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Alzheimer’s disease is a neurodegenerative dementia characterized by the presence of neurofibrillary tangles and senile plaques in the brain.
The intraneuronale neurofibrillary tangles are composed of paired helical filaments (PHF) containing the microtubule associated protein TAU.
Senile plaques are extracellular lesions containing an amyloid core surrounded by dystrophic neuritis and glial cells. The major constituent of the amyloid core is a 39-43 amino acid peptide, Aβ, which is derived from a transmembrane protein, the amyloid precursor protein (APP).
In this work, we have analyzed the effects induced by the expression of different forms of human APP in rat cultured neurons.
The adenoviral expression of APP695 in rat cortical neurons induces neurotoxicity. Neuronal death is not triggered by soluble APP or extracellular Aβ.
Expression of the C-terminal fragment of APP, or APP deleted in its C-terminal domain in neurotoxic. Those different APP isoforms accumulate similar levels of intraneuronale Aβ. Treatment of neurons with a specific γ-secretase inhibitor decreases intracellular Aβ accumulation and allows recovery of neuronal survival. These results demonstrate that intraneuronale Aβ accumulation is responsible for the neurotoxicity observed in our model.
To better characterize the observed neurotoxicity, we measured the activity of caspase 3, a maker of apoptosis. Expression of APP in neurons induces caspase 3 activity as compared to untreated neurons. This suggests that intraneuronale Aβ accumulation activated caspase 3.
Surprisingly, treatment of neurons expressing human APP695 with a specific caspase 3 inhibitor has not effect on neuronal survival. Therefore, caspase 3 doesn’t seem to be the only effector responsible for neuronal death observed in our model La maladie d’Alzheimer est une démence dégénérative caractérisée par la présence, dans le tissus cérébral, de deux types de lésions : les dégénérescences neurofibrillaires et les plaques séniles.
Les dégénérescences neurofibrillaires intraneuronales sont composées de paires hélicoïdales de filaments (PHF) dont le constituant majeur est une protéine associée aux microtubes : la protéine TAU.
Les plaques séniles sont des lésions extracellulaires constituées d’un noyau de fibres amyloïdes entouré de neurites dystrophiques et de cellules gliales. Le constituant majeur du noyau amyloïde est un peptide de 39 à 42 acides aminés appelé peptide amyloïde β ou Aβ. Il résulte d’un clivage protéolytique d’un précurseur transmembranaire : le précurseur du peptide amyloïde (APP). Ce peptide Aβ s’accumule également dans les neurones de patients atteints de la maladie d’Alzheimer.
Au cours de ce travail, nous avons analysés, les effets induits par l’expression de l’APP humain dans des neurones de rat en culture.
L’expression d’APP humain des neurones corticaux de rat à l’aide d’adénovirus provoque une neurotoxicité importante. La production d’Aβ-40 et d’APP soluble extracellulaires ne sont pas responsables de la mort neuronale observée.
L’expression du fragment C-terminal de l’APP (C99) ou encore de l’APP délaité de son domaine C-terminal intracellulaire induisent une neurotoxicité comparable à celle de l’APP. L’expression de ces trois formes d’APP provoque l’accumulation intraneuronale par un inhibiteur spécifique de la γ-sécrétase (DAPT) diminue la production d’Aβ1-42 intracellulaire et restaure la survie neuronale. Ces résultats indiquent que l’accumulation intraneuronale d’Aβ1-42 est responsable de la neurotoxicité observée dans notre modèle.
Afin de mieux caractériser cette neurotoxicité, nous avons mesuré l’activité d’un effecteur de l’apoptose, la caspase 3. L’expression de l’APP humain induit de manière importante l’activité de la caspase 3. Les neurones traités par la DAPT présentent une activité de la caspase 3 réduite par rapport à celle des neurones non-traités. Ceci suggère que l’accumulation d’Aβ1-42 intracellulaire active la caspase 3.
Cependant, le traitement des neurones exprimant l’APP humain avec un inhibiteur spécifique de la caspase 3 (Z-DEVD-FMK) n’exerce aucun effet sur la survie neuronale. La caspase 3 ne semble donc pas être un effecteur majeur de la neurotoxicité observée dans notre modèle

Neurotoxicity Syndromes --- Amyloid beta-Peptides --- Blotting, Western --- Enzyme-Linked Immunosorbent Assay

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Nervous System --- Behavior --- Neurotoxicity Syndromes --- Food --- Environmental Pollutants --- Behavioral toxicology --- Neurotoxic agents --- drug effects --- toxicity --- Nervous System - drug effects --- Behavior - drug effects --- Food - toxicity --- Environmental Pollutants - toxicity --- NERVOUS SYSTEM --- FOOD --- ENVIRONMENTAL POLLUTANTS --- BEHAVIOR --- DRUG EFFECTS --- TOXICITY

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Mercury, arsenic, antimony, lead, and thallium can be lethal, as many a poisoner knew too well. Emsley explores the gruesome history of these elements and those who have succumbed to them in a fascinating narrative that weaves together stories of true crime, enduring historical mysteries, tragic accidents, and the science behind it all. The colourful cast includes ancient alchemists, kings, leaders, a pope, several great musicians, and a motley crew of murderers. Among the intriguing accounts is that of the 17th century poet Sir Thomas Overbury, who survived four attempts to poison him with mercury but died when given the poison in enema form - under whose direction remains uncertain. Here, too, is detailed the celebrated case of Florence Maybrick, convicted of poisoning her violent husband James with arsenic, but widely believed at the time to be innocent. The question of her guilt is still disputed.

toxines --- popularisering wetenschap --- Criminology. Victimology --- wetenschapsgeschiedenis --- Toxicology --- Heavy Metal Poisoning, Nervous System --- Specialty Uses of Chemicals --- Neurotoxicity Syndromes --- Arsenic Poisoning --- Metals, Heavy --- Toxicology & Public Health --- Poisonous chemicals --- Poisonous substances --- Toxic chemicals --- Toxic substances --- Toxicants --- Toxics --- Poisoning. --- Poisons. --- Toxicology. --- Chemicals --- Medicine --- Pharmacology --- Poisoning --- Poisons --- Bioactive compounds --- Hazardous substances --- Toxicological emergencies --- Therapeutic use. --- History.

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This book evaluates the effects of arsine to human health. The information presented focuses on effects associated with short-term exposure to arsine. Arsine is a colourless non-irritating gas with a mild garlic-like odour. Arsine is extensively used in the semiconductor. The acute toxicity of arsine in different species including humans is high. The target organ of arsine poisoning is the haematopoietic system in particular the erythrocytes.

Air --Analysis. --- Arsenic compounds -- Health aspects. --- Arsenic compounds -- Toxicology. --- Risk Management --- Inorganic Chemicals --- Risk --- Organometallic Compounds --- Poisoning --- Environmental Pollution --- Heavy Metal Poisoning, Nervous System --- Epidemiologic Measurements --- Risk Assessment --- Environmental Exposure --- Arsenicals --- Arsenic Poisoning --- Chemicals and Drugs --- Organic Chemicals --- Probability --- Substance-Related Disorders --- Public Health --- Organization and Administration --- Neurotoxicity Syndromes --- Health Services Administration --- Nervous System Diseases --- Statistics as Topic --- Environment and Public Health --- Disease. --- Epidemiologic Methods --- Delivery of Health Care. --- Health Care Evaluation Mechanisms --- Investigative Techniques --- Quality of Health Care --- Analytical, Diagnostic and Therapeutic Techniques and Equipment --- Health Care Quality, Access, and Evaluation

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Malalties del sistema nerviós --- Quimioteràpia --- Farmacoteràpia --- Immunoquimioteràpia --- Terapèutica medicamentosa --- Terapèutica per agents químics (Medicina) --- Tractament amb medicaments --- Tractament per agents químics (Medicina) --- Us terapèutic dels medicaments --- Terapèutica --- Administració de medicaments --- Antibiòtics --- Diürètics --- Fotoquimioteràpia --- Pirogens --- Psicofarmacologia --- Prescripció de medicaments --- Quimioteràpia del càncer --- Utilització de medicaments --- Farmacologia --- Medicaments --- Malalties dels nervis --- Neuropatia --- Neuropatologia --- Trastorns del sistema nerviós --- Malalties --- Convulsions --- Infermeria neurològica --- Malalties del sistema nerviós autònom --- Malalties del sistema nerviós central --- Malalties neurodegeneratives --- Malalties neuromusculars --- Manifestacions neurològiques de les malalties --- Neurologia veterinària --- Neuropaties perifèriques --- Trastorns de la comunicació --- Trastorns de la percepció --- Trastorns motors --- Malformacions del sistema nerviós --- Nerves, Peripheral --- Drugs --- Diseases. --- Side effects. --- Adverse drug reactions --- Adverse reactions to drug therapy --- Chemotherapy --- Drug-induced disease --- Drug side effects --- Side effects of drugs --- Iatrogenic diseases --- Drug interactions --- Peripheral neuropathies --- Complications --- Adverse reactions --- Physiological effect --- Drug-Related Side Effects and Adverse Reactions. --- Peripheral Nervous System Diseases. --- Neurotoxicity Syndromes --- Antineoplastic Agents --- adverse effects. --- Adverse Drug Event --- Adverse Drug Reaction --- Drug Side Effects --- Drug Toxicity --- Side Effects of Drugs --- Toxicity, Drug --- Adverse Drug Events --- Adverse Drug Reactions --- Drug Event, Adverse --- Drug Events, Adverse --- Drug Reaction, Adverse --- Drug Reactions, Adverse --- Drug Related Side Effects and Adverse Reactions --- Drug Side Effect --- Drug Toxicities --- Effects, Drug Side --- Reactions, Adverse Drug --- Side Effect, Drug --- Side Effects, Drug --- Toxicities, Drug --- Drug Therapy --- Pharmaceutical Preparations --- Contraindications, Drug --- Drug Interactions --- Clinical Trials, Phase IV as Topic --- Encephalopathy, Toxic --- Nervous System Poisoning --- Neurotoxic Disorders --- Neurotoxin Diseases --- Neurotoxin Disorders --- Toxic Encephalitis --- Poisoning, Nervous System --- Encephalitides, Toxic --- Encephalitis, Toxic --- Encephalopathies, Toxic --- Nervous System Poisonings --- Neurotoxic Disorder --- Neurotoxicity Syndrome --- Neurotoxin Disease --- Neurotoxin Disorder --- Poisonings, Nervous System --- Syndrome, Neurotoxicity --- Syndromes, Neurotoxicity --- Toxic Encephalitides --- Toxic Encephalopathies --- Toxic Encephalopathy --- PNS (Peripheral Nervous System) Diseases --- PNS Diseases --- Peripheral Nervous System Disease --- Peripheral Nervous System Disorders --- Peripheral Nerve Diseases --- Peripheral Neuropathies --- Nerve Disease, Peripheral --- Nerve Diseases, Peripheral --- Neuropathy, Peripheral --- PNS Disease --- Peripheral Nerve Disease --- Peripheral Neuropathy --- adverse effects --- toxicity --- Neurotoxicity Syndromes. --- Malalties del sistema nerviós.