| 1. |
|
|
| 2. |
- Seita, D., et al.
(författare)
-
Large-scale supervised learning of the grasp robustness of surface patch pairs
- 2017
-
Ingår i: 2016 IEEE International Conference on Simulation, Modeling, and Programming for Autonomous Robots, SIMPAR 2016. - : Institute of Electrical and Electronics Engineers Inc.. - 9781509046164 ; , s. 216-223
-
Konferensbidrag (refereegranskat)abstract
- The robustness of a parallel-jaw grasp can be estimated by Monte Carlo sampling of perturbations in pose and friction but this is not computationally efficient. As an alternative, we consider fast methods using large-scale supervised learning, where the input is a description of a local surface patch at each of two contact points. We train and test with disjoint subsets of a corpus of 1.66 million grasps where robustness is estimated by Monte Carlo sampling using Dex-Net 1.0. We use the BIDMach machine learning toolkit to compare the performance of two supervised learning methods: Random Forests and Deep Learning. We find that both of these methods learn to estimate grasp robustness fairly reliably in terms of Mean Absolute Error (MAE) and ROC Area Under Curve (AUC) on a held-out test set. Speedups over Monte Carlo sampling are approximately 7500x for Random Forests and 1500x for Deep Learning.
|
|
| 3. |
|
|
| 4. |
- Rossi, Derrick J, et al.
(författare)
-
Deficiencies in DNA damage repair limit the function of haematopoietic stem cells with age
- 2007
-
Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 447:7145, s. 725-729
-
Tidskriftsartikel (refereegranskat)abstract
- A diminished capacity to maintain tissue homeostasis is a central physiological characteristic of ageing. As stem cells regulate tissue homeostasis, depletion of stem cell reserves and/or diminished stem cell function have been postulated to contribute to ageing. It has further been suggested that accumulated DNA damage could be a principal mechanism underlying age-dependent stem cell decline. We have tested these hypotheses by examining haematopoietic stem cell reserves and function with age in mice deficient in several genomic maintenance pathways including nucleotide excision repair, telomere maintenance and non-homologous end-joining. Here we show that although deficiencies in these pathways did not deplete stem cell reserves with age, stem cell functional capacity was severely affected under conditions of stress, leading to loss of reconstitution and proliferative potential, diminished self-renewal, increased apoptosis and, ultimately, functional exhaustion. Moreover, we provide evidence that endogenous DNA damage accumulates with age in wild-type stem cells. These data are consistent with DNA damage accrual being a physiological mechanism of stem cell ageing that may contribute to the diminished capacity of aged tissues to return to homeostasis after exposure to acute stress or injury.
|
|
| 5. |
- Rossi, Derrick J., et al.
(författare)
-
Hematopoietic stem cell quiescence attenuates DNA damage response and permits DNA damage accumulation during aging
- 2007
-
Ingår i: Cell Cycle. - 1551-4005. ; 6:19, s. 2371-2376
-
Tidskriftsartikel (refereegranskat)abstract
- The aging of tissue-specific stem and progenitor cells is believed to be central to the pathophysiological conditions arising in aged individuals. While the mechanisms driving stem cell aging are poorly understood, mounting evidence points to age-dependent DNA damage accrual as an important contributing factor. While it has been postulated that DNA damage may deplete stem cell numbers with age, recent studies indicate that murine hematopoietic stem cell (HSC) reserves are in fact maintained despite the accrual of genomic damage with age. Evidence suggests this to be a result of the quiescent (G(0)) cell cycle status of HSC, which results in an attenuation of checkpoint control and DNA damage responses for repair or apoptosis. When aged stem cells that have acquired damage are called into cycle under conditions of stress or tissue regeneration however, their functional capacity was shown to be severely impaired. These data suggest that age-dependent DNA damage accumulation may underlie the diminished capacity of aged stem cells to mediate a return to homeostasis after acute stress or injury. Moreover, the cytoprotection afforded by stem cell quiescence in stress-free, steady-state conditions suggests a mechanism through which potentially dangerous lesions can accumulate in the stem cell pool with age.
|
|
