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Journal articles on the topic 'Neurotoxicity assessment'

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Published: 13 September 2022

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1

Kulig, Beverly M. "Comprehensive Neurotoxicity Assessment." Environmental Health Perspectives 104 (April 1996): 317. http://dx.doi.org/10.2307/3432651.

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2

Kulig, B. M. "Comprehensive neurotoxicity assessment." Environmental Health Perspectives 104, suppl 2 (April 1996): 317–22. http://dx.doi.org/10.1289/ehp.96104s2317.

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3

Parng, Chuenlei, Nicole Marie Roy, Christopher Ton, Yingxin Lin, and Patricia McGrath. "Neurotoxicity assessment using zebrafish." Journal of Pharmacological and Toxicological Methods 55, no. 1 (January 2007): 103–12. http://dx.doi.org/10.1016/j.vascn.2006.04.004.

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4

GREENBERG, B. D., P. A. MOORE, R. LETZ, and E. L. BAKER. "Computerized Assessment of Human Neurotoxicity." Survey of Anesthesiology 30, no. 4 (August 1986): 189. http://dx.doi.org/10.1097/00132586-198608000-00010.

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5

Boyes, William K., Michael L. Dourson, Jacqueline Patterson, Hugh A. Tilson, William F. Sette, Robert C. MacPhail, Abby A. Li, and John L. O'Donoghue. "EPA's Neurotoxicity Risk Assessment Guidelines." Toxicological Sciences 40, no. 2 (1997): 175–84. http://dx.doi.org/10.1093/toxsci/40.2.175.

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6

Boyes, W. "EPA's Neurotoxicity Risk Assessment Guidelines, ,." Fundamental and Applied Toxicology 40, no. 2 (December 1997): 175–84. http://dx.doi.org/10.1006/faat.1997.2388.

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7

Kodell, R. L., J. J. Chen, and D. W. Gaylor. "Neurotoxicity Modeling for Risk Assessment." Regulatory Toxicology and Pharmacology 22, no. 1 (August 1995): 24–29. http://dx.doi.org/10.1006/rtph.1995.1064.

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8

Jacobson, Joseph L., and Sandra W. Jacobson. "Prospective, Longitudinal Assessment of Developmental Neurotoxicity." Environmental Health Perspectives 104 (April 1996): 275. http://dx.doi.org/10.2307/3432647.

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9

Jacobson, J. L., and S. W. Jacobson. "Prospective, longitudinal assessment of developmental neurotoxicity." Environmental Health Perspectives 104, suppl 2 (April 1996): 275–83. http://dx.doi.org/10.1289/ehp.96104s2275.

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10

Giardina, William J. "Assessment of temafloxacin neurotoxicity in rodents." American Journal of Medicine 91, no. 6 (December 1991): S42—S44. http://dx.doi.org/10.1016/0002-9343(91)90310-t.

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11

Shirakawa, Takafumi, and Ikuro Suzuki. "Approach to Neurotoxicity using Human iPSC Neurons: Consortium for Safety Assessment using Human iPS Cells." Current Pharmaceutical Biotechnology 21, no. 9 (June 9, 2020): 780–86. http://dx.doi.org/10.2174/1389201020666191129103730.

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Neurotoxicity, as well as cardiotoxicity and hepatotoxicity, resulting from administration of a test article is considered a major adverse effect both pre-clinically and clinically. Among the different types of neurotoxicity occurring during the drug development process, seizure is one of the most serious one. Seizure occurrence is usually assessed using in vivo animal models, the Functional Observational Battery, the Irwin test or electroencephalograms. In in vitro studies, a number of assessments can be performed using animal organs/cells. Interestingly, recent developments in stem cell biology, especially the development of Human-Induced Pluripotent Stem (iPS) cells, are enabling the assessment of neurotoxicity in human iPS cell-derived neurons. Further, a Multi-Electrode Array (MEA) using rodent neurons is a useful tool for identifying seizure-inducing compounds. The Consortium for Safety Assessment using Human iPS Cells (CSAHi; http://csahi.org/en/) was established in 2013 by the Japan Pharmaceutical Manufacturers Association (JPMA) to verify the application of human iPS cell-derived neuronal cells to drug safety evaluation. The Neuro Team of CSAHi has been attempting to evaluate the seizure risk of compounds using the MEA platform. Here, we review the current status of neurotoxicity and recent work, including problems related to the use of the MEA assay with human iPS neuronal cell-derived neurons, and future developments.
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12

Broxup, B. "Neuropathology As a Screen for Neurotoxicity Assessment." Journal of the American College of Toxicology 10, no. 6 (November 1991): 689–95. http://dx.doi.org/10.3109/10915819109078661.

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Pathology has been a cornerstone of toxicity testing for many years and is an integral part of the primary tier screen in the testing of drugs and chemicals for neurotoxicity. Because of the special nature of nervous tissue and its anatomical complexity, the approach to the evaluation can influence in a major way the effectiveness of the task. This report discusses issues which may account for variation in the degree of neuropathological assessment between laboratories. Both systematic and flexible approaches to the evaluation of neuropathology are discussed.
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13

Atli, O., U. Demir-Ozkay, S. Ilgin, H. Aydin, E. N. Akbulut, and E. Sener. "Neurotoxicity assessment of amoxicillin in juvenile rats." Toxicology Letters 238, no. 2 (October 2015): S272. http://dx.doi.org/10.1016/j.toxlet.2015.08.784.

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14

Authier, Nicolas, E. Dupuis, A. Kwasiborski, A. Eschalier, and F. Coudoré. "Behavioural assessment of dimethylsulfoxide neurotoxicity in rats." Toxicology Letters 132, no. 2 (June 2002): 117–21. http://dx.doi.org/10.1016/s0378-4274(02)00052-8.

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15

Kraft, Andrew, and Ambuja Bale. "Ex vivo models and chemical neurotoxicity assessment." Neurotoxicology and Teratology 34, no. 3 (May 2012): 379–80. http://dx.doi.org/10.1016/j.ntt.2012.05.037.

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16

Beckman, David A., Maureen Youreneff, and Mark T. Butt. "Neurotoxicity Assessment of Artemether in Juvenile Rats." Birth Defects Research Part B: Developmental and Reproductive Toxicology 98, no. 2 (March 11, 2013): 183–99. http://dx.doi.org/10.1002/bdrb.21054.

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17

He, Fengsheng, Soulin Zhang, Gang Li, Shucong Zhang, Jinxiang Huang, and Yiqin Wu. "An electroneurographic assessment of subclinical lead neurotoxicity." International Archives of Occupational and Environmental Health 61, no. 1-2 (October 1988): 141–46. http://dx.doi.org/10.1007/bf00381618.

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18

Boyes, William K., Virginia C. Moser, Andrew M. Geller, Vernon A. Benignus, Philip J. Bushnell, and Freya Kamel. "Integrating epidemiology and toxicology in neurotoxicity risk assessment." Human & Experimental Toxicology 26, no. 4 (April 2007): 283–93. http://dx.doi.org/10.1177/0960327106070481.

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Neurotoxicity risk assessments depend on the best available scientific information, including data from animal toxicity studies, human experimental studies and human epidemiology studies. There are several factors to consider when evaluating the comparability of data from studies. Regarding the epidemiology literature, issues include choice of study design, use of appropriate controls, methods of exposure assessment, subjective or objective evaluation of neurological status, and assessment and statistical control of potential confounding factors, including co-exposure to other agents. Animal experiments must be evaluated regarding factors such as dose level and duration, procedures used to assess neurological or behavioural status, and appropriateness of inference from the animal model to human neurotoxicity. Major factors that may explain apparent differences between animal and human studies include: animal neurological status may be evaluated with different procedures than those used in humans; animal studies may involve shorter exposure durations and higher dose levels; and most animal studies evaluate a single substance whereas humans typically are exposed to multiple agents. The comparability of measured outcomes in animals and humans may be improved by considering functional domains rather than individual test measures. The application of predictive models, weight of evidence considerations and meta-analysis can help evaluate the consistency of outcomes across studies. An appropriate blend of scientific information from toxicology and epidemiology studies is necessary to evaluate potential human risks of exposure to neurotoxic substances. Human & Experimental Toxicology (2007) 26, 283-293
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19

Amano, T., Y. Shimada, T. Nishina, K. Shinozaki, T. Esaki, Y. Komatsu, H. Akita, K. Shimozuma, Y. Ohashi, and F. H. Hausheer. "Prospective Validation of Patient Neurotoxicity Questionnaire (PNQ) for Assessment of Oxaliplatin Neurotoxicty: CSP-HOR 16." Annals of Oncology 23 (September 2012): ix512—ix513. http://dx.doi.org/10.1016/s0923-7534(20)34137-5.

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20

Pirovano, Carlo, Augusta Balzarini, Silvia Böhm, Saro Oriana, Gian Battista Spatti, and Franco Zunino. "Peripheral Neurotoxicity following High-Dose Cisplatin with Glutathione: Clinical and Neurophysiological Assessment." Tumori Journal 78, no. 4 (August 1992): 253–57. http://dx.doi.org/10.1177/030089169207800408.

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The use of high-dose cisplatin is limited by development of severe peripheral neurotoxicity and gradual worsening of renal function. In an ongoing study of high-dose cisplatin glutathione has been employed with the aim of preventing major cisplatin-induced toxicities. Neurotoxicity was examined in detail in 32 patients with ovarian cancer treated with cisplatin (160 mg/m2) and cyclophosphamide (600 mg/m2) every 3-4 weeks for five courses. In addition to serial complete neurological examination, sensory action potentials (SAPs) and motor conduction velocities (MCVs) were also assessed. We confirmed the development of a predominant sensory involvement, characterized by mild distal paresthesias and decrease in vibratory sensibility and in deep tendon reflexes, with a slight reduction of SAPs, observed after three courses of treatment. After five courses, distal paresthesias and disesthesias, decreased proprioception and loss of vibratory sensibility with ataxic signs, absence of deep tendon reflexes, unobtainable SAPs and only moderately reduced MCVs were seen. We did not observe any case of disabling neuropathy. There was a tendency to a more severe involvement of peripheral nerves in patients aged more than fifty. The 3 patients presenting the most serious neuropathy were the oldest in the whole group. Low degree of neurotoxicity observed in this study supports a glutathione protection against cisplatin-induced neurotoxicity. As the urinary excretion of platinum indicated no changes in the renal clearance of cisplatin following repeated courses, the lack of drug accumulation and high plasma peak due to preserved renal function might explain the reduced neurotoxicity observed.
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21

Eremina, N. V., L. G. Kolik, R. U. Ostrovskaya, and A. D. Durnev. "Preclinical in vivo Neurotoxicity Studies of Drug Candidates." Bulletin of the Scientific Centre for Expert Evaluation of Medicinal Products 10, no. 3 (September 18, 2020): 164–76. http://dx.doi.org/10.30895/1991-2919-2020-10-3-164-176.

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Neurotoxic effects are one of the common reasons for discontinuation of preclinical and/or clinical studies. Preclinical evaluation of neurotoxic effects is complicated due to a wide range of manifestations and degrees of severity. Current experimental approaches to neurotoxicity assessment are cumbersome, laborious and not adapted enough for preclinical studies in the early stages of drug development. The aim of the study was to review existing approaches to experimental assessment of neurotoxic potential of new drugs and to discuss the need for and feasibility of developing and using integrated rapid neurotoxicity tests for early assessment of a pharmacological project’s potential. The authors reviewed scientific literature and guidance documents and analysed current approaches to chemical compound neurotoxicity assessment in laboratory animals. The paper analyses the main issues of neurotoxicity assessment for new drugs and compares Irwin tests with the functional observation battery. It analyses issues related to assessment of drugs’ effects on the development and maturation of central nervous system functions at pre- and postnatal stages. It was determined that the current practice is not sufficient for assessment of potential adverse effects on cognitive functions. The authors assessed factors affecting cognitive functions of rodents during studies. The “Acute suppression of the exploratory and orientation response” and “Extrapolation escape task” tests were proposed for validation as potential rapid tests for detection of an array of organic and functional neurotoxic disorders at early stages of preclinical studies.
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22

Tilson, Hugh A. "Evolution and Current Status of Neurotoxicity Risk Assessment." Drug Metabolism Reviews 28, no. 1-2 (January 1996): 121–39. http://dx.doi.org/10.3109/03602539608993995.

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23

Harry, G. Jean, Melvin Billingsley, Arend Bruinink, Iain L. Campbell, Werner Classen, David C. Dorman, Corrado Galli, David Ray, Robert A. Smith, and Hugh A. Tilson. "In Vitro Techniques for the Assessment of Neurotoxicity." Environmental Health Perspectives 106 (February 1998): 131. http://dx.doi.org/10.2307/3433917.

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24

El-Fawal, Hassan A. N., Stacey J. Waterman, Anthony De Feo, and Magdy Y. Shamy. "Neuroimmunotoxicology: Humoral Assessment of Neurotoxicity and Autoimmune Mechanisms." Environmental Health Perspectives 107 (October 1999): 767. http://dx.doi.org/10.2307/3434339.

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25

Spear, Linda Patia. "Assessment of adolescent neurotoxicity: Rationale and methodological considerations." Neurotoxicology and Teratology 29, no. 1 (January 2007): 1–9. http://dx.doi.org/10.1016/j.ntt.2006.11.006.

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26

Boyes, W. K. "A 21st century update on neurotoxicity risk assessment." Toxicology Letters 259 (October 2016): S51—S52. http://dx.doi.org/10.1016/j.toxlet.2016.07.125.

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27

Rodriguez-Rodriguez, A., L. Boyero, L. Sempere, and A. Vilches-Arenas. "Animal models for neurotoxicity assessment in cardiac arrest." Medicina Intensiva 43, no. 7 (October 2019): 450. http://dx.doi.org/10.1016/j.medin.2018.09.009.

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28

Rodriguez-Rodriguez, A., L. Boyero, L. Sempere, and A. Vilches-Arenas. "Animal models for neurotoxicity assessment in cardiac arrest." Medicina Intensiva (English Edition) 43, no. 7 (October 2019): 450. http://dx.doi.org/10.1016/j.medine.2018.09.013.

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29

Harry, G. J., M. Billingsley, A. Bruinink, I. L. Campbell, W. Classen, D. C. Dorman, C. Galli, D. Ray, R. A. Smith, and H. A. Tilson. "In vitro techniques for the assessment of neurotoxicity." Environmental Health Perspectives 106, suppl 1 (February 1998): 131–58. http://dx.doi.org/10.1289/ehp.98106s1131.

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30

El-Fawal, H. A., S. J. Waterman, A. De Feo, and M. Y. Shamy. "Neuroimmunotoxicology: humoral assessment of neurotoxicity and autoimmune mechanisms." Environmental Health Perspectives 107, suppl 5 (October 1999): 767–75. http://dx.doi.org/10.1289/ehp.99107s5767.

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31

Bailey, F. "Reexamining the developmental neurotoxicity study and risk assessment." Neurotoxicology and Teratology 49 (May 2015): 111–12. http://dx.doi.org/10.1016/j.ntt.2015.04.042.

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32

Kazunobu, Tsunemoto, Shigeru Yamada, and Yasunari Kanda. "Assessment of developmental neurotoxicity using human iPS cells." Proceedings for Annual Meeting of The Japanese Pharmacological Society 93 (2020): 3—P—374. http://dx.doi.org/10.1254/jpssuppl.93.0_3-p-374.

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33

SLIKKER, WILLIAM, and THOMAS J. SOBOTKA. "Current and Future Approaches to Neurotoxicity Risk Assessment." Annals of the New York Academy of Sciences 825, no. 1 Neuroprotecti (October 1997): 406–18. http://dx.doi.org/10.1111/j.1749-6632.1997.tb48452.x.

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34

Tkachuk, R. A., B. І. Yavorskyy, and A. F. Yanenko. "Problems of neurotoxicity assessment with using of electroretinography." Visnyk NTUU KPI Seriia - Radiotekhnika Radioaparatobuduvannia, no. 61 (June 30, 2015): 108–15. http://dx.doi.org/10.20535/radap.2015.61.108-115.

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35

Douglas, J. Fielding, Richard H. Mckee, Stuart Z. Cagen, Susan L. Schmitt, Patrick W. Beatty, Mark S. Swanson, Ceinwen A. Schreiner, Charles E. Ulrich, and Beverly Y. Cockrell. "A Neurotoxicity Assessment of High Flash Aromatic Naphtha." Toxicology and Industrial Health 9, no. 6 (November 1993): 1047–58. http://dx.doi.org/10.1177/074823379300900605.

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Catalytic reforming is a refining process that converts naphthenes to aromatics by dehydrogenation to make higher octane gasoline blending components. A portion of this wide-boiling range hydrocarbon stream can be separated by distillation and used for other purposes. One such application is a mixture of predominantly 9-carbon aromatic molecules (C9 Aromatics, primarily isomers of ethyltoluene and trimethylbenzene), which is removed and used as a solvent also known as High Flash Aromatic Naphtha (HFAN). A program was initiated to assess the toxicological properties of HFAN since there may be human exposure, especially in the workplace. The current study was conducted to assess the potential for neurotoxicity in the rat. Adult male Sprague-Dawley rats of approximately 300 grams body weight, in groups of twenty, were exposed by inhalation to HFAN for 90 days at concentrations of 0, 100, 500, and 1500 ppm. During this period the animals were tested monthly for motor activity and in afunctional observation battery. After three months of exposure, for 6 hours/day, 5 days/week, 10 animals/group/sex were sacrificed and selected nervous system tissue was examined histopathologically. No signs of neurotoxicity were seen in any of the evaluated parameters, nor was there evidence of pathologic changes in any of the examined tissues.
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36

Mousavi Ahmadian, Kazem, Núria Serra Cabañas, Christian Cordoba Herrera, Leonor Fayos de Arizon, Mónica Perez Mir, Lluís Guirado Perich, and Carme Facundo Molas. "Assessment of Tacrolimus Neurotoxicity Measured by Retinal OCT." Transplantation Proceedings 54, no. 1 (January 2022): 80–86. http://dx.doi.org/10.1016/j.transproceed.2021.10.013.

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37

Niu, Q. "Neurotoxicity Assessment of Chemicals on Exposed Workers — A Review of Neurobehavioral and Neurophysilogical Tests." European Journal of Inflammation 1, no. 2 (May 2003): 51–58. http://dx.doi.org/10.1177/1721727x0300100201.

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With the wide utilization of neurotoxic substances, more and more people are exposed to them occupationally or environmentally. Neurotoxicity has been defined as any adverse effect on the structure or function of the central and /or peripheral nervous system by biological, chemical and physical agent. Neurotoxic effect may be permanent or reversible, caused by neuropharmacological or neurodegenerative properties of a neurotoxicant. The nervous system is very sensitive and fragile to chemicals. The early adverse effects should be detected as early as possible because they are reversible, functional and chemical, not structural. A multidisciplinary approach is necessary to assess neurotoxicity because of the complexity and diverse functions of the nervous system. Many of the relevant effects can be measured directly by neurochemical, neurophysiological, and neuropathological techniques, whereas, others must be inferred from observed behavior and psychic performance. Neurotoxicity in humans is most commonly measured by relatively noninvasive neurophysiological and neurobehavioral methods that assess cognitive, affective, sensory, and motor function. The biomarker assay can be complement. In general, due to the speciality and difficult accessibility, the biomarkers that manifest the neurotoxicity of chemicals in nervous system are difficult to obtain, but a number of biochemical and molecular parameters similar to those involved as toxicity targets in the nervous system are also present in more easily accessible tissues, such as cerebrospinal fluid (CSF), blood, plasma and peripheral blood cells. These tissues can be surrogate indicators. With the multidisciplinary approach, the neurotoxicity of chemicals can be assessed or screened sensitively and practically.
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38

Moore, David H., James Donnelly, William P. McGuire, Lois Almadrones, David F. Cella, Thomas J. Herzog, and Steven E. Waggoner. "Limited Access Trial Using Amifostine for Protection Against Cisplatin- and Three-Hour Paclitaxel–Induced Neurotoxicity: A Phase II Study of the Gynecologic Oncology Group." Journal of Clinical Oncology 21, no. 22 (November 15, 2003): 4207–13. http://dx.doi.org/10.1200/jco.2003.02.086.

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Purpose: The purpose of this study was to determine whether amifostine (WR-2721) prevents or ameliorates clinically significant (grade 2 to 4) neurotoxicity associated with cisplatin and 3-hour paclitaxel chemotherapy. Materials and Methods: The chemotherapy program consisted of intravenous paclitaxel 175 mg/m2 over 3 hours followed by amifostine 740 mg/m2 and cisplatin 75 mg/m2 administered over 90 minutes beginning 15 minutes after amifostine administration. At baseline, before each treatment cycle, and for 3 months after completing chemotherapy, patients were evaluated for evidence of neurotoxicity and other treatment-related adverse effects using three methods: standard clinical evaluation (National Cancer Institute common toxicity criteria [CTC] grading), a neurotoxicity questionnaire to assess symptoms and limitations imposed by peripheral neuropathy, and vibration perception threshold (VPT) testing. Results: Four of 27 assessable patients developed grade 2 to 4 neurotoxicity based on clinical assessments and CTC grading. This number of neuropathic events exceeded the predetermined threshold level for a second stage of accrual and the study was closed. Conclusion: Amifostine’s level of activity in this trial was insufficient to warrant further study in a phase III trial. Based on the receiver operating characteristic analysis, it would appear that VPT measurements are less sensitive to the development of peripheral neuropathy than the neurotoxicity questionnaire. The questionnaire, referred to as the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group–Neurotoxicity, may be used instead of VPT measurements in future studies of chemotherapy-induced peripheral neuropathy.
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39

Walther, L., and J. Schulze. "Causality assessment of putative neurotoxicity – Proposal of a checklist." Toxicology Letters 238, no. 2 (October 2015): S151—S152. http://dx.doi.org/10.1016/j.toxlet.2015.08.472.

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40

Kulig, Beverly, Enrico Alleva, Giorgio Bignami, Jeffrey Cohn, Deborah Cory-Slechta, V. Landa, John O'Donoghue, and David Peakall. "Animal Behavioral Methods in Neurotoxicity Assessment: SGOMSEC Joint Report." Environmental Health Perspectives 104 (April 1996): 193. http://dx.doi.org/10.2307/3432641.

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41

Panter, S. S., K. D. Vandegriff, P. O. Van, and R. F. Regan. "Assessment of Hemoglobin-Dependent Neurotoxicity: Alpha-Alpha Crosslinked Hemoglobin." Artificial Cells, Blood Substitutes, and Biotechnology 22, no. 3 (January 1994): 399–413. http://dx.doi.org/10.3109/10731199409117870.

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42

Slikker, William, Andrew C. Scallet, and David W. Gaylor. "Biologically-based dose–response model for neurotoxicity risk assessment." Toxicology Letters 102-103 (December 1998): 429–33. http://dx.doi.org/10.1016/s0378-4274(98)00335-x.

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43

Nontprasert, Apichart, Sasithon Pukrittayakamee, Sompol Prakongpan, Wichai Supanaranond, Sornchai Looareesuwan, and Nicholas J. White. "Assessment of the neurotoxicity of oral dihydroartemisinin in mice." Transactions of the Royal Society of Tropical Medicine and Hygiene 96, no. 1 (January 2002): 99–101. http://dx.doi.org/10.1016/s0035-9203(02)90256-7.

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44

Parng, Chuenlei, Catherine Willett, and Patricia McGrath. "ASSESSMENT OF DEVELOPMENTAL NEUROTOXICITY IN ZEBRAFISH AFTER CHEMICAL EXPOSURE." Journal of Pharmacological and Toxicological Methods 56, no. 2 (September 2007): e41. http://dx.doi.org/10.1016/j.vascn.2007.02.082.

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45

Kulig, B., E. Alleva, G. Bignami, J. Cohn, D. Cory-Slechta, V. Landa, J. O'Donoghue, and D. Peakall. "Animal behavioral methods in neurotoxicity assessment: SGOMSEC joint report." Environmental Health Perspectives 104, suppl 2 (April 1996): 193–204. http://dx.doi.org/10.1289/ehp.96104s2193.

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46

Yamada, Shigeru, Kazunobu Tsunemoto, Kaoru Sato, and Yasunari Kanda. "Drug-induced neurotoxicity assessment using human iPS cell technology." Journal of Pharmacological and Toxicological Methods 105 (September 2020): 106847. http://dx.doi.org/10.1016/j.vascn.2020.106847.

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47

Soderlund, David M., John M. Clark, Larry P. Sheets, Linda S. Mullin, Vincent J. Piccirillo, Dana Sargent, James T. Stevens, and Myra L. Weiner. "Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment." Toxicology 171, no. 1 (February 2002): 3–59. http://dx.doi.org/10.1016/s0300-483x(01)00569-8.

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48

Wallace, Kendall B. "Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment." Toxicology 171, no. 1 (February 2002): 1. http://dx.doi.org/10.1016/s0300-483x(01)00574-1.

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49

Amin, Sanjiv B. "Clinical assessment of bilirubin-induced neurotoxicity in premature infants." Seminars in Perinatology 28, no. 5 (October 2004): 340–47. http://dx.doi.org/10.1053/j.semperi.2004.09.005.

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50

SLIKKER, WILLIAM, and DAVID W. GAYLOR. "Biologically Based Dose-Response Model for Neurotoxicity Risk Assessment." Annals of the New York Academy of Sciences 765, no. 1 Neuroprotecti (September 1995): 339. http://dx.doi.org/10.1111/j.1749-6632.1995.tb16611.x.

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