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. We then analyze the performance of a proof-of-principle software implementation. We imagined a geometrical model geared towards blood flow computation from a color flow Doppler signal, and we developed a software implementation requiring only a standard diagnostic ultrasound device. Detection performance was evaluated by computing flow and its determinants (flow speed, vessel area, and ultrasound beam angle of incidence) on purposely designed synthetic and phantom-based arterial flow simulations. Flow was appropriately detected in all cases. Errors on synthetic images ranged from nonexistent to substantial depending on experimental conditions. Mean errors on measurements from our phantom flow simulation ranged from 1.2 to 40.2% for angle estimation, and from 3.2 to 25.3% for real-time flow estimation. This study is a proof of concept showing that accurate measurement can be done from automated color flow Doppler signal extraction, providing the industry the opportunity for further optimization using raw ultrasound data.

Multifocal community-acquired necrotizing fasciitis caused by a Panton-Valentine leukocidin-producing methicillin-sensitive Staphylococcus aureus.

We describe a rare case of multifocal necrotizing fasciitis (NF) complicating a single vaccine injection. Injection of hepatitis B vaccine of a 16-year-old immunocompetent woman developed into rapidly spreading multifocal NF of the right arm and the thighs, with septic shock. Treatment with antimicrobial therapy and surgical debridements allowed amputation to be avoided with a favourable outcome. The etiological agent was a methicillin-sensitive Staphylococcus aureus (MSSA) isolate harboring the Panton-Valentine leukocidin (PVL) and five enterotoxins. PVL has recently been reported in large series of methicillin-resistant SA cases and has been associated with necrotizing infections. Some strains of MSSA could harbor PVL and enterotoxins. PCR investigation is not frequent but could improve the understanding of the mechanisms of lesions. This case is in keeping with the increasing incidence of MSSA harboring PVL and enterotoxins with multifocal dissemination NF and emphasizes the necessary precautions for skin decontamination before vaccine injection.

Regulation of store-operated calcium entries and mitochondrial uptake by minidystrophin expression in cultured myotubes.

Defective expression of dystrophin in muscle cells is the primary feature of Duchenne muscular dystrophy (DMD), which is accompanied by fiber necrosis and intracellular calcium mishandling. These features led to the hypothesis that dystrophin could control calcium movements. Calcium mishandling in human DMD myotubes is dependent on contraction and/or calcium release activity, suggesting the involvement of channels being activated during these processes. Forced expression of minidystrophin at the plasma membrane of dystrophin-deficient Sol8 myotubes reactivates appropriate sarcolemmal expression of dystrophin-associated proteins and results in normal calcium homeostasis. In active dystrophic myotubes, store-operated calcium channels could be responsible for a sustained calcium influx in muscle cells. We show here that depletion of calcium stores (sarcoplasmic reticulum) by repetitive activation of calcium release and blockade of SERCA leads to a calcium influx. In myotubes expressing recombinant minidystrophin, these store-dependent influxes were reduced to a level similar to that observed in myotubes expressing native dystrophin. High store-dependent calcium influxes in dystrophin-deficient myotubes were associated with sustained cytosolic calcium transients and high intramitochondrial entries, while lower store-dependent calcium influx in myotubes expressing minidystrophin resulted in shorter calcium transients and reduced calcium uptake into mitochondria. We propose that minidystrophin negatively regulates sarcolemmal store-dependent calcium channels, which reduces store-dependent calcium influx, as well as its mitochondrial uptake. Forced expression of minidystrophin in dystrophic cells might restore the regulation of sarcolemmal store-dependent channels, which could protect against calcium mishandling.