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A decrease in integrin-mediated adhesion in adult muscles led to a progressive loss of muscle function due to a failure to maintain normal sarcomeric cytoarchitecture.
Declining skeletal muscle function, due to injury and aging (sarcopenia), results in a significantly decreased quality of life and is a major cause of disability in the United States.
Therefore, this patient group might even be more susceptible to sustained exhaustion as a result of impaired muscle function due to chemotherapy-induced subcellular calcaemic disturbances.
In summary, we propose that lipid overload causes impaired skeletal muscle function due to a reduction of muscle mass and ultrastructural damage.
This phenotype was apparently aggravated by impaired muscle function due to structural changes reflected by ultrastructural morphology as illustrated by the irregularities of a representative sarcomere unit from M. gast.
It has been suggested that the lamina propria may have an important role in integrating epithelial and smooth muscle function due to its innervations and proximity to the urothelium and tunica muscularis propria [ 6].
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Pompe's disease is a fatal muscular disorder caused by lysosomal α-glucosidase deficiency; patients with this disease have a rapidly fatal or slowly progressive impairment of muscle functions due to concomitant storage of lysosomal glycogen in the muscles and massive cardiomegaly.
34, 35, 36, 37 We hypothesize that these changes in single muscle fiber function due to MHC isoform composition contribute to the negative alterations detected in skeletal muscle quality and function with chronic heart failure.
Obesity-related reductions in muscle function are due to a loss of muscle mass (i.e. sarcopenia), which occurs largely from an imbalance between the rates of protein synthesis and degradation [ 2, 3].
GAPDH over-expression may be attributed to compensate for the progressive decrease in muscle mitochondrial function due to FFA induced ROS and contribute to loss of glucose and lipid homeostasis and eventually obesity and T2D [113], [113].
transcriptional coactivators are potent regulators of skeletal muscle metabolic function due to their ability to facilitate transcription factor activation in response to a number of extrinsic stimuli (2).
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