ABSTRACT
INTRODUCTION: Postpartum depression (PPD) is a common and serious illness that affects up to 14% of women in the first month after childbirth. We present an update on the pharmacologic treatment of PPD, although there continues to be a lack of large, randomized controlled trials (RCTs). AREAS COVERED: A review of the literature on the use of antidepressants, hormonal supplements and omega-3 fatty acids for the prevention and the treatment of PPD published since the original review in 2009 and the authors' opinion on the current status of the pharmacological treatment of PPD are covered. An electronic search was performed by using PubMed, Medline and PsychINFO. Inclusion criteria were: i) empirical articles in peer-reviewed English-language journals; ii) well-validated measures of depression; and iii) a uniform scoring system for depression among the sample. EXPERT OPINION: Since the last Expert Opinion review, four antidepressant treatment studies and one prevention study of PPD have been published. Six RCTs evaluating the use of omega-3 fatty acids (four for prevention and two for treatment) have been published. There continues to be lack of data regarding the pharmacotherapy of PPD. However, serotonin reuptake inhibitors should be considered first-line for women with PPD after it has been determined that the proper diagnosis is not bipolar disorder. It is important to individualize treatment for women with PPD and consider the risks and benefits of treatment while breastfeeding.
Subject(s)
Antidepressive Agents/therapeutic use , Depression, Postpartum/drug therapy , Fatty Acids, Omega-3/therapeutic use , Animals , Breast Feeding , Depression, Postpartum/prevention & control , Dietary Supplements , Female , Humans , Randomized Controlled Trials as Topic , Selective Serotonin Reuptake Inhibitors/therapeutic use , Treatment OutcomeABSTRACT
The risk for drug addiction is partially heritable. Genes of the dopamine system are likely candidates to harbour risk variants, as dopamine neurotransmission is involved in mediating the rewarding effects of drugs of abuse. One functional single nucleotide polymorphism in dopamine receptor D2 (DRD2), rs1076560, is involved in regulating splicing of the gene and alters the ratio of DRD2 isoforms located pre- and postsynaptically. rs1076560 has been previously associated with cocaine abuse and we set out to confirm this association in a sample of European American (EA) (n = 336) and African American (AA) (n = 1034) cocaine addicts and EA (n = 656) and AA (n = 668) controls. We also analysed the role of rs1076560 in opioid dependence by genotyping EA (n = 1041) and AA (n = 284) opioid addicts. rs1076560 was found to be nominally associated with opioid dependence in EAs (p = 0.02, OR = 1.27) and AAs (p = 0.03, OR = 1.43). When both opioid-addicted ancestral samples were combined, rs1076560 was significantly associated with increased risk for drug dependence (p = 0.0038, OR = 1.29). This association remained significant after correction for multiple testing. No association was found with cocaine dependence. These data demonstrate the importance of dopamine gene variants in the risk for opioid dependence and highlight a functional polymorphism that warrants further study.
Subject(s)
Opioid-Related Disorders/genetics , Polymorphism, Single Nucleotide , Receptors, Dopamine D2/genetics , Black or African American/genetics , Alleles , Case-Control Studies , Cocaine-Related Disorders/genetics , Female , Gene Frequency , Genotype , Humans , Linkage Disequilibrium , Male , Risk Factors , White People/geneticsABSTRACT
Little is known about the molecules that mediate the attachment of proepicardial cells to the heart. Ephrins are cell surface ligands for Eph tyrosine kinase receptors, molecules known to play a role in cell adhesion and migration. Here, we detected EphrinB ligands in proepicardial and epicardial mesothelial cells (EMCs) using reverse transcriptase-polymerase chain reaction, immunoblotting, immunolocalization, and EphB-Fc binding. Aggregated EphB-Fc fragments clustered ephrinB1 ligands on living EMCs indicating that they are cell surface expressed. In vitro assays demonstrated that ephrinB ligands participate in EMC migration but not cell adhesion. Localization studies in hearts at Hamburger and Hamilton stage 30 and older revealed that ephrinB1 is expressed in the epicardium and subepicardial mesenchyme of the atrioventricular sulcus. EMCs treated with platelet-derived growth factor-BB expressed smooth muscle markers but not ephrinB1. Our study supports an early role for ephrinB ligands for migration of epicardial cells and a later role in perivascular fibroblasts of coronary vessels in the atrioventricular sulcus.
