107 research outputs found
Is fetal gender associated with adverse perinatal outcome in intrauterine growth restriction (IUGR)?
OBJECTIVE: The purpose of this study was to determine if there is a difference in perinatal outcome by gender among growth-restricted fetuses.
STUDY DESIGN: This was a retrospective cohort study of intrauterine growth restriction (IUGR) singleton pregnancies over a 5-year period. Clinical outcomes compared by gender included preterm delivery, perinatal mortality (PNM), respiratory distress syndrome (RDS), grade 3 or 4 intraventricular hemorrhage (IVH), necrotizing enterocolitis (NEC), and periventricular leukomalacia (PVL). Statistical analysis included bivariate and multivariable techniques.
RESULTS: Seven hundred and twenty-seven singleton pregnancies with IUGR were identified. Three hundred and forty-six (47.6%) were males. Birth weight was similar between the groups. After adjusting for maternal demographics, medical history, gestational age, mode of delivery, and antenatal corticosteroids, adverse perinatal outcomes were similar between the groups. Severity of outcomes was also similar between males and females (P = .66).
CONCLUSION: Male fetuses with IUGR have similar outcomes when compared with female IUGR fetuses. Gender does not play a role in perinatal outcome in the setting of fetal growth restriction
A Pilot Study Assessing the Value of an âEducational Hospitalistâ in an OBGYN Residency Program
The emergence of new psychoactive substance (NPS) benzodiazepines: a review
The market for new psychoactive substances has increased markedly in recent years and there is now a steady stream of compounds appearing every year. Benzodiazepines consist of only a fraction of the total number of these compounds but their use and misuse has rapidly increased. Some of these benzodiazepines have only been patented, some of them have not been previously synthesised and the majority have never undergone clinical trials or tests. Despite their structural and chemical similarity, large differences exist between the benzodiazepines in their pharmacokinetic parameters and metabolic pathways and so they are not easily comparable. As benzodiazepines have been clinically used since the 1960s many analytical methods exist to quantify them in a variety of biological matrices and it is expected that these methods would also be suitable for the detection of benzodiazepines that are new psychoactive substances. Illicitly obtained benzodiazepines have been found to contain a wide range of compounds such as opiates which presents a problem since the use of them in conjunction with each other can lead to respiratory depression and death. The aim of this review is to collate the available information on these benzodiazepines and to provide a starting point for the further investigation of their pharmacokinetics which is clearly required
Le complexe de remodelage de la chromatine CHD4/NuRD associe rĂ©gulation Ă©pigĂ©nĂ©tique, flux glycolytique et prolifĂ©ration dans les cellules de mĂ©lanome et dâautres cancers
The Nucleosome Remodelling and Deacetylation (NuRD) complex is an epigenetic regulator of gene expression that includes two mutually exclusive ATPase subunits CHD3 and CHD4. Our results show that NuRD associates with essential melanoma cell transcription factors namely MITF and SOX10. However, despite their physical association and genomic co-localization, CHD4-NuRD does not appear to act as a cofactor for MITF or SOX10 regulated gene expression. Nevertheless, CHD4 silencing leads to a slow growth phenotype and de-represses the expression of PADI1 (Protein Arginine DeIminase 1) and PADI3, two enzymes involved in converting arginines to citrullines in melanoma and multiple types of cancer cells. Increased expression of PADI1 and PADI3 enhances citrullination of arginines within the key glycolytic regulatory enzyme PKM2 then promoting excessive glycolysis, lowering ATP levels and slowing down proliferation. PKM2 citrullination lowers its sensitivity to allosteric inhibitors thus shifting equilibrium towards allosteric activators thereby bypassing the normal physiological regulation of glycolysis. Overall, our results lead to describe a novel pathway linking, epigenetic regulation of PADI1 and PADI3 expression by CHD4/NuRD and reprogramming of PKM2 allosteric regulation through arginines citrullination, to glycolytic flux and cancer cell proliferation.Le complexe de remodelage de la chromatine NuRD, composĂ© des sous-unitĂ©s catalytiques CHD3 et CHD4, est un rĂ©gulateur Ă©pigĂ©nĂ©tique de lâexpression gĂ©nique. Nos rĂ©sultats montrent que NuRD sâassocie avec les facteurs de transcription essentiels du mĂ©lanome que sont MITF et SOX10. Cependant, malgrĂ© une association physique et une co-localisation gĂ©nomique, CHD4/NuRD ne semble pas agir comme un cofacteur important pour MITF ou SOX10. NĂ©anmoins, la rĂ©pression de CHD4 conduit Ă un ralentissement de la prolifĂ©ration et dĂ©rĂ©prime lâexpression des enzymes PADI1 et PADI3 dans les cellules de mĂ©lanome ainsi que dans de nombreux types de cellules cancĂ©reuses. Ainsi, lâinduction de ces enzymes, responsables de la conversion des arginines en citrullines, entraĂźne la citrullination spĂ©cifique de PKM2, une enzyme glycolytique essentielle, diminuant ainsi sa sensibilitĂ© aux inhibiteurs allostĂ©riques, et donc altĂ©rant lâĂ©quilibre physiologique entre activateurs et inhibiteurs de lâenzyme. Lâensemble de ce travail de thĂšse a permis de mettre en Ă©vidence une nouvelle voie reliant, dâune part la rĂ©gulation Ă©pigĂ©nĂ©tique de lâexpression de PADI1 et PADI3 par CHD4/NuRD ainsi que la reprogrammation de la rĂ©gulation allostĂ©rique de PKM2 via la citrullination dâarginines, au flux glycolytique et au contrĂŽle de la prolifĂ©ration des cellules cancĂ©reuses dâautre part
Regulation of glycolysis and cancer cell proliferation by PKM2 citrullination
International audienceConversion of peptidyl-arginine to peptidyl citrulline, known as citrullination, is a posttranslational protein modification catalysed by the PADI (Protein Arginine Deiminase) family of enzymes. PADI1 and PADI3 catalyse citrullination of arginine 106 in the glycolytic enzyme pyruvate kinase M2 modulating its allosteric regulation, glycolysis and cancer cell proliferation
Peptide library purity by mass spectrometry (Coassolo et al., 2023)
The library was produced as crude peptides at a quantity of 1-4mg with a C-terminal amidation as the only modification for comparative studies between peptides. Identity and purity of the peptides used in vivo were verified by LC-MS using an Agilent Q-TOF LCâMS instrument. The raw mass spectrometry (MS1 spectra) data are deposited as Agilent .d file for the six synthesized peptides used in the in vivo screen (BRINP2_peptide 5.d, EDIL3_peptide 5.d, FGF3_peptide 4.d, FGF5_peptide 5.d, FSTL4_peptide 3.d and SCG1_peptide 9.d).THIS DATASET IS ARCHIVED AT DANS/EASY, BUT NOT ACCESSIBLE HERE. TO VIEW A LIST OF FILES AND ACCESS THE FILES IN THIS DATASET CLICK ON THE DOI-LINK ABOV
Sorption studies of dipotassium clorazepate salt (TranxĂšneÂź) and midazolam hydrochloride (HypnovelÂź) in polyvinyl chloride and glass infusion containers
RĂ©gulation Ă©pigĂ©nĂ©tique de lâexpression gĂ©nique dans le mĂ©lanome malin
Le mĂ©lanome malin est un cancer trĂšs agressif capable de gĂ©nĂ©rer des mĂ©tastases Ă des stades prĂ©coces de son dĂ©veloppement. La transformation oncogĂ©nique des mĂ©lanocytes rĂ©sulte principalement de mutations dans BRAF, NRAS ou NF1 qui activent de façon constitutive la voie de signalisation des MAP kinases et la prolifĂ©ration cellulaire. Dâautres mutations inactivant CDKN2A ou PTEN, des mutations activatrices dans la voie bĂ©ta-catĂ©nine ainsi que des altĂ©rations de lâĂ©pigĂ©nome permettent aux cellules dâĂ©chapper Ă la sĂ©nescence induite par les oncogĂšnes. Quelle que soit la nature des mutations activatrices, la physiologie des cellules de mĂ©lanome est rĂ©gulĂ©e par des facteurs de transcription et des mĂ©canismes Ă©pigĂ©nĂ©tiques. MITF (Microphthalmia-associated Transcription Factor) et SOX10 sont deux facteurs de transcription jouant Ă©galement un rĂŽle essentiel dans la physiologie des mĂ©lanocytes normaux. Par une combinaison dâapproches incluant la gĂ©nĂ©tique de la souris, la biochimie et la gĂ©nomique Ă haut dĂ©bit, nous avons identifiĂ© des protĂ©ines partenaires de MITF et analysĂ© les mĂ©canismes de rĂ©gulation de la transcription par MITF, SOX10 et leurs partenaires
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