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Dissertations / Theses on the topic 'Unresponsiveness'

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1

Losson, B. J. "Immunological unresponsiveness to gastrointestinal nematodes." Thesis, University of Cambridge, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372886.

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2

Mahmood, Khalid Hassan. "The immunological unresponsiveness of badgers to mycobactera." Thesis, University College London (University of London), 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319747.

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3

Rankin, Alasdair Menzies. "An investigation of CD28/B7 family binding interactions and costimulation, using immunoglobulin fusion proteins." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360469.

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4

Tavernor, Angela Susan. "The immune unresponsiveness of the lamb and infection with Haemonchus contortus." Thesis, University of Cambridge, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292862.

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5

Khalaf, Rana. "Nontypeable Haemophilus influenzae-induced inflammation, corticosteroids unresponsiveness and functional polarisation in COPD alveolar macrophages." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/nontypeable-haemophilus-influenzaeinduced-inflammation-corticosteroids-unresponsiveness-and-functional-polarisation-in-copd-alveolar-macrophages(bcbe33db-3d70-4c0b-b39d-805d448ef693).html.

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COPD is a chronic inflammatory disease of the airways where many patients have recurrent lower airway bacterial infection, most commonly nontypeable Haemophilus influenzae (NTHi). Corticosteroids are commonly used anti-inflammatory drugs in COPD with limited clinical benefit. Previous studies focused on corticosteroid responsiveness in COPD did not consider the role of airway NTHi infection. Alveolar macrophages are the main inflammatory cells in COPD pathogenesis, a shift in their phenotype was highlighted in COPD patients. Some bacteria can modify alveolar macrophage phenotype to persist in the lower airways. I have optimised a clinically relevant in vitro model of NTHi infection; human alveolar macrophages were stimulated with an increasing load of live NTHi clinical isolate (R2846). NTHi provoked time-dependent release of TNF-α, IL-6, CXCL8 and IL-10 from alveolar macrophages, which was correlated with bacterial growth, lysis and phagocytosis in the model. Furthermore, NTHi load was inversely correlated with IL-10 release. These findings suggest that NTHi infection is a dynamic inflammatory process in human alveolar macrophages and pointed to the possible role of IL-10 in the NTHi persistence in the lower airways. NTHi-induced cytokines in alveolar macrophages showed reduced corticosteroid responsiveness, CXCL8 was particularly corticosteroid unresponsive cytokine. NTHi-induced glucocorticoid receptor (GR) phosphorylation at ser 226 residue, which would encourage GR nuclear exportation. This might be one possible mechanism of reduced corticosteroid response in the model. In line with the latter finding, NTHi impaired the corticosteroid-induced GR nuclear localisation, which was partially reversed by p38 MAPK inhibitor (BIRB-796). These results suggest the role of NTHi in corticosteroid unresponsiveness in COPD alveolar macrophages. NTHi-induced cytokine release in alveolar macrophages was mediated by NF-κB, p38 and ERK MAPK pathways. Combination of corticosteroid (dexamethasone) with p38 and ERK MAPK inhibitors (BIRB-796 and AZD6244 respectively) showed a potential synergistic anti-inflammatory effect in the model. Therefore, inhibitors of MAPK pathways might serve as future anti-inflammatory therapies in NTHi-infected COPD patients. NTHi in vitro infection caused upregulation of the pro-inflammatory (TNF-α, CXCL8, CD38) and the anti-inflammatory (IL-10) markers’ mRNA levels in COPD alveolar macrophages. Meanwhile, NTHi downregulated the antigen-presentation molecule (HLA-DR) and the scavenger receptors (CD14, CD36, CD163 and CD206) mRNA levels in COPD alveolar macrophages. Moreover, sputum macrophages from NTHi-infected stable COPD patients showed lower mRNA levels of CD36 and HLA-DR. These findings suggest that the NTHi modification of alveolar macrophage functions, especially antigen presentation and efferocytosis, might be a possible mechanism of NTHi chronic infection and COPD disease progression.
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6

Bell, Yvonne Louise. "An investigation into the induction of specific immunological unresponsiveness using donor major histompatibility complex antigens." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386871.

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7

Quigley, R. L. "Investigation of the mechanism of induction of immunologic unresponsiveness to renal allografts by blood transfusion." Thesis, University of Oxford, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233514.

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8

Madsen, Joren Christian. "A genetic analysis of antigen-induced specific unresponsiveness using recipient cells transfected with donor MHC genes." Thesis, University of Oxford, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302818.

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9

Fry, Jeremy. "Delivery of a donor MHC class I gene using a recombinant adenovirus to induce immunological unresponsiveness." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343471.

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10

Niimi, Masanori. "An investigation to determine the ability of allogeneic resting B cells to induce specific unresponsiveness in vivo." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244813.

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11

Foster, Serene. "Induction of immunologic unresponsiveness by class I MHC antigen : a study in a rat renal allograft model." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.279990.

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12

Billing, John Stephen. "Strategies for the induction of unresponsiveness to allografts using bone marrow as a vehicle for donor alloantigen delivery." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393427.

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13

Åkerman, Daniel. "Politics of Unresponsiveness : The effects of issue salience and party convergence on radical right-wing success in Sweden." Thesis, Uppsala universitet, Statsvetenskapliga institutionen, 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-417793.

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14

Mazur, Artur, Katrin Köhler, Markus Schülke, Mandy Skunde, Mariusz Ostański, and Angela Hübner. "Familial Glucocorticoid Deficiency Type 1 due to a Novel Compound Heterozygous MC2R Mutation." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-134512.

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Objective: Description of the clinical, biochemical and genetic features of a Polish patient with familial glucocorticoid deficiency. Methods: Detailed clinical investigation, hormonal analysis and sequencing of the coding region of the melanocortin 2 receptor (MC2R) gene in this patient. Results: We report on a 3-month-old boy with familial glucocorticoid deficiency who presented at the age of 3 months with skin hyperpigmentation, muscle weakness, mild jaundice and constipation. Hormonal analyses revealed high ACTH and TSH serum concentrations, low serum cortisol concentration along with normal blood electrolytes. On hydrocortisone supplementation, the disease symptoms disappeared and the child recovered completely. His physical and mental development progresses normally. Genetic analysis disclosed a novel compound heterozygous MC2R mutation p.Leu46fs and p.Val49Met. Conclusion: The heterozygous p.Leu46fs mutation adds to the small number of MC2R nonsense mutations and is the first frameshift mutation within the first transmembrane domain of the receptor. According to molecular modeling the Val49Met mutation results in a structural change of the first transmembrane domain and in a potential novel interaction of the transmembrane domains I and VII
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich
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15

Ávila, Faleolo Iturbide, and Garduño Francisco Javier López. "El valor pronostico de la escala de puntaje de Goma de Full Outline of Unresponsiveness Score (four) en el Traumatismo Cráneo Encefálico en pacientes ingresados a la Unidad de Choque del Centro Médico Lic. Adolfo López Mateos." Tesis de Licenciatura, Medicina-Quimica, 2013. http://ri.uaemex.mx/handle/123456789/13849.

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16

Mazur, Artur, Katrin Köhler, Markus Schülke, Mandy Skunde, Mariusz Ostański, and Angela Hübner. "Familial Glucocorticoid Deficiency Type 1 due to a Novel Compound Heterozygous MC2R Mutation." Karger, 2008. https://tud.qucosa.de/id/qucosa%3A27575.

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Objective: Description of the clinical, biochemical and genetic features of a Polish patient with familial glucocorticoid deficiency. Methods: Detailed clinical investigation, hormonal analysis and sequencing of the coding region of the melanocortin 2 receptor (MC2R) gene in this patient. Results: We report on a 3-month-old boy with familial glucocorticoid deficiency who presented at the age of 3 months with skin hyperpigmentation, muscle weakness, mild jaundice and constipation. Hormonal analyses revealed high ACTH and TSH serum concentrations, low serum cortisol concentration along with normal blood electrolytes. On hydrocortisone supplementation, the disease symptoms disappeared and the child recovered completely. His physical and mental development progresses normally. Genetic analysis disclosed a novel compound heterozygous MC2R mutation p.Leu46fs and p.Val49Met. Conclusion: The heterozygous p.Leu46fs mutation adds to the small number of MC2R nonsense mutations and is the first frameshift mutation within the first transmembrane domain of the receptor. According to molecular modeling the Val49Met mutation results in a structural change of the first transmembrane domain and in a potential novel interaction of the transmembrane domains I and VII.
Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.
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17

Hsu, Yu-Che, and 許毓哲. "Senescence Causes Cellular Unresponsiveness to IFN-γ Immunosurveillance in Phagocytes." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/qskjnd.

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18

Anhalt, Cindy. "Evaluation of responsiveness/unresponsiveness patterns to GLPhe in inbred and congenic mouse strains." 1987. http://hdl.handle.net/1993/15426.

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19

陳茂良. "The effect of dendritic cells stimulation on immunosuppressive cytokines-induced T-cell unresponsiveness." Thesis, 1999. http://ndltd.ncl.edu.tw/handle/30701221656788556896.

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20

Chung, I.-Hsin, and 鍾依新. "Epigenetic mechanisms of selective IFN-γ unresponsiveness of HLA class I alleles in melanoma." Thesis, 2011. http://ndltd.ncl.edu.tw/handle/fwd694.

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碩士
國立清華大學
分子與細胞生物研究所
99
Tumor immune evasion plays an important role in cancer cell progression, and lack of human MHC class I molecules HLA on the surface of cancer cells renders them insensitive to recognition and destruction by CD8+ cytotoxic T lymphocytes (CTLs). It has been hypothesized that lack or downregulation of the expression of single or multiple components of MHC class I complex and/or of the antigen processing machinery (APM) prevents proper assembly and transport of HLA class I to the surface of cancer cells, and therefore contributes to cancer cell escape from CD8+ CTL immune surveillance. Understanding the mechanisms will facilitate the development of rational, patient-based immunotherapy with improved clinical efficacy. We have analyzed a model melanoma cell line COPA-159 with marked total HLA class I down-regulation, which had been derived from a patient who failed both chemotherapy and T cell-based immunotherapy with a highly progressive clinical course. Immunohistochemical staining, flow cytometry and Western blotting revealed deficient HLA-A, HLA-B,-C, TAP1, TAP2 and tapasin expression in COPA-159 cells. Treatment of COPA-159 cells with IFN-gamma?nincreased the expression of HLA-B,-C and TAP but not that of HLA-A and tapasin. However, combined treatment with IFN-gamma and the DNA-demethylating agent 5-aza-2’deoxycytidine (5-aza-dC) restored the expression of HLA-A, whereas combined treatment with IFN-gamma and with or without 5-aza-dC and the histone deacetylase inhibitor, trichostatin A (TSA) or IFN-alpha 2B suppressed the HLA-A re-expression and treatment with TNF-alpha had no effect. Notably, marked STAT and HLA-A3 promoter activity was detected in IFN-gamma-treated COPA159 cells by luciferase reporter gene assay, indicating that the HLA-A gene is silenced in COPA-159 not by transcription factor-mediated mechanisms but by epigenetic mechanisms targeting the endogenous HLA-A gene promoter. Using methylation-specific PCR (MSP), bisulfite sequencing (BSP), pyrosequencing with primers designed to determine the methylation status of the COPA-159 HLA-A gene promoter, we found that combined IFN-gamma and 5-aza-dC treatment correlated with a decrease in CpG methylation in the HLA-A gene promoter in COPA-159 cells with re-expressed HLA-A. In addition, chromatin immunoprecipitation assay revealed that histone H3 is acetylated, and H3 lysine (K) 4 is dirmethylated at the HLA-A promoter in COPA-159 cells with obvious re-expressed HLA-A. These data suggest that promoter hypermethylation and chromatin modification represent two mechanisms leading to HLA class I down-regulation in COPA159 cells. Interestingly, HLA class I down-regulation did not make COPA-159 cells more sensitive to NK cell-mediated cytolysis, since COPA-159 cells resisted NK cell killing in a cytotoxicity assay. The resistance to NK cell killing correlated with the lack of NK cell-activating ligand MIC expression in COPA-159 cells. Taken together, COPA-159 cells have developed strategies to escape both CTL- and NK cell-mediated immune attacks through both IFN-gamma-correctable and -uncorrectable epigenetic mechanisms
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21

Feijó, Leonor dos Inocentes. "Avaliação do Estado de Consciência. Tradução e Validação da Escala FOUR (Full Outline of UnResponsiveness)." Dissertação, 2015. https://repositorio-aberto.up.pt/handle/10216/90400.

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22

Feijó, Leonor dos Inocentes. "Avaliação do Estado de Consciência. Tradução e Validação da Escala FOUR (Full Outline of UnResponsiveness)." Master's thesis, 2015. https://repositorio-aberto.up.pt/handle/10216/90400.

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23

"Associations between Openness, Relationship Satisfaction, and Perceived Partner Unresponsiveness and Topic Avoidance: Moderating Effects of Dogmatism for Individuals in a Romantic Relationship." Master's thesis, 2019. http://hdl.handle.net/2286/R.I.54823.

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abstract: Individuals in a romantic relationship may avoid discussing certain topics with their partner, often to avoid relational and emotional risk. This strategy is known as topic avoidance and may be an important factor for individuals in turbulent romantic relationship to consider due to the importance of communicating with a partner. The associations between characteristics such as openness, relationship satisfaction, and perceived partner unresponsiveness, and topic avoidance have not been directly studied within dogmatism literature. However, dogmatism, defined as a person’s relative openness (or closedness) to new information, may be an important construct associated with topic avoidance that strengthens the associations between perceived partner unresponsiveness, and topic avoidance, and weakens the association between openness, relationship satisfaction, and topic avoidance. Using data from 334 individuals in romantic relationships, results revealed that perceived partner unresponsiveness was positively associated with State of the Relationship, relationship satisfaction was positively associated with Conflict-Inducing and Negative Life Experiences, such that as scores on relationship satisfaction and perceived partner unresponsiveness increased, topic avoidance scores also increased. Openness was not associated with Topic Avoidance. Additionally, as predicted, dogmatism moderated the association between relationship satisfaction and State of the Relationship Topic Avoidance, the associations between perceived partner unresponsiveness and State of the Relationship Topic Avoidance and Negative Life Experiences Topic Avoidance. This research has important implications for clinicians working with individuals who present with relational concerns and exhibit dogmatic behavior. Limitations and future directions are discussed.
Dissertation/Thesis
Masters Thesis Counseling 2019
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