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Search Results: 1 - 10 of 467621 matches for " Lisa A Lopez "
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IL-2 Receptor Antagonist (Basiliximab) Is Associated with Rapid Fibrosis Progression in Patients with Recurrent Hepatitis C after Liver Transplantation
Ibrahim A. Hanouneh,Nizar N. Zein,Rocio Lopez,Lisa Yerian
International Journal of Organ Transplantation Medicine , 2010,
Abstract: Background: Recurrence of hepatitis C virus (HCV) infection following orthotopic liver transplantation (OLT) is universal. There is paucity of data on the safety and efficacy of interleukin (IL)-2 receptor antagonist (IL-2RA) when added to the standard immunosuppression regimen in OLT recipients with recurrent HCV infection.Objectives: To evaluate the efficacy of IL-2RA (Basiliximab) in preventing acute cellular rejection (ACR) in patients with recurrent HCV infection after OLT and to assess the impact of IL-2RA in promoting fibrosis progression in post-OLT recurrent HCV infection.Methods: Using an electronic pathology database, we identified all OLT/HCV patients with at least 2 post-OLT liver biopsies (1998–2006). Standard immunosuppression consisted of steroids and calcineurin inhibitor with and without mycophenolate mofetil. All patients who were transplanted after May 2004 received IL-2RA induction therapy. The Ludwig-Batts system was used to stage all biopsies (593 biopsies from 124 patients). The first biopsy that showed post-OLT fibrosis or the last follow-up biopsy was used for time-to-progression analysis. Univariate and multivariate Cox proportional hazards regression analyses were performed to identify factors associated with the progression of fibrosis.Results: ACR was significantly (p<0.001) lower in patients who received IL-2RA (20 of 70, 29%) compared to those who did not (33 of 54, 61%). The median (25%ile, 75%ile) follow-up was 12.1 (6.1, 23.9) months during which 61% of patients had progression of fibrosis. Univariate analysis revealed that a higher HCV RNA load at 4 months post-OLT (p=0.002), cytomegalovirus (CMV) infection (p<0.001), use of steroid therapy for ACR (p=0.043), and use of IL-2RA (p<0.001) were associated with higher hazards for the progressionof fibrosis. Viral load at 4 months post-OLT was significantly (p=0.025) higher in patients who had IL-2RA therapy (median [25%ile, 75%ile]: 2.9 [1.0, 5.0] ×106 vs. 1.4 [1.0, 2.3] ×106). In multivariate analysis, patients who received IL-2RA therapy were 3.1 (95% CI: 1.8–5.3) times more likely to develop fibrosisthan those who did not treated with IL-2RA. Steroid therapy for ACR remained significantly (Hazard Ratio=2.9, p=0.002) associated with the progression of fibrosis.Conclusion: IL-2RA (Basiliximab) decreases the rate of ACR. However, it may be associated with more rapid histological progression of the disease in post-OLT recurrent HCV.
Anti-tetherin activities in Vpu-expressing primate lentiviruses
Su Yang, Lisa A Lopez, Heiko Hauser, Colin M Exline, Kevin G Haworth, Paula M Cannon
Retrovirology , 2010, DOI: 10.1186/1742-4690-7-13
Abstract: We found that despite the close relatedness of HIV-1 and SIVcpz, the chimpanzee viruses use Nef instead of Vpu to counteract tetherin. Furthermore, SIVcpz Nef proteins had activity against chimpanzee but not human tetherin. This specificity mapped to a short sequence that is present in the cytoplasmic tail of primate but not human tetherins, and this also accounts for the specificity of SIVsm/mac Nef for primate but not human tetherins. In contrast, Vpu proteins from four diverse members of the SIVsyk lineage all displayed an anti-tetherin activity that was active against macaque tetherin. Interestingly, Vpu from a SIVgsn isolate was also found to have activity against human tetherin.Primate lentiviruses show a high degree of flexibility in their use of anti-tetherin factors, indicating a strong selective pressure to counteract tetherin restriction. The identification of an activity against human tetherin in SIVgsn Vpu suggests that the presence of Vpu in the ancestral SIVmus/mon/gsn virus believed to have contributed the 3' half of the HIV-1 genome may have played a role in the evolution of viruses that could counteract human tetherin and infect humans.The release of HIV-1 and other enveloped viruses from the surface of infected cells is reduced by the activity of the interferon-inducible cell surface protein BST-2/CD317/HM1.24/"tetherin" [1-6]. The importance of overcoming this restriction for virus replication is reflected in the growing list of viral proteins that have been shown to possess anti-tetherin activities, with the primate lentiviruses in particular having evolved diverse approaches that include the HIV-1 Vpu, HIV-2 Env and certain SIV Nef and Env proteins [2,3,7-12].Analyses of the interactions between tetherins from different primate species and the anti-tetherin proteins used by viruses that infect those hosts have revealed a high degree of specificity. For example, although all tetherins analyzed to date can block HIV-1 particle release as efficien
Lack of adaptation to human tetherin in HIV-1 Group O and P
Su Jung Yang, Lisa A Lopez, Colin M Exline, Kevin G Haworth, Paula M Cannon
Retrovirology , 2011, DOI: 10.1186/1742-4690-8-78
Abstract: We found a lack of activity against human tetherin for both the Vpu and Nef proteins from group O and P viruses. Furthermore, we found no evidence of anti-human tetherin activity in a fully infectious group O proviral clone, ruling out the possibility of an alternative anti-tetherin factor in this virus. Interestingly, an activity against primate tetherins was retained in the Nef proteins from both a group O and a group P virus. By making chimeras between a functional group M and non-functional group O Vpu protein, we were able to map the first 18 amino acids of group M Vpu as playing an essential role in the ability of the protein to antagonize human tetherin. We further demonstrated the importance of residue alanine-18 for the group M Vpu activity. This residue lies on a diagonal face of conserved alanines in the TM domain of the protein, and is necessary for specific Vpu-tetherin interactions.The absence of human specific anti-tetherin activities in HIV-1 group O and P suggests a failure of these viruses to adapt to human hosts, which may have limited their spread.Tetherin (BST-2/CD317/HM1.24) is an interferon-inducible plasma membrane protein that can inhibit the release of enveloped viruses by physical tethering nascent virions at the cell surface [1,2]. Within the primate lentiviruses, this restriction is counteracted by anti-tetherin activities present in either the Vpu, Nef or Env proteins [1-11]. Several of these interactions are species-specific, suggesting that selection to evolve and maintain anti-tetherin functions has been part of the adaptation of the viruses to their hosts. For example, HIV-1 clade B Vpu counteracts human, but not primate or rodent tetherins [7,12,13], while the SIVmac and SIVcpz Nef proteins antagonize macaque and chimpanzee tetherin, but not the human protein [3-5,7].HIV-1 is classified into four distinct groups that maintain a similar genome organization but are highly divergent in their sequences: M (major), O (outlier), N (non-m
AA versus pp and dA: A puzzling scaling in HBT@RHIC
Z. Chajecki,T. D. Gutierrez,M. A. Lisa,M. Lopez-Noriega,for the STAR Collaboration
Physics , 2005,
Abstract: A nontrivial space-time structure of the hot system created at RHIC is the defining aspect of the physics of relativistic heavy ion collisions. Femtoscopy through pion intensity interferometry provides direct access to the dynamic geometric substructure of the freeze-out stage, and appears to confirm source evolution via collective flow. Since flow is usually considered to be a bulk phenomenon, it is surpring to find a simple scaling in preliminary HBT radii from p+p, d+Au and Au+Au collisions. Investigating the light system data in detail, we discuss a new way to visualize the ``fine structure'' of 3D correlation functions and the potential importance of long range correlations.
HIV-1 Vpu and HIV-2 Env counteract BST-2/tetherin by sequestration in a perinuclear compartment
Heiko Hauser, Lisa A Lopez, Su Yang, Jill E Oldenburg, Colin M Exline, John C Guatelli, Paula M Cannon
Retrovirology , 2011, DOI: 10.1186/1742-4690-8-85
HIV-1 Vpu and HIV-2 Env counteract BST-2/tetherin by sequestration in a perinuclear compartment
Heiko Hauser, Lisa A Lopez, Su Yang, Jill E Oldenburg, Colin M Exline, John C Guatelli, Paula M Cannon
Retrovirology , 2010, DOI: 10.1186/1742-4690-7-51
Abstract: We observed that a fraction of tetherin is located at the surface of restricting cells, and that co-expression of both HIV-1 Vpu and HIV-2 Env reduced this population. In addition, Vpu, but not the HIV-2 Env, reduced total cellular levels of tetherin. An additional effect observed for both Vpu and the HIV-2 Env was to redirect tetherin to an intracellular perinuclear compartment that overlapped with markers for the TGN (trans-Golgi network). Sequestration of tetherin in this compartment was independent of tetherin's normal endocytosis trafficking pathway.Both HIV-1 Vpu and HIV-2 Env redirect tetherin away from the cell surface and sequester the protein in a perinuclear compartment, which likely blocks the action of this cellular restriction factor. Vpu also promotes the degradation of tetherin, suggesting that it uses more than one mechanism to counteract tetherin restriction.Viral pathogens frequently disable components of both intrinsic and adaptive host immune responses. The human immunodeficiency virus (HIV) expresses accessory proteins that play essential roles to counteract such host defenses [1]. Strategies include targeting the host anti-viral proteins or restriction factors for degradation through the recruitment of cullin-RING finger ubiquitin ligases, as occurs when Vif counteracts APOBEC3G, or Vpu targets CD4. Alternatively, the trafficking pathways used by the host factors can be altered to prevent expression at the cell surface, as occurs with Nef and CD4 or MHC class I. The HIV-1 Vpu protein also counteracts an α-interferon-inducible host cell restriction, BST-2/CD317/HM1.24 ("tetherin"), that prevents the release of newly formed virions from the cell surface [2-4]. Virions lacking Vpu accumulate at the cell surface and in intracellular compartments, leading to a correspondingly reduced ability of the virus to spread [3,5,6].Tetherin restriction of virus release is also active against other enveloped viruses including retroviruses, filoviruses and are
Concerns about child subject research in Botswana: a call for establishing structures and guidelines that protect children
Tapologo Maundeni, Lisa Lopez Levers
African Sociological Review / Revue Africaine de Sociologie , 2005,
Some consequences of the effective low-energy lagrangian for gravity
A. Dobado,A. Lopez
Physics , 1993, DOI: 10.1016/0370-2693(93)90322-9
Abstract: We consider the minimal low-energy action for gravity up to six derivatives which is renormalizable at the two-loop level modulo higher derivative corrections. Then we study the classical solutions corresponding to the Schwarzschild and the Robertson-Walker metrics. In the first case we find a singularity close to the gravitational radius and in the second case we find inflationary de Sitter solutions in absence of any matter or cosmological constant.
Inflatonless inflation
A. Dobado,A. Lopez
Physics , 1994, DOI: 10.1103/PhysRevD.53.2262
Abstract: Whichever could be the real theory of gravitation, the corresponding low-energy effective lagrangian will probably contain higher derivative terms. In this work we study the general conditions on those terms in order to produce enough inflation to solve some of the problems of the standard Friedmann-Robertson-Walker cosmology in absence of any inflaton field. We apply our results to some particular scenarios where higher derivative terms appear in the effective lagrangian for gravity like those coming from graviton (two)-loops or integrating out ordinary matter (like the one present in the Standard Model).
Formation, Repair, and Genotoxic Properties of Bulky DNA Adducts Formed from Tobacco-Specific Nitrosamines
Lisa A. Peterson
Journal of Nucleic Acids , 2010, DOI: 10.4061/2010/284935
Abstract: 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and -nitrosonornicotine (NNN) are tobacco-specific nitrosamines present in tobacco products and smoke. Both compounds are carcinogenic in laboratory animals, generating tumors at sites comparable to those observed in smokers. These Group 1 human carcinogens are metabolized to reactive intermediates that alkylate DNA. This paper focuses on the DNA pyridyloxobutylation pathway which is common to both compounds. This DNA route generates 7-[4-(3-pyridyl)-4-oxobut-1-yl]- -deoxyguanosine, -[4-(3-pyridyl)-4-oxobut-1-yl]- -deoxycytosine, -[4-(3-pyridyl)-4-oxobut-1-yl]- -deoxythymidine, and -[4-(3-pyridyl)-4-oxobut-1-yl]- -deoxyguanosine as well as unstable adducts which dealkylate to release 4-hydroxy-1- -1-butanone or depyriminidate/depurinate to generate abasic sites. There are multiple repair pathways responsible for protecting against the genotoxic effects of these adducts, including adduct reversal as well as base and nucleotide excision repair pathways. Data indicate that several DNA adducts contribute to the overall mutagenic properties of pyridyloxobutylating agents. Which adducts contribute to the carcinogenic properties of this pathway are likely to depend on the biochemistry of the target tissue. 1. Introduction Tobacco use has been linked to a variety of human cancers, including lung, oral cavity, esophagus, pharynx, larynx, urinary bladder, pancreas, and liver cancers [1]. Lung cancer alone is responsible for the deaths of 1.3 million people annually worldwide [2]. It is the leading cause of cancer deaths in the United States, with 80%–90% of this cancer associated with tobacco use [1]. Environmental tobacco smoke (second-hand smoke) has also been associated with human lung cancer but the risks are significantly lower than those associated with smoking [1]. There are more than 5000 identified chemicals present in cigarette smoke [1, 3–5]. More than 60 of these compounds are demonstrated chemical carcinogens in animal models [1, 3, 4, 6]. An important group of tobacco carcinogens are the tobacco-specific nitrosamines. These compounds are formed from tobacco alkaloids like nicotine during the curing process of tobacco [7]. 4(Methylnitrosamino)-1-(3pyridyl)-1-butanone (NNK) and -nitrosonornicotine (NNN) are two of the most potent tobacco-specific nitrosamines present in tobacco products and smoke [8]. Both compounds are carcinogenic in laboratory animals, generating tumors at sites comparable to those observed in smokers [8]. NNK is a potent lung carcinogen, which also induces liver and nasal tumors
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