Lower Extremity Kinematic Profile of Gait of Patients After Ankle Fracture: A Case-Control Study.

The present study examined the differences in the lower extremity gait kinematic profile of patients recovering from ankle fracture compared with healthy controls. In addition, we inquired whether the profile would differ among fracture severity groups. A total of 48 patients participated in the present prospective, case-control study. The gait of 24 patients recovering from an ankle fracture injury and 24 healthy matched controls was examined using an inertial measurement unit sensor system. The following gait parameters were evaluated: knee range of motion (ROM) during the swing phase, maximum knee flexion angle during stance, thigh and calf ROM, and stride duration. Statistically significant differences were found between the ankle fracture group and the control group for all parameters. The patients with ankle fracture had a lower knee ROM during swing phase compared with the control group (mean ± standard deviation 43.0° ± 15.5° compared with 66.7° ± 5.1°, respectively; p < .001). The maximum knee flexion angle during stance was lower in the patients with ankle fracture than in the control group (mean ± standard deviation 10.5° ± 6.1° compared with 21.2° ± 4.5°, respectively; p < .001). Patients with ankle fracture also had lower gait cycle thigh and calf ROM angles (p < .001) and a longer stride duration (p < .001) compared with the control group. No statistically significant differences were found among the severity groups. These results suggest that the gait kinematic characteristics vary between healthy people and patients recovering from an ankle fracture injury during the short-term period after injury.

A mitochondrial GABA permease connects the GABA shunt and the TCA cycle, and is essential for normal carbon metabolism.

In plants, γ-aminobutyric acid (GABA) accumulates in the cytosol in response to a variety of stresses. GABA is transported into mitochondria, where it is catabolized into TCA cycle or other intermediates. Although there is circumstantial evidence for mitochondrial GABA transporters in eukaryotes, none have yet been identified. Described here is an Arabidopsis protein similar in sequence and topology to unicellular GABA transporters. The expression of this protein complements a GABA-transport-deficient yeast mutant. Thus the protein was termed AtGABP to indicate GABA-permease activity. In vivo localization of GABP fused to GFP and immunobloting of subcellular fractions demonstrate its mitochondrial localization. Direct [(3) H]GABA uptake measurements into isolated mitochondria revealed impaired uptake into mitochondria of a gabp mutant compared with wild-type (WT) mitochondria, implicating AtGABP as a major mitochondrial GABA carrier. Measurements of CO(2) release, derived from radiolabeled substrates in whole seedlings and in isolated mitochondria, demonstrate impaired GABA-derived input into the TCA cycle, and a compensatory increase in TCA cycle activity in gabp mutants. Finally, growth abnormalities of gabp mutants under limited carbon availability on artificial media, and in soil under low light intensity, combined with their metabolite profiles, suggest an important role for AtGABP in primary carbon metabolism and plant growth. Thus, AtGABP-mediated transport of GABA from the cytosol into mitochondria is important to ensure proper GABA-mediated respiration and carbon metabolism. This function is particularly essential for plant growth under conditions of limited carbon.