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Firdaus, Riyadh, Sandy Theresia, Ryan Austin, and Rani Tiara. "Propofol effects in rodent models of traumatic brain injury: a systematic review." Asian Biomedicine 15, no. 6 (December 1, 2021): 253–65. http://dx.doi.org/10.2478/abm-2021-0032.
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Abstract Background Traumatic brain injury (TBI) causes high mortality and disability worldwide. Animal models have been developed to explore the complex processes in TBI. Propofol is used to manage head injuries during surgical intervention and mechanical ventilation in patients with TBI. Many studies have investigated the neuroprotective effect of propofol on TBI. However, other studies have shown neurotoxic effects. Objectives To review systematically the literature regarding the neuroprotective and neurotoxic effects of propofol in rodent models of TBI. Methods Data from rodents as models of TBI with propofol as one of the intervention agents, and/or comparing the neuroprotective effects of propofol with the other substances in rodent models of TBI, were obtained from PubMed, EBSCO Host, and ProQuest databases. The PRISMA 2020 statement recommendations were followed and research questions were developed based on PICOS guidelines. Data was extracted from the literature using a standardized Cochrane method. Results We analyzed data from 12 articles on physiological changes of experimental animals before and after trauma, the effects of propofol administration, and the observed neurotoxic effects. The effects of propofol administration were observed in terms of changes in traumatic lesion volume, the release of antioxidants and inflammatory factors, and the neurological function of rodent models of TBI. Conclusion Propofol has neuroprotective and neurotoxic effects via several mechanisms, and various doses have been used in research to determine its effects. The timing of administration, the dose administered, and the duration of administration contribute to determine the effect of propofol in rodent models of TBI. However, the doses that produce neuroprotective and neurotoxic effects are not yet clear and further research is needed to determine them.
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Zengerle, Michael, Florian Brandhuber, Christian Schneider, Franz Worek, Georg Reiter, and Stefan Kubik. "Highly efficient cyclosarin degradation mediated by a β-cyclodextrin derivative containing an oxime-derived substituent." Beilstein Journal of Organic Chemistry 7 (November 22, 2011): 1543–54. http://dx.doi.org/10.3762/bjoc.7.182.
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The potential of appropriately substituted cyclodextrins to act as scavengers for neurotoxic organophosphonates under physiological conditions was evaluated. To this end, a series of derivatives containing substituents with an aldoxime or a ketoxime moiety along the narrow opening of the β-cyclodextrin cavity was synthesized, and the ability of these compounds to reduce the inhibitory effect of the neurotoxic organophosphonate cyclosarin on its key target, acetylcholinesterase, was assessed in vitro. All compounds exhibited a larger effect than native β-cyclodextrin, and characteristic differences were noted. These differences in activity were correlated with the structural and electronic parameters of the substituents. In addition, the relatively strong effect of the cyclodextrin derivatives on cyclosarin degradation and, in particular, the observed enantioselectivity are good indications that noncovalent interactions between the cyclodextrin ring and the substrate, presumably involving the inclusion of the cyclohexyl moiety of cyclosarin into the cyclodextrin cavity, contribute to the mode of action. Among the nine compounds investigated, one exhibited remarkable activity, completely preventing acetylcholinesterase inhibition by the (−)-enantiomer of cyclosarin within seconds under the conditions of the assay. Thus, these investigations demonstrate that decoration of cyclodextrins with appropriate substituents represents a promising approach for the development of scavengers able to detoxify highly toxic nerve agents.
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Sekeres, Melanie J., Meenakshie Bradley-Garcia, Alonso Martinez-Canabal, and Gordon Winocur. "Chemotherapy-Induced Cognitive Impairment and Hippocampal Neurogenesis: A Review of Physiological Mechanisms and Interventions." International Journal of Molecular Sciences 22, no. 23 (November 24, 2021): 12697. http://dx.doi.org/10.3390/ijms222312697.
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A wide range of cognitive deficits, including memory loss associated with hippocampal dysfunction, have been widely reported in cancer survivors who received chemotherapy. Changes in both white matter and gray matter volume have been observed following chemotherapy treatment, with reduced volume in the medial temporal lobe thought to be due in part to reductions in hippocampal neurogenesis. Pre-clinical rodent models confirm that common chemotherapeutic agents used to treat various forms of non-CNS cancers reduce rates of hippocampal neurogenesis and impair performance on hippocampally-mediated learning and memory tasks. We review the pre-clinical rodent literature to identify how various chemotherapeutic drugs affect hippocampal neurogenesis and induce cognitive impairment. We also review factors such as physical exercise and environmental stimulation that may protect against chemotherapy-induced neurogenic suppression and hippocampal neurotoxicity. Finally, we review pharmacological interventions that target the hippocampus and are designed to prevent or reduce the cognitive and neurotoxic side effects of chemotherapy.
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Sorci, Guglielmo, Roberta Bianchi, Francesca Riuzzi, Claudia Tubaro, Cataldo Arcuri, Ileana Giambanco, and Rosario Donato. "S100B Protein, a Damage-Associated Molecular Pattern Protein in the Brain and Heart, and Beyond." Cardiovascular Psychiatry and Neurology 2010 (August 18, 2010): 1–13. http://dx.doi.org/10.1155/2010/656481.
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S100B belongs to a multigenic family of -binding proteins of the EF-hand type and is expressed in high abundance in the brain. S100B interacts with target proteins within cells thereby altering their functions once secreted/released with the multiligand receptor RAGE. As an intracellular regulator, S100B affects protein phosphorylation, energy metabolism, the dynamics of cytoskeleton constituents (and hence, of cell shape and migration), homeostasis, and cell proliferation and differentiation. As an extracellular signal, at low, physiological concentrations, S100B protects neurons against apoptosis, stimulates neurite outgrowth and astrocyte proliferation, and negatively regulates astrocytic and microglial responses to neurotoxic agents, while at high doses S100B causes neuronal death and exhibits properties of a damage-associated molecular pattern protein. S100B also exerts effects outside the brain; as an intracellular regulator, S100B inhibits the postinfarction hypertrophic response in cardiomyocytes, while as an extracellular signal, (high) S100B causes cardiomyocyte death, activates endothelial cells, and stimulates vascular smooth muscle cell proliferation.
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Haryanto, Budi. "Indonesia: country report on children’s environmental health." Reviews on Environmental Health 35, no. 1 (March 26, 2020): 41–48. http://dx.doi.org/10.1515/reveh-2019-0088.
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AbstractChildren’s bodies are in dynamic stages of development that make them more susceptible to harm from exposure to environmental agents. Children’s physical, physiological and behavioral traits can lead to increased exposure to toxic chemicals or pathogens. In addition, the social determinants of health interact with this exposure and create an increasing risk for further disparities among children. In Indonesia, the fourth most populated country in the world, children are under threat of exposure to contaminated water, air, food and soil, which can cause gastrointestinal and respiratory diseases, birth defects and neurodevelopmental disorders. A safe and balanced nutrition is still an unmet need for too many children. At the same time, the prevalence of obesity and the risk of later development of metabolic diseases, including diabetes and cardiovascular diseases, are increasing as a consequence of both unhealthy diets and inadequate physical activity. The risks of potential long-term toxicity, including carcinogenic, neurotoxic, immunotoxic, genotoxic, endocrine-disrupting and allergenic effects of many chemicals, are also close to their lives. This paper provides an overview of common disease risks in Indonesian children, including: acute hepatitis A, diarrheal diseases, dengue and malaria due to lack of water supply and sanitation, vectors, and parasites; asthma, bronchopneumonia, chronic obstructive pulmonary disease (COPD) and acute respiratory infections (ARIs) due to air pollution and climate change; some chronic diseases caused by toxic and hazardous waste; and direct or indirect consequences due to the occurrence of disasters and health emergencies.
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Nemecz, Dorota, Maciej Ostrowski, Marc Ravatin, Frederick Saul, and Grazyna Faure. "Crystal Structure of Isoform CBd of the Basic Phospholipase A2 Subunit of Crotoxin: Description of the Structural Framework of CB for Interaction with Protein Targets." Molecules 25, no. 22 (November 13, 2020): 5290. http://dx.doi.org/10.3390/molecules25225290.
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Crotoxin, from the venom of the South American rattlesnake Crotalus durissus terrificus, is a potent heterodimeric presynaptic β-neurotoxin that exists in individual snake venom as a mixture of isoforms of a basic phospholipase A2 (PLA2) subunit (CBa2, CBb, CBc, and CBd) and acidic subunit (CA1–4). Specific natural mutations in CB isoforms are implicated in functional differences between crotoxin isoforms. The three-dimensional structure of two individual CB isoforms (CBa2, CBc), and one isoform in a crotoxin (CA2CBb) complex, have been previously reported. This study concerns CBd, which by interaction with various protein targets exhibits many physiological or pharmacological functions. It binds with high affinity to presynaptic receptors showing neurotoxicity, but also interacts with human coagulation factor Xa (hFXa), exhibiting anticoagulant effect, and acts as a positive allosteric modulator and corrector of mutated chloride channel, cystic fibrosis transmembrane conductance regulator (CFTR), implicated in cystic fibrosis. Thus, CBd represents a novel family of agents that have potential in identifying new drug leads related to anticoagulant and anti-cystic fibrosis function. We determined here the X-ray structure of CBd and compare it with the three other natural isoforms of CB. The structural role of specific amino acid variations between CB isoforms are analyzed and the structural framework of CB for interaction with protein targets is described.
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Husstedt, IW, D. Reichelt, U. Oelker-Grueneberg, and S. Evers. "Neurotoxic effect of antiretroviral agents on CNS." Journal of the International AIDS Society 11, Suppl 1 (2008): P163. http://dx.doi.org/10.1186/1758-2652-11-s1-p163.
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Kurnik-Łucka, Magdalena, Gniewomir Latacz, Adrian Martyniak, Andrzej Bugajski, Katarzyna Kieć-Kononowicz, and Krzysztof Gil. "Salsolinol—neurotoxic or Neuroprotective?" Neurotoxicity Research 37, no. 2 (November 15, 2019): 286–97. http://dx.doi.org/10.1007/s12640-019-00118-7.
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AbstractSalsolinol (6,7-dihydroxy-1-methyl-1,2,3,4-tetrahydroisoquinoline), widely available in many edibles, is considered to alter the function of dopaminergic neurons in the central nervous system and thus, multiple hypotheses on its either physiological and/or pathophysiological role have emerged. The aim of our work was to revisit its potentially neurotoxic and/or neuroprotective role through a series of both in vitro and in vivo experiments. Salsolinol in the concentration range 10–250 μM did not show any significant release of lactate dehydrogenase from necrotic SH-SY5Y cells and was able in the concentration of 50 and 100 μM to rescue SH-SY5Y cells from death induced by H2O2. Its neuroprotective effect against neurotoxin 6-hydroxydopamine was also determined. Salsolinol was found to decrease significantly the reactive oxygen species level in SH-SY5Y cells treated by 500 μM H2O2 and the caspase activity induced by 300 μM of H2O2 or 100 μM of 6-hydroxydopamine. Serum levels of TNFα and CRP of salsolinol-treated rats were not significantly different from control animals. Both TNFα and CRP served as indirect markers of neurotoxicity and/or neuroprotection. Although the neurotoxic properties of salsolinol have numerously been emphasized, its neuroprotective properties should not be neglected and need greater consideration.
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Moro, Nicola, Lolita Dokshokova, Induja Perumal Vanaja, Valentina Prando, Sophie Julie A. Cnudde, Anna Di Bona, Riccardo Bariani, et al. "Neurotoxic Effect of Doxorubicin Treatment on Cardiac Sympathetic Neurons." International Journal of Molecular Sciences 23, no. 19 (September 21, 2022): 11098. http://dx.doi.org/10.3390/ijms231911098.
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Doxorubicin (DOXO) remains amongst the most commonly used anti-cancer agents for the treatment of solid tumors, lymphomas, and leukemias. However, its clinical use is hampered by cardiotoxicity, characterized by heart failure and arrhythmias, which may require chemotherapy interruption, with devastating consequences on patient survival and quality of life. Although the adverse cardiac effects of DOXO are consolidated, the underlying mechanisms are still incompletely understood. It was previously shown that DOXO leads to proteotoxic cardiomyocyte (CM) death and myocardial fibrosis, both mechanisms leading to mechanical and electrical dysfunction. While several works focused on CMs as the culprits of DOXO-induced arrhythmias and heart failure, recent studies suggest that DOXO may also affect cardiac sympathetic neurons (cSNs), which would thus represent additional cells targeted in DOXO-cardiotoxicity. Confocal immunofluorescence and morphometric analyses revealed alterations in SN innervation density and topology in hearts from DOXO-treated mice, which was consistent with the reduced cardiotropic effect of adrenergic neurons in vivo. Ex vivo analyses suggested that DOXO-induced denervation may be linked to reduced neurotrophic input, which we have shown to rely on nerve growth factor, released from innervated CMs. Notably, similar alterations were observed in explanted hearts from DOXO-treated patients. Our data demonstrate that chemotherapy cardiotoxicity includes alterations in cardiac innervation, unveiling a previously unrecognized effect of DOXO on cardiac autonomic regulation, which is involved in both cardiac physiology and pathology, including heart failure and arrhythmias.
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Shah, Arya, E. Matthew Hoffman, Michelle L. Mauermann, Charles L. Loprinzi, Anthony J. Windebank, Christopher J. Klein, and Nathan P. Staff. "Incidence and disease burden of chemotherapy-induced peripheral neuropathy in a population-based cohort." Journal of Neurology, Neurosurgery & Psychiatry 89, no. 6 (February 8, 2018): 636–41. http://dx.doi.org/10.1136/jnnp-2017-317215.
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ObjectiveTo assess disease burden of chemotherapy-induced peripheral neuropathy (CIPN), which is a common dose-limiting side effect of neurotoxic chemotherapy. Late effects of CIPN may increase with improved cancer survival.MethodsOlmsted County, Minnesota residents receiving neurotoxic chemotherapy were identified and CIPN was ascertained via text searches of polyneuropathy symptoms in the medical record. Clinical records were queried to collect data on baseline characteristics, risk factors, signs and symptoms of CIPN, medications, impairments and International Classification of Diseases, Ninth Revision (ICD-9) diagnostic codes for all subjects.ResultsA total of 509 individuals with incident exposure to an inclusive list of neurotoxic chemotherapy agents between 2006 and 2008 were identified. 268 (52.7%) of these individuals were determined to have CIPN. The median time from incident exposure to first documented symptoms was 71 days. Patients with CIPN received a neuropathy ICD-9 diagnosis in only 37 instances (13.8%). Pain symptoms and use of pain medications were observed more often in patients with CIPN. Five-year survival was greater in those with CIPN (55.2%) versus those without (36.1%). Those with CIPN surviving greater than 5 years (n=145) continued to have substantial impairments and were more likely to be prescribed opioids than those without CIPN (OR 2.0, 1.06–3.69).ConclusionsResults from our population-based study are consistent with previous reports of high incidence of CIPN in the first 2 years following incident exposure to neurotoxic chemotherapeutic agents, and its association with significant pain symptomatology and accompanied long-term opioid use. Increased survival following exposure to neurotoxic chemotherapy and its long-term disease burden necessitates further study among survivors.
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Ratnakumari, Lingamaneni, and Hugh C. Hemmings. "Inhibition of Presynaptic Sodium Channels by Halothane." Anesthesiology 88, no. 4 (April 1, 1998): 1043–54. http://dx.doi.org/10.1097/00000542-199804000-00025.
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Background Recent electrophysiologic studies indicate that clinical concentrations of volatile general anesthetic agents inhibit central nervous system sodium (Na+) channels. In this study, the biochemical effects of halothane on Na+ channel function were determined using rat brain synaptosomes (pinched-off nerve terminals) to assess the role of presynaptic Na+ channels in anesthetic effects. Methods Synaptosomes from adult rat cerebral cortex were used to determine the effects of halothane on veratridine-evoked Na+ channel-dependent Na+ influx (using 22Na+), changes in intrasynaptosomal [Na+] (using ion-specific spectrofluorometry), and neurotoxin interactions with specific receptor sites of the Na+ channel (by radioligand binding). The potential physiologic and functional significance of these effects was determined by measuring the effects of halothane on veratridine-evoked Na+ channel-dependent glutamate release (using enzyme-coupled spectrofluorometry). Results Halothane inhibited veratridine-evoked 22Na+ influx (IC50 = 1.1 mM) and changes in intrasynaptosomal [Na+] (concentration for 50% inhibition [IC50] = 0.97 mM), and it specifically antagonized [3H]batrachotoxinin-A 20-alpha-benzoate binding to receptor site two of the Na+ channel (IC50 = 0.53 mM). Scatchard and kinetic analysis revealed an allosteric competitive mechanism for inhibition of toxin binding. Halothane inhibited veratridine-evoked glutamate release from synaptosomes with comparable potency (IC50 = 0.67 mM). Conclusions Halothane significantly inhibited Na+ channel-mediated Na influx, increases in intrasynaptosomal [Na+] and glutamate release, and competed with neurotoxin binding to site two of the Na+ channel in synaptosomes at concentrations within its clinical range (minimum alveolar concentration, 1-2). These findings support a role for presynaptic Na+ channels as a molecular target for general anesthetic effects.
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Gettins, P. G. W., M. Simonovic, and K. Volz. "Pigment Epithelium-Derived Factor (PEDF), a Serpin with Potent Anti-Angiogenic and Neurite Outgrowth-promoting Properties." Biological Chemistry 383, no. 11 (November 13, 2002): 1677–82. http://dx.doi.org/10.1515/bc.2002.188.
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Abstract Pigment epitheliumderived factor is a member of the serpin superfamily of proteins, but one that lacks inhibitory properties against either serine or cysteine proteinases. Nevertheless it possesses a number of physiological properties that make it a potentially important protein in regulation of angiogenesis, in neuronal cell survival and in protection of neurons from neurotoxic agents. It is also a protein that is highly up regulated in the G0 phase of earlypassage cells compared with rapidly proliferating cells or senescent cells, and so is also linked to both the cell cycle and cell senescence. The determination of a high resolution Xray crystal structure of native PEDF provides insight into regions of the protein that may be involved in one or more of these functions.
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OLIVEIRA, MARCOS ROBERTO DE. "The neurotoxic effects of vitamin A and retinoids." Anais da Academia Brasileira de Ciências 87, no. 2 suppl (August 4, 2015): 1361–73. http://dx.doi.org/10.1590/0001-3765201520140677.
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Vitamin A (retinol) and its congeners - the retinoids - participate in a panoply of biological events, as for instance cell differentiation, proliferation, survival, and death, necessary to maintain tissue homeostasis. Furthermore, such molecules may be applied as therapeutic agents in the case of some diseases, including dermatological disturbances, immunodeficiency, and cancer (mainly leukemia). In spite of this, there is a growing body of evidences showing that vitamin A doses exceeding the nutritional requirements may lead to negative consequences, including bioenergetics state dysfunction, redox impairment, altered cellular signaling, and cell death or proliferation, depending on the cell type. Neurotoxicity has long been demonstrated as a possible side effect of inadvertent consumption, or even under medical recommendation of vitamin A and retinoids at moderate to high doses. However, the exact mechanism by which such molecules exert a neurotoxic role is not clear yet. In this review, recent data are discussed regarding the molecular findings associated with the vitamin A-related neurotoxicity.
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Shimada, Hiroshi, Shiori Noguchi, Masahiro Yamamoto, Katsuhiko Nishiyama, Yusuke Kitamura, and Toshihiro Ihara. "Electrochemical Sensing of Neurotoxic Agents Based on Their Electron Transfer Promotion Effect on an Au Electrode." Analytical Chemistry 89, no. 11 (May 16, 2017): 5742–47. http://dx.doi.org/10.1021/acs.analchem.6b04229.
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Komolafe, Kayode, Tolulope M. Olaleye, Rodrigo L. Seeger, Fabiano B. Carvalho, Aline A. Boligon, Margareth L. Athayde, Claudia V. Klimaczewski, Akintunde A. Akindahunsi, and Joao B. T. Rocha. "Parkia biglobosaImproves Mitochondrial Functioning and Protects against Neurotoxic Agents in Rat Brain Hippocampal Slices." BioMed Research International 2014 (2014): 1–15. http://dx.doi.org/10.1155/2014/326290.
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Objective. Methanolic leaf extracts ofParkia biglobosa, PBE, and one of its major polyphenolic constituents, catechin, were investigated for their protective effects against neurotoxicity induced by different agents on rat brain hippocampal slices and isolated mitochondria.Methods. Hippocampal slices were preincubated with PBE (25, 50, 100, or 200 µg/mL) or catechin (1, 5, or 10 µg/mL) for 30 min followed by further incubation with 300 µM H2O2, 300 µM SNP, or 200 µM PbCl2for 1 h. Effects of PBE and catechin on SNP- or CaCl2-induced brain mitochondrial ROS formation and mitochondrial membrane potential (ΔΨm) were also determined.Results. PBE and catechin decreased basal ROS generation in slices and blunted the prooxidant effects of neurotoxicants on membrane lipid peroxidation and nonprotein thiol contents. PBE rescued hippocampal cellular viability from SNP damage and caused a significant boost in hippocampus Na+, K+-ATPase activity but with no effect on the acetylcholinesterase activity. Both PBE and catechin also mitigated SNP- or CaCl2-dependent mitochondrial ROS generation. Measurement by safranine fluorescence however showed that the mild depolarization of theΔΨmby PBE was independent of catechin.Conclusion. The results suggest that the neuroprotective effect of PBE is dependent on its constituent antioxidants and mild mitochondrial depolarization propensity.
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Sharma, Abha, Colby Adams, Benjamin D. Cashdollar, Zheng Li, Nam V. Nguyen, Himasri Sai, Jiachun Shi, Gautham Velchuru, Kevin Z. Zhu, and Gerald H. Pollack. "Effect of Health-Promoting Agents on Exclusion-Zone Size." Dose-Response 16, no. 3 (July 1, 2018): 155932581879693. http://dx.doi.org/10.1177/1559325818796937.
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It is now well-confirmed that hydrophilic surfaces including those within the cell generate structural changes in water. This interfacial water is ordered and acquires features different from the bulk. Amongst those features is the exclusion of colloidal and molecular solutes from extensive regions next to the hydrophilic surface, thereby earning it the label of “exclusion zone” (EZ) water. The transition of ordered EZ water to bulk serves as an important trigger of many cellular physiological functions, and in turn cellular health. We tested physiological doses of half a dozen agents generally identified to restore or build health on the extent to which they build EZs. All agents known to enhance biological function resulted in EZ expansion. On the other hand, the weed killer, glyphosate, considerably diminished EZ size. While the expansion effect of the health-promoting agents was observed over a wide range of concentrations, excessive doses ultimately reduced EZ size. We hypothesize that EZ buildup may be a mechanistic feature underlying many health-promoting agents, while agents that impair health may act by diminishing the amount of EZ water.
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Andeden, Enver Ersoy, Sahlan Ozturk, and Belma Aslim. "Antiproliferative, neurotoxic, genotoxic and mutagenic effects of toxic cyanobacterial extracts." Interdisciplinary Toxicology 11, no. 4 (December 1, 2018): 267–74. http://dx.doi.org/10.2478/intox-2018-0026.
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Abstract Cyanobacteria are the rich resource of various secondary metabolites including toxins with broad pharmaceutical significance. The aim of this work was to evaluate the antiproliferative, neurotoxic, genotoxic and mutagenic effects of cyanobacterial extracts containing Microcystin-LR (MCLR) in vitro. ELISA analysis results showed that MCLR contents of five cyanobacterial extracts were 2.07 ng/mL, 1.43 ng/mL, 1.41 ng/mL, 1.27 ng/mL, and 1.12 ng/mL for Leptolyngbya sp. SB1, Phormidium sp. SB4, Oscillatoria earlei SB5, Phormidium sp. SB2, Uncultured cyanobacterium, respectively. Phormidium sp. SB4 and Phormidium sp. SB2 extracts had the lowest neurotoxicity (86% and 79% cell viability, respectively) and Oscillatoria earlei SB5 extracts had the highest neurotoxicity (47% cell viability) on PC12 cell at 1000 µg/ml extract concentration. Leptolyngbya sp. SB1 and Phormidium sp. SB2 showed the highest antiproliferative effect (92% and 77% cell death) on HT29 cell. On the other hand, all concentrations of five toxic cyanobacterial extracts induced DNA damage between 3.0% and 1.3% of tail intensity and did not cause any direct mutagenic effect at the 1000 µg/plate cyanobacterial extracts. These results suggest that cyanobacteria-derived MCLR is a promising candidate for development of effective agents against colon cancer.
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Bartnik, B. L., B. HJ Juurlink, and R. M. Devon. "Macrophages: their myelinotrophic or neurotoxic actions depend upon tissue oxidative stress." Multiple Sclerosis Journal 6, no. 1 (February 2000): 37–42. http://dx.doi.org/10.1177/135245850000600108.
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There are still questions regarding whether macrophages found in MS lesions are agents of recovery or of destruction. To address this, we examined in aggregate cultures prepared from dissociated embryonic spinal cord tissue, with or without addition of exogenous macrophages, the effect of menadione-induced oxidative stress. Similar to findings of other laboratories, we observed that in the absence of oxidative stress macrophage enrichment promoted myelinogenesis. In macrophage-poor cultures, menadione at 5 μM had very little effect upon the status of the aggregate cultures; however, increasing this to 10 and 20 μM did result in some damage to axons and myelin. By contrast, in macrophage enriched cultures, menadione at a concentration as little as 5 μM caused the complete destruction of the aggregates. We suggest that in neural tissues that have sufficiently high macrophage numbers, oxidative stress results in a positive inflammatory feedback loop that results in massive tissue destruction. We further suggest that what we see in macrophage-enriched aggregates subjected to oxidative stress may represent what happens in the Marburg-type of MS lesion.
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KARAKAYALI, Emine Müge, Duygu KEKEÇ, Tuna ÖNAL, and Mehmet İbrahim TUĞLU. "Investigation of the moderate toxicity of agricultural pesticides cyantraniliprole, boscalid and spiromesifen in vitro using neurotoxicity screening test." Anatomy 15, no. 1 (2021): 1–10. http://dx.doi.org/10.2399/ana.21.911509.
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Objectives: Although industrial products used as agricultural pesticides are considered safe, they are likely to lead to chronic problems due to their long-term effects. The neurotoxicity screening test (NST) is a method based on the inhibition of neurite extension of neurons that do not not die with toxic effects. In this study, we aimed to investigate the moderate neurotoxic effects and reveal the potential dangers of agricultural pesticides in vitro using NST. Methods: Cyantraniliprole, boscalid and spiromesifen were used as agricultural pesticides on the mouse neuroblastoma cell line N2a. Neurite extension of neurons was performed by taking them into the proliferation medium followed by the differentiation medium. Cell viability and proliferation were analyzed using the MTT test. The percentage of neurite inhibition was calculated by measuring neurite outgrowth by NST. Oxidative stress was analyzed by NOS staining with h-score and apoptosis was shown using the apoptotic index in TUNEL staining. Results: Cyantraniliprole, boscalid and spiromesifen at high concentrations caused neurite inhibition, decreased proliferation and reduced the viability of cultured neurons. These agricultural pesticides were found to be significantly moderate toxic for neurons by increasing oxidative stress and apoptosis. Conclusion: We conclude neurite inhibition may be important in early recognition for detecting and preventing the neurotoxic effect of pesticides, and NST is an important in vitro test that can predict the long-term effects of neurotoxic agents. In the present study, we observed cyantraniliprole, boscalid and spiromesifen had moderate neurotoxic effects in varying degrees using NST. This means that pesticides may behave toxic even in permissible limits for chronic exposure.
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Gouveia, Geraldo Candido Cabral, Flávio Ferreira da Silva Binotti, and Edilson Costa. "Priming effect on the physiological potential of maize seeds under abiotic stress1." Pesquisa Agropecuária Tropical 47, no. 3 (September 2017): 328–35. http://dx.doi.org/10.1590/1983-40632016v4746560.
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ABSTRACT Abiotic stress directly influences seed performance, so poor-vigor seeds under adverse conditions tend to show lower germination speed and rate. By controlling the hydration level of seeds (i.e., priming) with the addition of chemical agents, it is possible to elicit the maximum physiological potential of seeds, even under stress conditions. This study aimed to evaluate the priming effect of different chemical agents on the physiological potential of maize seeds under abiotic stress (polyethylene glycol induced water stress, hypoxia, low temperature and salt stress after controlled deterioration). The experimental design was completely randomized, in a 5 x 2 factorial scheme, consisting of different chemical agents used to hydrate the seeds [control without priming; control primed with water; calcium nitrate (0.2 %); amino acid L-phenylalanine (0.05 %); amino acid L-phenylalanine (0.5 %) + calcium nitrate (0.2 %)] and 2 seed lots, with four replicates. Priming with calcium nitrate lead to a greater germination and higher emergence rate of the seedlings under suboptimal temperature conditions, and seeds that underwent controlled deterioration showed greater germination levels with the use of calcium nitrate + phenylalanine in the priming process, regardless of the lot used. In general, seed priming allowed a greater expression of seed vigor, even though an interaction with lots was observed in some variables.
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Zubova, Svetlana V., Yaroslav V. Radzyukevich, Sergey V. Grachev, and Isabela R. Prokhorenko. "Effect of Various Agents on the Direction of THP-1 Cell Differentiation." Serbian Journal of Experimental and Clinical Research 19, no. 3 (September 1, 2018): 263–69. http://dx.doi.org/10.2478/sjecr-2018-0029.
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AbstractThe ability of physiological (1α,25-dihydroxyvitamin D3, retinoic acid) and non-physiological (various LPS) agents and their combinations to influence the direction of promonocytic THP-1 cell differentiation was studied.The differentiating activity of the agents was evaluated by the expression and the ratio of surface receptors (TLR4, CD11b, and CD14) as well as by the change in THP-1 cell phagocytic activity of different degree of differentiation by Flow cytometry.The THP-1 cell differentiation by VD3 was shown to lead probably to the formation of classical monocytes.Summarizing we can conclude that VD3 induces the THP-1 cells differentiation with the formation of classical monocytes and the sequence of 1α, 25-dihydroxyvitamin D3 and non-toxic LPS R. capsulatus PG causes the THP-1 cells differentiation with the formation of inflammatory or intermediate monocytes.
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Mruk, Allison L., Karen L. Garlitz, and Noelle R. Leung. "Levetiracetam in Neonatal Seizures: A Review." Journal of Pediatric Pharmacology and Therapeutics 20, no. 2 (April 1, 2015): 76–89. http://dx.doi.org/10.5863/1551-6776-20.2.76.
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Phenobarbital and phenytoin have been the mainstay treatment modalities for neonatal seizures. Studies have revealed these agents control seizures in less than half of neonates, can cause neuronal apoptosis in vitro, and have highly variable pharmacokinetics in neonates. In contrast, there have been no reports of levetiracetam causing these neurotoxic effects. Due to its favorable side effect and pharmacokinetic profiles and positive efficacy outcomes in neonatal studies to date, there is great interest in the use of levetiracetam for neonatal seizures. This article reviews the literature regarding the safety of levetiracetam in neonates and its efficacy in neonatal seizures.
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Adams, Yvonne, and J. Alexandra Rowe. "The Effect of Anti-Rosetting Agents against Malaria Parasites under Physiological Flow Conditions." PLoS ONE 8, no. 9 (September 16, 2013): e73999. http://dx.doi.org/10.1371/journal.pone.0073999.
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Mozhokina, G. N., A. G. Samoylova, I. A. Vasilyeva, and I. A. Burmistrova. "Specific Manifestations of Neurotoxicity of Some Drug Combinations for Treatment of Drug Resistant Tuberculosis from the Perspective of Experimental Studies." Tuberculosis and Lung Diseases 100, no. 12 (January 12, 2023): 28–32. http://dx.doi.org/10.21292/2075-1230-2022-100-12-28-32.
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The objective: to evaluate comparative neurotoxicity of combinations of anti-tuberculosis and antimicrobial drugs with different and similar toxic potentials assessing behavioral changes in rats.Subjects and Methods: non-linear female rats divided in 3 groups were used in this study. For 14 days, the rats received a daily combinations of drugs: Group 1 – Mxf + Lzd + Cs + Pto, Group 2 – Mxf + Bdq + Cs + Z , and Group 3 – Bdq + Lzd + Cfz + Z. Neurotoxicity was assessed by changes in behavioral responses using Open Field Test. The number of crossed squares and racks was recorded which characterized horizontal and vertical activity, also peeping into burrows (exploratory activity), the number of groomings (washing and scratching) and physiological functions were registered.Results. In rats of Group 1 versus baseline parameters, we observed a significant limitation of horizontal motor activity and a sharp decrease (by 5 times) in exploratory activity, a 2.8-fold decrease in the number of groomings which indicated emotional suppression. In rats of Groups 2 and 3, the decrease in motor and exploratory activity was insignificant but there was a more pronounced emotional depression. The use of the Mxf + Lzd + Cs + Pto combination in which all drugs possessed a neurotoxic potential, led to diverse and profound changes in behavioral responses which indicated a pronounced neurotoxic effect.
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Aulić, Suzana, Maria Laura Bolognesi, and Giuseppe Legname. "Small-Molecule Theranostic Probes: A Promising Future in Neurodegenerative Diseases." International Journal of Cell Biology 2013 (2013): 1–19. http://dx.doi.org/10.1155/2013/150952.
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Prion diseases are fatal neurodegenerative illnesses, which include Creutzfeldt-Jakob disease in humans and scrapie, chronic wasting disease, and bovine spongiform encephalopathy in animals. They are caused by unconventional infectious agents consisting primarily of misfolded, aggregated,β-sheet-rich isoforms, denoted prions, of the physiological cellular prion protein (PrPC). Many lines of evidence suggest that prions (PrPSc) act both as a template for this conversion and as a neurotoxic agent causing neuronal dysfunction and cell death. As such,PrPScmay be considered as both a neuropathological hallmark of the disease and a therapeutic target. Several diagnostic imaging probes have been developed to monitor cerebral amyloid lesions in patients with neurodegenerative disorders (such as Alzheimer’s disease, Parkinson’s disease, and prion disease). Examples of these probes are Congo red, thioflavin T, and their derivatives. We synthesized a series of styryl derivatives, denoted theranostics, and studied their therapeutic and/or diagnostic potentials. Here we review the salient traits of these small molecules that are able to detect and modulate aggregated forms of several proteins involved in protein misfolding diseases. We then highlight the importance of further studies for their practical implications in therapy and diagnostics.
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VONTAS, John G., Graham J. SMALL, and Janet HEMINGWAY. "Glutathione S-transferases as antioxidant defence agents confer pyrethroid resistance in Nilaparvata lugens." Biochemical Journal 357, no. 1 (June 25, 2001): 65–72. http://dx.doi.org/10.1042/bj3570065.
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Selection of a laboratory colony of the brown planthopper Nilaparvata lugens with the pyrethroids permethrin and λ-cyhalothrin increased its resistance to both insecticides. Biochemical analysis and synergistic studies with metabolic inhibitors indicated that elevated glutathione S-transferases (GSTs) with a predominant peroxidase activity conferred resistance to both pyrethroids, whereas esterases conferred part of the resistance to permethrin. Purified esterases hydrolysed permethrin at a slow rate, but incubation of either pyrethroid or their primary metabolites with partially purified GSTs had no effect on the metabolic profile. Although GSTs were sensitive to inhibition by both pyrethroids, they did not serve as binding proteins, as previously hypothesized [Grant and Matsumura (1988) Insect Biochem. 18, 615–622]. We demonstrate that pyrethroids, in addition to their neurotoxic effect, induce oxidative stress and lipid peroxidation in insects. Pyrethroid exposure induced lipid peroxides, protein oxidation and depleted reduced glutathione. Elevated GSTs in the resistant strains attenuated the pyrethroid-induced lipid peroxidation and reduced mortality, whereas their in vivo inhibition eliminated their protective role. We therefore hypothesize that the main role of elevated GSTs in conferring resistance in N. lugens is through protecting tissues from oxidative damage. Our study extends the GSTs' range of efficacy to pyrethroid insecticides and possibly explains the role of elevated GSTs in other pyrethroid-resistant insects.
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Servent, Denis, Sophie Creuzet, Carole Malgorn, Vincent Dive, Armen Zakarian, and Jordi Molgó. "Pinnatoxins, an emergent class of marine toxins interacting with nAChRs. Pharmacological characterization, biodistribution and musculo-skeletal effect of these neurotoxic agents." Toxicon 177 (April 2020): S3. http://dx.doi.org/10.1016/j.toxicon.2019.10.015.
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Ferlazzo, Nadia, Santa Cirmi, Alessandro Maugeri, Caterina Russo, Giovanni Enrico Lombardo, Sebastiano Gangemi, Gioacchino Calapai, Vincenzo Mollace, and Michele Navarra. "Neuroprotective Effect of Bergamot Juice in 6-OHDA-Induced SH-SY5Y Cell Death, an In Vitro Model of Parkinson’s Disease." Pharmaceutics 12, no. 4 (April 5, 2020): 326. http://dx.doi.org/10.3390/pharmaceutics12040326.
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Much evidence suggests that both oxidative stress and apoptosis play a key role in the pathogenesis of Parkinson’s disease (PD). The present study aims to evaluate the protective effect of bergamot juice (BJ) against 6-hydroxydopamine (6-OHDA)- or H2O2-induced cell death. Treatment of differentiated SH-SY5Y human neuroblastoma cells with 6-OHDA or H2O2 resulted in cell death that was significantly reduced by the pre-treatment with BJ. The protective effects of BJ seem to correlate with the reduction of intracellular reactive oxygen species and nitric oxide generation caused by 6-OHDA or H2O2. BJ also attenuated mitochondrial dysfunction, caspase-3 activation, imbalance of pro- and anti-apoptotic proteins, MAPKs activation and reduced NF-ĸB nuclear translocation evoked by neurotoxic agents. Additionally, BJ exhibited excellent antioxidant capability in cell-free assays. Collectively, our results suggest that BJ exerts neuroprotective effect through the interplay with specific cell targets and its antioxidant activity, making it worthy of consideration for the management of neurodegenerative diseases.
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Miroshnikov, V. M., A. V. Kokhanov, and A. A. Nyrkin. "Toward an explanation of the clinical effect when using industrial albumin preparations." Kazan medical journal 69, no. 4 (August 15, 1988): 301–2. http://dx.doi.org/10.17816/kazmj99701.
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Currently, in clinical medicine, preparations of donor and placental albumin are widely used, which are highly effective therapeutic agents for many pathological conditions. It is believed that placental albumin by its physico-chemical properties and physiological effect does not differ from donor albumin, but there are good reasons to doubt this statement.
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Greenberg, J., and E. E. Goldschmidt. "Acidifying Agents, Uptake, and Physiological Activity of Gibberellin A3 in Citrus." HortScience 24, no. 5 (October 1989): 791–93. http://dx.doi.org/10.21273/hortsci.24.5.791.
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Abstract Acidification of treatment solutions from pH 7 to 4, with either citrate-phosphate (CP) buffer or with dimethylglutaric acid–NaOH (DMG) buffer, increased [14C]GA3 uptake by ‘Marsh’ grapefruit (Citrus paradisi Macf.) peel. Acidification was effective also when wax was removed with organic solvents and under low and high relative humidity. The GA3-induced delay of coloration of ‘Minneola’ (Citrus paradisi × C. reticulata Blanco) tangelo and ‘Ortanique’ (C. sinensis × C. reticulata) was increased similarly by acidification with either buffer. Acidification with either buffer permitted the use of lower GA3 concentrations than those required to obtain the same physiological effect with neutral solutions. Acidification also delayed fruit senescence in field trials with ‘Clementine’ (Citrus reticulata Blanco) tangerines sprayed with 5 ppm GA3 + 0.1% H3PO4. Uptake of [14C]GA3 progressively increased by reducing pH from 7 to 3. With [3H]GA4, acidification improved the uptake only in the range of pH 8 to 5. This difference seems to be related to the more lipophilic nature of GA4.
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Apolloni, Savina, Paola Fabbrizio, Susanna Amadio, Giulia Napoli, Mattia Freschi, Francesca Sironi, Paolo Pevarello, et al. "Novel P2X7 Antagonist Ameliorates the Early Phase of ALS Disease and Decreases Inflammation and Autophagy in SOD1-G93A Mouse Model." International Journal of Molecular Sciences 22, no. 19 (September 30, 2021): 10649. http://dx.doi.org/10.3390/ijms221910649.
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Amyotrophic lateral sclerosis (ALS) is a disease with a resilient neuroinflammatory component caused by activated microglia and infiltrated immune cells. How to successfully balance neuroprotective versus neurotoxic actions through the use of anti-inflammatory agents is still under debate. There has been a boost of awareness regarding the role of extracellular ATP and purinergic receptors in modulating the physiological and pathological mechanisms in the nervous system. Particularly in ALS, it is known that the purinergic ionotropic P2X7 receptor plays a dual role in disease progression by acting at different cellular and molecular levels. In this context, we previously demonstrated that the P2X7 receptor antagonist, brilliant blue G, reduces neuroinflammation and ameliorates some of the pathological features of ALS in the SOD1-G93A mouse model. Here, we test the novel, noncommercially available, and centrally permeant Axxam proprietary P2X7 antagonist, AXX71, in SOD1-G93A mice, by assessing some behavioral and molecular parameters, among which are disease progression, survival, gliosis, and motor neuron wealth. We demonstrate that AXX71 affects the early symptomatic phase of the disease by reducing microglia-related proinflammatory markers and autophagy without affecting the anti-inflammatory markers or motor neuron survival. Our results suggest that P2X7 modulation can be further investigated as a therapeutic strategy in preclinical studies, and exploited in ALS clinical trials.
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Chiodini, Florence C., Edomer Tassonyi, Thomas Fuchs-Buder, Marc Fathi, Daniel Bertrand, and Dominique Muller. "Effects of Neuromuscular Blocking Agents on Excitatory Transmission and γ-Aminobutyric Acid-A-mediated Inhibition in the Rat Hippocampal Slice." Anesthesiology 88, no. 4 (April 1, 1998): 1003–13. http://dx.doi.org/10.1097/00000542-199804000-00021.
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Background Although neuromuscular blocking agents do not cross the blood-brain barrier, they may penetrate the central nervous system under particular circumstances and eventually cause neurotoxic consequences. Methods The effects of neuromuscular blocking agents on excitatory and inhibitory transmission in area CA1 of rat hippocampal slices were investigated using extracellular and intracellular recording techniques. Results Application of atracurium in the perfusion medium resulted in a dose-dependent enhancement of excitatory synaptic responses averaging 48.7 +/- 4.3% at a concentration of 10 nM. This effect was correlated with an increase in the size of the presynaptic fiber volley. Laudanosine, but not pancuronium bromide or vecuronium bromide, produced similar changes. In addition, atracurium and laudanosine blocked inhibitory transmission and reduced intracellularly recorded gamma-aminobutyric acidA receptor-mediated potentials. These effects were observed only at concentrations >1 microM and were not reproduced by pancuronium bromide and vecuronium bromide. Conclusions Atracurium and its metabolite, laudanosine, contrary to pancuronium bromide and vecuronium bromide, produce two distinct effects on hippocampal slices. They enhance excitatory transmission and neuronal excitability and they block inhibitory gamma-aminobutyric acidA-mediated synaptic responses.
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Tang, Yinshan, Shujun Shao, Yu Guo, You Zhou, Jin Cao, Anping Xu, Jihong Wu, Zhigang Li, and Dulian Xiang. "Electroacupuncture Mitigates Hippocampal Cognitive Impairments by Reducing BACE1 Deposition and Activating PKA in APP/PS1 Double Transgenic Mice." Neural Plasticity 2019 (May 15, 2019): 1–12. http://dx.doi.org/10.1155/2019/2823679.
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Increased amyloid-β (Aβ) plaque deposition is thought to be the main cause of Alzheimer’s disease (AD). β-Site amyloid precursor protein cleaving enzyme 1 (BACE1) is the key protein involved in Aβ peptide generation. Excessive expression of BACE1 might cause overproduction of neurotoxins in the central nervous system. Previous studies indicated that BACE1 initially cleaves the amyloid precursor protein (APP) and may subsequently interfere with physiological functions of proteins such as PKA, which is recognized to be closely associated with long-term potentiation (LTP) level and can effectively ameliorate cognitive impairments. Therefore, revealing the underlying mechanism of BACE1 in the pathogenesis of AD might have a significant impact on the future development of therapeutic agents targeting dementia. This study examined the effects of electroacupuncture (EA) stimulation on BACE1, APP, and p-PKA protein levels in hippocampal tissue samples. Memory and learning abilities were assessed using the Morris water maze test after EA intervention. Immunofluorescence, immunohistochemistry, and western blot were employed to assess the distribution patterns and expression levels of BACE1, APP, and p-PKA, respectively. The results showed the downregulation of BACE1 and APP and the activation of PKA by EA. In summary, EA treatment might reduce BACE1 deposition in APP/PS1 transgenic mice and regulate PKA and its associated substrates, such as LTP to change memory and learning abilities.
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Ogbuehi, H. C. "Effect of nodumax inoculant on morpho-physiological parameters, nutrient content and yield of soybean (Glycine max. L)." Journal of Agriculture and Food Sciences 18, no. 2 (February 24, 2021): 54–72. http://dx.doi.org/10.4314/jafs.v18i2.4.
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The field study was carried out at the Teaching and Research Farm of Faculty of Agriculture and Veterinary Medicine of Imo State University, Owerri, to investigate the effect of Nodumax inoculants on Morpho-Pysiological parameters, Nutrient content and yield of Soybean (Glycine max). The experimental design was Randomized Complete Block Design with five treatments and four replications. Treatments consist of Gum Arabic Slurry, Honey Slurry, Powdered milk Slurry, Sugar Slurry ( as adhesive agents) and control. The results obtained indicated that Nodumax inoculation, with adhesive agents especially Gum Arabic improved the Morpho- Physiological parameters such as plant heights, leaf area, leaf area index, leaf area ratio, Relative Growth Rate (RGR) and Net Assimilation Rate (NAR) and shoot dry weight compare to the control. Inoculation increased soybean grain yield across the various adhesive agents ranging from 909.45kg/ha for non-inoculated control to 1002.99kg/ha for inoculated using Gum Arabic, as sticker agent. Proximate composition of inoculated seeds was significantly (P<0.05) improved compare to the control. However, it was observed that Nodumax inoculation correspond to increase in soybean growth characteristics which subsequently increased the yield and improved the nutritional status of soybean. This study has shown that the type of adhesive for coating of seed during rhizobium inoculation could impact positive change in growth parameters, Nutritional status and yield of soybean.
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Barsoumian, Hampartsoum, Fadi El-Rami, and Alexander M. Abdelnoor. "The effect of five antibacterial agents on the physiological levels of serum nitric oxide in mice." Immunopharmacology and Immunotoxicology 33, no. 4 (March 22, 2011): 652–55. http://dx.doi.org/10.3109/08923973.2011.558095.
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Godha, Sonal. "EFFECT OF ENVIRONMENTAL STRESS ON HUMAN HEALTH." International Journal of Research -GRANTHAALAYAH 3, no. 9SE (September 30, 2015): 1–4. http://dx.doi.org/10.29121/granthaalayah.v3.i9se.2015.3180.
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Over the past three or four decades, there have been important advances in the understanding of the actions, exposure-response characteristics, and mechanisms of action of many common air pollutants. Environmental physiology is the study of the physiological mechanisms that allow animals to cope with and adapt to changes in temperature, humidity, atmospheric pressure, and other natural factors of their physical environment these ideal test conditions are clearly not representative of the fluctuations in the natural environment encountered by humans and other animals on a day-to-day basis. How variations in the natural environment will alter physiological responses to toxicants. Temperature and exercise are the two well-studied parameters in the fields of environmental physiology and toxicology. In general, high temperatures exacerbate the toxic effects of many environmental toxicants. Quantitative and qualitative understanding of the effects of a small group of air pollutants/ toxicants has advanced considerably, but the understanding is by no means complete, and the breadth of effects of all air pollutants is only partially understood. The prospect of global warming also warrants a better assessment of how higher environmental temperatures may impact on the response of humans and other species to toxic chemicals. Hence, this paper focuses on the salient aspects of the interaction between environmental stress and physiological response to toxic agents with particular emphasis on temperature.
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Lee, Jinhyuk, and Mira Jun. "Dual BACE1 and Cholinesterase Inhibitory Effects of Phlorotannins from Ecklonia cava—An In Vitro and in Silico Study." Marine Drugs 17, no. 2 (February 1, 2019): 91. http://dx.doi.org/10.3390/md17020091.
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Alzheimer′s disease (AD) is one of the most common neurodegenerative diseases with a multifactorial nature. β-Secretase (BACE1) and acetylcholinesterase (AChE), which are required for the production of neurotoxic β-amyloid (Aβ) and the promotion of Aβ fibril formation, respectively, are considered as prime therapeutic targets for AD. In our efforts towards the development of potent multi-target, directed agents for AD treatment, major phlorotannins such as eckol, dieckol, and 8,8′-bieckol from Ecklonia cava (E. cava) were evaluated. Based on the in vitro study, all tested compounds showed potent inhibitory effects on BACE1 and AChE. In particular, 8,8′-bieckol demonstrated the best inhibitory effect against BACE1 and AChE, with IC50 values of 1.62 ± 0.14 and 4.59 ± 0.32 µM, respectively. Overall, kinetic studies demonstrated that all the tested compounds acted as dual BACE1 and AChE inhibitors in a non-competitive or competitive fashion, respectively. In silico docking analysis exhibited that the lowest binding energies of all compounds were negative, and specifically different residues of each target enzyme interacted with hydroxyl groups of phlorotannins. The present study suggested that major phlorotannins derived from E. cava possess significant potential as drug candidates for therapeutic agents against AD.
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Sytnikov, D., N. Vorobey, and S. Kots. "Physiological reaction of legume plants to inoculation with algal-rhizobial associations." Acta Agronomica Hungarica 57, no. 2 (June 1, 2009): 239–44. http://dx.doi.org/10.1556/aagr.57.2009.2.15.
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The physiological reaction of legume plants to inoculation with algal-rhizobial associations was studied, based on the nodule bacteria, their Tn5 mutants and the cyanobacterium Nostoc punctiforme . It was shown that binary inoculation with rhizobia and cyanobacteria may have a positive effect if the inoculation agents and their ratio are correctly chosen. The data obtained on the effect of complex bacterization on the development and productivity of plants under legume-rhizobial symbiotic conditions indicate the prospects of bacterial preparations based on cyanobacteria and rhizobia, including their genetically modified strains.
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Engelke, Anna D., Anika Gonsberg, Simrika Thapa, Sebastian Jung, Sarah Ulbrich, Ralf Seidel, Shaon Basu, et al. "Dimerization of the cellular prion protein inhibits propagation of scrapie prions." Journal of Biological Chemistry 293, no. 21 (April 10, 2018): 8020–31. http://dx.doi.org/10.1074/jbc.ra117.000990.
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A central step in the pathogenesis of prion diseases is the conformational transition of the cellular prion protein (PrPC) into the scrapie isoform, denoted PrPSc. Studies in transgenic mice have indicated that this conversion requires a direct interaction between PrPC and PrPSc; however, insights into the underlying mechanisms are still missing. Interestingly, only a subfraction of PrPC is converted in scrapie-infected cells, suggesting that not all PrPC species are suitable substrates for the conversion. On the basis of the observation that PrPC can form homodimers under physiological conditions with the internal hydrophobic domain (HD) serving as a putative dimerization domain, we wondered whether PrP dimerization is involved in the formation of neurotoxic and/or infectious PrP conformers. Here, we analyzed the possible impact on dimerization of pathogenic mutations in the HD that induce a spontaneous neurodegenerative disease in transgenic mice. Similarly to wildtype (WT) PrPC, the neurotoxic variant PrP(AV3) formed homodimers as well as heterodimers with WTPrPC. Notably, forced PrP dimerization via an intermolecular disulfide bond did not interfere with its maturation and intracellular trafficking. Covalently linked PrP dimers were complex glycosylated, GPI-anchored, and sorted to the outer leaflet of the plasma membrane. However, forced PrPC dimerization completely blocked its conversion into PrPSc in chronically scrapie-infected mouse neuroblastoma cells. Moreover, PrPC dimers had a dominant-negative inhibition effect on the conversion of monomeric PrPC. Our findings suggest that PrPC monomers are the major substrates for PrPSc propagation and that it may be possible to halt prion formation by stabilizing PrPC dimers.
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Merlino, John, and Jon Iredell. "Molecular science of antimicrobial resistance." Microbiology Australia 28, no. 4 (2007): 160. http://dx.doi.org/10.1071/ma07160.
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The study of bacterial resistance to antimicrobial agents is a complex science that requires an understanding of the genetic, molecular and physiological mechanisms of resistance, and the effect of antibiotic selection pressures on bacterial populations in different environments.
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Jadhav, Shrinivas S., and David M. "EFFECT OF FLUBENDIAMIDE ON MORPHOLOGY, AVOIDANCE BEHAVIOUR AND ACETYLCHOLINESTERASE ACTIVITY IN EARTHWORM EUDRILUS EUGENIAE." International Journal of Pharmacy and Pharmaceutical Sciences 9, no. 9 (July 22, 2017): 233. http://dx.doi.org/10.22159/ijpps.2017v9i9.20684.
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Objective: Flubendiamide is extensively used in agriculture practices as foliar application pesticide. Due to long persistency in the soil, flubendiamide pose serious health concern in non-target organisms. Our main objective was to examine flubendiamide impact on burrowing animal Eudrilus eugeniae with special emphasis on avoidance behaviour and neurotoxicity.Methods: Acute toxicity study of flubendiamide (Diamide pesticide) was conducted on earthworm, Eudrilus eugeniae through direct paper contact method and artificial soil method. Median lethal concentration (LC50) of flubendiamide was calculated by following probit analysis. The neurotoxic potential of flubendiamide was studied with marker enzyme Acetyl cholinesterase (AChE) levels in both In vivo and In vitro experiments.Results: LC50 in earthworms was found to be 94.4 µg cm-2 at 48h paper contact test and 332.21 mg kg-1and 238.31 mg kg-1 respectively at 7 and 14 d artificial soil exposure. Morphological and physiological alterations in earthworms attribute to inhibition of AChE levels. The kinetic study of AChE activity in presence and absence of inhibitor suggests the enzyme reaction is competitive in nature.Conclusion: Present study establishes concentration-dependent flubendiamide toxicity in earthworm E. eugeniae. No clear conclusive remarks were made on earthworm avoidance behaviour as the worms were located both in toxic and control soil after 48h of exposure. Further studies may be needed in this aspect to establish clear understanding on avoidance nature of E. eugeniae in different soil types.
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Packham, M. A., N. L. Bryant, M. A. Guccione, R. L. Kinlough-Rathbone, and J. F. Mustard. "Effect of the Concentration of Ca2+ in the Suspending Medium on the Responses of Human and Rabbit Platelets to Aggregating Agents." Thrombosis and Haemostasis 62, no. 03 (1989): 968–76. http://dx.doi.org/10.1055/s-0038-1651037.
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SummaryThe effect of the concentration of Ca2+ in the suspending medium of human and rabbit platelets on aggregation, release of 14C-serotonin, and TXB2 formation in response to ADP, thrombin, l-0-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine (PAF), collagen and arachidonic acid was studied in either platelet-rich plasma anticoagulated with D-phenylalanyl-prolyl-arginyl chloromethylketone (PPACK) or citrate, or suspensions of washed platelets in modified Tyrode-albumin solutions containing 1 mM Mg2+ and concentrations of added Ca2+ ranging from 0 to 5 mM. In response to ADP, thrombin, or PAF, human platelets were stimulated to form TXA2 by close platelet contact in a low- Ca2+ medium; at physiological concentrations of Ca2+, TXB 2formation was much less and declined progressively as the concentration of Ca2+ was raised. When the formation of TXA 2was blocked with aspirin or indomethacin, aggregation and release by human platelets were strongest at physiological concentrations of Ca2+. Rabbit platelet responses differed markedly from those of human platelets because close contact of rabbit platelets in a low-Ca2+ medium did not promote TXA2 formation. Rabbit platelet responses were more strongly inhibited by the lack of added Ca2+ in the medium than the responses of human platelets, possibly because rabbit platelets do not contain releasable Ca2+.In all studies of human platelets in media with low concentrations of Ca2+, the additional contribution to platelet responses of TXA2 formed because of close platelet contact should be considered because TXA2 formation is not usually stimulated in this way at physiological concentrations of Ca2+. When TXA2 formation is blocked, aggregation and release responses to all agonists are greatest at physiological concentrations of Ca2+. Thus, the responses of human platelets in media with low concentrations of Ca2+ (citrated platelet-rich plasma or artificial media to which no Ca2+ has been added) are abnormal in at least two ways, and do not correspond to the responses at physiological concentrations of Ca2+.
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Forsby, Anna, and Bas Blaauboer. "Integration of in vitro neurotoxicity data with biokinetic modelling for the estimation of in vivo neurotoxicity." Human & Experimental Toxicology 26, no. 4 (April 2007): 333–38. http://dx.doi.org/10.1177/0960327106072994.
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Risk assessment of neurotoxicity is mainly based on in vivo exposure, followed by tests on behaviour, physiology and pathology. In this study, an attempt to estimate lowest observed neurotoxic doses after single or repeated dose exposure was performed. Differentiated human neuroblastoma SH-SY5Y cells were exposed to acrylamide, lindane, parathion, paraoxon, phenytoin, diazepam or caffeine for 72 hours. The effects on protein synthesis and intracellular free Ca2+concentration were studied as physiological endpoints. Voltage operated Ca2 +channel function, acetylcholine receptor function and neurite degenerative effects were investigated as neurospecific endpoints for excitability, cholinergic signal transduction and axonopathy, respectively. The general cytotoxicity, determined as the total cellular protein levels after the 72 hours exposure period, was used for comparison to the specific endpoints and for estimation of acute lethality. The lowest concentration that induced 20% effect (EC 20) obtained for each compound, was used as a surrogate for the lowest neurotoxic level (LOEL) at the target site in vivo. The LOELs were integrated with data on adsorption, distribution, metabolism and excretion of the compounds in physiologically-based biokinetic (PBBK) models of the rat and the lowest observed effective doses (LOEDs) were estimated for the test compounds. A good correlation was observed between the estimated LOEDs and experimental LOEDs found in literature for rat for all test compounds, except for diazepam. However, when using in vitro data from the literature on diazepam's effect on gamma-amino butyric acid (GABA)A receptor function for the estimation of LOED, the correlation between the estimated and experimental LOEDs was improved from a 10 000-fold to a 10-fold difference. Our results indicate that it is possible to estimate LOEDs by integrating in vitro toxicity data as surrogates for lowest observed target tissue levels with PBBK models, provided that some knowledge about toxic mechanisms is known. Human & Experimental Toxicology (2007) 26, 333—338
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Khodanovich, Marina, Anna Zelenskaya, Elizaveta Gul, Dmitry Sukhanov, and Elena Krutenkova. "Reduction of Locomotor and Brain Activity of Wistar Rats after Serial Administration of Titanium Dioxide." Advanced Materials Research 1085 (February 2015): 400–405. http://dx.doi.org/10.4028/www.scientific.net/amr.1085.400.
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Nanoparticles of titanium dioxide (TiO2) are widely used nanomaterial with particle size below 100 nanometers TiO2 is applied as a pigment to provide whiteness to such products as paints, paper, foodstuffs, medicines, toothpastes, etc. However, neurotropic properties of titanium dioxide remains unclear. This work aimed evaluation of neurotoxic effects of titanium dioxide nanoparticles (12 nm particle size) serially administered to Wistar rats in dose of 250 mg/kg for 7 days. Behavioral and physiological observations were registered immediately after treatment. Results showed that nanoTiO2 particles caused reducing of general motor activity in rats and a shift of the electroencephalogram (EEG) power toward low frequencies of (EEG), while aggressive behavior, and open field behavior did not change. The depressive effect of titanium dioxide nanoparticles on the central nervous system (CNS) observed in our study might be related to neuronal damage caused by an increase in reactive oxygen species (ROS) as well as the impairment of synaptic transmission.
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Ferris, Mark J., Charles F. Mactutus, and Rosemarie M. Booze. "Neurotoxic profiles of HIV, psychostimulant drugs of abuse, and their concerted effect on the brain: Current status of dopamine system vulnerability in NeuroAIDS." Neuroscience & Biobehavioral Reviews 32, no. 5 (July 2008): 883–909. http://dx.doi.org/10.1016/j.neubiorev.2008.01.004.
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Serafini, Mauro, Ilaria Peluso, and Anna Raguzzini. "Flavonoids as anti-inflammatory agents." Proceedings of the Nutrition Society 69, no. 3 (June 23, 2010): 273–78. http://dx.doi.org/10.1017/s002966511000162x.
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Epidemiological evidence suggests that a high intake of plant foods is associated with lower risk of chronic diseases. However, the mechanism of action and the components involved in this effect have not been identified clearly. In recent years, the scientific community has agreed to focus its attention on a class of secondary metabolites extensively present in a wide range of plant foods: the flavonoids, suggested as having different biological roles. The anti-inflammatory actions of flavonoids in vitro or in cellular models involve the inhibition of the synthesis and activities of different pro-inflammatory mediators such as eicosanoids, cytokines, adhesion molecules and C-reactive protein. Molecular activities of flavonoids include inhibition of transcription factors such as NF-κB and activating protein-1 (AP-1), as well as activation of nuclear factor-erythroid 2-related factor 2 (Nrf2). However, the in vitro evidence might be somehow of limited impact due to the non-physiological concentrations utilized and to the fact that in vivo flavonoids are extensively metabolized to molecules with different chemical structures and activities compared with the ones originally present in the food. Human studies investigating the effect of flavonoids on markers of inflammation are insufficient, and are mainly focused on flavonoid-rich foods but not on pure molecules. Most of the studies lack assessment of flavonoid absorption or fail to associate an effect on inflammation with a change in circulating levels of flavonoids. Human trials with appropriate placebo and pure flavonoid molecules are needed to clarify if flavonoids represent ancillary ingredients or key molecules involved in the anti-inflammatory properties of plant foods.
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Miwa, M., and K. Morizane. "Effect of Chelating Agents on the Growth of Blue-Green Algae and the Release of Geosmin." Water Science and Technology 20, no. 8-9 (August 1, 1988): 197–203. http://dx.doi.org/10.2166/wst.1988.0243.
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The effect of chelating agents on the growth of Anabaenamacrospora, a planktonic blue-green algae, and on its production of geosmin was studied. When A.macrospora was cultured in CT medium containing EDTA (an artificial chelator), the maximum cell numbers were about 1×106 cells/ml. However, in an EDTA-free CT medium, the maximum cell numbers were a tenth of the normal growth level in the complete medium. In addition the chlorophyll-a content was reduced almost a fourth and the color of the algal cell bodies changed from green to yellow. These results showed that growth of this alga in a chelator-free medium was not healthy. At this time, though the geosmin content was constant and in the same range of 1.0-4.0×10−5 ng/cell as in the complete medium, the ratio of the extracellular geosmin concentration in the medium to the gross concentration was 2:10 to 3:10 and 2 to 3 times its normal level. It was considered that the deterioration of alga's physiological condition increased the release of geosmin to the medium. These results suggested that the extracellular concentration of geosmin produced by A.macrospora was affected by the alga's physiological condition. Finally EDTA can be substituted by humic acid. When this alga was grown in a medium containing humic acid instead of EDTA, the maximum cell numbers and the release ratio of geosmin was of the same level as in the case of the complete medium.
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Kadyseva, Oksana V., Vladimir N. Bykov, Olga Y. Strelova, and Alexander N. Grebenyuk. "STUDY OF THE EFFECT OF THE PHYSICOCHEMICAL PROPERTIES OF CHITOSAN ON ITS HAEMOSTATIC ACTIVITY." Progress on Chemistry and Application of Chitin and its Derivatives 26 (September 30, 2021): 112–20. http://dx.doi.org/10.15259/pcacd.26.010.
Full textAbstract:
Chitosan are biopolymers that are actively used for the production of local haemostatic agents. The physicochemical characteristics that determine its biological properties include the molecular weight and the deacetylation degree. However, there is no linear relationship between these parameters and haemostatic activity. The most reliable method of confirming the effectiveness is still in vivo experiments. The ability to initiate haemostasis depends on the conformational transition of chitosan macromolecules. The highest efficiency in vitro was for samples in which the transition of a significant part of the molecules from the ‘rigid rod’ state to the ‘globule’ occurred at physiological pH. It is proposed to expand the list of indicators of chitosan that can be controlled to evaluate the quality of raw materials, related to haemostatic activity, to include the definition of the conformational transition at physiological pH.
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Sahyoun, Christina, Wojciech Krezel, César Mattei, Jean-Marc Sabatier, Christian Legros, Ziad Fajloun, and Mohamad Rima. "Neuro- and Cardiovascular Activities of Montivipera bornmuelleri Snake Venom." Biology 11, no. 6 (June 9, 2022): 888. http://dx.doi.org/10.3390/biology11060888.
Full textAbstract:
The complications following snake bite envenoming are due to the venom’s biological activities, which can act on different systems of the prey. These activities arise from the fact that snake venoms are rich in bioactive molecules, which are also of interest for designing drugs. The venom of Montivipera bornmuelleri, known as the Lebanon viper, has been shown to exert antibacterial, anticancer, and immunomodulatory effects. However, the venom’s activity on the nervous system has not yet been studied, and its effect on the cardiovascular system needs further investigation. Because zebrafish is a convenient model to study tissue alterations induced by toxic agents, we challenged it with the venom of Montivipera bornmuelleri. We show that this venom leads to developmental toxicity but not teratogenicity in zebrafish embryos. The venom also induces neurotoxic effects and disrupts the zebrafish cardiovascular system, leading to heartbeat rate reduction and hemorrhage. Our findings demonstrate the potential neurotoxicity and cardiotoxicity of M. bornmuelleri’s venom, suggesting a multitarget strategy during envenomation.
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Grasso, Chiara, Vanessa Marchesini, and Nicola Disma. "Applications and Limitations of Neuro-Monitoring in Paediatric Anaesthesia and Intravenous Anaesthesia: A Narrative Review." Journal of Clinical Medicine 10, no. 12 (June 15, 2021): 2639. http://dx.doi.org/10.3390/jcm10122639.
Full textAbstract:
Safe management of anaesthesia in children has been one of the top areas of research over the last decade. After the large volume of articles which focused on the putative neurotoxic effect of anaesthetic agents on the developing brain, the attention and research efforts shifted toward prevention and treatment of critical events and the importance of peri-anaesthetic haemodynamic stability to prevent negative neurological outcomes. Safetots.org is an international initiative aiming at raising the attention on the relevance of a high-quality anaesthesia in children undergoing surgical and non-surgical procedures to guarantee a favourable outcome. Children might experience hemodynamic instability for many reasons, and how the range of normality within brain autoregulation is maintained is still unknown. Neuro-monitoring can guide anaesthesia providers in delivering optimal anaesthetic drugs dosages and also correcting underling conditions that can negatively affect the neurological outcome. In particular, it is referred to EEG-based monitoring and monitoring for brain oxygenation.