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Very preterm infants more likely exhibit deficient executive functions than term born controls.
Consistent with the phenotype of STAT5a and STAT5b singly deficient mice, the doubly deficient animals exhibit defective development of mammary glands and impaired T cell proliferation in response to IL-2.
Importantly, these vessels exhibited deficient adenosine-mediated vasorelaxation when subjected to myograph studies, suggesting impaired Kv7 ion channels.
Several NPC2 mutants exhibited deficient sterol transport properties in a set of fluorescence-based assays.
Li, Q. et al. IKK1-deficient mice exhibit abnormal development of skin and skeleton.
Notch4-deficient mice exhibit normal development without any vascular abnormality [ 83].
In addition CXCR5-deficient mice exhibit impaired development of lymph nodes and Peyer's patches, and the tissue architecture of these organs is severely disturbed showing a lack of B-cell follicles [ 27, 28].
Nrf2-deficient cells exhibit a deficient stress response [ 116].
These endothelial-specific CD146-deficient mice exhibited normal development, suggesting that CD146 is dispensable for vasculogenesis in the process of embryogenesis; these animals had the ability to reproduce, which also suggests that CD146 does not play an essential role during physiological angiogenesis in adult mice, such as the adult female reproductive cycle.
In vitro studies of para-aortic splanchnopleural explants showed that AML-1-deficient mice also exhibit defective vascular development (Takakura et al, 2000).
UCHL1-deficient mice, known as gracile axonal dystrophy mice, show neuronal loss in the spinal gracile tract and exhibit early development sensory ataxia and progressive motor ataxia (10).
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