Improving geometric accuracy of 3D printed parts using 3D metrology feedback and mesh morphing

ABSTRACT: Additive manufacturing (AM), also known as 3D printing, has gained significant interest due to the freedom it offers in creating complex-shaped and highly customized parts with little lead time. However, a current challenge of AM is the lack of geometric accuracy of fabricated parts. To improve the geometric accuracy of 3D printed parts, this paper presents a three-dimensional geometric compensation method that allows for eliminating systematic deviations by morphing the original surface mesh model of the part by the inverse of the systematic deviations. These systematic deviations are measured by 3D scanning multiple sacrificial printed parts and computing an average deviation vector field throughout the model. We demonstrate the necessity to filter out the random deviations from the measurement data used for compensation. Case studies demonstrate that printing the compensated mesh model based on the average deviation of five sacrificial parts produces a part with deviations about three times smaller than measured on the uncompensated parts. The deviation values of this compensated part based on the average deviation vector field are less than half of the deviation values of the compensated part based on only one sacrificial part

Clinico-pathological and biomolecular findings in Italian patients with multiple cutaneous neurofibromas

<p>Abstract</p> <p>Background</p> <p>Neurofibroma occurs as isolated or multiple lesions frequently associated with neurofibromatosis type 1 (NF1), a common autosomal dominant disorder affecting 1 in 3500 individuals. It is caused by mutations in the <it>NF1 </it>gene, which comprises 60 exons and is located on chromosome 17q11.2. <it>NF1 </it>is a fully penetrant gene exhibiting a mutation rate some 10-fold higher compared with most other disease genes. As a consequence, a high number of cases (up to 50%) are sporadic. Mutation detection is complex due to the large size of the <it>NF1 </it>gene, the presence of pseudogenes and the great variety of lesions.</p> <p>Methods</p> <p>110 patients with at least two neurofibroma lesions recorded in the files of the Pathology Department of the University of Modena during the period 1999-2010, were included in this study. Through interviews and examination of clinical charts, pedigrees were drawn for all patients who were affected by at least two neurofibromas. We attempted to delineate the clinical features of NF1 and the mutational spectrum in the cohort of 11 NF1 families identified. For each proband, the whole coding sequence and all splice sites were studied for mutations, either by the protein truncation test (PTT), or, more frequently, by denaturing high performance liquid chromatography (DHPLC). Two GIST tumors of NF1 patients were tested for somatic NF1 mutations.</p> <p>Results</p> <p>NF1 germline mutations were identified in 7 (68%) patients. A novel mutation, c.3457_3460delCTCA in exon 20, was detected in two unrelated patients and was associated with different clinical features. No NF1 somatic mutations were detected in the GIST tumors. A wide phenotypic and genotypic variability was registered, both in the spectrum of skin lesions and visceral neoplasms, even among members of the same family who had different clinical manifestations. A proclivity to multiple tumors arising in the same subject, and a higher tumor burden per family were the most relevant findings observed in patients affected with the NF1 mutation.</p> <p>Conclusions</p> <p>We report a novel NF1 mutation and we contribute data for the refinement of the NF1 genotype-phenotype spectrum.</p

SS18 Together with Animal-Specific Factors Defines Human BAF-Type SWI/SNF Complexes

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