australia (PASA

    Z-string global gauge anomaly and Lorentz non-invariance

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    Certain (3+1)-dimensional chiral non-Abelian gauge theories have been shown to exhibit a new type of global gauge anomaly, which in the Hamiltonian formulation is due to the fermion zero-modes of a Z-string-like configuration of the gauge potential and the corresponding spectral flow. Here, we clarify the relation between this Z-string global gauge anomaly and other anomalies in both 3+1 and 2+1 dimensions. We then point out a possible trade-off between the (3+1)-dimensional Z-string global gauge anomaly and the violation of CPT and Lorentz invariance.Comment: 11 pages, LaTe

    Nav1.5 regulates breast tumor growth and metastatic dissemination in vivo

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    Voltage-gated Na(+) channels (VGSCs) mediate action potential firing and regulate adhesion and migration in excitable cells. VGSCs are also expressed in cancer cells. In metastatic breast cancer (BCa) cells, the Na(v)1.5 α subunit potentiates migration and invasion. In addition, the VGSC-inhibiting antiepileptic drug phenytoin inhibits tumor growth and metastasis. However, the functional activity of Na(v)1.5 and its specific contribution to tumor progression in vivo has not been delineated. Here, we found that Na(v)1.5 is up-regulated at the protein level in BCa compared with matched normal breast tissue. Na(+) current, reversibly blocked by tetrodotoxin, was retained in cancer cells in tumor tissue slices, thus directly confirming functional VGSC activity in vivo. Stable down-regulation of Na(v)1.5 expression significantly reduced tumor growth, local invasion into surrounding tissue, and metastasis to liver, lungs and spleen in an orthotopic BCa model. Na(v)1.5 down-regulation had no effect on cell proliferation or angiogenesis within the in tumors, but increased apoptosis. In vitro, Na(v)1.5 down-regulation altered cell morphology and reduced CD44 expression, suggesting that VGSC activity may regulate cellular invasion via the CD44-src-cortactin signaling axis. We conclude that Na(v)1.5 is functionally active in cancer cells in breast tumors, enhancing growth and metastatic dissemination. These findings support the notion that compounds targeting Na(v)1.5 may be useful for reducing metastasis

    Discounting Future Reward in an Uncertain World

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    Humans discount delayed relative to more immediate reward. A plausible explanation is that impatience arises partly from uncertainty, or risk, implicit in delayed reward. Existing theories of discounting-as-risk focus on a probability that delayed reward will not materialize. By contrast, we examine how uncertainty in the magnitude of delayed reward contributes to delay discounting. We propose a model wherein reward is discounted proportional to the rate of random change in its magnitude across time, termed volatility. We find evidence to support this model across three experiments (total N = 158). First, using a task where participants chose when to sell products, whose price dynamics they previously learned, we show discounting increases in line with price volatility. Second, we show that this effect pertains over naturalistic delays of up to 4 months. Using functional magnetic resonance imaging, we observe a volatility-dependent decrease in functional hippocampal–prefrontal coupling during intertemporal choice. Third, we replicate these effects in a larger online sample, finding that volatility discounting within each task correlates with baseline discounting outside of the task.We conclude that delay discounting partly reflects time-dependent uncertainty about reward magnitude, that is volatility. Our model captures how discounting adapts to volatility, thereby partly accounting for individual differences in impatience. Our imaging findings suggest a putative mechanism whereby uncertainty reduces prospective simulation of future outcomes

    The sodium channel-blocking antiepileptic drug phenytoin inhibits breast tumour growth and metastasis.

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    Background Voltage-gated Na+ channels (VGSCs) are heteromeric protein complexes containing pore-forming ? subunits and smaller, non-pore-forming ? subunits. VGSCs are classically expressed in electrically excitable cells, e.g. neurons. VGSCs are also expressed in tumour cells, including breast cancer (BCa) cells, where they enhance cellular migration and invasion. However, despite extensive work defining in detail the molecular mechanisms underlying the expression of VGSCs and their pro-invasive role in cancer cells, there has been a notable lack of clinically relevant in vivo data exploring their value as potential therapeutic targets. Findings We have previously reported that the VGSC-blocking antiepileptic drug phenytoin inhibits the migration and invasion of metastatic MDA-MB-231 cells in vitro. The purpose of the present study was to establish whether VGSCs might be viable therapeutic targets by testing the effect of phenytoin on tumour growth and metastasis in vivo. We found that expression of Nav1.5, previously detected in MDA-MB-231 cells in vitro, was retained on cells in orthotopic xenografts. Treatment with phenytoin, at a dose equivalent to that used to treat epilepsy (60 mg/kg; daily), significantly reduced tumour growth, without affecting animal weight. Phenytoin also reduced cancer cell proliferation in vivo and invasion into surrounding mammary tissue. Finally, phenytoin significantly reduced metastasis to the liver, lungs and spleen. Conclusions This is the first study showing that phenytoin reduces breast tumour growth and metastasis in vivo. We propose that pharmacologically targeting VGSCs, by repurposing antiepileptic or antiarrhythmic drugs, should be further studied as a potentially novel anti-cancer therapy
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