The Experts below are selected from a list of 1011 Experts worldwide ranked by ideXlab platform
Jiayin Dai - One of the best experts on this subject based on the ideXlab platform.
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perfluoropolyether carboxylic acids novel alternatives to pfoa impair zebrafish posterior swim Bladder development via thyroid hormone disruption
Environment International, 2020Co-Authors: Jinxing Wang, Guohui Shi, Jingzhi Yao, Nan Sheng, Ruina Cui, Yong Guo, Jiayin DaiAbstract:Abstract Perfluoropolyether carboxylic acids (PFECAs, CF3(OCF2)nCOO−, n = 2–5) are novel alternatives to perfluorooctanoic acid (PFOA) and are widely used in industrial production. However, although they have been detected in surface water and human blood, their toxicities on aquatic organisms remain unknown. We used zebrafish embryos to compare the developmental toxicities of various PFECAs (e.g., perfluoro (3,5,7-trioxaoctanoic) acid (PFO3OA), perfluoro (3,5,7,9-tetraoxadecanoic) acid (PFO4DA), and perfluoro (3,5,7,9,11-pentaoxadodecanoic) acid (PFO5DoDA)) with that of PFOA and to further reveal the key events related to toxicity caused by these chemicals. Results showed that, based on half maximal effective concentrations (EC50), toxicity increased in the order: PFO5DoDA > PFO4DA > PFOA > PFO3OA, with uninflated posterior swim Bladders the most frequently observed Malformation. Similar to PFOA, PFECA exposure significantly lowered thyroid hormone (TH) levels (e.g., T3 (3,5,3′-L-triiodothyronine) and T4 (L-thyroxine)) in the whole body of larvae at 5 d post-fertilization following disrupted TH metabolism. In addition, the transcription of UDP glucuronosyltransferase 1 family a, b (ugt1ab), a gene related to TH metabolism, increased dose-dependently. Exogeneous T3 or T4 supplementation partly rescued PFECA-induced posterior swim Bladder Malformation. Our results further suggested that PFECAs primarily damaged the swim Bladder mesothelium during early development. This study is the first to report on novel emerging PFECAs as thyroid disruptors causing swim Bladder Malformation. Furthermore, given that PFECA toxicity increased with backbone OCF2 moieties, they may not be safer alternatives to PFOA.
Janine Altmuller - One of the best experts on this subject based on the ideXlab platform.
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muscarinic acetylcholine receptor m3 mutation causes urinary Bladder disease and a prune belly like syndrome
American Journal of Human Genetics, 2011Co-Authors: Stefanie Weber, Holger Thiele, Sevgi Mir, Mohammad R Toliat, Betul Sozeri, Heiko Reutter, Markus Draaken, Michael Ludwig, Janine AltmullerAbstract:Urinary Bladder Malformations associated with Bladder outlet obstruction are a frequent cause of progressive renal failure in children. We here describe a muscarinic acetylcholine receptor M3 (CHRM3) (1q41-q44) homozygous frameshift mutation in familial congenital Bladder Malformation associated with a prune-belly-like syndrome, defining an isolated gene defect underlying this sometimes devastating disease. CHRM3 encodes the M3 muscarinic acetylcholine receptor, which we show is present in developing renal epithelia and Bladder muscle. These observations may imply that M3 has a role beyond its known contribution to detrusor contractions. This Mendelian disease caused by a muscarinic acetylcholine receptor mutation strikingly phenocopies Chrm3 null mutant mice.
Heiko Reutter - One of the best experts on this subject based on the ideXlab platform.
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muscarinic acetylcholine receptor m3 mutation causes urinary Bladder disease and a prune belly like syndrome
American Journal of Human Genetics, 2011Co-Authors: Stefanie Weber, Holger Thiele, Sevgi Mir, Mohammad R Toliat, Betul Sozeri, Heiko Reutter, Markus Draaken, Michael Ludwig, Janine AltmullerAbstract:Urinary Bladder Malformations associated with Bladder outlet obstruction are a frequent cause of progressive renal failure in children. We here describe a muscarinic acetylcholine receptor M3 (CHRM3) (1q41-q44) homozygous frameshift mutation in familial congenital Bladder Malformation associated with a prune-belly-like syndrome, defining an isolated gene defect underlying this sometimes devastating disease. CHRM3 encodes the M3 muscarinic acetylcholine receptor, which we show is present in developing renal epithelia and Bladder muscle. These observations may imply that M3 has a role beyond its known contribution to detrusor contractions. This Mendelian disease caused by a muscarinic acetylcholine receptor mutation strikingly phenocopies Chrm3 null mutant mice.
Jinxing Wang - One of the best experts on this subject based on the ideXlab platform.
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perfluoropolyether carboxylic acids novel alternatives to pfoa impair zebrafish posterior swim Bladder development via thyroid hormone disruption
Environment International, 2020Co-Authors: Jinxing Wang, Guohui Shi, Jingzhi Yao, Nan Sheng, Ruina Cui, Yong Guo, Jiayin DaiAbstract:Abstract Perfluoropolyether carboxylic acids (PFECAs, CF3(OCF2)nCOO−, n = 2–5) are novel alternatives to perfluorooctanoic acid (PFOA) and are widely used in industrial production. However, although they have been detected in surface water and human blood, their toxicities on aquatic organisms remain unknown. We used zebrafish embryos to compare the developmental toxicities of various PFECAs (e.g., perfluoro (3,5,7-trioxaoctanoic) acid (PFO3OA), perfluoro (3,5,7,9-tetraoxadecanoic) acid (PFO4DA), and perfluoro (3,5,7,9,11-pentaoxadodecanoic) acid (PFO5DoDA)) with that of PFOA and to further reveal the key events related to toxicity caused by these chemicals. Results showed that, based on half maximal effective concentrations (EC50), toxicity increased in the order: PFO5DoDA > PFO4DA > PFOA > PFO3OA, with uninflated posterior swim Bladders the most frequently observed Malformation. Similar to PFOA, PFECA exposure significantly lowered thyroid hormone (TH) levels (e.g., T3 (3,5,3′-L-triiodothyronine) and T4 (L-thyroxine)) in the whole body of larvae at 5 d post-fertilization following disrupted TH metabolism. In addition, the transcription of UDP glucuronosyltransferase 1 family a, b (ugt1ab), a gene related to TH metabolism, increased dose-dependently. Exogeneous T3 or T4 supplementation partly rescued PFECA-induced posterior swim Bladder Malformation. Our results further suggested that PFECAs primarily damaged the swim Bladder mesothelium during early development. This study is the first to report on novel emerging PFECAs as thyroid disruptors causing swim Bladder Malformation. Furthermore, given that PFECA toxicity increased with backbone OCF2 moieties, they may not be safer alternatives to PFOA.
Stefanie Weber - One of the best experts on this subject based on the ideXlab platform.
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muscarinic acetylcholine receptor m3 mutation causes urinary Bladder disease and a prune belly like syndrome
American Journal of Human Genetics, 2011Co-Authors: Stefanie Weber, Holger Thiele, Sevgi Mir, Mohammad R Toliat, Betul Sozeri, Heiko Reutter, Markus Draaken, Michael Ludwig, Janine AltmullerAbstract:Urinary Bladder Malformations associated with Bladder outlet obstruction are a frequent cause of progressive renal failure in children. We here describe a muscarinic acetylcholine receptor M3 (CHRM3) (1q41-q44) homozygous frameshift mutation in familial congenital Bladder Malformation associated with a prune-belly-like syndrome, defining an isolated gene defect underlying this sometimes devastating disease. CHRM3 encodes the M3 muscarinic acetylcholine receptor, which we show is present in developing renal epithelia and Bladder muscle. These observations may imply that M3 has a role beyond its known contribution to detrusor contractions. This Mendelian disease caused by a muscarinic acetylcholine receptor mutation strikingly phenocopies Chrm3 null mutant mice.