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1

Léonard, Nancy Jacynthe. "Ectoparasitism of odonate hosts, host response to parasitism and host sex bias in parasitism." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ36940.pdf.

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De, Hondt Piers. "Guest-host mixtures using novel host-mimicking fluorescent dyes in ferroelectric and flexoelectric liquid crystal hosts." Thesis, University of Southampton, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418076.

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Casey, Abigail Nyree Jane. "The population dynamics of host-host-parasitoid system." Thesis, University of Liverpool, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366395.

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Grundling, Hendrik, and hendrik@maths unsw edu au. "Host Algebras." ESI preprints, 2000. ftp://ftp.esi.ac.at/pub/Preprints/esi896.ps.

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Conocimiento, Dirección de Gestión del. "Ebsco Host." Ebsco, 2004. http://hdl.handle.net/10757/655293.

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Amarillo-Suárez, Angela Rocío. "INFLUENCES OF HOST SIZE AND HOST QUALITY ON HOST USE IN A SEED-FEEDING BEETLE." UKnowledge, 2006. http://uknowledge.uky.edu/gradschool_diss/352.

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For insects that develop inside discrete hosts both host size and host quality constrain offspring growth, influencing the evolution of body size and life history traits. This dissertation examines the effects of host size, host quality, and intraspecific competition on life history and associated traits of populations of the seed-feeding beetle S. limbatus adapted to different host plants, and quantifies population differences in phenotypic plasticity. Populations of the study correspond to divergent clades of the species phylogeography (Colombia and United States). Clades compared differ genetically for all traits when beetles were raised in a common garden. Contrary to expectations from the local adaptation hypothesis, beetles from all populations were larger, developed faster and had higher survivorship when reared in Acacia greggii, the larger host. Two host-plant mediated maternal effects were found: offspring matured sooner, regardless of their rearing host, when their mothers were reared on Pseudosamanea guachapele and females laid larger eggs on Ps. guachapele. These results also show that this species in addition to be a smaller is a low quality host. Females also laid more eggs and sooner on A. greggii than in Ps. guachapele and, laid more eggs on P. guachapele when A. greggii seeds were small than when they were large. Eggs were larger when laid on Ps. guachapele and Parkinsonia florida, two hosts that reduce survivorship in all populations. However, Colombia females laid eggs of similar size on Ps. guachapele and Pa. florida, while USA females laid the largest eggs on Pa. florida. Larger beetles were most affected when larval competition was increased and seed size decreased. The responses of different body sized females were asymmetrical showing significant variation in plasticity. Although differences between populations in growth and life history traits appear to be adaptations to the size and quality of their host plants, host-associated maternal effects, partly mediated by maternal egg size plasticity play an important role in the evolution of S. limbatus’ diet breadth. More generally, phenotypic plasticity mediates the fitness consequences of using novel hosts, likely facilitating colonization of new hosts but also buffering herbivores from selection post-colonization.
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de, Klerk Nele. "Host-bacteria interactions : Host cell responses and bacterial pathogenesis." Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-126425.

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Helicobacter pylori colonizes the human stomach, where it causes gastritis that may develop into peptic ulcer disease or cancer when left untreated. Neisseria gonorrhoeae colonizes the urogenital tract and causes the sexually transmitted disease gonorrhea. In contrast, Lactobacillus species are part of the human microbiota, which is the resident microbial community, and are considered to be beneficial for health. The first host cell types that bacteria encounter when they enter the body are epithelial cells, which form the border between the inside and the outside, and macrophages, which are immune cells that engulf unwanted material.       The focus of this thesis has been the interaction between the host and bacteria, aiming to increase our knowledge of the molecular mechanisms that underlie the host responses and their effects on bacterial pathogenicity. Understanding the interactions between bacteria and the host will hopefully enable the development of new strategies for the treatment of infectious disease. In paper I, we investigated the effect of N. gonorrhoeae on the growth factor amphiregulin in cervical epithelial cells and found that the processing and release of amphiregulin changes upon infection. In paper II, we examined the expression of the transcription factor early growth response-1 (EGR1) in epithelial cells during bacterial colonization. We demonstrated that EGR1 is rapidly upregulated by many different bacteria. This upregulation is independent of the pathogenicity, Gram-staining type and level of adherence of the bacteria, but generally requires viable bacteria and contact with the host cell. The induction of EGR1 is mediated primarily by signaling through EGFR, ERK1/2 and β1-integrins. In paper III, we described the interactions of the uncharacterized protein JHP0290, which is secreted by H. pylori, with host cells. JHP0290 is able to bind to several cell types and induces apoptosis and TNF release in macrophages. For both of these responses, signaling through Src family kinases and ERK is essential. Apoptosis is partially mediated by TNF release. Finally, in paper IV, we showed that certain Lactobacillus strains can reduce the colonization of H. pylori on gastric epithelial cells. Lactobacilli decrease the gene expression of SabA and thereby inhibit the binding mediated by this adhesin.

At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 2: Manuscript. Paper 4: Manuscript.

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8

Hasan, Zehra. "Mycobacterium - host interactions : trafficking of mycobacteria within the host cell." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.264976.

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Fryer, Helen. "Within-host evolution and between-host transmission of HIV variants." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510958.

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Mabbott, Neil A. "Nitric oxide : host-protective or host-destructive during African trypanosomiasis." Thesis, University of Aberdeen, 1995. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU543723.

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The aims of the research presented in this thesis were concerned with investigating the effect of inducible nitric oxide (NO) synthase expression during Trypanosoma brucei infections on both host and parasite. NO was shown to exhibit a potent cytostatic effect on parasite proliferation. Oxyhaemoglobin is a potent scavenger of NO. The cytostatic effects of NO on the trypanosomes were completely prevented through the addition of erythrocytes to the cultures. This implies that in the host blood-stream, NO is unlikely to be involved in the eradication of the parasites. Through the adoptive transfer of suppressor macrophages from T.brucei-infected donor mice to naive recipients, it was demonstrated that NO mediates a suppressive effect on host lymphocyte responses in vivo. Furthermore, suppressor macrophages were shown to have a finite life-span and undergo NO-mediated apoptosis. Evidence also suggested that elevated NO production in the bone marrow of T.brucei -infected mice is likely to play a significant role in the anaemia resulting from T.brucei infection. Experiments demonstrated that a soluble lysate prepared from freeze-thawed blood-stream form T.brucei, activated interferon (IFN)-gamma primed macrophages to express high levels of NO synthase. Experiments also demonstrated that viable blood-stream forms, but not procyclic form trypanosomes, released a soluble factor which in combination with IFN-gamma induced NO synthase. The absolute requirement of IFN-gamma priming for NO synthase activation by T.brucei was studied using macrophages from mutant mice lacking functional IFN-gamma receptors (IFN-gamma R -/- mutant mice). In comparison to macrophages from wild-type mice, cells from IFN-gamma-R-/- mutant mice were unable to produce NO following stimulation in vitro or infection in vivo. Finally, utilising mice with specific immunodeficiencies it was demonstrated that natural killer cells and a/b T-lymphocytes were important sources of IFN-gamma during murine T.brucei infections.
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Nerakis, Eleftherios. "IPv6 host fingerprint." Thesis, Monterey, Calif. : Springfield, Va. : Naval Postgraduate School ; Available from National Technical Information Service, 2006. http://library.nps.navy.mil/uhtbin/hyperion/06Sep%5FNerakis.pdf.

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Thesis (M.S. in Computer Science)--Naval Postgraduate School, September 2006.
Thesis Advisor(s): Geoffrey Xie, John Gibson. "September 2006." Includes bibliographical references (p. 101-102). Also available in print.
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Wright, Susan Clare. "Blazar host galaxies." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.243088.

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Sandfer, Jordan. "Host City, Inishmore." Digital Commons at Loyola Marymount University and Loyola Law School, 2019. https://digitalcommons.lmu.edu/etd/785.

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Wilson, F. D., and H. M. Flint. "Host Plant Resistance." College of Agriculture, University of Arizona (Tucson, AZ), 1985. http://hdl.handle.net/10150/203923.

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Wilson, F. D., and H. M. Flint. "Host Plant Resistance." College of Agriculture, University of Arizona (Tucson, AZ), 1986. http://hdl.handle.net/10150/219754.

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The 1985 and 1986 Cotton Reports have the same publication and P-Series numbers.
Cotton breeding stocks were evaluated for resistance to pink bollworm. Resistance is being transferred into improved agronomic stocks.
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Pugh-Humphreys, R. G. P. "A histopathological investigation of the host inflammatory response and tumour invasion into host tissues following transplantation of ascites tumours within murine hosts." Thesis, University of Aberdeen, 1988. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU020632.

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The LAC and EL4 ascites tumour cells contained both Type A and Type C virions. These virions replicated within the ascites tumour cells. However, neither the tumour cells nor their murine hosts were contaminated with LDV virions. Intraperitoneal transplantation of the LAC and EL4 ascites tumours provoked an oedematous inflammatory response which was accompanied by histological changes within the lymphoid organs of their hosts. Intraperitoneal transplantation of the LAC tumour within MF1 mice induced histopathological changes within the spleens and mediastinal lymph nodes compatible with an immune response. Intraperitoneal transplantation of the EL4 ascites lymphoma within C57BL10 mice culminated in infiltration of EL4 cells into both the spleen and mediastinal lymph nodes. Both the LAC and EL4 ascites tumours induced thymic involution and inflammation within the livers of their murine hosts. Growth of the LAC and EL4 ascites tumours within the peritoneal cavity was accompanied by infiltration of ascites tumour cells into the adipose tissues, pancreas, diaphragm and mesenteries. Whereas successful transplantation of the EL4 ascites lymphoma was achieved in both intraperitoneal and subcutaneous locations, the LAC tumour was only transplanted successfully intraperitoneally but not in subcutaneous locations. Subcutaneous transplantation of EL4 cells within the hind limbs of C57BL10 mice provoked an inflammatory response culminating in angiogenesis and fibroplasia around the transplants. As the growing transplants invaded the surrounding host tissue there was extensive remodelling of the connective tissue matrix followed by degradation of the connective tissue. Host inflammatory cells infiltrated the growing EL4 tumours but ultrastructural studies did not reveal any obvious indications that the host cells exerted an antitumour effect. Instead the macrophages appeared to phagocytose degraded materials within the tumours and therefore behaved as traditional phagocytes. The macrophages within the EL4 tumours had a well developed endoplasmic reticulum and Golgi apparatus, indicative of a secretory status for the cells, and it has been suggested that the macrophages within the EL4 tumours may have a trophic role. Any cytotoxic functions of the macrophages may have been suppressed by tumour derived or host cell derived factors generated within the complex ecosystem of the EL4 tumours. Subcutaneous transplantation of LAC cells within the hind limbs of MF1 mice did not provoke an intense inflammatory response and angiogenesis and fibroplasia was not apparent around the tumours soon after transplantation. It has been speculated that the LAC cells may have suppressed angiogenesis and fibroblast proliferation through production of anti-inflammatory factors. As a consequence of the lack of angiogenesis, the transplanted LAC cells necrosed and only then provoked an inflammatory response from their hosts. The inflammatory response resulted in the formation of scar tissue which gradually replaced the necrosed LAC cells at the site of transplantation. Intraperitoneal transplantation of LAC and EL4 ascites tumour cells provoked an inflammatory response. The inflammatory leucocytes did not appear to impair the viability of the LAC and EL4 cells and although the host inflammatory cells established contacts with the tumour cells they did not appear to sustain any damage and the transplants proliferated to establish ascites tumours. Within the MF1 mice some of the peritoneal macrophages appeared to be damaged and it is suggested that the LAC cells release a factor cytotoxic for macrophages. Within the C57BL10 mice ip injection of the EL4 cells provoked fibrin deposition and the fibrin was phagocytosed by the macrophages. During the course of tumour growth the LAC and EL4 cells bound alpha and gamma globulins to their sufaces and it is believed that these molecules may have afforded the ascites cells 'immunological protection' by masking cell surface antigenic determinants. During the course of the inflammatory response which attended the growth of the ascitic tumours the mesothelial cells covering the mesenteries and adipose tissue underwent a retraction response and exfoliated thus allowing the LAC and EL4 cells to invade these tissues. Whereas ip transplantation of LAC cells into normal MF1 mice resulted in the formation of ascites tumours, ip transplantation of LAC cells into mice which had already injected a subcutaneous transplant of LAC cells, resulted in rejection of the ip transplanted cells. Lymphocytes and macrophages participated in the rejection response and during the course of this event the macrophages became activated.
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Kingdom, Heather. "AY-WB phytoplasma manipulations of host and non-host leafhopper interactions." Thesis, University of East Anglia, 2012. https://ueaeprints.uea.ac.uk/40581/.

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In plant hosts, phytoplasmas induce physiological changes and in both hosts modulate plant-insect interactions. Previously, interactions have been examined with both hosts infected with phytoplasmas. Thus, it is unclear which organism the effect stems from or how phytoplasmas facilitate changes. To investigate phytoplasma manipulations of insect-plant interactions, the model Arabidopsis thaliana was used together with the fully sequenced Aster Yellows phytoplasma strain Witches’ Broom (AY-WB) and vector leafhopper Macrosteles quadrilineatus. I demonstrate possibility to differentiate effects of phytoplasma infection within plant and within insect hosts. To assess root cause of changes, AY-WB secreted effector proteins were examined, their roles within plants, and in manipulations of vector fecundity. One of the 56 secreted AY-WB proteins (SAPs) identified, SAP11, carries a nuclear localization signal and accumulates in plant cell nuclei (Bai et al. 2009). SAP11 is shown to reduce production of plant defense hormone jasmonic acid (Sugio et al. 2011). Stable expression of SAP11 and 3 other SAPs in Arabidopsis increase fecundity of M. quadrilineatus. In addition, phytoplasmas are known to affect non-host insect-plant interactions. Using the same approach, I demonstrate D. maidis survives and produces nymphs only on AY-WB-infected Arabidopsis. Furthermore, I show that whilst SAP11 has no effect on D. maidis survival, 3 other SAPs increase D. maidis survival and oviposition. These data suggest phytoplasmas utilize a suite of effector proteins to manipulate both host and non-host insect-plant interactions. Thus, AY-WB effector functions extend beyond direct interaction with plant hosts; they stimulate generation of insect vectors, and increase chance of uptake by novel insect hosts. This project highlights the value of using a model system in studying phytoplasma manipulation of their hosts and gives insight into development of evolutionary associations between phytoplasmas and vectors.
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Nakase, Yuta. "Manipulation of host behavior and host-associated diversification in strepsipteran insects." Kyoto University, 2014. http://hdl.handle.net/2433/188795.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(人間・環境学)
甲第18357号
人博第670号
新制||人||161(附属図書館)
25||人博||670(吉田南総合図書館)
31215
京都大学大学院人間・環境学研究科相関環境学専攻
(主査)教授 加藤 眞, 教授 松井 正文, 教授 市岡 孝朗
学位規則第4条第1項該当
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Rogers, Lindsay Deborah. "Proteomic analysis of Salmonella-host interactions reveals novel host targets of SopB." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/33597.

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Salmonella enterica is an intracellular bacterium causing gastroenteritis and typhoid fever. Virulence is achieved by two type III secretion systems (T3SS) encoded on Salmonella pathogenicity islands 1 and 2 (SPI-1 and SPI-2) that translocate effector proteins into host cells where they mimic or block host protein function. Effectors translocated by T3SS-1 facilitate internalization of the bacteria into the Salmonella-containing vacuole (SCV), actively stimulate intracellular signaling cascades, and regulate trafficking of the SCV to avoid degradation. A T3SS-1 effector, SopB has been shown to regulate a vast array of host processes important for pathogenesis, but only a few host proteins have been identified as targets of this effector. Here quantitative mass spectrometry-based proteomics and bioinformatics techniques have been employed to identify novel host targets of SopB. Quantitative immunoprecipitation experiments identified Cell division control protein 42 (Cdc42) as a direct SopB binding partner, and the binding site within SopB was localized to residues 117-168. SopB and active Cdc42 were shown to colocalize at membrane ruffles on the host cell surface, and two SopB monoubiquitylation sites were identified. To globally analyze host protein phosphorylation events regulated by SopB, a phosphoproteomics method employing heat and chaotropic denaturation for phosphatase inactivation, peptide fractionation by in-solution isoelectric focusing, and phosphopeptide enrichment by metal oxide chromatography was developed. Quantitative analysis of host protein phosphorylation during the initial 20 minutes post Salmonella infection identified >9000 phosphorylation sites, >2000 of which were dynamic. Signaling cascades downstream of T3SS-1 were compared to those induced by growth factor simulation, revealing stark differences between these signaling mechanisms. Kinase prediction upstream of dynamic phosphosites revealed protein kinases B and C as master host regulators during Salmonella infection, and phosphorylation dynamics following wild type versus ΔsopB infection were compared to identify novel host targets of SopB. This work has greatly improved our understanding of SopB’s activity within host cells. It has also provided the first global view of host protein phosphorylation dynamics during bacterial infection, and developed several techniques that can be widely applied within the field of pathogen-host interactions.
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Rooney, Michael Steven. "Integrative genomic approaches to dissecting host-tumor and host-pathogen immune processes." Thesis, Massachusetts Institute of Technology, 2015. http://hdl.handle.net/1721.1/98722.

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Thesis: Ph. D., Harvard-MIT Program in Health Sciences and Technology, 2015.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 243-263).
Two parallel research efforts were pursued. First, we conducted a systematic exploration of how the genomic landscape of cancer shapes and is shaped by anti-tumor immunity. Using large-scale genomic data sets of solid tissue tumor biopsies, we quantified the cytolytic activity of the local immune infiltrate and identified associated properties across 18 tumor types. The number of predicted MHC Class I-associated neoantigens was correlated with cytolytic activity and was lower than expected in colorectal and other tumors, suggesting immune-mediated elimination. We identified recurrently mutated genes that showed positive association with cytolytic activity, including beta-2- microglobulin (B2M), HLA-A, -B and -C and Caspase 8 (CASP8), highlighting loss of antigen presentation and blockade of extrinsic apoptosis as key strategies of resistance to cytolytic activity. Genetic amplifications were also associated with high cytolytic activity, including immunosuppressive factors such as PDL1/2 and ALOX12B/15B. Our genetic findings thus provide evidence for immunoediting in tumors and uncover mechanisms of tumor-intrinsic resistance to cytolytic activity. Second, we combined measurements of protein production and degradation and mRNA dynamics so as to build a quantitative genomic model of the differential regulation of gene expression in lipopolysaccharide-stimulated mouse dendritic cells. Changes in mRNA abundance play a dominant role in determining most dynamic fold changes in protein levels. Conversely, the preexisting proteome of proteins performing basic cellular functions is remodeled primarily through changes in protein production or degradation, accounting for more than half of the absolute change in protein molecules in the cell. Thus, the proteome is regulated by transcriptional induction for newly activated cellular functions and by protein lifecycle changes for remodeling of preexisting functions.
by Michael Steven Rooney.
Ph. D.
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21

Kapoor, Manisha. "Host-pathogen interaction in metarhizium anisopliae and its insect host helicoverpa armigera." Thesis(Ph.D.), CSIR-National Chemical Laboratory, Pune, 2012. http://dspace.ncl.res.in:8080/xmlui/handle/20.500.12252/2147.

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Bruhin, Dominik. "Haftung des Host-Providers." St. Gallen, 2007. http://www.biblio.unisg.ch/org/biblio/edoc.nsf/wwwDisplayIdentifier/01649094005/$FILE/01649094005.pdf.

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Murphy, Helen. "Host Responses to Campylobacter." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.520636.

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Jones, Amanda L. "Burkholderia pseudomallei, host interactions." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq20744.pdf.

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Murray, Shannon. "Foamy virus-host interactions /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/4987.

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Storer, Andrew John. "Host exploitation in Scolytidae." Thesis, University of Oxford, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335804.

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Morgan, Andrew. "Experimental host-parasite coevolution." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424864.

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Maguire, Glenn E. M. "Optically responsive host systems." Thesis, Queen's University Belfast, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.482023.

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Kundu, Ranajit. "Host alternation in aphids." Thesis, University of East Anglia, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241092.

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Lane, Trevor Glen. "Metalloporphyrins as host molecules." Thesis, University of Liverpool, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314481.

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Dale, Denver Dudley Stanton. "Parasites and host nutrition." Thesis, University of Oxford, 1993. http://ora.ox.ac.uk/objects/uuid:5bc8aebc-fcfa-4301-8d04-4ebc89fb1c8a.

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Quax, Tessa. "Archaeal virus-host interactions." Paris 6, 2013. http://www.theses.fr/2013PA066637.

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The work presented in this thesis provides novel insights in several aspects of the molecular biology of Archaea, Bacteria and their viruses. The archaeal virus Sulfolobus islandicus rod-shaped virus 2 (SIRV2), has a remarkable infection cycle. Infection with SIRV2 results in the formation of large virus associated pyramids (VAPs) on the host cell surface. The pyramids open during the final step of the infection cycle, to allow the release of virions. This virus release mechanism is unique. The VAPs are formed by self-assembly of one virus-encoded protein, PVAP. VAPs exist as discrete particles, and are baseless pyramids with heptagonal perimeter. The assembly process of the VAPs is described, based on cryo-electron tomography experiments and mutational analysis of PVAP. VAPs consists of two layers of which the outer one continuous with the cell membrane. PVAP expression in bacterial and eukaryotic cells resulted in VAP formation on nearly all membranes, demonstrating that PVAP serves as a universal membrane remodeling system, which might be exploited for biotechnological purposes. Whole transcriptome sequencing allowed determination of a global map of virus and host gene expression during the infection cycle. Host genes involved in anti-viral defence are activated (i. E. CRISPR-Cas and toxin anti-toxin systems). The multi-subunit protein complexes crucial for CRISPR anti-viral defence have an uneven stoichiometry and are encoded on operons. It is shown that differential translation is a key determinant of modulated expression of genes clustered in operons and that codon bias generally is the best in silico indicator of unequal protein production
Le travail présenté dans cette thèse donne un nouveau regard sur plusieurs aspects de biologie moléculaire des archées, des bactéries et de leurs virus. Le virus Sulfolobus islandicus rod-shaped 2 (SIRV2) a un cycle d’infection remarquable. L’infection par SIRV2 aboutit à la formation sur la surface de la cellule hôte de grandes structures pyramidales associées à ce virus (VAP). Ce mécanisme de libération du virus SIRV2 est unique. Les VAPs sont formées par l’auto-assemblage de la protéine PVAP codée par le virus. Les VAPS peuvent être isolées sous forme de structures compactes et correspondent à des pyramides heptagonales creuses. Le processus d’assemblage des VAPs est décrit, d’après des expériences de cryo-tomographie et d’analyse mutationnelle de PVAP. Les VAPS sont constituées de deux couches dont celle extérieure continue avec la membrane cellulaire. L’expression des PVAP dans les cellules bactériennes et eucaryotiques conduit à la formation de VAPs sur presque toutes les membranes, ce qui démontre que PVAP sert comme un système universel de remodelage des membranes, qui pourrait être utilisé à des fins biotechnologiques. Le séquençage du transcriptome a permis la détermination d’une carte générale de l’expression génique du virus et de l’hôte pendant le cycle d’infection. Les gènes de l’hôte impliqués dans la défense anti-virale sont activés (systèmes CRISPR-Cas et toxine-antitoxine). Il a été démontré que la traduction différentielle est une clef déterminante de l’expression modulée des gènes groupés en opérons et que le biais de codon est généralement le meilleur indicateur in silico de production inégale de protéines
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Fraser, Liana. "Southern Host Organizations: At the Forefront of Discussions on International Volunteerism." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39482.

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Volunteers, governments, agencies and organizations from the North have too often defined the benefits and limitations of international volunteer programs without incorporating the perspectives of the organizations they seek to help. In fact, scholars and practitioners have relied on Northern experiences to develop a critical analysis of this development practice. As the experiences of the South are often absent from the conversations about international volunteerism, the goal of this thesis is to leverage the voices and the stories of Southern hosts to further understand the impact of international volunteerism. The research draws on the experiences of host organizations in Uganda. The interviewed participants are Ugandans who have worked with international volunteers to address various development issues. A review of the existing literature on international volunteerism, combined with the field research, support the analysis of the benefits and limitations of international volunteerism from the perspectives of host organizations. It also enables an exploration of the agency of volunteerism and determines key principles to empower host organizations and their employees. Thus, the analysis establishes the following conclusions: international volunteers are valuable actors for Southern hosts; volunteer programs must consider the impact, the challenges and the recommendations identified by host organizations and their communities; international volunteers enable alternative voices to be heard; and volunteerism fosters cooperation and partnerships within the Global South.
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Camp, Jeremy Vann. "Host attraction and host selection in the family Corethrellidae (Wood and Borkent) (Diptera)." Click here to access thesis, 2006. http://www.georgiasouthern.edu/etd/archive/fall2006/jeremy_v_camp/camp_jeremy_v_200608_ms.pdf.

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Thesis (M.S.)--Georgia Southern University, 2006.
"A dissertation submitted to the Graduate Faculty of Georgia Southern University in partial fulfillment of the requirements for the degree Master of Science" ETD. Includes bibliographical references (p. 64-68) and appendix.
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Ofong, Anthony Ukaobasi. "Rosellinia ring dying of Salix repens L. : host range; and host-parasite interactions." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279992.

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Perez, Belinda. "Host innate response and virus-host cell interactions in avian influenza virus infection." Thesis, University of Nottingham, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.606257.

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Highly pathogenic avian influenza (HP AI) H5Nl viruses cause devastating fatal disease in chickens, reaching nearly 100% mortality rate within 48 hours. In contrast, ducks show little or no clinical signs. This suggests that there are host species-specific differences in the innate immunity beMeen these two species. Large quantities of HP Al H5Nl viruses have been reported in skeletal muscle of infected chickens and ducks. An in vitro model comprising primary skeletal muscle cells from these two avian species was established to study host immune response 'to avian influenza. Infection with a low pathogenicity avian influenza (LP AI) virus in differentiated chicken muscle cells resulted in a vigorous induction of interferon-fJ and several interferon-inducible genes while two HP Al H5N 1 viruses effectively inhibited this antiviral response. Duck muscle cells did not appear to produce large amounts of type 1 interferons independent of the virus used.
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Beswetherick, John T. "An ultrastructural study of host and non-host resistance reactions in plant cells." Thesis, Open University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292658.

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38

Sharma, Anil. "Development of a host vulnerability checking tool and data analysis of host vulnerabilities." College Park, Md. : University of Maryland, 2004. http://hdl.handle.net/1903/1878.

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Thesis (M.S.) -- University of Maryland, College Park, 2004.
Thesis research directed by: Dept. of Mechanical Engineering. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
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Ng, Seang Khi Preston. "The Role of Distinct Host Glycans in the Evolution of Host Adapted Pathogens." Thesis, Griffith University, 2014. http://hdl.handle.net/10072/365445.

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Glycans are carbohydrate structures coating the cell surface of virtually all nucleated cells of vertebrates. A crucial function of glycans is in cell interaction and recognition, which is constantly exploited by bacteria and viral pathogens as targets for toxins, and as a receptor to aid recognition of and adhesion to host cells. Sialic acids, a 9-carbon compound commonly added as a terminal sugar on glycoconjugates is crucial to both bacteria and viruses causing a successful infection. Bacterial pathogens utilize sialic acids as a component of LOS and capsule, both key virulence factors. The decoration of the bacterial cell surface with sialic acid glycoconjugates has two roles; first, to mimic host glycans to evade the host immune system, second, in reducing the efficiency of complement mediated lysis and opsonophagocytosis. Several key bacterial pathogens including Haemophilus influenzae and Pneumococcus also utilize sialic acids as a carbon source. In viruses, host sialic acids glycoconjugates act as a receptor for viral recognition and adherence to host cells. In the case of influenza A virus, a viral neuraminidase is required to cleave and release newly formed viral particles from infected host cell. This thesis investigates the role of sialic acid glycoconjugates in pathogenesis to increase the understanding of sialic acid biology in human host adapted pathogens. The role sialic acids play in pathogenicity is investigated in the major human pathogens; non-typeable Haemophilus influenzae (NTHi) and Neisseria meningitidis and in human influenza A viral strains.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
Institute for Glycomics
Science, Environment, Engineering and Technology
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40

Bugila, Abdalbaset Abusalah Ali. "Host-parasitoid relationships of Anagyrus sp. near pseudococci (Girault), (Hymenoptera, Encyrtidae), as a basis to improve biological control of pest mealybugs (Hemiptera, Pseudococcidae)." Doctoral thesis, ISA/UL, 2014. http://hdl.handle.net/10400.5/7341.

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Doutoramento em Engenharia Agronómica - Instituto Superior de Agronomia
The host-parasitoid relationships of Anagyrus sp. nr. pseudococci were investigated, including host selection behavior, host defenses, host suitability and parasitoid functional response in relation to five mealybug species with different phylogenetic relationships and geographical origins: i) a Mediterranean native species, Planococcus ficus, with a long co-evolutionary history with the parasitoid; ii) three alien species, Planococcus citri, Pseudococcus calceolariae and Pseudococcus viburni, with a more recent co-evolutionary history; and iii) a fourth alien species, Phenacoccus peruvianus, with no previous common history with the parasitoid. The parasitoid recognized as potential hosts and complete development in all five mealybug species, but showed a clear preference for Planococcus spp. Host suitability of the studied mealybugs seems to fit a phylogenetic/biogeographic trend, showing the highest level in Pl. ficus and its closely related congener Pl. citri, followed by the Australasian Ps. calcelolariae, and the Neotropical Ps. viburni and Ph. peruvianus. The functional response of the parasitoid varied between host species, with a type II and type III responses observed for Ps. calceolariae and Pl. ficus, respectively. The results suggest that A. sp. nr. pseudococci has a broader host range and a more generalist behavior in comparison with other Anagyrus species.
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41

Hopkins, Skylar R. "Multi-scale Transmission Ecology: How Individual Host Characteristics, Host Population Density, and Community Structure Influence Transmission in a Multi-host Snail Symbiont System." Diss., Virginia Tech, 2017. http://hdl.handle.net/10919/85567.

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We live in an era of global change, where emerging infectious diseases such as Ebola, Zika, bird flu, and white nose syndrome are affecting humans, wildlife, and domesticated species at an increasing rate. To understand and predict the dynamic spread of these infectious agents and other symbionts through host populations and communities, we need dynamic mathematical models that accurately portray host-symbiont transmission. But transmission is an inherently difficult process to measure or study, because it is actually a series of interacting processes influenced by abiotic and biotic factors at multiple scales, and thus empirical tests of the transmission function within epidemiological models are rare. Therefore, in this dissertation, I explore factors at the individual, population, and community-levels that influence host contact rates or symbiont transmission success in a common snail-symbiont system, providing a detailed description of the multi-faceted nature of symbiont transmission. From a review of the ecological literature, I found that most models assume that transmission is a linear function of host population density, whereas most empirical studies describe transmission as a nonlinear function of density. I then quantified the net nonlinear transmission-density relationship in a system where ectosymbiotic oligochaetes are directly transmitted among snail hosts, and I explored the ecological mechanisms underlying the nonlinear transmission-density relationship observed in the field via intraspecific transmission success and contact rate experiments in the laboratory. I found that the field results could be explained by heterogeneity in transmission success among snails with different characteristics and nonlinear contact-density relationships caused by non-instantaneous handling times. After I 'unpacked'population-level transmission dynamics into those individual-level mechanistic processes, I used this same approach to examine higher-level ecological organization by describing the mechanistic underpinnings of interspecific or community-level transmission in the same snail-symbiont system. I found that low interspecific transmission rates in the field were the product of opposing interactions between high population densities, high prevalences of infection, and very low interspecific transmission success caused by strong symbiont preferences for their current host species. Unpacking transmission in this way resulted in one of the most detailed empirical studies of transmission dynamics in a wildlife system, and yielded many surprising new insights in symbiont ecology that would not have been discovered with a purely phenomenological or holistic view of transmission. Though simple, linear, and holistic epidemiological models will always be important tools in disease ecology, 'unpacking'transmission rates and adding heterogeneity and nonlinearity to models, as I have done here, will become increasingly important as we work to maximize model prediction accuracy in this era of increased disease emergence.
Ph. D.
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42

Howell, Jeffrey L. "Host location and host-associated divergence in parasitoids of the gall midge, Asteromyia carbonifera." Wright State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=wright1464032496.

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43

Kreutzfeldt, Kaj Maximiliane. "Characterisation of host determinants that influence host-pathogen interaction during infection with Mycobacterium tuberculosis." Thesis, University of Brighton, 2015. https://research.brighton.ac.uk/en/studentTheses/9c2b2ddd-2ae7-4a8e-934a-a7e1dd28369a.

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Tuberculosis is endemic in the Gambian population, in which the magnitude of mycobacterial antigen-driven interferon-γ (IFN-γ) response in BCG vaccinated neonates has been linked to regions on the genome that encode the RIP2 kinase, the toll-like receptor 4 adapter protein MD-2 and the NF-κB subunit NF-κB2 by genome-wide linkage analysis. The receptor interacting protein (RIP2) is an essential kinase downstream of the nucleotide-binding oligomerization domain-containing protein 1 (NOD1) and NOD2, both intracellular pattern-recognition receptors for peptidoglycan moieties that induce activation of NF-κB. To establish the significance of RIP2 kinase during Mycobacterium tuberculosis infection, RIP2 was depleted in THP-1- derived macrophages using small interfering RNAs. In the absence of RIP2, THP- 1-derived macrophages secreted significantly reduced levels of the proinflammatory cytokine IL-1β upon infection with M. tuberculosis.
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Swiecki, Melissa K. "Bacillus anthracis spore-host interactions." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. http://www.mhsl.uab.edu/dt/2007p/swiecki.pdf.

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45

Persson, Christer. "The Olympic host selection process /." Luleå, 2000. http://epubl.luth.se/1402-1544/2000/37/index.html.

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46

Tusell, Sonia M. "Coronavirus receptors and host range /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2007.

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Thesis (Ph.D. in Molecular Biology) -- University of Colorado Denver, 2007.
Typescript. Includes bibliographical references (leaves 198-221). Free to UCD affiliates. Online version available via ProQuest Digital Dissertations;
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47

Pollok, Richard. "Cryptosporidium parvum : host-parasite interactions." Thesis, Queen Mary, University of London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402442.

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48

Norton, Alice Joan. "Inter-specific host-schistosome interactions." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433669.

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49

Joiner, A. "Studies of guest-host chemistry." Thesis, University of Liverpool, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.384345.

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50

Stretton, Clare. "Alphaviruses and host cell interactions." Thesis, University of Liverpool, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441742.

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