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D.A. Van Vugt

Researcher at Queen's University

Publications -  23
Citations -  1734

D.A. Van Vugt is an academic researcher from Queen's University. The author has contributed to research in topics: (+)-Naloxone & Prolactin. The author has an hindex of 17, co-authored 23 publications receiving 1723 citations. Previous affiliations of D.A. Van Vugt include Michigan State University.

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Effects of naloxone, morphine and methionine enkephalin on serum prolactin, luteinizing hormone, follicle stimulating hormone, thyroid stimulating hormone and growth hormone.

TL;DR: It is suggested that endogenous morphinomimetic substances may participate in regulating secretion of anterior pituitary hormones through regulating the response to naloxone and morphine.
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Naloxone inhibition of stress-induced increase in prolactin secretion

TL;DR: It is concluded that endorphins may be responsible for increased release of PRL during stressful conditions and inhibited the stress-induced rises in serum prolactin.
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Lasting response to ovariectomy in severe intractable premenstrual syndrome

TL;DR: It is concluded that cyclic ovarian steroidogenesis is a powerful determinant for the expression of pre menstrual symptomatology and Ovariectomy with low-dose estrogen replacement is an effective alternative for the woman with debilitating premenstrual syndrome who does not respond to conventional interventions.
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The effects of estrogen and progesterone on corticotropin-releasing hormone and arginine vasopressin messenger ribonucleic acid levels in the paraventricular nucleus and supraoptic nucleus of the rhesus monkey.

TL;DR: E2 and E2 + P4 replacement to OVX monkeys exert different effects on CRH and AVP gene expression, as estrogen stimulation of CRH mRNA in the PVN was abrogated by progesterone, whereas no effect of ovarian steroids on AVP mRNA in either the PVn or SON was observed.
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Interaction between opiates and hypothalamic dopamine on prolactin release

TL;DR: Observations indicate that opiates stimulate PRL release by decreasing DA activity in the median eminence, and β-endorphin, an endogenous opioid peptide, decreased the rate of DA turnover in the Median eminence and increased serum PRL levels approximately 10 - fold.