Sonoprocessing of oil: Asphaltene declustering behind fine ultrasonic emulsions.

Despite the transition toward carbon-free energy carriers, liquid fossil fuels are expected to occupy an important market share in the future. Therefore, it is crucial to develop innovative technology for better combustion reducing the emissions of pollutants associated with their utilization. Water in oil (w/o) emulsions contribute to greener combustion, increasing carbon efficiency and reducing emissions. Water content, emulsions stability, and droplet size distributions are key parameters in targeting the efficient use of emulsions as combustibles. In particular, for fixed water content, the finer the emulsion, the better its beneficial effect on combustion. In this work, two emulsions, mechanically and ultrasonically generated, were compared. Cryogenic scanning electron microscopy (cryo-SEM) allowed the visualization of water droplets inside the oily matrix. No surfactants were added to the oil, due to its high asphaltenic content. Asphaltene molecular aggregates, namely clusters, act as natural surfactants stabilizing the emulsions by arranging at w/o interface and forming a rigid film. The asphaltenic rigid film is clearly visualized in this work and compared for the two emulsions. The results showed finer water droplets in the ultrasonically generated emulsion, together with a reduction in the thickness of the asphaltenic film. Ultrasonically induced cavitation favored the de-clustering (breakage of intermolecular forces) of asphaltene molecules. Thus, smaller clusters allowed to stabilize smaller water droplets resulting in an ultra-fine emulsion, which improves the combustion performances of the fuel.

Homozygous TNNI3 Mutations and Severe Early Onset Dilated Cardiomyopathy: Patient Report and Review of the Literature.

The TNNI3 gene encodes for the cardiac isoform of troponin I, a pivotal component of the sarcomeric structure of the myocardium. While heterozygous TNNI3 missense mutations have long been associated with autosomal dominant hypertrophic and restrictive cardiomyopathies, the role of TNNI3 null mutations has been more debated due to the paucity and weak characterization of reported cases and the low penetrance of heterozygous genotypes. In recent years, however, an increasing amount of evidence has validated the hypothesis that biallelic TNNI3 null mutations cause a severe form of neonatal dilated cardiomyopathy. Here, we expand the case series reporting two unrelated patients afflicted with early onset dilated cardiomyopathy, due to homozygosity for the p.Arg98* TNNI3 variant, which had thus far been documented only in heterozygous patients and apparently healthy carriers, and the recurrent p.Arg69Alafs*8 variant, respectively. A review of previously reported biallelic TNNI3 loss-of-function variants and their associated cardiac phenotypes was also performed.

Bone disease in medullary sponge kidney and effect of potassium citrate treatment.

BACKGROUND AND OBJECTIVES: In medullary sponge kidney (MSK)-a common malformative renal condition in patients with calcium nephrolithiasis-hypercalciuria, incomplete distal renal tubular acidosis, and hypocitraturia are common. Clinical conditions with concomitant hypercalciuria and/or incomplete distal renal tubular acidosis are almost invariably associated with bone disease, making osteopathy highly likely in MSK, too. Patients with MSK have never been investigated for osteopathy; neither has the potential effect of potassium citrate administration (CA) on their urinary metabolic risk factors and on bone mineralization. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: These issues were retrospectively analyzed in 75 patients with MSK and primary stone risk factor (PSRF; hypercalciuria, hypocitraturia, hyperuricosuria, and/or hyperoxaluria) on an outpatient basis; 65 received CA (2.9 +/- 0.8 g/d), whereas 10 received only general "stone clinic" suggestions. The 24-h urinary excretion of calcium, phosphate, oxalate, uric acid, and citrate; morning urine pH; serum biochemistry; and bone mineral density were investigated at baseline and at the end of follow-up (78 +/- 13 and 72 +/- 15 mo in groups A and B, respectively). RESULTS: CA led to a significant rise in urinary pH and citrate and decreased urinary calcium and phosphate (all P < 0.001). Patients with MSK and PSRF had reduced bone density. Bone density improved significantly in the group that was treated with oral CA. CONCLUSIONS: Bone disease is very frequent in patients with MSK and concomitant PSRF. Long-term CA improves bone density. The concurrent effects of treatment on PSRF suggest that the subtle acidosis plays a pivotal role in bone disease and hypercalciuria in patients with MSK.