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Background Clavicle nonunions in adolescent patients are exceedingly rare. The purpose of this study was to evaluate a series of clavicle nonunions from a pediatric multicenter study group to assess potential risk factors and treatment outcomes. Methods A retrospective review of all clavicle nonunions in patients younger than 19 years was performed at 9 pediatric hospitals between 2006 and 2016. Demographic and surgical data were documented. Radiographs were evaluated for initial fracture classification, displacement, shortening, angulation, and nonunion type. Clinical outcomes were evaluated, including rate of healing, time to union, return to sports, and complications. Risk factors for nonunion were assessed by comparing the study cohort with a separate cohort of age-matched patients with a diaphyseal clavicle fracture. Results There were 25 nonunions (mean age, 14.5 years; range, 10.0-18.9 years) identified, all of which underwent surgical fixation. Most fractures were completely displaced (68%) initially, but 21% were partially displaced and 11% were nondisplaced. Bone grafting was performed in 24 of 25 cases, typically using the hypertrophic callus. Radiographic healing was achieved in 96% of cases. One patient (4%) required 2 additional procedures to achieve union. The primary risk factor for development of a nonunion was a previous history of an ipsilateral clavicle fracture. Conclusions Clavicle nonunions can occur in the adolescent population but are an uncommon clinical entity. The majority occur in male patients with displaced fractures, many of whom have sustained previous fractures of the same clavicle. High rates of union were achieved with plate fixation and the use of bone graft.

During its first 2 years of operation, the gamma-ray AGILE satellite almost completed a full study of the gamma-ray sky. This paper presents the preliminary results of the systematic study performed on the AGILE data to search for GeV counterparts and to derive flux upper limits of the TeV sources detected by various instruments (MAGIC, HESS, VERITAS, Cangaroo, MILAGRO, ARGO, … .).

Since its early phases of operation, the AGILE mission is successfully observing Gamma Ray Bursts (GRBs) in the hard X-ray band with the SuperAGILE imager and in the MeV range with the Mini-Calorimeter. Up to now, three firm GRB detections were obtained above 25 MeV and some bursts were detected with lower statistical confidence in the same energy band. When a GRB is localized, either by SuperAGILE or Swift/BAT or INTEGRAL/IBIS or Fermi/GBM or IPN, inside the field of view of the Gamma Ray Imager of AGILE, a detection is searched for in the gamma ray band or an upper limit is provided. A promising result of AGILE is the detection of very short gamma ray transients, a few ms in duration and possibly identified with Terrestrial Gamma-ray Flashes. In this paper we show the current status of the observation of Gamma Ray Bursts and Terrestrial Gamma-ray Flashes with AGILE., Four pages and four figures

At the core of the AGILE scientific instrument, designed to operate on a satellite, there is the Gamma Ray Imaging Detector (GRID) consisting of a Silicon Tracker (ST), a Cesium Iodide Mini-Calorimeter and an Anti-Coincidence system of plastic scintillator bars. The ST needs an on-ground calibration with a g-ray beam to validate the simulation used to calculate the energy response function and the effective area versus the energy and the direction of the g rays. A tagged g-ray beam line was designed at the Beam Test Facility (BTF) of the INFN Laboratori Nazionali of Frascati (LNF), based on an electron beam generating g-rays through bremsstrahlung in a position-sensitive target. The g-ray energy is deduced by difference with the post-bremsstrahlung electron energy [1,2]. The electron energy is measured by a spectrometer consisting of a dipole magnet and an array of position sensitive silicon strip detectors, the Photon Tagging System (PTS). The use of the combined BTF-PTS system as tagged photon beam requires understanding the efficiency of g-ray tagging, the probability of fake tagging, the energy resolution and Contents lists available at SciVerse ScienceDirect

The acidosis of chronic renal failure is not due to bicarbonate wastage per se; rather, bicarbonate reabsorption per nephron is markedly enhanced. The ability to lower the urine pH is preserved. While overall ammonium production may be decreased in chronic renal failure, both ammonium production and excretion are markedly increased when expressed per remaining nephron. Titratable acid excretion in chronic renal failure is essentially maximal, owing to the effect of parathyroid hormone on phosphate excretion by the kidney. Thus, it appears that the acidosis of chronic renal failure is solely the consequence of the reduction in functional renal mass. Extrarenal buffering may contribute substantially to the maintenance of a near normal acid-base status in patients with marked reduction in glomerular filtration rate. That homeostasis is so well preserved until glomerular filtration rate falls to approximately 10 per cent of normal is remarkable; the price, however, may be considerable. Prolonged acidosis may magnify the tendency of renal failure to cause osteodystrophy. An obvious treatment for the acidosis of renal failure is exogenous alkali therapy. Most clinicians withhold alkali therapy until the bicarbonate concentration falls below 20 mEq per L. If the acidosis cannot be safely corrected with exogenous therapy, dialysis should be initiated.

Role of urinary concentrating ability in the generation of toxic papillary necrosis. We studied the pathogenesis of chemically induced papillary necrosis in six groups of rats. Papillary necrosis was produced by a single injection of 2-bromoethylamine hydrobromide (BEA), 50 mg, i.v.; the animals were followed for 7 to 10 days after the administration of the compound. Following BEA, heterozygous Brattleboro rats developed all the functional and morphologic lesions of papillary necrosis that we previously described in Sprague-Dawley rats. They were unable to maintain sodium balance when dietary sodium was withdrawn. Homozygous Brattleboro rats, on the other hand, developed none of the manifestations of papillary necrosis (that is, animals with central diabetes insipidus were protected completely from the nephrotoxic effects of BEA). They adapted normally to a zero sodium diet. Chronic administration of vasopressin to homozygous Brattleboro rats fully restored the toxic effects of BEA. Lowering urinary concentrating ability by inducing a water diuresis in Sprague-Dawley rats completely protected against BEA-induced papillary necrosis. Decreasing papillary solute concentration by furosemide or increasing urine flow after abrupt withdrawal of vasopressin to homozygous Brattleboro rats did not protect against BEA-induced papillary necrosis. We conclude that the combination, but not either alone, of increased urine flow and decreased papillary solute concentration protects against the development of BEA-induced papillary necrosis. Role du pouvoir de concentration urinaire sur l'apparition d'une necrose papillaire toxique. Nous avons etudie la physiopathologie d'une necrose papillaire induite chimiquement chez six groupes de rats. La necrose papillaire etait produite par une injection unique de 2-bromoethylamine hydrobromide (BEA), 50 mg, i.v.; les animaux etaient suivis pendant 7 a 10 jours apres administration du produit. Apres le BEA, des rats Brattleboro heterozygotes ont developpe toutes les lesions fonctionnelles et morphologiques d'une necrose papillaire telles que nous les avions deja decrites chez des rats Sprague-Dawley. Ils n'etaient pas capables d'assurer l'equilibre de la balance sodee lorsque le sodium alimentaire etait supprime. Par ailleurs, des rats Brattleboro homozygotes n'ont developpe aucune des manifestations de necrose papillaire (c'est-a-dire que les animaux ayant un diabete insipide central etaient completement proteges des effets nephrotoxiques du BEA). Ils s'adaptaient normalement a un regime sans sodium. L'administration chronique de vasopressine a des rats Brattleboro homozygotes a totalement restaure l'effet toxique du BEA. Le fait d'abaisser la capacite de concentration des urines en induisant une diurese aqueuse dans les rats Sprague-Dawley a completement protege contre la necrose papillaire induite par le BEA. La diminution de la concentration de solutes papillaires par le furosemide ou l'augmentation du debit urinaire apres arret brutal de la vasopressine chez des rats Brattleboro homozygotes ne protegeait pas contre la necrose papillaire induite par le BEA. Nous concluons que la combinaison, mais non chaque facteur separement, d'une augmentation du debit urinaire et d'une diminution de la concentration de solutes papillaires protegent contre le developpement d'une necrose papillaire induite par le BEA.