Results 221 to 230 of about 65,558 (345)
Abstract Exposure levels without appreciable human health risk may be determined by dividing a point of departure on a dose–response curve (e.g., benchmark dose) by a composite adjustment factor (AF). An “effect severity” AF (ESAF) is employed in some regulatory contexts.
Barbara L. Parsons+17 more
wiley +1 more source
Recombinant expression of receptor binding domains of all eight subtypes of botulinum neurotoxin type A for generation of antitoxins with broad reactivity. [PDF]
Quynh Pham N+11 more
europepmc +1 more source
Exploring biomarkers of neurodegeneration in epilepsy: Critical insights
Abstract The advent of biofluid biomarkers for neurodegenerative disorders has precipitated a surge in recent evidence regarding their role in epilepsy. In this literature review, we examine the diagnostic, prognostic, and therapeutic potential of several biomarkers, including amyloid‐beta (Aβ) protein, total (t‐tau), phosphorylated tau (p‐tau) protein,
Rida Farhan+7 more
wiley +1 more source
Sensorineural hearing loss from quinolinic acid: A neurotoxin in middle ear effusions [PDF]
Robert F. Yellon+8 more
openalex +1 more source
Molecular cloning of the Clostridium botulinum structural gene encoding the type B neurotoxin and determination of its entire nucleotide sequence [PDF]
Sarah M. Whelan+5 more
openalex +1 more source
Abstract The COX4I1 is responsible for encoding a crucial component of cytochrome c oxidase, integral to electron transport in the mitochondrial respiratory chain. Mutations in COX4I1 can result in a rare autosomal recessive disorder characterized by growth retardation, slow weight gain, microcephaly, and potentially, hematologic symptoms such as ...
Zhen Liu+5 more
wiley +1 more source
Inherited metabolic epilepsies–established diseases, new approaches
Abstract Inherited metabolic epilepsies (IMEs) represent the inherited metabolic disorders (IMDs) in which epilepsy is a prevailing component, often determining other neurodevelopmental outcomes associated with the disorder. The different metabolic pathways affected by individual IMEs are the basis of their rarity and heterogeneity.
Itay Tokatly Latzer, Phillip L. Pearl
wiley +1 more source