Pulmonary embolism presenting as flank pain: a case series.

BACKGROUND: Pulmonary embolism (PE) is a potentially fatal disease that can be effectively treated once diagnosed. Due to insidious and often cryptogenic presentations, the diagnosis of this disease can easily elude clinicians. Over the last several years the use of computed tomography (CT) scanning has improved the clinician's ability to diagnose PE. In addition, the widespread use of CT to investigate other complaints such as flank and abdominal pain could theoretically result in radiographic findings not previously identified that could point to the diagnosis of PE. The current case series reveals the unexpected and initially unrecognized CT finding of a pulmonary infarct in two patients presenting with flank pain; a third patient presented with flank pain and was also found to have a PE. OBJECTIVE: We describe three cases of patients who presented to the Emergency Department with flank pain who were diagnosed with pulmonary embolism. CASE REPORTS: The cases reported here discuss patients who presented with flank pain and were ultimately diagnosed with PE. In the first two cases, the patients had incidental findings of pulmonary infiltrates on abdominal CT scans, which prompted further diagnostic investigation. In the third case, the patient had risk factors for PE and presented with flank pain and the diagnosis was quickly made by CT imaging. CONCLUSION: Physicians should consider pulmonary embolism in the differential diagnosis of patients with isolated flank pain. Additionally, unexpected pulmonary findings on abdominal CT scans may help suggest the diagnosis of PE in the appropriate clinical setting.

Knockdown of m-calpain increases survival of primary hippocampal neurons following NMDA excitotoxicity.

The calpain family of cysteine proteases has a well-established causal role in neuronal cell death following acute brain injury. However, the relative contribution of calpain isoforms to the various forms of injury has not been determined as available calpain inhibitors are not isoform-specific. In this study, we evaluated the relative role of m-calpain and mu-calpain in a primary hippocampal neuron model of NMDA-mediated excitotoxicity. Baseline mRNA expression for the catalytic subunit of m-calpain (capn2 ) was found to be 50-fold higher than for the mu-calpain catalytic subunit (capn1) based on quantitative real-time PCR. Adeno-associated viral vectors designed to deliver short hairpin RNAs targeting capn1 or capn2 resulted in 60% and 90% knockdown of message respectively. Knockdown of capn2 but not capn1 increased neuronal survival after NMDA exposure at 21 days in vitro. Nuclear translocation of calpain substrates apoptosis inducing factor, p35/p25 and collapsin response mediator protein (CRMP) 2-4 was not detected after NMDA exposure in this model. However, nuclear translocation of CRMP-1 was observed and was prevented by capn2 knockdown. These findings provide insight into potential mechanisms of calpain-mediated neurodegeneration and have important implications for the development of isoform-specific calpain inhibitor therapy.