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Mimicking the extracellular muscle environment improves tools exploring the behavior of primary muscle cells.
We investigated the efficiency of autologous bone grafting in a well-vascularised muscle environment, and additionally when isolated from the muscle and connected only to the bony environment.
The ability of a muscle to produce force and power is determined by the interaction of biomechanical and physiological factors, such as muscle mechanics (e.g., type of muscle action) and morphological (e.g., muscle fiber type) and neural (e.g., motor unit recruitment) factors, and by the muscle environment itself (e.g., biochemical composition) [31].
As a step in furthering our understanding of satellite cell regulation, this study explored how TNF in the muscle environment represses the satellite cell program.
How these different injury regimes model the dystrophic muscle environment and to what extent the local environment, genetic background and immunological status of the host mouse affect muscle stem cell behavior are important to determine, for the identification of robust methodologies which could be reliably used for therapeutic trials in muscular dystrophies.
Inhibition of IL6 activity leads to changes in the dystrophic muscle environment.
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These combined results suggest that isoform L enzymes are designed to function under different metabolic conditions encountered in the non-striated muscle environments where they are expressed.
Considering that we express the human Dystrophin in a skeletal muscle embryonic environment it is not surprising, and it is even reassuring, that it would behave as in the human embryonic environment and be found in a cytoplasmic form.
Both biologically active, naturally derived materials (such as extracellular matrix) and carefully engineered synthetic polymers have been developed to provide such a muscle regenerative environment.
Conversely a sedentary lifestyle, associated with osteoarthritis-mediated physical inactivity, is associated with reduced mitochondrial function, dysregulation of cellular redox status and chronic systemic inflammation that renders the skeletal muscle intracellular environment prone to reactive oxygen species-mediated toxicity.
Adverse consequences of oxytocin augmentation may be, at least partially, related to the fact that the uterine muscle isoenzyme environment may not yet be optimized for uterine contraction activity when this intervention is implemented.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com