Outcomes following quadriceps tendon repair using transosseous tunnels versus suture anchors: A systematic review.

INTRODUCTION: Two major techniques are used to repair complete quadriceps tendon ruptures, transosseous tunnel (TT) and the suture anchor (SA). There are multiple studies comparing the biomechanical outcomes of repairs performed with TT or SA. Our purpose was to compare the clinical outcomes following quadriceps tendon repair using SA and TT fixation techniques. METHODS: Three major search engines were used with predetermined keyword searches to perform a systematic review of literature. These studies were independently scanned by two reviewers using PRISMA criterion. All included studies had to include at least one of the following outcome measures: range of motion (ROM), Lysholm score, complications, and/or re-ruptures. RESULTS: Using three major search engines, 1039 articles were identified. After removing duplicates and screening for inclusion, 49 articles were reviewed. Two independent reviewers searched the studies to meet the inclusion criteria, and eight studies were selected. These eight studies included 156 knees in the TT group and 54 knees in the SA group. The TT group had a significantly better ROM after QT repair (132.5° versus 127.0°, p = 0.02). There was no significant difference in Lysholm scores between the TT group (92.6) and SA group (91.0, p = 0.11). There were significantly more complications in SA groups (9.3% versus 1.3%, p = 0.013), but not a significant difference in re-rupture rate between those undergoing SA vs. TT repair (3.7% versus 0%, p = 0.065). The SA group had a significantly higher age at time of surgery (63.62 vs. 54.32) CONCLUSION: The current study suggests that, following quadriceps tendon rupture, there are no significant differences in functional outcome between TT and SA techniques. Those undergoing TT repair attained a statistically significantly greater final ROM but this difference may not be clinically relevant. There was a statistically significantly higher rate of post-operative complications using SA technique.

Non-Union After Multiple Lumbar Fusion Surgeries in a Patient With Facioscapulohumeral Muscular Dystrophy: A Case Report and Review of the Literature.

BACKGROUND: Facioscapulohumeral muscular dystrophy (FSHD) is a rare condition affecting 1/20,000 persons and the third most common muscular dystrophy condition, with an autosomal dominant pattern of inheritance characterized by progressive muscular weakness primarily involving the face, shoulder girdle, and upper arm. The condition is associated with atrophic musculature of the trunk and core leading to difficulties with gait, posture, and function. FSHD leaves as many as 20% of patients wheelchair-bound and most commonly presents with low back, neck, and shoulder pain. CASE DESCRIPTION: We present the case of a patient with FSHD who underwent multiple spinal fusion surgeries without relief in her back pain. Imaging studies serve to highlight the extent of paraspinal muscle atrophy and provides the basis for a discussion on the preoperative factors that may predict patients most likely to benefit from surgery. We then provide a brief review of the literature on the role of paraspinal muscle atrophy in back pain. CONCLUSIONS: This case adds to our understanding of the surgical management of patients with FSHD and patients with atrophic core musculature as a whole.

Blockade of MCU-Mediated Ca2+ Uptake Perturbs Lipid Metabolism via PP4-Dependent AMPK Dephosphorylation.

Mitochondrial Ca2+ uniporter (MCU)-mediated Ca2+ uptake promotes the buildup of reducing equivalents that fuel oxidative phosphorylation for cellular metabolism. Although MCU modulates mitochondrial bioenergetics, its function in energy homeostasis in vivo remains elusive. Here we demonstrate that deletion of the Mcu gene in mouse liver (MCUΔhep) and in Danio rerio by CRISPR/Cas9 inhibits mitochondrial Ca2+ (mCa2+) uptake, delays cytosolic Ca2+ (cCa2+) clearance, reduces oxidative phosphorylation, and leads to increased lipid accumulation. Elevated hepatic lipids in MCUΔhep were a direct result of extramitochondrial Ca2+-dependent protein phosphatase-4 (PP4) activity, which dephosphorylates AMPK. Loss of AMPK recapitulates hepatic lipid accumulation without changes in MCU-mediated Ca2+ uptake. Furthermore, reconstitution of active AMPK, or PP4 knockdown, enhances lipid clearance in MCUΔhep hepatocytes. Conversely, gain-of-function MCU promotes rapid mCa2+ uptake, decreases PP4 levels, and reduces hepatic lipid accumulation. Thus, our work uncovers an MCU/PP4/AMPK molecular cascade that links Ca2+ dynamics to hepatic lipid metabolism.