The Experts below are selected from a list of 1842 Experts worldwide ranked by ideXlab platform
Yu Ju Ding - One of the best experts on this subject based on the ideXlab platform.
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Evaluation of the teratogenic effects of three traditional Chinese medicines, Si Jun Zi Tang, Liu Jun Zi Tang and Shenling Baizhu San, during zebrafish pronephros development
'Japanese Society of Toxicologic Pathology', 2016Co-Authors: Yu Ju DingAbstract:[[abstract]]The aim of this study was to evaluate the teratogenic effects of three common Chinese medical prescriptions, Si Jun Zi Tang (SJZT), Liu Jun Zi Tang (LJZT) and Shenling Baizhu San (SLBS), during zebrafish pronephros development. We used the transgenic zebrafish line Tg(wt1b:EGFP) to assess the teratogenic effects using 12 different protocols, which comprised combinations of 4 doses (0, 25, 250, 1,250 ng/mL) and 3 exposure methods [methods I, 12–36 hours post fertilization (hpf), II, 24–48 hpf, and III, 24–36 hpf]. As a result, few defects in the Kidneys were observed in the embryos exposed to 25 ng/mL of each medical prescription. The percentage of Kidney Malformation phenotypes increased as the exposure concentrations increased (25 ng/mL, 0–10%; 250 ng/mL, 0–60%; 1,250 ng/mL, 80–100%). Immunohistochemistry for α6F, which is a basolateral and renal tubular differentiation marker, revealed no obvious defective phenotypes in either SJZT- or LJZT-treated embryos, indicating that these Chinese medical prescriptions had minimal adverse effects on the pronephric duct. However, SLBS-treated embryos displayed a defective phenotype in the pronephric duct. According to these findings, we suggest (1) that the Chinese medical prescriptions induced Kidney Malformation phenotypes that are dose dependent and (2) that the embryonic zebrafish Kidney was more sensitive to SLBS than SJZT and LJZT.[[notice]]補正完
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Evaluation of the teratogenic effects of three traditional Chinese medicines, Si Jun Zi Tang, Liu Jun Zi Tang and Shenling Baizhu San, during zebrafish pronephros development
Journal of Toxicologic Pathology, 2015Co-Authors: Yu Ju Ding, Ling-ling Yang, Bo-cheng Wang, Yau-hung ChenAbstract:: The aim of this study was to evaluate the teratogenic effects of three common Chinese medical prescriptions, Si Jun Zi Tang (SJZT), Liu Jun Zi Tang (LJZT) and Shenling Baizhu San (SLBS), during zebrafish pronephros development. We used the transgenic zebrafish line Tg(wt1b:EGFP) to assess the teratogenic effects using 12 different protocols, which comprised combinations of 4 doses (0, 25, 250, 1,250 ng/mL) and 3 exposure methods [methods I, 12-36 hours post fertilization (hpf), II, 24-48 hpf, and III, 24-36 hpf]. As a result, few defects in the Kidneys were observed in the embryos exposed to 25 ng/mL of each medical prescription. The percentage of Kidney Malformation phenotypes increased as the exposure concentrations increased (25 ng/mL, 0-10%; 250 ng/mL, 0-60%; 1,250 ng/mL, 80-100%). Immunohistochemistry for α6F, which is a basolateral and renal tubular differentiation marker, revealed no obvious defective phenotypes in either SJZT- or LJZT-treated embryos, indicating that these Chinese medical prescriptions had minimal adverse effects on the pronephric duct. However, SLBS-treated embryos displayed a defective phenotype in the pronephric duct. According to these findings, we suggest (1) that the Chinese medical prescriptions induced Kidney Malformation phenotypes that are dose dependent and (2) that the embryonic zebrafish Kidney was more sensitive to SLBS than SJZT and LJZT.
Yau-hung Chen - One of the best experts on this subject based on the ideXlab platform.
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Original Article Evaluation of the teratogenic effects of three traditional Chinese
2016Co-Authors: Si Jun, Ling-ling Yang, Zi Tang, Liu Jun, Shenling Baizhu, Fei-peng Lee, Yau-hung ChenAbstract:Abstract: The aim of this study was to evaluate the teratogenic effects of three common Chinese medical prescriptions, Si Jun Zi Tang (SJZT), Liu Jun Zi Tang (LJZT) and Shenling Baizhu San (SLBS), during zebrafish pronephros development. We used the transgenic zebrafish line Tg(wt1b:EGFP) to assess the teratogenic effects using 12 different protocols, which comprised combinations of 4 doses (0, 25, 250, 1,250 ng/mL) and 3 exposure methods [methods I, 12–36 hours post fertilization (hpf), II, 24–48 hpf, and III, 24–36 hpf]. As a result, few defects in the Kidneys were observed in the embryos exposed to 25 ng/mL of each medical prescription. The percentage of Kidney Malformation phenotypes increased as the exposure concentrations increased (25 ng/mL, 0–10%; 250 ng/mL, 0–60%; 1,250 ng/mL, 80–100%). Immunohistochemistry for α6F, which is a basolateral and renal tubular differentiation marker, revealed no obvi-ous defective phenotypes in either SJZT- or LJZT-treated embryos, indicating that these Chinese medical prescriptions had minima
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Evaluation of the teratogenic effects of three traditional Chinese medicines, Si Jun Zi Tang, Liu Jun Zi Tang and Shenling Baizhu San, during zebrafish pronephros development
Journal of Toxicologic Pathology, 2015Co-Authors: Yu Ju Ding, Ling-ling Yang, Bo-cheng Wang, Yau-hung ChenAbstract:: The aim of this study was to evaluate the teratogenic effects of three common Chinese medical prescriptions, Si Jun Zi Tang (SJZT), Liu Jun Zi Tang (LJZT) and Shenling Baizhu San (SLBS), during zebrafish pronephros development. We used the transgenic zebrafish line Tg(wt1b:EGFP) to assess the teratogenic effects using 12 different protocols, which comprised combinations of 4 doses (0, 25, 250, 1,250 ng/mL) and 3 exposure methods [methods I, 12-36 hours post fertilization (hpf), II, 24-48 hpf, and III, 24-36 hpf]. As a result, few defects in the Kidneys were observed in the embryos exposed to 25 ng/mL of each medical prescription. The percentage of Kidney Malformation phenotypes increased as the exposure concentrations increased (25 ng/mL, 0-10%; 250 ng/mL, 0-60%; 1,250 ng/mL, 80-100%). Immunohistochemistry for α6F, which is a basolateral and renal tubular differentiation marker, revealed no obvious defective phenotypes in either SJZT- or LJZT-treated embryos, indicating that these Chinese medical prescriptions had minimal adverse effects on the pronephric duct. However, SLBS-treated embryos displayed a defective phenotype in the pronephric duct. According to these findings, we suggest (1) that the Chinese medical prescriptions induced Kidney Malformation phenotypes that are dose dependent and (2) that the embryonic zebrafish Kidney was more sensitive to SLBS than SJZT and LJZT.
Norman D Rosenblum - One of the best experts on this subject based on the ideXlab platform.
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Kidney patterning genes disrupts renal morphogenesis
2014Co-Authors: Sita Bhella, Chichung Hui, Christopher W Wilson, Paotien Chuang, Norman D RosenblumAbstract:Truncating mutations in Gli3, an intracellular effector in the SHH-SMO-GLI signaling pathway, cause renal aplasia/dysplasia in humans and mice. Yet, the pathogenic mechanisms are undefined. Here, we report the effect of decreased SHH-SMO signaling on renal morphogenesis, the expression of SHH target genes and GLI binding to Shh target genes. Shh deficiency or cyclopaminemediated SMO inhibition disrupted renal organogenesis, decreased expression of GLI1 and GLI2 proteins, but increased expression of GLI3 repressor relative to GLI3 activator. Shh deficiency decreased expression of Kidney patterning genes (Pax2 and Sall1) and cell cycle regulators (cyclin D1 and MYCN). Elimination of Gli3 in Shh –/ – mice rescued Kidney Malformation and restored expression of Pax2, Sall1, cyclin D1, MYCN, Gli1 and Gli2. To define mechanisms by which SHH-SMO signaling controls gene expression, we determined the binding of GLI proteins to 5 � flanking regions containing GLI consensus binding sequences in Shh target genes using chromatin immunoprecipitation. In normal embryonic Kidney tissue, GLI1 and/or GLI2 were bound to each target gene. By contrast, treatment of embryonic Kidney explants with cyclopamine decreased GLI1 and/or GLI2 binding, and induced binding of GLI3. However, cyclopamine failed to decrease Gli1 and Gli2 expression and branching morphogenesis in Gli3-deficient embryonic Kidney tissue. Together, these results demonstrate that SHH-SMO signaling controls renal morphogenesis via transcriptional control of Gli, renal patterning and cell cycle regulator genes in a manner that is opposed by GLI3. KEY WORDS: Kidney development, Sonic Hedgehog, GLI
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gli3 dependent transcriptional repression of gli1 gli2 and Kidney patterning genes disrupts renal morphogenesis
Development, 2006Co-Authors: Sita Bhella, Chichung Hui, Christopher W Wilson, Paotien Chuang, Norman D RosenblumAbstract:Truncating mutations in Gli3 , an intracellular effector in the SHH-SMO-GLI signaling pathway, cause renal aplasia/dysplasia in humans and mice. Yet, the pathogenic mechanisms are undefined. Here, we report the effect of decreased SHH-SMO signaling on renal morphogenesis, the expression of SHH target genes and GLI binding to Shh target genes. Shh deficiency or cyclopamine-mediated SMO inhibition disrupted renal organogenesis, decreased expression of GLI1 and GLI2 proteins, but increased expression of GLI3 repressor relative to GLI3 activator. Shh deficiency decreased expression of Kidney patterning genes ( Pax2 and Sall1 ) and cell cycle regulators (cyclin D1 and MYCN). Elimination of Gli3 in Shh–/– mice rescued Kidney Malformation and restored expression of Pax2, Sall1 , cyclin D1, MYCN, Gli1 and Gli2 . To define mechanisms by which SHH-SMO signaling controls gene expression, we determined the binding of GLI proteins to 5′ flanking regions containing GLI consensus binding sequences in Shh target genes using chromatin immunoprecipitation. In normal embryonic Kidney tissue, GLI1 and/or GLI2 were bound to each target gene. By contrast, treatment of embryonic Kidney explants with cyclopamine decreased GLI1 and/or GLI2 binding, and induced binding of GLI3. However, cyclopamine failed to decrease Gli1 and Gli2 expression and branching morphogenesis in Gli3 -deficient embryonic Kidney tissue. Together, these results demonstrate that SHH-SMO signaling controls renal morphogenesis via transcriptional control of Gli , renal patterning and cell cycle regulator genes in a manner that is opposed by GLI3.
Renata Lorini - One of the best experts on this subject based on the ideXlab platform.
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Collectrin gene screening in Turner syndrome patients with Kidney Malformation
Journal of Genetics, 2009Co-Authors: L. Pasquali, Giuseppe D'annunzio, Roberto Gastaldi, E. Di Battista, Valeria Calcaterra, Daniela Larizza, Renata Lorini, Elena D’amatoAbstract:Turner syndrome (TS) affects one in 2500–3000 live-born girls, and is the most prevalent female sex chromosomal disorder in humans, resulting from the loss of all or part of one of the two X chromosomes (Sybert and McCauley 2004). About 50% of TS patients carry a 45, X monosomy, the rest being mosaics or structural chromosome abnormalities. TS patients’ phenotype is variable, and the wide spectrum of clinical features includes: short stature, ovarian dysgenesis, lymphedema, cardiovascular defects and renal Malformation. Diabetes mellitus is also present at a rate two to four times higher than in the general population (Elsheikh et al. 2002), consistent with the finding of a relative insulin deficiency in TS on a non-immune basis, suggesting that haploinsufficiency for X-chromosome gene(s) impairs beta-cell function predisposing to diabetes mellitus in TS (Bakalov et al. 2004). The loss of the short arm of chromosome X (Xp), common to all TS, generally results in the full syndrome phenotype (Elsheikh et al. 2002). So far, a correlation between karyotype and phenotype in TS patients has not been clearly defined. Haploinsufficiency of several genes mapped to the short arm of X chromosome has been related to the clinical signs observed in TS patients; for example, the SHOX (short stature homeobox-containing gene) responsible for the short stature characteristic of the patients. Association of renal abnormalities and TS varies from 33% to 70% (Matthies et al. 1971). These include horseshoe Kidney, duplication of collecting system, ectopic Kidney, ureteropelvic stenosis, renal agenesis and renal cysts. Two forms of cystic Kidney disease have been described in
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horseshoe Kidney Malformation in turner syndrome is not associated with hnf 1β gene mutations
Pediatric Nephrology, 2008Co-Authors: Elena Damato, Valeria Calcaterra, Daniela Larizza, Giuseppe Dannunzio, Vera Morsellino, Renata LoriniAbstract:Mutations in hepatocyte nuclear factor-1β (HNF-1β) gene cause a subtype of maturity-onset diabetes of the young (MODY5), whose clinical features are pancreatic β-cell dysfunction, renal Malformations, and in some females, internal genital Malformations. Recently, we reported the first case of MODY5 and horseshoe Kidney. The patient was the only male in a three-generation family with five affected females carrying renal cysts or dysplastic Kidney. Diabetes mellitus, horseshoe Kidney, and X chromosome monosomy or mosaicism can be observed in Turner syndrome (TS). In particular, diabetes mellitus affects about 50% and horseshoe Kidney occurs in approximately 16% of patients. To investigate whether mutations/polymorphisms of HNF-1β and X monosomy influence horseshoe Kidney development, we evaluated HNF-1β gene sequence in 13 patients with TS and several Kidney abnormalities. Analysis of the nine exons including intron–exon boundaries of HNF-1β revealed the presence in two subjects (15%) of a known intronic polymorphism, IV8+48insC. No specific variants were found. We conclude there is no direct relationship between horseshoe Kidney in TS and mutation or polymorphism of HNF-1β gene, but we speculate that target gene(s) of HNF-1β, likely mapped on the X chromosome, is/are responsible of the horseshoe Kidney formation in TS.
Ling-ling Yang - One of the best experts on this subject based on the ideXlab platform.
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Original Article Evaluation of the teratogenic effects of three traditional Chinese
2016Co-Authors: Si Jun, Ling-ling Yang, Zi Tang, Liu Jun, Shenling Baizhu, Fei-peng Lee, Yau-hung ChenAbstract:Abstract: The aim of this study was to evaluate the teratogenic effects of three common Chinese medical prescriptions, Si Jun Zi Tang (SJZT), Liu Jun Zi Tang (LJZT) and Shenling Baizhu San (SLBS), during zebrafish pronephros development. We used the transgenic zebrafish line Tg(wt1b:EGFP) to assess the teratogenic effects using 12 different protocols, which comprised combinations of 4 doses (0, 25, 250, 1,250 ng/mL) and 3 exposure methods [methods I, 12–36 hours post fertilization (hpf), II, 24–48 hpf, and III, 24–36 hpf]. As a result, few defects in the Kidneys were observed in the embryos exposed to 25 ng/mL of each medical prescription. The percentage of Kidney Malformation phenotypes increased as the exposure concentrations increased (25 ng/mL, 0–10%; 250 ng/mL, 0–60%; 1,250 ng/mL, 80–100%). Immunohistochemistry for α6F, which is a basolateral and renal tubular differentiation marker, revealed no obvi-ous defective phenotypes in either SJZT- or LJZT-treated embryos, indicating that these Chinese medical prescriptions had minima
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Evaluation of the teratogenic effects of three traditional Chinese medicines, Si Jun Zi Tang, Liu Jun Zi Tang and Shenling Baizhu San, during zebrafish pronephros development
Journal of Toxicologic Pathology, 2015Co-Authors: Yu Ju Ding, Ling-ling Yang, Bo-cheng Wang, Yau-hung ChenAbstract:: The aim of this study was to evaluate the teratogenic effects of three common Chinese medical prescriptions, Si Jun Zi Tang (SJZT), Liu Jun Zi Tang (LJZT) and Shenling Baizhu San (SLBS), during zebrafish pronephros development. We used the transgenic zebrafish line Tg(wt1b:EGFP) to assess the teratogenic effects using 12 different protocols, which comprised combinations of 4 doses (0, 25, 250, 1,250 ng/mL) and 3 exposure methods [methods I, 12-36 hours post fertilization (hpf), II, 24-48 hpf, and III, 24-36 hpf]. As a result, few defects in the Kidneys were observed in the embryos exposed to 25 ng/mL of each medical prescription. The percentage of Kidney Malformation phenotypes increased as the exposure concentrations increased (25 ng/mL, 0-10%; 250 ng/mL, 0-60%; 1,250 ng/mL, 80-100%). Immunohistochemistry for α6F, which is a basolateral and renal tubular differentiation marker, revealed no obvious defective phenotypes in either SJZT- or LJZT-treated embryos, indicating that these Chinese medical prescriptions had minimal adverse effects on the pronephric duct. However, SLBS-treated embryos displayed a defective phenotype in the pronephric duct. According to these findings, we suggest (1) that the Chinese medical prescriptions induced Kidney Malformation phenotypes that are dose dependent and (2) that the embryonic zebrafish Kidney was more sensitive to SLBS than SJZT and LJZT.
