A5011980037- Hypothalamic control of reproductive hormones
- Plant Reproductive Biology
- Thyroid Disorders and Treatments
- Metabolism, Diabetes, and Cancer
- Plant Molecular Biology Research
- Ion channel regulation and function
- Genetic and Clinical Aspects of Sex Determination and Chromosomal Abnormalities
- Growth Hormone and Insulin-like Growth Factors
- Pharmaceutical Practices and Patient Outcomes
- Cardiovascular Disease and Adiposity
- Adipose Tissue and Metabolism
- Neuropeptides and Animal Physiology
- Receptor Mechanisms and Signaling
- Hormonal and reproductive studies
- Ovarian function and disorders
- Reproductive Biology and Fertility
- Intramuscular injections and effects
- Muscle metabolism and nutrition
- Chemotherapy-induced cardiotoxicity and mitigation
- Regulation of Appetite and Obesity
- Patient Safety and Medication Errors
- Biochemical Analysis and Sensing Techniques
- Sexual Differentiation and Disorders
- Ion Channels and Receptors
- Anesthesia and Sedative Agents
University of Miami
2009-2022
American Pharmacists Association
2022
Brigham and Women's Hospital
2004-2011
Harvard University
2004-2010
Gonadotropin-dependent, or central, precocious puberty is caused by early maturation of the hypothalamic-pituitary-gonadal axis. In girls, this condition most often idiopathic. Recently, a G protein-coupled receptor, GPR54, and its ligand, kisspeptin, were described as an excitatory neuroregulator system for secretion gonadotropin-releasing hormone (GnRH). study, we have identified autosomal dominant GPR54 mutation--the substitution proline arginine at codon 386 (Arg386Pro)--in adopted girl...
Kisspeptin, encoded by the KISS1 gene, is a key stimulatory factor of GnRH secretion and puberty onset. Inactivating mutations its receptor (KISS1R) cause isolated hypogonadotropic hypogonadism (IHH). A unique KISS1R-activating mutation was described in central precocious (CPP).Our objective to investigate patients with idiopathic CPP normosmic IHH.Eighty-three children (77 girls) 61 IHH (40 men) were studied. The control group consisted 200 individuals normal pubertal development.The...
Objective Epicardial adipose tissue (EAT), the visceral fat depot of heart, is a modifiable cardiovascular risk factor and emerging therapeutic target. Liraglutide, an analog glucagon‐like peptide‐1, indicated for treatment type 2 diabetes mellitus. Liraglutide has recently been shown to reduce risk. Nevertheless, whether liraglutide could EAT unknown. Methods To test hypothesis, 6‐month randomized, open‐label, controlled study was performed in 95 diabetic subjects with body mass index (BMI)...
We report the phenotype of mice with targeted disruption Trpv6 (Trpv6 KO) epithelial calcium channel. The exhibit disordered Ca(2+) homeostasis, including defective intestinal absorption, increased urinary excretion, decreased BMD, deficient weight gain, and reduced fertility. Although our KO affects closely adjacent EphB6 gene, reported here is not related to dysfunction.
Disturbances in energy homeostasis can result obesity and other metabolic diseases. Here we report a pathway present normal human skeletal muscle myoblasts that is activated by the small polyphenolic molecule kaempferol (KPF). Treatment with KPF leads to an ∼30% increase myocyte oxygen consumption. The mechanism involves several-fold cyclic AMP (cAMP) generation protein kinase A activation, effect of be mimicked via treatment dibutyryl cAMP. Microarray real-time PCR studies identified set...
Cold-induced adaptive (or nonshivering) thermogenesis in small mammals is produced primarily brown adipose tissue (BAT). BAT has been identified humans and becomes more active after cold exposure. Heat production from requires sympathetic nervous system stimulation, T(3), uncoupling protein 1 (UCP1) expression. Our previous studies with a thyroid hormone receptor-beta (TR beta) isoform-selective agonist demonstrated that TR beta stimulation alone, was markedly impaired, although UCP-1...
The goal of this study was to investigate how the Arg386Pro mutation prolongs KiSS-1 receptor (KISS1R) responsiveness kisspeptin, contributing human central precocious puberty. Confocal imaging showed colocalization wild-type (WT) KISS1R with a membrane marker, which persisted for up 5 h stimulation. Conversely, no lysosome marker detected. Also, overnight treatment inhibitor did not affect WT protein, whereas proteasome increased protein levels by 24-fold. and time-dependent internalization...
KISS1 is a candidate gene for GnRH deficiency.Our objective was to identify deleterious mutations in KISS1.DNA sequencing and assessment of the effects rare sequence variants (RSV) were conducted 1025 probands with GnRH-deficient conditions.Fifteen harbored 10 heterozygous RSV seen less than 1% control subjects. Of that reside within mature kisspeptin peptide, p.F117L (but not p.S77I, p.Q82K, p.H90D, or p.P110T) reduces inositol phosphate generation. lie coding region but outside p.G35S...
Context Loss-of-function mutations of the kisspeptin-1 receptor gene, KISS1R , have been identified in patients with normosmic isolated hypogonadotropic hypogonadism (nIHH). Objective To investigate defects absent or delayed puberty. Patients We investigated gene a cohort 99 Brazilian nIHH constitutional delay puberty (CDP). Methods The entire coding region was amplified by PCR followed automatic sequencing. In addition, screening for exonic deletions performed multiplex ligation-dependent...
REVIEW article Front. Endocrinol., 13 December 2012 | https://doi.org/10.3389/fendo.2012.00149
Whereas many cardiac symptoms of thyrotoxicosis resemble those the hyperadrenergic state, circulating catecholamines are reduced or normal in this condition. To test hypothesis that thyrotoxic heart is hypersensitive to catechol-amines, we studied β-adrenergic signaling a transgenic (TG) mouse which human type 2 iodothyronine deiodinase (D2) gene expressed myocardium. Because D2 converts T4 T3, active form thyroid hormone, TG exhibits mild, chronic limited In current study, determined cAMP...
We investigated the physiological role of Gβ5, a unique G protein β subunit that dimerizes with regulators signaling (RGS) proteins R7 family instead Gβ. Gβ5 is essential for stability these complexes, so its knockout (KO)causes degradation entire Gβ5-R7 family. report Gβ5-KO mice remain leaner than wild type (WT) throughout their lifetime and are resistant to high-fat diet. They have 5-fold increase in locomotor activity, increased thermogenesis, lower serum insulin, all which correlate...
Altered glucose metabolism in the heart is an important characteristic of cardiovascular and metabolic disease. Because thyroid hormones have major effects on peripheral metabolism, we examined heart-selective increase T3 using transgenic mice expressing human type 2 iodothyronine deiodinase (D2) under control α-myosin heavy chain promoter (MHC-D2). Hyperinsulinemic-euglycemic clamps showed normal whole-body disposal but increased hepatic insulin action MHC-D2 as compared to wild-type (WT)...
Conference Abstract| February 01 1972 The Effects on Airways Conductance of Alpha-Adrenergic Stimulation and Blocking F. J. Prime; Prime 1Department Medicine, Institute Disease the Chest, Fulham Road, London, S.W.3 Search for other works by this author on: This Site PubMed Google Scholar S. Bianco; Bianco P. Griffin; Griffin L. Kamburoff Clin Sci (1972) 42 (2): 13P. https://doi.org/10.1042/cs042013Pa Views Icon Article contents Figures & tables Video Audio Supplementary Data Peer Review...
OPEN ACCESSMay 10, 2022Opioid Use Disorder Curriculum: Preclerkship Pharmacology Case-Based Learning Session Sabrina Taldone, MD, MBA, Sandra Lemmon, PhD, Suzy Bianco, PharmD, Joan St. Onge, MPH, Henri Ford, MHA, Lindsay Cox, David P. Serota, MSc, Sabita Roy, Jason Onugha, W. Forrest, Tyler Bartholomew, Hansel E. Tookes, MPH MBA Assistant Professor, Department of Medicine, University Miami Leonard M. Miller School Medicine , PhD Molecular and Cellular Pharmacology, Pharmacist, MHA Dean Chief...
Defects in a number of genes have been implicated the pathophysiology GnRH deficiency. Several lines evidence suggest that KISS1 is likely candidate gene for These include identification inactivating mutations KISS1R (a.k.a. GPR54) patients with deficiency, targeted deletions either or mice hypogonadotropic phenotypes, and demonstrated role kisspeptin stimulation neurons initiation puberty. However, no found The aim this study was to identify deleterious KISS1. After systematic evaluation...
The kisspeptin receptor (KISS1R) is a G protein-coupled recognized as the trigger of puberty and regulator reproductive competence in adulthood 1,2,3. Inactivating mutations KISS1R identified patients have been associated with iodiopathic hypogonadotropic hypogonadism (IHH) 1,2 precocious 4. Functional studies these mutants are crucial for our understanding mechanisms underlying regulation reproduction by this well those shaping disease outcomes, which result from abnormal signaling...
The kisspeptin receptor (KISS1R) is a G protein-coupled recognized as the trigger of puberty and regulator reproductive competence in adulthood 1,2,3. Inactivating mutations KISS1R identified patients have been associated with iodiopathic hypogonadotropic hypogonadism (IHH) 1,2 precocious 4. Functional studies these mutants are crucial for our understanding mechanisms underlying regulation reproduction by this well those shaping disease outcomes, which result from abnormal signaling...
Kisspeptin, encoded by the KISS1 gene, is a key stimulatory factor of GnRH secretion and puberty onset. Inactivating mutations its receptor (KISS1R) cause isolated hypogonadotropic hypogonadism (IHH). A unique KISS1R activating mutation was described in central precocious (CPP). To investigate patients with idiopathic CPP normosmic IHH. Eighty-three children (77 girls) 61 IHH (40 men) were studied. The control group consisted 200 individuals normal pubertal development. promoter region 3...