Mechanical (direct-drive) systems designed for high-speed and high-accuracy applications require control systems that eliminate the influence of disturbances like cogging forces and friction. One way to achieve additional disturbance rejection is to extend the usual (P(I)D) controller with a disturbance observer. There are two distinct ways to design, represent, and implement a disturbance observer, but in this paper it is shown that the one is a generalization of the other. A general systematic design procedure for disturbance observers that incorporates stability requirements is given. Furthermore, it is shown that a disturbance observer can be transformed into a classical feedback structure, enabling numerous well-known tools to be used for the design and analysis of disturbance observers. Using this feedback interpretation of disturbance observers, it will be shown that a disturbance observer based robot tracking controller can be constructed that is equivalent to a passivity based controller. By this equivalence not only stability proofs of the disturbance observer based controller are obtained, but it also provides more transparent controller parameter selection rules for the passivity based controller.

Cross-sectional as well as longitudinal studies indicate that the prevalence of periodontal disease in persons with Down's syndrome (DS) under the age of 30 years is extremely high. It is even noted in the deciduous dentition. The progression of the disease is rapid, especially in the younger age groups. Severe periodontal breakdown with horizontal bone loss is often present in the lower anteriors. The large amount of plaque and calculus alone cannot explain the severity of periodontal disease in DS persons. Many contributing factors are reported. Abnormal capillary morphology, disorders in connective tissue and anatomical aspects of teeth are some of those considered to be of influence. Alteration in immunological response may also play a role in the progression of the disease process. Disorders in the polymorphonuclear leucocyte function and monocyte function have been reported in persons with DS. T-cell functioning declines after the first 10 years of life. T-cell lymphocyte counts are low and an immature subset of T-lymphocytes is present. This latter effect occurs especially in institutions where the immunological system is under stress. The altered immune response together with higher calculus scores may explain the difference in severity of periodontal disease between institutionalized DS children and those living at home.

Background: To assess health-related quality of life (HRQoL) in children (8-11 years) and adolescents (12-18 years) who survived retinoblastoma (RB), by means of the KIDSCREEN self-report questionnaire and the proxy-report version.

The MLL-AF9 fusion gene is associated with aggressive leukemias of both the myeloid and lymphoid lineage in infants, whereas in adults, this translocation is mainly associated with acute myeloid leukemia. These observations suggest that differences exist between fetal and adult tissues in terms of the 'cell of origin' from which the leukemia develops. Here we show that depending on extrinsic cues, human neonatal CD34(+) cells are readily immortalized along either the myeloid or lymphoid lineage upon MLL-AF9 expression and give rise to mainly lymphoid leukemia in immunocompromised mice. In contrast, immortalization of adult bone marrow CD34(+) cells is more difficult to achieve and is myeloid-biased, even when MLL-AF9 is expressed in purified hematopoietic stem cells (HSCs). Transcriptome analysis identified enrichment of HSC but not progenitor gene signatures in MLL-AF9-expressing cells. Although not observed in adult cells, neonatal cells expressing MLL-AF9 were enriched for gene signatures associated with poor prognosis, resistance to chemotherapeutic agents and MYC signaling. These results indicate that neonatal cells are inherently more prone to MLL-AF9-mediated immortalization than adult cells and suggest that intrinsic properties of the cell of origin, in addition to extrinsic cues, dictate lineage of the immortalized cell.