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Sökning: WFRF:(Aberger Martin)

  • Resultat 1-3 av 3
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1.
  • Aberger, Martin (författare)
  • Effects of Nonlinearities in Black Box Identification of an Industrial Robot
  • 2000
  • Rapport (övrigt vetenskapligt/konstnärligt)abstract
    • This paper discusses effects of nonlinearities in black box identification of one axis of a robot. The used data come from a commercial ABB robot, IRB1400. A three-mass flexible model for the robot was built in MathModelica. The nonlinearities in the model are nonlinear friction and backlash in the gear box.
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2.
  • Norrlöf, Mikael, 1971-, et al. (författare)
  • Modeling and Identification of a Mechanical Industrial Manipulator
  • 2002
  • Ingår i: Proceedings of the 15th IFAC World Congress. - Linköping : Linköping University Electronic Press. - 9783902661746 ; , s. 852-852, s. 250-255
  • Rapport (övrigt vetenskapligt/konstnärligt)abstract
    • This paper covers modeling and identification of one joint of an industrial robot manipulator including flexibilities. It is shown how models can be built in the Modelica graphical environment and how these models can be transformed into a mathematical state space description which directly can be used for identification. A motivation to use linear models for modeling of the robot arm is given. This includes an analysis of the nonlinearities in the input/output data from the actual robot using a special kind of input signal. Identification and validation of the physically parameterized models are also covered.
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3.
  • Redmer, Torben, et al. (författare)
  • JUN mediates the senescence associated secretory phenotype and immune cell recruitment to prevent prostate cancer progression
  • 2024
  • Ingår i: Molecular Cancer. - : BioMed Central (BMC). - 1476-4598. ; 23:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Prostate cancer develops through malignant transformation of the prostate epithelium in a stepwise, mutation-driven process. Although activator protein-1 transcription factors such as JUN have been implicated as potential oncogenic drivers, the molecular programs contributing to prostate cancer progression are not fully understood.Methods: We analyzed JUN expression in clinical prostate cancer samples across different stages and investigated its functional role in a Pten-deficient mouse model. We performed histopathological examinations, transcriptomic analyses and explored the senescence-associated secretory phenotype in the tumor microenvironment.Results: Elevated JUN levels characterized early-stage prostate cancer and predicted improved survival in human and murine samples. Immune-phenotyping of Pten-deficient prostates revealed high accumulation of tumor-infiltrating leukocytes, particularly innate immune cells, neutrophils and macrophages as well as high levels of STAT3 activation and IL-1β production. Jun depletion in a Pten-deficient background prevented immune cell attraction which was accompanied by significant reduction of active STAT3 and IL-1β and accelerated prostate tumor growth. Comparative transcriptome profiling of prostate epithelial cells revealed a senescence-associated gene signature, upregulation of pro-inflammatory processes involved in immune cell attraction and of chemokines such as IL-1β, TNF-α, CCL3 and CCL8 in Pten-deficient prostates. Strikingly, JUN depletion reversed both the senescence-associated secretory phenotype and senescence-associated immune cell infiltration but had no impact on cell cycle arrest. As a result, JUN depletion in Pten-deficient prostates interfered with the senescence-associated immune clearance and accelerated tumor growth.Conclusions: Our results suggest that JUN acts as tumor-suppressor and decelerates the progression of prostate cancer by transcriptional regulation of senescence- and inflammation-associated genes. This study opens avenues for novel treatment strategies that could impede disease progression and improve patient outcomes. Graphical Abstract: (Figure presented.).
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