422 research outputs found

    Abiotic formation of O2 and O3 in high-CO2 terrestrial atmospheres

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    Previous research has indicated that high amounts of ozone (O3) and oxygen (O2) may be produced abiotically in atmospheres with high concentrations of CO2. The abiotic production of these two gases, which are also characteristic of photosynthetic life processes, could pose a potential "false-positive" for remote-sensing detection of life on planets around other stars.We show here that such false positives are unlikely on any planet that possesses abundant liquid water, as rainout of oxidized species onto a reduced planetary surface should ensure that atmospheric H2 concentrations remain relatively high, and that O2 and O3 remain low. Our aim is to determine the amount of O3 and O2 formed in a high CO2 atmosphere for a habitable planet without life. We use a photochemical model that considers hydrogen (H2) escape and a detailed hydrogen balance to calculate the O2 and O3 formed on planets with 0.2 of CO2 around the Sun, and 0.02, 0.2 and 2 bars of CO2 around a young Sun-like star with higher UV radiation. The concentrations obtained by the photochemical model were used as input in a radiative transfer model that calculated the spectra of the modeled planets. The O3 and O2 concentrations in the simulated planets are extremely small, and unlikely to produce a detectable signature in the spectra of those planets. We conclude that with a balanced hydrogen budget, and for planets with an active hydrological cycle, abiotic formation of O2 and O3 is unlikely to create a possible false positive for life detection in either the visible/near-infrared or mid-infrared wavelength regimes.Comment: 27 pages, 15 figures, Astronomy & Astrophysics accepte

    Architecturally diverse proteins converge on an analogous mechanism to inactivate Uracil-DNA glycosylase

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    Uracil-DNA glycosylase (UDG) compromises the replication strategies of diverse viruses from unrelated lineages. Virally encoded proteins therefore exist to limit, inhibit or target UDG activity for proteolysis. Viral proteins targeting UDG, such as the bacteriophage proteins ugi, and p56, and the HIV-1 protein Vpr, share no sequence similarity, and are not structurally homologous. Such diversity has hindered identification of known or expected UDG-inhibitory activities in other genomes. The structural basis for UDG inhibition by ugi is well characterized; yet, paradoxically, the structure of the unbound p56 protein is enigmatically unrevealing of its mechanism. To resolve this conundrum, we determined the structure of a p56 dimer bound to UDG. A helix from one of the subunits of p56 occupies the UDG DNA-binding cleft, whereas the dimer interface forms a hydrophobic box to trap a mechanistically important UDG residue. Surprisingly, these p56 inhibitory elements are unexpectedly analogous to features used by ugi despite profound architectural disparity. Contacts from B-DNA to UDG are mimicked by residues of the p56 helix, echoing the role of ugi’s inhibitory beta strand. Using mutagenesis, we propose that DNA mimicry by p56 is a targeting and specificity mechanism supporting tight inhibition via hydrophobic sequestration

    Resonant Electron Transfer And Excitation In Two-, Three-, And Four- Electron Caq +20 And Vq +23 Ions Colliding With Helium

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    Significant new evidence is reported for resonant transfer and excitation in ion-atom collisions. This process, which is analogous to dielectronic recombination, occurs when a target electron is captured simultaneously with the excitation of the projectile followed by photon emission. Strong resonant behavior with structure, in agreement with theoretical calculations, is observed in the cross section for projectile K x rays coincident with single electron capture for 100-360-MeV Ca16+,17+,18+20 and 180-460-MeV V19+,20+,21+23 ions colliding with helium. © 1984 The American Physical Society

    X-Rays from Accelerated Ion Interactions

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    We have developed in detail the theory of X-ray line and continuum production due to atomic interactions of accelerated ions, incorporating in our calculations information from a broad range of laboratory measurements. We applied our calculations to the Orion region from which nuclear gamma-ray lines were observed with the COMPTEL instrument on CGRO. The accelerated particles which produce this gamma-ray emission via nuclear reactions also produce X-ray lines via atomic interactions. We predict strong line emission in the range from 0.5 to 1 keV, mainly due to de-excitations in fast O ions. While much of the diffuse X-ray emission observed with ROSAT from Orion could be due to accelerated ions, the current X-ray data do not provide unambiguous signatures for such an origin. If future observations with high spectral resolution would confirm the predicted X-rays, the combined analysis of the X-ray and gamma-ray data will set important constraints on the origin of the accelerated particles and their interaction model.Comment: 26 pages, 14 figure

    Prostate Cancer-Specific and Potent Antitumor Effect of a DD3-Controlled Oncolytic Virus Harboring the PTEN Gene

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    Prostate cancer is a major health problem for men in Western societies. Here we report a Prostate Cancer-Specific Targeting Gene-Viro-Therapy (CTGVT-PCa), in which PTEN was inserted into a DD3-controlled oncolytic viral vector (OV) to form Ad.DD3.E1A.E1B(Δ55)-(PTEN) or, briefly, Ad.DD3.D55-PTEN. The woodchuck post-transcriptional element (WPRE) was also introduced at the downstream of the E1A coding sequence, resulting in much higher expression of the E1A gene. DD3 is one of the most prostate cancer-specific genes and has been used as a clinical bio-diagnostic marker. PTEN is frequently inactivated in primary prostate cancers, which is crucial for prostate cancer progression. Therefore, the Ad.DD3.D55-PTEN has prostate cancer specific and potent antitumor effect. The tumor growth rate was almost completely inhibited with the final tumor volume after Ad.DD3.D55-PTEN treatment less than the initial volume at the beginning of Ad.DD3.D55-PTEN treatment, which shows the powerful antitumor effect of Ad.DD3.D55-PTEN on prostate cancer tumor growth. The CTGVT-PCa construct reported here killed all of the prostate cancer cell lines tested, such as DU145, 22RV1 and CL1, but had a reduced or no killing effect on all the non-prostate cancer cell lines tested. The mechanism of action of Ad.DD3.D55-PTEN was due to the induction of apoptosis, as detected by TUNEL assays and flow cytometry. The apoptosis was mediated by mitochondria-dependent and -independent pathways, as determined by caspase assays and mitochondrial membrane potential
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