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  • 1
    Online Resource
    Online Resource
    Operation and performance of the ATLAS semiconductor tracker in LHC Run 2
    IOP Publishing ; 2022
    In:  Journal of Instrumentation Vol. 17, No. 01 ( 2022-01-01), p. P01013-
    Details
    In: Journal of Instrumentation, IOP Publishing, Vol. 17, No. 01 ( 2022-01-01), p. P01013-
    Abstract: The semiconductor tracker (SCT) is one of the tracking systems for charged particles in the ATLAS detector. It consists of 4088 silicon strip sensor modules. During Run 2 (2015–2018) the Large Hadron Collider delivered an integrated luminosity of 156 fb -1 to the ATLAS experiment at a centre-of-mass proton-proton collision energy of 13 TeV. The instantaneous luminosity and pile-up conditions were far in excess of those assumed in the original design of the SCT detector. Due to improvements to the data acquisition system, the SCT operated stably throughout Run 2. It was available for 99.9% of the integrated luminosity and achieved a data-quality efficiency of 99.85%. Detailed studies have been made of the leakage current in SCT modules and the evolution of the full depletion voltage, which are used to study the impact of radiation damage to the modules.
    Type of Medium: Online Resource
    ISSN: 1748-0221
    URL: Article
    DOI: 10.1088/1748-0221/17/01/P01013
    Language: Unknown
    Publisher: IOP Publishing
    Publication Date: 2022
    detail.hit.zdb_id: 2235672-1
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  • 2
    Online Resource
    Online Resource
    Proceedings of the Frontiers of Retrovirology Conference 2016
    Springer Science and Business Media LLC ; 2016
    In:  Retrovirology Vol. 13, No. S1 ( 2016-9)
    Details
    In: Retrovirology, Springer Science and Business Media LLC, Vol. 13, No. S1 ( 2016-9)
    Type of Medium: Online Resource
    ISSN: 1742-4690
    URL: Article
    DOI: 10.1186/s12977-016-0294-5
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2016
    detail.hit.zdb_id: 2142602-8
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Conduction Disturbances and Increased Atrial Vulnerability in Connexin40-Deficient Mice Analyzed by Transesophageal Stimulation
    Ovid Technologies (Wolters Kluwer Health) ; 1999
    In:  Circulation Vol. 99, No. 11 ( 1999-03-23), p. 1508-1515
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 99, No. 11 ( 1999-03-23), p. 1508-1515
    Abstract: Background —Recently, it has been reported that connexin40 (Cx40) deficiency in targeted mouse mutants is associated with a prolongation of P-wave and QRS complex duration on surface electrograms. The specific effects of Cx40 deficiency on sinus node function, sinoatrial, and atrioventricular conduction properties as well as on atrial vulnerability have not yet been investigated systematically by electrophysiological analysis. Methods and Results —Fifty-two mice (18 Cx40 +/+ , 15 Cx40 +/− , and 19 Cx40 −/− mice) were subjected to rapid atrial transesophageal stimulation after anesthesia with avertin. A significant prolongation of sinus node recovery time was noticed in Cx40 −/− mice compared with Cx40 +/− and Cx40 +/+ mice (287.8±109.0 vs 211.1±61.8 vs 204.4±60.9 ms; P 〈 0.05). In addition, Wenckebach periodicity occurred at significantly longer atrial pacing cycle lengths in Cx40 −/− mice than in Cx40 +/− or Cx40 +/+ mice (93.3±11.8 vs 83.9±9.7 vs 82.8±8.0 ms, P 〈 0.05). Analysis of 27 Cx40 −/− mice showed a significant increase in intra-atrial conduction time and atrioventricular conduction time compared with 52 Cx40 +/− and 31 wild-type (Cx40 +/+ ) mice. Furthermore, in Cx40 −/− mice, atrial tachyarrhythmias could be induced frequently by atrial burst pacing, whereas no atrial arrhythmias were inducible in heterozygous or wild-type mice. Conclusions —This study demonstrates that Cx40 deficiency is associated with sinoatrial, intra-atrial, and atrioventricular conduction disturbances. In atrial myocardium of the mouse, Cx40 deficiency results in increased atrial vulnerability and might contribute to arrhythmogenesis.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.99.11.1508
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1999
    detail.hit.zdb_id: 1466401-X
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  • 4
    Online Resource
    Online Resource
    Abnormal Cardiac Conduction and Morphogenesis in Connexin40 and Connexin43 Double-Deficient Mice
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Circulation Research Vol. 87, No. 5 ( 2000-09), p. 399-405
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 87, No. 5 ( 2000-09), p. 399-405
    Abstract: Abstract —Connexin40-deficient (Cx40 −/− /Cx43 +/+ ) and connexin43-heterozygous knockout mice (Cx40 +/+ /Cx43 +/− ) are viable but show cardiac conduction abnormalities. The ECGs of adult double heterozygous animals (Cx40 +/− /Cx43 +/− ) suggest additive effects of Cx40 and Cx43 haploinsufficiency on ventricular, but not on atrial, conduction. We also observed additive effects of both connexins on cardiac morphogenesis. Approximately half of the Cx40 −/− /Cx43 +/+ embryos died during the septation period, and an additional 16% died after birth. The majority of the latter mice had cardiac hypertrophy in conjunction with common atrioventricular junction or a ventricular septal defect. All Cx40 −/− /Cx43 +/− progeny exhibited cardiac malformations and died neonatally. The most frequent defect was common atrioventricular junction with abnormal atrioventricular connection, which was more severe than that seen in Cx40 −/− /Cx43 +/+ mice. Furthermore, muscular ventricular septal defects, premature closure of the ductus arteriosus, and subcutaneous edema were noticed in these embryos. Cx40 +/− /Cx43 −/− embryos showed the same phenotype (ie, obstructed right ventricular outflow tract) as reported for Cx40 +/+ /Cx43 −/− mice. These findings demonstrate that Cx43 haploinsufficiency aggravates the abnormalities observed in the Cx40 −/− phenotype, whereas Cx40 haploinsufficiency does not worsen the Cx43 −/− phenotype. We conclude that the gap-junctional proteins Cx40 and Cx43 contribute to morphogenesis of the heart in an isotype-specific manner.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.87.5.399
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
    detail.hit.zdb_id: 1467838-X
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  • 5
    Online Resource
    Online Resource
    Defective vascular development in connexin 45-deficient mice
    The Company of Biologists ; 2000
    In:  Development Vol. 127, No. 19 ( 2000-10-01), p. 4179-4193
    Details
    In: Development, The Company of Biologists, Vol. 127, No. 19 ( 2000-10-01), p. 4179-4193
    Abstract: In order to reveal the biological function(s) of the gap-junction protein connexin 45 (Cx45), we generated Cx45-deficient mice with targeted replacement of the Cx45-coding region with the lacZ reporter gene. Heterozygous Cx45+/− mice showed strong expression of the reporter gene in vascular and visceral smooth muscle cells. Cx45-deficient embryos exhibited striking abnormalities in vascular development and died between embryonic day (E) 9.5 and 10.5. Differentiation and positioning of endothelial cells appeared to be normal, but subsequent development of blood vessels revealed impaired formation of vascular trees in the yolk sac, impaired allantoic mesenchymal ingrowth and capillary formation in the labyrinthine part of the placenta, and arrest of arterial growth, including a failure to develop a smooth muscle layer surrounding the major arteries of the embryo proper. As a consequence, the hearts of most Cx45-deficient embryos were dilated. The abnormal development of the vasculature in the yolk sac of Cx45−/− embryos could be caused by defective TGFβ signalling, as the amount of TGF β1 protein in the epithelial layer of the yolk sac was largely decreased in the E9.5 Cx45−/− embryo, compared with the wild-type embryo. The defective vascular development was accompanied by massive apoptosis, which began in some embryos at E8.5 and was abundant in virtually all tissues of the embryos at E9.5. We conclude that in Cx45−/− embryos, vasculogenesis was normal, but subsequent transformation into mature vessels was interrupted. Development of different types of vessels was impaired to a varying extent, which possibly reflects the complementation by other connexin(s).
    Type of Medium: Online Resource
    ISSN: 0950-1991 , 1477-9129
    URL: Article
    DOI: 10.1242/dev.127.19.4179
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2000
    detail.hit.zdb_id: 2007916-3
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Biographical Feature: Bernhard Fleckenstein
    American Society for Microbiology ; 2021
    In:  Journal of Virology Vol. 95, No. 17 ( 2021-08-10)
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 95, No. 17 ( 2021-08-10)
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.00896-21
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2021
    detail.hit.zdb_id: 1495529-5
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  • 7
    Online Resource
    Online Resource
    Virology under the Microscope—a Call for Rational Discourse
    American Society for Microbiology ; 2023
    In:  Journal of Virology Vol. 97, No. 2 ( 2023-02-28)
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 97, No. 2 ( 2023-02-28)
    Abstract: Viruses have brought humanity many challenges: respiratory infection, cancer, neurological impairment and immunosuppression to name a few. Virology research over the last 60+ years has responded to reduce this disease burden with vaccines and antivirals. Despite this long history, the COVID-19 pandemic has brought unprecedented attention to the field of virology. Some of this attention is focused on concern about the safe conduct of research with human pathogens. A small but vocal group of individuals has seized upon these concerns – conflating legitimate questions about safely conducting virus-related research with uncertainties over the origins of SARS-CoV-2. The result has fueled public confusion and, in many instances, ill-informed condemnation of virology. With this article, we seek to promote a return to rational discourse. We explain the use of gain-of-function approaches in science, discuss the possible origins of SARS-CoV-2 and outline current regulatory structures that provide oversight for virological research in the United States. By offering our expertise, we – a broad group of working virologists – seek to aid policy makers in navigating these controversial issues. Balanced, evidence-based discourse is essential to addressing public concern while maintaining and expanding much-needed research in virology.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.00089-23
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2023
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  • 8
    Online Resource
    Online Resource
    Intrastructural Help: Harnessing T Helper Cells Induced by Licensed Vaccines for Improvement of HIV Env Antibody Responses to Virus-Like Particle Vaccines
    American Society for Microbiology ; 2018
    In:  Journal of Virology Vol. 92, No. 14 ( 2018-07-15)
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 92, No. 14 ( 2018-07-15)
    Abstract: Induction of persistent antibody responses by vaccination is generally thought to depend on efficient help by T follicular helper cells. Since the T helper cell response to HIV Env may not be optimal, we explored the possibility of improving the HIV Env antibody response to virus-like particle (VLP) vaccines by recruiting T helper cells induced by commonly used licensed vaccines to provide help for Env-specific B cells. B cells specific for the surface protein of a VLP can internalize the entire VLP and thus present peptides derived from the surface and core proteins on their major histocompatibility complex class II (MHC-II) molecules. This allows T helper cells specific for the core protein to provide intrastructural help for B cells recognizing the surface protein. Consistently, priming mice with an adjuvanted Gag protein vaccine enhanced the HIV Env antibody response to subsequent booster immunizations with HIV VLPs. To harness T helper cells induced by the licensed Tetanolpur vaccines, HIV VLPs that contained T helper cell epitopes of tetanus toxoid were generated. Tetanol-immunized mice raised stronger antibody responses to immunizations with VLPs containing tetanus toxoid T helper cell epitopes but not to VLPs lacking these epitopes. Depending on the priming immunization, the IgG subtype response to HIV Env after the VLP immunization could also be modified. Thus, harnessing T helper cells induced by other vaccines appears to be a promising approach to improve the HIV Env antibody response to VLP vaccines. IMPORTANCE Induction of HIV Env antibodies at sufficient levels with optimal Fc effector functions for durable protection remains a challenge. Efficient T cell help may be essential to induce such a desirable antibody response. Here, we provide proof of concept that T helper cells induced by a licensed vaccine can be harnessed to provide help for HIV Env-specific B cells and to modulate the Env-specific IgG subtype response.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.00141-18
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2018
    detail.hit.zdb_id: 1495529-5
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  • 9
    Online Resource
    Online Resource
    Vector Order Determines Protection against Pathogenic Simian Immunodeficiency Virus Infection in a Triple-Component Vaccine by Balancing CD4 + and CD8 + T-Cell Responses
    American Society for Microbiology ; 2017
    In:  Journal of Virology Vol. 91, No. 23 ( 2017-12)
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 91, No. 23 ( 2017-12)
    Abstract: An effective AIDS vaccine should elicit strong humoral and cellular immune responses while maintaining low levels of CD4 + T-cell activation to avoid the generation of target cells for viral infection. The present study investigated two prime-boost regimens, both starting vaccination with single-cycle immunodeficiency virus, followed by two mucosal boosts with either recombinant adenovirus (rAd) or fowlpox virus (rFWPV) expressing SIVmac239 or SIVmac251 gag/pol and env genes, respectively. Finally, vectors were switched and systemically administered to the reciprocal group of animals. Only mucosal rFWPV immunizations followed by systemic rAd boost significantly protected animals against a repeated low-dose intrarectal challenge with pathogenic SIVmac251, resulting in a vaccine efficacy (i.e., risk reduction per exposure) of 68%. Delayed viral acquisition was associated with higher levels of activated CD8 + T cells and Gag-specific gamma interferon (IFN-γ)-secreting CD8 + cells, low virus-specific CD4 + T-cell responses, and low Env antibody titers. In contrast, the systemic rFWPV boost induced strong virus-specific CD4 + T-cell activity. rAd and rFWPV also induced differential patterns of the innate immune responses, thereby possibly shaping the specific immunity. Plasma CXCL10 levels after final immunization correlated directly with virus-specific CD4 + T-cell responses and inversely with the number of exposures to infection. Also, the percentage of activated CD69 + CD8 + T cells correlated with the number of exposures to infection. Differential stimulation of the immune response likely provided the basis for the diverging levels of protection afforded by the vaccine regimen. IMPORTANCE A failed phase II AIDS vaccine trial led to the hypothesis that CD4 + T-cell activation can abrogate any potentially protective effects delivered by vaccination or promote acquisition of the virus because CD4 + T helper cells, required for an effective immune response, also represent the target cells for viral infection. We compared two vaccination protocols that elicited similar levels of Gag-specific immune responses in rhesus macaques. Only the animal group that had a low level of virus-specific CD4 + T cells in combination with high levels of activated CD8 + T cells was significantly protected from infection. Notably, protection was achieved despite the lack of appreciable Env antibody titers. Moreover, we show that both the vector and the route of immunization affected the level of CD4 + T-cell responses. Thus, mucosal immunization with FWPV-based vaccines should be considered a potent prime in prime-boost vaccination protocols.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.01120-17
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2017
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  • 10
    Online Resource
    Online Resource
    Vpu of a Simian Immunodeficiency Virus Isolated from Greater Spot-Nosed Monkey Antagonizes Human BST-2 via Two AxxxxxxxW Motifs
    American Society for Microbiology ; 2020
    In:  Journal of Virology Vol. 94, No. 2 ( 2020-01-06)
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 94, No. 2 ( 2020-01-06)
    Abstract: BST-2/CD317/tetherin is a host transmembrane protein that potently inhibits human immunodeficiency virus type 1 (HIV-1) virion release by tethering the nascent virions to the plasma membrane. Viral protein U (Vpu) is an accessory protein encoded by HIV-1 as well as by some simian immunodeficiency viruses (SIVs) infecting wild chimpanzees, gorillas, or monkeys (SIVcpz, SIVgor, or SIVgsn/SIVmon/SIVmus, respectively). HIV-1 Vpu directly binds to and downregulates human BST-2. The antagonism is highly species specific because the amino acid sequences of BST-2 are different among animal species. Here, we show that Vpu proteins from several SIVcpz, SIVgsn, SIVmon, or SIVmus isolates fail to antagonize human BST-2. Only Vpu from an SIVgsn isolate (SIVgsn-99CM71 [SIVgsn71]) was able to antagonize human BST-2 as well as BST-2 of its natural host, greater spot-nosed monkey (GSN). This SIVgsn Vpu interacted with human BST-2, downregulated cell surface human BST-2 expression, and facilitated HIV-1 virion release in the presence of human BST-2. While the unique 14 AxxxxxxxW 22 motif in the transmembrane domain of HIV-1 NL4-3 Vpu was reported to be important for antagonizing human BST-2, we show here that two AxxxxxxxW motifs (A 22 W 30 and A 25 W 33 ) exist in SIVgsn71 Vpu. Only the A 22 W 30 motif was needed for SIVgsn71 Vpu to antagonize GSN BST-2, suggesting that the mechanism of this antagonism resembles that of HIV-1 NL4-3 Vpu against human BST-2. Interestingly, SIVgsn71 Vpu requires two AxxxxxxxW (A 22 W 30 and A 25 W 33 ) motifs to antagonize human BST-2, suggesting an as-yet-undefined way that SIVgsn71 Vpu works against human BST-2. These results imply an evolutionary impact of primate BST-2 on lentiviral Vpu. IMPORTANCE Genetic alterations conferring a selective advantage in protecting from life-threating pathogens are maintained during evolution. In fact, the amino acid sequences of BST-2 differ among primate animals and their susceptibility to viral proteins is species specific, suggesting that such genetic diversity has arisen through the evolutionarily controlled balance between the host and pathogens. The M (main) group of HIV-1 is thought to be derived from SIVcpz, which utilizes Nef, but not Vpu, to antagonize chimpanzee BST-2. SIVcpz Nef is, however, unable to antagonize human BST-2, and Vpu was consequently chosen again as an antagonist against human BST-2 in the context of HIV-1. Studies on how Vpu lost and acquired this ability, together with the distinct mechanisms by which SIVgsn71 Vpu binds to and downregulates human or GSN BST-2, may help to explain the evolution of this lentiviral protein as a result of host-pathogen interactions.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.01669-19
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2020
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