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Nevertheless, this study is one of the few randomized studies studying EPO effects on renal function and is the only one testing the effect of EPO on inflammatory markers such as cytokines.
The persistent effect of EPO on cognition, lasting for over 3 weeks after cessation of treatment, indicates alterations in neuroplasticity induced by EPO that do not require its continuous presence.
Because erythropoietin (EPO) has been shown to have antioxidant, anti-inflammatory and neuroprotective effects in many previous studies, present study was designed to evaluate the effect of EPO on rotenone-induced dopaminergic neuronal loss.
EPO-TBI is a trial of EPO as cerebral protection after traumatic brain injury, and the renal substudy assesses the effect of EPO on the development of acute kidney injury (AKI) and the response to treatment using multiple renal biomarkers with different time profiles in patients with traumatic brain injury.
Therefore, the effect of EPO on intestinal IR injury was examined by the change of intestinal histology; the expression of pro-inflammatory cytokines tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and interferon γ (IFN-γ); and the protein levels of EPOR, p-EPOR, p85, p-p85, Akt, p-Akt, IκΒ-α, p-p65, and p65.
Our observation that rhEPO increased mature oligodendrocytes prompted us to examine the effect of EPO on myelinated axons.
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The present study was designed to determine the histological and ultrastructural changes in kidney cell of the rats after relatively long exhaustive exercise, evaluate the preventive and therapeutic effects of EPO on such a pathological conditions to provide empirical evidence for the application of EPO clinically.
The beneficial effects of EPO on renal dysfunction and hemodynamics have been recently confirmed in large-animal models of ischemic acute kidney injury (monkeys, pigs, and dogs [43 46]).
There are high-quality data on the effects of EPO on transfusion requirements in critical illness.
The beneficial effects of EPO on renal dysfunction and hemodynamics have been recently confirmed in large-animal models of ischemic acute kidney injury (monkeys, pigs, and dogs [ 43- 46]).
Because EPO has been reported to activate mitochondrial biogenesis (Carraway et al., 2010) and haemoglobin expression (Tezel et al., 2010) in non-haematopoietic cells, we assessed the effects of EPO on primary astrocytes and PC12 cells.
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