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Relevant bibliographies by topics / Neurotoxicity

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Academic literature on the topic 'Neurotoxicity'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 June 2025

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Journal articles on the topic "Neurotoxicity"

1

Rahiman K, Jassim. "Chemotherapy-Induced Neurotoxicity." International Journal of Science and Research (IJSR) 13, no. 8 (2024): 1250–54. http://dx.doi.org/10.21275/sr24820170848.

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Alkhatib, Ahed J., and Nayef Alzamel. "NEUROTOXICITY AND CRIMINAL BEHAVIOR." Indian Research Journal of Pharmacy and Science 5, no. 2 (2018): 1432–38. http://dx.doi.org/10.21276/irjps.2018.5.2.5.

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Lippmann, Maurice, and Timothy Van Natta. "Neurotoxicity." Anesthesiology 117, no. 4 (2012): 923–24. http://dx.doi.org/10.1097/aln.0b013e318267375d.

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Andrews, Jennifer C., John Bergsagel, and Glen Lew. "Acute Neurotoxicity In Children with Acute Lymphoblastic Leukemia: An Association with Day-36 Intrathecal Methotrexate In Delayed Intensification." Blood 116, no. 21 (2010): 3224. http://dx.doi.org/10.1182/blood.v116.21.3224.3224.

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Abstract Abstract 3224 Background: Methotrexate (MTX), both intrathecal (IT) and intravenous (IV) may induce acute neurotoxicity, typically manifested as seizures or stroke-like encephalopathy. The FRALLE 93 trial reported exposure to high-dose (HD) MTX as an independent risk factor for acute neurotoxicity in univariate analysis 1. Pediatric Oncology Group (POG) trial 9005 showed an association between IV MTX and acute neurotoxicity2. We investigate risk factors associated with acute neurotoxicity in children treated according to recent Children's Oncology Group (COG)-modified Berlin-Frankfurt-Munster (BFM)-based protocols, specifically whether number of doses of IT MTX therapy given during delayed intensification (DI) is an independent predictor. Patients and Methods: A retrospective cohort of 167 children ages 1–21 years with ALL treated at our institution according to COG-modified BFM-based therapy between January 2001 and December 2007 with complete records available were reviewed. Patients who received bone marrow transplant in first remission or died prior to DI were excluded. In patients who relapsed, only data regarding therapy prior to relapse was reviewed. Baseline characteristics between patients with acute neurotoxicity (n= 11) and patients without acute neurotoxicity (n= 156) were assessed for differences using the two-tailed student's t-test for continuous variables and the Chi-squared test or Fisher's exact test for categorical variables. Logistical regression analysis was performed using age, diagnosis (pre-B versus T-cell ALL), administration of HD MTX, administration of cranial irradiation (cXRT) and doses of IT MTX (two, on days 1/29, vs. three, on days 1/29/36) administered during DI as predictor variables. Interaction between doses of IT MTX and administration of HD MTX or cXRT was not able to be reliably assessed because of the rarity of the outcome event. Results: 4/136 (3%) patients who received two doses of IT MTX during DI experienced acute neurotoxicity either during DI or thereafter compared with 7/31 (23%) patients who received three doses of IT MTX (p = 0.0008). Univariate analysis showed no significant differences in diagnosis, administration of HD MTX, cranial radiation and relapse rate between patients with acute neurotoxicity vs. those without. Patients with acute neurotoxicity were more likely to be older (p = 0.05) and have received three doses of IT MTX during DI than patients without an event (see table). In multivariate analysis, patients who received three doses of IT MTX during DI were at increased risk of acute neurotoxicity (OR = 7.6, 95% confidence interval 1.7–33.7) adjusted for age, diagnosis, administration of HD MTX and cXRT. Older age was no longer a significant predictor of acute neurotoxicity (OR = 1.1, 95% confidence interval 0.94–1.3). Conclusion: In children with ALL treated per COG-modified BFM-based protocols at our institution, three doses of IT MTX during DI (Days 1/29/36) was associated with a higher risk for acute neurotoxicity compared to two IT MTX doses on Days 1/29. The association between Day 36 IT MTX and acute neurotoxicity was seen in both univariate and multivariate analysis adjusted for age, diagnosis, administration of HD MTX and cXRT. This association should be explored in a larger patient cohort, and if confirmed, warrants consideration of eliminating IT MTX on Day 36 of DI. 1. Dufourg NM et al. Age and high-dose methotrexate are associated to clinical acute encephalopathy in FRALLE 93 trial for acute lymphoblastic leukemia in children. Leukemia 2007; 21:238-47. 2. Mahoney DH et al. Acute neurotoxicity in children with B-precursor acute lymphoid leukemia: an association with intermediate-dose intravenous methotrexate and intrathecal triple therapy – a Pediatric Oncology Group study. J Clin Oncol 1998; 16:1712-22. Disclosures: No relevant conflicts of interest to declare.

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Puri, Vinod. "Metronidazole neurotoxicity." Neurology India 59, no. 1 (2011): 4. http://dx.doi.org/10.4103/0028-3886.76848.

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Lewin, Peter K. "Isoniazid Neurotoxicity." Pediatrics 97, no. 5 (1996): 782–83. http://dx.doi.org/10.1542/peds.97.5.782b.

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I read with great interest the article entitled "Acute Isoniazid Neurotoxicity in an Urban Hospital" in the May 1995 issue of Pediatrics.1 As noted by the authors, there has been a resurgence of tuberculosis in North America that is affecting increasing numbers of children and adolescents. Isoniazid (INH) is still the medication of choice in the management of early primary tuberculosis. However, because INH therapy interferes with pyridoxine metabolism, chronic INH neurotoxicity is also becoming much more prevalent.

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Millichap, J. Gordon. "Lead Neurotoxicity." Pediatric Neurology Briefs 9, no. 6 (1995): 42. http://dx.doi.org/10.15844/pedneurbriefs-9-6-2.

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Maloney, Terence, Robert O'Shannassy, and Donald Handley. "Vincristine neurotoxicity." Medical Journal of Australia 144, no. 1 (1986): 51. http://dx.doi.org/10.5694/j.1326-5377.1986.tb113639.x.

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DOBSON, ALLISON W., KEITH M. ERIKSON, and MICHAEL ASCHNER. "Manganese Neurotoxicity." Annals of the New York Academy of Sciences 1012, no. 1 (2004): 115–28. http://dx.doi.org/10.1196/annals.1306.009.

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Painter, Michael J. "BILIRUBIN NEUROTOXICITY." Developmental Medicine & Child Neurology 14, no. 3 (2008): 395–97. http://dx.doi.org/10.1111/j.1469-8749.1972.tb02607.x.

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Dissertations / Theses on the topic "Neurotoxicity"

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Zhou, Yan. "ß-amyloid neurotoxicity." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/nq23974.pdf.

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Al-Mousa, Fawaz Ali F. "Neurotoxicity of environmental pollutants." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/1461/.

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Brominated flame retardants (BFRs) and alkylphenols (APs) are pollutants commonly found within the environment and have human health concerns due to their endocrine disrupting and cytotoxic effects. BFRs are used to reduce the flammability of a variety of consumer products such as foam furnishings, whereas APs are found in plastic products used by the food industry. This study investigated the neurotoxicity of the most commonly used groups of BFRs and APs on SH-SY5Y human neuroblastoma cells. The results presented in this thesis showed (using cell viability assays) that these pollutants are toxic at low concentrations. Some compounds such as hexabromocyclododecane (HBCD) and 4-nonylphenol (4-NP) induce cell death (apoptosis) by caspases activation (Casp-8, Casp-9 and Casp-3) and cytochrome c release at low micromolar concentrations (IC50 ~ 4μM and 6μM, respectively). Consequently this study also showed that these compounds increased intracellular [Ca2+] levels and the production of reactive oxygen species (ROS) within SH-SY5Y cells by causing Ca2+-dependent depolarization of the mitochondria. In support of a Ca2+-mediated mechanism, the data presented here shows that some BFRs and APs inhibit Sarcoplasmic/ Endoplasmic Ca2+-ATPase (SERCA) and to corroborate this over-expressing SERCA1 improved cell viability especially in cells exposed to certain cytotoxic chemicals such as HBCD; this study is the first experiment of this type to be performed. This study also showed that some of these chemicals, at low concentrations had amyloidgenic effects causing the cleavage amyloid precursor protein (APP) into Beta-amyloid (Aβ) and could therefore be implicated in Alzheimer‟s disease (AD).

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Child, Tim. "The neurotoxicity of acrylamide." Thesis, Aston University, 1996. http://publications.aston.ac.uk/10934/.

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The experiments described in this thesis compared conventional methods of screening for neurotoxins with potential electrophysiological and pharmacological tests in an attempt to improve the sensitivity of detection of progressive distal neuropathy. Adult male albino mice were dosed orally with the neurotoxicant acylamide and subjected to a test of limb strength and co-ordination and a functional observational battery. These methods established a no observable effect level of 10 mg/kg. A dose of 200 mg/kg resulted in abnormalities of gait and reduced limb strength and/or co-ordination. The evoked and spontaneous twitch responses of the hemidiaphragm preparation following in vitro exposure to the organophosphorous anticholinesterase compound ecothiopate were altered by in vivo pre treatment with acrylamide. Acrylamide caused an increase in the time course of the potentiation of stimulated twitches and a decrease in the maximum potentiation. Spontaneous twitches were reduced in amplitude and frequency. These effects occurred at an acrylamide dose level insufficient to cause clinical signs of neuropathy. Investigations into the mechanisms underlying these observations yielded the following observations. Analysis of miniature endplate potentials at this dose level indicated prolongation of the life of acetylcholine in the synaptic cleft but the implied decrease in cholinesterase activity could not be demonstrated biochemically or histologically. The electrical excitability of the nerve terminal region of phrenic motor nerves was reduced following acrylamide although a possible compromise of antidromic action potential conduction could not be confirmed. There was no histopathological evidence of neuropathy at this dose level. Further exploration of this phenomenon is desirable in order to ascertain whether the effect is specific to acrylamide and/or ecothiopate and to elucidate the mechanisms behind these novel observations.

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Kern, Cynthia H. "Neurotoxicity of neonatal manganese exposure /." Diss., Digital Dissertations Database. Restricted to UC campuses, 2009. http://uclibs.org/PID/11984.

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Menton, Kevin. "Intracellular mechanisms of manganese neurotoxicity." Thesis, University of Sunderland, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311078.

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Dick, Finlay D. "The neurotoxicity of paint solvents." Thesis, University of Aberdeen, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288257.

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<i>Objectives</i>- To investigate the relationship between neuropsychological symptoms, as measured by questionnaire, and formal measurements of neurological and psychological function. To investigate the relationship between neuropsychological symptoms and solvent exposure estimates. To test the hypothesis that neuropsychological disorder in solvent exposed workers is more likely to those with genetic predisposition. <i>Methods </i>- A nested case-control study was carried out in a cohort of former dockyard painters and community controls. The 78 painters and 42 community controls had previously participated in a postal study that had shown an excess of neuropsychological symptoms amongst painters. The 120 participants in the nested - case control study underwent detailed neuropsychological testing, colour vision testing, estimation of solvent exposure indices and genetic testing for GSTM1, GSTT1, NAT1 and NAT2 enzyme polymorphisms. <i>Results </i>- A case-control analysis of 68 patients failed to demonstrate significant differences in neuropsychological function between symptomatic and asymptomatic painters as measured by the Q16. Subsequent regression analyses of all 120 subjects showed a range of neuropsychological deficits with an exposure response relationship. There was no convincing evidence of risk modification by any of the enzyme polymorphisms studied. During the study a pattern of deficits was recognised, sufficient to constitute a syndrome of impaired colour vision, cognitive impairment impaired vibration perception and resting tremor. <i>Conclusions </i>- Exposure to mixed solvents is associated with neuropsychological impairment, the risk increasing with increasing intensity of exposure. The risk of impairment was not altered in this study by the presence of different enzyme polymorphisms.

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Abdulla, Elizabeth McFarlane. "In vitro studies of neurotoxicity." Thesis, King's College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248040.

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Alm, Henrik. "Proteomic Characterization of Induced Developmental Neurotoxicity." Doctoral thesis, Uppsala universitet, Institutionen för farmaceutisk biovetenskap, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-99652.

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The developing brain goes through a number of developmental periods during which it displays an increased sensitivity to exogenous disturbances. On such period is the so called “Brain growth spurt” (BGS) which in humans takes place starting from the third trimester of pregnancy and throughout the first few years of life. The corresponding period in rats and mice is the first postnatal weeks. Exposure to relatively modest concentrations of the brominated flame retardant PBDE-99 during the second week of life in mice causes a more or less permanent impairment in the ability of the animals to adjust properly to environmental changes at adulthood. This “late response on early exposure” reflects the long-term consequences of disrupting the developing brain during a sensitive time period. The cellular mechanisms underlying the behavioral effects are far from clear. To address the initial damage occurring around the time of exposure, the approach used in this thesis is to use proteomics to analyze the effects of PBDE-99 on protein expression soon (24 hours) after exposure of the neonatal mouse on postnatal day (PND) 10.The thesis comprises the effects on the proteome in three distinct brain parts: cerebral cortex, striatum and the hippocampus. In addition, an in vitro model was developed and used to evaluate the PBDE-99 effects on cultured cerebral cortex cells from embryonic rat brains. Gel-based proteomics (2D-DIGE) coupled to MALDI- or ESI-MS has been used throughout for the proteomics experiments, but other techniques aimed at analyzing both proteins and mRNA have also been used to better characterize the effects. Even if the protein complements expressed by the different brain parts and separated with 2D-DIGE are seemingly similar, the effects are apparently specific for the different brain regions. In hippocampus, PBDE induces effects on proteins involved in metabolism and energy production, while the effects in striatum point towards effects on neuroplasticity. PBDE-99 changes the expression of cytoskeletal proteins in the cerebral cortex 24 hours after exposure. Interestingly, in vitro exposure of cerebral cortex cells to a PBDE-99 concentration in the same order of magnitude as in the in vivo neonatal brain also induces cytoskeletal effects, in the absence of cytotoxicity. This may suggest effects on regulatory aspects of cytoskeletal dynamics such as those involved in neurite sprouting. This thesis also addresses the problems involved in presenting proteomics data. Many of the available methods and approaches for presenting transcriptomics data are not suitable for isoform rich protein data. Modifications of existing methods and the development of a new approach (DEPPS) is also presented. Most importantly, the thesis presents the application and usefulness of proteomics as hypothesis generating techniques in neurotoxicology.

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Campbell, Sonja Gray. "Methylmercury Neurotoxicity and Interactions with Selenium." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/33173.

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Methylmercury (MeHg) is a ubiquitous contaminant and potent neurotoxicant with no completely effective therapy, although selenium antagonises MeHg toxicity. Furthermore, nanoparticles are promising as a novel drug delivery system. We researched the potential of selenium nanoparticles (SeNPs) in antagonising MeHg neurotoxicity compared to selenomethionine (SeMet) using primary astrocyte cell cultures and examining outcomes related to oxidative stress. We found that SeNPs were more toxic than SeMet. Increasing SeNPs significantly decreased MeHg cellular uptake and MeHg significantly decreased uptake of SeNPs at the highest concentration. Finally, SeNPs alone produced significantly higher reactive oxidative species and altered the ratio of reduced-to-oxidised glutathione, but MeHg, SeMet, and co-exposures did not. There were no significant effects on glutathione peroxidase or reductase activity. This suggests that SeNPs are more toxic than MeHg in cerebellar astrocytes and that they may not be suitable as a therapy at the doses and formulation used in this research.

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Axelrad, Janie Clodah. "Neurotoxicity of organophosphates : synergy and interactions." Thesis, University of Liverpool, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.250224.

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Books on the topic "Neurotoxicity"

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Herken, Hans, and Ferdinand Hucho, eds. Selective Neurotoxicity. Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-85117-9.

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C, Bondy Stephen, and Prasad Kedar N, eds. Metal neurotoxicity. CRC Press, 1988.

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Arlien-Søborg, Peter. Solvent neurotoxicity. CRC Press, 1992.

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K, Aktories, Herken Hans, and Hucho Ferdinand 1939-, eds. Selective neurotoxicity. Springer-Verlag, 1992.

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Hans, Herken, and Hucho Ferdinand 1939-, eds. Selective neurotoxicity. Springer-Verlag, 1994.

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Kostrzewa, Richard M., ed. Handbook of Neurotoxicity. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-71519-9.

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Aschner, Michael, and Lucio G. Costa, eds. Neurotoxicity of Metals. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60189-2.

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Niu, Qiao, ed. Neurotoxicity of Aluminum. Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1370-7.

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Morimoto, Yuji, ed. Anesthesia and Neurotoxicity. Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-55624-4.

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Ceccatelli, Sandra, and Michael Aschner, eds. Methylmercury and Neurotoxicity. Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-2383-6.

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Book chapters on the topic "Neurotoxicity"

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Leonardi, M., and R. Agati. "Neurotoxicity." In Trends in Contrast Media. Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59814-2_9.

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Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, et al. "Neurotoxicity." In Encyclopedia of Psychopharmacology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1406.

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Dewar, A. J. "Neurotoxicity." In The Future of Predictive Safety Evaluation. Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3201-2_7.

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Abou-Donia, Mohamed B. "Neurotoxicity." In Mammalian Toxicology. John Wiley & Sons, Inc., 2015. http://dx.doi.org/10.1002/9781118683484.ch18.

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Gould, A. Lawrence. "Neurotoxicity." In Statistical Methods for Evaluating Safety in Medical Product Development. John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118763070.ch10.

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Viberg, Henrik, and Espen Mariussen. "Neurotoxicity." In Toxicological Effects of Perfluoroalkyl and Polyfluoroalkyl Substances. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-15518-0_9.

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Aschner, Michael, Marcelo Farina, and João B. T. Rocha. "Mercury Neurotoxicity." In Encyclopedia of Metalloproteins. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_315.

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Sharma, Hari Shanker, and Aruna Sharma. "Silver, Neurotoxicity." In Encyclopedia of Metalloproteins. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_551.

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Metcalf, James S., Rachael Anne Dunlop, Paul Alan Cox, and Sandra Anne Banack. "BMAA Neurotoxicity." In Handbook of Neurotoxicity. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-15080-7_225.

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Ávila, Daiana Silva, João Batista Teixeira Rocha, Yousef Tizabi, et al. "Manganese Neurotoxicity." In Handbook of Neurotoxicity. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-15080-7_3.

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Conference papers on the topic "Neurotoxicity"

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Stelmashchuk, O. A., V. V. Dremin та A. Y. Abramov. "Singlet Oxygen Prevents the Mitochondrial NADH Depletion in β-amyloid Induced Neurotoxicity". У 2024 International Conference Laser Optics (ICLO). IEEE, 2024. http://dx.doi.org/10.1109/iclo59702.2024.10624450.

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Agapito, Giuseppe, Marianna Milano, Francesca Scionti, et al. "Modeling UGT2B7 and NR1I3 genes through multilayer network to highlight hidden link with taxane neurotoxicity." In 2024 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2024. https://doi.org/10.1109/bibm62325.2024.10822206.

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Di Trapani, Rachel, and William D. Freeman. "Dronedarone-Induced Neurotoxicity." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3880.

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Souza, Larissa Baccoli de, Marcella Canato Toloi, Kassia Braga Canzian, Isabela de Almeida Stella, Marcele Schettini de Almeida, and Roberta Arb Saba. "Manganese neurotoxicity: a case report." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.786.

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A 51-year-old female patient, teacher, presented initially with hematemesis associated with hemodynamic instability, with recurrence of the condition for two times and other several clinical complications. During hospitalizations, she developed progressive weight loss and alteration of the mental state, in addition to reduced strength in the four limbs, cognitive decline of rapid evolution and loss of functionality and independency for basic activities of life daily. The cognitive exam revealed significant alterations with impaired sustained attention and verbal fluency, loss of executive and visuospatial functions. The somatic exam showed rigidity and bradykinesia in the four limbs, with reduction of blinking, in addition to important postural instability, with Cock-Walk Gait. Laboratory and abdominal imaging pointed signs of chronic liver disease and magnetic resonance imaging (MRI) of the brain showed a hypersignal on T1 sequence in bilateral globus pallidus (GP) with a symmetrical appearance. Such changes could be related to an acquired hepatocerebral degeneration associated with manganese (Mn) deposition in the GP. Treatment for parkinsonism and hepatic encephalopaty were established In outpatient return, an important improvement was seen, especially in the cognitive tests. The association between chronic liver disease and parkinsonism added cock-walk gait suggest the clinical of chronic acquired hepatocerebral degeneration, a rare case of deposit of Mn in the central nervous system (CNS), which causes neurotoxicity, neurological disorders and MRI findings. Chronic liver disease is associated with Mn clearance and binding mechanisms, as well as metal transport across the blood-brain barrier. Associated, there are several neurotoxicity mechanisms still under investigation, which cause the deposition of the metal in the GP. More investigations are needed to delineate the complex nature of the mechanisms of Mn-induced CNS toxicity.

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Brewer, Janet. "Involuntary Neurotoxicity and Criminal Responsibility." In 12th International Conference on Humanities, Psychology and Social Sciences. Acavent, 2021. http://dx.doi.org/10.33422/12th.hpsconf.2021.05.25.

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Grandjean, Philippe. "Developmental Effects of Metal Neurotoxicity." In Proceedings of the 18th International Conference on Heavy Metals in the Environment. openjournals ugent, 2016. http://dx.doi.org/10.21825/ichmet.71395.

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Okon, Emmanuel E., Anthony Isedeh, Christian A. Engell, and Eliahu Bishburg. "Atypical Presentation Of Tacrolimus Associated Neurotoxicity." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3164.

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Li, B. "156. Effects of Styrene on Neurotoxicity." In AIHce 2005. AIHA, 2005. http://dx.doi.org/10.3320/1.2758506.

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Anger, WK. "1639c Organophosphorus pesticide neurotoxicity in egyptian applicators." In 32nd Triennial Congress of the International Commission on Occupational Health (ICOH), Dublin, Ireland, 29th April to 4th May 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/oemed-2018-icohabstracts.821.

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Niu, Q., Q. Zhang, H. Li, L. Wang, and X. Lu. "1708b The immunotoxicity and neurotoxicity of aluminium." In 32nd Triennial Congress of the International Commission on Occupational Health (ICOH), Dublin, Ireland, 29th April to 4th May 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/oemed-2018-icohabstracts.139.

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Reports on the topic "Neurotoxicity"

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Jortner, Bernard. Multifactorial Assessment of Depleted Uranium Neurotoxicity. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada435240.

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Jortner, Bernard S. Multifactorial Assessment of Depleted Uranium Neurotoxicity. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada419521.

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Lasley, Stephen M. Neurotoxicity From Chronic Exposure to Depleted Uranium. Defense Technical Information Center, 2006. http://dx.doi.org/10.21236/ada457731.

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Wilson, Barry W. Low-Level Sarin Neurotoxicity and Its Modulation by Pyridostigmine. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada399150.

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Janowsky, Jeri. Exploration of Prostate Cancer Treatment Induced Neurotoxicity with Neuroimaging. Defense Technical Information Center, 2008. http://dx.doi.org/10.21236/ada484214.

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Janowsky, Jenri. Exploration of Prostate Cancer Treatment Induced Neurotoxicity with Neuroimaging. Defense Technical Information Center, 2007. http://dx.doi.org/10.21236/ada472360.

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O'Malley, Karen L. Fundamental Patterns Underlying Neurotoxicity Revealed by DNA Microarray Expression Profiling. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada409422.

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O'Malley, Karen L. Fundamental Patterns Underlying Neurotoxicity Revealed by DNA Microarray Expression Profiling. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada429295.

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Kinkead, E. R., S. R. Bunger, R. E. Wolfe, and H. G. Wall. The Acute, Delayed Neurotoxicity Evaluation of Two Jet Engine Oil Formulations. Defense Technical Information Center, 1990. http://dx.doi.org/10.21236/ada222018.

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Fremouw, Thane, Maxwell Hennings, Christy Fessler, Hawk Cambron, Teresa Collins, and Moriah Greer. Chemotherapy, Neurotoxicity, and Cognitive Decline: Developing a Mouse Model and Potential Interventions. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada568167.

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