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Cholinergic Toxicity

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2. Protective effects of voltage-gated calcium channel antagonists against zinc toxicity in SN56 neuroblastoma cholinergic cells. (PubMed)

Protective effects of voltage-gated calcium channel antagonists against zinc toxicity in SN56 neuroblastoma cholinergic cells. One of the pathological site effects in excitotoxic activation is Zn2+ overload to postsynaptic neurons. Such an effect is considered to be equivalent to the glutamate component of excitotoxicity. Excessive uptake of Zn2+ by active voltage-dependent transport systems in these neurons may lead to significant neurotoxicity. The aim of this study was to investigate whether

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2018 PLoS ONE

3. Cholinergic Toxicity

Cholinergic Toxicity Cholinergic Toxicity Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Cholinergic Toxicity Cholinergic Toxicity (...) Aka: Cholinergic Toxicity , Cholinergic Overdose , Cholinergic , Cholinergic Agent , Cholinomimetic , Parasympathomimetic Agent II. Causes III. Findings: Symptoms and Signs (Mnemonic: DUMBELLS or SLUDGe) (and Diaphoresis) and abdominal cramping Urination (pinpoint pupils) (muscarinic) or (nicotinic) ( and ) Lethargy tion IV. Findings: Symptoms and Signs: Other (not covered by mnemonic) Anxiety or s Muscle fasciculations (including respiratory muscles) V. Diagnostics VI. Management See Images

2018 FP Notebook

4. Toxic ingestions in children

with resultant toxicity or risk of toxicity. Agents consumed may be pharmaceutical substances; drugs of abuse (including alcohol); toxic plants, berries, or mushrooms; or chemicals. History and exam medication error in infants witnessed ingestion or child found with empty bottle or pill hx of deliberate ingestion hx of substance abuse sympathomimetic toxidrome antimuscarinic toxidrome opioid toxidrome sedative-hypnotic toxidrome cholinergic toxidrome nausea, vomiting, or diarrhoea altered mental status fever (...) Toxic ingestions in children Toxic ingestions in children - Symptoms, diagnosis and treatment | BMJ Best Practice You'll need a subscription to access all of BMJ Best Practice Search  Toxic ingestions in children Last reviewed: February 2019 Last updated: March 2018 Summary Children may ingest a toxic substance accidentally while exploring their environment, or deliberately in response to stress or underlying mental problems, or in an attempt to get 'high'. A regional poison-control centre

2018 BMJ Best Practice

5. Potentiating a non-neuronal cardiac cholinergic system reinforces the functional integrity of the blood brain barrier associated with systemic anti-inflammatory responses. (PubMed)

integrity in vitro confirmed the consolidation of ChAT tg. ChAT tg were also resistant to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neuronal toxicity due to lower mortality rate and neuronal loss of substantia nigra. Additionally, ChAT tg subjected to MPTP showed attenuated BBB disruption, as evident from reduced sodium fluorescein levels in the brain parenchyma. The activated central cholinergic pathway of ChAT tg lead to anti-convulsive effects like vagus nerve stimulation. However, DSP-4 (...) Potentiating a non-neuronal cardiac cholinergic system reinforces the functional integrity of the blood brain barrier associated with systemic anti-inflammatory responses. We previously reported that the heart-specific choline acetyltransferase (ChAT) gene overexpressing mice (ChAT tg) show specific phenotypes including ischemic tolerance and the CNS stress tolerance. In the current study, we focused on molecular mechanisms responsible for systemic and localized anti-inflammatory phenotypes

2019 Brain, behavior, and immunity

6. Single copy/knock-in models of ALS SOD1 in C. elegans suggest loss and gain of function have different contributions to cholinergic and glutamatergic neurodegeneration (PubMed)

Single copy/knock-in models of ALS SOD1 in C. elegans suggest loss and gain of function have different contributions to cholinergic and glutamatergic neurodegeneration Mutations in Cu/Zn superoxide dismutase 1 (SOD1) lead to Amyotrophic Lateral Sclerosis (ALS), a neurodegenerative disease that disproportionately affects glutamatergic and cholinergic motor neurons. Previous work with SOD1 overexpression models supports a role for SOD1 toxic gain of function in ALS pathogenesis. However (...) yielded single-copy/knock-in ALS SOD1 models. These differ from previously reported overexpression models in multiple assays. In single-copy/knock-in models, we observed differential impact of sod-1 ALS alleles on glutamatergic and cholinergic neurodegeneration. A4V, H71Y, G85R, and G93A animals showed increased SOD1 protein accumulation and oxidative stress induced degeneration, consistent with a toxic gain of function in cholinergic motor neurons. By contrast, H71Y, L84V, and G85R lead

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2018 PLoS genetics

7. Pathological Increases in Neuronal Hyperactivity in Selective Cholinergic and Noradrenergic Pathways May Limit the Efficacy of Amyloid-β-Based Interventions in Mild Cognitive Impairment and Alzheimer’s Disease (PubMed)

of toxic aggregated and soluble Aβ species. Before abandoning both the hypothesis and approach, there is a need to examine some overlooked factors that may have contributed to the lack of efficacy, such as the potential drug-induced increases in neuronal hyperactivity leading to adverse cognitive effects. In particular, we posit that selective cholinergic and noradrenergic pathways will be especially vulnerable to this adverse effect. If confirmed, this idea could help identify a potentially (...) Pathological Increases in Neuronal Hyperactivity in Selective Cholinergic and Noradrenergic Pathways May Limit the Efficacy of Amyloid-β-Based Interventions in Mild Cognitive Impairment and Alzheimer’s Disease In spite of compelling evidence linking amyloid-β (Aβ) disturbances to the pathophysiology of Alzheimer's disease (AD), Aβ-based treatments have consistently failed to produce any beneficial effects both in mild cognitive impairment (MCI) and AD, even with successful reductions

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2018 Journal of Alzheimer's Disease Reports

8. Management of Toxicities from Immunotherapy: ESMO Clinical Practice Guidelines

Management of Toxicities from Immunotherapy: ESMO Clinical Practice Guidelines CLINICAL PRACTICE GUIDELINES Management of toxicities from immunotherapy: ESMO Clinical Practice Guidelines for diagnosis, treatment and follow-up † J. B. A. G. Haanen 1 , F. Carbonnel 2 , C. Robert 3 , K. M. Kerr 4 , S. Peters 5 , J. Larkin 6 & K. Jordan 7 , on behalf of the ESMO Guidelines Committee * 1 Netherlands Cancer Institute, Division of Medical Oncology, Amsterdam, The Netherlands; 2 Department (...) ligand PD-L1 has become standard of care for an increasing number of indications (Table 1). Therefore, an increasing number of patients will be exposed to these drugs with a chance of developing toxicities from these treatments. Depending on the immune checkpoint that is targeted, the incidence of toxicity varies. Toxicities from immune checkpoint inhibitors (ICPis) can be divided into infu- sion reactions and immune-related adverse events (irAEs) or ad- verse events of special interest (AEoSI

2017 European Society for Medical Oncology

9. Neuroprotection of N-benzylcinnamide on scopolamine-induced cholinergic dysfunction in human SH-SY5Y neuroblastoma cells (PubMed)

properties against amyloid-β-induced neuronal toxicity in rat cortical primary cell culture and to improve spatial learning and memory of aged rats through alleviating oxidative stress. We proposed a hypothesis that PT3 has a neuroprotective effect against scopolamine-induced cholinergic dysfunction. PT-3 (125-200 nM) pretreatment was performed in human neuroblastoma SH-SY5Y cell line following scopolamine induction. PT-3 (125-200 nM) inhibited scopolamine (2 mM)-induced generation of reactive oxygen (...) Neuroprotection of N-benzylcinnamide on scopolamine-induced cholinergic dysfunction in human SH-SY5Y neuroblastoma cells Alzheimer's disease, a progressive neurodegenerative disease, affects learning and memory resulting from cholinergic dysfunction. Scopolamine has been employed to induce Alzheimer's disease-like pathology in vivo and in vitro through alteration of cholinergic system. N-benzylcinnamide (PT-3), purified from Piper submultinerve, has been shown to exhibit neuroprotective

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2017 Neural Regeneration Research

10. Effects of Aged Garlic Extract on Cholinergic, Glutamatergic and GABAergic Systems with Regard to Cognitive Impairment in Aβ-Induced Rats (PubMed)

then euthanized to investigate any changes to the cholinergic neurons, vesicular glutamate transporter 1 and 2 proteins (VGLUT1 and VGLUT2), and glutamate decarboxylase (GAD) in the hippocampus. The results showed that AGE significantly improved the working memory and tended to improve the reference memory in cognitively-impaired rats. In addition, AGE significantly ameliorated the loss of cholinergic neurons and increased the VGLUT1 and GAD levels in the hippocampus of rat brains with Aβ-induced toxicity (...) Effects of Aged Garlic Extract on Cholinergic, Glutamatergic and GABAergic Systems with Regard to Cognitive Impairment in Aβ-Induced Rats Alzheimer's disease (AD) has been linked to the degeneration of central cholinergic and glutamatergic transmission, which correlates with progressive memory loss and the accumulation of amyloid-β (Aβ). It has been claimed that aged garlic extract (AGE) has a beneficial effect in preventing neurodegeneration in AD. Therefore, the objective of this study

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2017 Nutrients

11. Cholinergic Mechanisms of Gait Dysfunction in Parkinson's Disease

Cholinergic Mechanisms of Gait Dysfunction in Parkinson's Disease Cholinergic Mechanisms of Gait Dysfunction in Parkinson's Disease - Proj#3 - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. Cholinergic (...) Assignment Masking: Triple (Participant, Care Provider, Investigator) Primary Purpose: Treatment Official Title: Cholinergic Mechanisms of Gait Dysfunction in Parkinson's Disease - Proj#3 Study Start Date : February 2015 Estimated Primary Completion Date : January 2020 Estimated Study Completion Date : April 2020 Resource links provided by the National Library of Medicine related topics: related topics: available for: Arms and Interventions Go to Arm Intervention/treatment Experimental: Measuring Brain

2016 Clinical Trials

12. Treatment of beta amyloid 1–42 (Aβ1–42)-induced basal forebrain cholinergic damage by a non-classical estrogen signaling activator in vivo (PubMed)

Treatment of beta amyloid 1–42 (Aβ1–42)-induced basal forebrain cholinergic damage by a non-classical estrogen signaling activator in vivo In Alzheimer's disease (AD), there is a loss in cholinergic innervation targets of basal forebrain which has been implicated in substantial cognitive decline. Amyloid beta peptide (Aβ(1-42)) accumulates in AD that is highly toxic for basal forebrain cholinergic (BFC) neurons. Although the gonadal steroid estradiol is neuroprotective, the administration (...) is associated with risk of off-target effects. Previous findings suggested that non-classical estradiol action on intracellular signaling pathways has ameliorative potential without estrogenic side effects. After Aβ(1-42) injection into mouse basal forebrain, a single dose of 4-estren-3α, 17β-diol (estren), the non-classical estradiol pathway activator, restored loss of cholinergic cortical projections and also attenuated the Aβ(1-42)-induced learning deficits. Estren rapidly and directly phosphorylates c

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2016 Scientific reports

13. An In Vivo Pharmacological Screen Identifies Cholinergic Signaling as a Therapeutic Target in Glial-Based Nervous System Disease (PubMed)

, including many FDA-approved drugs and natural products. We identify four compounds capable of dose-dependent inhibition of nervous system toxicity. Focusing on one of these hits, glycopyrrolate, we confirm the role for muscarinic cholinergic signaling in pathogenesis using additional pharmacologic reagents and genetic approaches. We further demonstrate that muscarinic cholinergic signaling works through downstream Gαq to control oxidative stress and death of neurons and glia. Importantly, we document (...) An In Vivo Pharmacological Screen Identifies Cholinergic Signaling as a Therapeutic Target in Glial-Based Nervous System Disease The role that glia play in neurological disease is poorly understood but increasingly acknowledged to be critical in a diverse group of disorders. Here we use a simple genetic model of Alexander disease, a progressive and severe human degenerative nervous system disease caused by a primary astroglial abnormality, to perform an in vivo screen of 1987 compounds

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2016 The Journal of Neuroscience

14. The Role of Nicotine Dose and Route of Delivery in Affecting Adoption of E-cigarettes and Reducing Exposure to Toxic Combustion Products

The Role of Nicotine Dose and Route of Delivery in Affecting Adoption of E-cigarettes and Reducing Exposure to Toxic Combustion Products The Role of Nicotine Dose and Route of Delivery in Affecting Adoption of E-cigarettes and Reducing Exposure to Toxic Combustion Products - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study (...) Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. The Role of Nicotine Dose and Route of Delivery in Affecting Adoption of E-cigarettes and Reducing Exposure to Toxic Combustion Products (ENDS-Switch) The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. of clinical studies and talk to your

2018 Clinical Trials

15. Cholinergic Toxicity

Cholinergic Toxicity Cholinergic Toxicity Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Cholinergic Toxicity Cholinergic Toxicity (...) Aka: Cholinergic Toxicity , Cholinergic Overdose , Cholinergic , Cholinergic Agent , Cholinomimetic , Parasympathomimetic Agent II. Causes III. Findings: Symptoms and Signs (Mnemonic: DUMBELLS or SLUDGe) (and Diaphoresis) and abdominal cramping Urination (pinpoint pupils) (muscarinic) or (nicotinic) ( and ) Lethargy tion IV. Findings: Symptoms and Signs: Other (not covered by mnemonic) Anxiety or s Muscle fasciculations (including respiratory muscles) V. Diagnostics VI. Management See Images

2015 FP Notebook

16. Gelidiella acerosa protects against Aβ 25–35-induced toxicity and memory impairment in Swiss Albino mice: an in vivo report (PubMed)

Gelidiella acerosa protects against Aβ 25–35-induced toxicity and memory impairment in Swiss Albino mice: an in vivo report Alzheimer's disease (AD) is believed to develop due to deposition of β-amyloid (Aβ) peptide. Hence, efforts are being made to develop potent drug that target amyloid hypothesis.The present study explores the effect of the seaweed Gelidiella acerosa (Forsskål) Feldmann & Hamel (Gelidiellaceae) against Aβ 25-35 peptide in Swiss albino mice.The animals were administered (...) and protein oxidation significantly (p < 0.05). The extract protected the mice from cholinergic deficit significantly (p < 0.05) by inhibiting the activities of AChE and BuChE, which was about 0.116 ± 0.0088 U/mg of protein and 0.011 ± 0.0014 U/mg of protein respectively, which was otherwise increased in peptide-treated group (0.155 ± 0.007 U/mg of protein and 0.015 ± 0.0012 U/mg of protein respectively). Interestingly, G. acerosa benzene extract inhibited β-secretase and MAO-B activity. Reduction (p

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2017 Pharmaceutical biology

17. Distribution of uridine diphosphate glucuronosyltransferase 1A polymorphisms and their role in irinotecan-induced toxicity in patients with cancer (PubMed)

(1,601, 76.5%), TA6/TA7 (463, 22.1%) and TA7/TA7 (29, 1.4%) for UGT1A1*28 (n=2,093); and G/G (286, 66.4%), G/A (124, 28.8%) and A/A (21, 4.9%) for UGT1A1*6 (n=431). The most frequent severe hematological toxicity was neutropenia, and the predominant non-hematological toxicities were diarrhea and cholinergic syndrome. In toxicity comparisons, grade 3-4 leukopenia and neutropenia were significantly higher in TA6/TA7 compared with TA6/TA6 (P<0.05). The UGT1A1*6 polymorphism was associated with a higher (...) Distribution of uridine diphosphate glucuronosyltransferase 1A polymorphisms and their role in irinotecan-induced toxicity in patients with cancer Uridine diphosphate glucuronosyltransferase 1A (UGT1A1), which affects irinotecan metabolism, has been associated with severe adverse reactions in patients with cancer treated with irinotecan. However, neither large-scale analysis of the distribution of UGT1A1 polymorphisms, nor standardized assessment of how UGT1A1 polymorphisms affect irinotecan

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2017 Oncology letters

18. Zebrafish is a predictive model for identifying compounds that protect against brain toxicity in severe acute organophosphorus intoxication (PubMed)

Zebrafish is a predictive model for identifying compounds that protect against brain toxicity in severe acute organophosphorus intoxication Acute organophosphorus (OP) intoxication is a worldwide clinical and public health problem. In addition to cholinergic crisis, neurodegeneration and brain damage are hallmarks of the severe form of this toxidrome. Recently, we generated a chemical model of severe acute OP intoxication in zebrafish that is characterized by altered head morphology and brain (...) degeneration. The pathophysiological pathways resulting in brain toxicity in this model are similar to those described in humans. The aim of this study was to assess the predictive power of this zebrafish model by testing the effect of a panel of drugs that provide protection in mammalian models. The selected drugs included "standard therapy" drugs (atropine and pralidoxime), reversible acetylcholinesterase inhibitors (huperzine A, galantamine, physostigmine and pyridostigmine), N-methyl-D-aspartate (NMDA

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2016 Archives of toxicology

19. Solifenacin Succinate for Treatment of Urinary Toxicity Occurring During Radiotherapy of Prostatic Cancer

Solifenacin Succinate for Treatment of Urinary Toxicity Occurring During Radiotherapy of Prostatic Cancer Solifenacin Succinate for Treatment of Urinary Toxicity Occurring During Radiotherapy of Prostatic Cancer - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100 (...) ). Please remove one or more studies before adding more. Solifenacin Succinate for Treatment of Urinary Toxicity Occurring During Radiotherapy of Prostatic Cancer (VesiCaP) The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our for details. ClinicalTrials.gov Identifier: NCT02805452 Recruitment Status : Terminated (Target of recruitment not reachable) First

2016 Clinical Trials

20. Anticholinergic Toxicity

Anticholinergic Toxicity Anticholinergic Toxicity Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Anticholinergic Toxicity (...) Anticholinergic Toxicity Aka: Anticholinergic Toxicity , Anticholinergic Poisoning , Anticholinergic Symptoms , Anticholinergic , Anticholinergic Syndrome , Anticholinergic Reaction II. Causes See s s s s: BZ Ingested items Jimsonweed Amanita muscaria mushrooms Parasympatholytic medications Scopolamine III. Symptoms: Mnemonic (antimuscarinic) Hot as a hare (Hyperthermia) Dry as a bone ( ) Red as a beet (Flushed) Blind as bat ( ) Mad as a hatter ( ) IV. Symptoms: Complete List (antimuscarinic) Speech may

2018 FP Notebook

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