A5076619105- Pesticide Exposure and Toxicity
- Amyotrophic Lateral Sclerosis Research
- Parkinson's Disease Mechanisms and Treatments
- Neurological diseases and metabolism
- Nerve injury and regeneration
- Marine Toxins and Detection Methods
- Cholinesterase and Neurodegenerative Diseases
- Potato Plant Research
- Neuroscience and Neuropharmacology Research
- Cassava research and cyanide
- Genetic Neurodegenerative Diseases
- Carcinogens and Genotoxicity Assessment
- Neurogenesis and neuroplasticity mechanisms
- Climate Change and Health Impacts
- Parasitic Diseases Research and Treatment
- Mitochondrial Function and Pathology
- Botulinum Toxin and Related Neurological Disorders
- Neurological disorders and treatments
- Botany and Geology in Latin America and Caribbean
- Skin and Cellular Biology Research
- Health, Environment, Cognitive Aging
- Alcoholism and Thiamine Deficiency
- Botanical Research and Chemistry
- Hereditary Neurological Disorders
- Nerve Injury and Rehabilitation
Oregon Health & Science University
2016-2025
Shenzhen Center for Disease Control and Prevention
2023
Federal Scientific Center for Medical and Preventive Health Risk Management Technologies
2022
Public Health England
2020-2021
University of Cambridge
2020
Lancaster University
2018
Technical University of Munich
2018
Mater Misericordiae University Hospital
2016
Gulu University
2016
B.C. Women's Hospital & Health Centre
2015
The decline in the high incidence of amyotrophic lateral sclerosis, parkinsonism, and Alzheimer-type dementia among Chamorro population western Pacific islands Guam Rota, coupled with absence demonstrable viral hereditable factors this disease, suggests gradual disappearance an environmental factor selectively associated culture. One candidate is seed neurotoxic plant Cycas circinalis L., a traditional source food medicine which has been used less Americanization people after World War II....
The spatio-temporal pattern of distal peripheral nerve, sensory and motor nerve terminal, degeneration in experimental acrylamide neuropathy has been examined. Tissue was sampled from limbs cats throughout various stages intoxication (e.g. 7–32 days 10 mg/kg/day up to 294 3 acrylamide) examined by light electron microscopy. Nerve terminals a few Pacinian corpuscles hindfoot forefoot toepads displayed the first abnormalities, before onset clinical signs; filopod axon processes were lost,...
The spatio-temporal evolution of peripheral giant axonal degeneration has been studied in rats during the development concurrent (PNS) and central (CNS) nervous system dying-back disease after chronic intoxication with neurotoxic hexacarbons n-hexane (CH3CH2CH2CH2CH2CH3), methyl n-butyl ketone (MBK) (CH3COCH2CH2CH2CH3), or 2,5-hexanedione (CH3COCH2CH2COCH3), a metabolite MBK. Each compound caused animals insidiously to develop identical, symmetrical neuropathies characterized by eversion...
A companion paper in this issue (46) described the evolution of peripheral nervous system dying-back disease giant axonal type animals chronically intoxicated with neurotoxic hexacarbons n-hexane (CH3CH2CH2CH2CH2CH3), methyl n-butyl ketone or MBK (CH3COCH2-CH2CH2CH3), and 2,5-hexanedione (CH3COCH2CH2COCH3). The present study compares distribution pattern (PNS) central (CNS) produced by these three that acrylamide (CH2CHCONH2), and, addition, employs compounds to address unresolved issues...
We conducted an exploratory study of young-onset Parkinson's disease (YOPD) to examine occupational and environmental factors associated with risk. This case-control included 63 YOPD patients (diagnosis on or before age 50); controls (n = 68) were diagnosed rheumatoid arthritis. Crude odds ratios (ORs) computed identify exposure variables for logistic regression analyses. After controlling the race, educational level, sex, age, at diagnosis, family history (PD), PD was positively insecticide...
Abstract A number of chemically unrelated neurotoxic compounds and several types f metabolic abnormalities cause strikingly similar patterns distal symmetrical polyneuropathy in humans animals. Experimental studies with laboratory species have demonstrated that many toxic polyneuropathies are associated retrograde axonal degeneration occurring vulnerable nerve fiber tracts the central as well peripheral nervous system. This has been termed central‐peripheral axonopathy . Recent observations...
Journal Article DEGENERATION IN CENTRAL AND PERIPHERAL NERVOUS SYSTEMS PRODUCED BY PURE n-HEXANE: AN EXPERIMENTAL STUDY Get access HERBERT H. SCHAUMBURG, SCHAUMBURG From the Saul R. Korey Department of Neurology and Pathology (Neuropathology), Albert Einstein College MedicineThe Bronx, New York, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar PETER S. SPENCER Brain, Volume 99, Issue 2, June 1976, Pages 183–192, https://doi.org/10.1093/brain/99.2.183...
Chronic exposure of rats to 2,5-hexanedione (CH3COCH2CH2COCH3), a major metabolite the neurotoxic industrial solvent methyl n-buryl ketone (CH3COCH2CH2CH2CH3), has been shown cause clinical peripheral neuropathy with dying-back and central nervous system degeneration characterized by giant axonal swellings filled neurofilaments. This pattern disease is similar that produced n-butyl ketone.
Because of a number cases peripheral neuropathy that occurred in factory workers employed fabricprinting plant 1973, chronic inhalation experiments have been conducted using the printing-ink solvents methyl n-butyl ketone (MBK) and iso-butyl (MIBK). After four months intermittent respiratory exposure to 1,300 parts per million (ppm) MBK, all six rats tested developed severe symmetric weakness hindlimbs. Morphological studies showed massive focal axonal enlargements containing abnormally...