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Recent advances in genetical engineering of the mouse have highlighted the importance of reproducible and less invasive models of cerebral ischemia in mice.
These studies of sub-optimal pregnancy in the spiny mouse have highlighted numerous sex-specific differences including placental gene expression and structural development [ 15, 16, 18], postnatal growth and survival after birth asphyxia [ 11] and susceptibility to adult renal dysfunction [ 17] after excess maternal glucocorticoid exposure in utero.
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Furthermore, studies on genetically engineered animals, especially knockout and transgenic mice, have highlighted a number of molecules essential for liver development.
Tissue-specific gene deletions in mice have highlighted the importance of the peripheral clocks in female reproduction.
Studies on knockout mice have highlighted that expression of the ERα isoform has been identified as critically important to cell proliferation in the uterus and breast,.
The skeleto-hematopoietic disease phenotype of the collagen X Tg and KO mice has highlighted an intimate link between endochondral skeletal elements, specifically growth plate hypertrophic chondrocytes and trabecular bone, and blood cell differentiation within the marrow.
More recently, the increased release of high-mobility group box protein 1 (HMGB1) and splenic apoptosis in septic CKD mice has highlighted these pathways in the CKD/sepsis interaction [ 28].
33 Recent work in transgenic sickle mice has highlighted the central role played by hypoxia in generating multi-organ damage by increased adenosine signalling via the G-protein coupled adenosine receptor ADORA2B.
Numerous findings, ranging from epidemiological studies to molecular analyses of mouse models, have highlighted a strong contribution of chronic inflammation to tumour development [ 1, 2].
Mouse model studies have highlighted functional links between these genes.
Comparative studies performed in mouse for HDL concentrations have highlighted that there are remarkable concordances between human and murine QTL maps [ 1] as well as between QTL (mouse) and GWAS (human) trait-associated regions (TARs) [ 2].
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