Thomas W Geisber, an expert on Ebola and siRNAs at The University of Texas Medical Branch, said the research was «highly significant because it shows protection against Ebola in
a robust model of human disease: non-human primates.»
Not exact matches
«If
human organs on chips can be shown to be
robust and consistently recapitulate complex
human organ physiology and
disease phenotypes in unrelated laboratories around the world, as suggested by early proof -
of - concept studies, then we will see them progressively replace one animal
model at a time.
Molecular mechanism underlying
diseases (conformational
diseases, cystic kidney disorders, neuromuscular
diseases, inflammation, iron - related
diseases, disorders
of human reproduction, osteoporosis and bone
diseases) are being investigated by many groups with
robust animal and cellular
models and patients» biological samples.
Human primary hepatocytes and immortalized cell lines (e.g., HepaRG) are used to study these disorders, but due to these cells» high variability, low availability, short assay window, or lack
of physiological relevance, researchers studying metabolic
diseases are searching for more
robust and reliable
models.
These studies allow the construction
of robust in vitro
human disease models, and also provide a path towards precision medicine and therapeutic genome editing.
There are currently no
disease - modifying treatments that have been shown to slow the progression or delay the onset
of HD in
humans; however, several compounds have demonstrated promise in animal
models of HD.1
Robust and sensitive markers
of disease progression are required to assess their efficacy in
humans.