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Greater knowledge of the cellular and axonal anatomy of heterotopia of the PF has important implications toward our understanding of normal cerebellar development as well as cerebellar disorders with defective neuronal migration and altered lamination.
We believe that such migration and altered cell differentiation caused the development of fibrotic tissue on the sternum of one patient in group B. Thus, we conclude that centrifuged fat combined with ASCs as cell pellets (group C procedure) was best among the three methods used in this study.
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Particularly, a peptide that specifically blocked HA-RHAMM binding but not HA-CD44 or HA-TLR binding was able to block fibroblast migration and alter wound repair in wild-type but not RHAMM-knockout mice.
ANGPTL4-deficient mice exhibit delayed wound reepithelialization with impaired keratinocyte migration, angiogenesis and altered inflammatory response [ 43, 44].
Mice with Bergmann glial defects during development have severe abnormalities including pial rupture, disrupted neuronal migration and layering, and altered connectivity [6], [7].
Metastasis is a multistep process and involves increased migration, protease secretion and altered adhesion of cancer cells to allow their dissemination from primary tumor sites [ 22].
Pharmacological inhibition of dynamin in neurons migrating in a three-dimensional (3D) ECM substrate produces significant disruptions in migration and alters the subcellular distribution of adhesion molecules.
EOPK inhibits cell migration and alters cytoskeletal structure, through the reduction of basal spread and cell elongation and increased cell rounding.
Cytochalasin B dramatically inhibited the extent of migration and also altered cell morphology; nonetheless, urokinase was detected in the limited number of cells that moved into the wounded area, even in the presence of cytochalasin B. A small but consistent enhancement (36% +/- 9) of plasminogen activator activity was observed in the supernatant of wounded cultures.
CD44 resides in lipid rafts [ 6, 26, 27], organisation centres for molecules that play key roles in cell migration and whose altered functional behaviour has been implicated in diseases including breast cancer [ 12].
The observation that BTG2 suppression did not markedly affect cell viability or cell proliferation of bladder cancer cells, as assessed by BrdU and cell cycle analyses, provides strong evidence that the results of the migration assays reflect real cell migration and not altered cell proliferation.
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