A5063737321- Neurological disorders and treatments
- Botulinum Toxin and Related Neurological Disorders
- Hereditary Neurological Disorders
- Amyotrophic Lateral Sclerosis Research
- Ion channel regulation and function
- Neurobiology and Insect Physiology Research
- Prion Diseases and Protein Misfolding
- Traumatic Brain Injury Research
- Insect and Pesticide Research
- Microtubule and mitosis dynamics
- RNA Research and Splicing
- Insect Pest Control Strategies
- TGF-β signaling in diseases
- Genetics and Neurodevelopmental Disorders
- Alzheimer's disease research and treatments
- RNA modifications and cancer
- Mitochondrial Function and Pathology
- Traumatic Brain Injury and Neurovascular Disturbances
- Genetics, Aging, and Longevity in Model Organisms
- Intracranial Aneurysms: Treatment and Complications
- Healthcare and Venom Research
- Developmental Biology and Gene Regulation
- Protist diversity and phylogeny
- Pesticide Exposure and Toxicity
- Neurogenetic and Muscular Disorders Research
United States Army Medical Research Institute of Infectious Diseases
2017-2023
BASF (United States)
2023
Triangle
2023
Research Triangle Park Foundation
2023
United States Army
2016-2021
Johns Hopkins University
2012-2018
Johns Hopkins Medicine
2012-2018
University of Alabama at Birmingham
2012
University of Washington
1987-1993
Psychosocial outcome and recovery of a group 31 consecutive adult patients with moderate to severe head injuries were prospectively investigated over 2-year period. A friend control was used for comparison purposes. We conclude that have significant long-term impact on psychosocial functioning. More specifically, although there is an increase time in the number subjects who resume former levels activity, many severely head-injured people remain unable work, support themselves financially,...
Pyridazine pyrazolecarboxamides (PPCs) are a novel insecticide class discovered and optimized at BASF. Dimpropyridaz is the first PPC to be submitted for registration controls many aphid species as well whiteflies other piercing-sucking insects.Dimpropyridaz tertiary amide PPCs proinsecticides that converted in vivo into secondary active forms by N-dealkylation. Active metabolites of potently inhibit function insect chordotonal neurons. Unlike Group 9 29 insecticides, which hyperactivate...
Neuronal function depends on the retrograde relay of growth and survival signals from synaptic terminal, where neuron interacts with its targets, to nucleus, gene transcription is regulated. Activation Bone Morphogenetic Protein (BMP) pathway at Drosophila larval neuromuscular junction results in nuclear accumulation phosphorylated form factor Mad motoneuron nucleus. This turn regulates genes that control growth. How BMP signaling terminal relayed cell body nucleus regulate unknown. We show...
One hundred and two consecutive head injured patients were studied at 1 12 months after injury. Their performances compared with a group of uninjured friends. The results indicate that impairment in memory depends on the type task used, time from injury to testing, severity (that is, degree impaired consciousness). Head indices are more closely related behavioural outcome early as later At year, only those deep or prolonged consciousness (as represented by greater than day coma, Glasgow Coma...
Mutations in the RNA binding protein Fused sarcoma (FUS) are estimated to account for 5-10% of all inherited cases amyotrophic lateral sclerosis (ALS), but function FUS motor neurons is poorly understood.Here, we investigate early functional consequences overexpressing wild-type or ALS-associated mutant proteins Drosophila neurons, and compare them phenotypes arising from loss homolog FUS, Cabeza (Caz).We find that lethality locomotor correlate with levels transgene expression, indicating...
Intraneuronal delivery of a therapeutic, single-domain antibody reverses botulism symptoms and increases survival mice, guinea pigs, monkeys.
Botulinum neurotoxins (BoNTs) are potent neuroparalytic toxins that cause mortality through respiratory paralysis. The approved medical countermeasure for BoNT poisoning is infusion of antitoxin immunoglobulins. However, antitoxins have poor therapeutic efficacy in symptomatic patients; thus, there an urgent need treatments reduce the artificial ventilation. We report US Food and Drug Administration-approved potassium channel blocker 3,4-diaminopyridine (3,4-DAP) reverses depression...
Abstract Botulinum neurotoxins (BoNTs) are highly potent, select agent toxins that inhibit neurotransmitter release at motor nerve terminals, causing muscle paralysis and death by asphyxiation. Other than post-exposure prophylaxis with antitoxin, the only treatment option for symptomatic botulism is intubation supportive care until recovery, which can require weeks or longer. In previous studies, we reported FDA-approved drug 3,4-diaminopyridine (3,4-DAP) reverses early symptoms prolongs...
Botulinum neurotoxins (BoNTs) are highly potent toxins that cleave neuronal SNARE proteins required for neurotransmission, causing flaccid paralysis and death by asphyxiation. Currently, there no clinical treatments to delay or reverse BoNT-induced blockade of neuromuscular transmission. While aminopyridines have demonstrated varying efficacy in transiently reducing following BoNT poisoning, the precise mechanisms which symptomatically treat botulism not understood. Here we found...
Introduction Botulinum neurotoxin (BoNT) causes neuroparalytic disease and death by blocking neuromuscular transmission. There are no specific therapies for clinical botulism the only treatment option is supportive care until function spontaneously recovers, which can take weeks or months after exposure. The highly specialized junction (NMJ) between phrenic motor neurons diaphragm muscle fibers main target of BoNT. Due to difficulty in eliciting respiratory paralysis without a high mortality...