The Experts below are selected from a list of 52371 Experts worldwide ranked by ideXlab platform

George P. Chrousos - One of the best experts on this subject based on the ideXlab platform.

  • Neuroimmunomodulation in Asthma: Focus on the Hypothalamic-Pituitary-Adrenal Axis - Neuroimmunomodulation in Asthma: Focus on the Hypothalamic-Pituitary-Adrenal Axis
    Neuroimmunomodulation, 2009
    Co-Authors: Kostas N. Priftis, George P. Chrousos
    Abstract:

    Introduction Neuroimmunomodulation in Asthma: Focus on the Hypothalamic-Pituitary-Adrenal Axis: Priftis, K.N. Chrousos, G.P. Regulation of the Hypothalamic-Pituitary-Adrenal Axis: Papadimitriou, A. Priftis, K.N. Evaluation of the Hypothalamic-Pituitary-Adrenal Axis Function in Childhood and Adolescence: Chrousos, G.P. Kino, T. Charmandari, E. Salivary Cortisol for Assessment of Hypothalamic-Pituitary-Adrenal Axis Function: Tornhage, C.-J. Glucocorticoid Receptor in Human Respiratory Epithelial Cells: Pujols, L. Mullol, J. Picado, C. Enhancing versus Suppressive Effects of Stress on Immune Function: Implications for Immunoprotection and Immunopathology: Dhabhar, F.S. Stress and Airway Reactivity in a Murine Model of Allergic Airway Inflammation: Quarcoo, D. Pavlovic, S. Joachim, R.A. Cortisol Responses to Stress in Allergic Children: Interaction with the Immune Response: Buske-Kirschbaum, A. Endocrine-Immune Interactions in Adrenal Function of Asthmatic Children on Inhaled Corticosteroids: Priftis, K.N. Papadimitriou, A. Anthracopoulos, M.B. Fretzayas, A. Chrousos, G.P. Single Nucleotide Polymorphisms Related to HPA Axis Reactivity: DeRijk, R.H. Intranasal Corticosteroids and Adrenal Suppression: Bruni, F.M. De Luca, G. Venturoli, V. Boner, A.L. Author Index Subject Index.

  • Hypothalamic-Pituitary-Adrenal Axis activity in obese men with and without sleep apnea: effects of continuous positive airway pressure therapy.
    The Journal of Clinical Endocrinology & Metabolism, 2007
    Co-Authors: Alexandros N Vgontzas, Edward O Bixler, Slobodanka Pejovic, E. Zoumakis, Hung-mo Lin, Christina M. Bentley, Alexios Sarrigiannidis, Maria Basta, George P. Chrousos
    Abstract:

    Context: Previous studies on the association between the Hypothalamic-Pituitary-Adrenal Axis activity and sleep apnea (SA) and obesity are inconsistent and/or limited. Objective: In this study, we evaluated the activity of the Hypothalamic-Pituitary-Adrenal Axis in nonpsychologically distressed obese subjects with and without SA and examined the impact of continuous positive airway pressure (CPAP) in SA patients. Design and Participants: In study I, four-night sleep laboratory recordings and serial 24-h plasma measures of cortisol were obtained in 45 obese men with and without apnea and nonobese controls. Sleep apneic patients were reassessed after 3 months of CPAP use. In study II, 38 obese men with and without sleep apnea and nonobese controls were challenged with ovine CRH administration after four nights in the sleep laboratory. Results: The sleep patterns were similar between obese and nonobese controls. Twenty-four-hour plasma cortisol levels were highest in nonobese controls, intermediate in obese ...

  • chronic insomnia is associated with nyctohemeral activation of the hypothalamic pituitary adrenal Axis clinical implications
    The Journal of Clinical Endocrinology and Metabolism, 2001
    Co-Authors: Alexandros N Vgontzas, Edward O Bixler, Paolo Prolo, George Mastorakos, Antonio Velabueno, Anthony Kales, George P. Chrousos
    Abstract:

    Although insomnia is, by far, the most commonly encountered sleep disorder in medical practice, our knowledge in regard to its neurobiology and medical significance is limited. Activation of the Hypothalamic-Pituitary-Adrenal Axis leads to arousal and sleeplessness in animals and humans; however, there is a paucity of data regarding the activity of the Hypothalamic-Pituitary-Adrenal Axis in insomniacs. We hypothesized that chronic insomnia is associated with increased plasma levels of ACTH and cortisol. Eleven young insomniacs (6 men and 5 women) and 13 healthy controls (9 men and 4 women) without sleep disturbances, matched for age and body mass index, were monitored in the sleep laboratory for 4 consecutive nights, whereas serial 24-h plasma measures of ACTH and cortisol were obtained during the fourth day. Insomniacs, compared with controls, slept poorly (significantly higher sleep latency and wake during baseline nights). The 24-h ACTH and cortisol secretions were significantly higher in insomniacs, c...

  • Chronic Insomnia Is Associated with Nyctohemeral Activation of the Hypothalamic-Pituitary-Adrenal Axis: Clinical Implications
    The Journal of Clinical Endocrinology & Metabolism, 2001
    Co-Authors: Alexandros N Vgontzas, Edward O Bixler, Paolo Prolo, George Mastorakos, Anthony Kales, Hung-mo Lin, Antonio Vela-bueno, George P. Chrousos
    Abstract:

    Although insomnia is, by far, the most commonly encountered sleep disorder in medical practice, our knowledge in regard to its neurobiology and medical significance is limited. Activation of the Hypothalamic-Pituitary-Adrenal Axis leads to arousal and sleeplessness in animals and humans; however, there is a paucity of data regarding the activity of the Hypothalamic-Pituitary-Adrenal Axis in insomniacs. We hypothesized that chronic insomnia is associated with increased plasma levels of ACTH and cortisol. Eleven young insomniacs (6 men and 5 women) and 13 healthy controls (9 men and 4 women) without sleep disturbances, matched for age and body mass index, were monitored in the sleep laboratory for 4 consecutive nights, whereas serial 24-h plasma measures of ACTH and cortisol were obtained during the fourth day. Insomniacs, compared with controls, slept poorly (significantly higher sleep latency and wake during baseline nights). The 24-h ACTH and cortisol secretions were significantly higher in insomniacs, compared with normal controls (4.2 +/- 0.3 vs. 3.3 +/- 0.3 pM, P = 0.04; and 218.0 +/- 11.0 vs. 190.4 +/- 8.3 nM, P = 0.07). Within the 24-h period, the greatest elevations were observed in the evening and first half of the night. Also, insomniacs with a high degree of objective sleep disturbance (% sleep time < 70), compared with those with a low degree of sleep disturbance, secreted a higher amount of cortisol. Pulsatile analysis revealed a significantly higher number of peaks per 24 h in insomniacs than in controls (P < 0.05), whereas cosinor analysis showed no differences in the temporal pattern of ACTH or cortisol secretion between insomniacs and controls. We conclude that insomnia is associated with an overall increase of ACTH and cortisol secretion, which, however, retains a normal circadian pattern. These findings are consistent with a disorder of central nervous system hyperarousal rather than one of sleep loss, which is usually associated with no change or decrease in cortisol secretion or a circadian disturbance. Chronic activation of the Hypothalamic-Pituitary-Adrenal Axis in insomnia suggests that insomniacs are at risk not only for mental disorders, i.e. chronic anxiety and depression, but also for significant medical morbidity associated with such activation. The therapeutic goal in insomnia should be to decrease the overall level of physiologic and emotional arousal, and not just to improve the nighttime sleep.

  • interactions between the hypothalamic pituitary adrenal Axis and the female reproductive system clinical implications
    Annals of Internal Medicine, 1998
    Co-Authors: George P. Chrousos, David J Torpy, Philip W Gold
    Abstract:

    The Hypothalamic-Pituitary-Adrenal Axis exerts profound, multilevel inhibitory effects on the female reproductive system. Corticotropin-releasing hormone (CRH) and CRH-induced proopiomelanocortin p...

Philip W Gold - One of the best experts on this subject based on the ideXlab platform.

  • interactions between the hypothalamic pituitary adrenal Axis and the female reproductive system clinical implications
    Annals of Internal Medicine, 1998
    Co-Authors: George P. Chrousos, David J Torpy, Philip W Gold
    Abstract:

    The Hypothalamic-Pituitary-Adrenal Axis exerts profound, multilevel inhibitory effects on the female reproductive system. Corticotropin-releasing hormone (CRH) and CRH-induced proopiomelanocortin p...

  • Interactions between the Hypothalamic-Pituitary-Adrenal Axis and the Female Reproductive System: Clinical Implications
    Annals of Internal Medicine, 1998
    Co-Authors: George P. Chrousos, David J Torpy, Philip W Gold
    Abstract:

    The Hypothalamic-Pituitary-Adrenal Axis exerts profound, multilevel inhibitory effects on the female reproductive system. Corticotropin-releasing hormone (CRH) and CRH-induced proopiomelanocortin peptides inhibit hypothalamic gonadotropin-releasing hormone secretion, whereas glucocorticoids suppress pituitary luteinizing hormone and ovarian estrogen and progesterone secretion and render target tissues resistant to estradiol. The Hypothalamic-Pituitary-Adrenal Axis is thus responsible for the "hypothalamic" amenorrhea of stress, which is also seen in melancholic depression, malnutrition, eating disorders, chronic active alcoholism, chronic excessive exercise, and the hypogonadism of the Cushing syndrome. Conversely, estrogen directly stimulates the CRH gene promoter and the central noradrenergic system, which may explain adult women's slight hypercortisolism; preponderance of affective, anxiety, and eating disorders; and mood cycles and vulnerability to autoimmune and inflammatory disease, both of which follow estradiol fluctuations. Several components of the Hypothalamic-Pituitary-Adrenal Axis and their receptors are present in reproductive tissues as autacoid regulators. These include ovarian and endometrial CRH, which may participate in the inflammatory processes of the ovary (ovulation and luteolysis) and endometrium (blastocyst implantation and menstruation), and placental CRH, which may participate in the physiology of pregnancy and the timing of labor and delivery. The hypercortisolism of the latter half of pregnancy can be explained by high levels of placental CRH in plasma. This hypercortisolism causes a transient postpartum adrenal suppression that, together with estrogen withdrawal, may partly explain the depression and autoimmune phenomena of the postpartum period.

  • evidence for impaired activation of the hypothalamic pituitary adrenal Axis in patients with chronic fatigue syndrome
    The Journal of Clinical Endocrinology and Metabolism, 1991
    Co-Authors: Mark A Demitrack, George P. Chrousos, Janet K Dale, Stephen E Straus, Louisa Laue, Sam J Listwak, Markus J P Kruesi, Philip W Gold
    Abstract:

    Chronic fatigue syndrome is characterized by persistent or relapsing debilitating fatigue for at least 6 months in the absence of a medical diagnosis that would explain the clinical presentation. Because primary glucocorticoid deficiency states and affective disorders putatively associated with a deficiency of the arousal-producing neuropeptide CRH can be associated with similar symptoms, we report here a study of the functional integrity of the various components of the Hypothalamic-Pituitary-Adrenal Axis in patients meeting research case criteria for chronic fatigue syndrome. Thirty patients and 72 normal volunteers were studied. Basal activity of the Hypothalamic-Pituitary-Adrenal Axis was estimated by determinations of 24-h urinary free cortisol-excretion, evening basal plasma total and free cortisol concentrations, and the cortisol binding globulin-binding capacity. The adrenal cortex was evaluated indirectly by cortisol responses during ovine CRH (oCRH) stimulation testing and directly by cortisol r...

K Ebner - One of the best experts on this subject based on the ideXlab platform.

  • Medial prefrontal cortex suppression of the Hypothalamic-Pituitary-Adrenal Axis response to a physical stressor, systemic delivery of interleukin-1β
    European Journal of Neuroscience, 2003
    Co-Authors: James W Crane, K Ebner, Trevor A. Day
    Abstract:

    Previous studies have shown that the medial prefrontal cortex can suppress the Hypothalamic-Pituitary-Adrenal Axis response to stress. However, this effect appears to vary with the type of stressor. Furthermore, the absence of direct projections between the medial prefrontal cortex and corticotropin-releasing factor cells at the apex of the Hypothalamic-Pituitary-Adrenal Axis suggest that other brain regions must act as a relay when this inhibitory mechanism is activated. In the present study, we first established that electrolytic lesions involving the prelimbic and infralimbic medial prefrontal cortex increased plasma adrenocorticotropic hormone levels seen in response to a physical stressor, the systemic delivery of interleukin-1beta. However, medial prefrontal cortex lesions did not alter plasma adrenocorticotropic hormone levels seen in response to a psychological stressor, noise. To identify brain regions that might mediate the effect of medial prefrontal cortex lesions on Hypothalamic-Pituitary-Adrenal Axis responses to systemic interleukin-1beta, we next mapped the effects of similar lesions on interleukin-1beta-induced Fos expression in regions previously shown to regulate the Hypothalamic-Pituitary-Adrenal Axis response to this stressor. It was found that medial prefrontal cortex lesions reduced the number of Fos-positive cells in the ventral aspect of the bed nucleus of the stria terminalis. However, the final experiment, which involved combining retrograde tracing with Fos immunolabelling, revealed that bed nucleus of the stria terminalis-projecting medial prefrontal cortex neurons were largely separate from medial prefrontal cortex neurons recruited by systemic interleukin-1beta, an outcome that is difficult to reconcile with a simple medial prefrontal cortex-bed nucleus of the stria terminalis-corticotropin-releasing factor cell control circuit.

  • medial prefrontal cortex suppression of the hypothalamic pituitary adrenal Axis response to a physical stressor systemic delivery of interleukin 1β
    European Journal of Neuroscience, 2003
    Co-Authors: James W Crane, K Ebner
    Abstract:

    Previous studies have shown that the medial prefrontal cortex can suppress the hypothalamic–pituitary–adrenal Axis response to stress. However, this effect appears to vary with the type of stressor. Furthermore, the absence of direct projections between the medial prefrontal cortex and corticotropin-releasing factor cells at the apex of the hypothalamic–pituitary–adrenal Axis suggest that other brain regions must act as a relay when this inhibitory mechanism is activated. In the present study, we first established that electrolytic lesions involving the prelimbic and infralimbic medial prefrontal cortex increased plasma adrenocorticotropic hormone levels seen in response to a physical stressor, the systemic delivery of interleukin-1β. However, medial prefrontal cortex lesions did not alter plasma adrenocorticotropic hormone levels seen in response to a psychological stressor, noise. To identify brain regions that might mediate the effect of medial prefrontal cortex lesions on hypothalamic–pituitary–adrenal Axis responses to systemic interleukin-1β, we next mapped the effects of similar lesions on interleukin-1β-induced Fos expression in regions previously shown to regulate the hypothalamic–pituitary–adrenal Axis response to this stressor. It was found that medial prefrontal cortex lesions reduced the number of Fos-positive cells in the ventral aspect of the bed nucleus of the stria terminalis. However, the final experiment, which involved combining retrograde tracing with Fos immunolabelling, revealed that bed nucleus of the stria terminalis-projecting medial prefrontal cortex neurons were largely separate from medial prefrontal cortex neurons recruited by systemic interleukin-1β, an outcome that is difficult to reconcile with a simple medial prefrontal cortex–bed nucleus of the stria terminalis–corticotropin-releasing factor cell control circuit.

James W Crane - One of the best experts on this subject based on the ideXlab platform.

  • Medial prefrontal cortex suppression of the Hypothalamic-Pituitary-Adrenal Axis response to a physical stressor, systemic delivery of interleukin-1β
    European Journal of Neuroscience, 2003
    Co-Authors: James W Crane, K Ebner, Trevor A. Day
    Abstract:

    Previous studies have shown that the medial prefrontal cortex can suppress the Hypothalamic-Pituitary-Adrenal Axis response to stress. However, this effect appears to vary with the type of stressor. Furthermore, the absence of direct projections between the medial prefrontal cortex and corticotropin-releasing factor cells at the apex of the Hypothalamic-Pituitary-Adrenal Axis suggest that other brain regions must act as a relay when this inhibitory mechanism is activated. In the present study, we first established that electrolytic lesions involving the prelimbic and infralimbic medial prefrontal cortex increased plasma adrenocorticotropic hormone levels seen in response to a physical stressor, the systemic delivery of interleukin-1beta. However, medial prefrontal cortex lesions did not alter plasma adrenocorticotropic hormone levels seen in response to a psychological stressor, noise. To identify brain regions that might mediate the effect of medial prefrontal cortex lesions on Hypothalamic-Pituitary-Adrenal Axis responses to systemic interleukin-1beta, we next mapped the effects of similar lesions on interleukin-1beta-induced Fos expression in regions previously shown to regulate the Hypothalamic-Pituitary-Adrenal Axis response to this stressor. It was found that medial prefrontal cortex lesions reduced the number of Fos-positive cells in the ventral aspect of the bed nucleus of the stria terminalis. However, the final experiment, which involved combining retrograde tracing with Fos immunolabelling, revealed that bed nucleus of the stria terminalis-projecting medial prefrontal cortex neurons were largely separate from medial prefrontal cortex neurons recruited by systemic interleukin-1beta, an outcome that is difficult to reconcile with a simple medial prefrontal cortex-bed nucleus of the stria terminalis-corticotropin-releasing factor cell control circuit.

  • medial prefrontal cortex suppression of the hypothalamic pituitary adrenal Axis response to a physical stressor systemic delivery of interleukin 1β
    European Journal of Neuroscience, 2003
    Co-Authors: James W Crane, K Ebner
    Abstract:

    Previous studies have shown that the medial prefrontal cortex can suppress the hypothalamic–pituitary–adrenal Axis response to stress. However, this effect appears to vary with the type of stressor. Furthermore, the absence of direct projections between the medial prefrontal cortex and corticotropin-releasing factor cells at the apex of the hypothalamic–pituitary–adrenal Axis suggest that other brain regions must act as a relay when this inhibitory mechanism is activated. In the present study, we first established that electrolytic lesions involving the prelimbic and infralimbic medial prefrontal cortex increased plasma adrenocorticotropic hormone levels seen in response to a physical stressor, the systemic delivery of interleukin-1β. However, medial prefrontal cortex lesions did not alter plasma adrenocorticotropic hormone levels seen in response to a psychological stressor, noise. To identify brain regions that might mediate the effect of medial prefrontal cortex lesions on hypothalamic–pituitary–adrenal Axis responses to systemic interleukin-1β, we next mapped the effects of similar lesions on interleukin-1β-induced Fos expression in regions previously shown to regulate the hypothalamic–pituitary–adrenal Axis response to this stressor. It was found that medial prefrontal cortex lesions reduced the number of Fos-positive cells in the ventral aspect of the bed nucleus of the stria terminalis. However, the final experiment, which involved combining retrograde tracing with Fos immunolabelling, revealed that bed nucleus of the stria terminalis-projecting medial prefrontal cortex neurons were largely separate from medial prefrontal cortex neurons recruited by systemic interleukin-1β, an outcome that is difficult to reconcile with a simple medial prefrontal cortex–bed nucleus of the stria terminalis–corticotropin-releasing factor cell control circuit.

David J Torpy - One of the best experts on this subject based on the ideXlab platform.

  • interactions between the hypothalamic pituitary adrenal Axis and the female reproductive system clinical implications
    Annals of Internal Medicine, 1998
    Co-Authors: George P. Chrousos, David J Torpy, Philip W Gold
    Abstract:

    The Hypothalamic-Pituitary-Adrenal Axis exerts profound, multilevel inhibitory effects on the female reproductive system. Corticotropin-releasing hormone (CRH) and CRH-induced proopiomelanocortin p...

  • Interactions between the Hypothalamic-Pituitary-Adrenal Axis and the Female Reproductive System: Clinical Implications
    Annals of Internal Medicine, 1998
    Co-Authors: George P. Chrousos, David J Torpy, Philip W Gold
    Abstract:

    The Hypothalamic-Pituitary-Adrenal Axis exerts profound, multilevel inhibitory effects on the female reproductive system. Corticotropin-releasing hormone (CRH) and CRH-induced proopiomelanocortin peptides inhibit hypothalamic gonadotropin-releasing hormone secretion, whereas glucocorticoids suppress pituitary luteinizing hormone and ovarian estrogen and progesterone secretion and render target tissues resistant to estradiol. The Hypothalamic-Pituitary-Adrenal Axis is thus responsible for the "hypothalamic" amenorrhea of stress, which is also seen in melancholic depression, malnutrition, eating disorders, chronic active alcoholism, chronic excessive exercise, and the hypogonadism of the Cushing syndrome. Conversely, estrogen directly stimulates the CRH gene promoter and the central noradrenergic system, which may explain adult women's slight hypercortisolism; preponderance of affective, anxiety, and eating disorders; and mood cycles and vulnerability to autoimmune and inflammatory disease, both of which follow estradiol fluctuations. Several components of the Hypothalamic-Pituitary-Adrenal Axis and their receptors are present in reproductive tissues as autacoid regulators. These include ovarian and endometrial CRH, which may participate in the inflammatory processes of the ovary (ovulation and luteolysis) and endometrium (blastocyst implantation and menstruation), and placental CRH, which may participate in the physiology of pregnancy and the timing of labor and delivery. The hypercortisolism of the latter half of pregnancy can be explained by high levels of placental CRH in plasma. This hypercortisolism causes a transient postpartum adrenal suppression that, together with estrogen withdrawal, may partly explain the depression and autoimmune phenomena of the postpartum period.