Tesi sul tema "Hypothalmic diseases"
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Näsman, Birgitta. "The limbic-hypothalamic-pituitary-adrenal axis in Alzheimer's disease". Doctoral thesis, Umeå universitet, Geriatrik, 1994. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-140822.
Testo completodigitalisering@umu
Dembek, Katarzyna Agnieszka. "Hypothalamic-pituitary-adrenal axis dysfunction in critically ill foals". The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1479220019340433.
Testo completoO'Brien, John Tiernan. "Magnetic resonance imaging and hypothalmic-pituitary-adrenal axis function in depression and Alzheimer's disease". Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308774.
Testo completoHawkins, Paul. "Nutritional influences on development of the cardiovascular system and the hypothalamic-pituitary-adrenal axis". Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.325124.
Testo completoNguyen, Elizabeth T. "Sex differences in stress responsivity, glucocorticoid signaling, and disease". University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin156327275069323.
Testo completoAbebe, Getachew. "The integrity of the hypothalamic-pituitary-adrenal axis in Boran (Bos indicus) cattle infected with Trypanosoma congolense". Thesis, Brunel University, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292991.
Testo completoDromey, Jasmin Rachel. "Elucidating novel aspects of hypothalamic releasing hormone receptor regulation". University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0133.
Testo completoNye, Elisabeth Jane. "Dynamic stimulation tests in the assessment of hypothalamic-pituitary-adrenal axis function in pituitary disease and obesity /". St. Lucia, Qld, 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17166.pdf.
Testo completoGordon, Jennifer. "Depression, the dynamic function of the autonomic nervous system and hypothalamic-pituitary-adrenal (HPA) axis, and cardiovascular disease". Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110429.
Testo completoLa dépression est associée à un risque élevé de maladie cardiaque. Un mécanisme qui pourrait expliquer cette association est la dysfonction du système nerveux autonome (SNA) et l'axe hypothalamo-hypophyso-surrénalien (HHS), qui sont les deux systèmes impliqués dans la réaction physiologique au stress. Cette thèse avait comme but de mieux comprendre la relation entre la dépression et ces deux systèmes. Dans la première étude, l'effet de la dépression majeure sur le rétablissement de la fréquence cardiaque après l'exercice, un marqueur de la balance autonome, a été examiné chez des patients cardiaques. La dépression était associée à un pauvre rétablissement cardiaque immédiatement après l'exercice, ce qui suggère un délai dans l'activation du système parasympathique. Dans la deuxième étude, qui incluait des participants en santé, on examinait l'effet des symptômes dépressifs cognitifs et somatiques en relation avec le rétablissement de la fréquence cardiaque et la variabilité de la fréquence cardiaque, deux marqueurs de l'activation du SNA, en réaction à des stress interpersonnels de laboratoire. Les deux types de symptômes étaient associés avec un moins bon rétablissement cardiaque après les stress. Finalement, la troisième étude examinait la relation entre la dépression majeure et l'activité du SNA et de l'axe HHS en réaction à un test diagnostique stressant. De plus, l'étude a eu comme but de déterminer si les antidépresseurs sont efficaces dans le rétablissement d'une réponse normale au stress chez les dépressifs. Les patients cardiaques dépressifs avaient un niveau de cortisol plus élevé tout au long du test, ce qui indique une activation plus forte de l'axe HHS. Cet effet n'a pas été observé chez les dépressifs qui prenaient des antidépresseurs; par contre, ni la dépression ni l'utilisation des antidépresseurs étaient associées à la variabilité de la fréquence cardiaque. Ces études suggèrent une relation modeste et inconsistante entre la dépression et une activation altérée du SNA. Par contre, la relation entre la dépression et la suractivation de l'axe HHS apparait relativement forte. Finalement, les antidépresseurs semblent être efficaces en annulant la suractivation de l'axe HHS chez les dépressifs.
Sonner, Patrick M. "FUNCTIONAL INTERPLAY BETWEEN SUBTHRESHOLD ION CHANNELS IN PREAUTONOMIC NEURONS OF THE HYPOTHALAMIC PARAVENTRICULAR NUCLEUS IN HEALTH AND DISEASE CONDITIONS". Wright State University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=wright1197577443.
Testo completoMonteiro, Davolli Gabriel. "REVERSIBLE DOWNREGULATION OF HYPOTHALAMIC-PITUITARY-GONADAL AXIS IN THE STALLION WITH A THIRD-GENERATION GNRH ANTAGONIST". UKnowledge, 2015. http://uknowledge.uky.edu/gluck_etds/22.
Testo completoSouza, Patrícia Reis de. "Participação do eixo hipotálamo-pituitária-adrenal na Doença Inflamatória Intestinal induzida experimentalmente". Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/60/60135/tde-26102015-164051/.
Testo completoInflammatory bowel diseases (IBD) are caused by imbalance between regulatory and effector immune responses in the intestinal mucosa and can be modulated by the hypothalamic-pituitary-adrenal (HPA) axis via neuroimmune endocrine interactions and secretion of cortisol. Although glucocorticoids (GC) are used to treat IBD, cortisol produced by the adrenals glands is also involved in the stress response, which can lead to uncontrolled inflammatory diseases. Therefore, the aim of this study was to evaluate the HPA axis in the modulation of the immune response of intestinal mucosa. C57BL/6 mice were subjected to removal of the adrenal glands followed by induction of colitis by administration of water containing 3% dextran sulfate sodium (DSS). The results showed that the absence of adrenals led to increased susceptibility to disease and early mortality, a phenomenon that was not prevented by GC replacement. Adrenalectomized animals exposed to DSS had significantly lower levels of LPS, concomitantly to increased IL-6 in the serum when compared to non-adrenalectomized mice. In addition, adrenalectomized animals had lower cellularity in the lamina propria (LP), less erosion areas and less histopathologic score associated with increased IFN-? and FasL in the intestine, without compensatory local production of corticosterone. There was an increase in the activity of the myeloperoxidase (MPO) enzyme, N- acetilglicosaminidase (NAG) and eosinophil-peroxidase (EPO) in the intestines of DSS-exposed animals when compared to the healthy control group of mice, regardless of the presence of intact HPA axis, while treatment with GC led to significantly reduced MPO activity. It was also observed in the LP of adrenalectomized mice significant increase in the frequency of tolerogenic dendritic cells CD11b+CD11c+CD103+, helper T (CD3+ CD4+), cytolytic T (CD3+ CD8+) and NKT (CD3+ CD49b+) besides significant reduction in the population of pro-inflammatory dendritic cells CD11c+ CD11b+ CD103-, leukocyte CD11b+ and intraepithelial lymphocytes, GC-dependent manner. The absence HPA intact carried decrease in total leukocytes in spleen when compared to the group with colitis, related mainly to significant reduction in the frequency of NKT cells (CD3+CD49b+), which were restored in the GC treated mice. During exposure to DSS there was increased Th2 and Th1 cells in the spleen of non-adrenalectomized mice, while the removal of the adrenals was associated to a marked reduction in the population of CD4 T cells producing IL-4, IL-10, IFN-? or IL-17 with increased Th17 cells and significant decrease in Th1 cells in the spleen of adrenalectomized mice treated with GC. Interestingly there was less accumulation of regulatory T cells together to a reduction in mean fluorescence intensity (MFI) of FOXP3 in CD4+CD25+ T cells in the spleen of mice exposed to DSS after adrenalectomy, most dependent on GC. Finally, the decline of regulatory mechanisms was accompanied by lower rates of proliferation and increased IL-10 in the supernatant culture of splenocytes of mice with disrupted HPA axis, indicating that the absence of endogenous GC altered significantly the homeostasis of the immune system. Together, our results demonstrate that the HPA axis is important in modulating the immune response during experimentally induced colitis
Glasper, Erica Renee. "Psychobiological factors alter health outcome". Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1148415999.
Testo completoGrover, Sanita. "Role of hypothalamic pituitary adrenal axis in prenatal programming of adult disease". 2008. http://hdl.handle.net/2440/48490.
Testo completoThesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproductive Health, 2008
Castro-Diehl, Olga Cecilia. "Association of Sleep Duration and Quality with Activation of Two Neuroendocrine Systems: Hypothalamic-Pituitary-Adrenal Axis and Sympathetic Nervous System. The Multi-Ethnic Study of Atherosclerosis (MESA)". Thesis, 2016. https://doi.org/10.7916/D8TH8MKR.
Testo completoBerntson, Jessica. "Depressive Symptom Severity, Stressful Life Events, and Subclinical Atherosclerosis in African American Adults". Thesis, 2015. http://hdl.handle.net/1805/8476.
Testo completoProspective epidemiologic evidence indicates that both stressful life events (SLEs) and depression are associated with an increased risk of subclinical atherosclerosis and cardiovascular disease (CVD) events. Even though stressful life events (SLEs) and depression co-occur and may act together to influence cardiovascular disease (CVD) risk, these psychosocial factors have been mainly examined in isolation. For instance, depression may moderate the relationship between SLEs and CVD outcomes. I hypothesized that depressive symptoms would potentiate the deleterious effect of SLEs on subclinical atherosclerosis. This hypothesis is plausible, given that depressed adults exhibit exaggerated and prolonged sympathetic nervous system, hypothalamic-pituitary-adrenal (HPA) axis, and inflammatory responses to stress, which in turn could promote atherosclerosis. As compared to their nondepressed counterparts, depressed individuals may also be more likely to engage in maladaptive methods to cope with SLEs (e.g., increased tobacco use, alcohol use, and consumption of low-nutrient, energy dense foods), which could also promote atherosclerosis. I examined cross-sectional data from 274 to 279 (depending on the outcome measure) older, African American adults (mean age = 66 years, 67% female) with no evidence of clinical CVD or dementia who participated in the St. Louis African American Health-Heart study (2009–2011). Number of SLEs was assessed using the Life Events Calendar, a structured interview. From this interview, a continuous SLEs variable was computed (number of adult SLEs: 0, 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, or 11+). Severity of depression symptoms was measured using the 17-item Hamilton Rating Scale for Depression (HAM-D). Two measures of subclinical atherosclerosis were obtained: carotid intima-media thickness (CIMT; assessed by ultrasonography) and coronary artery calcification (CAC; assessed by multi-detector computerized tomography). I conducted linear (CIMT) and logistic (CAC) regression models, first adjusted for demographics (age, sex, education) and then fully-adjusted (demographics; mean arterial pressure; low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C); hemoglobin A1c; BMI; tobacco use; diabetes diagnosis; and use of antihypertensitve, lipid lowering, antidiabetic, and antidepressant medications). No main effects of SLEs or HAM-D were found for CIMT or CAC. There were also no SLEs by HAM-D interactions for CIMT or CAC. Because the current results are largely inconsistent with prior literature and there is a paucity of studies utilizing African American samples, future research is needed to examine the independent and interactive associations of SLEs and depressive symptoms with measures of subclinical atherosclerosis. If the present results are replicated, it may suggest that SLEs, depressive symptoms, and their interactive effect are not cardiotoxic among African American adults.
Connor, Kristin Leanne. "Effect of maternal periconceptional undernutrition on the development of the fetal hypothalamic-pituitary-adrenal axis and placenta: Implications for the timing of birth and postnatal disease risk". 2009. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=968397&T=F.
Testo completoRumball, Christopher William Henry. "Effects of periconceptional undernutrition and twinning on ovine pregnancy". 2008. http://hdl.handle.net/2292/3290.
Testo completoAuckland Medical Research Foundation, Health Research Council of New Zealand