Superluminal Localized Solutions to Maxwell Equations propagating along a waveguide: The finite-energy case

In a previous paper of ours [Phys. Rev. E64 (2001) 066603, e-print physics/0001039] we have shown localized (non-evanescent) solutions to Maxwell equations to exist, which propagate without distortion with Superluminal speed along normal-sized waveguides, and consist in trains of "X-shaped" beams. Those solutions possessed therefore infinite energy. In this note we show how to obtain, by contrast, finite-energy solutions, with the same localization and Superluminality properties. [PACS nos.: 41.20.Jb; 03.50.De; 03.30.+p; 84.40.Az; 42.82.Et. Keywords: Wave-guides; Localized solutions to Maxwell equations; Superluminal waves; Bessel beams; Limited-dispersion beams; Finite-energy waves; Electromagnetic wavelets; X-shaped waves; Evanescent waves; Electromagnetism; Microwaves; Optics; Special relativity; Localized acoustic waves; Seismic waves; Mechanical waves; Elastic waves; Guided gravitational waves.]Comment: plain LaTeX file (12 pages), plus 10 figure

The use of 68Ga-EDTA PET allows detecting progressive decline of renal function in rats.

Evaluation of glomerular filtration rate is very important in both preclinical and clinical setting, especially in the context of chronic kidney disease. It is typically performed using <sup>51</sup> Cr-EDTA or by imaging with <sup>123</sup> I-Hippuran scintigraphy, which has a significantly lower resolution and sensitivity as compared to PET. <sup>68</sup> Ga-EDTA represents a valid alternative due to its quick availability using a <sup>68</sup> Ge/ <sup>68</sup> Ga generator, while PET/CT enables both imaging of renal function and accurate quantitation of clearance of activity from both plasma and urine. Therefore, we aimed at investigating the use of <sup>68</sup> Ga-EDTA as a preclinical tracer for determining renal function in a knock-in rat model known to present progressive decline of renal function. <sup>68</sup> Ga-EDTA was injected in 23 rats, either wild type (n=10) or knock-in (n=13). By applying a unidirectional, two-compartment model and Rutland-Patlak Plot linear regression analysis, split renal function was determined from the age of 6 weeks to 12 months. Glomerular filtration ranged from 0.025±0.01 ml/min at 6 weeks to 0.049±0.05 ml/min at 6 months in wild type rats. Glomerular filtration was significantly lower in knock-in rats at 6 and 12 months (P<0.01). No significant difference was observed in renal volumes between knock-in and wild type animals, based on imaging-derived volume calculations. <sup>68</sup> Ga-EDTA turned out to be a very promising PET/CT tracer for the evaluation of split renal function. This method allowed detection of progressive renal impairment in a knock-in rat model. Additional validation in a human cohort is warranted to further assess clinical utility in both, healthy individuals and patients with renal impairment

A knock-in rat model unravels acute and chronic renal toxicity in glutaric aciduria type I.

Glutaric aciduria type I (GA-I, OMIM # 231670) is an autosomal recessive inborn error of metabolism caused by deficiency of the mitochondrial enzyme glutaryl-CoA dehydrogenase (GCDH). The principal clinical manifestation in GA-I patients is striatal injury most often triggered by catabolic stress. Early diagnosis by newborn screening programs improved survival and reduced striatal damage in GA-I patients. However, the clinical phenotype is still evolving in the aging patient population. Evaluation of long-term outcome in GA-I patients recently identified glomerular filtration rate (GFR) decline with increasing age. We recently created the first knock-in rat model for GA-I harboring the mutation p.R411W (c.1231 C>T), corresponding to the most frequent GCDH human mutation p.R402W. In this study, we evaluated the effect of an acute metabolic stress in form of high lysine diet (HLD) on young Gcdh <sup>ki/ki</sup> rats. We further studied the chronic effect of GCDH deficiency on kidney function in a longitudinal study on a cohort of Gcdh <sup>ki/ki</sup> rats by repetitive <sup>68</sup> Ga-EDTA positron emission tomography (PET) renography, biochemical and histological analyses. In young Gcdh <sup>ki/ki</sup> rats exposed to HLD, we observed a GFR decline and biochemical signs of a tubulopathy. Histological analyses revealed lipophilic vacuoles, thinning of apical brush border membranes and increased numbers of mitochondria in proximal tubular (PT) cells. HLD also altered OXPHOS activities and proteome in kidneys of Gcdh <sup>ki/ki</sup> rats. In the longitudinal cohort, we showed a progressive GFR decline in Gcdh <sup>ki/ki</sup> rats starting at young adult age and a decline of renal clearance. Histopathological analyses in aged Gcdh <sup>ki/ki</sup> rats revealed tubular dilatation, protein accumulation in PT cells and mononuclear infiltrations. These observations confirm that GA-I leads to acute and chronic renal damage. This raises questions on indication for follow-up on kidney function in GA-I patients and possible therapeutic interventions to avoid renal damage