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Nathan Goodyear

PsychiatryOnline | The Journal of Neuropsychiatry and Clinical Neurosciences | The Neur... - 0 views

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    Understanding the neuroendocrine effects of TBI. This article discusses all hormonal effects as a result of TBI.
Nathan Goodyear

Octreotide - A Review of its Use in Treating Neuroendocrine Tumours - PMC - 0 views

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    Octreotide prolongs time interval to tumor progression in neuroendocrine tumors.
Nathan Goodyear

Mood Disorders and Obesity: Understanding Inflammation as a Pathophysiological Nexus | ... - 0 views

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    good review of the interaction between the immune system and the neuroendocrine system in obesity and mood disorders.  
Nathan Goodyear

Neuroendocrine disorders after... [J Neurol Neurosurg Psychiatry. 2008] - PubMed - NCBI - 0 views

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    The majority of people with PTHP after TBI remain undiagnosed.  The current thought, is that 25% of those with TBI have at least one pituitary hormone deficiency.  It does not have to be total pituitary failure.  Deficiencies can be isolated.
Nathan Goodyear

PsychiatryOnline | The Journal of Neuropsychiatry and Clinical Neurosciences | The Neur... - 0 views

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    TBI results in hormone disruption in 25-69% of those effected.  The major cause is a pituitary/neuro-endocrine effect.  This has been described since the early 20th century.
Nathan Goodyear

Hypothalamic-pituitary-adrenal axis, neuroendorine factors and stress - 0 views

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    Great review on how stress effects the neuroimmunoendocrine systems.
Nathan Goodyear

Delayed Neuroendocrine Sexual Maturation in Female Rats After a Very Low Dose of Bisphe... - 0 views

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    low dose of BPA in rat model finds delayed sexual maturation.
Nathan Goodyear

Evaluating obesity in fibromyalgia: neuroendocrine biomarkers, symptoms, and functions - 0 views

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    It is no suprise that obesity is found to be associated with Fibromyalgia.  They are both inflammatory conditions.    This study goes even further and suggests that obesity plays a role in fibromyalgia
Nathan Goodyear

Prevalence of Neuroendocrine Dysfunction in Patients Recovering from Traumatic Brain In... - 0 views

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    TBI results in pituitary dysfunction.  The result in low cortisol, low thyroid, and low HGH.  Other hormones appeared to be unaffected
Nathan Goodyear

The natural history of neuroendocrine change... [Biol Psychiatry. 2007] - PubMed - NCBI - 0 views

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    salivary evaluation of cortisol levels in children after MVA reveals slow normalization of elevated cortisol over time (6-18 months), yet catecholamines stay elevated
Nathan Goodyear

Perinatal exposure to low-dose bisphenol A affects the neuroendocrine stress response i... - 0 views

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    intra uterine exposure to BPA disrupts stress response in rat model.
Nathan Goodyear

The Estrogen Receptor β Subtype: A Novel Mediator of Estrogen Action in Neuro... - 0 views

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    Estrogen receptors are one mechanism of the transmission of the estrogen signal.  The signal can be from estrogens themselves, estrogenic like compounds (xenoestrogens) and via non-estrogens like 3-beta androstane idol that interacts with ER beta to decrease prostate cancer cell proliferation.
Nathan Goodyear

Metabolic influences on neuroendocrine regulation of reproduction - 0 views

  • Energy storage occurs mainly at the level of white adipose tissue, where adipocytes secrete the anorexigenic adipokine leptin
  • humans and laboratory animals with leptin or insulin deficiency or resistance and/or increased ghrelin levels exhibit delayed or absent puberty and frequently display hypogonadotropic hypogonadism, which prevents fertility
  • Ghrelin suppresses pulsatile gonadotropin-releasing hormone (GnRH) release [14,15], thus serving as a signal to suppress reproduction in times of famine
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  • GnRH neurons have been shown to express insulin receptor mRNA and protein [27] and are activated by insulin
  • AgRP and NPY have the opposite (orexigenic) effect, inducing food intake.
  • Neuropeptides derived from POMC/CART neurons exert a potent anorectic action, thus decreasing food intake and body weight
  • Kisspeptins (encoded by KISS1) have been identified in the last decade as the most potent secretagogues of GnRH release.
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    Good, although brief, discussion of the interaction between metabolism and hormones.  Kisspeptin is a GNRH secreatagogue "upstream".   Insulin, Leptin, and Gherlin can inhibit GNRH through resistance and low levels.  Probably a U shaped graph of optimal activity.
Nathan Goodyear

Acute Effects of Triiodothyronine (T3) Replacement Therapy in Patients with Chronic Hea... - 0 views

  • In DC patients, short-term synthetic L-T3 replacement therapy significantly improved neuroendocrine profile and ventricular performance
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    T3 provides significant improvement in cardiac function in those with dilated cardiomyopathy
Nathan Goodyear

ScienceDirect - Journal of Psychiatric Research : Neuroendocrine effects of S-adenosyl-... - 0 views

  • Our results, at least in depressed men, seem to support the hypothesis of a stimulating effect of SAMe on the dopaminergic system
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    SAMe stimulates dopamine secretion in depressed men
Nathan Goodyear

Leptin stimulates fatty-acid oxidation by activati... [Nature. 2002] - PubMed result - 0 views

  • Leptin is a hormone secreted by adipocytes that plays a pivotal role in regulating food intake, energy expenditure and neuroendocrine function. Leptin stimulates the oxidation of fatty acids and the uptake of glucose, and prevents the accumulation of lipids in nonadipose tissues, which can lead to functional impairments known as "lipotoxicity"
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    Leptin and fat accumulation called "lipotoxicity"
Nathan Goodyear

Leptin Levels Are Dependent on Sleep Duration: Relationships with Sympathovagal Balance... - 0 views

  • sleep modulates a major component of the neuroendocrine control of appetite.
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    sleep controls your appetite
Nathan Goodyear

Hypercalcemia of malignancy and new treatment options - 0 views

  • Hypercalcemia of malignancy occurs as the result of direct bone metastasis and via humoral mechanisms such as parathyroid hormone-related protein (PTHrP) or 1,25-dihydroxyvitamin D mediated pathways
  • ectopic secretion of parathyroid hormone (PTH) has been implicated
  • Hypercalcemia due to osteolytic bone lesions is common in multiple myeloma, leukemia, and breast cancer
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  • Humoral hypercalcemia is predominant in squamous cell, renal cell and ovarian cancers, and lymphomas are associated with 1,25-dihydroxyvitamin D mediated hypercalcemia
  • 20% of cases of hypercalcemia of malignancy and is frequently encountered in multiple myeloma, metastatic breast cancer, and to a lesser extent in leukemia and lymphoma
  • Physiologic bone turnover requires the complementary activity of osteoblasts – mesenchymal stem cell-derived bone-forming cells – and bone-resorbing cells of monocyte and macrophage lineage known as osteoclasts
  • In local osteolytic hypercalcemia, the RANKL/RANK interaction results in excessive osteoclast activation leading to enhanced bone resorption and thus hypercalcemia
  • In addition, osteoclast activation is also mediated by malignancy secreted cytokines, including interleukin-1, initially termed “osteoclast stimulating factor”
  • Macrophage inflammation protein 1-alpha (MIP 1-alpha)
  • hypercalcemia is through extra-renal 1,25-dihydroxyvitamin D (calcitriol) production
  • 1% of cases
  • increased production of 1,25-dihydroxyvitamin D occurs nearly exclusively in Hodgkin and non-Hodgkin lymphoma with case reports of the same in ovarian dysgerminoma
  • 1-α-hydroxylase in the kidney, a process regulated by PTH
  • in 1,25-dihydroxyvitamin D induced hypercalcemia, malignant cells likely recruit and induce adjacent macrophages to express 1-α-hydroxylase, converting endogenous calcidiol into calcitriol.31 Calcitriol then binds to receptors in the intestine leading to heightened enteric calcium reabsorption with resultant hypercalcemia
  • this mechanism of disease is best conceptualized as an absorptive form of hypercalcemia
  • Ectopic production of PTH by malignant cells has been described in a handful of cases involving cancer of the ovary and lung, as well as neuroendocrine tumors and sarcoma
  • primary hyperparathyroidism and malignancy comprising nearly 90% of cases of hypercalcemia
  • an initial panel consisting of PTH, PTHrP, phosphorus, 25-hydroxyvitamin D, and 1,25-dihydroxyvitamin D should be obtained
  • Lymphoma, a hypercalcemia due to 1,25-dihydroxyvitamin D mediated pathways, is implied by elevations in 1,25-dihydroxyvitamin D without concomitant elevations in 25-hydroxyvitamin D. In such cases, PTH is low and PTHrP undetectable
  • Treatment of hypercalcemia of malignancy is aimed at lowering the serum calcium concentration by targeting the underlying disease, specifically by inhibiting bone resorption, increasing urinary calcium excretion, and to a lesser extent by decreasing intestinal calcium absorption
  • mildly symptomatic disease
  • marked symptoms
  • hydration with isotonic fluid (if admitted), avoidance of thiazide diuretics, and a low-calcium diet
  • denosumab
  • Denosumab is an RANKL antibody that inhibits osteoclast maturation, activation, and function
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    hypercalcemia in cancer and treatments.
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