Institution
Montreal Children's Hospital
Healthcare•Montreal, Quebec, Canada•
About: Montreal Children's Hospital is a healthcare organization based out in Montreal, Quebec, Canada. It is known for research contribution in the topics: Population & Poison control. The organization has 3842 authors who have published 4816 publications receiving 200198 citations.
Topics: Population, Poison control, Gene, Medicine, Kidney
Papers published on a yearly basis
Papers
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TL;DR: Lineweaver-Burk plots of data from saturable transport phenomena often yield a line of two linear segments, and it is possible to resolve the original plot into plots for each mechanism and to determine the V max and the Michaelis constant for each mechanisms.
104 citations
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TL;DR: A new classification of PA-VSD is proposed based on the characterization of the pulmonary circulation and efforts were made to include all relevant nomenclature categories using synonyms where appropriate.
103 citations
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TL;DR: It is postulate that haploinsufficiency of this riboflavin transporter causes mild rib oflavin deficiency, and when coupled with nutritional riboflavin deficiency in pregnancy, resulted in the transient ribOflavin‐responsive disease seen in her newborn infant.
Abstract: Riboflavin, or vitamin B2, is a precursor to flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN) molecules, required in biological oxidation-reduction reactions. We previously reported a case of a newborn female who had clinical and biochemical features of multiple acyl-CoA dehydrogenation deficiency (MADD), which was corrected by riboflavin supplementation. The mother was then found to be persistently riboflavin deficient, suggesting that a possible genetic defect in riboflavin transport in the mother was the cause of the transient MADD seen in the infant. Two recently-identified riboflavin transporters G protein-coupled receptor 172B (GPR172B or RFT1) and riboflavin transporter 2 (C20orf54 or RFT2) were screened for mutations. Two missense sequence variations, c.209A>G [p.Q70R] and c.886G>A [p.V296M] were found in GPR172B. In vitro functional studies of both missense variations showed that riboflavin transport was unaffected by these variations. Quantitative real-time PCR revealed a de novo deletion in GPR172B spanning exons 2 and 3 in one allele from the mother. We postulate that haploinsufficiency of this riboflavin transporter causes mild riboflavin deficiency, and when coupled with nutritional riboflavin deficiency in pregnancy, resulted in the transient riboflavin-responsive disease seen in her newborn infant. This is the first report of a genetic defect in riboflavin transport in humans.
103 citations
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TL;DR: This study provides no evidence that common MTR and MTRR mutations are associated with alterations in plasma homocysteine, and investigates subjects from two of the NHLBI Family Heart Study field centers.
103 citations
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TL;DR: Understanding CTC biology and host–tumor ‘complementarities’ will help define metastasis-related biomarkers providing formidable and tailored novel therapeutic targets.
Abstract: Disseminated malignancy is responsible for the vast majority of cancer-related deaths. During this process, circulating tumor cells (CTC) are generated, spread from the primary tumor, colonize distant organs and lead to overt metastatic disease. CTC are essential for establishing metastasis; however, they are not sufficient as this process is highly inefficient and most will fail to grow in target sites. Several CTC die during migration while others remain dormant for several years and very few grow into macrometastases. CTC have been well documented in the bloodstream of cancer patients; however, the clinical relevance of this detection is still the subject of controversies and their biology is poorly understood. Indeed, available markers fail to distinguish between subgroups of CTC, and several current methods lack sensitivity, specificity or reproducibility in CTC characterization and detection. The advent of more precise technologies is renewing the interest in CTC biology. We will review herein recent findings on CTC biology, on the role of host-tumor interactions in CTC shedding and implantation, available methods of CTC detection and future perspectives for the molecular characterization of the CTC subset(s) responsible for the development of metastasis. Ultimately, understanding CTC biology and host-tumor 'complementarities' will help define metastasis-related biomarkers providing formidable and tailored novel therapeutic targets.
103 citations
Authors
Showing all 3844 results
Name | H-index | Papers | Citations |
---|---|---|---|
Paul M. Matthews | 140 | 617 | 88802 |
Joost J. Oppenheim | 130 | 454 | 59601 |
Michael Camilleri | 125 | 1084 | 58867 |
James M. Swanson | 117 | 415 | 47131 |
Rhian M. Touyz | 114 | 620 | 43738 |
Ian Roberts | 112 | 714 | 51933 |
William D. Foulkes | 108 | 682 | 45013 |
Stephen P. Hinshaw | 106 | 330 | 37336 |
Michael S. Kramer | 104 | 568 | 43803 |
Liam Smeeth | 104 | 753 | 53433 |
Eric Fombonne | 100 | 336 | 44447 |
Douglas L. Arnold | 100 | 624 | 37040 |
Erwin W. Gelfand | 99 | 675 | 36059 |
Frederick Andermann | 90 | 365 | 25638 |
Robert W. Platt | 88 | 638 | 31918 |