Intrinsic graft laxity variation with open kinetic chain exercise after anterior cruciate ligament reconstruction: A non-randomized controlled study.

Objectives: To determine whether quadriceps and hamstring strengthening in a rehabilitation program involving early open kinetic chain (OKC) and/or closed kinetic chain (CKC) knee joint exercises had an influence on graft laxity at 1, 3, and 6 months after anterior cruciate ligament reconstruction (ACLR).

Design: Retrospective study.

Methods: Two groups (n = 53) of ACLR patients (combination of OKC and CKC exercises group compared to a CKC exercise group) were recruited.

Evaluation of Muscle Strength and Graft Laxity With Early Open Kinetic Chain Exercise After ACL Reconstruction: A Cohort Study.

Background: Open kinetic chain (OKC) exercise is an effective method to improve muscle function during rehabilitation after anterior cruciate ligament reconstruction (ACLR); however, there is controversy about its use in the early phase of rehabilitation.

Purpose: To determine (1) whether the use of OKC and closed kinetic chain (CKC) exercises improves quadriceps and hamstring strength in the early phase of rehabilitation after ACLR and (2) whether the early use of OKC exercise affects graft laxity at 3 and 6 months postoperatively in patients with a hamstring tendon graft.

Study Design: Cohort study; Level of evidence, 3.

A feasability study of color flow doppler vectorization for automated blood flow monitoring.

An ongoing issue in vascular medicine is the measure of the blood flow. Catheterization remains the gold standard measurement method, although non-invasive techniques are an area of intense research. We hereby present a computational method for real-time measurement of the blood flow from color flow Doppler data, with a focus on simplicity and monitoring instead of diagnostics.

Congenital muscular dystrophy type 1D (MDC1D) due to a large intragenic insertion/deletion, involving intron 10 of the LARGE gene.

Mutation of the LARGE gene is the rarest of the six known genetic causes of α-dystroglycanopathy. We report further a family with MDC1D due to a complex genomic rearrangement that was not apparent on standard sequencing of LARGE. Two sisters in a consanguineous family had moderate mental retardation and cerebellar malformations, together with dystrophic changes and markedly reduced α-dystroglycan glycosylation staining on muscle biopsy.

In vitro analysis of rod composition and actin dynamics in inherited myopathies.

Rods are the pathological hallmark of nemaline myopathy, but they can also occur as a secondary phenomenon in other disorders, including mitochondrial myopathies such as complex I deficiency. The mechanisms of rod formation are not well understood, particularly when rods occur in diverse disorders with very different structural and metabolic defects. We compared the characteristics of rods associated with abnormalities in structural components of skeletal muscle thin filament (3 mutations in the skeletal actin gene ACTA1) with those of rods induced by the metabolic cell stress of adenosine triphosphate depletion.