This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. This project has two sets of hypotheses: Treatment Hypotheses and Neuro-Biological Correlates of Treatment Hypotheses. Treatment Hypotheses include: 1. Treatment with Fluoxetine and Divalproes will be more efficacious than Placebo in reducing impulsive aggressive behavior in subjects with Intermittent Explosive Disorder (IED) overall and, 2. 'High Aggressive' IED Subjects will respond preferentially to treatment with Fluoxetine (both aims/hypotheses to be funded by NIMH). The Neuobiological Correlates Hypotheses include: 1. Platelet 5-HT Transporter binding will correlate with the anti-aggressive response to Fluoxetine but not to Divalproex; 2. Plasma GABA will correlate with the anti-aggressive response to Divalproex but not to Fluoxetine; 3. Assessment of aggression impulsivity, and social/emotional information processing will correlate with the anti-aggressive response to both Fluoxetine and Divalproex and, 4. DNA Polymorphisms of 5-Htrelevant genes will correlate with the anti-aggressive response to Fluoxetine and DNA Polymorphisms of GABA relevant genes will correlate with the anti-aggressive response to Divalproex. The design of the study is a fourteen week (twelve-weeks for active drug), double-blind, randomized, placebo-controlled trial of fluoxetine and divaloproex in IED subjects stratified by lifetime aggressiveness (I.e. Life History of Aggression Score: 'Moderate Aggression'=LHA<17, 'High Aggression'=LHA>18). CRC resources are requested primarily for ancillary services in obtaining medical screening and medical surveillance testing and in obtaining samples for Platelet 5-HT Transporter Binding, Plasma GABA Concentration, and in obtaining blood samples for DNA Extraction for pharmacogenetic analysis.
| Rosenfield, Robert L; Ehrmann, David A (2016) The Pathogenesis of Polycystic Ovary Syndrome (PCOS): The Hypothesis of PCOS as Functional Ovarian Hyperandrogenism Revisited. Endocr Rev 37:467-520 |
| Garyu, Justin W; Meffre, Eric; Cotsapas, Chris et al. (2016) Progress and challenges for treating Type 1 diabetes. J Autoimmun 71:1-9 |
| Rosenfield, Robert L (2015) The Polycystic Ovary Morphology-Polycystic Ovary Syndrome Spectrum. J Pediatr Adolesc Gynecol 28:412-9 |
| Maitland, Michael L; Xu, Chun-Fang; Cheng, Yu-Ching et al. (2015) Identification of a variant in KDR associated with serum VEGFR2 and pharmacodynamics of Pazopanib. Clin Cancer Res 21:365-72 |
| Bershad, Anya K; Jaffe, Jerome H; Childs, Emma et al. (2015) Opioid partial agonist buprenorphine dampens responses to psychosocial stress in humans. Psychoneuroendocrinology 52:281-8 |
| Fleming, Gini F; Schumm, Philip; Friberg, Greg et al. (2015) Circadian variation in plasma 5-fluorouracil concentrations during a 24 hour constant-rate infusion. BMC Cancer 15:69 |
| Refetoff, Samuel; Bassett, J H Duncan; Beck-Peccoz, Paolo et al. (2014) Classification and proposed nomenclature for inherited defects of thyroid hormone action, cell transport, and metabolism. J Clin Endocrinol Metab 99:768-70 |
| Kirkpatrick, Matthew G; Francis, Sunday M; Lee, Royce et al. (2014) Plasma oxytocin concentrations following MDMA or intranasal oxytocin in humans. Psychoneuroendocrinology 46:23-31 |
| Copinschi, Georges; Leproult, Rachel; Spiegel, Karine (2014) The important role of sleep in metabolism. Front Horm Res 42:59-72 |
| Müller, Peter; Quintana, Fernando A; Rosner, Gary L et al. (2014) Bayesian inference for longitudinal data with non-parametric treatment effects. Biostatistics 15:341-52 |
Showing the most recent 10 out of 244 publications
