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Fig. 6 Forest plot comparison of sway magnitude between the ACL-non-injured and ACL-matched control leg.
Fig. 2 Forest plot comparison of sway magnitude between the ACL-injured and ACL-matched control leg.
The present meta-analysis found no differences of postural sway between the non-injured and matched control leg.
1Second ACL group in the same study Fig. 3 Forest plot comparison of anteroposterior sway magnitude between the ACL-injured and ACL-matched control leg.
standardized, SE standard error, IV inverse variance, CI confidence interval, df degrees of freedom, ACL anterior cruciate ligament Fig. 7 Forest plot comparison of sway velocity between the ACL-non-injured leg and ACL-matched control leg.
standardized, SE standard error, IV inverse variance, CI confidence interval, df degrees of freedom, ACL anterior cruciate ligament Fig. 5 Forest plot comparison of sway velocity between the ACL-injured and ACL-matched control leg.
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The impairments typically affect the ability to control legs, trunk, arms and hands.
In histopathological sections, the soft callus area in treatment legs was significantly more than the control legs.
Our defect model resulted in a loss of muscle function, with injured legs generating less than 55% of muscle strength from the contralateral uninjured control legs, even at 4 weeks post-injury.
Remarkably, overexpressing DGAT1 led to a ∼30% increase in DAG content in the HFD-DGAT1 overexpressing leg and a ∼35% increase in DAG content in CHOW-DGAT1 overexpressing leg, compared to control legs of the animals (p = 0.073, HFD-DGAT1 vs. HFD-control leg, and p = 0.045, CHOW-DGAT1 vs. CHOW-control leg).
The DGAT1 overexpression was associated with a ∼52% increase in intramyocellular lipids in the HFD-DGAT1 overexpressing leg and a ∼66% increase in muscle triglyceride content in the CHOW-DGAT1 overexpressing leg, compared to control legs of the animals (p = 0.018, HFD-DGAT1 vs. HFD-control leg, and p = 0.044, CHOW-DGAT1 vs. CHOW-control leg, figure 1).
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