Novel Electromagnetic Characterization Methods for New Materials and Structures in Aerospace Platforms.

The tendency over the last decades in the aerospace industry is to substitute classic metallic materials with new composite materials such as carbon fiber composites (CFC), fiber glass, etc., as well as adding electronic devices to ensure the safety and proper platform operation. Due to this, to protect the aircraft against the Electromagnetic Environmental Effects (E3), it is mandatory to develop accurate electromagnetic (EM) characterization measurement systems to analyze the behavior of new materials and electronic components.

Characterization of Joints between Carbon Fiber Composite Parts Using a Microstrip Transmission Line Method.

The electromagnetic performance of aerial platforms, which are composed mostly of nonmetallic materials, is a subject of great interest at present time. The behavior of this type of composite structure against electromagnetic environmental effects (E3), such as lightning, is not well-studied as in the case of metalic structures. The purpose of this article is to characterize the joints present in aerial platforms constructed mainly of nonmetallic composite materials.

[Prader Willi syndrome patients: study of 77 patients].

Background: The Prader-Willi syndrome (PWS) is a disease of genetic origin. It is characterized by neonatal hypotonia, hypogonadism, hiperfagia leading to obesity, low stature, developmental delay, moderate mental retardation, abnormal behavior and characteristic facial appearance. It is caused by the loss or the inactivation of paternal genes of the imprinted region 15q11-13.

Imprinting center analysis in Prader-Willi and Angelman syndrome patients with typical and atypical phenotypes.

Prader-Willi syndrome (PWS) and Angelman syndrome (AS) are genetic disorders caused by a deficiency of imprinted gene expression from the paternal or maternal chromosome 15, respectively. This deficiency is due to the deletion of the 15q11-q13 region, parental uniparental disomy of the chromosome 15, or imprinting defect (ID). Mutation of the UBE3A gene causes approximately 10% of AS cases.