1,2-Ethylenebis(oxyethyleneoxyethyleneoxy)benzene/Benzo-18-crown-6/CROWN ETHER/BENZO-18-CROWN-6 FOR SYNTHES/B18C6/CROWN ETHER/BENZO-18-CROWN-6/2,3-Benzo-1,4,7,10,13,16-hexaoxaoctadec-2-ene/1,4,7,10,13,16-HEXAHYDROXY-16-ORTHOCYCLOPHANE/benzo-1,4,7,10,13,16-hexaoxacyclooctadecane/2,3-benzo-1,4,7,10,13,16-hexaoxacyclooctadec-2-ene/2,3,5,6,8,9,11,12,14,15-Decahydro-1,4,7,10,13,16-benzohexaoxacyclooctadecine/benzo-18-C-6/2,3,5,6,8,9,11,12,14,15-decahydro-1,4,7,10,13,16-benzohexaoxacyclooctadecin/1,4,7,10,13,16-Benzohexaoxacyclooctadecin, 2,3,5,6,8,9,11,12,14,15-decahydro-/Benzo-18-crown 6-Ether
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MicroRNAs (miRNAs) are small non-coding RNAs that have shown promise as noninvasive biomarkers in cardiac disease. This study was undertaken to investigate the miRNA expression profile in dogs with myxomatous mitral valve disease (MMVD). 277 miRNAs were quantified using RT-qPCR from six normal dogs (American College of Veterinary Internal Medicine Stage A), six dogs with MMVD mild to moderate cardiac enlargement (ACVIM Stage B1/B2) and six dogs with MMVD and congestive heart failure (ACVIM Stage C/D). Eleven miRNAs were differentially expressed (False Discovery Rate < 0.05). Dogs in Stage B1/B2 or C/D had four upregulated miRNAs, including three cfa-let-7/cfa-miR-98 family members, while seven others were downregulated, compared to Stage A. Expression of six of the 11 miRNAs also were significantly different between dogs in Stage C/D and those in Stage B1/B2. The expression changes were greater as disease severity increased. These miRNAs may be candidates for novel biomarkers and may provide insights into genetic regulatory pathways in canine MMVD
microRNA, dog, congestive heart failure, biomarker, myxomatous mitral valve disease, RT-qPCR
Expression Profiling of Circulating MicroRNAs in Canine Myxomatous Mitral Valve Disease
Qinghong Li,1,* Lisa M. Freeman,2 John E. Rush,2 and Dorothy P. Laflamme1
Mutations in the SMARCA4/BRG1 gene resulting in complete loss of its protein (BRG1) occur frequently in non-small cell lung cancer (NSCLC) cells. Currently, no single therapeutic agent has been identified as synthetically lethal with SMARCA4/BRG1 loss. We identify AURKA activity as essential in NSCLC cells lacking SMARCA4/BRG1. In these cells, RNAi-mediated depletion or chemical inhibition of AURKA induces apoptosis and cell death in vitro and in xenograft mouse models. Disc large homologue-associated protein 5 (HURP/DLGAP5), required for AURKA-dependent, centrosome-independent mitotic spindle assembly is essential for the survival and proliferation of SMARCA4/BRG1 mutant but not of SMARCA4/BRG1 wild-type cells. AURKA inhibitors may provide a therapeutic strategy for biomarker-driven clinical studies to treat the NSCLCs harbouring SMARCA4/BRG1-inactivating mutations.
SMARCA4-inactivating mutations increase sensitivity to Aurora kinase A inhibitor VX-680 in non-small cell lung cancers
Vural Tagal,1 Shuguang Wei,1 Wei Zhang,2,3 Rolf A. Brekken,3,4,5 Bruce A. Posner,1,5 Michael Peyton,3 Luc Girard,3,4 TaeHyun Hwang,6 David A. Wheeler,7 John D. Minna,3,4,5,8 Michael A. White,5,9 Adi F. Gazdar,2,3,5 and Michael G. Rotha,1,5
Inherited metabolic disorders (IMDs) in neonates are a diagnostic and therapeutic challenge for the neonatologist, with the priority being to rapidly flag the treatable diseases. The objective of this study was to evaluate the contribution of targeted metabolic testing for diagnosing suspected IMDs on the basis of suggestive clinical setting or family history in neonates. We conducted an observational study over five years, from January 1st, 2010 to December 31, 2014 in the neonatal intensive care unit (NICU) at Robert Debre University Hospital, Paris, France. We assessed the number of neonates for whom a metabolic testing was performed, the indication for each metabolic test and the diagnostic yield of this selected metabolic workup for diagnosing an IMD. Metabolic testing comprised at least one of the following testings: plasma, urine or cerebrospinal fluid amino acids, urine organic acids, plasma acylcarnitine profile, and urine mucopolysaccharides and oligosaccharides. 11,301 neonates were admitted at the neonatal ICU during the study period. One hundred and ninety six neonates underwent metabolic testing. Eleven cases of IMDs were diagnosed. This diagnostic approach allowed the diagnosis, treatment and survival of 4 neonates (maple syrup urine disease, propionic acidemia, carnitine-acylcarnitine translocase deficiency and type 1 tyrosinemia). In total, metabolic testing was performed for 1.7% of the total number of neonates admitted in the NICU over the study period. These included 23% finally unaffected neonates with transient abnormalities, 5.6% neonates suffering from an identified IMD, 45.4% neonates suffering from a non-metabolic identified disease and 26% neonates with chronic abnormalities but for whom no final causal diagnosis could be made. In conclusion, as expected, such a metabolic targeted workup allowed the diagnosis of classical neonatal onset IMDs in symptomatic newborns. However, this workup remained normal or unspecific for 94.4% of the tested patients. It allowed excluding an IMD in 68.4% of the tested neonates. In spite of the high rate of normal results, such a strategy seems acceptable due to the severity of the symptoms and the need for immediate treatment when available in neonatal IMDs. However, its cost-effectiveness remains low especially in a clinically targeted population in a country where newborn screening is still unavailable for IMDs except for phenylketonuria in 2019.
Subject terms: Metabolic disorders, Paediatric research
Diagnostic contribution of metabolic workup for neonatal inherited metabolic disorders in the absence of expanded newborn screening
Alexandra Bower,1,2 Apolline Imbard,3,4 Jean-Francois Benoist,3,4 Samia Pichard,2 Odile Rigal,3 Olivier Baud,1,5 and Manuel Schiffcorresponding author2,5