Osteosynthesis using a plate lacking the anterior component and canulated cancellous screws to treat an avulsion fracture of the calcaneal tuberosity: A case report.

INTRODUCTION: Avulsion fractures of the calcaneal tuberosity with significant displacement can cause soft tissue complications in the heel. However, a treatment strategy for calcaneal tuberosity fractures with poor heel-skin condition is yet to be established. Here, we report a case involving avulsion fracture of the calcaneal tuberosity presenting with superficial skin necrosis that was treated with a plate lacking the anterior component and screws inserted percutaneously. PRESENTATION OF CASE: A 74-year-old woman presented with progressive right heel pain following an injury to her heel sustained approximately six weeks previously. She had experienced difficulty walking due to heel pain and superficial necrosis was observed on the posterior surface of the heel. Radiography and computed tomography revealed an avulsion fracture of the calcaneal tuberosity with superior displacement. Open reduction was performed using a lateral L-shaped incision. After inserting two cancellous screws percutaneously into the calcaneal tuberosity, we fixed a plate lacking the anterior component to the lateral surface of the calcaneus. The superficial necrosis healed gradually post-operatively. Bone union was confirmed using radiography six months post-operatively. DISCUSSION: We developed a novel surgical procedure to treat avulsion fractures of the calcaneal tuberosity with poor skin condition. The combination of a plate lacking the anterior component and the percutaneous insertion of canulated cancellous screws can reduce the risk of post-operative soft tissue complications while maintaining fixation of the fractured fragment. CONCLUSION: Our findings provide a novel surgical method for the treatment of avulsion fractures of the calcaneal tuberosity with soft tissue complications.

Uncoupling protein 2 and aldolase B impact insulin release by modulating mitochondrial function and Ca2+ release from the ER.

Uncoupling protein 2 (UCP2), a mitochondrial protein, is known to be upregulated in pancreatic islets of patients with type 2 diabetes (T2DM); however, the pathological significance of this increase in UCP2 expression is unclear. In this study, we highlight the molecular link between the increase in UCP2 expression in ß-cells and ß-cell failure by using genetically engineered mice and human islets. ß-cell-specific UCP2-overexpressing transgenic mice (ßUCP2Tg) exhibited glucose intolerance and a reduction in insulin secretion. Decreased mitochondrial function and increased aldolase B (AldB) expression through oxidative-stress-mediated pathway were observed in ßUCP2Tg islets. AldB, a glycolytic enzyme, was associated with reduced insulin secretion via mitochondrial dysfunction and impaired calcium release from the endoplasmic reticulum (ER). Taken together, our findings provide a new mechanism of ß-cell dysfunction by UCP2 and AldB. Targeting the UCP2/AldB axis is a promising approach for the recovery of ß-cell function.

Improvement of Predictivity of Teicoplanin Serum Trough Concentrations at Steady State Calculated by Vancomycin Pharmacokinetic Parameter.

According to a recent study and meta-analysis, trough levels of >10 µg/mL teicoplanin (TEIC) may be acceptable for the treatment of uncomplicated infection, but no method of TEIC personalized medicine has been established. Vancomycin (VCM) and TEIC are glycopeptide antibiotic agents effective against methicillin-resistance Staphyloccocus aureus. This study aimed to establish TEIC personalized medicine at a steady state calculated by VCM pharmacokinetic parameters. Bayesian forecasting and population mean methods were employed to estimate individual total VCM clearance (CL) using existing population pharmacokinetics (PPK) parameter, and the differences between the CL calculated by these two methods were defined as ΔCL. Serum drug concentration data for patients treated with TEIC were collected at a steady state concentration (>96 h post infusion). There was a significant relationship between the prediction error of TEIC trough level and ΔCL. The relation between ΔCL and TEIC trough concentration at steady state was used to develop the following equation to determine the maintenance dose: TEIC (µg/mL)=1.1119X-6.124ΔCL+3.9164 (X is defined as TEIC trough concentration calculated from the PPK parameter). The results of this study indicated that it is possible to improve the prediction error of TEIC trough concentration at a steady state for patients who have received VCM therapy.

MAOA/B deletion syndrome in male siblings with severe developmental delay and sudden loss of muscle tonus.

Deletion of the monoamine oxidase (MAO)-A and MAO-B was detected in two male siblings and in their mother. The approximately 800-kb deletion, extending from about 43.0MB to 43.8MB, was detected by array comparative genomic hybridization analysis. The MAOA and MAOB genes were included in the deletion, but the adjacent Norrie disease gene, NDP, was not deleted. The boys had short stature, hypotonia, severe developmental delays, episodes of sudden loss of muscle tone, exiting behavior, lip-smacking and autistic features. The serotonin levels in their cerebrospinal fluid were extremely elevated. Another set of siblings with this deletion was reported previously. We propose recognition of MAOA/B deletion syndrome as a distinct disorder.