Gotowe bibliografie tematyczne / Hypothalamic-pituitary-adrenal axis

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Gotowa bibliografia na temat „Hypothalamic-pituitary-adrenal axis”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 23 lutego 2023

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Artykuły w czasopismach na temat "Hypothalamic-pituitary-adrenal axis"

Kirnap, Mehmet, Hulusi Atmaca, Fatih Tanriverdi, Osman Ozsoy, Kursad Unluhizarci i Fahrettin Kelestimur. "Hypothalamic-pituitary-adrenal axis in patients with ankylosing spondylitis". HORMONES 7, nr 3 (15.07.2008): 255–58. http://dx.doi.org/10.14310/horm.2002.1206.

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Honour, J. W. "Hypothalamic-pituitary-adrenal axis". Respiratory Medicine 88 (sierpień 1994): 9–15. http://dx.doi.org/10.1016/s0954-6111(05)80035-6.

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Chez, Ronald A. "Fetal hypothalamic-pituitary-adrenal axis". American Journal of Obstetrics and Gynecology 183, nr 5 (listopad 2000): 1310. http://dx.doi.org/10.1067/mob.2000.107737.

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Gordon, D., C. G. Semple, G. H. Beastall i J. A. Thomson. "A study of hypothalamic-pituitary-adrenal suppression following curative surgery for Cushing's syndrome due to adrenal adenoma". Acta Endocrinologica 114, nr 2 (luty 1987): 166–70. http://dx.doi.org/10.1530/acta.0.1140166.

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Abstract. The hypothalamic-pituitary-adrenal axis was investigated in all six patients requiring glucocorticoid replacement 2.5–11 years after unilateral adrenalectomy for adrenal adenomas causing Cushing's syndrome. The hypothalamic-pituitary-adrenal axis was assessed by insulin induced hypoglycaemia and CRF testing in each patient. Two patients showed normal cortisol and ACTH responses to hypoglycaemia. Two patients showed subnormal cortisol responses to hypoglycaemia in the presence of high or normal basal ACTH concentrations. ACTH concentrations increased with both hypoglycaemia and CRF. Two patients showed subnormal cortisol responses to hypoglycaemia and CRF. One of these patients showed an ACTH rise following hypoglycaemia but not CRF. Defects at either hypothalamic-pituitary or adrenal levels were demonstrated and recovery of the axis appears to commence at the hypothalamic-pituitary level.

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Zapanti, Evangelia, Konstantinos Terzidis i George Chrousos. "Dysfunction of the Hypothalamic-Pituitary-Adrenal axis in HIV infection and disease". HORMONES 7, nr 3 (15.07.2008): 205–16. http://dx.doi.org/10.14310/horm.2002.1200.

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ARATÓ, MIHÁLY, CSABA M. BANKI, CHARLES B. NEMEROFF i GARTH BISSETTE. "Hypothalamic-Pituitary-Adrenal Axis and Suicide". Annals of the New York Academy of Sciences 487, nr 1 Psychobiology (grudzień 1986): 263–70. http://dx.doi.org/10.1111/j.1749-6632.1986.tb27905.x.

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BATEMAN, ANDREW, AVA SINGH, THOMAS KRAL i SAMUEL SOLOMON. "The Immune-Hypothalamic-Pituitary-Adrenal Axis*". Endocrine Reviews 10, nr 1 (luty 1989): 92–112. http://dx.doi.org/10.1210/edrv-10-1-92.

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Altamura, A. Carlo. "Hypothalamic-pituitary-adrenal axis in schizophrenia". Biological Psychiatry 40, nr 6 (wrzesień 1996): 560–61. http://dx.doi.org/10.1016/0006-3223(96)85271-1.

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Lilly, Michael P. "The Hypothalamic-Pituitary-Adrenal—Immune Axis". Archives of Surgery 127, nr 12 (1.12.1992): 1463. http://dx.doi.org/10.1001/archsurg.1992.01420120097017.

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Watson, Paddy Burges. "The hypothalamic/pituitary/adrenal axis revisited". Stress Medicine 5, nr 3 (lipiec 1989): 141–43. http://dx.doi.org/10.1002/smi.2460050303.

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Rozprawy doktorskie na temat "Hypothalamic-pituitary-adrenal axis"

Evuarherhe, Obaro. "Gender, puberty and the hypothalamic-pituitary-adrenal axis". Thesis, University of Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.618813.

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The hypothalamo-pituitary-adrenal (HPA) axis, a neuroendocrine pathway involved in the stress response is well studied in both human beings and rodents. Major gender-related neuroendocrine changes take place during pubcl1y (days 30 - 60 in rats) including a robust increase in the levels of gonadal steroids which are thought to underlie numerous neural and behavioural changes brought on after puberty. Evidence suggests the HPA axis undergoes significant changes over the pubertal period. This project investigated the effects of gonadal steroids on the HPA axis before and after puberty and the role of the pubertal surge in endogenous gonadal steroids in both sexes; specifically looking at the sensitivity of the resulting adult HPA axis to exogenous gonadal steroids. There was a significant effect of both age and sex on the adrenocorticotrophic hormone (ACTH) and corticosterone response to restraint stress. Sexual dimorphism in the endocrine stress response became more pronounced after puberty. Adult physiological levels of gonadal steroids reduced the corticosterone and ACTH response to restraint stress in both male and female prepubertal rats. In adult males, testosterone reduced the ACTH response to stress while in adult females, there was a s significant effect of ovariectomy (OVX) on the stress response. 1:estosterone treatment did not significantly affect overall corticosterone release over the 24hr period in adult animals castrated (CSX) before puberty. In contrast, testosterone significantly suppressed corticosterone secretion in animals CSX in adulthood. Animals CSX prepubertally displayed significantly lower glucocorticoid receptor levels in the dentate gyrus of the dorsal hippocampus than animals CSX in adulthood. [n females, prepubertal OVX did not affect the ability of oestradiol to affect basal HPA activity in adulthood. Overall, the data suggest vital roles of peripubertal gonadal steroids on the adult HPA axis; although the pubertal maturation of the female HP A phenotype appears to be independent of peripubertal oestrogens.

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Stirrat, Laura Ingram. "Hypothalamic pituitary adrenal axis dysregulation in obese pregnancy". Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/28979.

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There has been a global rise in obesity in the last three decades, and at present one in five women are obese at antenatal booking. Maternal obesity is associated with an increased risk of adverse pregnancy outcomes, including increased fetal size and prolonged pregnancy. In the longer-term, offspring of obese are at increased risk of premature death from a cardiovascular event in their adulthood. One mechanism that has been linked to these outcomes is fetal exposure to glucocorticoids in utero. During normal pregnancy, the maternal hypothalamic pituitary adrenal (HPA) axis undergoes major changes, resulting in exponentially increasing levels of the major circulating glucocorticoid cortisol, and other HPA axis hormones, such as corticotrophin releasing hormone (CRH). Cortisol and CRH are vital for normal fetal growth and length of gestation, but in excess they are associated with fetal growth restriction and preterm labour. In non-pregnant obesity, it is thought that the HPA axis is dysregulated, although evidence is inconclusive. Little is known about the effects of maternal obesity in pregnancy on the HPA axis. The work in this Thesis used clinical studies to test the hypothesis that the HPA axis is dysregulated in obese pregnant women with altered release, clearance and placental metabolism of cortisol. Associations with clinical outcomes related to fetal size and length of gestation were also studied. The HPA axis activity during pregnancy was investigated in a prospective case-control study cohort. Fasting serum cortisol levels were measured at 16, 28 and 36 weeks of gestation (obese n=276, lean n=135). In a subset (obese n=20, lean n=20), corticosteroid binding globulin (CBG), CRH, estrogens and progesterone were measured. Salivary cortisol was measured in samples collected at bedtime, waking and 30 minutes after waking at 16 weeks. Urinary glucocorticoid metabolites were measured at 19 weeks and 36 weeks (obese n=6, lean n=5) and non-pregnant (obese n=7, lean n=7) subjects. All circulating hormone levels rose similarly in obese and lean during pregnancy, but were significantly lower in obese women. The diurnal rhythm of cortisol was maintained. Urinary glucocorticoids increased with gestation in lean, but not in obese, indicating a lesser activation of the HPA axis in obese compared with lean pregnancy. These findings associated with increased birthweight and longer gestation in obese pregnancy, suggesting that decreased HPA axis activity may underlie these obese related adverse pregnancy outcomes. Whether or not lower glucocorticoids in obese pregnancies are maintained at delivery was investigated by measuring active glucocorticoids (cortisol and corticosterone) and their inactive versions (cortisone and 11- dehydrocorticosterone, respectively) from matched maternal and cord plasma samples (n=259, BMI 18 – 55 kg/m2). Active glucocorticoids were significantly higher in maternal than cord blood, and inactive versions were significantly higher in cord than maternal blood. Increased maternal BMI associated with lower maternal cortisol, corticosterone and 11-dehydrocorticosterone. Despite significant correlations between maternal and cord blood glucocorticoid levels, increased maternal BMI did not associate with lower cord blood glucocorticoids. This suggests that conditions at delivery may overcome any potential negative effects of low maternal glucocorticoids on the fetus in the short-term. However, it may not preclude the longer-term effects of fetal exposure to lower glucocorticoid levels during obese pregnancy, and offspring follow-up studies are required. Potential mechanisms leading to altered HPA axis activity in obese pregnancy were explored by studying the pulsatile release and placental metabolism of glucocorticoid hormones. Glucocorticoid pulsatility is thought to be important for transcriptional regulation of glucocorticoid responsive genes, and disruptions to pulsatility have been reported in some disease processes. Glucocorticoids were measured in 10-minute serum sampling between 08.00h-11.00h and 16.00h- 19.00h. Peripheral tissue cortisol was measured from 20-minute sampling of interstitial fluid, over 24-hours, at 16-24 weeks and 30-36 weeks (obese n=7, lean n=8), and non-pregnant controls (obese n=4, lean n=3). Total circulating serum cortisol levels were higher in pregnancy than non-pregnancy in lean and obese, and increased significantly with advancing gestation in lean but not in obese. Pulsatility of cortisol was demonstrated in interstitial fluid in both non-pregnancy and pregnancy. In obese pregnancy, interstitial fluid pulse frequency was lower with advancing gestation. This may be a novel mechanism underlying the observed decreased HPA axis activity in obese pregnancy. Placental cortisol metabolism and transport was studied using an ex vivo placental perfusion model, perfused with a deuterium-labelled cortisol tracer combined with computational modeling. The findings challenge the concept that maternal cortisol diffuses freely across the placenta, but confirmed that 11β- HSD2 acts as major ‘barrier’ to cortisol transfer to the fetus, protecting the fetus from the high maternal circulating cortisol levels. In addition we showed preliminary evidence of local cortisol production within the placenta. The model is able to predict maternal-fetal cortisol transfer and can now be used in future experimental design. In conclusion, in obese pregnancy, lower maternal cortisol and urinary clearance suggested reduced HPA axis activity. Altered glucocorticoid pulsatility may underlie this change. Future studies of placental cortisol metabolism in maternal obesity could be conducted using an ex vivo perfusion model. The lower HPA axis activity in obese pregnancy represents a novel pathway underlying increased fetal growth.

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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.

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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.
digitalisering@umu

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Watson, Stuart. "Hypothalamic-pituitary-adrenal axis function in mood disorder patients". Thesis, University of Newcastle upon Tyne, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413260.

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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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Gillich, Anton. "The role of histamine in the hypothalamic - pituitary - adrenal axis /". Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=55496.

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Histamine appears to act as a neurotransmitter within the CNS and may be involved in the regulation of a number of physiological systems including the Hypothalamic-Pituitary-Adrenal (HPA) axis. We conducted a series of experiments in rats to examine the role of histamine within the HPA axis. We first determined if histamine undergoes diurnal variations in the paraventricular nucleus, the periventricular nucleus, and the ventro-medial nucleus of the hypothalamus, the frontal cortex, septal nucleus, median eminence, posterior hypothalamus, mammillary bodies, supraoptic nucleus, suprachiasmatic nucleus, bed nucleus of the stria terminalis, dentate gyrus, and the CA1, CA2, and CA3 cell fields of the hippocampus. We further examined the effect of adrenalectomy and corticosterone replacement in these areas to determine if the histaminergic system is susceptible to glucocorticoid negative feedback inhibition. Finally, histamine levels in the paraventricular hypothalamic nucleus, the periventricular nucleus, the median eminence, the posterior hypothalamus, the mammillary bodies, the supraoptic nucleus, and the suprachiasmatic nucleus were measured in rats that were either intact, adrenalectomized (ADX), or ADX and treated with corticosterone and were stressed for various periods of time.
The results suggest that (1) histamine may mediate basal plasma levels of ACTH through the regulation of paraventricular hypothalamic activity, (2) the histaminergic system may not be susceptible to glucocorticoid negative feedback inhibition under normal, non-stress conditions, (3) histaminergic neurons stimulate the HPA axis but may not be able to maintain their activity for extended periods of time, and (4) glucocorticoid negative feedback inhibition can occur but may only be effective within a specific period after HPA activation due to stress.

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Zollner, Ekkehard Werner Arthur. "Hypothalamic-pituitary-adrenal axis suppression in asthmatic children on corticosteroids". Thesis, Stellenbosch : Stellenbosch University, 2013. http://hdl.handle.net/10019.1/95468.

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Thesis (PhD)-- Stellenbosch University, 2013.
ENGLISH ABSTRACT: Although the effect of inhaled corticosteroids (ICS) on the hypothalamic- pituitary-adrenal axis (HPA) has been regarded as a “benign physiological response”, a survey published in 2002 suggested that adrenal crisis is more common in asthmatic children on ICS than previously thought. Relying on clinical features to detect chronic adrenal insufficiency secondary to corticosteroids may not be wise, as these are non-specific and can therefore easily be missed. Accurate biochemical assessment of the whole axis to detect subclinical HPA suppression (HPAS) is thus desirable. A review of the literature indicates that basal adrenal function tests, including plasma cortisol profiles, do not identify which children can appropriately respond to stress. There is no evidence to suggest that the degree of the physiological adjustment of the HPA to ICS and/or nasal steroids (by reducing basal cortisol production), predicts HPAS. Cortisol profiles should therefore only be used to demonstrate differences in systemic activity of various ICS and delivery devices. Only two tests, considered as gold standard adrenal function tests [the insulin tolerance test (ITT) and the metyrapone test] can assess the integrity of the whole axis.
AFRIKAANSE OPSOMMING: Die outeurs van ´n opname wat in 2002 gepubliseer is stel voor dat ´n bynierkrisis meer algemeen by asmatiese kinders, wat inhalasie kortikosteroïede ontvang, voorkom as wat voorheen gedink is. Dit is strydig met die gevestigde opvatting dat die effek van IKS op die hipotalamiese-hipofise-bynier-as (HHB) ’n “goedaardige fisiologiese reaksie” is. Die kliniese kenmerke van kroniese bynierontoereikendheid sekondêr tot die gebruik van kortikosteroïede (KS) is nie-spesifiek en gevolglik onbetroubaar. ´n Akkurate biochemiese toets van subkliniese HBB onderdrukking (HHBO) sou gevolglik waardevol wees. ´n Literatuur oorsig toon dat toetse van basale bynierfunksie, insluitend plasma kortisol (K) profiele, nie kinders uitken wat toepaslik op stres sal reageer nie. Daar is geen bewyse dat die graad van fisiologiese aanpassing van die HHB, soos aangedui deur laer K-vlakke, na die gebruik van IKS en/of nasale steroïede (NS), HHBO voorspel nie. Serum K profiele is dus slegs van waarde om die sistemiese aktiwiteit van verskillende IKS en toedieningsstelsels te ondersoek. Slegs twee toetse, naamlik die insulien toleransie toets (ITT) en die metyrapone -(MTP)-toets (wat beide as die goue standaard van bynier funksie beskou word), kan die integriteit van die hele as meet.
Stellenbosch University
Medical Research Council
SA Thoracic Society
Harry Crossley Foundation
Red Cross Children’s Hospital.

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Kalyani, Manu. "Interaction between Prolactin and the Hypothalamic-Pituitary-Adrenal (HPA) axis". Miami University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=miami1397233916.

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Reynolds, Rebecca M. "Programming of the hypothalamic-pituitary-adrenal axis during fetal life". Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/23168.

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The aim of this thesis was to study the HPA axis in detail, examining aspects of both activity of the axis and cortisol action, in order to determine variations that could explain the link between low birthweight and subsequent development of cardiovascular risk factors. The principal findings were that men aged 66-77 years, who were of low birthweight and/or with the Metabolic Syndrome, have activation of the HPA axis with increased cortisol response to ACTH_1-24 and increased urinary cortisol metabolite excretion. In contrast to rats programmed by dexamethasone administration during pregnancy, there was no evidence of altered central feedback sensitivity to low dose dexamethasone. However, dexamethasone may not cross the blood-brain barrier at low doses in man, so that this only tests the pituitary component of the negative feedback loop. Alternatively, rather than impaired central negative feedback, the activation of the HPA axis could be due to increased forward drive to ACTH and cortisol secretion from higher centres. Consistent with this hypothesis there was lack of habituation to the stress of repeated venepuncture in diabetic subjects. In contrast to the central GR changes, peripheral (liver) GR expression is increased in the rodent model. Tissue-specific differences in GR levels are a potential mechanism whereby subtle abnormalities in cortisol action could contribute to variations in insulin sensitivity in the population. Using competitive quantitative RT-PCR, GR mRNA levels were determined in total RNA extracted from skeletal muscle biopsies from 23 men in Uppsala, Sweden who had been studied at age 70 years with an oral glucose tolerance test and a euglycaemic hyperinsulinaemic clamp. Increased GR expression was associated with resistance to insulin-mediated glucose uptake, independent of obesity.

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Heinzmann, Jan-Michael. "Central and peripheral aspects of hypothalamic-pituitary-adrenal (HPA) axis dysfunction". Diss., lmu, 2012. http://nbn-resolving.de/urn:nbn:de:bvb:19-150032.

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Książki na temat "Hypothalamic-pituitary-adrenal axis"

Print͡s︡ipy i mekhanizmy reguli͡a︡t͡s︡ii gipofizarno-adrenokortikalʹnoĭ sistemy. Leningrad: Izd-vo "Nauka," Leningradskoe otd-nie, 1987.

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

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Arkadʹevich, Filaretov Anatoliĭ, Mezhdunarodnai͡a problemnai͡a komissii͡a "Intervist͡ser.", Institut fiziologii im. I.P. Pavlova. i Institut ėvoli͡ut͡sionnoĭ fiziologii i biokhimii im. I.M. Sechenova., red. Mezhdunarodnyĭ simpozium Fiziologii͡a gipofizarno-adrenokortikalʹnoĭ sistemy, Leningrad, 1-4 okti͡abri͡a 1990 g.: Tezisy dokladov. Leningrad: Akademii͡a nauk SSSR, 1990.

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T, Podvigina T., i Filaretova L. P, red. Adaptat͡s︡ii͡a︡ kak funkt͡s︡ii͡a︡ gipofizarno-adrenokortikalʹnoĭ sistemy. Sankt-Peterburg: "Nauka", 1994.

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

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F, Ganong William, Dallman M. F, Roberts James Lewis 1951, Krieger Dorothy T, Herbert E. 1926- i New York Academy of Sciences., red. The Hypothalamic-pituitary-adrenal axis revisited: A symposium in honor of Dorothy Krieger and Edward Herbert. New York, N.Y: New York Academy of Sciences, 1987.

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Abebe, Getachew. The integrity of the hypothalamic-pituitary-adrenal axis in Boran (Bos indicus) cattle infected with Trypanosoma congolense. Uxbridge: Brunel University, 1991.

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de, Kloet E. R., Azmitia Efrain C, Landfield Philip W i New York Academy of Sciences., red. Brain corticosteroid receptors: Studies on the mechanism, function, and neurotoxicity of corticosteroid action. New York, N.Y: New York Academy of Sciences, 1994.

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Young, Allan H., i 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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Części książek na temat "Hypothalamic-pituitary-adrenal axis"

Kyrou, Ioannis, i Constantine Tsigos. "Hypothalamic-Pituitary-Adrenal Axis". W Adrenal Glands, 19–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-26861-8_3.

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Heaney, Jennifer. "Hypothalamic-Pituitary-Adrenal Axis". W Encyclopedia of Behavioral Medicine, 1127–28. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_460.

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Orbell, Sheina, Havah Schneider, Sabrina Esbitt, Jeffrey S. Gonzalez, Jeffrey S. Gonzalez, Erica Shreck, Abigail Batchelder i in. "Hypothalamic-Pituitary-Adrenal Axis". W Encyclopedia of Behavioral Medicine, 1017–18. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_460.

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Bloch, Michael H., Michael H. Bloch, Mark A. Geyer, David C. S. Roberts, Eileen M. Joyce, Jonathan P. Roiser, John H. Halpern i in. "Hypothalamic–Pituitary–Adrenal Axis". W Encyclopedia of Psychopharmacology, 615. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1697.

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Heaney, Jennifer. "Hypothalamic-Pituitary-Adrenal Axis". W Encyclopedia of Behavioral Medicine, 1–2. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6439-6_460-2.

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Woods, Douglas W., Matthew R. Capriotti, Madison Pilato, Carolyn A. Doyle, Christopher J. McDougle, Beth Springate, Deborah Fein i in. "Hypothalamic-Pituitary-Adrenal Axis". W Encyclopedia of Autism Spectrum Disorders, 1530–35. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_213.

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Wirtz, Petra H. "Hypothalamic-Pituitary-Adrenal Axis". W Handbook of Cardiovascular Behavioral Medicine, 941–74. New York, NY: Springer New York, 2022. http://dx.doi.org/10.1007/978-0-387-85960-6_39.

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Geronikolou, Styliani A., George Chrousos i Christina Kanaka-Gantenbein. "Hypothalamic–Pituitary–Adrenal Axis". W Encyclopedia of Personality and Individual Differences, 2110–12. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-24612-3_765.

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Geronikolou, Styliani A., George Chrousos i Christina Kanaka-Gantenbein. "Hypothalamic–Pituitary–Adrenal Axis". W Encyclopedia of Personality and Individual Differences, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-28099-8_765-1.

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Glover, Dorie. "Hypothalamic-Pituitary-Adrenal Axis". W Encyclopedia of Autism Spectrum Disorders, 2378–83. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-91280-6_213.

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Streszczenia konferencji na temat "Hypothalamic-pituitary-adrenal axis"

Oliveria, John Paul, Abbey Torek, Tara Strinich, Karen Howie, John Bienenstock i Gail Gauvreau. "The Hypothalamic-Pituitary-Adrenal Axis In Subjects With Allergic Asthma". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5650.

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Rigatos, Gerasimos. "Differential flatness properties and adaptive control of the hypothalamic-pituitary-adrenal axis model". W INTERNATIONAL CONFERENCE OF COMPUTATIONAL METHODS IN SCIENCES AND ENGINEERING 2016 (ICCMSE 2016). Author(s), 2016. http://dx.doi.org/10.1063/1.4968674.

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Perov, S. Yu, i S. A. Askerova. "THE NEUROENDOCRINE SYSTEM RESPONSE OF 2-5 G COMMUNICATION ELECTROMAGNETIC FIELD ANIMAL EXPOSURE". W The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-398-402.

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Abstract: Background. The neuroendocrine effect on the hypothalamus-pituitary-adrenal cortex axis is significant example stressor of electromagnetic exposure for biological object. Aim. The neuroendocrine effect investigation of multi-frequency electromagnetic field laboratory animals’ exposure from 2-5 generations cellular base stations Methods. The neuroendocrine status evaluated by corticosterone and adrenocorticotropic hormone (ACTH) concentrations in blood exposed and sham rats. ACTH and corticosterone rat blood assessed by immunoenzyme method. Results. The results of the multi-frequency electromagnetic field laboratory animals’ exposure from 2-5 generations cellular base stations in a chronic experiment showed wave-like changes in the hypothalamic-pituitary-adrenal function. These changes are manifested in an immediate increase in corticosteroids secretion and depression of the corticosteroid response to normal or subnormal levels. After 3 month chronic exposure there was a secondary rise in hormonal secretion.

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Chakrabarty, Ankush, Gregery T. Buzzard, Martin J. Corless, Stanislaw H. Zak i Ann E. Rundell. "Correcting hypothalamic-pituitary-adrenal axis dysfunction using observer-based explicit nonlinear model predictive control". W 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6944359.

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Kaslik, Eva, Dan Bogdan Navolan i Mihaela Neamţu. "Stability analysis of a hypothalamic-pituitary-adrenal axis model with inclusion of glucocorticoid receptor and memory". W ICNPAA 2016 WORLD CONGRESS: 11th International Conference on Mathematical Problems in Engineering, Aerospace and Sciences. Author(s), 2017. http://dx.doi.org/10.1063/1.4972703.

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Soroceanu, Radu-Petru, Ioana Silistraru, Anamaria Ciubara, Doina Azoicai, Daniel Timofte, Liviu Răzvan Platon, Bogdan Ciuntu i Mădălina Maxim. "OBESITY AND DEPRESSION INTERTWINED – A NARRATIVE REVIEW". W The European Conference of Psychiatry and Mental Health "Galatia". Archiv Euromedica, 2023. http://dx.doi.org/10.35630/2022/12/psy.ro.18.

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Both pathologies—obesity and depression—have high prevalence rates and have serious negative effects on the public's health. In recent meta-analyses, clinical trials, and epidemiological studies, they have been observed in people of all races. Both obesity and major depression are risk factors related to one another. In this paper, we suggest an overview of the two interconnected biological processes, including genetic influences and changes to the systems in charge of energy synthesis and consumption (hypothalamic-pituitary-adrenal axis, and inflammation, neuroendocrine regulators, and gut microbiota). Additionally, we look into how people perceive their bodies and social stigma, as well as the potential benefits of physical activity and weight-loss surgery on comorbid conditions and quality of life.

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RAVIZZA, L., R. G. MASERA, P. PROLO, A. H. STAURENGHI, E. ZANALDA, M. L. SARTORI i A. ANGELI. "MODULATION OF NATURAL KILLER (NK) CELL ACTIVITY BY HORMONES OF THE HYPOTHALAMIC-PITUITARY-ADRENAL AXIS IN ANOREXIA NERVOSA". W IX World Congress of Psychiatry. WORLD SCIENTIFIC, 1994. http://dx.doi.org/10.1142/9789814440912_0012.

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Olsson, Petter, Claus Vogelmeier, Kenneth Chapman, Angel FowlerTaylor, Tim Ayers, Chau Thach, Robert Fogel, Francesco Patalano i Donald Banerji. "Effect of indacaterol/glycopyrronium versus salmeterol/fluticasone on hypothalamic pituitary-adrenal axis function in moderate-to-very severe COPD patients: Results from the FLAME study". W ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa984.

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Corpuz, Abigail. "Adverse Childhood Experiences and complex PTSD: A Theoretical Model Exploring Psychedelic Drugs as a Therapeutic Treatment". W 7th International Conference on Spirituality and Psychology. Tomorrow People Organization, 2022. http://dx.doi.org/10.52987/icsp.2022.001.

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Abstract Complex posttraumatic stress disorder (cPTSD) has several detrimental consequences, including severe anxiety, emotional detachment, mood irregularities, and vivid flashbacks to trauma. In many cases, cPTSD can be linked back to adverse childhood experiences (ACEs). Treatments for cPTSD that involve psychedelic drugs are potentially beneficial, but unfortunately they are understudied in psychology labs due to their classification as a Schedule I substance. Thus, theoretical work is needed to explain potential mechanisms involved in treatment programs. In this new theoretical model, I clarify the mechanistic links between ACEs and cPTSD and then examine why psychedelic drugs may be an ideal therapeutic tool for the treatment of cPTSD. Toxic stress theory posits that exposure to extreme, frequent, and persistent ACEs without the presence of a supportive caretaker chronically activates the stress response system (Jones et al., 2021). Toxic stress results in dysregulation of the limbic-hypothalamic-pituitary-adrenal (LHPA) axis, elevating levels of catecholamines, cortisol, and proinflammatory cytokines (Thermo Fisher Scientific, n.d.). The toxic stress induced by ACEs causes cPTSD due to the persistent exposure to multiple adverse events leading to re-experience of the traumatic events, avoidance behaviors, and paranoia. Psychedelic drugs unlock repressed memories, engaging positively with negative self-concept and dysregulated emotions, which are both characteristic of the Disturbances of Self-Organization symptom cluster of cPTSD. Presentation of this theoretical model would allow for public recognition of the potential benefits of this treatment and further exploration into this topic. Keywords: PTSD, psychedelics, adverse childhood experiences, stress

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Aflahiyah, Shiva, Didik Gunawan Tamtomo i Hanung Prasetya. "A Meta-Analysis on the Effectiveness of Prenatal Yoga in Reducing Cortisol Hormone in Pregnancy". W The 7th International Conference on Public Health 2020. Masters Program in Public Health, Universitas Sebelas Maret, 2020. http://dx.doi.org/10.26911/the7thicph.05.47.

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ABSTRACT Backgrund: A growing body of evidence suggests that activity of the stress-responsive hypothalamic-pituitary-adrenal axis and its end-product cortisol also may be associated with perinatal emotional well-being. A number of preventive interventions, such as Yoga, targeting psychosocial and physiological risk factors for perinatal depression have utilized mind-body practices, which embody the idea that the mind interacts with the body to influence physical functioning, improve symptoms, and promote health. This study aimed to investigate effectiveness of prenatal yoga in reducing cortisol hormone in pregnancy Subjects and Method: This was a meta-analysis and systematic review. This study collected published articles during 2000 to 2020 from PubMed, Science Direct, Springer, Proquest, and Chocrane electronic databases. The inclusion criteria were full text, randomized controlled trial, and prenatal yoga intervention. The study subjects were pregnant women who received prenatal yoga for 8 to 20 weeks. Outcome was cortisol hormone reduction during pregnancy. The selected articles were analyzed by PRISMA flow chart and RevMan 5.3. Results: 5 articles from America and Asia were met the inclusion criteria. This study had high heterogeneity (I2=88%; p<0.001). Therefore, this study used random effect model (REM). Prenatal yoga reduced cortisol level 0.59 times in pregnancy (Mean Difference= -0.59; 95% CI= 1.18 to 0.01; p= 0.050). Conclusion: Prenatal yoga is effective to reduce cortisol level in pregnant women. Keywords: prenatal yoga, cortisol hormone, pregnant women Correspondence: Shiva Aflahiyah. Masters Program in Public Health, Universitas Sebelas Maret. Jl. Ir. Sutami 36 A, Surakarta 57126, Central Java. Email: shivaafla@gmail.com. DOI: https://doi.org/10.26911/the7thicph.05.47

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