Not exact matches
By studying how these genes cause defects in fly and
mouse models, we can
improve our insights into the mechanisms related to
human disease,» said corresponding author and Dr. Hugo J. Bellen, professor
of neuroscience and molecular and
human genetics at Baylor College
of Medicine and an investigator at the Howard Hughes Medical Institute.
«If the
mouse models are indicative
of human disease, the combination therapy can increase the proportion
of patients who respond to therapy without additional adverse side effects and can
improve the quality
of life for cancer patients.»
«We think that by restoring the natural «microbial identity»
of laboratory
mice, we will
improve the
modeling of complex
diseases of free - living mammals, which includes
humans and their
diseases,» said Barbara Rehermann, M.D., senior author
of the paper.
These experiments are innovative because they seek to
improve a
mouse model based on current knowledge from
human disease, while also testing novel therapies that could be
of benefit for affected individuals.
These
mouse models are useful tools to
improve our understanding
of the biological significance and functional relevance
of these polymorphisms in
human disease, particularly when validated with controlled exposures and environmental challenges.
In rodents, ketogenic diets reduce reactive oxygen species in the brain34 and reduce central inflammation and reactive oxygen species in a
model of multiple sclerosis.35 Two clinical papers have found that ketogenic diet feeding
of 12 weeks to 6 months reduced signs
of liver inflammation in obese patients with nonalcoholic fatty liver
disease (in addition to
improving various other physiological and biochemical variables).36, 37 Unfortunately, basic research into non-alcoholic fatty liver
disease has been hampered by species differences between
mice and
humans in their hepatic reaction to ketogenic diets.38