19 research outputs found

    EuPRAXIA conceptual design report

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    This report presents the conceptual design of a new European research infrastructure EuPRAXIA. The concept has been established over the last four years in a unique collaboration of 41 laboratories within a Horizon 2020 design study funded by the European Union. EuPRAXIA is the first European project that develops a dedicated particle accelerator research infrastructure based on novel plasma acceleration concepts and laser technology. It focuses on the development of electron accelerators and underlying technologies, their user communities, and the exploitation of existing accelerator infrastructures in Europe. EuPRAXIA has involved, amongst others, the international laser community and industry to build links and bridges with accelerator science — through realising synergies, identifying disruptive ideas, innovating, and fostering knowledge exchange. The Eu-PRAXIA project aims at the construction of an innovative electron accelerator using laser- and electron-beam-driven plasma wakefield acceleration that offers a significant reduction in size and possible savings in cost over current state-of-the-art radiofrequency-based accelerators. The foreseen electron energy range of one to five gigaelectronvolts (GeV) and its performance goals will enable versatile applications in various domains, e.g. as a compact free-electron laser (FEL), compact sources for medical imaging and positron generation, table-top test beams for particle detectors, as well as deeply penetrating X-ray and gamma-ray sources for material testing. EuPRAXIA is designed to be the required stepping stone to possible future plasma-based facilities, such as linear colliders at the high-energy physics (HEP) energy frontier. Consistent with a high-confidence approach, the project includes measures to retire risk by establishing scaled technology demonstrators. This report includes preliminary models for project implementation, cost and schedule that would allow operation of the full Eu-PRAXIA facility within 8—10 years

    Three-dimensional evaluation of upper anterior alveolar bone dehiscence after incisor retraction and intrusion in adult patients with bimaxillary protrusion malocclusion*

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    Objective: The purpose of this study was to evaluate three-dimensional (3D) dehiscence of upper anterior alveolar bone during incisor retraction and intrusion in adult patients with maximum anchorage. Methods: Twenty adult patients with bimaxillary dentoalveolar protrusion had the four first premolars extracted. Miniscrews were placed to provide maximum anchorage for upper incisor retraction and intrusion. A computed tomography (CT) scan was performed after placement of the miniscrews and treatment. The 3D reconstructions of pre- and post-CT data were used to assess the dehiscence of upper anterior alveolar bone. Results: The amounts of upper incisor retraction at the edge and apex were (7.64±1.68) and (3.91±2.10) mm, respectively, and (1.34±0.74) mm of upper central incisor intrusion. Upper alveolar bone height losses at labial alveolar ridge crest (LAC) and palatal alveolar ridge crest (PAC) were 0.543 and 2.612 mm, respectively, and the percentages were (6.49±3.54)% and (27.42±9.77)%, respectively. The shape deformations of LAC-labial cortex bending point (LBP) and PAC-palatal cortex bending point (PBP) were (15.37±5.20)° and (6.43±3.27)°, respectively. Conclusions: Thus, for adult patients with bimaxillary protrusion, mechanobiological response of anterior alveolus should be taken into account during incisor retraction and intrusion. Pursuit of maximum anchorage might lead to upper anterior alveolar bone loss

    Fluoride therapy of type I osteoporosis.

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    Sodium Fluoride (NaF) is the only medication so far clinically available with a bone formation stimulating property, through its peculiar mitogenic dose-dependent action on the osteoblast cell line. Bone strength is commensurate to bone mass, and in a condition with fragility fractures, like osteoporosis, it seems logical to restore bone mass without weakening bone strength. However, as with any active drug. NaF therapy requires adhesion to elementary rules if drawbacks are to be prevented. A first mandatory rule is not to prescribe NaF without calcium supplementation, if bone loss at the appendicular skeleton is to be avoided; to prevent this, the availability of monofluorophosphate (MFP), containing the fluoride and calcium salts in the same preparation has enhanced the compliance to calcium supplementation. A second rule is not to give supraphysiological doses of vitamin D, for the same reason. Third, if one wants to avoid a calcium shift from cortical to trabecular bone and osteomalacia, one should use small doses of NaF, of the order of 50 mg/day. With this in mind, the bioavailability of the drug has to be taken into account, particularly its gastrointestinal absorption which is dramatically enhanced if a plain non entericoated (EC) capsule is used, as compared to that of an EC tablet with the same face value. Too much NaF is deleterious to bone, a fact known for years. Already in 1972, it was noted that in all patients receiving 60 mg or more of NEC NaF, daily, morphologically abnormal bone developed and which appeared irregular and contained areas of incompletely mineralized bone. The bone was histologically and microradiographically normal in patients receiving 45 mg or less of NEC NaF/day. Fourth, NaF therapy is contraindicated in renal insufficiency owing to an enhanced retention in the skeleton. NaF is, however, by no means the ideal medication, because its therapeutic window is narrow. It has many bothersome drawbacks, and notably it is irritating for the gastric mucosa, a hazard which may be partly circumvented by the use of an Ec or slow release tablet. Furthermore, peripheral stress fractures may occur, and, in our experience, they were seen in 17% of patients, almost exclusively in females with a low lumbar BMD. Their occurrence should be curtailed by not allowing an increase in alkaline phosphatase activity of more than 50%. This is a relatively benign complication, because no stress fracture degenerated into a complete fracture. In all cases, the stress fractures healed after a transitory drug discontinuation. If there is some concern about cortical bone, NaF therapy may be associated with an antiresorber like estrogens which will prevent any further bone loss, and does not impair the response to NaF. NaF therapy should be reserved for patients suffering chiefly from trabecular osteoporosis and should be avoided in senile osteoporosis, because of a frequently impaired renal function. Currently, we would recommend in clinical practice a daily dose of 50 mg EC-NaF or 150 mg Ca-MFP as the therapy of involutional osteoporosis in women, reserving the dose of 75 mg EC-NAF or 200 mg MFP for males or female patients resistant to lower dose. The therapy should be maintained for 2 to 3 years, or more, according to the bone response, taking into account that patients with the vertebral crush fracture syndrome have lost on average 30%, as compard to the young adult mean
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