| 1. |
- Filieri, Antonio, et al.
(author)
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Automated Design of Self-Adaptive Software with Control-Theoretical Formal Guarantees
- 2015
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In: Software Engineering and Management 2015 : Multikonferenz der GI-Fachbereiche Softwaretechnik (SWT) und Wirtschaftsinformatik (WI), FA WI-MAW - Multikonferenz der GI-Fachbereiche Softwaretechnik (SWT) und Wirtschaftsinformatik (WI), FA WI-MAW. - 1617-5468. - 9783885796336 ; P-239, s. 112-113
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Conference paper (peer-reviewed)abstract
- Self-adaptation enables software to execute successfully in dynamic, unpredictable, and uncertain environments. However, most of the current approaches lack formal guarantees on the effectiveness and dependability of the adaptation mechanisms, limiting their applicability in practice. Control theory established a broad set of mathematically grounded techniques for the control of dynamic systems for several engineering fields. While control shares self-evident similarities with software adaptation, modeling software behavior as a system of differential or difference equations is not straightforward, nor is mastering the mathematical background needed for synthesizing a suitable controller. In this paper we focus on the automatic modeling and controller synthesis for systems with a single knob affecting the satisfaction of a quantitative requirements. Effectiveness and performance of the controller are guaranteed by construction. The approach is fully automated and implemented in several programming languages, empowering non-experts with the ability of applying control principles to a wide range of software adaptation problems.
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| 2. |
- Wittnam, Jessica L, et al.
(author)
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Pyroglutamate amyloid β (Aβ) aggravates behavioral deficits in transgenic amyloid mouse model for Alzheimer disease.
- 2012
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In: The Journal of biological chemistry. - 1083-351X. ; 287:11, s. 8154-62
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Journal article (peer-reviewed)abstract
- Pyroglutamate-modified Aβ peptides at amino acid position three (Aβ(pE3-42)) are gaining considerable attention as potential key players in the pathogenesis of Alzheimer disease (AD). Aβ(pE3-42) is abundant in AD brain and has a high aggregation propensity, stability and cellular toxicity. The aim of the present work was to study the direct effect of elevated Aβ(pE3-42) levels on ongoing AD pathology using transgenic mouse models. To this end, we generated a novel mouse model (TBA42) that produces Aβ(pE3-42). TBA42 mice showed age-dependent behavioral deficits and Aβ(pE3-42) accumulation. The Aβ profile of an established AD mouse model, 5XFAD, was characterized using immunoprecipitation followed by mass spectrometry. Brains from 5XFAD mice demonstrated a heterogeneous mixture of full-length, N-terminal truncated, and modified Aβ peptides: Aβ(1-42), Aβ(1-40), Aβ(pE3-40), Aβ(pE3-42), Aβ(3-42), Aβ(4-42), and Aβ(5-42). 5XFAD and TBA42 mice were then crossed to generate transgenic FAD42 mice. At 6 months of age, FAD42 mice showed an aggravated behavioral phenotype compared with single transgenic 5XFAD or TBA42 mice. ELISA and plaque load measurements revealed that Aβ(pE3) levels were elevated in FAD42 mice. No change in Aβ(x)(-42) or other Aβ isoforms was discovered by ELISA and mass spectrometry. These observations argue for a seeding effect of Aβ(pE-42) in FAD42 mice.
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