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55 results for “neurotoxin”
S43 | NEUROTOXINS | Neurotoxicants Collection from Public Resources
<p>This is the collection associated with list S43 NEUROTOXINS on the NORMAN Suspect List Exchange.</p> <p><a href="https://www.norman-network.com/?q=suspect-list-exchange">https://www.norman-network.com/?q=suspect-list-exchange</a></p> <p>S43</p> <p>NEUROTOXINS</p> <p><strong>Neurotoxicants Collection from Public Resources</strong></p> <p>NEUROTOXINS <a href="https://www.norman-network.com/sites/default/files/files/suspectListExchange/120219Update/NEUROTOXINS_14022019.xlsx">XLSX</a>, <a href="https://www.norman-network.com/sites/default/files/files/suspectListExchange/120219Update/NEUROTOXINS_14022019.csv">CSV</a> (14/02/2019)<br> CompTox <a href="https://comptox.epa.gov/dashboard/chemical_lists/neurotoxins">NEUROTOXINS List</a></p> <p>NEUROTOXINS <a href="https://www.norman-network.com/sites/default/files/files/suspectListExchange/120219Update/NEUROTOXINS_InChIKeys_14022019.txt">InChIKeys</a> (14/02/2019)</p> <p>A list of neurotoxicants compiled from public resources, details on CompTox and Schymanski <em>et al. </em>(submitted). </p>
S24 | HUMANNEUROTOX | List of Human Neurotoxins
<p>This is the collection associated with list S24 HUMANNEUROTOX on the NORMAN Suspect List Exchange.</p> <p><a href="https://www.norman-network.com/?q=suspect-list-exchange">https://www.norman-network.com/?q=suspect-list-exchange</a></p> <p>S24</p> <p>HUMANNEUROTOX</p> <p><strong>List of Human Neurotoxins</strong></p> <p>Human Neurotoxin List <a href="https://www.norman-network.com/sites/default/files/files/suspectListExchange/190618Update/HUMANNEUROTOX-2018-06-19-15-34-35.xls">XLS</a> (19/06/2018)<br> CompTox <a href="https://comptox.epa.gov/dashboard/chemical_lists/humanneurotox">HUMANNEUROTOX List </a></p> <p>Human Neurotox <a href="https://www.norman-network.com/sites/default/files/files/suspectListExchange/190618Update/HUMANNEUROTOX-2018-06-19_InChIKeys.txt">InChIKeys</a> (19/06/2018)</p> <p>A set of chemicals listed as neurotoxicants by Grandjean and Landrigan, DOI: <a href="https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(06)69665-7/fulltext">10.1016/S0140-6736(06)69665-7</a>. List provided by Emma Schymanski/Antony Williams.</p> <p>Nov 14 update: added CSV</p>
Efficacy of Functional Electrical Stimulation (FES) in Persons Receiving Botulinum Neurotoxin for Upper Extremity Spasticity
ClinicalTrials.gov study NCT00462449. IPD Sharing: Not stated. Countries: 1. Publications: 25.
Safety Study of DWP-450 (Botulinum Purified Neurotoxin, Type A) Injection to Treat Glabellar Lines
ClinicalTrials.gov study NCT02184988. IPD Sharing: NO. Countries: 1. Publications: 1.
Eosinophil-derived neurotoxin (EDN): a biologically and analytically attractive asthma biomarker
<p>There is a growing body of evidence for the utility of eosinophil-derived neurotoxin (EDN) as a biomarker in asthma, including association with eosinophilic airway inflammation, assessment of disease severity and potential for predicting pathogenic risks, including exacerbations. However, to interpret any biomarker data with confidence, it is first important to understand the preanalytical factors and biological variation that may affect its reliable measurement and results interpretation. In this study we defined the healthy serum EDN reference range for men and women as 1.98 to 26.10 ng/mL, with no significant gender differences. Smoking did not impact the mean EDN levels and no circadian rhythm was identified for EDN, unlike blood eosinophils (EOS) where levels peaked at 00:00h. EDN expression in different cell types was investigated and shown to occur primarily in eosinophils, indicating they are likely to be the main cellular repository for EDN. We also confirm that the quantification of serum EDN is not influenced by the type of storage tube used, and it is stable at ambient temperature or when refrigerated for at least 7 days and for up to one year when frozen at -20°C or -80°C. In summary, EDN is a stable biomarker that may prove useful in precision medicine approaches by enabling the identification of a subpopulation of asthma patients with activated eosinophils and a more severe form of the disease. </p>
Data from: What caused over a century of decline in general intelligence? Testing predictions from the genetic selection and neurotoxin hypotheses
Several converging lines of evidence indicate that general intelligence (g) has declined in Western populations. The causes of these declines are debated. Here, two hypotheses are tested: (1) selection acting against genetic variants that promote g causes the decline and (2) the presence of neurotoxic pollution in the environment causes the decline. A linear mixed model was devised to test (1) and (2), in which the secular decline in a "heritable g" (g.h) chronometric factor (comprised of convergent indicators of simple reaction time, working memory, utilization frequencies of high difficulty and also social-intelligence-indicating vocabulary items and per capita macro-innovation rates) was predicted using a neurotoxin chronometric factor (comprised of convergent secular trends among measures of lead, mercury and dioxin + furan pollution, in addition to alcohol consumption) and a polygenic score chronometric factor (comprised of polygenic score means for genetic variants predictive of g, sourced from US and Icelandic age-stratified cohorts). Bivariate correlations revealed that (other than time) only the polygenic score factor was significantly associated with declining g.h (r = .393, p < .05 vs. .033, ns for the neurotoxin factor). Using a hierarchical linear mixed model approach incorporating 25 year lags between the predictors and g.h, time period, operationalized categorically as fifths of a century, accounted for the majority of the variance in the decline in g.h (partial η^2 = .584, p < .05). Net of time period and neurotoxins, changing levels of polygenic scores also significantly predicted variance in the decline in g.h (partial η^2 = .253, p < .05); however, changing levels of neurotoxins did not significantly predict variance in g.h net of time (partial η^2 = .027 ns). Within-period analysis indicates that the independent significant positive effect of the polygenic score factor on g.h was restricted to the third fifth of a century period (β = .202, p < .05).
Fig. 4 in Genomic insights into the biosynthesis and physiology of the cyanobacterial neurotoxin 2,4-diaminobutanoic acid (2,4-DAB)
Fig. 4. The biochemical pathway to schizokinen. The established route to rhizobactin 1021 in Sinorhizobium meliloti (Lynch et al., 2001) includes schizokinen as its immediate precursor. (The enzyme responsible for the biosynthesis of rhizobactin 1021 from schizokinen is currently unknown). Nomenclature is from www.bren da-enzymes.org. The genes rhbA and rhbB (Lynch et al., 2001), correspond to the enzymes diaminobutanoate-2-oxo-glutarate transaminase (RhbA, EC 2.6.1.76) and diaminobutanoate decarboxylase (RhbB, EC 4.1.1.86). The enzymes RhbD (an acetylase), RhbE (which catalyses the oxidation of a single amino group of 1,3-diaminopropane), RhbC and RhbF (which catalyse condensation reactions) are unclassified. Redrawn from Lynch et al. (2001). The molecule in square brackets* represents 2,4-diaminobutanoate (2,4-diaminobutanoic acid) after rotation of the amino and carboxylate functions about carbon-2 to allow visual alignment of the amino groups in 1,3-diaminopropane and subsequent derivatives.
Fig. 8 in Genomic insights into the biosynthesis and physiology of the cyanobacterial neurotoxin 2,4-diaminobutanoic acid (2,4-DAB)
Fig. 8. The localisation of the enzymes diaminobutanoate-2-oxo-glutarate transaminase, the downstream decarboxylase, and ectoine synthase within siderophore clusters and incomplete ectoine clusters. The top three clusters correspond to NIS clusters and the bottom cluster corresponds to an incomplete ectoine cluster. The organisation of NIS clusters follows the same pattern: diaminobutanoate-2-oxo-glutarate transaminase (EC 2.6.1.76), followed by diaminobutanoate decarboxylase (EC 4.1.1.86) and IucA/IucC (EC 6.3.2.38, EC 6.3.2.39) family siderophore biosynthesis protein. Arrows point to the orientation of transcription. AntiSMASH was used to identify and annotate specialised metabolite clusters containing both 2,4-DAB transaminase and decarboxylase or 2,4-DAB transaminase and ectoine synthase (EC 4.2.1.108).
Fig. 3 in Genomic insights into the biosynthesis and physiology of the cyanobacterial neurotoxin 2,4-diaminobutanoic acid (2,4-DAB)
Fig. 3. The synthesis of 1,3-diaminopropane from 2,4-DAB. Established route to 1,3-diaminopropane. The nomenclature is from www.brenda-enzymes.org; the Enzyme Commission numbers are as follows: (1) diaminobutanoate-2-oxo-glutarate transaminase: EC 2.6.1.76; (2) diaminobutanoate decarboxylase: EC 4.1.1.86.
Fig. 2. The aspartate 4 in Genomic insights into the biosynthesis and physiology of the cyanobacterial neurotoxin 2,4-diaminobutanoic acid (2,4-DAB)
Fig. 2. The aspartate 4-phosphate pathway. Established routes to 2,4-diaminobutanoate (2,4-diaminobutanoic acid) and derivatives. The nomenclature is from www.brenda-enzymes.org; the Enzyme Commission numbers are as follows: (1) aspartate transaminase: EC 2.6.1.1; (2) aspartate kinase: EC 2.7.2.4; (3) aspartate-semialdehyde dehydrogenase: EC 1.2.1.11; (4) diaminobutanoate- 2-oxo-glutarate transaminase: EC 2.6.1.76; (5) diaminobutanoate acetyltransferase: EC 2.3.1.178; (6) ectoine synthase: EC 4.2.1.108; and (7) ectoine hydroxylase: EC 1.14.11.55. Multiple-step pathways are indicated by *.
Fig. 1 in Genomic insights into the biosynthesis and physiology of the cyanobacterial neurotoxin 2,4-diaminobutanoic acid (2,4-DAB)
Fig. 1. Structure of 2,4-diaminobutanoic acid in the ionised form (2,4- diaminobutanoate). This form is present at physiological pH values. The carboxyl group is then completely ionised and positive charge is shared between the two amino groups.
Fig. 6 in Genomic insights into the biosynthesis and physiology of the cyanobacterial neurotoxin 2,4-diaminobutanoic acid (2,4-DAB)
Fig. 6. The pathway to 2,4-DAB derived from S-adenosylmethionine (SAM). The formation of 2,4-diaminobutanoate (2,4-diaminobutanoic acid) from S-adenosylmethionine (SAM) and isoxazolin-5-one in Lathyrus sylvestris (Callebaut and Lambein, 1977; Ikegami and Murakoshi, 1994). ACI: 2-(3-amino-3-carboxypropyl)-isoxazolin-5-one (Kuo et al., 1982). The enzymes catalysing the two reactions are unclassified.
Fig. 7 in Genomic insights into the biosynthesis and physiology of the cyanobacterial neurotoxin 2,4-diaminobutanoic acid (2,4-DAB)
Fig. 7. Species phylogeny showing the cross-species distribution of specialised metabolite clusters containing a gene coding for diaminobutanoate-2-oxoglutarate transaminase (EC 2.6.1.76). The enzymes encoded by each species are indicated by coloured circles, next to the species name. For enzymes' accession numbers, see Supplementary Tables S12-S17. See Supplementary Fig. S2 for bootstrap support of each branch.
Head-to-Head Comparison of All Botulinum Neurotoxin Type A Products for Glabellar Rhytides
ClinicalTrials.gov study NCT06448676. IPD Sharing: Not stated. Countries: 0. Publications: 19.
Effects of Botulinum Neurotoxin Type A (BoNT/A) Free of Complexing Proteins in the Spastic Equinovarus Foot
ClinicalTrials.gov study NCT03044080. IPD Sharing: NO. Countries: 1. Publications: 4.
Botulism Antitoxin Effects on Paralysis Induced by Botulinum Neurotoxins in the EDB Muscle
ClinicalTrials.gov study NCT00636519. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Exposure to Neurotoxins as Risk Factors for ALS
ClinicalTrials.gov study NCT00340301. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Depth of Botulinum Neurotoxin Injection for Treatment of Glabellar Lines
ClinicalTrials.gov study NCT05766683. IPD Sharing: Not stated. Countries: 1. Publications: 7.
Data from: What caused over a century of decline in general intelligence? Testing predictions from the genetic selection and neurotoxin hypotheses
Open the record for dataset details and reuse information.
Eosinophil-derived neurotoxin (EDN): a biologically and analytically attractive asthma biomarker
Open the record for dataset details and reuse information.
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