The Experts below are selected from a list of 249 Experts worldwide ranked by ideXlab platform

Sally A. Camper - One of the best experts on this subject based on the ideXlab platform.

  • Aged PROP1 deficient dwarf mice maintain ACTH production.
    PloS one, 2011
    Co-Authors: Igor O. Nasonkin, Robert D Ward, Amanda H. Mortensen, David L. Bavers, Felix Beuschlein, Catherine E. Keegan, Gary D. Hammer, Sally A. Camper
    Abstract:

    Humans with PROP1 mutations have multiple Pituitary hormone deficiencies (MPHD) that typically advance from growth insufficiency diagnosed in infancy to include more severe growth hormone (GH) deficiency and progressive reduction in other Anterior Pituitary Hormones, eventually including adrenocorticotropic hormone (ACTH) deficiency and hypocortisolism. Congenital deficiencies of GH, prolactin, and thyroid stimulating hormone have been reported in the Prop1null (Prop1-/-) and the Ames dwarf (Prop1df/df) mouse models, but corticotroph and Pituitary adrenal axis function have not been thoroughly investigated. Here we report that the C57BL6 background sensitizes mutants to a wasting phenotype that causes approximately one third to die precipitously between weaning and adulthood, while remaining homozygotes live with no signs of illness. The wasting phenotype is associated with severe hypoglycemia. Circulating ACTH and corticosterone levels are elevated in juvenile and aged Prop1 mutants, indicating activation of the Pituitary-adrenal axis. Despite this, young adult Prop1 deficient mice are capable of responding to restraint stress with further elevation of ACTH and corticosterone. Low blood glucose, an expected side effect of GH deficiency, is likely responsible for the elevated corticosterone level. These studies suggest that the mouse model differs from the human patients who display progressive hormone loss and hypocortisolism.

Maureen Kelly - One of the best experts on this subject based on the ideXlab platform.

  • The acute effects of cocaine on Anterior Pituitary Hormones in ovariectomized rhesus monkeys.
    The Journal of pharmacology and experimental therapeutics, 1995
    Co-Authors: Nancy K. Mello, Zoltán Sarnyai, Jack H. Mendelson, J M Drieze, Maureen Kelly
    Abstract:

    Cocaine stimulates a rapid release of gonadotropins in intact rhesus males and females and human males and enhances synthetic luteinizing hormone-releasing hormone (LHRH), stimulated luteinizing hormone (LH) and follicle-stimulating hormone (FSH). This report describes the effects of acute cocaine administration on basal and synthetic LHRH-stimulated Anterior Pituitary Hormones [LH, FSH and prolactin (PRL)] in five ovariectomized female rhesus monkeys. Integrated blood samples were collected every 10 min for 40 min before i.v. administration of cocaine (0.4 or 0.8 mg/kg) or an equal volume of vehicle control solution and for 110 min after cocaine or placebo administration. Synthetic LHRH (100 micrograms i.v.) was administered 10 min after cocaine or placebo-cocaine injection. In contrast to previous observations in rhesus and human males and in early follicular and midluteal phase rhesus females, cocaine did not change basal levels of gonadotropins or PRL in long-term ovariectomized females. LHRH stimulated a significant and sustained increase in LH (P < .01) within 20 min and FSH (P < .05) within 40 min after placebo-cocaine administration. LHRH also stimulated significant increases in LH and FSH after 0.4 and 0.8 mg/kg cocaine administration. Significant increases in LH (P < .05) and FSH (P < .01) were measured 10 min sooner after 0.8 mg/kg cocaine than after placebo-cocaine, but cocaine did not significantly increase the magnitude or duration of LHRH-stimulated increases in gonadotropins in ovariectomized females as it did in follicular phase females. Basal PRL levels (3.6 +/- 0.2 and 5.5 +/- 0.7 ng/ml) did not change after administration of cocaine alone.(ABSTRACT TRUNCATED AT 250 WORDS)

  • Acute effects of cocaine on Anterior Pituitary Hormones in male and female rhesus monkeys.
    The Journal of pharmacology and experimental therapeutics, 1993
    Co-Authors: Nancy K. Mello, Zoltán Sarnyai, Jack H. Mendelson, J M Drieze, Maureen Kelly
    Abstract:

    The effects of acute cocaine administration (0.4 or 0.8 mg/kg) on Anterior Pituitary Hormones were studied in four male and six female adult rhesus monkeys during the midluteal phase of the menstrual cycle (days 20-23). Progesterone levels averaged 15.7 +/- 3 and 10.6 +/- 2.8 ng/ml before low and high dose cocaine administration. Integrated plasma samples were collected every 10 min for 40 min before i.v. administration of cocaine, and 11 postcocaine samples were collected over 110 min. Cocaine (0.8 mg/kg) stimulated a significant increase in luteinizing hormone (LH) within 10 to 20 min (P < .01) and LH reached peak levels (59-60% above base line) within 30 min after cocaine administration in both males and females. Plasma cocaine levels averaged 289 +/- 23 and 346 +/- 73 ng/ml at 10 min after i.v. cocaine (0.8 mg/kg) administration in males and females, respectively. Follicle stimulating hormone levels were unchanged in midluteal females. Male testosterone increased by 50% above average base-line levels 50 min after the LH peak (80 min postcocaine). These data are consistent with our previous findings that cocaine increased LH and enhanced luteinizing hormone-releasing hormone-stimulated LH in early follicular females. The low dose of cocaine did not change basal levels of LH and follicle stimulating hormone in midluteal females and both LH and testosterone were unaffected in males. Cocaine plasma levels averaged 97.6 +/- 29 and 68.3 +/- 9.1 ng/ml at 10 min after 0.4 mg/kg of cocaine in males and females, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Igor O. Nasonkin - One of the best experts on this subject based on the ideXlab platform.

  • Aged PROP1 deficient dwarf mice maintain ACTH production.
    PloS one, 2011
    Co-Authors: Igor O. Nasonkin, Robert D Ward, Amanda H. Mortensen, David L. Bavers, Felix Beuschlein, Catherine E. Keegan, Gary D. Hammer, Sally A. Camper
    Abstract:

    Humans with PROP1 mutations have multiple Pituitary hormone deficiencies (MPHD) that typically advance from growth insufficiency diagnosed in infancy to include more severe growth hormone (GH) deficiency and progressive reduction in other Anterior Pituitary Hormones, eventually including adrenocorticotropic hormone (ACTH) deficiency and hypocortisolism. Congenital deficiencies of GH, prolactin, and thyroid stimulating hormone have been reported in the Prop1null (Prop1-/-) and the Ames dwarf (Prop1df/df) mouse models, but corticotroph and Pituitary adrenal axis function have not been thoroughly investigated. Here we report that the C57BL6 background sensitizes mutants to a wasting phenotype that causes approximately one third to die precipitously between weaning and adulthood, while remaining homozygotes live with no signs of illness. The wasting phenotype is associated with severe hypoglycemia. Circulating ACTH and corticosterone levels are elevated in juvenile and aged Prop1 mutants, indicating activation of the Pituitary-adrenal axis. Despite this, young adult Prop1 deficient mice are capable of responding to restraint stress with further elevation of ACTH and corticosterone. Low blood glucose, an expected side effect of GH deficiency, is likely responsible for the elevated corticosterone level. These studies suggest that the mouse model differs from the human patients who display progressive hormone loss and hypocortisolism.

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

  • The acute effects of cocaine on Anterior Pituitary Hormones in ovariectomized rhesus monkeys.
    The Journal of pharmacology and experimental therapeutics, 1995
    Co-Authors: Nancy K. Mello, Zoltán Sarnyai, Jack H. Mendelson, J M Drieze, Maureen Kelly
    Abstract:

    Cocaine stimulates a rapid release of gonadotropins in intact rhesus males and females and human males and enhances synthetic luteinizing hormone-releasing hormone (LHRH), stimulated luteinizing hormone (LH) and follicle-stimulating hormone (FSH). This report describes the effects of acute cocaine administration on basal and synthetic LHRH-stimulated Anterior Pituitary Hormones [LH, FSH and prolactin (PRL)] in five ovariectomized female rhesus monkeys. Integrated blood samples were collected every 10 min for 40 min before i.v. administration of cocaine (0.4 or 0.8 mg/kg) or an equal volume of vehicle control solution and for 110 min after cocaine or placebo administration. Synthetic LHRH (100 micrograms i.v.) was administered 10 min after cocaine or placebo-cocaine injection. In contrast to previous observations in rhesus and human males and in early follicular and midluteal phase rhesus females, cocaine did not change basal levels of gonadotropins or PRL in long-term ovariectomized females. LHRH stimulated a significant and sustained increase in LH (P < .01) within 20 min and FSH (P < .05) within 40 min after placebo-cocaine administration. LHRH also stimulated significant increases in LH and FSH after 0.4 and 0.8 mg/kg cocaine administration. Significant increases in LH (P < .05) and FSH (P < .01) were measured 10 min sooner after 0.8 mg/kg cocaine than after placebo-cocaine, but cocaine did not significantly increase the magnitude or duration of LHRH-stimulated increases in gonadotropins in ovariectomized females as it did in follicular phase females. Basal PRL levels (3.6 +/- 0.2 and 5.5 +/- 0.7 ng/ml) did not change after administration of cocaine alone.(ABSTRACT TRUNCATED AT 250 WORDS)

  • Acute effects of cocaine on Anterior Pituitary Hormones in male and female rhesus monkeys.
    The Journal of pharmacology and experimental therapeutics, 1993
    Co-Authors: Nancy K. Mello, Zoltán Sarnyai, Jack H. Mendelson, J M Drieze, Maureen Kelly
    Abstract:

    The effects of acute cocaine administration (0.4 or 0.8 mg/kg) on Anterior Pituitary Hormones were studied in four male and six female adult rhesus monkeys during the midluteal phase of the menstrual cycle (days 20-23). Progesterone levels averaged 15.7 +/- 3 and 10.6 +/- 2.8 ng/ml before low and high dose cocaine administration. Integrated plasma samples were collected every 10 min for 40 min before i.v. administration of cocaine, and 11 postcocaine samples were collected over 110 min. Cocaine (0.8 mg/kg) stimulated a significant increase in luteinizing hormone (LH) within 10 to 20 min (P < .01) and LH reached peak levels (59-60% above base line) within 30 min after cocaine administration in both males and females. Plasma cocaine levels averaged 289 +/- 23 and 346 +/- 73 ng/ml at 10 min after i.v. cocaine (0.8 mg/kg) administration in males and females, respectively. Follicle stimulating hormone levels were unchanged in midluteal females. Male testosterone increased by 50% above average base-line levels 50 min after the LH peak (80 min postcocaine). These data are consistent with our previous findings that cocaine increased LH and enhanced luteinizing hormone-releasing hormone-stimulated LH in early follicular females. The low dose of cocaine did not change basal levels of LH and follicle stimulating hormone in midluteal females and both LH and testosterone were unaffected in males. Cocaine plasma levels averaged 97.6 +/- 29 and 68.3 +/- 9.1 ng/ml at 10 min after 0.4 mg/kg of cocaine in males and females, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Felix Beuschlein - One of the best experts on this subject based on the ideXlab platform.

  • Aged PROP1 Deficient Dwarf Mice Maintain ACTH Production
    2016
    Co-Authors: Igor Nasonkin. O. ¤a, David L. Bavers, Felix Beuschlein, Robert Ward. D. ¤b, Mortensen Catherine E. Keegan
    Abstract:

    Humans with PROP1 mutations have multiple Pituitary hormone deficiencies (MPHD) that typically advance from growth insufficiency diagnosed in infancy to include more severe growth hormone (GH) deficiency and progressive reduction in other Anterior Pituitary Hormones, eventually including adrenocorticotropic hormone (ACTH) deficiency and hypocortiso-lism. Congenital deficiencies of GH, prolactin, and thyroid stimulating hormone have been reported in the Prop1null (Prop1-/-) and the Ames dwarf (Prop1df/df) mouse models, but corticotroph and Pituitary adrenal axis function have not been thoroughly investigated. Here we report that the C57BL6 background sensitizes mutants to a wasting phenotype that causes approximately one third to die precipitously between weaning and adulthood, while remaining homozygotes live with no signs of illness. The wasting phenotype is associated with severe hypoglycemia. Circulating ACTH and corticosterone levels are elevated in juvenile and aged Prop1 mutants, indicating activation of the Pituitary-adrenal axis. Despite this, young adult Prop1 deficient mice are capable of responding to restraint stress with further elevation of ACTH and corticosterone. Low blood glucose, an expected side effect of GH deficiency, is likely responsible for the elevated corticosterone level. These studies suggest that the mouse model differs from the human patients who display progressiv

  • Aged PROP1 deficient dwarf mice maintain ACTH production.
    PloS one, 2011
    Co-Authors: Igor O. Nasonkin, Robert D Ward, Amanda H. Mortensen, David L. Bavers, Felix Beuschlein, Catherine E. Keegan, Gary D. Hammer, Sally A. Camper
    Abstract:

    Humans with PROP1 mutations have multiple Pituitary hormone deficiencies (MPHD) that typically advance from growth insufficiency diagnosed in infancy to include more severe growth hormone (GH) deficiency and progressive reduction in other Anterior Pituitary Hormones, eventually including adrenocorticotropic hormone (ACTH) deficiency and hypocortisolism. Congenital deficiencies of GH, prolactin, and thyroid stimulating hormone have been reported in the Prop1null (Prop1-/-) and the Ames dwarf (Prop1df/df) mouse models, but corticotroph and Pituitary adrenal axis function have not been thoroughly investigated. Here we report that the C57BL6 background sensitizes mutants to a wasting phenotype that causes approximately one third to die precipitously between weaning and adulthood, while remaining homozygotes live with no signs of illness. The wasting phenotype is associated with severe hypoglycemia. Circulating ACTH and corticosterone levels are elevated in juvenile and aged Prop1 mutants, indicating activation of the Pituitary-adrenal axis. Despite this, young adult Prop1 deficient mice are capable of responding to restraint stress with further elevation of ACTH and corticosterone. Low blood glucose, an expected side effect of GH deficiency, is likely responsible for the elevated corticosterone level. These studies suggest that the mouse model differs from the human patients who display progressive hormone loss and hypocortisolism.