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Tuft Cells Inhibit Pancreatic Tumorigenesis in Mice by Producing Prostaglandin D.
Gastroenterology
November 2020
Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California. Electronic address:
Background & Aims: Development of pancreatic ductal adenocarcinoma (PDA) involves acinar to ductal metaplasia and genesis of tuft cells. It has been a challenge to study these rare cells because of the lack of animal models. We investigated the role of tuft cells in pancreatic tumorigenesis.
View Article and Find Full Text PDFPre-symptomatic targeted treatment of patent ductus arteriosus in preterm newborns: A systematic review and meta-analysis.
J Neonatal Perinatal Med
September 2019
George & Fay Yee Center for HealthcareInnovation, University of Manitoba/Winnipeg Regional Health Authority, Winnipeg, Manitoba, Canada.
Background: A clinically significant patent ductus arteriosus (PDA) is associated with significant morbidity and mortality in premature newborns. Symptomatic PDAs are often treated with prostaglandin synthesis inhibitors (PSI), but controversy remains if PSIs should also be used to manage early, asymptomatic PDAs.
Objective: To systematically identify, critically appraise, and evaluate the efficacy and safety of pharmacological management of pre-symptomatic PDA in preterm newborns after confirmed patency by echocardiography.
Prediction of Therapeutic Response to Cyclooxygenase Inhibitors in Preterm Infants with Patent Ductus Arteriosus.
Pediatr Cardiol
April 2018
Department of Pediatrics, Peking University First Hospital, Beijing, 100034, China.
Patent ductus arteriosus (PDA) is a morbid condition commonly seen in premature infants. Cyclooxygenase (COX) inhibitors, such as indomethacin and ibuprofen, are often used for the treatment of PDA in preterm infants, and they work by reducing the production of prostaglandin. However, as observed in clinical practice, not all PDAs in preterm infants can be closed using COX inhibitors.
View Article and Find Full Text PDFPatterns of gene expression in the ductus arteriosus are related to environmental and genetic risk factors for persistent ductus patency.
Pediatr Res
October 2010
Pharmaceutical Discovery Division, SRI International, Menlo Park, California 94025, USA.
Three independent risk factors (immature gestation, absence of antenatal glucocorticoid exposure, and presence of the rs2817399(A) allele of the gene TFAP2B) are associated with patent ductus arteriosus (PDAs) that fail to close during prostaglandin inhibition. We hypothesized that these three factors may affect a common set of genes that increase the risk of persistent PDA after birth. We studied baboon ductus from term, preterm, and glucocorticoid-treated preterm fetuses and found that both immature gestation and absence of antenatal glucocorticoid exposure decreased RNA expression of calcium- and potassium-channel genes involved in oxygen-induced constriction, and phosphodiesterase genes (that modulate cAMP/cGMP signaling).
View Article and Find Full Text PDFProphylactic closure of the patent ductus arteriosus has been recommended as a means of decreasing the morbidity of the very low birth weight neonate. This study was undertaken in order to determine potential risk factors involved in the development of the silent ductus, its impact upon both the early cardiorespiratory symptomatology and the subsequent morbidity of the premature neonate, and finally the potential benefit to be derived from prophylactic closure in this presymptomatic stage. Infants with birth weights of 1000 g or less were studied on days 2-3 of life echocardiographically, clinically, and with determination of plasma dilator prostaglandin levels.
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