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Other markers of muscle damage, such as aldolase, troponin, carbonic anhydrase type 3 and fatty acid-binding protein (FABP), are mainly used in chronic muscle diseases.
Extensive muscle damage, such as caused by exercise or in muscular disease, requires a stem cell-mediated response.
It is concluded that theracurmin ingestion attenuates some aspects of muscle damage such as MVC loss and CK activity increase.
First, indirect indicators of muscle damage, such as the decreases in MVC, electrically induced knee extension torques, and low-frequency fatigue measured immediately after stretch-shortening cycle exercise, did not differ between phases of the menstrual phase.
However, the muscle biopsy remains invaluable in at least one regard - understanding the pathogenesis of Pompe disease and the mechanisms of skeletal muscle damage; such information may justify the need for earlier therapy and assist in the development of a better therapy.
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The Chinese studies of rosuvastatin always monitored liver, kidney and muscle damage markers, such as ALT, AST, serum creatinine, and CK.
These authors speculated that anti-inflammatory and/or anti-oxidant effect of the substances decreased secondary muscle damage responses such as increases in vascular permeability, neutrophil and free radical, attenuating muscle fibre disruption (Connolly et al. 2006; Trombold et al. 2010).
This could be beneficial in conditions associated with muscle damage or atrophy, such as faecal incontinence, where the use of bulking materials or cell transplantation alone has proven to be ineffective.
Quantification of histological damage is more difficult, but has been shown to be reliable when there is an established set of criteria to quantify muscle damage [ 51], such as inflammatory cell infiltration on H&E sections [ 15].
An increased signal in T2-weighted images, which is linked to T2 relaxation time (T2-rt) lengthening, is a well-known MR sign of cardiac and skeletal muscle damage, reflecting heterogeneous phenomena such as oedema and inflammation.
Another possibility is that the DNA damage signaling that is the trigger for activation of p53 in old muscle originates from chromosomal damage, such as double-strand breaks or telomere shortening, rather than from oxidative alterations.
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