Small UAS Detect and Avoid Requirements Necessary for Limited Beyond Visual Line of Sight (BVLOS) Operations

Potential small Unmanned Aircraft Systems (sUAS) beyond visual line of sight (BVLOS) operational scenarios/use cases and Detect And Avoid (DAA) approaches were collected through a number of industry wide data calls. Every 333 Exemption holder was solicited for this same information. Summary information from more than 5,000 exemption holders is documented, and the information received had varied level of detail but has given relevant experiential information to generalize use cases. A plan was developed and testing completed to assess Radio Line Of Sight (RLOS), a potential key limiting factors for safe BVLOS ops. Details of the equipment used, flight test area, test payload, and fixtures for testing at different altitudes is presented and the resulting comparison of a simplified mathematical model, an online modeling tool, and flight data are provided. An Operational Framework that defines the environment, conditions, constraints, and limitations under which the recommended requirements will enable sUAS operations BVLOS is presented. The framework includes strategies that can build upon Federal Aviation Administration (FAA) and industry actions that should result in an increase in BVLOS flights in the near term. Evaluating approaches to sUAS DAA was accomplished through five subtasks: literature review of pilot and ground observer see and avoid performance, survey of DAA criteria and recommended baseline performance, survey of existing/developing DAA technologies and performance, assessment of risks of selected DAA approaches, and flight testing. Pilot and ground observer see and avoid performance were evaluated through a literature review. Development of DAA criteria—the emphasis here being well clear— was accomplished through working with the Science And Research Panel (SARP) and through simulations of manned and unmanned aircraft interactions. Information regarding sUAS DAA approaches was collected through a literature review, requests for information, and direct interactions. These were analyzed through delineation of system type and definition of metrics and metric values. Risks associated with sUAS DAA systems were assessed by focusing on the Safety Risk Management (SRM) pillar of the SMS (Safety Management System) process. This effort (1) identified hazards related to the operation of sUAS in BVLOS, (2) offered a preliminary risk assessment considering existing controls, and (3) recommended additional controls and mitigations to further reduce risk to the lowest practical level. Finally, flight tests were conducted to collect preliminary data regarding well clear and DAA system hazards

Deletion 17q12 is a recurrent copy number variant that confers high risk of autism and schizophrenia

Autism spectrum disorders (ASD) and schizophrenia are neurodevelopmental disorders for which recent evidence indicates an important etiologic role for rare copy number variants (CNVs) and suggests common genetic mechanisms. We performed cytogenomic array analysis in a discovery sample of patients with neurodevelopmental disorders referred for clinical testing. We detected a recurrent 1.4 Mb deletion at 17q12, which harbors HNF1B, the gene responsible for renal cysts and diabetes syndrome (RCAD), in 18/15,749 patients, including several with ASD, but 0/4,519 controls. We identified additional shared phenotypic features among nine patients available for clinical assessment, including macrocephaly, characteristic facial features, renal anomalies, and neurocognitive impairments. In a large follow-up sample, the same deletion was identified in 2/1,182 ASD/neurocognitive impairment and in 4/6,340 schizophrenia patients, but in 0/47,929 controls (corrected p = 7.37 × 10?5). These data demonstrate that deletion 17q12 is a recurrent, pathogenic CNV that confers a very high risk for ASD and schizophrenia and show that one or more of the 15 genes in the deleted interval is dosage sensitive and essential for normal brain development and function. In addition, the phenotypic features of patients with this CNV are consistent with a contiguous gene syndrome that extends beyond RCAD, which is caused by HNF1B mutations only.<br/