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This specific association between UCP2 and mitochondrial GSH levels regulation was further confirmed using lipopolysaccharide models of peripheral inflammation, and in purified peritoneal macrophages.
Neuron-microglial signaling including purinergic, fractalkine, and neuroregulin-1 signaling have been implicated in regulating the proliferation of resident microglia in models of peripheral nerve injury [58, 59].
Our results showing an increased number of microglia cells in the TNC after repetitive closed head injury may be from resident microglia in line with those for models of peripheral nerve injury.
Increased expression of PKCγ is clearly documented in animal models of peripheral neuropathy [69], [70] as well as increased phosphorylation of cyclic AMP response element-binding protein in dorsal horn neurons expressing PKCγ [71].
Angiogenic factors have also shown promise in experimental models of peripheral ischemia.
Improving clinical outcome requires reliable and reproducible experimental models of peripheral nerve injuries and their reconstruction [ 55, 58, 59].
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Speech Encoding in a Model of Peripheral Auditory Processing: Quantitative Assessment by Means of Automatic Speech Recognition.
The therapeutic potential of CEP 03 was further evaluated in a mouse model of peripheral arterial disease by quantification of blood perfusion recovery and capillary density.
In this paper, an extended dynamic model of peripheral milling process including process damping, structural and cutting force nonlinearities is presented.
Failure of stroke volume to rise during a progressive simulated swim test is consistent with a model of peripheral facilitation of circulatory responses to exercise.
In a mouse hindlimb ischemia model of peripheral arterial disease, MITCH-PEG co-delivery of hiPSC-ECs and VEGF was found to reduce inflammation and promote muscle tissue regeneration compared to a saline control.
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