Relevant bibliographies by topics / Adenoviral

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Adenoviral'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 February 2022

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Journal articles on the topic "Adenoviral"

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Asaoka, Katsuyuki, Mitsuhiro Tada, Yutaka Sawamura, Jun Ikeda, and Hiroshi Abe. "Dependence of efficient adenoviral gene delivery in malignant glioma cells on the expression levels of the Coxsackievirus and adenovirus receptor." Journal of Neurosurgery 92, no. 6 (June 2000): 1002–8. http://dx.doi.org/10.3171/jns.2000.92.6.1002.

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Object. Recombinant adenovirus is used as a competent vector in a wide spectrum of cancer gene therapies because of its high efficiency in gene delivery. To study the feasibility of gene therapy in malignant gliomas, the authors examined the antiproliferative effect of the adenovirally transduced wild-type p53 tumor suppressor gene by using 15 different high-grade glioma cell lines.Methods. Although growth suppression in association with a high adenoviral p53 transduction efficiency was seen in five of 15 cell lines, it was not observed in the remaining 10 cell lines. To clarify the underlying mechanism, we examined the expression levels of the Coxsackievirus and adenovirus receptor (CAR), which is the primary receptor for adenovirus, and of the integrins αvβ3 and αvβ5, which promote adenoviral internalization. The expression level of the CAR gene showed a close correlation to adenoviral gene transduction efficiency in the tested cell lines, whereas the expression levels of the integrins did not. The CAR expression was decreased by wild-type p53 transduction in U251MG cells harboring mutant p53 and increased by antisense inhibition of p53 in LN443 cells with endogenous wild-type p53.Conclusions. The results of this study indicate that CAR expression is a critical determinant of transduction efficiencies in adenovirus-based gene therapy for human malignant gliomas.
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O'Prey, Jim, Simon Wilkinson, and Kevin M. Ryan. "Tumor Antigen LRRC15 Impedes Adenoviral Infection: Implications for Virus-Based Cancer Therapy." Journal of Virology 82, no. 12 (April 2, 2008): 5933–39. http://dx.doi.org/10.1128/jvi.02273-07.

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ABSTRACT Adenoviruses for gene or oncolytic therapy are under development. Notable among these strategies is adenoviral delivery of the tumor suppressor p53. Since all therapeutics have limitations in certain settings, we have undertaken retroviral suppressor screens to identify genes conferring resistance to adenovirus-delivered p53. These studies identified the tumor antigen LRRC15, which is frequently overexpressed in multiple tumor types, as a repressor of cell death due to adenoviral p53. LRRC15, however, does not impede p53 function per se but impedes adenoviral infection. Specifically, LRRC15 causes redistribution of the coxsackievirus-adenovirus receptor away from the cell surface. This effect is manifested in less adenoviral binding to the surfaces of LRRC15-expressing cells. This discovery, therefore, not only is important for understanding adenoviral biology but also has potentially important implications for adenovirus-based anticancer therapeutics.
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Jogler, Christian, Dennis Hoffmann, Dirk Theegarten, Thomas Grunwald, Klaus Überla, and Oliver Wildner. "Replication Properties of Human Adenovirus In Vivo and in Cultures of Primary Cells from Different Animal Species." Journal of Virology 80, no. 7 (April 1, 2006): 3549–58. http://dx.doi.org/10.1128/jvi.80.7.3549-3558.2006.

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ABSTRACT Oncolytic adenoviruses have emerged as a promising approach for the treatment of tumors resistant to other treatment modalities. However, preclinical safety studies are hampered by the lack of a permissive nonhuman host. Screening of a panel of primary cell cultures from seven different animal species revealed that porcine cells support productive replication of human adenovirus type 5 (Ad5) nearly as efficiently as human A549 cells, while release of infectious virus by cells from other animal species tested was diminished by several orders of magnitude. Restriction of productive Ad5 replication in rodent and rabbit cells seems to act primarily at a postentry step. Replication efficiency of adenoviral vectors harboring different E1 deletions or mutations in porcine cells was similar to that in A549 cells. Side-by-side comparison of the viral load kinetics in blood of swine and mice injected with Ad5 or a replication-deficient adenoviral vector failed to provide clear evidence for virus replication in mice. In contrast, evidence suggests that adenovirus replication occurs in swine, since adenoviral late gene expression produced a 13.5-fold increase in viral load in an individual swine from day 3 to day 7 and 100-fold increase in viral DNA levels in the Ad5-infected swine compared to the animal receiving a replication-deficient adenovirus. Lung histology of Ad5-infected swine revealed a severe interstitial pneumonia. Although the results in swine are based on a small number of animals and need to be confirmed, our data strongly suggest that infection of swine with human adenovirus or oncolytic adenoviral vectors is a more appropriate animal model to study adenoviral pathogenicity or pharmacodynamic and toxicity profiles of adenoviral vectors than infection of mice.
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Harrod, Kevin S., Bruce C. Trapnell, Kazuhisa Otake, Thomas R. Korfhagen, and Jeffrey A. Whitsett. "SP-A enhances viral clearance and inhibits inflammation after pulmonary adenoviral infection." American Journal of Physiology-Lung Cellular and Molecular Physiology 277, no. 3 (September 1, 1999): L580—L588. http://dx.doi.org/10.1152/ajplung.1999.277.3.l580.

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Surfactant protein A (SP-A) is a member of the collectin family of host defense molecules expressed primarily in the epithelial cells of the lung. To determine the role of SP-A in pulmonary adenoviral infection, SP-A-deficient (SP-A −/−) mice were intratracheally infected with a replication-deficient recombinant adenovirus, Av1Luc1. Lung inflammation was markedly increased in SP-A −/− compared with SP-A +/+ mice and was associated with increased hemorrhage and epithelial cell injury. Polymorphonuclear cells in bronchoalveolar lavage fluid (BALF) were increased in SP-A −/− mice after administration of adenovirus. Coadministration of adenovirus and purified human SP-A ameliorated adenoviral-induced lung inflammation in SP-A −/− mice. Concentrations of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β were increased in BALF of SP-A −/− mice. Likewise, TNF-α, IL-6, macrophage inflammatory protein (MIP)-1α, monocyte chemotactic protein-1, and MIP-2 mRNAs were increased in lung homogenates from SP-A −/− mice 6 and 24 h after viral administration. Clearance of adenoviral DNA from the lung and uptake of fluorescent-labeled adenovirus by alveolar macrophages were decreased in SP-A −/− mice. SP-A enhances viral clearance and inhibits lung inflammation during pulmonary adenoviral infection, providing support for the importance of SP-A in antiviral host defense.
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Zhu, Jiangao, Xiaopei Huang, and Yiping Yang. "Innate Immune Response to Adenoviral Vectors Is Mediated by both Toll-Like Receptor-Dependent and -Independent Pathways." Journal of Virology 81, no. 7 (January 17, 2007): 3170–80. http://dx.doi.org/10.1128/jvi.02192-06.

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ABSTRACT Recombinant adenoviral vectors have been widely used for gene therapy applications and as vaccine vehicles for treating infectious diseases such as human immunodeficiency virus disease. The innate immune response to adenoviruses represents the most significant hurdle in clinical application of adenoviral vectors for gene therapy, but it is an attractive feature for vaccine development. How adenovirus activates innate immunity remains largely unknown. Here we showed that adenovirus elicited innate immune response through the induction of high levels of type I interferons (IFNs) by both plasmacytoid dendritic cells (pDCs) and non-pDCs such as conventional DCs and macrophages. The innate immune recognition of adenovirus by pDCs was mediated by Toll-like receptor 9 (TLR9) and was dependent on MyD88, whereas that by non-pDCs was TLR independent through cytosolic sensing of adenoviral DNA. Furthermore, type I IFNs were pivotal in innate and adaptive immune responses to adenovirus in vivo, and type I IFN blockade diminished immune responses, resulting in more stable transgene expression and reduction of inflammation. These findings indicate that adenovirus activates innate immunity by its DNA through TLR-dependent and -independent pathways in a cell type-specific fashion, and they highlight a critical role for type I IFNs in innate and adaptive immune responses to adenoviral vectors. Our results that suggest strategies to interfere with type I IFN pathway may improve the outcome of adenovirus-mediated gene therapy, whereas approaches to activate the type I IFN pathway may enhance vaccine potency.
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Lee, Minhyeok, Seulgi Kim, Oh Jung Kwon, Ji Hye Kim, Inbeom Jeong, Ji Woong Son, Moon Jun Na, Yoo Sang Yoon, Hyun Woong Park, and Sun Jung Kwon. "Treatment of Adenoviral Acute Respiratory Distress Syndrome Using Cidofovir With Extracorporeal Membrane Oxygenation." Journal of Intensive Care Medicine 32, no. 3 (November 30, 2016): 231–38. http://dx.doi.org/10.1177/0885066616681272.

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Adenovirus infections are associated with respiratory (especially upper respiratory) infection and gastrointestinal disease and occur primarily in infants and children. Although rare in adults, severe lower respiratory adenovirus infections including pneumonia are reported in specific populations, such as military recruits and immunocompromised patients. Antiviral treatment is challenging due to limited clinical experience and lack of well-controlled randomized trials. Several previously reported cases of adenoviral pneumonia showed promising efficacy of cidofovir. However, few reports discussed the efficacy of cidofovir in acute respiratory distress syndrome (ARDS). We experienced 3 cases of adenoviral pneumonia associated with ARDS and treated with cidofovir and respiratory support, including extracorporeal membrane oxygenation (ECMO). All 3 patients showed a positive clinical response to cidofovir and survival at 28 days. Cidofovir with early ECMO therapy may be a therapeutic option in adenoviral ARDS. A literature review identified 15 cases of adenovirus pneumonia associated with ARDS.
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Debey, B. M., H. D. Lehmkuhl, C. Chard-Bergstrom, and L. A. Hobbs. "Ovine Adenovirus Serotype 7-associated Mortality in Lambs in the United States." Veterinary Pathology 38, no. 6 (November 2001): 644–48. http://dx.doi.org/10.1354/vp.38-6-644.

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Adenoviral infections were diagnosed in three neonatal lambs that died spontaneously, and no other etiologic agents were identified. Clinical signs were anorexia, weakness, abdominal distention, and sudden death. Microscopic lesions consisted of multifocal necrotizing hepatitis, multifocal subacute interstitial nephritis, and loss of enterocytes from intestinal villi. Adenovirus inclusions were identified by light microscopy in the kidneys only. Adenoviral antigen, however, was identified in the liver, kidney, and intestine of the lambs by immunohistochemical techniques. An ovine adenovirus serotype 7, not previously isolated from sheep in the United States, was characterized from these lambs.
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Bayer, Wibke, Matthias Tenbusch, Ruth Lietz, Lena Johrden, Simone Schimmer, Klaus Überla, Ulf Dittmer, and Oliver Wildner. "Vaccination with an Adenoviral Vector That Encodes and Displays a Retroviral Antigen Induces Improved Neutralizing Antibody and CD4+ T-Cell Responses and Confers Enhanced Protection." Journal of Virology 84, no. 4 (December 9, 2009): 1967–76. http://dx.doi.org/10.1128/jvi.01840-09.

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ABSTRACT We present a new type of adenoviral vector that both encodes and displays a vaccine antigen on the capsid, thus combining in itself gene-based and protein vaccination; this vector resulted in an improved vaccination outcome in the Friend virus (FV) model. For presentation of the envelope protein gp70 of Friend murine leukemia virus on the adenoviral capsid, gp70 was fused to the adenovirus capsid protein IX. When compared to vaccination with conventional FV Env- and Gag-encoding adenoviral vectors, vaccination with the adenoviral vector that encodes and displays pIX-gp70 combined with an FV Gag-encoding vector resulted in significantly improved protection against systemic FV challenge infection, with highly controlled viral loads in plasma and spleen. This improved protection correlated with improved neutralizing antibody titers and stronger CD4+ T-cell responses. Using a vector that displays gp70 without encoding it, we found that while the antigen display on the capsid alone was sufficient to induce high levels of binding antibodies, in vivo expression was necessary for the induction of neutralizing antibodies. This new type of adenovirus-based vaccine could be a valuable tool for vaccination.
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B, Tadesse. "Review on Adeno Virus; As a Vaccine Vehicle." Open Access Journal of Veterinary Science & Research 2, no. 3 (2017): 1–12. http://dx.doi.org/10.23880/oajvsr-16000138.

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Adenoviruses have moved to the forefront of vaccinology and are showing substantial prom ise as vehicles for antigen delivery for a number of vaccines currently being developed. Most studies to date have focused on human serotype adenoviruses, particularly human adenovirus type 5. Human serotype adenovirus vaccine vectors are particularly usef ul for development of veterinary vaccines as neutralizing antibodies to the vector will not usually be present in the vaccinates. Most vectors currently used as vaccine carriers are deleted in E1 gene. The original E1 deleted adenoviral vectors were constr ucted by homologous recombination. Replication incompetent vectors contain an antigen expression cassette substituted for the deleted E1A – E1B region. These replication incompitant adenoviruses can not replicate because of the deletion of the essential vir al E1 gene region containing two genes. Replication competent adenoviral vectors encode all of the remaining adenoviral antigens in addition to the transgene product, i.e., the vaccine antigen. The potential for adenoviruses to elicit powerful B cell and T cell responses in the mammalian host are the main reason for the use of these vectors in vaccine development. For effective veterinary use, extensive research on adenoviral vaccine vectors should be undertaken.
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Jakubczak, John L., Michele L. Rollence, David A. Stewart, Jonathon D. Jafari, Dan J. Von Seggern, Glen R. Nemerow, Susan C. Stevenson, and Paul L. Hallenbeck. "Adenovirus Type 5 Viral Particles Pseudotyped with Mutagenized Fiber Proteins Show Diminished Infectivity of Coxsackie B-Adenovirus Receptor-Bearing Cells." Journal of Virology 75, no. 6 (March 15, 2001): 2972–81. http://dx.doi.org/10.1128/jvi.75.6.2972-2981.2001.

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ABSTRACT A major limitation of adenovirus type 5 (Ad5)-based gene therapy, the inability to target therapeutic genes to selected cell types, is attributable to the natural tropism of the virus for the widely expressed coxsackievirus-adenovirus receptor (CAR) protein. Modifications of the Ad5 fiber knob domain have been shown to alter the tropism of the virus. We have developed a novel system to rapidly evaluate the function of modified fiber proteins in their most relevant context, the adenoviral capsid. This transient transfection/infection system combines transfection of cells with plasmids that express high levels of the modified fiber protein and infection with Ad5.βgal.ΔF, an E1-, E3-, and fiber-deleted adenoviral vector encoding β-galactosidase. We have used this system to test the adenoviral transduction efficiency mediated by a panel of fiber protein mutants that were proposed to influence CAR interaction. A series of amino acid modifications were incorporated via mutagenesis into the fiber expression plasmid, and the resulting fiber proteins were subsequently incorporated onto adenoviral particles. Mutations located in the fiber knob AB and CD loops demonstrated the greatest reduction in fiber-mediated gene transfer in HeLa cells. We also observed effects on transduction efficiency with mutations in the FG loop, indicating that the binding site may extend to the adjacent monomer in the fiber trimer and in the HI loop. These studies support the concept that modification of the fiber knob domain to diminish or ablate CAR interaction should result in a detargeted adenoviral vector that can be combined simultaneously with novel ligands for the development of a systemically administered, targeted adenoviral vector.
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Dissertations / Theses on the topic "Adenoviral"

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Rauma-Pinola, T. (Tanja). "Adenovirus endocytosis and adenoviral gene transfer in cardiovascular and dermatologic disease models." Doctoral thesis, University of Oulu, 2004. http://urn.fi/urn:isbn:9514274342.

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Abstract Adenoviral gene transfer is a valuable tool in molecular biology research. In order to be an efficient and safe vector, adenovirus structure and infection mechanism as well as molecular biology of the used transgene need to be well studied. The aim of this study was to evaluate the role of adenovirus as a gene transfer vector from several perspectives. Adenovirus uses receptor-mediated endocytosis in order to enter the target cell. The effect of Rab5 GTPase on adenovirus entry and gene transfer efficiency was examined first. Next, adenovirus was used as an investigatory tool in the cardiovascular research, focused on clarifying the role of adrenomedullin (AM) in heart and vascular remodeling. Finally, a model of adenoviral gene transfer into skin fibroblasts was used. The role of Rab5 GTPase in the adenovirus endocytosis was examined in HeLa cells using Cy3-labeled adenovirus, and gene transfer efficiency using β-galactosidase encoding adenovirus. Rab5 increased both adenovirus uptake and gene transfer, whereas dominant negative Rab5S34N decreased both endocytosis and gene transfer. The data indicate that Rab5 is needed in mediating the adenovirus uptake into the target cell. In the rat heart, adenovirus-mediated AM gene transfer transiently improved systolic function both in vivo and in vitro. AM caused activation of translocation of protein kinases C ε and δ, whereas phosphorylation of p38 mitogen activated protein kinase was decreased in the left ventricle. AM significantly attenuated the development of angiotensin II-induced cardiac hypertrophy. In rats with myocardial infarction, AM enhanced dilatation of left ventricle and thinning of anterior wall. The role of AM in neointima formation was evaluated in rat artery after endothelial injury. Intravascular AM gene transfer decreased neointimal growth and increased neointimal myofibroblasts apoptosis. These results show that AM regulates left ventricular systolic function and remodeling in the heart, and plays a role in pathological vascular remodeling. Adenovirus-mediated lysyl hydroxylase (LH) gene transfer into skin fibroblasts of type VI Ehlers-Danlos syndrome patient and rat skin increased functional LH production, elevated LH activity, and human LH mRNA production both in vitro and in vivo. LH gene replacement therapy may thus lead to possibilities to improve skin wound healing in Ehlers-Danlos syndrome patients.
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Rauschhuber, Christina. "Analysis of Adenovirus-Host Interactions to Improve Recombinant Adenoviral Vectors for Gene Therapy." Diss., lmu, 2011. http://nbn-resolving.de/urn:nbn:de:bvb:19-128560.

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Wiles, Karen Anna, and n/a. "Coxsackie and Adenovirus Receptor (CAR) expression is a potential limiting factor in adenoviral oncotheraphy." University of Otago. Dunedin School of Medicine, 2007. http://adt.otago.ac.nz./public/adt-NZDU20070619.161353.

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Novel approaches to cancer treatment in the context of Gene Therapy have been gaining popularity as an alternative to conventional therapies which have proven to lack specificity, resulting in tumour cell resistance, tumour progression and mortality. As a consequence the use of adenoviruses has been widely developed not only as a replication deficient vector for gene therapy but also as a replication competent oncolytic agent designed to selectively target and kill tumour cells. Unfortunately their success in clinical application has been limited, and it has been suggested that a lack of the primary viral attachment receptor 'CAR' could be a barrier to infection by limiting access to target cells. If Ad/CAR binding is the rate limiting step for successful Ad therapy, it is essential to establish a CAR expression profile in normal and tumour tissue, and in tumour progression, to enable more effective targeted therapy. Furthermore, in the context of using adenovirus as an anticancer strategy by exploiting its replicative lysis, it is important to explore whether Ad success is affected by CAR expression and to identify factors downstream of CAR that may be influential in this process. In the first experimental chapter, an in vivo immunohistochemical analysis of tissue array slides determined CAR expression in a range of normal and tumour tissue. CAR was differentially expressed dependent on cell of origin, with normal stem cells and basal cells displaying very high CAR, signifying its importance in early development and differentiation. Epithelial cells were also high in CAR but its expression was negligible in mesenchymal, lymphoid and neural cells. This trend was also reflected in most tumour tissue albeit with a general decrease in CAR compared to corresponding normal tissue of the same organ. An exception was the blastic tumours which displayed high CAR reflecting their embryonic state of derivation. CAR expression also decreased in high grade, poorly differentiated tumours of the prostate, stomach and breast compared to their well differentiated counterparts. In the second experimental chapter, a more comprehensive study of breast cancer biopsy specimens was undertaken, to determine both the expression of CAR and the tumour suppressor gene p53 in relation to tumour grade. The rationale being that both loss of CAR expression and p53 mutation (resulting in loss of function), have been associated with tumour progression. It is possible that CAR and p53 interact directly or indirectly and may be modulated by each other. This study revealed a decrease in both CAR and hormone receptor expression and an increase in p53 'mutational' status with increasing tumour grade. These three factors when compared independently to tumour grade are statistically significant associations, implying that CAR expression and hormone responsiveness decrease with tumour progression and p53 function is compromised or lost via mutation. There was also a significant association between CAR expression and hormone receptor status, however a significant association between CAR expression and p53 status within the tumour grades was not found. Treatment outcome with Ads will also depend on defining factors downstream of CAR attachment that affect adenovirus 'permissivity', which is ultimately measured by viral replication and cell death, relying on the bystander effect to eradicate all tumour cells. The in vitro analysis revealed statistically significant associations between CAR receptor expression, 'infectivity' (virus infection) and permissivity. Cell lines that were more susceptible to Ad5 were generally of epithelial origin, had high CAR, and were easily infected. However there were exceptions and CAR was not the sole determinant in adenovirus cell entry nor in its ability to replicate and kill the cell. Permissivity was also related to p53 status. Thus, although CAR expression may indeed be a limiting factor, it is apparent that a combination of other events contributes to a deficient infection, especially in the deregulated tumour environment. The results presented in this thesis clearly demonstrate that there is more to the story of 'CAR' which hints that its role in viro-oncotherapy is not limited solely to its function as an attachment receptor for adenovirus but may also involve its function as a cell adhesion molecule and signal transducer. The further elucidation of these aspects of CAR�s potential role in the scheme of tumour biology may alter the course and strategy of cancer therapy in the future.
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Jäger, Lorenz. "The persistence of recombinant adenoviral vectors." Diss., lmu, 2009. http://nbn-resolving.de/urn:nbn:de:bvb:19-100490.

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Watkins, Sarah Jane. "Adenoviral targeting with antibody fusion proteins." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624907.

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Shahbazi, Bijan [Verfasser], and Leonhard [Akademischer Betreuer] Mohr. "Adenovirale Überexpression von Glycoprotein gp 96 in Tumorzellen = Adenoviral overexpression of Ggycoprotein gp 96 in tumor cells." Freiburg : Universität, 2014. http://d-nb.info/1114669784/34.

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Knapp, Mark. "Development of dopamine receptor-expressing adenoviral vectors." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0001/MQ28801.pdf.

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Cassivi, Stephen David. "Adenoviral-mediated gene therapy in lung transplantation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0002/MQ40800.pdf.

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Finlay, Siân. "Modulation of macrophage phenotype using adenoviral transfection." Thesis, University of Aberdeen, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409252.

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The initial aim of this study was to examine the nature of the interaction between adenovirus and transfected macrophage, and to characterise the molecular mechanisms underlying macrophage response to adenoviral infection. Results showed that adenoviral transfection activated macrophages, promoting production of pro-inflammatory mediators and priming an enhanced response to other inflammatory stimuli.  Activation was dependent on the nuclear factor kappa B (NFkB) signalling pathway, which was activated within two hours of transfection, and could be prevented using an inhibitory adenovirus which blocked NFkB signalling.  The ultimate phenotype of the transfected macrophage was determined both by non-specific viral activation and by the properties of the transgene expressed. The second aim of this research was to investigate the effect of the local cytokine milieu on transgene expression in vitro.  Results showed that transgene expression under the control of two different promoter constructs was subject to regulation by pro-inflammatory mediators, by mechanisms at least partly dependent on the NFkB signalling pathway.  the results have important implications for the use of these promoters in gene therapy applications where the gene of interest is delivered into an inflammatory environment. The final stage of the project focused on the use of transfected macrophages in vivo, in a rat model of glomerulonephritis.  Results showed that transfected macrophages expressing the anti-inflammatory cytokine IL-4 localised with enhanced efficiency to inflamed glomeruli after intra-renal artery injection of the mechanisms for this were examined.  Better understanding of the mechanisms which promote localisation may ultimately permit the design of genetically-modified macrophages which selectively target sites of injury for delivery of anti-inflammatory cytokines.
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Fulco, Enzo Augusto Medeiros 1982. "Corticosteróides tópicos para ceratoconjuntivite adenoviral = revisão sistemática." [s.n.], 2011. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311821.

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Orientador: Rodrigo Pessoa Cavalcanti Lira
Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-19T10:10:15Z (GMT). No. of bitstreams: 1 Fulco_EnzoAugustoMedeiros_M.pdf: 625645 bytes, checksum: 871772c97dcfc7b49d6bc56d1a72c439 (MD5) Previous issue date: 2011
Resumo: Introdução: Corticosteróides tópicos são utilizados comumente no tratamento da ceratoconjuntivite viral aguda. Tem sido sugerida a utilidade dos corticosteróides no tratamento sintomático da conjuntivite alívio dos sinais e/ou sintomas e prevenção dos infiltrados subepiteliais. Por outro lado, observou-se o relato dos possíveis efeitos colaterais, como o prolongamento da transmissão invitro do vírus e, no âmbito da medicina clínica, ensaios clínicos revelaram a eficácia duvidosa dos colírios de corticosteróides. O objetivo deste estudo foi comparar o uso dos corticosteróides tópicos, com quaisquer drogas usadas nos ensaios clínicos com o placebo. Objetivo: Avaliar se os corticosteróides tópicos são eficazes e seguros para o tratamento da ceratoconjuntivite adenoviral para melhorar os sintomas e evitar ou minimizar complicações relacionadas à doença. Desenho: Revisão sistemática. Métodos: Pesquisa documental na Cochrane Central Register of Controlled Trials (CENTRAL) (que contém o Cochrane Eyes and Vision Group Trials Register), MEDLINE, EMBASE, PubMed, nas listas de referência de relatórios de ensaio identificados e no o Science Citation Index. Foram incluídos ensaios clínicos aleatorizados comparando quaisquer apresentações de corticosteróides tópico com quaisquer outras formas de tratamentos da ceratoconjuntivite adenoviral aguda. Resultados: Foram incluídos ensaios clínicos randomizados onde os corticosteróides tópicos foram comparados com placebo no tratamento da ceratoconjuntivite adenoviral aguda. A busca digital inicial identificou quatro ensaios clínicos comparando corticosteroides e placebo no manejo da ceratoconjuntivite epidêmica somando 243 pacientes. Uma revisão sistemática foi realizada. Conclusão: Nenhum estudo mostrou melhora no alívio dos sinais ou sintomas. A prevenção dos infiltrados subepiteliais permanece controversa, mostrando mais comumente um adiamento na história natural da doença do que uma modificação nela. O uso destes colírios deve ser recomendado com cautela e novos ensaios clínicos são necessários para comprovar sua eficácia
Abstract: Introduction: Topical corticosteroids are commonly used in the treatment of acute viral keratoconjunctivitis. It has been suggested the usefulness of corticosteroids in symptomatic relief of the signs of conjunctivitis and / or symptoms and prevention of subepithelial infiltrates. On the other hand, we observed the reported possible side effects, such as the extension of transmission of the virus in vitro, and beside that, clinical trials showing the effectiveness of corticosteroids eye drops. The aim of this study was to compare the use of topical corticosteroids, with any drugs used in clinical trials with placebo. Objective: To assess whether topical corticosteroids are effective and safe for the treatment of adenoviral keratoconjunctivitis to improve symptoms and prevent or minimize complications related to the disease. Design: Systematic review. Methods: We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (which contains the Cochrane Eyes and Vision Group Trials Register), MEDLINE, EMBASE, PubMed and the reference lists of identified trial reports. We used the Science Citation Index to look for articles that cited the relevant studies. We included masked randomized controlled trials in which any form of topical corticosteroid treatment had been compared with placebo in the management of acute adenoviral ceroconjuctivitis. Results: Were included randomized controlled trials in which any form of topical corticosteroid treatment had been compared with placebo in the management of acute adenoviral keratoconjunctivitis. The initial digital search identified 4 clinical trials comparing corticosteroids and placebo in the management of Epidemic keratoconjunctivitis totaling 243 patients. A narrative review was conducted. Conclusion: No study has shown improvement in relief of the signs or symptoms. Prevention of subepithelial infiltrates remains controversial, most commonly showing a delay in the natural history of disease than a change in it. The use of eye drops should be recommended with caution and new clinical trials are needed to prove its effectiveness
Mestrado
Oftalmologia
Mestre em Ciências Médicas
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Books on the topic "Adenoviral"

1

Knapp, Mark. Development of dopamine receptor expressing adenoviral vectors. Ottawa: National Library of Canada, 1997.

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Cassivi, Stephen David. Adenoviral-mediated gene therapy in lung transplantation. Ottawa: National Library of Canada, 1998.

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Forrest, Zoe Darroch. Gene therapy of CNS malignancies using adenoviral vectors and cytotoxic gene systems. Manchester: University of Manchester, 1997.

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Weinrib, Laura M. Cisplatin chemotherapy plus adenoviral p53 gene therapy in EBV-positive and -negative nasopharyngeal carcinoma. Ottawa: National Library of Canada, 2000.

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Weedon, Sarah Jane. Development and characterisation of nitroreductase-expressing adenoviral vectors for enzyme-prodrug gene therapy of cancer. Birmingham: University of Birmingham, 1998.

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James Anthony Edward Harris Latham. PSA promoter driven vectors for gene therapy - construction and testing of tissue specific adenoviral vectors. Birmingham: University of Birmingham, 1999.

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Negrete-Virgen, Juan Alejandro. Manufacture of adenoviral vectors for gene therapy applications: Critical comparison of solvent extraction and adsorption-based processes. Birmingham: University of Birmingham, 2003.

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Chillón, Miguel, and Assumpció Bosch, eds. Adenovirus. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-679-5.

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Doerfler, Walter, ed. Adenovirus DNA. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2293-1.

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Wold, William S. M., and Ann E. Tollefson, eds. Adenovirus Methods and Protocols. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-277-9.

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Book chapters on the topic "Adenoviral"

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Alharbi, Ziyad, and Majed Alkharashi. "Adenoviral Keratoconjunctivitis." In Encyclopedia of Ophthalmology, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-35951-4_745-1.

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Seth, Prem. "Adenoviral Vectors." In Advances in Experimental Medicine and Biology, 13–22. New York, NY: Springer US, 2002. http://dx.doi.org/10.1007/0-306-46817-4_2.

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Alharbi, Ziyad, and Majed Alkharashi. "Adenoviral Keratoconjunctivitis." In Encyclopedia of Ophthalmology, 38–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 2018. http://dx.doi.org/10.1007/978-3-540-69000-9_745.

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Lee, Martin G., Eric J. Kremer, and Michel Perricaudet. "Adenoviral vectors." In Molecular and Cell Biology of Human Gene Therapeutics, 20–32. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0547-7_2.

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Peterson, Per A. "Adenoviral Immune Suppression." In Concepts in Viral Pathogenesis III, 121–29. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4613-8890-6_14.

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Brunetti-Pierri, Nicola, and Philip Ng. "Helper-dependent adenoviral vectors." In Gene Therapy for Autoimmune and Inflammatory Diseases, 193–207. Basel: Springer Basel, 2010. http://dx.doi.org/10.1007/978-3-0346-0165-8_13.

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Havenga, Menzo J. E., Ronald Vogels, Abraham Bout, and Majid Mehtali. "Pseudotyping of Adenoviral Vectors." In Vector Targeting for Therapeutic Gene Delivery, 87–121. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2003. http://dx.doi.org/10.1002/0471234303.ch5.

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Hillenkamp, Jost, Rainer Sundmacher, and Thomas Reinhard. "Treatment of Adenoviral Keratoconjunctivitis." In Essentials in Ophthalmology, 163–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-31226-9_12.

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Parker, Alan L., Angela C. Bradshaw, Raul Alba, Stuart A. Nicklin, and Andrew H. Baker. "Capsid Modification Strategies for Detargeting Adenoviral Vectors." In Adenovirus, 45–59. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-679-5_3.

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Jones, N. C. "Genetic Elements Governing Adenoviral Gene Expression." In Adenovirus DNA, 161–91. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2293-1_5.

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Conference papers on the topic "Adenoviral"

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Wang, Shutao, Amanda Buch, Syed Abid Hussaini, Camilo Acosta, and Elisa Konofagou. "Focused ultrasound facilitated adenoviral delivery for optogenetic stimulation." In 2015 IEEE International Ultrasonics Symposium (IUS). IEEE, 2015. http://dx.doi.org/10.1109/ultsym.2015.0207.

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Oliveira, Daniel Vieira C., Eugenia Costanzi-Strauss, and Bryan E. Strauss. "Abstract B26: AdCDKN2aIRESp53: A bicistronic adenoviral vector for glioblastoma gene therapy." In Abstracts: AACR International Conference held in cooperation with the Latin American Cooperative Oncology Group (LACOG) on Translational Cancer Medicine; May 4-6, 2017; São Paulo, Brazil. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1557-3265.tcm17-b26.

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Kishimoto, Hiroyuki, Yasuo Urata, Toshiyoshi Fujiwara, Michael Bouvet, and Robert M. Hoffman. "Abstract 1454: Telomerase-specific adenoviral labeling and treatment of hepatocellular carcinoma." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1454.

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Gunay, Melih, Evgin Goceri, and Taner Danisman. "Automated Detection of Adenoviral Conjunctivitis Disease from Facial Images using Machine Learning." In 2015 IEEE 14th International Conference on Machine Learning and Applications (ICMLA). IEEE, 2015. http://dx.doi.org/10.1109/icmla.2015.232.

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Saini, Reshu, Jason Warram, Anna Goblirsch Sorace, Heidi Umphrey, Kurt R. Zinn, and Kenneth Hoyt. "Validation of controlled receptor expression using adenoviral techniques and targeted ultrasound imaging." In 2010 IEEE Ultrasonics Symposium (IUS). IEEE, 2010. http://dx.doi.org/10.1109/ultsym.2010.5935763.

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Crosby, Erika J., Gangjun Lei, Junping Wei, Xiao Yi Yang, Tao Wang, Cong-Xiao Liu, H. Kim Lyerly, and Zachary C. Hartman. "Abstract A22: Augmentation of a novel adenoviral vaccine strategy by checkpoint inhibitors." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-a22.

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Zhang, Lingzhi, Farah Hedjran, Christopher Larson, Min Yan, and Tony Reid. "Abstract B50: A novel immunocompetent murine model for replicating oncolytic adenoviral therapy." In Abstracts: AACR Special Conference: The Translational Impact of Model Organisms in Cancer; November 5-8, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1557-3125.modorg-b50.

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Pertzborn, M., S. Pasala, M. Moore, U. K. Chalwadi, R. M. Qaqish, J. Fett, Z. Ghazala, E. Ararat, A. Agarwal, and A. Berlinski. "Diffuse Alveolar Hemorrhage in the Setting of Adenoviral Infection in an Immunocompetent Child." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1993.

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Stoff-Khalili, MA, A. Nedeljkovic-Kurepa, JS Jung, BV Glover, B. Wappenschmidt, K. Rhiem, K. Bosse, et al. "Combination of oncolytic adenoviral therapy with chemotherapy for enhanced breast cancer cell killing." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-2129.

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Del Valle, Paulo Roberto, Daniela B. Zanatta, and Bryan E. Strauss. "Abstract 3539: Modifications of adenoviral structure and genome improves transduction efficiency and transgene expression." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3539.

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Reports on the topic "Adenoviral"

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VonSeggern, Daniel J. Adenoviral Gene Therapy Vectors Targeted to Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada417951.

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Von Seggern, Daniel J. Adenoviral Gene Therapy Vectors Targeted to Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada429389.

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Huang, Shuang. Endothelial Cell-Targeted Adenoviral Vector for Suppressing Breast Malignancies. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada436940.

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Rogers, Buck E. Enhanced Peptide of Prostate Cancer Using Targeted Adenoviral Vectors. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada442988.

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Huang, Shuang. Endothelial Cell-Targeted Adenoviral Vector for Suppressing Breast Tumors. Fort Belvoir, VA: Defense Technical Information Center, April 2003. http://dx.doi.org/10.21236/ada416751.

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Vora, Gary J., Baochuan Lin, Kevin Gratwick, Carolyn Meador, Donald Seto, Anjan Purkayastha, Nikki E. Freed, Kevin Russell, and David Metzgar. Coinfections of Multiple Virulent Adenoviral Species in Previously Vaccinated Patients. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada433544.

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Rogers, Buck E. Enhanced Peptide Radiotherapy of Prostate Cancer Using Targeted Adenoviral Vectors. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada428235.

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Rogers, Buck E. Enhanced Peptide Radiotherapy of Prostate Cancer Using Targeted Adenoviral Vectors. Fort Belvoir, VA: Defense Technical Information Center, June 2003. http://dx.doi.org/10.21236/ada420846.

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Woo, Savio L. Adenoviral Mediated Interleudkin-12 Gene Therapy for Metastatic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, November 2004. http://dx.doi.org/10.21236/ada433855.

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Douglas, Joanne T. Treatment of Primary and Metastatic Breast Cancer by an Armed Replicating Adenoviral Vector. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada430586.

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