Background: Anterior cruciate ligament (ACL) injury can lead to changes in tibiofemoral kinematics during gait, but the detailed short-term kinematic changes after ACL injury are still unknown.... Show moreBackground: Anterior cruciate ligament (ACL) injury can lead to changes in tibiofemoral kinematics during gait, but the detailed short-term kinematic changes after ACL injury are still unknown. Purpose: To measure tibiofemoral kinematics during gait in ACL-deficient (ACLD) knees over time after ACL injury. Study Design: Controlled laboratory study. Methods: The authors categorized 76 patients with unilateral ACLD knees into 4 groups based on the time from injury: <3 months (group 1), 3 to 6 months (group 2), >6 to 12 months (group 3), and >12 months (group 4). The controls were 20 participants with ACL-intact knees. Changes in the knee kinematics and range of motion during gait were compared among ACLD groups and those with ACL-intact knees. Results: Compared with controls, the range of motion of flexion in group 1 was significantly lower (6 degrees; P = .033), and the mean knee flexion was significantly increased (0.7 degrees-3.4 degrees) in groups 1 to 4 (all P <= .004). There was more internal tibial rotation (2.9 degrees-4.3 degrees) in group 1 and 2, and more anterior tibial translation (4.3 mm) in group 1 during the stance or swing phases than in controls (P <= .049 for all). The mean internal tibial rotation and anterior tibial translation significantly decreased from group 1 to group 4 (P < .001 for both). Compared with controls, the mean medial tibial translation was significantly greater (1.2-2.5 mm) in all groups, and more medial tibial translations (2.4-3.7 mm) were observed during the stance phase in groups 1, 3, and 4 (P <= .047 for all). Conclusion: ACLD knees displayed a motion impairment walking strategy within 3 months, and a higher-flexion walking strategy increased with time after injury. Excessive anterior translation and internal rotation of the tibia tended to return to normal, while excessive medial translation of the tibia increased in ACLD knees after 6 months postinjury. These results may provide new insight into the compensatory mechanisms and risk factors for premature osteoarthritis in ACLD knees. Show less
Sark, A.D.; Fromme, M.; Olejnicka, B.; Welte, T.; Strnad, P.; Janciauskiene, S.; Stolk, J. 2022
Alpha-1-Antitrypsin (AAT) is a protein of the SERPINA1 gene. A single amino acid mutation (Lys342Glu) results in an expression of misfolded Z-AAT protein, which has a high propensity to intra- and... Show moreAlpha-1-Antitrypsin (AAT) is a protein of the SERPINA1 gene. A single amino acid mutation (Lys342Glu) results in an expression of misfolded Z-AAT protein, which has a high propensity to intra- and extra-cellular polymerization. Here, we asked whether levels of circulating Z-AAT polymers are associated with the severity of lung disease, liver disease, or both. We obtained cross sectional data from the Dutch part of the Alpha1 International Registry of 52 ZZ-AAT patients who performed a pulmonary function test and donated a blood sample on the same day. From the Alpha-1 Liver Aachen Registry, we obtained a cohort of 40 ZZ-AAT patients with available data on their liver function. The levels of plasma Z-AAT polymers were determined using a LG96 monoclonal antibody-based sandwich ELISA. In a Dutch cohort, the median plasma level of Z-AAT polymers of patients diagnosed for pulmonary disease was 947.5 mu g/mL (733.6-1218 mu g/mL (95% CI)), which did not correlate with airflow obstruction or gas transfer value. In the Alpha-1 liver patient cohort, the median polymer level was 1245.9 mu g/mL (753-2034 mu g/mL (95% CI)), which correlated with plasma gamma-glutamyl transferase (GGT, rs = 0.57, p = 0.001), glutamate dehydrogenase (GLDH, rs = 0.48, p = 0.002) and triglycerides (TG, rs = 0.48, p = 0.0046). A Wilcoxon rank test showed higher Z-AAT polymer values for the liver over the lung group (p < 0.0001). These correlations support a possible link between plasma Z-AAT polymers and the liver function. Show less
Sokol, J.; Timp, J.F.; Cessie, S. le; Hylckama-Vlieg, A. van; Rosendaal, F.R.; Kubisz, P.; ... ; Lijfering, W.M. 2018
