Impact of Hospitalist-Led Interdisciplinary Antimicrobial Stewardship Interventions at an Academic Medical Center.

Background: Approximately 20%-50% of antimicrobial use in hospitals is inappropriate. Limited data exist on the effect of frontline provider engagement on antimicrobial stewardship outcomes.

Methods: A three-arm pre-post quality improvement study was conducted on three adult internal medicine teaching services at an urban academic hospital.

Twist on a classic: vitamin D and hypercalcaemia of malignancy.

Malignancy is the most common cause of hypercalcaemia in the inpatient setting. Most cases are caused by tumour production of parathyroid hormone-related protein and osseous metastases. In less than 1% of cases, hypercalcaemia is driven by increased production of 1,25-dihydroxyvitamin D (1,25(OH)D), a mechanism most commonly seen in haematological malignancies.

Altered serum levels of the osteoclast-specific TRACP 5b isoform in Chinese children undergoing orthodontic treatment.

Orthodontic tooth movement is dependent upon the ability of mechanical forces to induce remodelling activity within the tooth-supporting alveolar bone. In view of the importance of bone resorption in mediating tooth movement, the aim of this study was to establish if alterations in the osteoclast-specific bone marker tartrate-resistant acid phosphatase (TRACP) 5b could be detected in the sera of patients undergoing orthodontic treatment. The sample consisted of 14 subjects (10 girls and 4 boys) aged 10.

Polyglutamine proteins at the pathogenic threshold display neuron-specific aggregation in a pan-neuronal Caenorhabditis elegans model.

The basis of neuron-specific pathogenesis, resulting from the expression of misfolded proteins, is poorly understood and of central importance to an understanding of the cell-type specificity of neurodegenerative disease. In this study, we developed a new model for neuron-specific polyQ pathogenesis in Caenorhabditis elegans by pan-neuronal expression that exhibits polyQ length-dependent aggregation, neurotoxicity, and a pathogenic threshold at a length of 35-40 glutamines. Analysis of specific neurons in C.