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Lesley M. E. Mccowan - One of the best experts on this subject based on the ideXlab platform.
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Corticotropin-Releasing Hormone, Corticotropin-Releasing Hormone-binding protein, and activin A in maternal serum: prediction of preterm delivery and response to glucocorticoids in women with symptoms of preterm labor.
American Journal of Obstetrics and Gynecology, 2000Co-Authors: Matthew A.g. Coleman, Jean-claude Schellenberg, Valentin Ananiev, Jeffrey A. Keelan, Nigel P Groome, Kevin M. Townend, Lesley M. E. MccowanAbstract:OBJECTIVE: The aim of this study was to determine prospectively whether serum concentrations of Corticotropin-Releasing Hormone, Corticotropin-Releasing Hormone-binding protein, and activin A (1) predict preterm birth within 10 days of hospital admission or at
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Corticotropin-Releasing Hormone, Corticotropin-Releasing Hormone-binding protein, and activin A in maternal serum: prediction of preterm delivery and response to glucocorticoids in women with symptoms of preterm labor.
American journal of obstetrics and gynecology, 2000Co-Authors: Matthew A.g. Coleman, Jean-claude Schellenberg, Valentin Ananiev, Jeffrey A. Keelan, Nigel P Groome, Kevin M. Townend, Lesley M. E. MccowanAbstract:Abstract Objective: The aim of this study was to determine prospectively whether serum concentrations of Corticotropin-Releasing Hormone, Corticotropin-Releasing Hormone–binding protein, and activin A (1) predict preterm birth within 10 days of hospital admission or at Study Design: Serum concentrations of Corticotropin-Releasing Hormone and activin A were measured in 94 women with symptoms of preterm labor between 24 and 34 weeks' gestation, and delivery outcomes were monitored. Corticotropin-Releasing Hormone–binding protein concentrations were measured in 71 of these women. In a subgroup of 15 women the serum analytes were assayed in conjunction with estriol before and 12 to 24 hours after administration of dexamethasone. Results: Forty-six percent (6/13) of the women who were delivered within 10 days of hospital admission had a raised serum Corticotropin-Releasing Hormone level, but the predictive relationship was not significant (χ 2 = 1.7; P =.2). Among the 31 women (including the 6 previously mentioned) who were delivered at 2 = 9; P =.003), the predictive diagnostic value was poor, with sensitivity, specificity, and positive and negative predictive values of 39%, 90%, 67%, and 75%, respectively. The serum concentrations of Corticotropin-Releasing Hormone–binding protein and activin A were unrelated to gestational age at delivery. Dexamethasone markedly lowered the serum estriol level ( P Conclusion: Serum concentrations of Corticotropin-Releasing Hormone, Corticotropin-Releasing Hormone–binding protein, and activin A are not clinically useful for the prediction of preterm delivery among women with symptoms of preterm labor and are not affected by administration of glucocorticoids. (Am J Obstet Gynecol 2000;183:643-8.)
Joseph A. Majzoub - One of the best experts on this subject based on the ideXlab platform.
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Comprehensive Physiology - Regulation and Actions of Corticotropin-Releasing Hormone
Comprehensive Physiology, 2011Co-Authors: Stacie C. Weninger, Joseph A. MajzoubAbstract:The sections in this article are: 1 Corticotropin-Releasing Hormone Expression 2 Corticotropin-Releasing Hormone Receptors 3 Corticotropin-Releasing Hormone-Binding Protein 4 Corticotropin-Releasing Hormone-Like Molecules 5 Regulation of Corticotropin-Releasing Hormone Expression 5.1 Corticotropin-Releasing Hormone Gene Structure 5.2 Intracellular Second Messengers That Regulate Corticotropin-Releasing Hormone Gene Expression 5.3 Extracellular Ligands That Regulate Corticotropin-Releasing Hormone Expression and Release 6 Regulation of the Hypothalamic-Pituitary-Adrenal Axis 6.1 Role of Corticotropin-Releasing Hormone in Stimulating Corticotropin Synthesis and Release 6.2 Other Corticotropin-Releasing Factors 6.3 Role of Corticotropin-Releasing Hormone in Circadian Rhythm Generation of the Hypothalamic-Pituitary-Adrenal Axis 6.4 Role of Corticotropin-Releasing Hormone in Fetal Development 7 Role of Corticotropin-Releasing Hormone in Responses to Physiological and Psychological Stressors 7.1 Acute Stressors 7.2 Chronic Stressors 8 Role of Corticotropin-Releasing Hormone in Regulating Other Neuroendocrine Functions 8.1 Behavior 8.2 Appetite 8.3 Reproduction 8.4 Autonomic Function 9 Conclusion
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Corticotropin-Releasing Hormone, Placenta
Encyclopedia of Endocrine Diseases, 2004Co-Authors: Katia Karalis, Joseph A. MajzoubAbstract:Corticotropin-Releasing Hormone (CRH) is a 41-amino acid neuropeptide identified in the central nervous system as well as in several peripheral tissues. CRH has been found in the placentae of different primates. In humans, CRH can be measured in the maternal circulation, with very high levels as labor approaches, suggesting its usefulness as a marker of the timing of parturition. In this article, the regulation of placental CRH during human pregnancy, its maternal effects, and its putative significance for the fetus are discussed.
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Corticotropin-Releasing Hormone stimulates angiogenesis and epithelial tumor growth in the skin.
Journal of Investigative Dermatology, 1999Co-Authors: Jack L. Arbiser, Katia Karalis, Akila N. Viswanathan, Chieko Koike, Bela Anand-apte, Evelyn Flynn, Bruce R. Zetter, Joseph A. MajzoubAbstract:The hypothalamic neuropeptide Corticotropin-Releasing Hormone is the major hypothalamic regulator of the endocrine pituitary–adrenal axis. Corticotropin-Releasing Hormone is also expressed in many peripheral sites, where its functions are unclear. It is also secreted by diverse neoplasms, where it may be associated with malignant behavior. To provide information regarding the function of Corticotropin-Releasing Hormone in peripheral sites and in tumors, we asked whether Corticotropin-Releasing Hormone has angiogenic properties. In vitro, we found that human Corticotropin-Releasing Hormone specifically stimulates endothelial chemotaxis via a Corticotropin-Releasing Hormone receptor-dependent mechanism. In vivo, subcutaneous inoculation of nude mice with human epithelial tumor cells engineered to secrete Corticotropin-Releasing Hormone was associated with significantly enhanced angiogenesis (2.3-fold over control) and tumor growth (5-fold over control). Peripheral Corticotropin-Releasing Hormone may thus enhance local angiogenesis, which may provide clues to its function outside of the nervous system.
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Placental Corticotropin-Releasing Hormone: Function and regulation
American Journal of Obstetrics and Gynecology, 1999Co-Authors: Joseph A. Majzoub, Katia KaralisAbstract:Corticotropin-Releasing Hormone is a neuropeptide placentally expressed among mammals only in primates. Its expression increases as much as 100 times during the last 6 to 8 weeks of pregnancy and is paradoxically stimulated by glucocorticoids. Increasing evidence suggests that placental Corticotropin-Releasing Hormone may have evolved in primates to stimulate fetal adrenocorticotropin release and adrenal steroidogenesis, thus satisfying the high demand for synthesis of dehydroepiandrosterone, the predominant source of placental estradiol. Concomitant stimulation by placental Corticotropin-Releasing Hormone of fetal cortisol and dehydroepiandrosterone would couple the glucocorticoid effects on fetal organ maturation with the timing of parturition, an obvious benefit in postnatal survival. (Am J Obstet Gynecol 1999;180:S242-6.)
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A central theory of preterm and term labor: Putative role for Corticotropin-Releasing Hormone
American Journal of Obstetrics and Gynecology, 1999Co-Authors: Joseph A. Majzoub, C J Lockwood, Roger Smith, James A. Mcgregor, Martha Snyder Taggart, Jay SchulkinAbstract:Near the end of human pregnancy the concentration of placental Corticotropin-Releasing Hormone in maternal blood rises exponentially. The rate of elevation of Corticotropin-Releasing Hormone and its duration through time have been linked to the time of onset of labor. Paradoxically, although glucocorticoids are known to inhibit Corticotropin-Releasing Hormone production within the hypothalamic-pituitary-adrenal axis, cortisol actually increases Corticotropin-Releasing Hormone levels in several areas outside the hypothalamus, including the placenta. Placental Corticotropin-Releasing Hormone may be an important component of a system that controls the normal maturation of the fetus and signals the initiation of labor. Abnormal elevations in Corticotropin-Releasing Hormone, which may be a hormonal response to stressors arising in either the mother, placenta, or fetus, may prove to participate in the premature onset of parturition.
George P Chrousos - One of the best experts on this subject based on the ideXlab platform.
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Potential Uses of Corticotropin‐Releasing Hormone Antagonists
Annals of the New York Academy of Sciences, 2006Co-Authors: E Zoumakis, Phillip W. Gold, Kenner C. Rice, George P ChrousosAbstract:Corticotropin-Releasing Hormone (CRH), its natural homologs urocortins (UCN) 1, 2, and 3, and several types of CRH receptors (R), coordinate the behavioral, endocrine, autonomic, and immune responses to stress. The potential use of CRH antagonists is currently under intense investigation. Selective antagonists have been used experimentally to clarify the role of CRH-related peptides in anxiety and depression, addictive behavior, inflammatory disorders, acute and chronic neurodegeneration, and sleep disorders, as well as preterm labor.
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Nonpeptide Corticotropin-Releasing Hormone receptor type 1 antagonists and their applications in psychosomatic disorders.
Neuroendocrinology, 2004Co-Authors: Carlo Contoreggi, Kenner C. Rice, George P ChrousosAbstract:Overproduction of Corticotropin-Releasing Hormone (CRH) and stress system abnormalities are seen in psychiatric diseases such as depression, anxiety, eating disorders, and addiction. Investigations of
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Roles of reproductive Corticotropin-Releasing Hormone.
Annals of the New York Academy of Sciences, 2003Co-Authors: Sophia N. Kalantaridou, George Mastorakos, Antonis Makrigiannakis, George P ChrousosAbstract:: Corticotropin-Releasing Hormone (CRH), the principal regulator of the hypothalamic-pituitary-adrenal axis, as well as its receptors, have been identified in most female reproductive tissues, including the uterus, placenta, and ovary. Endometrial CRH may participate in decidualization, implantation, and early maternal tolerance; placental CRH may participate in the physiology of pregnancy and the onset of parturition, and ovarian CRH may participate in follicular maturation, ovulation, and luteolysis. The hypercortisolism of the latter half of pregnancy can be explained by increased levels of placental CRH in plasma. This hypercortisolism is followed by a transient suppression of hypothalamic CRH secretion in the postpartum period, which may explain the blues or depression and autoimmune phenomena frequently observed during this period.
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Fas/Fas ligand-associated apoptosis in experimental autoimmune uveoretinitis in rodents: role of proinflammatory Corticotropin-Releasing Hormone.
Experimental Eye Research, 2001Co-Authors: Vassiliki Poulaki, Nicholas Mitsiades, George Mastorakos, Rachel R Caspi, George P Chrousos, Evrydiki A BouzasAbstract:We have previously shown that Corticotropin-Releasing Hormone plays an important proinflammatory role in the induction of experimental autoimmune uveoretinitis. In this study, we examined the role of apoptosis in the destruction of the retina during experimental autoimmune uveoretinitis, and the role of Corticotropin-Releasing Hormone as a local regulator of Fas and Fas Ligand expression in this condition. We evaluated apoptosis by the terminal deoxynucleotidyl transferase dUTP nick end labeling method and Fas and Fas Ligand presence by immunohistochemistry. We examined formalin-fixed, paraffin-embedded eye sections from female Lewis rats or B10.A mice immunized with the major pathogenetic epitope (R16 peptide) of the interphotoreceptor retinoid-binding protein. Female B10.A mice similarly immunized were treated with intraperitoneal injections of the rabbit anti-Corticotropin-Releasing Hormone antibody TS-2 or nonimmune rabbit serum. The percentage of retinal cells undergoing apoptosis and the expression of Fas and Fas Ligand were increased in inflamed retinas in immunized Lewis rats and B10.A mice, compared to controls. Retinas from immunized B10.A mice treated with anti-Corticotropin-Releasing Hormone antibody showed significantly lower apoptosis and Fas and Fas Ligand expression than placebo-treated animals. In conclusion, retinal cells in experimental autoimmune uveoretinitis undergo apoptosis associated with concurrent upregulation of Fas and Fas Ligand. The local presence of Corticotropin-Releasing Hormone appears to be of pivotal importance in this process.
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cerebrospinal fluid levels of corticotropin releasing Hormone in women with functional hypothalamic amenorrhea
American Journal of Obstetrics and Gynecology, 2000Co-Authors: Sarah L Berga, Tammy L Loucksdanielsa, Lauri J Adler, Judy L Cameron, Karen A Matthews, George P Chrousos, Marsha D MarcusAbstract:Abstract Objective: Women with functional hypothalamic amenorrhea are anovulatory because of reduced gonadotropin-releasing Hormone drive. Several studies have documented hypercortisolemia, which suggests that functional hypothalamic amenorrhea is stress-induced. Further, with recovery (resumption of ovulation), cortisol decreased and gonadotropin-releasing Hormone drive increased. Corticotropin-Releasing Hormone can increase cortisol and decrease gonadotropin-releasing Hormone. To determine its role in functional hypothalamic amenorrhea, we measured Corticotropin-Releasing Hormone in cerebrospinal fluid along with arginine vasopressin, another potent adrenocorticotropic Hormone secretagog, and β-endorphin, which is released by Corticotropin-Releasing Hormone and can inhibit gonadotropin-releasing Hormone. Study Design: Corticotropin-Releasing Hormone, vasopressin, and β-endorphin levels were measured in cerebrospinal fluid from 14 women with eumenorrhea and 15 women with functional hypothalamic amenorrhea. Results: Levels of Corticotropin-Releasing Hormone in cerebrospinal fluid and of vasopressin were comparable and β-endorphin levels were lower in women with functional hypothalamic amenorrhea. Conclusions: In women with established functional hypothalamic amenorrhea, increased cortisol and reduced gonadotropin-releasing Hormone are not sustained by elevated cerebrospinal-fluid Corticotropin-Releasing Hormone, vasopressin, or β-endorphin. These data do not exclude a role for these factors in the initiation of functional hypothalamic amenorrhea. (Am J Obstet Gynecol 2000;182:776-84.)
C J Lockwood - One of the best experts on this subject based on the ideXlab platform.
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Stress-associated preterm delivery: the role of Corticotropin-Releasing Hormone.
American journal of obstetrics and gynecology, 1999Co-Authors: C J LockwoodAbstract:The study's objective was to provide an introduction to the role of Corticotropin-Releasing Hormone in preterm delivery associated with stress. A selective review of the current literature relevant to the objective was undertaken. Published data were analyzed for relevance to the biochemical model presented. Preterm delivery is a leading cause of neonatal morbidity and mortality. Efforts to prevent preterm delivery have been greatly hampered by a poor understanding of the underlying pathophysiology. There is increasing clinical and laboratory evidence that many preterm deliveries result from maternal and fetal stress, which activates cells in the placenta, decidua, and fetal membranes to produce Corticotropin-Releasing Hormone. Corticotropin-Releasing Hormone in turn enhances prostaglandin production in these tissues to promote parturition. Corticotropin-Releasing Hormone plays an important role in the etiology of preterm delivery associated with maternal or fetal stress.
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Stress-associated preterm delivery: The role of Corticotropin-Releasing Hormone☆☆☆
American Journal of Obstetrics and Gynecology, 1999Co-Authors: C J LockwoodAbstract:Abstract Objective: The study's objective was to provide an introduction to the role of Corticotropin-Releasing Hormone in preterm delivery associated with stress. Study Design: A selective review of the current literature relevant to the objective was undertaken. Published data were analyzed for relevance to the biochemical model presented. Results: Preterm delivery is a leading cause of neonatal morbidity and mortality. Efforts to prevent preterm delivery have been greatly hampered by a poor understanding of the underlying pathophysiology. There is increasing clinical and laboratory evidence that many preterm deliveries result from maternal and fetal stress, which activates cells in the placenta, decidua, and fetal membranes to produce Corticotropin-Releasing Hormone. Corticotropin-Releasing Hormone in turn enhances prostaglandin production in these tissues to promote parturition. Conclusion: Corticotropin-Releasing Hormone plays an important role in the etiology of preterm delivery associated with maternal or fetal stress. (Am J Obstet Gynecol 1999;180:S264-6.)
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A central theory of preterm and term labor: Putative role for Corticotropin-Releasing Hormone
American Journal of Obstetrics and Gynecology, 1999Co-Authors: Joseph A. Majzoub, C J Lockwood, Roger Smith, James A. Mcgregor, Martha Snyder Taggart, Jay SchulkinAbstract:Near the end of human pregnancy the concentration of placental Corticotropin-Releasing Hormone in maternal blood rises exponentially. The rate of elevation of Corticotropin-Releasing Hormone and its duration through time have been linked to the time of onset of labor. Paradoxically, although glucocorticoids are known to inhibit Corticotropin-Releasing Hormone production within the hypothalamic-pituitary-adrenal axis, cortisol actually increases Corticotropin-Releasing Hormone levels in several areas outside the hypothalamus, including the placenta. Placental Corticotropin-Releasing Hormone may be an important component of a system that controls the normal maturation of the fetus and signals the initiation of labor. Abnormal elevations in Corticotropin-Releasing Hormone, which may be a hormonal response to stressors arising in either the mother, placenta, or fetus, may prove to participate in the premature onset of parturition.
Matthew A.g. Coleman - One of the best experts on this subject based on the ideXlab platform.
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Corticotropin-Releasing Hormone, Corticotropin-Releasing Hormone-binding protein, and activin A in maternal serum: prediction of preterm delivery and response to glucocorticoids in women with symptoms of preterm labor.
American Journal of Obstetrics and Gynecology, 2000Co-Authors: Matthew A.g. Coleman, Jean-claude Schellenberg, Valentin Ananiev, Jeffrey A. Keelan, Nigel P Groome, Kevin M. Townend, Lesley M. E. MccowanAbstract:OBJECTIVE: The aim of this study was to determine prospectively whether serum concentrations of Corticotropin-Releasing Hormone, Corticotropin-Releasing Hormone-binding protein, and activin A (1) predict preterm birth within 10 days of hospital admission or at
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Corticotropin-Releasing Hormone, Corticotropin-Releasing Hormone-binding protein, and activin A in maternal serum: prediction of preterm delivery and response to glucocorticoids in women with symptoms of preterm labor.
American journal of obstetrics and gynecology, 2000Co-Authors: Matthew A.g. Coleman, Jean-claude Schellenberg, Valentin Ananiev, Jeffrey A. Keelan, Nigel P Groome, Kevin M. Townend, Lesley M. E. MccowanAbstract:Abstract Objective: The aim of this study was to determine prospectively whether serum concentrations of Corticotropin-Releasing Hormone, Corticotropin-Releasing Hormone–binding protein, and activin A (1) predict preterm birth within 10 days of hospital admission or at Study Design: Serum concentrations of Corticotropin-Releasing Hormone and activin A were measured in 94 women with symptoms of preterm labor between 24 and 34 weeks' gestation, and delivery outcomes were monitored. Corticotropin-Releasing Hormone–binding protein concentrations were measured in 71 of these women. In a subgroup of 15 women the serum analytes were assayed in conjunction with estriol before and 12 to 24 hours after administration of dexamethasone. Results: Forty-six percent (6/13) of the women who were delivered within 10 days of hospital admission had a raised serum Corticotropin-Releasing Hormone level, but the predictive relationship was not significant (χ 2 = 1.7; P =.2). Among the 31 women (including the 6 previously mentioned) who were delivered at 2 = 9; P =.003), the predictive diagnostic value was poor, with sensitivity, specificity, and positive and negative predictive values of 39%, 90%, 67%, and 75%, respectively. The serum concentrations of Corticotropin-Releasing Hormone–binding protein and activin A were unrelated to gestational age at delivery. Dexamethasone markedly lowered the serum estriol level ( P Conclusion: Serum concentrations of Corticotropin-Releasing Hormone, Corticotropin-Releasing Hormone–binding protein, and activin A are not clinically useful for the prediction of preterm delivery among women with symptoms of preterm labor and are not affected by administration of glucocorticoids. (Am J Obstet Gynecol 2000;183:643-8.)
