Bibliografie tematiche / Hypothalmic diseases

Letteratura scientifica selezionata sul tema "Hypothalmic diseases"

Autore: Grafiati
Pubblicato: 27 luglio 2024
Ultima modifica: 29 luglio 2024

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Articoli di riviste sul tema "Hypothalmic diseases"

1

Haug, R. H. "Recovery of the hypothalmic-pituitary adrenal (HPA) axis in patients with rheumatic diseases receiving low-dose prednisone". Journal of Oral and Maxillofacial Surgery 52, n. 2 (febbraio 1994): 203. http://dx.doi.org/10.1016/0278-2391(94)90422-7.

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Kim, Ye Jin, Thai Hien Tu, Sunggu Yang, Jae Kwang Kim e Jae Geun Kim. "Characterization of Fatty Acid Composition Underlying Hypothalamic Inflammation in Aged Mice". Molecules 25, n. 14 (11 luglio 2020): 3170. http://dx.doi.org/10.3390/molecules25143170.

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Abstract (sommario):
Degenerative diseases, which can develop during aging, are underlined by inflammatory processes. Hypothalamic inflammation triggered by elevation in circulating fatty acid levels is directly coupled to metabolic disorders. The present study aimed to investigate and characterize the hypothalamic inflammation and composition of fatty acids in the hypothalami of aged mice. We verified that inflammation and microglial activation occur in the hypothalami of aged mice by performing quantitative real-time PCR and using immunohistochemistry methods. In addition, we observed increased levels of various saturated fatty acids in the hypothalami of aged mice, whereas no major changes in the levels of circulating fatty acids were detected using gas chromatography with a flame ionization detector. Collectively, our current findings suggest that increases in saturated fatty acid levels are coupled to hypothalamic inflammation and thereby cause perturbations in energy metabolism during the aging process.
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3

Zapanti, Evangelia, Konstantinos Terzidis e George Chrousos. "Dysfunction of the Hypothalamic-Pituitary-Adrenal axis in HIV infection and disease". HORMONES 7, n. 3 (15 luglio 2008): 205–16. http://dx.doi.org/10.14310/horm.2002.1200.

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Mravec, Boris, e Alena Szelle Černáčková. "Hypothalamic inflammation and somatic diseases". Česká a slovenská neurologie a neurochirurgie 81/114, n. 3 (31 maggio 2018): 278–83. http://dx.doi.org/10.14735/amcsnn2018278.

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von Werder, K., e O. A. Müller. "Medical therapy of hypothalamic diseases". Acta Neurochirurgica 75, n. 1-4 (marzo 1985): 147–51. http://dx.doi.org/10.1007/bf01406335.

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Salvio, Gianmaria, Marianna Martino, Giulia Giancola, Giorgio Arnaldi e Giancarlo Balercia. "Hypothalamic–Pituitary Diseases and Erectile Dysfunction". Journal of Clinical Medicine 10, n. 12 (9 giugno 2021): 2551. http://dx.doi.org/10.3390/jcm10122551.

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Abstract (sommario):
Several hormones contribute to ensure penile erection, a neurovascular phenomenon in which nitric oxide plays a major role. Erectile dysfunction (ED), which is defined as the persistent inability to obtain or maintain penile erection sufficient for a satisfactory sexual performance, may be due to arteriogenic, neurogenic, iatrogenic, but also endocrinological causes. The hypothalamus–pituitary axis plays a central role in the endocrine system and represents a fundamental link between the brain and peripheral glands, including gonads. Therefore, the hormonal production of the hypothalamic–pituitary axis can control various aspects of sexual function and its dysregulation can compromise erectile function. In addition, excess and deficiency of pituitary hormones or metabolic alterations that are associated with some pituitary diseases (e.g., Cushing’s disease and acromegaly, hypopituitarism) can determine the development of ED with different mechanisms. Thus, the present review aimed to explore the relationship between hypothalamic and pituitary diseases based on the most recent clinical and experimental evidence.
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Swaab, Dick F. "Hypothalamic Peptides in Human Brain Diseases". Trends in Endocrinology & Metabolism 10, n. 6 (agosto 1999): 236–44. http://dx.doi.org/10.1016/s1043-2760(99)00158-7.

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Reimann, Hobart A. "HYPOTHALAMIC-HYPOPHYSEAL-NEURAL INFLUENCE IN PERIODIC DISEASES". Annals of the New York Academy of Sciences 117, n. 1 (16 dicembre 2006): 589–94. http://dx.doi.org/10.1111/j.1749-6632.1964.tb48210.x.

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Rychlik, A., M. Nowicki, A. Kolodziejska-Sawerska e M. Szweda. "The effect of orally administered Budesonide on the hypothalamic-pituitary-adrenal axis in dogs with inflammatory bowel disease". Veterinární Medicína 62, No. 5 (9 maggio 2017): 261–68. http://dx.doi.org/10.17221/130/2015-vetmed.

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The aim of this study was to evaluate the effect of Budesonide on the hypothalamic-pituitary-adrenal (HPA) axis in dogs with inflammatory bowel disease. The effect of orally administered Budesonide (Entocort) on the HPA axis was analysed in 21 dogs with inflammatory bowel disease. Biochemical analyses were carried out to evaluate the activity levels of alanine aminotransferase, asparagine aminotransferase, alkaline phosphatase, cortisol and endogenous adrenocorticotropic hormone. Urine samples were collected from each patient before the study and after 30 days of the experiment to determine the composition and the physical and chemical properties of urine sediments. Considerably lower serum concentrations of cortisol and endogenous adrenocorticotropic hormone were observed after 30 days of treatment. A significant increase in alkaline phosphatase levels was noted on Day 30. In the studied dogs, the drop in HPA axis activity was correlated with side effects associated with the administered glucocorticosteroid (polyuria, polydipsia). In conclusion, we have shown that oral administration of Budesonide to dogs diagnosed with inflammatory bowel disease significantly suppressed the activity of the HPA axis.
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Lapko, Inna V., Alla V. Zheglova, Kristina V. Klimkina e Inessa A. Bogatyreva. "Neurohumoral regulation under exposure to vibration and physical overloads". Hygiene and sanitation 101, n. 10 (23 ottobre 2022): 1200–1205. http://dx.doi.org/10.47470/0016-9900-2022-101-10-1200-1205.

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Introduction. In response to the action of various occupational factors, central regulatory mechanisms, including the hypothalamus, are involved. Clarification of the influence of the hypothalamus on the indicators of peripheral blood circulation, peripheral innervation and bone metabolism under the influence of vibration and physical overloads is relevant for the diagnosis and treatment of occupational diseases of a neurological profile. The aim of the study. To establish the relationship between hypothalamic disorders and functional indicators of occupational diseases of the peripheral nervous system under the influence of vibration and physical overloads. Material and methods. One hundred fifteen tunnellers and machinists of the drilling rig of JSC “KMAruda Combine”, 26 tunnellers of the drainage mine of JSC “Stoilensky Mining and Processing Plant”, 65 workers of auxiliary occupations were examined. Depending on the influencing factor, they were divided into four groups with occupational neurological pathology, the fifth group was control Examined cases were divided into subgroups: A - without hypothalamic disorders and B - with hypothalamic syndrome. The criteria for the diagnosis of hypothalamic syndrome are clinical. All the examined patients underwent rheovasography, stimulation electroneuromyography of the extremities, ultrasound densitometry. Results. It was found that in patients with vibration disease from the effects of local or general vibration, especially when combined with lumbosacral radiculopathy during rheovasography, there are decrements in pulse blood filling, changes in vascular tone in vessels of various calibers and venous dysfunction, which are aggravated against the background of hypothalamic disorders. Hypothalamic disorders contribute to the aggravation of peripheral nerve indices: a decrease in the amplitude of the M-response, the rate of propagation of excitation along sensory axons and an increase in the value of residual latency. Functional assessment of bone tissue revealed the greatest prevalence of osteopenia syndrome in patients with vibration disease and its combined forms with lumbosacral radiculopathy in subgroups with hypothalamic-pituitary dysfunction (up to 33.6%). The frequency of detected functional disorders was established to increase with the progression of occupational diseases. Limitations. The study was conducted in workers with neurological occupational diseases exposed to vibration and physical overloads. Conclusions. Neurohumoral disorders, manifested by hypothalamic syndrome caused by exposure to general and local vibration in combination with physical overloads, contribute to the development or aggravation of functional changes in the body of workers, aggravating the course of occupational diseases of the peripheral nervous system, which can be used to develop diagnostic and treatment methods, and study the pathogenesis of diseases.
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Tesi sul tema "Hypothalmic diseases"

1

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.

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Dysfunction of the limbic-hypothalamic-pituitary-adrenal (LHPA) axis is a common finding in advanced dementia. In this study, the function of the LHPA axis at different levels was investigated in patients with dementia and in healthy elderly. A subtle disturbance in the feedback regulation of the LHPA axis was found in patients with early (i.e., mild to moderate) Alzheimer’s disease (AD). After 0.5 mg dexamethasone, serum cortisol levels were less suppressed in AD patients and plasma adrenocorticotropin (ACTH) levels were lower as compared with healthy elderly. After stimulation with human corticotropin-releasing hormone a blunted ACTH response was found in AD patients while relative serum cortisol, dehydroepiandrosterone, and androstenedione responses were increased. Significant correlations were found between low plasma ACTH levels and temporal lobe atrophy and between low peak plasma ACTH levels and hippocampal atrophy measured with computer tomography. Patients with advanced AD and multi-infarct dementia had lower basal levels of dehydroepiandrosterone sulphate in combination with no difference in cortisol levels, resulting in a high cortisol/DHAS ratio. The difference persisted after adjustments for age and sex in a multivariate analysis. In patients with early AD, basal serum levels of dehydroepiandrosterone and androstenedione were increased, and this increase was accentuated after stimulation with ACTH. Peripheral glucocorticoid sensitivity was examined by skin vasoconstrictor blanching tests. Patients with AD and patients treated with glucocorticoids showed skin blanching at higher clobetasol concentrations than healthy elderly. These findings justify further investigations on the role of LHPA axis dysfunction in Alzheimer’s disease and its possible importance for the pathophysiology of the disease.
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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.

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O'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.

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Hawkins, 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.

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Nguyen, 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.

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Abebe, 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.

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Dromey, 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.

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[Truncated abstract] G-protein coupled receptors (GPCRs) form one of the largest superfamilies of cell-surface receptors and respond to a vast range of stimuli including light, hormones and neurotransmitters. Although structurally similar, GPCRs are regulated by many diverse proteins, which allow the specific functions of each receptor to be carried out. This thesis focussed on two well-documented GPCRs, the thyrotropin releasing hormone receptor (TRHR) and gonadotrophin-releasing hormone receptor (GnRHR), which control the thyroid and reproductive endocrine pathways respectively. Although each of these anterior pituitary receptors is responsible for distinct physiological responses, both are integral to normal development and homeostasis. This thesis focused on three areas of GPCR regulation: ?-arrestin recruitment, transcription factor regulation and receptor up-regulation. The role of the cytoplasmic protein, ?-arrestin, has perhaps been previously underestimated in GPCR regulation, but it is now increasingly apparent that ?-arrestins not only inhibit further G-protein activation and assist in GPCR internalisation but also act as complex scaffolding platforms to mediate and amplify downstream signalling networks for hours after initial GPCR activation. It is therefore becoming increasingly important to be able to monitor such complexes in live cells over longer time-frames. ... Members of the E2F transcription family have been previously identified by this laboratory as potential GnRHR interacting proteins, via a yeast-2-hybrid screen and BRET. This thesis further investigated the role of E2F family members and demonstrates that a range of GPCRs are able to activate E2F transcriptional activity when stimulated by agonist. However, despite GnRHR displaying robust E2F transcriptional activation upon agonist stimulation, this did not result in any conclusive evidence for functional regulation, although it is possible E2F may modulate and assist in GnRHR trafficking. Furthermore it is apparent that E2F family members are highly redundant, as small effects in GnRHR binding and cell growth were only observed when protein levels of both E2F4 and E2F5 were altered. During the course of the investigation into the effect of E2F transcription on GPCR function, it was evident that long-term agonist stimulation of GnRHR had a profound effect on its expression. As this was explored further, it became clear that this agonist-induced up-regulation was both dose- and time-dependent. Furthermore, altering levels of intracellular calcium and receptor recycling/synthesis could modulate GnRHR up-regulation. In addition, an extremely sensitive CCD camera has been used for the first time to visualise the luciferase activity attributed to GnRHR up-regulation. Overall, this thesis demonstrates the complex nature of GPCR regulation. For the first time, long-term BRET analysis on ?-arrestin interactions with both classes of GPCRs has been examined in a variety of cellular formats. This has given valuable insights into the roles of phosphorylation and internalisation on ?-arrestin interaction. Additionally, this thesis has revealed that prolonged agonist exposure increases receptor expression levels, which has major implications for drug therapy regimes in the treatment of endocrine-related disorders and tumours.
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Nye, 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.

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Gordon, 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.

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Depression is associated with an increased risk of cardiovascular disease (CVD). One possible mechanism of this effect is dysregulation of the biological stress systems, the autonomic nervous system (ANS) and hypothalamic-pituitary-adrenal (HPA) axis. The current thesis aimed to better understand the relationship between depression and these two systems. In the first study, the effect of major depression on heart rate recovery following exercise, a marker of ANS tone, was examined in cardiac patients. Depression was associated with poor early heart rate recovery, suggesting reduced post-exercise parasympathetic activation. The second study, which included healthy participants, examined the effect of cognitive and somatic depressive symptoms in relation to recovery of heart rate and heart rate variability, two markers of ANS tone, in response to interpersonal laboratory stressors. Both types of symptoms were found to predict post-stress recovery. The third study aimed to examine the relationship between major depression both ANS and HPA axis activity in response to a stressful diagnostic test. Furthermore, it aimed to determine whether antidepressant medication is effective in restoring a normal stress response in depressed individuals. Depressed cardiac patients exhibited elevated cortisol levels in response to the test but this effect was not seen among depressed individuals taking antidepressant medication. However, neither depression nor antidepressant use was associated with heart rate variability. As a whole, these studies suggest a modest and inconsistent relationship between depression and prolonged post-stress ANS activation. On the other hand, the relationship between depression and exaggerated HPA axis activity appears to be relatively strong. Finally, antidepressant medication may be effective in reversing the excessive HPA axis activation observed in depressed individuals.
La 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.
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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.

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Libri sul tema "Hypothalmic diseases"

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Casanueva, Felipe F., e Ezio Ghigo, a cura di. Hypothalamic-Pituitary Diseases. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-44444-4.

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Casanueva, Felipe F., e Ezio Ghigo, a cura di. Hypothalamic-Pituitary Diseases. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-38681-2.

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Dina, Nerozzi, Goodwin Frederick K. 1936-, Costa Erminio e International Congress on "Hypothalamic Dysfunction in Neuropsychiatric Disorders" (1986 : Rome, Italy), a cura di. Hypothalamic dysfunction in neuropsychiatric disorders. New York: Raven Press, 1987.

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Geer, Eliza B., a cura di. The Hypothalamic-Pituitary-Adrenal Axis in Health and Disease. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-45950-9.

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Kurup, Ravikumar. Hypothalamic digoxin, cerebral dominance and brain function in health and diseases. New York: Nova Science Publishers, Inc., 2003.

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C, Gaillard Rolf, a cura di. The ACTH axis: Pathogenesis, diagnosis, and treatment. Boston: Kluwer Academic Publishers, 2003.

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Martin, Joseph B. Clinical neuroendocrinology. 2a ed. Philadelphia: Davis, 1987.

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Ghigo, Ezio, e Felipe F. Casanueva. Hypothalamic-Pituitary Diseases. Springer International Publishing AG, 2018.

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Hypothalamic-Pituitary Diseases. Springer, 2018.

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Young, Allan H., e Mario F. Juruena. Hypothalamic–pituitary–adrenal axis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.003.0006.

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Increased adrenocortical secretion of hormones, primarily cortisol in depression, is one of the most consistent findings in neuropsychiatry. The maintenance of the internal homeostatic state of an individual is facilitated by the ability to circulate glucocorticoids to exert negative feedback on the secretion of hypothalamic–pituitary–adrenal (HPA) hormones through binding to mineralocorticoid and glucocorticoid receptors, thus limiting the vulnerability to diseases related to psychological stress in genetically predisposed individuals. The HPA axis response to stress can be thought of as a crucial part of the organism’s response to stress: acute responses are generally adaptive, but excessive or prolonged responses can lead to deleterious effects. A spectrum of conditions may be associated with increased and prolonged activation of the HPA axis, including depression, poorly controlled diabetes mellitus, and metabolic syndrome. HPA axis dysregulation and hypercortisolaemia may further contribute to a hyperglycaemic or poorly controlled diabetic state.
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Capitoli di libri sul tema "Hypothalmic diseases"

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Reyes, Francisco I. "Hypothalamic-Pituitary Disease". In Gynecologic Endocrinology, 349–67. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2157-6_16.

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Kelley, Roger E. "Traumatic and Degenerative Hypothalamic Diseases". In The Human Hypothalamus, 479–95. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-62187-2_21.

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Tiedemann, Anne, Catherine Sherrington, Daina L. Sturnieks, Stephen R. Lord, Mark W. Rogers, Marie-Laure Mille, Paavo V. Komi et al. "Functional Hypothalamic Amenorrhea". In Encyclopedia of Exercise Medicine in Health and Disease, 350. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2420.

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Bulsara, Ketan R., Joshua Knopf, Rebecca Calafiore e Anzhela D. Moskalik. "Neurosurgical Aspects of Hypothalamic Disease". In The Human Hypothalamus, 171–80. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-62187-2_9.

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Sainburg, Robert L., Andrew L. Clark, George E. Billman, Zachary J. Schlader, Toby Mündel, Kevin Milne, Earl G. Noble et al. "Hypothalamic-Pituitary-Cortisol Hypothesis". In Encyclopedia of Exercise Medicine in Health and Disease, 428. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2522.

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Bronstein, Marcello D., Malebranche B. C. Cunha Neto e Nina Rosa de C. Musolino. "Diagnosis and Treatment of Hypothalamic Disease". In Neuroendocrinology in Physiology and Medicine, 475–97. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-707-9_27.

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Lovera, Jesus, Olinda Verdecie Feria e Vaniolky Losada Leon. "Infectious Diseases of the Hypothalamic-Pituitary Axis". In The Human Hypothalamus, 415–35. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-62187-2_19.

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Kaltsas, Gregory, Anthony S. Zannas e George P. Chrousos. "Hypothalamic–Pituitary–Adrenal Axis and Cardiovascular Disease". In Stress and Cardiovascular Disease, 71–87. London: Springer London, 2011. http://dx.doi.org/10.1007/978-1-84882-419-5_5.

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Proske, Uwe, David L. Morgan, Tamara Hew-Butler, Kevin G. Keenan, Roger M. Enoka, Sebastian Sixt, Josef Niebauer et al. "Exercise-Associated Functional Hypothalamic Amenorrhea". In Encyclopedia of Exercise Medicine in Health and Disease, 324. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_4207.

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Zarzour, Hekmat, Margaret Pain, Joshua Bederson e Kalmon D. Post. "Surgical Treatment of Cushing’s Disease". In The Hypothalamic-Pituitary-Adrenal Axis in Health and Disease, 149–64. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45950-9_8.

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Atti di convegni sul tema "Hypothalmic diseases"

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Oliveira, Jefferson Borges de, Caroline Berthier Zanin, Gustavo Carreira Henriques, Maiévi Liston, Rafael Glória Zatta, Rodrigo de Faria Martins e Tatiana Pizzolotto Bruch. "Pallister-Hall Syndrome - case report". In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.575.

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In 1980, Hall et all described a syndrome characterized by “hamartoblastoma”, hypopituitarism, unperfurated anus, polydactyly postaxial and numerous visceral anomalies, today known as Pallister-Hall Syndrome. On the study, Hall et all reported six cases of children with that malformation syndrome - lethal on neonatal period. None of the newborns had anterior hypophysis and the hypothalamic tumor was apparent in the inferior part of the brain, going from the optic chiasm to the interpeduncular fossa. Besides, other anomalies were found, such as: laryngeal split, abnormal pulmonary lobation, renal agenesis or dysplasia, shorts fourth metacarpals, nail dysplasia, multiple mouth frenulum, hypoadrenalism, congenital cardiomyopathy and intrauterine growth retardation. Every case was sporadic, the chromosome were apparently normal, without consaguinity relations. Several similar, milder and even asymptomatic cases were described later on. Kletter and Biesecker (1992), Topf et all (1993) and Penman Splitt et all (1994), define the disease as dominant autosomal inheritance. Kettler and Biesecker (1992) stated that most cases as sporadic as a result of a gene mutation with variable expressiveness. According to Biesecker et al (1996), an international workshop determined diagnostic criteria to the Syndrome: Hypothalamic Hamartroma and Central Polydactyly; First degree relative with hypothalamic hamartroma and polydactyly; Dominant autosomal parrent inheritance or in a consistent form with germaine mosaicism. The radiological changes are important for differential diagnosis between Pallister-Hall Syndrome and other hamartroma-present diseases. The hypothalamic hamartroma isolated has phenotypical features and causes hormonal disorders such as early puberty. On the MRI (Magnetic resonance imaging) it shows hyperintese sign on attenuated fluid. On the other hand, the Pallister-Hall Syndrome the hamartroma shows itself as a isointense signs along with other deformities as polydactyly, for example. According to Kuo et al (1999), on MRI, the classic hypothalamic hamartroma isn’t calcified, is homogenous and isointense to the grey matter on weight images in T1, and isointense and often hyperintense on weight images in T2. Those findings are pretty distinctive and help distinguish the hypothalamic hamartroma from ordinary lesions, as craniopharyngioma and hypothalamic/opticalchiasmic glioma, observed in children. Case report: The patient ALDV, male, born in 30/12/1995, was referred to evaluation on the Medical Genetic Service from HCPA. At the time, aged one year and 8 months, he was the only son of a young, healthy couple with no consanguinity. The family history of similar cases or other genetic pathologies are unknown. The prenatal happened with no intercurrences, unless the smoking mother. It was a natural birth; Birth Weight: 2kg; High: 42cm; PC: 32cm. APGAR 9. At 8 months, starts an investigation for precocious puberty, and a karyotype was performed in her hometown: 46, XY (normal). He presents convulsive crises since one year old. DNPM: cephalic support when he had 8 months, sat without support at the age of one. Physical examination: Head circumference in the 97th percentile, length above the 97th percentile. Good general condition, dysmorphic, facies with fusion of eyebrows (sinofre), epicanthus, small nose, dysplastic ears with a broad shield, three café-au-lait spots on the body. Presence of pubic hair. Increase in length and diameter of the penis, as well as of the testicles, in relation to chronological age. In the hands, significant brachydactyly with bitateral hexadactyly. In the feet, bilateral hexadactyly. Proximal cutaneous syndactyly between the 2nd and 3rd bilateral arthroids, mainly on the right. Additional exams: Rx of hands and wrists for bone age: 7 years; Chronological Age: 1 year and 10 months. Normal abdominal ultrasound; Computed Tomography of Skull/Magnetic Resonance of Skull: hypothalamic expansive lesion (3 cm), compatible with hamartoma; triventricular hydrocephalus; Cavum septum pellucidum. Endocrinological Evaluation: compatible with precocious puberty of central cause. High resolution karyotype: 46, XY (normal). Computed tomography of the brain: Examination for neurological control, performed on 10/12/2014, 18-year-old patient. It was observed solid nodular formation in the hypothalamic region, hypodense, with well-defined limits, in close contact with the mesencephalon, without impregnation by contrast medium administered intravenously, measuring about 2.9 X 2.4 X 3.0 cm, in the respective laterolateral, anteroposterior and craniocaudal planes, which in correlation with the patient’s clinical history may be related to hypothalamic Hamartoma.
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Giani, Teresa, Francesca Falorni e Rolando Cimaz. "AB0979 CORTICOSTEROID TREATMENT IN PEDIATRIC RHEUMATIC DISEASES AND SUPPRESSION OF THE HYPOTHALAMIC-PITUITARY AXIS". In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.2744.

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Gabery, Sanaz, Barbara Baldo, Rana Soylu-Kucharz, Rachel Y. Cheong, Jo B. Henningsen, Elisabet Englund, Catriona McLean, Deniz Kirik, Glenda Halliday e Åsa Petersén. "A52 SIRT1 is increased in affected brain regions in huntington disease impacting hypothalamic metabolic pathways". In EHDN 2018 Plenary Meeting, Vienna, Austria, Programme and Abstracts. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/jnnp-2018-ehdn.50.

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Soylu-Kucharz, Rana, Natalie Adlesic, Jo Henningsen, Marcus Davidsson, Tomas Bjorklund, Maria Björkqvist e Åsa Petersén. "A53 Effects of hypothalamic circuitries on pathology in the ventral striatum in mouse models of huntington disease". In EHDN 2018 Plenary Meeting, Vienna, Austria, Programme and Abstracts. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/jnnp-2018-ehdn.51.

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Dickson, Elna, Rana Soylu Kucharz, Åsa Petersén e Maria Björkqvist. "A15 Hypothalamic expression of huntingtin causes distinct metabolic changes in the R6/2 and bachd mouse models of huntington’s disease". In EHDN Abstracts 2021. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/jnnp-2021-ehdn.14.

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Shpigel, A. S., e N. V. Vakurowa. "Features of the response of the pituitary-thyroid complex to the introduction of synthetic hypothalamic tyroliberin in vibration disease (VD) from the effects of local vibration". In II Международная конференция, посвящеенная 100- летию И.А. Држевецкой. СКФУ, 2022. http://dx.doi.org/10.38006/9612-62-6.2022.348.350.

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