ABSTRACT
Nocturnal enuresis is a common disorder in childhood, but its pathophysiological mechanisms have not been fully elucidated. Iatrogenic nocturnal enuresis has been described following treatment with several psychotropic medications. Herein, we describe a 6-year-old child who experienced nocturnal enuresis during treatment with the antihistamine cetirizine. Drug rechallenge was positive. Several neurotransmitters are implicated in the pathogenesis of nocturnal enuresis, including noradrenaline, serotonin and dopamine. Antihistamine treatment may provoke functional imbalance of these pathways resulting in incontinence.
Subject(s)
Cetirizine/therapeutic use , Histamine H1 Antagonists, Non-Sedating/therapeutic use , Nocturnal Enuresis/chemically induced , Rhinitis/drug therapy , Cetirizine/adverse effects , Child , Female , Histamine H1 Antagonists, Non-Sedating/adverse effects , Humans , Iatrogenic Disease , Treatment OutcomeABSTRACT
miRNAs act as oncogenes or tumor suppressors in a wide variety of human cancers, including prostate cancer (PCa). We found a severe and consistent downregulation of miRNAs, miR-154, miR-299-5p, miR-376a, miR-376c, miR-377, miR-381, miR-487b, miR-485-3p, miR-495 and miR-654-3p, mapped to the 14q32.31 region in metastatic cell lines as compared with normal prostatic epithelial cells (PrEC). In specimens of human prostate (28 normals, 99 primary tumors and 13 metastases), lower miRNA levels correlated significantly with a higher incidence of metastatic events and higher prostate specific antigen (PSA) levels, with similar trends observed for lymph node invasion and the Gleason score. We transiently transfected 10 members of the 14q32.31 cluster in normal prostatic epithelial cell lines and characterized their affect on malignant cell behaviors, including proliferation, apoptosis, migration and invasion. Finally, we identified FZD4, a gene important for epithelial-to-mesenchymal transition in (PCa), as a target of miR-377.
Subject(s)
Chromosomes, Human, Pair 14 , MicroRNAs/genetics , Prostatic Neoplasms/genetics , Prostatic Neoplasms/pathology , Apoptosis/genetics , Cell Line, Tumor , Cell Movement/genetics , Cell Proliferation , Down-Regulation , Epigenesis, Genetic , Epithelial-Mesenchymal Transition , Frizzled Receptors/genetics , Gene Expression Regulation, Neoplastic , Humans , Male , Prostate/physiology , Reference ValuesABSTRACT
Toll-like receptors (TLR) are important innate immune proteins for the identification and clearance of invading pathogen. TLR signal through adaptor proteins, most commonly myeloid differentiation primary response gene 88 (MyD88). Inappropriate response of specific TLR has been implicated in certain autoimmune diseases, such as multiple sclerosis (MS). Activation of TLR2, TLR4, TLR7 and TLR9 plays a role in experimental allergic encephalomyelitis (EAE), a murine model of MS, while TLR3 activation protects from disease. Therefore, TLR-modulation could be an important adjuvant to current treatments. Here, we focus on TLR involved in EAE and MS pathogenesis highlighting specific components targeting TLR that might offer further therapeutic possibilities.
