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  • 1
    Book
    Book
    Cambridge, Mass. [u.a.] : Productivity Press
    UID:
    (DE-627)303121041
    Format: XXI, 249 S , Ill., Kt
    ISBN: 091529916X
    Language: English
    Subjects: Economics
    RVK:
    Keywords: Japan ; Management ; Methode
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  • 2
    UID:
    (DE-627)1633172589
    ISSN: 0118-8534
    In: Asian journal of pentecostal studies, Baguio City : Sem., 1998, 14(2011), 1, Seite 74-92, 0118-8534
    In: volume:14
    In: year:2011
    In: number:1
    In: pages:74-92
    Language: English
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  • 3
    UID:
    (DE-627)1757456821
    ISSN: 0165-1765
    In: Economics letters, Amsterdam [u.a.] : Elsevier, 1978, 193(2020) vom: Aug., Seite 1-5, 0165-1765
    In: volume:193
    In: year:2020
    In: month:08
    In: pages:1-5
    Additional Edition: 10.1016/j.econlet.2020.109329
    Language: English
    Keywords: Aufsatz in Zeitschrift
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  • 4
    UID:
    (DE-627)1878306960
    In: ASEE Annual Conference (129. : 2022 : Minneapolis, Minn.), Excellence through diversity ; Volume 6 of 30, Red Hook, NY : Curran Associates, Inc., 2023, (2023), Seite 4181-4188
    In: year:2023
    In: pages:4181-4188
    Language: English
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  • 5
    UID:
    (DE-627)260909971
    ISSN: 0743-7951
    In: Wisconsin international law journal, Madison, Wis., 1983, 13 (1995),2, S. 565-584, 0743-7951
    In: volume:13
    In: year:1995
    In: number:2
    In: pages:565-584
    Language: English
    Keywords: Aufsatz in Zeitschrift
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  • 6
    Online Resource
    Online Resource
    [Erscheinungsort nicht ermittelbar] : EuroPython
    Show associated volumes
    UID:
    (DE-627)1820987442
    Format: 1 Online-Ressource (118 MB, 00:42:31:09)
    Content: With the increase in computing power, harnessing and controlling one’s code out of the single-threaded realm becomes an ever-increasing problem, coupled with the desire to stay in the Python layer. With the recent tools and frameworks that have been published, escaping the GIL cleanly is much easier than before, allow one’s Python code to effectively utilize multi-core and many core architectures in the most Pythonic ways possible. In this talk, learn about how to utilize static multiprocessing for process pinning, and effectively balancing thread pools with a monkey-patched import of threading modules. Overview: Introduction to multithreading and multiprocessing in Python History of multithreading+multiprocessing in Python, classic frameworks Problems that can occur (oversubscription, nested parallelism issues, process hopping, pool resource on shared machines) Python accessing bigger hardware over the last few years (28+ cores, etc) When to stay in the GIL, and when to escape it The advantages and safety of the GIL Python-level exiting of the GIL; analysis of when to return to single-threaded, and when threading is a deceivingly bad idea Accountability of frameworks that natively exit the GIL The new multithreading and multiprocessing libraries and techniques static multiprocessing module (smp) (and monkey patching of multiprocessing) thread pool control with command line calls of Python ( python -m tbb -p 8) Putting it all together Examples of using static multiprocessing on a large machine to stop oversubscription Example of pseudo-daemon process on 4-core machine by processor pinning Thread pool control on a simple NumPy example Summary - Best practices for using above methods to control multithreading+multiprocessing What needs to be done in the space (frameworks and things that need to be exposed) Problems that still exist in the area Q&A
    Note: Audiovisuelles Material
    In: EuroPython 2018, (Jan. 2018)
    Language: English
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  • 7
    Book
    Book
    Hongkong : Internat. Studies Group
    UID:
    (DE-604)BV006548864
    Format: 50 S.
    Language: English
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  • 8
    UID:
    (DE-627)507378555
    Format: graph. Darst.
    ISBN: 0071460748
    In: The handbook of mortgage-backed securities, New York, NY [u.a.] : McGraw-Hill, 2006, (2006), Seite 333-362, 0071460748
    In: year:2006
    In: pages:333-362
    Language: English
    Keywords: Aufsatz im Buch
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  • 9
    UID:
    (DE-627)1067381902
    Format: Illustrationen
    ISBN: 9781482264081
    Note: Literaturverzeichnis: Seite 349
    In: Additive manufacturing handbook, Boca Raton : CRC Press, 2017, (2017), Seite 329-349, 9781482264081
    In: year:2017
    In: pages:329-349
    Language: English
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  • 10
    Online Resource
    Online Resource
    [Erscheinungsort nicht ermittelbar] : eScholarship, University of California
    UID:
    (DE-627)1803315636
    Content: Cardiac remodeling is an essential process that facilitates heart development and wound healing responses post-injury. Cardiac fibroblasts (CFs) are the primary cell type responsible for maintaining myocardial structure and the cardiac extracellular matrix (ECM). CFs contribute to both basal ECM synthesis and its enhanced generation in response to cardiac injury: unregulated, these actions can lead to cardiac fibrosis and decreased cardiac performance. Soluble factors and mechanical cues can stimulate the transformation of CFs into myofibroblasts that increase ECM synthesis, proliferation and migration and that express numerous pro-fibrogenic genes. The work to be described here investigates a novel pro-fibrotic signaling pathway initiated by the release of cellular adenosine triphosphate (ATP) from CFs via connexin (Cx) gap junction hemi-channels following mechanical perturbations (Chapter 3). Importantly, released ATP functions as an autocrine/paracrine signaling molecule, which activates P2Y₂ nucleotide receptors and drives myofibroblast transformation, as indicated by increased collagen synthesis, CF migration and proliferation and the up-regulation of pro-fibrotic genes including [alpha]- smooth muscle actin ([alpha]-SMA) and plasminogen activator inhibitor (PAI)-1 (Chapters 3 & 4). Collagen synthesis and PAI-1 expression are sensitive to MAPK/ERK inhibition, while [alpha]-SMA expression and CF contractile responses are sensitive to RhoA/ROCK inhibition; both pathways are activated upon P2Y₂ stimulation by ATP. However, attenuating this signaling are ectonucleoside triphosphate diphosphohydrolases (ENTPDs), extracellular enzymes that hydrolyze ATP and play an essential role in regulating pro-fibrotic nucleotide signaling. ENTPD inhibition with siRNA or pharmacological agents increased basal extracellular ATP concentration and was sufficient to drive CF collagen synthesis and myofibroblast transformation (Chapter 5). Furthermore, ENTPD activity not only hydrolyzes pro- fibrotic ATP but also facilitates the generation of adenosine, a bioactive molecule that activates A2B adenosine receptors with anti-fibrotic effects. Together, these findings identify an autocrine/paracrine mechanism of CF regulation initiated by cellular ATP release and integrating pro-fibrotic ATP-P2Y and anti-fibrotic adenosine-P1 signaling, which are mediated by nucleotidase activity. This regulatory system contributes to both basal CF phenotype and response to acute cellular stress. These findings not only have direct implications in the understanding of cardiac fibrosis, but they may represent a general mechanism underlying the regulation of cellular homeostasis and response to injury
    Note: Dissertation eScholarship, University of California
    Language: Undetermined
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