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Books on the topic 'Hypothalamic hormones'

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Published: 4 June 2021
Last updated: 29 July 2024

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1

Kenkyūjo, Gunma Daigaku Naibunpi, and Gunma Symposium on Endocrinology (22nd : 1984 : Maebashi-shi, Japan), eds. Hypothalamic peptides in endocrinology: Morphological and physiological aspects. Tokyo: Center for Academic Publications Japan, 1985.

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2

Shennan, Kathleen I. J. Regulation of hypothalamic neurotensin by thyroid hormones. Birmingham: University of Birmingham, 1985.

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3

P, Beck-Peccoz, ed. Syndromes of hormone resistance on the hypothalamic-pituitary-thyroid axis. Boston: Kluwer Academic Publishers, 2004.

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4

Liposits, Zsolt. Ultrastructural immunocytochemistry of the hypothalamic corticotropin releasing hormone synthesizing system: Anatomical basis of neuronal and humoral regulatory mechanisms. Stuttgart: Gustav Fischer Verlag, 1990.

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5

Rasmussen, Jane Elliott. The trophic effects of estradiol on virally transformed hypothalamic cell lines. [New Haven: s.n.], 1990.

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6

International Symposium on Protirelin Tartrate (TRH-T) (1988 Taormina, Italy). Protirelin tartrate (TRH-T): Pharmacological and clinical studies : recent advances and perspectives. London: Libbey, 1988.

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7

Ferring Symposium on Brain and Pituitary Peptides (3rd 1985 Noordwijk, Netherlands). Pulsatile GnRH 1985: Proceedings of the 3rd Ferring Symposium, Noordwijk, September 11-13, 1985. Edited by Coelingh Bennink, Herman Jan Tymen, 1943-. Haarlem: Ferring, 1985.

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8

B, Bercu Barry, Walker Richard F. 1939-, and International Symposium on Growth Hormone Secretagogues (1994 : Saint Petersburg Beach, Fla.), eds. Growth hormone secretagogues. New York: Springer, 1996.

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9

Beck-Peccoz, Paolo, ed. Syndromes of Hormone Resistance on the Hypothalamic-Pituitary-Thyroid Axis. Boston, MA: Springer US, 2004. http://dx.doi.org/10.1007/978-1-4020-7852-1.

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10

F, Schatzberg Alan, Nemeroff Charles B, and American College of Neuropsychopharmacology. Meeting, eds. The Hypothalamic-pituitary-adrenal axis: Physiology, pathophysiology, and psychiatric implications. New York: Raven Press, 1988.

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11

Wimersma Greidanus, Tj. B. van., ed. and Lamberts, Steven W. J., ed., eds. Regulation of pituitary function. Basel: Karger, 1985.

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12

R, D'Agata, and Chrousos George P, eds. Recent advances in adrenal regulation and function. New York: Raven Press, 1987.

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13

Leng, G. Computational neuroendocrinology. Chichester, West Sussex, UK: John Wiley & Sons, Inc., 2016.

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14

Hähnle, Bettina Anna. Der Kortikotropin-Releasing-Hormon-Stimulationstest in der Untersuchung der Hypothalamus-Hypophysen-Nebennierenrinden-Achse bei klinisch gesunden Hunden und Hunden mit Cushing-Syndrom. München: [s.n.], 1992.

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15

K, Lüdecke Dieter, Chrousos George P, Tolis George, and International Symposium on Challenges of Hypersecretion: ACTH, Cushing's Syndrome, and Other Hypercortisolemic States (2nd : 1989 : Crete, Greece), eds. ACTH, Cushing's syndrome, and other hypercortisolemic states. New York: Raven Press, 1990.

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16

F, Mantero, ed. The Adrenal and hypertension: From cloning to clinic. New York: Raven Press, 1989.

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17

Fulder, Stephen. The tao of medicine: Ginseng and other Chinese herbs for inner equilibrium and immune power. Rochester, Vt: Healing Arts Press, 1990.

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18

Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.

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19

Li, Choh Hao. Hypothalamic Hormones. Elsevier Science & Technology Books, 2012.

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20

Ultrastructural Immunocytochemistry of the Hypothalamic Corticotropin Releasing Hormone Synthesizing System (Progress in Histochemistry and Cytochemi). Lubrecht & Cramer, Limited, 1990.

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21

Hypothalamic Peptide Hormones and Pituitary Regulation. Springer, 2012.

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22

John, Porter. Hypothalamic Peptide Hormones and Pituitary Regulation. Springer London, Limited, 2012.

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23

John, Porter. Hypothalamic Peptide Hormones and Pituitary Regulation. Springer, 2012.

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24

Hypothalamic peptides in endocrinology: Morphological and physiological aspects (Gunma symposia and endocrinology). VNU Science Press BV, 1985.

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25

McKerns, Kenneth W. Hormonal Control of the Hypothalamo-Pituitary-Gonadal Axis. Springer, 2012.

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26

McKerns, Kenneth W. Hormonal Control of the Hypothalamo-Pituitary-Gonadal Axis. Springer, 2013.

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27

McKerns, Kenneth W. Hormonal Control of the Hypothalamo-Pituitary-Gonadal Axis. Springer, 2012.

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28

Young, Allan H., and 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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29

Jürimäe, Jaak. Hormones and training. Edited by Neil Armstrong and Willem van Mechelen. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198757672.003.0033.

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Physical exercise regulates energy balance and is important to growth and maturation. These processes are regulated by the endocrine system. Endocrine mechanisms in the response to sport training include growth hormone-insulin-like growth factor-1 (GH-IGF-1), hypothalamic-pituitary-gonadal and hypothalamic-pituitary-adrenal axes, and peripheral markers of energy homeostasis. Physical performance is associated with anabolic adaptations of the GH-IGF-1 system in child athletes alongside spontaneous growth, while heavy training does not affect basal testosterone levels. In female adolescent athletes, the major factor altering reproductive hormone secretion is energy deficiency, rather than exercise stress or increase in exercise energy expenditure. Ghrelin is another indicator of energy imbalance across the menstrual cycle. Pubertal onset decreases ghrelin, and leptin levels are reduced and may remain unchanged between prepuberty and maturation in athletes. To better understand the influence of high training load on hormonal markers responsible for overall growth and energy homeostasis, growing athletes should be monitored often.
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30

Patisaul, Heather B., and Scott M. Belcher. The Neuroendocrine System and General Mechanisms of Endocrine Disruption. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780199935734.003.0004.

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The neuroendocrine system is the interface between the endocrine and nervous systems. This chapter presents an overview of the neuroendocrine system and endogenous hormones, with a primary focus on the hypothalamic-pituitary-gonadal (HPG) axis, the hypothalamic-pituitary-adrenal (HPA) axis and the hypothalamic-pituitary-thyroid axis (HPT). The importance of impacts of exogenous compounds, both natural and man-made, on the neuroendocrine system is discussed, with a focus on endocrine-disruptive actions of plant-derived phytoestrogens and the role of the aryl hydrocarbon receptor as an environmental sensor. The impacts of EDCs on feed-forward and negative feedback regulation of neuroendocrine functions, including those mediated by estrogen, androgen, and thyroid pathways, as well as other less studied pathways of hormonal signaling that involve disruption of neurosteroids, peptide hormones, and adrenal hormone signaling are also presented.
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31

Shah, Nandkumar S., and Alexander G. Donald. Psychoneuroendocrine Dysfunction. Springer, 2012.

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32

Psychoneuroendocrine Dysfunction. Springer London, Limited, 2013.

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33

Gainer, Harold. Peptides in Neurobiology. Springer, 2012.

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34

Gainer, Harold. Peptides in Neurobiology. Springer, 2011.

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35

Steiger, Axel. Sleep in endocrine disorders. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0044.

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Related to bidirectional interaction between electrophysiological and endocrine activity during sleep, which are assessed by sleep electroencephalography (EEG) and hormone profiles, respectively, sleep changes occur frequently in endocrine disorders. In most of these disorders, sleep is impaired. Only in patients with prolactinoma is slow-wave sleep elevated. This chapter summarizes the current knowledge on sleep in disorders of the hypothalamic–pituitary–adrenocortical (HPA) and hypothalamic–pituitary–somatotropic (HPS) systems, in hypo- and hyperthyroidism, in diabetes mellitus, in prolactinoma, in disorders related to gonadal hormones, and with regard to disturbed endocrine rhythms related to environmental influences.
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36

Steckler, T., N. H. Kalin, and J.M.H.M. Reul. Handbook of Stress and the Brain Part 1: The Neurobiology of Stress, Volume 15, Part 1 (Techniques in the Behavioral and Neural Sciences). Elsevier Science, 2005.

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37

Mottram, Linda-Jayne, and Gavin G. Lavery. The metabolic and nutritional response to critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0202.

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The metabolic response to critical illness is complex and affects every body system. The first phase of this response is characterized by increased hypothalamic pituitary activity and resistance (decreased response) to effector hormones in many target tissues. Cytokines released in the early stages of such illness may be important as they appear to stimulate the hypothalamic pituitary axis directly as part of this ‘stress response’. This phase is considered ‘adaptive’ (helpful), increasing the availability of glucose, free fatty acids, and amino acids as substrates for vital organs. However, in prolonged illness, the neuroendocrine response is very different with damped hypothalamic responses, leading to a state in which catabolism predominates, leading to what might be termed the critical illness wasting syndrome. The gastrointestinal (GI) failure often associated with prolonged critical illness appears to be due, at least in part, to an altered neuroendocrine environment. The poor nutritional state associated with GI failure exacerbates the catabolic response, prolonging illness and the period of intensive care management required by the patient. The result is increased mortality and, in survivors, a more prolonged recovery/rehabilitation process.
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38

(Editor), Efrain C. Azmitia, E. R. De Kloet (Editor), New York Academy of Sciences (Corporate Author), and Philip W. Landfield (Editor), eds. Brain Corticosteroid Receptors: Studies on the Mechanism, Function, and Neurotoxicity of Corticosteroid Action (Annals of the New York Academy of). New York Academy of Sciences, 1995.

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39

Steckler, T., N. H. Kalin, and J.M.H.M. Reul. Handbook of Stress and the Brain Part 2: Stress: Integrative and Clinical Aspects, Volume 15, Part 2 (Techniques in the Behavioral and Neural Sciences). Elsevier Science, 2005.

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40

Steckler, T., N. H. Kalin, and J.M.H.M. Reul. Handbook of Stress and the Brain (Two-Volume Set) (Techniques in the Behavioral and Neural Sciences). Elsevier Science, 2005.

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41

Newell-Price, John, Alia Munir, and Miguel Debono. Normal function of the endocrine system. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0182.

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Endocrinology is the study of hormones (and their glands of origin), their receptors, the intracellular signalling pathways they invoke, and their associated diseases. The clinical specialty of endocrinology focuses specifically on the endocrine organs, that is, the organs whose primary function is hormone secretion, including the hypothalamus, the pituitary, the thyroid, the parathyroid, the adrenal glands, the pancreas, and the reproductive organs.
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42

O’Neal, M. Angela. Acute Headache in Pregnancy. Edited by Angela O’Neal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190609917.003.0020.

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The case illustrates the characteristics of pituitary apoplexy. This anatomy of the pituitary, which predisposes to the condition, is described. The most common clinical feature is headache. Visual disturbance related to optic chiasm or optic nerve involvement is also common. Pituitary apoplexy is a neuroendocrine emergency. The most important hormone involved is adrenocorticotropic hormone, ACTH. However, there are often multiple hormonal deficiencies: growth hormone, hypothyroidism, and hypogonadotropic deficiency. A high prolactin level may reflect a prolactinoma or be due to hypothalamic inhibition. Diabetes insipidus (DI) is also common. The most urgent issue in treating pituitary apoplexy is prompt assessment of fluid and electrolyte imbalance and the replacement of corticosteroids.
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43

Leng, Gareth. Heart of the Brain: The Hypothalamus and Its Hormones. MIT Press, 2018.

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44

Leng, Gareth. Heart of the Brain: The Hypothalamus and Its Hormones. MIT Press, 2018.

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45

Leng, Gareth. Heart of the Brain: The Hypothalamus and Its Hormones. MIT Press, 2018.

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46

Ganong, William F., and Mary F. Dallman. Hypothalamic-Pituitary-Adrenal Axis Revisited: A Symposium in Honor of Dorothy Krieger and Edward Herbert (Annals of the New York Academy of Sciences). New York Academy of Sciences, 1988.

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47

Yehuda, Rachel. Neuroendocrinology of PTSD. Edited by Charles B. Nemeroff and Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0020.

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Initial studies on the neuroendocrine basis of post-traumatic stress disorder (PTSD) showed a biological dysregulation of stress response systems that appeared to be incompatible with the stress response theories that had prevailed when PTSD was first established as a diagnosis. Cortisol levels were found to be lower and catecholamine higher in patients with PTSD than in those with major depression and other psychiatric disorders. There was no explanation for why levels of two stress hormones that are generally correlated—cortisol and norepinephrine—would be different, and it was also not clear why cortisol levels would be on the low end of the normal spectrum, when the classic stress response paradigms suggested stress results in elevated cortisol. The study of neuroendocrinology and hypothalamic–pituitary–adrenal (HPA) axis alterations in PTSD provides an object lesson in how paradoxical observations might be pursued toward a better understanding of the pathophysiology of a disorder. This chapter reviews HPA findings in PTSD in cross-sectional and prospective longitudinal studies.
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48

Bercu, Barry B., and Richard F. Walker. Growth Hormone Secretagogues. Springer, 2011.

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49

Bercu, Barry B., and Richard F. Walker. Growth Hormone Secretagogues. Springer, 2012.

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50

Heart of the Brain: The Hypothalamus and Its Hormones. MIT Press, 2024.

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