Dissertations / Theses: 'Endocrine'

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Monges-Ranchin, Geneviève. "Les cellules endocrines de l'estomac et leur pathologie." Aix-Marseille 2, 1987. http://www.theses.fr/1987AIX21917.

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Sharma, Vinay. "Endocrine and non-endocrine factors affecting the outcome of assisted conception." Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244126.

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Delgado, Verdugo Alberto. "Genetic Aspects of Endocrine Tumorigenesis : A Hunt for the Endocrine Neoplasia Gene." Doctoral thesis, Uppsala universitet, Endokrinkirurgi, 2014. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-224111.

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Endocrine tumors arise from endocrine glands. Most endocrine tumors are benign but malignant variants exist. Several endocrine neoplasms display loss of parts of chromosome 11 or 18, produce hormones and responds poorly to conventional chemotherapeutics. The multiple endocrine neoplasia syndromes are mainly confined to endocrine tumors. This opens the question if there exists a single or several endocrine tumor genes. The aim of the study was to describe genetic derangements in endocrine tumors. Paper I: Investigation of mutational status of SDHAF2 in parathyroid tumors. SDHAF2 is located in the proximity of 11q13, a region that frequently displays loss in parathyroid tumors. We established that mutations in SDHAF2 are infrequent in parathyroid tumors. Paper II: Study of SDHAF2 gene expression in a cohort of benign pheochromocytomas (PCC) (n=40) and malignant PCC (n=10). We discovered a subset of benign PCC (28/40) and all malignant PCC (10/10) with significantly lower SDHAF2 expression. Benign PCC with low SDHAF2 expression and malignant tumors consistently expressing low levels of SDHAF2 were methylated in the promoter region. SDHAF2 expression was restored in vitro after treatment with 5- aza-2-deoxycytidine. Paper III: HumanMethylation27 array (Illumina) covering 27578 CpG sites spanning over 14495 genes were analyzed in a discovery cohort of 10 primary small neuroendocrine tumors (SI-NETs) with matched metastases. 2697 genes showed different methylation pattern between the primary tumor and its metastasis. We identified several hypermethylated genes in key regions. Unsupervised clustering of the tumors identified three distinct clusters, one with a highly malignant behavior. Paper IV: Loss of chromosome 18 is the most frequent genetic aberration in SI-NETs. DNA from SI-NETs were subjected to whole exome capture sequencing and high resolution SNP array. Genomic profiling revealed loss of chromosome 18 in 5 out of 7 SI-NETs. No tumor-specific somatic mutation on chromosome 18 was identified which suggests involvement of other mechanisms than point mutations in SI-NET tumorigenesis. Paper V: The cost for diagnostic genetic screening of common susceptibility genes in PCC is expensive and labor intensive. Three PCC from three patients with no known family history were chosen for exome capture sequencing. We identified three variants in known candidate genes. We suggest that exome-capture sequencing is a quick and cost-effective tool.

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Симоненко, Наталія Олександрівна, Наталия Александровна Симоненко, Nataliia Oleksandrivna Symonenko, and N. Vasko. "Endocrine system and disorders." Thesis, Вид-во СумДУ, 2009. http://essuir.sumdu.edu.ua/handle/123456789/16782.

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Kohler, Romain. "Collection de cas d'auto-enseignement en imagerie des glandes endocrines (thyroïde, parathyroïdes, surrénales, pancréas endocrine) /." Genève : [s.n.], 2006. http://www.unige.ch/cyberdocuments/theses2006/KohlerR/these.pdf.

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Martínez, Rodríguez María Ángeles. "Endocrine disruption assessment: exposure, biomonitoring and potential activity of widespread endocrine disruptors during pregnancy and early stages of life." Doctoral thesis, Universitat Rovira i Virgili, 2020. http://hdl.handle.net/10803/669420.

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Els disruptors endocrins (DEs) són substàncies o mescles exògenes que alteren les funcions de sistema endocrí i, en conseqüència, causen efectes adversos per a la salut en un organisme intacte, o la seva progènie, o (sub) poblacions. Entre aquests DEs, hi ha un grup que es caracteritza per estar àmpliament estès i present en envasos i materials en contacte amb aliments. L'envasament protegeix de les alteracions, però es poden donar migracions de les substàncies químiques als aliments. Tenint en compte això, s'han seleccionat els següents compostos químics: bisfenols (BPA, BPS i BPF); plastificants ftalats i no ftalats; substàncies perfluorooalquiladas (PFOS i PFOA) i tetrabromobisfenol A (TBBPA). La hipòtesi general d'aquesta tesi és que hi ha exposició durant les etapes primerenques de la vida. Aquesta exposició pot causar efectes adversos. Per tant, l'objectiu general d'aquesta tesi és avaluar els nivells d'exposició a diferents DEs en una població de dones embarassades (EXHES) a Tarragona, Espanya. A més a més, estudiar com aquests químics poden afectar el desenvolupament cel·lular. Per abordar-lo, es va estimar l'exposició prenatal als DEs mitjançant el model integrat de dosimetria externa i interna (PBPK). Seguit per la biomonitorització d'aquests químics en diferents matrius (orina, sang, llet materna), i de la reconstrucció i simulació de l'exposició. finalment, es van realitzar estudis in vitro per avaluar l'activitat potencial endocrina de DE àmpliament distribuïts. Els resultats d'aquesta tesi confirmen que l'exposició a DEs pot observar-se en poblacions adultes i en el període prenatal. Aquesta exposició pot causar efectes adversos. Per aquesta raó, han d'establir-se alternatives segures als DEs. Seguit d’unes regulacions concises respecte a l'exposició de la població més vulnerable.
Los disruptores endocrinos (DEs) son sustancias o mezclas exógenas que alteran las funciones del sistema endocrino y, en consecuencia, causan efectos adversos para la salud en un organismo intacto, o su progenie, o (sub)poblaciones. Entre estos DEs, hay un grupo que se caracteriza por estar ampliamente extendido y presentes en envases y materiales en contacto con alimentos. El envasado protege al producto de las alteraciones, pero se pueden dar migraciones de las substancias químicas a los alimentos. En base a esto, se han seleccionado los siguientes compuestos químicos: bisfenoles (BPA, BPS y BPF); plastificantes ftalatos y no ftalatos; sustancias perfluorooalquiladas (PFOS y PFOA) y tetrabromobisfenol A (TBBPA). La hipótesis general de esta tesis es que existe exposición a DE en etapas tempranas de la vida. Esta exposición puede causar efectos adversos. Por lo tanto, el objetivo general de esta tesis es evaluar los niveles de exposición a diferentes DE en una población de mujeres embarazadas (EXHES) en Tarragona, España, y a su vez, estudiar cómo estos químicos pueden afectar al desarrollo celular. Para abordarlo, se estimó la exposición prenatal a los DEs mediante el modelo integrado de dosimetría externa e interna (PBPK). Seguido por el biomonitoreo de estos químicos en diferentes matrices (orina, sangre, leche materna), y de la reconstrucción y simulación de la exposición. finalmente, se realizaron estudios in vitro para evaluar la actividad potencial endocrina de DE ampliamente distribuidos. Los resultados de esta tesis confirman que la exposición a DEs puede observarse en poblaciones adultas y en el periodo prenatal. Esta exposición puede causar efectos adversos. Por esa razón, se necesitan alternativas seguras a estos DE. Deben de establecerse unas regulaciones concisas respecto a la exposición de la población más vulnerable.
Endocrine disruptors (EDs) are exogenous substances or mixtures that alters function(s) of the endocrine system and consequently causes adverse health effects in an intact organism, or its progeny, or (sub) populations. Among these EDs, there is a group that takes an important place due to their widespread distribution and their presence in food-packaging or food contact materials. Packaging protects food from alterations. However, the packaging could be a source of contamination as migration can occur from these materials with the transfer of chemicals into the food. According to that, some bisphenols (BPA, BPS and BPF); phthalates and non-phthalate plasticizers; perfluorooalkilated substances (PFOS and PFOA) and tetrabromobisphenol A (TBBPA) were selected in this thesis. The general hypothesis of this thesis is that there is EDs exposure during prenatal and early stages of life and this exposure can cause adverse outcomes. Therefore, the general objective of this thesis is to assess the exposure levels to different EDs from a pregnant women EXHES cohort in Tarragona, Spain and to study how these chemicals can affect normal cellular development. To address that, prenatal exposure to EDs was estimated by integrated external and internal dosimetry modelling, physiologically based pharmacokinetic (PBPK) model. Followed by biomonitoring of these chemicals in different matrices (urine, blood, breast milk), reconstructed exposure and reconstructed-PBPK simulations and finally, in vitro studies to assess the endocrine potential activity for different widespread EDs were performed. Results from this thesis confirm that exposure to EDs can be observed in adult populations and in the early stages of life. This exposure can cause adverse effects. For that reason, safe alternatives to these EDs are needed. Regulations regarding the most vulnerable exposure population should be established in the endocrine disruption context.

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Bruïne, Adriaan Pieter de. "Endocrine differentiation in colorectal cancer." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1993. http://arno.unimaas.nl/show.cgi?fid=6579.

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Bensing, Sophie. "Pituitary autoantibodies in endocrine disorders /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-478-3/.

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Olsson, Tommy. "Endocrine studies in stroke patients." Doctoral thesis, Umeå universitet, Medicin, 1989. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-101772.

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There are a number of links between the endocrine system and the nervous system. In this study, the impact of ischemic stroke on the endocrine system was investigated. Elderly volunteers were studied because data regarding the influence of advanced age on endocrine parameters were lacking. Only small differences in pituitary-thyroid and pituitary-adrenal hormone axes were found between two groups of elderly patients, 60 and 80 years of age. The 80-year-old age group had a lower thyrotropin response to thyrotropin releasing hormone (TRH) and a decline in dopamine excretion. Patients with acute ischemic stroke showed a pronounced hypercortisolism studied by the dexamethasone test and urine free cortisol measurements. In multiple regression analyses, postdexamethasone cortisol levels were positively correlated to proximity of the lesion to the frontal pole of the brain and disorientation. Urine cortisol levels were predicted by limb paresis, disorientation and body temperature. High cortisol excretion was associated with a worse functional outcome. Norepinephrine excretion was correlated to urine cortisol levels and to motor impairment. Patients with acute stroke had elevated free thyroxin indices. A paradoxical growth hormone response to TRH was found in the majority of stroke patients. In a multiple regression model disorientation was negatively correlated to thyrotropin response after TRH and positively correlated to prolactin response. Growth hormone response to TRH was associated with extensive paresis. In a cohort study diabetic and non-diabetic patients were prospectively studied after an initial stroke. Diabetes mellitus adversely influenced survival, the risk for a recurrent stroke and myocardial infarction.

S. 1-66: sammanfattning, s. 69-190: 6 uppsatser

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Hidayat, Egi. "On identification of endocrine systems." Licentiate thesis, Uppsala universitet, Avdelningen för systemteknik, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-227630.

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System identification finds nowadays application in various areas of biomedical research as a tool of empiric mathematical modeling and model individualization. Hormone regulation is a classical example of biological feedback where control theories, in general, and system identification, in particular, are indispensable in unraveling the regulation mechanisms and explicating the complex dynamical phenomena arising in endocrine systems. The main function of endocrine feedback regulation is to maintain the hormone levels within a particular physiological range as well as to sustain an appropriate hormone secretion pattern. Therefore, a natural operating mode of a closed-loop endocrine system is a stable periodic cycle. This property significantly reduces the repertoire of readily available identification techniques, not least due to the fact that the regulation (input) signal is immeasurable in many practical cases. There are two approaches to blind identification of hormone dynamics presented in this thesis. The first one is based on constrained nonlinear least-squares method. Weighting functions play an important role in satisfying the biological conditions on the identified model. The second approach is derived from a novel time-delay system identification method in Laguerre domain. In the latter, the time delay appears due to a specific input signal model and is estimated along with the finite-dimensional dynamics of hormone kinetics.

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Vaidya, Bijayeswar. "Genetics of autoimmune endocrine disorders." Thesis, University of Newcastle Upon Tyne, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341439.

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Masutomi, Naoya. "Evaluation of endocrine active chemicals on endocrine/reproductive systems following transplacental and lactational exposure in rats." Kyoto University, 2004. http://hdl.handle.net/2433/147783.

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Mantovani, G. "Ruolo delle diverse subunità regolatorie della PKA nella regolazione della proliferazione di cellule endocrine ed endocrino-relate." Doctoral thesis, Università degli Studi di Milano, 2006. http://hdl.handle.net/2434/30895.

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The two regulatory subunits (R1 and R2) of PKA are differentially expressed in several cancer cell lines and studies indicate distinct roles for these subunits in growth control. In recent years, mutations of genes involved in cAMP signalling and resulting in the constitutive activation of cAMP formation have been identified as cause of endocrine neoplasia. In particular, activating mutations of the ? subunit of the stimulatory G protein gene have been found in about 30-40% of GH secreting pituitary adenomas and in subsets of thyroid, adrenocortical, ovarian and testicular Leydig cell tumors, while mutations of the PKA regulatory subunit 1A gene (PRKAR1A) have been identified in patients with Carney complex, a familial multiple endocrine neoplasia syndrome. This thesis evaluated the expression of the different PKA regulatory subunits (R1A, R2A, R2B) in human pituitary adenomas, cortisol-secreting adrenocortical tumors and melanomas, as well as the effects of selective subunit activation on cell proliferation. Our data indicate that altered PKA R1/R2 ratio characterize most endocrine tumors, when compared with the normal counterpart, and that pharmacological and genetic manipulations able to revert this unbalanced expression are able to induce significant anti-proliferative and pro-apoptotic effectis in human tumoral cells.

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Jones, Maren Bell. "Effects and interactions of endocrine disrupting chemicals and diet on the mouse reproductive system." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/5006.

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Thesis (M.A.)--University of Missouri-Columbia, 2007.
The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on October 29, 2007) Vita. Includes bibliographical references.

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Larsson, Anders. "Androgen receptors and endocrine disrupting substances /." Örebro : Örebro University, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-9679.

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Myrelid, Åsa. "Down syndrome : Growth and endocrine impact." Doctoral thesis, Uppsala universitet, Pediatrik, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-106756.

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Down syndrome (DS) is associated with psychomotor retardation, short stature and endocrine dysfunction. Statural growth is a well-known indicator of health. The growth in DS differs markedly from that of other children and there is a 20 cm reduction of final height as compared to target height. We developed growth charts specific for Swedish children with DS, in order to facilitate early diagnosis of concomitant diseases that influence growth. The growth charts are available for paediatricians and child health care professionals in Sweden. The mechanism underlying the impaired growth in DS is unknown. Height is influenced by parental factors, energy intake, hormone balance and general health. In DS, genetic factors deriving from the extra chromosome 21 further affect growth. Children with DS seem to have reasonable levels of growth hormone (GH), even though GH treatment for limited periods of time improves growth velocity. Within the present project, the subjects of a previous study on early GH therapy in DS were followed up regarding late effects. We found a larger adult head circumference and better psychomotor abilities in the previously treated subjects despite a lack of effect on final height. In adult life, GH has effects on psychological well-being and metabolism. The clinical features in adults with DS might indicate impaired GH secretion. Ten young adults with DS were studied and compared with ten healthy controls. The GH secretion in the DS subjects did not differ from that in the controls. The fat body mass percentage was increased in DS, in line with the high prevalence of overweight/obesity. The finding of an increased HOMA index as well as a high relative rate of hepatic glucose production in DS indicates reduced insulin sensitivity both peripherally and in the liver. Thyroid dysfunction is common in DS. There is a 30-fold increase in congenital hypothyroidism, and acquired hypothyroidism has been reported to be present in up to 50% of adults with DS. We collected neonatal screening results and hospital records for the first ten years of life of 68 children with DS. The mean TSH concentration was increased neonatally, indicating marginal hypothyroidism early in life in DS. However, the neonatal TSH level did not predict development of manifest hypothyroidism later in life.
Downs syndrom (DS) är en vanlig kromosomavvikelse. Kortvuxenhet och psykomotorisk utvecklingsstörning är kardinaltecken vid DS. Endokrina avvikelser är också frekvent förekommande. Tillväxt är en bra indikator på barns hälsa. Nyfödda barn med DS är kortare än andra nyfödda, och skillnaden i längd ökar under barndomen. Sjukdomar som påverkar tillväxten upptäcks ofta via ett förändrat tillväxtmönster. Detta kan lätt förbises vid DS eftersom tillväxten redan är avvikande. Användning av syndromspecifika tillväxtkurvor ökar möjligheterna till diagnostik av sjukdomar som stör längdtillväxten. Vi har framställt tillväxtkurvor för barn med DS, vilka finns tillgängliga inom svensk barnsjukvård och barnhälsovård. Längdtillväxt styrs av nedärvda faktorer från föräldrarna liksom av nutrition, hälsa och hormoner. Genetiska faktorer, kopplade till kromosom 21, kan påverka tillväxten vid DS, men tillväxtstörningens exakta bakgrund är inte känd. I vuxen ålder är personer med DS ungefär 20 cm kortare än förväntat med hänsyn till föräldralängder. Trots att barn med DS har relativt normala nivåer av tillväxthormon (STH eller GH) förbättras deras tillväxt vid STH-behandling. Inom avhandlingsarbetet följde vi upp ungdomar med DS, vilka behandlats med STH i tidig barndom. Vi kunde påvisa större huvudomfång samt förbättrad kognitiv och motorisk förmåga, trots avsaknad av effekt på slutlängden. Tillväxthormon har i vuxen ålder effekt både på ämnesomsättning och psykologiskt välbefinnande. Vuxna individer med DS uppvisar flera tecken förenliga med STH-brist. Vi jämförde tio unga vuxna med DS med tio friska kontrollindivider avseende förmågan att insöndra STH. STH-insöndringen hos individerna med DS skiljde sig inte från den hos kontrollerna. Vid samtidig undersökning av kroppssammansättning påvisades en ökad andel kroppsfett hos individerna med DS, resultat i linje med den frekventa förekomsten av övervikt/fetma. Individerna med DS hade en förhöjd glukosproduktion, som tillsammans med ett ökat HOMA-index talar för förekomst av minskad insulinkänslighet både på levernivå och perifert. Brist på sköldkörtelhormon är mycket vanligt vid DS och upp till hälften av vuxna med DS kan ha hypotyreos. Vi studerade 68 barn med DS avseende nivåer av tyroideastimulerande hormon (TSH) vid PKU-provtagning. Vi följde också barnens journalhandlingar från de tio första levnadsåren i syfte att undersöka om den neonatala TSH-nivån kan prediktera framtida underfunktion av sköldkörteln. Resultaten visade att barn med DS har en förhöjd nivå av TSH neonatalt, vilket indikerar en brist på sköldkörtelhormon redan i nyföddhetsperioden, men nivån förutsäger inte utveckling av manifest hypotyreos senare under barndomen.

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Takamiya, Minako. "Endocrine disrupting chemical impacts on eukaryotes." Thesis, Cranfield University, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487012.

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Endocrine Disrupting Chemicals (EDCs) are exogenous substances or mixtures that might lead to endocrine disruption in humans and wildlife. Bispheriol (BPA) was chosen as a model EDC and assessed for its toxic impacts on two eukaryotic test systems: (1) A fungal test system - white-rot basidiomycete, Trametes versicolor T. versicolor was tolerant of high concentrations of BPA (up to 300 ppm). The ligninolytic enzymes produced by the fungi were stimulated by 300 ppm of BPA. Of the three ligninolytic enzyme encoding genes examined, lignin peroxidase showed the greatest increase in expression in the presence ofBPA. (2) A mammalian test system - mouse Leydig tumor cell lines (mLTC-l) Time- and dose-responses of the cells stimulated with gonadotrophin to BPA demonstrated the clearest response in the expression of the steroidogenic genes without a marked effect on cell viability. The studies on the response of global gene expression to BPA by microarray analysis of mLTC-l cells showed 24 genes were differentially expressed in the presence of BPA (8 were increased and 16 were decreased). Several of these genes were related to steroid/cholesterol metabolism, transport and cell cycle regulation. In addition a study of male reproductive impairment was carried out to understand the reproductive toxicity of EDCs and likely effects on male infertility - one of the serious effects caused by EDCs. Human testicular tissues from fertile and infertile patients were examined by a microarray and 2642 genes were differentially expressed between the testes of fertile and infertile patients (955 genes were increased and 1687 genes were decreased in infertile patients). These genes are related to steroidogenesis, Leydig cell function, spermatid metamorphosis, cell cycle, and ribosome function. The array data exhibited phenotype-specific gene expression patterns. The most significant gene expression differences between fertile and infertile. patients were observed in spermatocyte- and spermatid- stages. Though further analysis is required, it is thought that BPA has weak modulatory impacts on eukaryotic test systems used in this study, however, its reproductive toxicity may not be negligible.

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Gambelunghe, Giovanni. "Immunogenetic studies in autoimmune endocrine diseases /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-691-x/.

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Hessman, Ola. "Genetic studies of endocrine abdominal tumors." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-5026-1/.

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Pottinger, T. G. "Endocrine control of the salmonid integument." Thesis, Lancaster University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235253.

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Pannett, Anna Alexandra Josephine. "Molecular genetic studies of endocrine cancers." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392892.

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Clifford, Katy A. "Endocrine mechanisms of early pregnancy loss." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597778.

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Ritchie, Catherine Marian. "Aspects of hypertension in endocrine disease." Thesis, Queen's University Belfast, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357488.

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Owen, Catherine Jane. "Genetic determinants of autoimmune endocrine disease." Thesis, University of Newcastle Upon Tyne, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440584.

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Gosney, J. R. "Histopathology of endocrine organs in hypoxia." Thesis, University of Liverpool, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356277.

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Ogilvy-Stuart, Amanda Lesley. "Endocrine sequelae of irradiation in childhood." Thesis, University of Southampton, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296367.

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Schoeman, Johan P. "Endocrine changes in canine critical illness." Thesis, University of Cambridge, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.611343.

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Göthlin, Eremo Anna. "Biological profiles of endocrine breast cancer." Doctoral thesis, Örebro universitet, Institutionen för hälsovetenskap och medicin, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-43963.

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Funding: Magnus Bergvall Cancer Foundation; Percy Falk foundation for research in breast and prostate cancer; Nyckelfonden; Örebro University Hospital; Lions cancer research foundation, Region Uppsala-Örebro

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Cazabat, Sage Laure. "Tumorigenèse endocrine et voie de l'AMPc." Paris 11, 2009. http://www.theses.fr/2009PA11T079.

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Kleimberg, Didier. "L'entite cystopathie endocrine existe-t-elle ?" Université Louis Pasteur (Strasbourg) (1971-2008), 1986. http://www.theses.fr/1986STR1M113.

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Barrow, John. "Transcriptional control of the endocrine pancreas." Thesis, University of Aberdeen, 2005. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU487870.

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Transcription factors are vitally important to the developmental biology of all life. They also define many of the developmental stages of organs within the body. Their expression allows for the activation of developmentally important cues and signalling cascades, through activation of specific subsets of genes. When transcription factor function is disrupted, it can have serious repercussions on the development and function of organ systems. This dysfunction, in many cases, leads to the onset of diseases such as cancer and diabetes. The general objectives of this thesis were to describe the role and function of several transcription factors vitally important in the development and maintenance of the pancreas through three lines of research. Firstly, neurogenin3 (ngn3) is vitally important to the development of the islets of Langerhans. Knocking out this gene prevents mice from developing endocrine cells of the pancreas (islets of Langerhans). This thesis set out to label the ngn3 positive precursor cell population in developing mice, and characterise their phenotype. Detailed immunohistochemistry and fluorescence activated cell sorting coupled with reverse transcriptase (RT)-PCR were employed to fully characterise the EGFP positive cell population at embryonic day (E)15.5 and E l8.5. EGFP positive cells were able to be isolated at both E l5.5 and E l8.5 and were found to co-express endocrine markers both in immunohistochemical and RT-PCR based assays. Marking cells that are developmentally important to pancreas function, and being able to identify their phenotype, may provide clues to markers that could be exploited as targets for future diabetes therapies. Secondly, pancreatic duodenal homeobox-1 (PDX-1) is another critically important transcription factor in both pancreas development and in maintaining the insulin expression of the beta cells in the islets of Langerhans. Preventing PDX-1 function causes severe agenesis of the pancreas, and mutations in the gene cause one form of diabetes. This thesis describes the production of a super-activated form of the PDX-1 protein using the transactivation domain VP 16. The main objective of this work was to drive PDX-1 function in a non-beta cell. Using chromatin immunoprecipitation (ChIP) assays, the PDX-1 VP 16 protein appeared to increase the acetylation state of the insulin promoter in the mouse non-beta cell line (alpha-TCI.6), particularly through altering the acetylation state of the insulin 2 promoter. The use of the PDX-1VP16 protein could provide a potential starting point for research into driving differentiation of stem cells to a pancreatic phenotype. Finally, there are four transcription factors that are known to drive expression of the insulin gene synergistically. They are the homeodomain protein PDX-1, the leucine zipper protein MafA, and the basic helix loop helix heterodimer beta2/E47. All of these proteins have binding sites within 300 bp of the transcriptional start site of the insulin gene. Through the use of ChIP assays this thesis shows, for the first time, the ordered cyclical binding of these four transcription factors on the insulin 2 gene promoter in the mouse beta cell line MIN-6. Understanding how the transcription factors that drive insulin expression interact on the promoter in vivo could be used for future studies to understand the process of insulin gene transcription both in healthy and diabetic patients. This may then shed light on the processes that cause the perturbations in insulin transcription seen with certain forms of diabetes.

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Petrasek, Danny Cohen Donald S. "Diffusion-mediated regulation of endocrine networks /." Diss., Pasadena, Calif. : California Institute of Technology, 2002. http://resolver.caltech.edu/CaltechETD:etd-12052003-095049.

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Reutman, Susan Simpson. "ENDOCRINE DISRUPTION RELATED TO FUEL EXPOSURE AMONGST WOMEN IN THE MILITARY AND RACIAL DIFFERENCES IN ENDOCRINE LEVELS." University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin985628877.

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Merani, Salima A. "Development of a specific and sensitive assay for cholecystokinin, and applications thereof." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37619.

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Cholecystokinin, or "CCK" peptides, originally identified in the gastrointestinal tract, are now considered to be one of the most abundant peptide systems in the mammalian central nervous system. Prompted by recent findings that implicated the cholecystokinergic system in the pathophysiology of various illnesses, we developed a novel assay system to measure the various forms of cholecystokinin peptides in human plasma and cerebrospinal fluid. The system detects CCK-4, sulfated CCK-8 (CCK-8s) and nonsulfated CCK-8 (CCK-8ns) with equal affinity, with the lower detection limit of 2.7 fmol and an ED50 of 10.6 +/- 2.2 fmol. Using the assay system, we determined that mean CCK-like immunoreactivity (CCK-LI) in the plasma of 12 healthy subjects was 12.9 +/- 2.1 pM CCK-4 equivalents.
After developing the cholecystokinin assay system, we were able to combine our unique methodology with other established techniques to investigate the role of CCK in illnesses such as premenstrual dysphoric disorder (PMDD), anxiety, bulimia nervosa, and cardiomyopathy.
Briefly, we observed no significant differences in plasma CCK levels between women with PMDD and healthy volunteers. However, we found that, independent of diagnosis, plasma cholecystokinin concentrations were higher in women during their first visit to the clinic to participate in the study, as compared to later visits.
In addition, application of our assay system allowed us to determine that oral ingestion of caffeine increased plasma CCK-LI levels 2--4 fold in humans. Moreover, we observed substantial variation in post-caffeine cholecystokinin levels among individuals.
In another study of cholecystokinin and anxiety, we used our CCK assay to determine the effects of ondansetron, a serotonin receptor antagonist, on cholecystokinin levels in plasma. We found that multiple oral doses of ondansetron influence the pharmacokinetic parameters of exogenous CCK.
We also used the three-step assay system to measure CCK-LI in patients with the eating disorder, bulimia nervosa. Baseline fasted cholecystokinin plasma levels were lower in bulimic women as compared to control subjects. However, at "satiety", or the post-binge stage, CCK levels in bulimic women were similar to those of control women.
Finally, our investigation into the role of cholecystokinin in cardiomyopathy revealed that neuronal cholecystokinin receptor density was altered in the cardiomyopathic hamster brain, as compared to age- and sex-matched control animals. (Abstract shortened by UMI.)

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Park, June-Woo. "Development and validation of novel molecular techniques to elucidate mechanisms of endocrine disruption." Diss., Connect to online resource - MSU authorized users, 2008.

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Thesis (Ph. D.)--Michigan State University. Dept. of Zoology-Environmental Toxicology, 2008.
Title from PDF t.p. (viewed on Mar. 30, 2009) Includes bibliographical references. Also issued in print.

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Martínez, López Rubén Francisco. "Integrative analysis of endocrine disruption in zebrafish (Danio rerio)." Doctoral thesis, Universitat de Barcelona, 2020. http://hdl.handle.net/10803/672727.

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Understanding the mode of action of different pollutants and xenobiotics in human and wildlife is a key step in environmental risk assessment. Omic technologies allow the study of the global status at different biological levels (transcriptome, metabolome, lipidome...) from a holistic and integrative point of view. The omic data fusion and integration of the effects at these different levels is an extremely useful method to elucidate the mode of action (MoA) of the pollutants and to propose adverse outcome pathways (AOPs). In this way, the aim of this thesis is to determine molecular and phenotypical signatures of exposure of several endocrine disrupting chemicals (EDCs) on zebrafish (Danio rerio) eleutheroembryos, which constitutes an excellent model for endocrine disruption. Morphometric and transcriptomic (RNA-Sequencing) studies were carried out in individuals exposed to bisphenol A (BPA), perfluorooctanesulfonate (PFOS) and tributyltin (TBT). Further metabolic, epigenetic (DNA methylation and miRNAs) and lipidomic (thin layer chromatography and high performance liquid chromatography – mass spectrometry) studies were performed only in BPA-exposed individuals. Main effects of BPA included lipid metabolism disruption, yolk sac malabsorption syndrome and lipid retention (obesogenicity), visual system alteration, and estrogenicity. Some of its effects were long-term persistent and could be mediated by epigenetic mechanisms. PFOS had immunosuppressive and anorexic-like properties, it disrupted the transcription of genes related to cell adhesion molecules (CAMs), and the exposed eleutheroembryos presented muscle-skeletal alterations (scoliosis and kyphosis). Finally, TBT disrupted the transcription of genes related to steroid and cell cycle metabolism, and elicited a general developmental delay (diapause-arrest effect) in the exposed individuals. Phenotypic observations were related to their transcriptomic alterations and their proposed molecular initiation event (MIE), allowing the design of an AOP for each of the studied EDCs. Overall, this thesis shows the usefulness of transcriptomics and of data integration at different biological levels to discern AOPs and MIE, therefore contributing to a deeper comprehension of the toxicity and the mode of action of BPA, PFOS and TBT. We consider that these results can be extrapolated to understand the toxic effects of these compounds in other animals, including humans.
Comprender el modo de acción de los diferentes contaminantes y xenobióticos en humanos y en la vida silvestre constituye un paso clave en la evaluación del riesgo ambiental. Las tecnologías “ómicas” permiten el estudio global de los diferentes niveles biológicos (transcriptoma, metaboloma, lipidoma...) desde un punto de vista holístico e integrado. La fusión de datos ómicos y la integración de los efectos observados a estos diferentes niveles es un método extremadamente útil para dilucidar el modo de acción (MoA) de los contaminantes y proponer “mecanismos explicativos de efectos adversos” (AOP). De este modo, el objetivo de esta tesis es determinar las firmas moleculares y fenotípicas de exposición a varios disruptores endocrinos (EDC) en eleuteroembriones de pez cebra (Danio rerio), el cual constituye un excelente modelo para estudiar la disrupción endocrina. Se realizaron estudios morfométricos y transcriptómicos (RNA- Seq) en individuos expuestos a bisfenol A (BPA), perfluorooctanosulfonato (PFOS) y tributilestaño (TBT). Adicionalmente, otros estudios metabólicos, epigenéticos (metilación de ADN y miRNAs) y lipidómicos (mediante cromatografía de capa fina y cromatografía líquida de alta eficacia – espectrometría de masas) se realizaron específicamente en individuos expuestos a BPA. Los principales efectos causados por el BPA incluyeron la alteración del metabolismo de lípidos, síndrome de malabsorción del saco vitelino y retención de lípidos (obesogenicidad), alteración del sistema visual y estrogenicidad. Algunos de sus efectos fueron persistentes a largo plazo y podrían estar regulados por mecanismos epigenéticos. El PFOS presentó propiedades inmunosupresoras y pseudo-anoréxicas, alteró la transcripción de genes relacionados con las moléculas de adhesión celular (MAC) y los eleuteroembriones expuestos a él presentaron alteraciones músculo-esqueléticas (escoliosis y cifosis). Finalmente, el TBT alteró la transcripción de genes relacionados con el metabolismo de esteroides y del ciclo celular, y provocó un retraso general del desarrollo (efecto “pseudo-diapáusico”) en los individuos expuestos. Las observaciones fenotípicas se pudieron relacionar con las alteraciones transcriptómicas y el evento molecular de iniciación (MIE) propuesto para cada EDC estudiado, permitiendo así el diseño de un AOP específico para cada uno de ellos. En conclusión, esta tesis muestra la utilidad de la transcriptómica y de la integración de datos a diferentes niveles biológicos para la propuesta de AOPs y MIEs, contribuyendo a una comprensión más profunda de la toxicidad y el modo de acción del BPA, PFOS y TBT. Consideramos que estos resultados pueden extrapolarse para comprender los efectos tóxicos de estos compuestos en otros animales, incluidos los humanos.
Comprendre el mode d'acció dels diferents contaminants i xenobiòtics en humans i en la vida silvestre constitueix un pas clau en l'avaluació del risc ambiental. Les tecnologies "òmiques" permeten l'estudi global dels diferents nivells biològics (transcriptoma, metaboloma, lipidoma...) des d'un punt de vista holístic i integrat. La fusió de dades òmiques i la integració dels efectes observats a aquests diferents nivells és un mètode extremadament útil per dilucidar el mode d'acció (MoA) dels contaminants i proposar "mecanismes explicatius d'efectes adversos" (AOP). D'aquesta manera, l'objectiu d'aquesta tesi és determinar les signatures moleculars i fenotípiques d'exposició a diversos disruptors endocrins (EDC) a eleuteroembrions de peix zebra (Danio rerio), el qual constitueix un excel·lent model per estudiar la disrupció endocrina. Es van realitzar estudis morfomètrics i transcriptòmics (RNA-Seq) en individus exposats a bisfenol A (BPA), perfluorooctanosulfonat (PFOS) i tributilestany (TBT). Addicionalment, altres estudis metabòlics, epigenètics (metilació d'ADN i miRNAs) i lipidòmics (mitjançant cromatografia de capa fina i cromatografia líquida d'alta eficàcia - espectrometria de masses) es van realitzar específicament en individus exposats a BPA. Els principals efectes causats pel BPA van incloure l'alteració del metabolisme de lípids, síndrome de malabsorció del sac vitel·lí i retenció de lípids (obesogenicitat), alteració del sistema visual i estrogenicitat. Alguns dels seus efectes van ser persistents a llarg termini i podrien estar regulats per mecanismes epigenètics. El PFOS va presentar propietats immunosupressores i pseudo-anorèxiques, va alterar la transcripció de gens relacionats amb les molècules d'adhesió cel·lular (MAC) i els eleuteroembrions exposats a ell van presentar alteracions músculo-esquelètiques (escoliosi i cifosi). Finalment, el TBT va alterar la transcripció de gens relacionats amb el metabolisme d'esteroides i del cicle cel·lular, i va provocar un retard general de desenvolupament (efecte “pseudo- diapàusic”) en els individus exposats. Les observacions fenotípiques es van poder relacionar amb les alteracions transcriptòmiques i l'esdeveniment molecular d'iniciació (MIE) proposat per a cada EDC estudiat, permetent així el disseny d'un AOP específic per a cada un d'ells. En conclusió, aquesta tesi mostra la utilitat de la transcriptòmica i de la integració de dades a diferents nivells biològics per a la proposta d'AOPs i MIEs, contribuint a una comprensió més profunda de la toxicitat i el mode d'acció de l'BPA, PFOS i TBT. Considerem que aquests resultats poden extrapolar-se per comprendre els efectes tòxics d'aquests compostos en altres animals, inclosos els humans.

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Miskimon, Amy K. "Healthy aging and the endocrine environment the association between the endocrine environment and body composition in postmenopausal women /." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2009. https://www.mhsl.uab.edu/dt/2009m/miskimon.pdf.

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Johansson, Térèse A. "Pancreatic Endocrine Tumourigenesis : Genes of potential importance." Doctoral thesis, Uppsala University, Department of Medical Sciences, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9294.

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Understanding signalling pathways that control pancreatic endocrine tumour (PET) development and proliferation may reveal novel targets for therapeutic intervention. The pathogenesis for sporadic and hereditary PETs, apart from mutations of the MEN1 and VHL tumour suppressor genes, is still elusive. The protein product of the MEN1 gene, menin, regulates many genes. The aim of this thesis was to identify genes involved in pancreatic endocrine tumourigenesis, with special reference to Notch signalling.

Messenger RNA and protein expression of NOTCH1, HES1, HEY1, ASCL1, NEUROG3, NEUROD1, DLK1, POU3F4, PDX1, RPL10, DKK1 and TPH1 were studied in human PETs, sporadic and MEN 1, as well as in tumours from heterozygous Men1 mice. For comparison, normal and MEN1 non-tumourous human and mouse pancreatic specimens were used. Nuclear expression of HES1 was consistently absent in PETs. In mouse tumours this coincided with loss of menin expression, and there was a correlation between Men1 expression and several Notch signalling factors. A new phenotype consisting of numerous menin-expressing endocrine cell clusters, smaller than islets, was found in Men1 mice. Expression of NEUROG3 and NEUROD1 was predominantly localised to the cytoplasm in PETs and islets from MEN 1 patients and Men1 mice, whereas expression was solely nuclear in wt mice. Differences in expression levels of Pou3f4, Rpl10 and Dlk1 between islets of Men1 and wt mice were observed.

In addition, combined RNA interference and microarray expression analysis in the pancreatic endocrine cell line BON1 identified 158 target genes of ASCL1. For two of these, DKK1 (a negative regulator of the WNT/β-catenin signalling pathway) and TPH1, immunohistochemistry was performed on PETs. In concordance with the microarray finding, DKK1 expression showed an inverse relation to ASCL1 expression.

Altered subcellular localisation of HES1, NEUROD1 and NEUROG3 and down-regulation of DKK1 may contribute to tumourigenesis.

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Holmbäck, Ulf. "Metabolic and Endocrine Responses to Nocturnal Eating." Doctoral thesis, Uppsala universitet, Institutionen för medicinska vetenskaper, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2956.

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An increasing amount of people have their work hours displaced to the night and there are indications that shift work and other irregular working schedules are associated with an increased risk of developing the metabolic syndrome and other pathological conditions. It is therefore important to address the consequences of eating at irregular hours, especially nighttime. Papers I-III refer to a study in which 7 males were given a high-carbohydrate diet (HC) or a high-fat diet (HF), using a cross-over design. Subjects were kept awake for 24 h and food was provided as 6 equally spaced isocaloric meals. Higher energy expenditure and non-esterified fatty acids (NEFA) concentration, as well as lower glucose and triacylglycerol (TAG) concentrations were observed with the HF-diet, compared to the HC-diet. With the HF-diet, fat oxidation, heat release, heart rate, glucose, NEFA and TAG concentrations differed depending on time of day. The highest postprandial TAG concentrations were seen after the 04.00 meal with both diets. Insulin and leptin responses to meal intake differed with respect to diet and time of day. Time of day affected glucagon, thyroid stimulating hormone, free thyroxin, total triiodothyronine (tT3), cortisol, chromogranin A and pancreatic polypeptide (PP) concentrations. PP’s postprandial increase was greater during 08.00 – 16.00 compared to 20.00 – 08.00. Furthermore, the subjects felt less irritated when eating the HF-diet but hunger was not related to macronutrient composition. Hunger and thirst decreased throughout the 24 h period despite constant activity and energy intake; and were correlated with several endocrine and metabolic variables. In paper IV 7 males were studied twice during 24-h either given 6 isocaloric meals throughout the 24-h period, or 4 isocaloric meals from 08.00 to 20.00, followed by a nocturnal fast. Energy expenditure, glucose, TAG, insulin and glucagon concentrations were lower; and NEFA concentrations were higher during the nocturnal fast compared to nocturnal eating; although no 24 h differences between the protocols were apparent. The subjects were more passive during the fasting period compared to when food was given. Stepwise regression showed that correlations between metabolic variables and hormones differed between daytime and nighttime. The decreased evening/nocturnal responses of cortisol and PP to meal intake suggest that nocturnal eating might have health implications and that the body reacts unfavorably to nocturnal eating. Smaller meals around the clock, however, showed marginally better effects on postprandial TAG concentrations and mental energy compared to larger meals during daytime. Further studies (long term) are needed before dietary guidelines can be given to shift workers, especially regarding the impact of nocturnal eating on gastrointestinal response and cortisol.

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Micallef, Rachel Antonia. "Wnt signalling in endocrine resistant breast cancer." Thesis, Cardiff University, 2012. http://orca.cf.ac.uk/41274/.

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Wnt signalling components are reported to be deregulated in breast cancer but the contribution of this pathway in endocrine resistance is less clearly defined. Endocrine resistance is an important clinical challenge affecting up to a quarter of all breast cancer patients and is associated with a poorer clinical prognosis. This project focussed on exploring the role of Wnt signalling in endocrine resistant breast cancer cell models. Wnt pathway elements were deregulated in the acquired tamoxifen resistant cell line (Tam-R) compared to tamoxifen sensitive parental cells (MCF-7), with changes supportive of Wnt signalling activation in this tamoxifen resistant model apparent from Affymetrix HGU-133A gene microarray data and Western blot analysis. In contrast, Wnt signalling appeared to be suppressed based on Affymetrix data for MCF-7 cells treated with oestradiol for 10 days, with equivocal changes in MCF-7 cells treated with tamoxifen for 10 days or a faslodex resistant cell model (Fas-R). Excitingly, Tam-R cells were also more sensitive than MCF-7 cells to pharmacological manipulation of Wnt signalling. While Wnt activation using Wnt3a and LiCl did not affect cell growth or migration, inhibition of Wnt signalling usingIWP2, PNU 74654 and iCRT14 suppressed Tam-R cell growth and migration. There is mounting evidence of cross talk between Wnt and EGFR signalling in breast cancer, and EGFR activity is upregulated in Tam-R cells. The project’s findings tentatively supported cross-talk between the two signalling pathways in this model. Thus, targeting of the Wnt pathway alongside EGFR blockade was superior in suppressing cell growth and migration in Tam-R cells. The effect appeared to be more pronounced when Wnt signalling was inhibited at the nuclear level using iCRT14. Collectively, these data suggest that Wnt signalling may play an important role in tamoxifen resistance where it may offer an opportunity for more effective therapeutic intervention to control relapse and associated tumour aggressiveness.

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Biggs, Christine. "Endocrine and ovarian function in Meishan pigs." Thesis, University of Nottingham, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334798.

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Pearce, Sarah. "Endocrine and environmental manipulation of adipose tissue." Thesis, University of Nottingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.410411.

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Shelton, K. "Endocrine studies on the bovine corpus luteum." Thesis, University of Nottingham, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376416.

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Higham, Andrew Damian. "Neuroendocrine regulation of gastric endocrine cell function." Thesis, University of Liverpool, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266054.

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Bridges, Nicola Anne. "The endocrine and physical events of puberty." Thesis, University of Southampton, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295696.

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L', Hopital François. "Tumeur endocrine pancréatique secrétant calcitonine et glucagon." Clermont-Ferrand 1, 1987. http://www.theses.fr/1987CLF11048.

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Après urappel sur les tumeurs endocrines du pancréas, la somatostatine, la calcitonine et le calcitonine gene related peptide (CGRP), l' auteur décrit une observation de tumeurs endocrines pancréatiques sécrétant calcitonine et glucagon (dosages radio-immunologiques et immunocytochimie), s' exprimant sous la forme : d' un processus tumoral hépatique (métastases), de diarrhée, de flushs, d' épisodes d' hypoglycémie, et traitées par la somatostatine retard. Il s' agit de la première observation décrite de tumeur pancréatique associant calcitonine et glucagon, les épisodes d' hypoglycémie sont expliqués par une sécrétion inappropriée d' insuline. L' auteur note enfin l' absence d' efficacité de la somatostine retard sur l' hyperglucagonémie (en opposition avec les données de la littérature) et sur l' hypercalcitoninémie (en accord avec les données de la littérature).

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Wieduwild, Elisabeth. "Neuro-endocrine regulation of innate immune responses." Thesis, Aix-Marseille, 2019. http://www.theses.fr/2019AIXM0551.

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L'axe hypothalamo-hypophyso-surrénalien (HHS) et le système nerveux sympathique (SNS) sont nécessaires à l’équilibre entre immunité et immunopathologie. Ils stimulent respectivement la production de glucocorticoïdes (GC) ou d'adrénaline/noradrénaline, qui se lient au récepteur des glucocorticoïdes (GR) ou au récepteur β2-adrénergique (β2-AR), exprimés par les cellules immunitaires. Durant ma thèse, j’ai analysé le rôle du β2-AR dans un modèle d’infection virale ainsi que le rôle intrinsèque du GR dans les cellules Natural Killer (NK). La délétion du β2-AR entraîne une charge virale réduite et une plus grande résistance à l'infection par le cytomégalovirus murin (MCMV), corrélée à une diminution des lésions tissulaires et à une augmentation des taux d'IFN-γ dans le sang. Nous avons identifié les NK comme étant la source de cette production accrue d’IFN-γ. Enfin, nous avons démontré que l’effet protecteur de la délétion du β2-AR est médié par les cellules non hématopoïétiques.La signalisation GR intrinsèque aux NK a également des effets régulateurs sur leur production d'IFN-γ. Lors d’une infection MCMV, les GC endogènes induisent l'expression sélective du PD-1 sur les NK spléniques, limitant ainsi leur production d'IFN-γ et prévenant l’histopathogenèse. De plus, dans un modèle de choc endotoxique, l’expression du GR dans les NK spléniques permet l’induction d’une tolérance dépendante de l'IL-10.En résumé, ces t révèlent un nouveau rôle du SNS dans la régulation des réponses immunitaires antivirales et fournissent des informations sur le mécanisme de protection de l'hôte contre l'immunopathologie grâce à l'axe HHS
The Hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (SNS) are important for the balance between immunity and immunopathology. The HPA axis and the SNS stimulate the release of glucocorticoids or adrenaline and noradrenaline, respectively. They bind to the glucocorticoid receptor (GR) and the β2-adrenergic receptor (β2-AR) that are expressed by immune cells. In my thesis, I analysed the role of the β2-AR in viral infections and the intrinsic role of the GR in NK cells. I revealed tissue dependent differences in the regulation of NK cells by the nervous system that are essential for host survival. Systemic β2-AR-deficiancy resulted in reduced viral load and greater resistance to murine cytomegalovirus (MCMV) infection, which correlated with decreased tissue damage and higher systemic IFN-γ levels. Liver NK cells were a major source of this additional IFN-γ in β2-AR-deficient mice. Interestingly, β2-AR deletion in non-haematopoietic cells increased IFN-γ levels and promoted resistance to MCMV.GR signalling intrinsic to NK cells also regulated their IFN-γ production, required for host protection against MCMV infection. Mechanistically, endogenous glucocorticoids induced the selective expression of PD-1 on splenic NK cells, which limited their IFN-γ production and prevented lethal immunopathology. Furthermore, the expression of the GR in splenic NK cells was required for the development of IL-10–dependent endotoxin tolerance, by limiting their IFN-γ production. In this thesis I reveal, a novel role of the SNS in regulating anti-viral immune responses and provide mechanistic insights into host protection from immunopathology by the HPA axis

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Mayeux, Patrick. "Recherches sur la regulation endocrine de l'erythropoiese." Reims, 1988. http://www.theses.fr/1988REIMS002.

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Bilous, Iryna Ivanivna. "Neurological disorders of patients with endocrine pathology." Thesis, Буковинський деравний медичний університет, 2018. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/14444.

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Kulkarni, Saurabh S. "Endocrine Mechanisms Underlying Phenotypic Evolution in Frogs." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1342106009.

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Dissertations / Theses on the topic 'Endocrine'

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