6 results on '"Tinwell, Helen"'
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2. List of Contributors
- Author
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Abe, Y., primary, Anspaugh, Douglas D., additional, Aoki, Takao, additional, Aponte, Raphael, additional, Arimori, Sadayuki, additional, Armel, Gregory, additional, Banba, Shinichi, additional, Barreteau, Fabien, additional, Barry, James, additional, Bartholomaeus, Anika, additional, Bartlett, Dave, additional, Berthon, Guillaume, additional, Bindschaedler, Pascal, additional, Blythe, Judith, additional, Boussemghoune, Mohamed, additional, Bowerman, Peter, additional, Bravo-Altamirano, Karla, additional, Briddell, Twyla A., additional, Buchan, Zachary, additional, Buchholz, A., additional, Campe, Ruth, additional, Cao, Xiaofeng, additional, Cassayre, Jérôme, additional, Cederbaum, Fredrik, additional, Chang, Kang, additional, Chang, Yaning, additional, Chen, Lai, additional, Chen, Xiulei, additional, Chen, Yuzhong, additional, Cheng, Jiagao, additional, Churcher, Thomas S., additional, Cordova, Daniel, additional, Cui, Dongliang, additional, Daeuble, John F., additional, Dahmen, Peter, additional, Daido, H., additional, Daniels, M., additional, DeKorver, Kyle, additional, DeLorbe, Jonathan, additional, De Mesmaeker, Alain, additional, Desbordes, Philippe, additional, Desmedt, Willem, additional, Dickhaut, Joachim, additional, Dong, Jingao, additional, El Qacemi, Myriem, additional, Essigmann, Bernd, additional, Fan, Zhijin, additional, Fehr, Marcus, additional, Flaeschel, Michael, additional, Flemming, A.J., additional, Fonné-Pfister, Raymonde, additional, Fukatsu, Kosuke, additional, Furukawa, Y., additional, Gary, Stephanie, additional, Gockel, Birgit, additional, Godfrey, C.R., additional, Godineau, E., additional, Godineau, Edouard, additional, Guan, Aiying, additional, Gutbrod, Oliver, additional, Haas, Hans Ulrich, additional, Hamada, Takahiro, additional, Hamamoto, Taku, additional, Hamer, M., additional, Hamon, Nick, additional, Harayama, Hiroto, additional, Havens, Patrick L., additional, He, Hong-Wu, additional, Heemstra, Ron, additional, Henry, Yewande T., additional, Hermann, Katrin, additional, Herrera, Rafael, additional, Herrick, Jessica, additional, Hirase, Kangetsu, additional, Hisamatsu, Akihiro, additional, Hoegger, Patrik, additional, Holyoke, Caleb W., additional, Hoppé, M., additional, Hueter, O., additional, Hughes, Kenneth A., additional, Hunter, James S., additional, Huwyler, Nikolas, additional, Inoue, Takuya, additional, Ito, Mai, additional, Iwahashi, Fukumatsu, additional, Iwasa, M., additional, Iwata, Atsushi, additional, Jia, Haowu, additional, Jones, David, additional, Kadotani, Junji, additional, Kasahara, Ryota, additional, Katsuta, H., additional, Kawahara, A., additional, Kiguchi, So, additional, Kikuchi, T., additional, Kleemann, Jochen, additional, Kloer, D.P., additional, Kobayashi, Y., additional, Komoda, M., additional, Koradin, Christopher, additional, Koyanagi, Toru, additional, Kyndt, Tina, additional, Lachia, Mathilde, additional, Lahm, George P., additional, Lal, Mukul, additional, Lamberth, Clemens, additional, Lancashire, Peter, additional, Laughlin, Laura A., additional, Leighty, Robert M., additional, Li, BaoJu, additional, Li, Honglin, additional, Li, Pengfei, additional, Li, Wei, additional, Li, Yongqiang, additional, Li, Zhong, additional, Lin, Hong-Yan, additional, Liu, Changling, additional, Loy, Brian A., additional, Lu, Aidang, additional, Lu, Yu, additional, Luksch, Torsten, additional, Lumbroso, Alexandre, additional, Ma, Hongjuan, additional, Maienfisch, Peter, additional, Mangelinckx, Sven, additional, Marrone, Pamela G., additional, Masala, Simonetta, additional, Matsumoto, M., additional, Matsuzaki, Yuichi, additional, Maue, Michael, additional, McCann, Stephen F., additional, Meng, Charles, additional, Meregalli, Giovanna, additional, Meyer, Kevin G., additional, Michrowska-Pianowska, Anna, additional, Mietzner, Thomas, additional, Mita, T., additional, Mitani, S., additional, Molt, Andrea, additional, Morell, Mauricio, additional, Morita, Masayuki, additional, Muehlebach, M., additional, Murata, Tetsuya, additional, Nakamoto, Kenichi, additional, Nakamura, Y., additional, Nakao, T., additional, Nan, Jia-Xu, additional, Newton, Trevor, additional, Nokura, Yoshihiko, additional, Nomura, M., additional, Nourani, R., additional, Oliver, S., additional, Ōmura, Satoshi, additional, Oyama, Kazuhiko, additional, Pahutski, Thomas F., additional, Papineni, Sabitha, additional, Patre, Rupesh, additional, Paulini, Ralph, additional, Peng, Hao, additional, Perruccio, F., additional, Pitterna, Thomas, additional, Pohlman, Matthias, additional, Popp, C., additional, Porri, Aimone, additional, Prasanna, C.S., additional, Qian, Xuhong, additional, Qu, Ren-Yu, additional, Rajan, Ramya, additional, Rankl, Nancy B., additional, Rawal, Girish, additional, Rendine, Stefano, additional, Renold, Peter, additional, Rigoli, Jared, additional, Röckl, Johannes, additional, Sakaguchi, Hiroshi, additional, Salgado, Vincent L., additional, Satoh, Eikoh, additional, Schaetzer, J., additional, Schröder, Hartwig, additional, Schwarz, Hans-Georg, additional, Screpanti, Claudio, additional, Seitz, Thomas, additional, Senn, R., additional, Shan, Guomin, additional, Shao, Xusheng, additional, Shen, Hongfeng, additional, Sherrard-Smith, Ellie, additional, Shi, Qinjie, additional, Shi, Yanxia, additional, Shigematsu, Yoshio, additional, Shino, Mamiko, additional, Sierotzki, Helge, additional, Simon, Anja, additional, Slater, R., additional, Smejkal, Tomas, additional, Smits, Helmars, additional, Soergel, Sebastian, additional, Song, Hongjian, additional, Stafford, D., additional, Stierli, Daniel, additional, Strickman, Daniel, additional, Sulzer-Mosse, Sarah, additional, Suwa, Akiyuki, additional, Takahashi, Masaki, additional, Tan, Xiao-song, additional, Tinwell, Helen, additional, Tong, My-Hanh T., additional, Tsukamoto, Masamitsu, additional, Tsukamoto, Yoshihisa, additional, Tsukuda, S., additional, Vanholme, Bartel, additional, Viner, Russell, additional, Vock-Hatt, F., additional, Vogt, Juliane, additional, Wakita, T., additional, Walter, Harald, additional, Wang, Gaolei, additional, Wang, Nick X., additional, Wang, Qingmin, additional, Wang, Tao, additional, Wang, Ziwen, additional, Wege, P., additional, Weimer, Monte R., additional, Wenger, J., additional, Wildsmith, L., additional, Willis, Derek W., additional, Wilmot, Jeremy, additional, Winter, Christian, additional, Witschel, Matthias, additional, Wu, Qiao, additional, Xiao, Youxin, additional, Xu, Ming, additional, Xu, Xiaoyong, additional, Xu, Yufang, additional, Xu, Zheng, additional, Yamada, Hiroji, additional, Yan, Yao-Chao, additional, Yang, Guang-Fu, additional, Yang, Jichun, additional, Yang, Wen-Chao, additional, Yao, Chenglin, additional, Yoneda, T., additional, Yoshimoto, Yuya, additional, Young, David, additional, Yuan, Jun-Lin, additional, Zambach, W., additional, Zhang, Jingjing, additional, Zhang, Jingwei, additional, Zhang, Ruifeng, additional, Zhang, Wenming, additional, Zhao, Bin, additional, Zhao, Zhenjiang, additional, Zhou, Cong, additional, Zhou, Yuan, additional, and Zhu, Weiping, additional
- Published
- 2021
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3. Nervous system development related gene expression regulation in the zebrafish embryo after exposure to valproic acid and retinoic acid: A genome wide approach.
- Author
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Samrani LMM, Dumont F, Hallmark N, Bars R, Tinwell H, Pallardy M, and Piersma AH
- Subjects
- Animals, Humans, Valproic Acid toxicity, Gene Expression Regulation, Teratogens toxicity, Biomarkers, Nervous System metabolism, Gene Expression Regulation, Developmental, Embryo, Nonmammalian, Tretinoin toxicity, Zebrafish genetics, Zebrafish metabolism
- Abstract
The evaluation of chemical and pharmaceutical safety for humans is moving from animal studies to New Approach Methodologies (NAM), reducing animal use and focusing on mechanism of action, whilst enhancing human relevance. In developmental toxicology, the mechanistic approach is facilitated by the assessment of predictive biomarkers, which allow mechanistic pathways perturbation monitoring at the basis of human hazard assessment. In our search for biomarkers of maldevelopment, we focused on chemically-induced perturbation of the retinoic acid signaling pathway (RA-SP), a major pathway implicated in a plethora of developmental processes. A genome-wide expression screening was performed on zebrafish embryos treated with two teratogens, all-trans retinoic acid (ATRA) and valproic acid (VPA), and a non-teratogen reference compound, folic acid (FA). Each compound was found to have a specific mRNA expression profile with 248 genes commonly dysregulated by both teratogenic compounds but not by FA. These genes were implicated in several developmental processes (e.g., the circulatory and nervous system). Given the prominent response of neurodevelopmental gene sets, and the crucial need to better understand developmental neurotoxicity, our study then focused on nervous system development. We found 62 genes that are potential early neurodevelopmental toxicity biomarker candidates. These results advance NAM-based safety assessment evaluation by highlighting the usefulness of the RA-SP in providing early toxicity biomarker candidates., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Laura Samrani reports financial support was provided by French National Association of Technical Research., (Copyright © 2023 Elsevier B.V. All rights reserved.)
- Published
- 2023
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4. Metribuzin-induced non-adverse liver changes result in rodent-specific non-adverse thyroid effects via uridine 5'-diphospho-glucuronosyltransferase (UDPGT, UGT) modulation.
- Author
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Bomann W, Tinwell H, Jenkinson P, and Kluxen FM
- Subjects
- Animals, Cell Line, Dose-Response Relationship, Drug, Female, Male, Rats, Thyroxine biosynthesis, Thyroxine blood, Glucuronosyltransferase drug effects, Herbicides pharmacology, Thyroid Gland drug effects, Thyroxine drug effects, Triazines pharmacology
- Abstract
Metribuzin is a herbicide that inhibits photosynthesis and has been used for over 40 years. Its main target organ is the liver and to some extent the kidney in rats, dogs, and rabbits. Metribuzin shows a specific thyroxine (T4) profile in rat studies with T4 increases at low doses and T4 decreases at higher doses. Only the T4 decreases occur together with histopathological changes in the thyroid and weight changes of liver and thyroid. A set of experiments was conducted to investigate metribuzin's endocrine disruptor potential according to European guidance and regulations. The results indicate that a liver enzyme modulation, i.e. of the uridine 5'-diphospho-glucuronosyltransferase (UDPGT, UGT), is most likely responsible for both increased and decreased plasma thyroxine level and for thyroid histopathological observations. Animals with high T4 levels show low UGT activity, while animals with low T4 levels show high UGT activity. A causal relationship was inferred, since other potentially human-relevant mode of action (MOA) pathways were excluded in dedicated studies, i.e. inhibition of deiodinases (DIO), inhibition of thyroid peroxidase (TPO) or of the sodium importer system (NIS). This liver metabolism-associated MOA is considered not relevant for human hazard assessment, due to species differences in thyroid homeostasis between humans and rats and, more importantly, based on experimental data showing that metribuzin affects UGT activity in rat but not in human hepatocytes. Further, we discuss whether or not increased T4 levels in the rat, in the absence of histopathological changes, should be considered as adverse and therefore used as an appropriate hazard model for humans. Based on a weight of evidence approach, metribuzin should not be classified as an endocrine disruptor with regard to the thyroid modality., (Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.)
- Published
- 2021
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5. Minimum datasets to establish a CAR-mediated mode of action for rodent liver tumors.
- Author
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Peffer RC, LeBaron MJ, Battalora M, Bomann WH, Werner C, Aggarwal M, Rowe RR, and Tinwell H
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- Animals, Biomarkers, Tumor analysis, Constitutive Androstane Receptor, Cyclopropanes, Fluorobenzenes, Liver Neoplasms chemically induced, Liver Neoplasms pathology, Mice, Picolines, Rats, Receptors, Cytoplasmic and Nuclear analysis, Biomarkers, Tumor metabolism, Datasets as Topic, Liver Neoplasms metabolism, Receptors, Cytoplasmic and Nuclear metabolism
- Abstract
Methods for investigating the Mode of Action (MoA) for rodent liver tumors via constitutive androstane receptor (CAR) activation are outlined here, based on current scientific knowledge about CAR and feedback from regulatory agencies globally. The key events (i.e., CAR activation, altered gene expression, cell proliferation, altered foci and increased adenomas/carcinomas) can be demonstrated by measuring a combination of key events and associative events that are markers for the key events. For crop protection products, a primary dataset typically should include a short-term study in the species/strain that showed the tumor response at dose levels that bracket the tumorigenic and non-tumorigenic dose levels. The dataset may vary depending on the species and the test compound. As examples, Case Studies with nitrapyrin (in mice) and metofluthrin (in rats) are described. Based on qualitative differences between the species, the key events leading to tumors in mice or rats by this MoA are not operative in humans. In the future, newer approaches such as a CAR biomarker signature approach and/or in vitro CAR3 reporter assays for mouse, rat and human CAR may eventually be used to demonstrate a CAR MoA is operative, without the need for extensive additional studies in laboratory animals., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)
- Published
- 2018
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6. Potential new targets involved in 1,3-dinitrobenzene induced testicular toxicity.
- Author
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Ludwig S, Tinwell H, Rouquié D, Schorsch F, Pallardy M, and Bars R
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- Animals, Apoptosis drug effects, Cell Cycle drug effects, Cell Line, Tumor, Cell Survival drug effects, Dinitrobenzenes administration & dosage, Dose-Response Relationship, Drug, Estradiol metabolism, Gene Expression Profiling, Humans, Male, Progesterone metabolism, Random Allocation, Rats, Rats, Wistar, Sertoli Cells cytology, Sertoli Cells drug effects, Sertoli Cells metabolism, Testis cytology, Testis metabolism, Testosterone metabolism, Dinitrobenzenes toxicity, Testis drug effects
- Abstract
1,3-Dinitrobenzene (DNB) causes testicular injury, particularly to Sertoli cells, and induces apoptosis in the surrounding germinal cells in rodents; however, the mechanisms causing this toxicity are poorly understood. Our studies, using standard and molecular tools, were conducted to better understand the pathogenesis of the testicular effects. Four daily oral doses of 0.1-8mg/kg/day caused marked testicular lesions in rats from 4mg/kg/day. Global transcriptomics revealed cell cycle and cell death as the major biological processes affected with the expression of genes associated with cell cycle progression ("mitotic roles of polo-like kinase") being particularly altered. In a single dose time course study (4mg/kg), no adverse changes were recorded; however, in contrast to the data from the multiple dose study, plasma testosterone and testicular steroidogenesis-related gene expression were affected. These steroid hormone effects were confirmed in vitro using the H295R steroidogenesis assay. With this global approach we show that DNB not only induces apoptosis and interferes with cell cycle in the testes but that DNB can also modulate steroid hormone biosynthesis, suggesting an interference with the endocrine system. However, the contribution of the endocrine changes to the severe testicular lesions is presently unknown and requires further investigation., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)
- Published
- 2012
- Full Text
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