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These results are the first to demonstrate prolonged chimerism in primates treated with CD28/mTOR blockade and nondepletional CD40 blockade, and support further investigation of combined costimulation blockade targeting the CD28 and CD40 pathways.
Models that have been established for in vivo study of vascular neoplasias include mice and non-human primates treated with chemical carcinogens or infected with KSHV.
Similarly, non-human primates treated with anti-miR-33 oligonucleotides also exhibit increased HDL-C levels (Rayner et al, 2011a; Rottiers et al, 2013).
Furthermore, fracture healing has been found to be improved in rodents and non-human primates treated with an anti-sclerostin antibody (Agholme et al. 2010, Ominsky et al. 2011).
Rafael de Cabo further illuminated the role of SIRT1 in regulating metabolism and promoting healthy aging, describing longitudinal studies in mice and primates treated with resveratrol and other SIRT1-activating compounds (STACs).
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Nonetheless, the role of humoral immunity is in fact supported by studies showing consistent delay in death or protection of primates therapeutically treated with EBOV-neutralizing antibodies (16, 29, 30).
Astrogliosis and Alzheimer type II astrocytes have been demonstrated in nonhuman primates treated acutely (Pentschew et al. 1963) and chronically (Guilarte et al. 2008a; Olanow et al. 1996) with Mn.
Non-human primates (NHP, Cynomolgus) treated with two structurally distinct LRRK2 inhibitors for up to 1 month developed similar lamellar body formation in the lung and decreased LRRK2 in the lung of treated animals [ 33].
In primates, offspring of mothers treated with dexamethasone during late pregnancy have elevated basal and stress-stimulated cortisol levels [55,278].
Here we show that human iPS cell-derived dopaminergic progenitor cells survived and functioned as midbrain dopaminergic neurons in a primate model of PD (Macaca fascicularis) treated with the neurotoxin MPTP.
Expanding upon data previously reported in rats, adult nonhuman primates were subjected to spinal cord injury and then treated with a neutralizing antibody against Nogo-A.
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