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  • 1
    Publication Date: 2014-07-22
    Description: The viral reservoir represents a critical challenge for human immunodeficiency virus type 1 (HIV-1) eradication strategies. However, it remains unclear when and where the viral reservoir is seeded during acute infection and the extent to which it is susceptible to early antiretroviral therapy (ART). Here we show that the viral reservoir is seeded rapidly after mucosal simian immunodeficiency virus (SIV) infection of rhesus monkeys and before systemic viraemia. We initiated suppressive ART in groups of monkeys on days 3, 7, 10 and 14 after intrarectal SIVMAC251 infection. Treatment with ART on day 3 blocked the emergence of viral RNA and proviral DNA in peripheral blood and also substantially reduced levels of proviral DNA in lymph nodes and gastrointestinal mucosa as compared with treatment at later time points. In addition, treatment on day 3 abrogated the induction of SIV-specific humoral and cellular immune responses. Nevertheless, after discontinuation of ART following 24 weeks of fully suppressive therapy, virus rebounded in all animals, although the monkeys that were treated on day 3 exhibited a delayed viral rebound as compared with those treated on days 7, 10 and 14. The time to viral rebound correlated with total viraemia during acute infection and with proviral DNA at the time of ART discontinuation. These data demonstrate that the viral reservoir is seeded rapidly after intrarectal SIV infection of rhesus monkeys, during the 'eclipse' phase, and before detectable viraemia. This strikingly early seeding of the refractory viral reservoir raises important new challenges for HIV-1 eradication strategies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4126858/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4126858/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Whitney, James B -- Hill, Alison L -- Sanisetty, Srisowmya -- Penaloza-MacMaster, Pablo -- Liu, Jinyan -- Shetty, Mayuri -- Parenteau, Lily -- Cabral, Crystal -- Shields, Jennifer -- Blackmore, Stephen -- Smith, Jeffrey Y -- Brinkman, Amanda L -- Peter, Lauren E -- Mathew, Sheeba I -- Smith, Kaitlin M -- Borducchi, Erica N -- Rosenbloom, Daniel I S -- Lewis, Mark G -- Hattersley, Jillian -- Li, Bei -- Hesselgesser, Joseph -- Geleziunas, Romas -- Robb, Merlin L -- Kim, Jerome H -- Michael, Nelson L -- Barouch, Dan H -- AI060354/AI/NIAID NIH HHS/ -- AI078526/AI/NIAID NIH HHS/ -- AI084794/AI/NIAID NIH HHS/ -- AI095985/AI/NIAID NIH HHS/ -- AI096040/AI/NIAID NIH HHS/ -- AI100645/AI/NIAID NIH HHS/ -- R01 AI084794/AI/NIAID NIH HHS/ -- R56 AI091514/AI/NIAID NIH HHS/ -- T32 AI007245/AI/NIAID NIH HHS/ -- U19 AI078526/AI/NIAID NIH HHS/ -- U19 AI095985/AI/NIAID NIH HHS/ -- U19 AI096040/AI/NIAID NIH HHS/ -- UM1 AI100645/AI/NIAID NIH HHS/ -- UM1 AI100663/AI/NIAID NIH HHS/ -- England -- Nature. 2014 Aug 7;512(7512):74-7. doi: 10.1038/nature13594. Epub 2014 Jul 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA [2] Ragon Institute of MGH, MIT and Harvard, Cambridge, Massachusetts 02139, USA. ; Program for Evolutionary Dynamics, Harvard University, Cambridge, Massachusetts 02138 USA. ; Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA. ; Bioqual, Rockville, Maryland 20852, USA. ; Gilead Sciences, Foster City, California 94404, USA. ; US Military HIV Research Program, Walter Reed Army Institute of Research, Silver Spring, Maryland 20910, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25042999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Retroviral Agents/administration & dosage/pharmacology/therapeutic use ; Carrier State/drug therapy/virology ; DNA, Viral/analysis/biosynthesis/blood ; Disease Models, Animal ; Female ; Kinetics ; Macaca mulatta/immunology/*virology ; Male ; Proviruses/genetics ; RNA, Viral/blood ; Rectum/virology ; Simian Acquired Immunodeficiency Syndrome/drug therapy/immunology/*virology ; Simian Immunodeficiency Virus/drug effects/*growth & ; development/immunology/physiology ; Time Factors ; Treatment Failure ; *Viral Load/drug effects ; Viremia/drug therapy/*virology ; Virus Replication/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2015-01-17
    Description: CD4 T cells promote innate and adaptive immune responses, but how vaccine-elicited CD4 T cells contribute to immune protection remains unclear. We evaluated whether induction of virus-specific CD4 T cells by vaccination would protect mice against infection with chronic lymphocytic choriomeningitis virus (LCMV). Immunization with vaccines that selectively induced CD4 T cell responses resulted in catastrophic inflammation and mortality after challenge with a persistent strain of LCMV. Immunopathology required antigen-specific CD4 T cells and was associated with a cytokine storm, generalized inflammation, and multi-organ system failure. Virus-specific CD8 T cells or antibodies abrogated the pathology. These data demonstrate that vaccine-elicited CD4 T cells in the absence of effective antiviral immune responses can trigger lethal immunopathology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4382081/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4382081/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Penaloza-MacMaster, Pablo -- Barber, Daniel L -- Wherry, E John -- Provine, Nicholas M -- Teigler, Jeffrey E -- Parenteau, Lily -- Blackmore, Stephen -- Borducchi, Erica N -- Larocca, Rafael A -- Yates, Kathleen B -- Shen, Hao -- Haining, W Nicholas -- Sommerstein, Rami -- Pinschewer, Daniel D -- Ahmed, Rafi -- Barouch, Dan H -- AI007245/AI/NIAID NIH HHS/ -- AI030048/AI/NIAID NIH HHS/ -- AI07387/AI/NIAID NIH HHS/ -- AI078526/AI/NIAID NIH HHS/ -- AI096040/AI/NIAID NIH HHS/ -- P51 OD011132/OD/NIH HHS/ -- T32 AI007245/AI/NIAID NIH HHS/ -- U19 AI078526/AI/NIAID NIH HHS/ -- U19 AI096040/AI/NIAID NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2015 Jan 16;347(6219):278-82. doi: 10.1126/science.aaa2148.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. ; Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. ; Department of Microbiology and Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA. ; Department of Pathology and Immunology, WHO Collaborating Centre for Vaccine Immunology, University of Geneva, 1211 Geneva, Switzerland. ; Department of Pathology and Immunology, WHO Collaborating Centre for Vaccine Immunology, University of Geneva, 1211 Geneva, Switzerland. Department of Biomedicine-Haus Petersplatz, Division of Experimental Virology, University of Basel, 4009 Basel, Switzerland. ; Emory Vaccine Center and Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322, USA. ; Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. Ragon Institute of MGH, MIT, and Harvard, Boston, MA 02114, USA. dbarouch@bidmc.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25593185" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; Antibodies, Viral/immunology ; Antigens, Viral/immunology ; Arenaviridae Infections/*immunology/virology ; CD4-Positive T-Lymphocytes/*immunology ; CD8-Positive T-Lymphocytes/immunology ; Cytokines/blood ; Epitopes, T-Lymphocyte/immunology ; Immune System Diseases/*etiology/immunology/pathology ; Immunologic Memory ; Inflammation/*etiology/immunology/pathology ; Lymphocytic choriomeningitis virus/*immunology/physiology ; Mice, Inbred C57BL ; Multiple Organ Failure/etiology ; Vaccination ; Viral Load ; Viral Vaccines/*adverse effects/*immunology ; Virus Replication
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2015-07-04
    Description: Preclinical studies of viral vector-based HIV-1 vaccine candidates have previously shown partial protection against neutralization-resistant virus challenges in rhesus monkeys. In this study, we evaluated the protective efficacy of adenovirus serotype 26 (Ad26) vector priming followed by purified envelope (Env) glycoprotein boosting. Rhesus monkeys primed with Ad26 vectors expressing SIVsmE543 Env, Gag, and Pol and boosted with AS01B-adjuvanted SIVmac32H Env gp140 demonstrated complete protection in 50% of vaccinated animals against a series of repeated, heterologous, intrarectal SIVmac251 challenges that infected all controls. Protective efficacy correlated with the functionality of Env-specific antibody responses. Comparable protection was also observed with a similar Ad/Env vaccine against repeated, heterologous, intrarectal SHIV-SF162P3 challenges. These data demonstrate robust protection by Ad/Env vaccines against acquisition of neutralization-resistant virus challenges in rhesus monkeys.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4653134/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4653134/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barouch, Dan H -- Alter, Galit -- Broge, Thomas -- Linde, Caitlyn -- Ackerman, Margaret E -- Brown, Eric P -- Borducchi, Erica N -- Smith, Kaitlin M -- Nkolola, Joseph P -- Liu, Jinyan -- Shields, Jennifer -- Parenteau, Lily -- Whitney, James B -- Abbink, Peter -- Ng'ang'a, David M -- Seaman, Michael S -- Lavine, Christy L -- Perry, James R -- Li, Wenjun -- Colantonio, Arnaud D -- Lewis, Mark G -- Chen, Bing -- Wenschuh, Holger -- Reimer, Ulf -- Piatak, Michael -- Lifson, Jeffrey D -- Handley, Scott A -- Virgin, Herbert W -- Koutsoukos, Marguerite -- Lorin, Clarisse -- Voss, Gerald -- Weijtens, Mo -- Pau, Maria G -- Schuitemaker, Hanneke -- AI060354/AI/NIAID NIH HHS/ -- AI078526/AI/NIAID NIH HHS/ -- AI080289/AI/NIAID NIH HHS/ -- AI084794/AI/NIAID NIH HHS/ -- AI095985/AI/NIAID NIH HHS/ -- AI096040/AI/NIAID NIH HHS/ -- AI102660/AI/NIAID NIH HHS/ -- AI102691/AI/NIAID NIH HHS/ -- OD011170/OD/NIH HHS/ -- P30 AI060354/AI/NIAID NIH HHS/ -- R01 AI080289/AI/NIAID NIH HHS/ -- R01 AI084794/AI/NIAID NIH HHS/ -- R01 AI102660/AI/NIAID NIH HHS/ -- R01 AI102691/AI/NIAID NIH HHS/ -- R01 OD011170/OD/NIH HHS/ -- R37 AI080289/AI/NIAID NIH HHS/ -- U19 AI078526/AI/NIAID NIH HHS/ -- U19 AI095985/AI/NIAID NIH HHS/ -- U19 AI096040/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2015 Jul 17;349(6245):320-4. doi: 10.1126/science.aab3886. Epub 2015 Jul 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard University, Cambridge, MA 02139, USA. dbarouch@bidmc.harvard.edu. ; Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard University, Cambridge, MA 02139, USA. ; Thayer School of Engineering at Dartmouth, Hanover, NH 03755, USA. ; Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. ; University of Massachusetts Medical School, Worcester, MA 01605, USA. ; New England Primate Research Center, Southborough, MA 01772, USA. ; Bioqual, Rockville, MD 20852, USA. ; Children's Hospital, Boston, MA 02115, USA. ; JPT Peptide Technologies GmbH, 12489 Berlin, Germany. ; AIDS and Cancer Virus Program, Leidos Biomedical Research, Frederick National Laboratory, Frederick, MD 21702, USA. ; Washington University School of Medicine, St. Louis, MO 63110, USA. ; GSK Vaccines, 1330 Rixensart, Belgium. ; Janssen Infectious Diseases and Vaccines (formerly Crucell), 2301 Leiden, Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26138104" target="_blank"〉PubMed〈/a〉
    Keywords: AIDS Vaccines/*immunology ; Adenovirus Vaccines/*immunology ; Adoptive Transfer ; Animals ; Antibodies, Neutralizing/immunology ; Female ; Gene Products, env/*immunology ; Gene Products, gag/immunology ; Gene Products, pol/immunology ; Genetic Vectors/immunology ; HIV-1/*immunology ; Histocompatibility Antigens Class I/genetics/immunology ; Immunization, Secondary ; Macaca mulatta ; Male ; SAIDS Vaccines/*immunology ; Simian Acquired Immunodeficiency Syndrome/*prevention & control ; Simian Immunodeficiency Virus/immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Electronic Resource
    Electronic Resource
    College Park, Md. : American Institute of Physics (AIP)
    The Journal of Chemical Physics 109 (1998), S. 8635-8640 
    ISSN: 1089-7690
    Source: AIP Digital Archive
    Topics: Physics , Chemistry and Pharmacology
    Notes: Anion desorption stimulated by the impact of 0–20 eV electrons on O2/hydrocarbon mixed films is reported. It is shown that part of the H−, OH−, CH−, and CH2〈sup ARRANGE="STAGGER"〉− desorption yields from O2/hydrocarbon films is the result of reactive scattering of O− fragments produced via dissociative electron attachment (DEA) in the alkane and alkene thin films. These results support the interpretation that the DEA O− react with the hydrocarbon molecules to form a transient molecular anion complex which, in addition to autodetachment, may decay by dissociation into various anion and neutral fragments, and thus cause chemical modification of the solid. © 1998 American Institute of Physics.
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  • 5
    Electronic Resource
    Electronic Resource
    College Park, Md. : American Institute of Physics (AIP)
    The Journal of Chemical Physics 105 (1996), S. 6032-6042 
    ISSN: 1089-7690
    Source: AIP Digital Archive
    Topics: Physics , Chemistry and Pharmacology
    Notes: We have studied electron stimulated desorption (ESD) of positive ions from PF3 molecules adsorbed on a Pt substrate over a wide electron energy range (0–175 eV). Electron bombardment of 1 ML PF3 adsorbed on the Pt surface gives rise mainly to an F+ signal, whereas ESD from 6 ML thick PF3 film (thick PF3 layer) leads to P+, PF+, and PF+2 signals, in addition to F+. We find that the onset for F+ desorption from the 1-ML PF3/Pt is at ∼26.5 eV, while the F+ threshold from the thick PF3 layer is ∼28.5 eV. The P+ appearance potential from the thick PF3 layer is ∼23 eV. The ESD F+ ion energy distribution has a peak energy of ∼4 eV for all electron impact energies and a full width at half maximum (FWHM) of ∼3 eV. The P+ ions desorb with a peak energy of ∼2 eV under 55 eV electron impact; the FWHM of the P+ energy distribution is ∼2 eV. We suggest that the near threshold P+ formation from PF3 corresponds to the excitations of the 6a1 level, while the F+ threshold for adsorbed PF3 on the Pt surface is due to the excitation of the F 2s level. Our results suggest that beyond near threshold ((approximately-greater-than)32 eV), the excitation of the F 2s level also contributes significantly to the formation of P+ and PF+ ions from adsorbed PF3. © 1996 American Institute of Physics.
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  • 6
    Electronic Resource
    Electronic Resource
    College Park, Md. : American Institute of Physics (AIP)
    The Journal of Chemical Physics 105 (1996), S. 6043-6051 
    ISSN: 1089-7690
    Source: AIP Digital Archive
    Topics: Physics , Chemistry and Pharmacology
    Notes: We have studied electron stimulated desorption (ESD) of negative ions from PF3 molecules adsorbed on a Pt substrate over a wide electron energy range (0–175 eV). ESD from adsorbed PF3 gives rise to several negative ion fragments: F− (predominantly), F−2, P−, and PF−. The F− yield produced in the electron energy range 0–15 eV proceeds via dissociative electron attachment (DEA); the F− yield exhibits a peak around 11.5 eV with an onset around 7.5 eV. At electron energies above ∼15 eV, F− ions are produced via dipolar dissociation (DD). We have found that the F− ions produced from a 1 ML PF3/Pt surface via a DEA process with 11.5 eV electron impact desorb with a peak kinetic energy of ∼0.7 eV, while the F− ions generated via DD by 175 eV electron impact desorb with a peak kinetic energy of ∼1.2 eV. The F−2 yield curve also shows a peak at ∼11.5 eV; the onset of the F−2 yield from adsorbed PF3 is ∼9 eV. The F−2 yield in the electron range 9–15 eV is initiated via DEA. The P− signal from PF3 adsorbed on Pt has an onset at ∼16 eV. We have identified some possible DEA and DD processes leading to desorption of negative ions from adsorbed PF3. We suggest that Rydberg core-excited (1-hole, 2-electron) transient anion states of PF3, formed by capture of low energy electrons, dissociate to produce the F− and F−2 ions for E(e)〈15 eV. © 1996 American Institute of Physics.
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  • 7
    Electronic Resource
    Electronic Resource
    College Park, Md. : American Institute of Physics (AIP)
    The Journal of Chemical Physics 103 (1995), S. 6775-6782 
    ISSN: 1089-7690
    Source: AIP Digital Archive
    Topics: Physics , Chemistry and Pharmacology
    Notes: We report electron stimulated desorption (ESD) measurements of O− yields produced by dissociative electron attachment (DEA) to physisorbed CO2. The molecules are condensed at about 17–20 K on polycrystalline Pt, either as pure multilayer films, or in submonolayer (ML) quantities onto thick rare gas substrates. For the pure disordered multilayer solids, we observe four peaks in the O− yield function at incident electron energies, E(e), of about 4.1, 8.5, 11.2, and 15 eV. The lowest two are assigned, respectively, to the 2Πu and 2Πg resonance states of CO−2, which dissociate into O−(2P)+CO(X 1Σ+), and are known to dominate the gas phase DEA O− production cross section for E(e)≤20 eV. Measurements of ESD CO* metastable yields from similar CO2 multilayer solids on Pt(111), also presented here, suggest that the 11.2 and 15 eV O− peaks are associated with the manifold of close-lying CO2*− states which dissociate into O−(2P)+CO* (a 3Π, a′ 3Σ+, or d 3Δ). For 0.15 ML of CO2 physisorbed on 20 ML thick rare gas substrate films significant sharp enhancements (fwhm ≤0.5 eV) are observed in the ESD O− yields at about 0.3–0.4 eV below the lowest substrate exciton energy. These enhancements are attributed to a coupling of the (electron plus exciton) core-excited anion resonances of the rare gas atoms to the dissociative Rydberg anion states of the coadsorbed CO2 at the solid's surface. This is followed by a transfer of the charge and excitation energy to the coadsorbate. © 1995 American Institute of Physics.
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  • 8
    Electronic Resource
    Electronic Resource
    College Park, Md. : American Institute of Physics (AIP)
    The Journal of Chemical Physics 87 (1987), S. 2292-2296 
    ISSN: 1089-7690
    Source: AIP Digital Archive
    Topics: Physics , Chemistry and Pharmacology
    Notes: Energy analysis of Cl− ions produced by dissociative attachment in electron stimulated desorption from Cl2 condensed on a platinum substrate is reported. The electron energy dependence of the Cl− signal exhibits two peaks around 2 and 5 eV which arise, respectively, from the 2Πg and 2Πu core-excited Cl−@B|2 resonant states. At higher Cl2 coverages, a third peak is observed around 11.5 eV. From kinetic energy distributions, it is possible to ascribe this latter peak to Cl− ions formed via the 2Πu resonance by electrons which have suffered energy losses through the excitation of low-lying electronic states of molecular chlorine. In the energy range of the 2Πu Cl−*2 resonance, we observe that multiple scattering processes are also important and that the curve representing the kinetic energy of Cl− ions formed via a single scattering process as a function of incident electron energy is a straight line with a slope 1/2. This indicates that the chlorine lattice is not involved in the dissociation dynamics.
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  • 9
    Electronic Resource
    Electronic Resource
    College Park, Md. : American Institute of Physics (AIP)
    The Journal of Chemical Physics 115 (2001), S. 4811-4818 
    ISSN: 1089-7690
    Source: AIP Digital Archive
    Topics: Physics , Chemistry and Pharmacology
    Notes: We investigate the effects of the geometrical structure (phase and porosity) of multilayer benzene films on the desorption of O− induced by 2–20 eV electron impact on varying quantities of absorbed O2. Differences in the yield of O− from O2 doped amorphous and crystalline benzene films are attributed to the ability of O2 to diffuse into the amorphous solid via pores and defects formed during its deposition at 20 K. In contrast, diffusion into crystalline benzene is limited and deposited O2 molecules remain at the surface of the film. Thermal desorption measurements support this analysis. The data are also compared with results of similar experiments for O2 on water. While it is apparent that some of the variation in O− yield observed from ice films is similarly related to morphology, a substantial suppression of the O− yield is likely to result from energy loss by electrons prior to dissociation. Quenching of intermediate O2− states by water ice may also contribute to this suppression in the range 5–12 eV. © 2001 American Institute of Physics.
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  • 10
    Electronic Resource
    Electronic Resource
    College Park, Md. : American Institute of Physics (AIP)
    The Journal of Chemical Physics 94 (1991), S. 8570-8576 
    ISSN: 1089-7690
    Source: AIP Digital Archive
    Topics: Physics , Chemistry and Pharmacology
    Notes: Low energy (0–12 eV) electron impact on condensed amorphous H2O and D2O films is shown to induce electron stimulated desorption of H− and D−, respectively, via dissociative electron attachment. The onsets for H− and D− detection are at 5.5 eV, with a maximum yield for anion desorption at ∼7.4 eV. The kinetic energy distributions of the desorbing anions are peaked near 0 eV, indicating that the anions suffer post-dissociation collisions at or near the surface, with a large probability of anion trapping on the surface. The present results provide direct information on the dissociation products, prior to the interferences of subsequent reaction processes in the condensed film.
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