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Cross-regulation

What are the best guess maximum and minimum limits of the load current and are there any intermittent characteristics in its current demand such as those presented by motors, video monitors, pulsed loads, and so forth Always add 50 percent more to what is told to you since these estimates always turn out to be low. Also what are the maximum excursions in supply voltage that the designer feels that the circuit can withstand. This dictates the design approaches of the cross-regulation of the outputs, and feedback compensation in order to provide the needs of the loads. [Pg.2]

During the prototype stage, verify its operation with respect to the level of voltage spikes, cross regulation, output accuracy and ripple, and RFI, etc., and make corrections where necessary. [Pg.38]

Within multiple-output forward converters, it is possible to easily combine the filter chokes of complementary outputs (i.e., +/- 5V, etc.) together on the same core (see Figure 3-2f). This offers several advantages it saves space, vastly improves cross-regulation of those outputs, and exliibits superior ripple voltage levels on both outputs. [Pg.47]

In order to enhance the cross-regulation of the multiple outputs, it is desired to sense a portion of all the positive output voltages. To do this, one must investigate the technology of the circuits that must draw their power from the outputs. The hypothetical loads, in this case, are... [Pg.109]

Purine and pyrimidine biosynthesis parallel one another mole for mole, suggesting coordinated control of their biosynthesis. Several sites of cross-regulation characterize purine and pyrimidine nucleotide biosynthesis. The PRPP synthase reaction (reaction 1, Figure 34-2), which forms a precursor essential for both processes, is feedback-inhibited by both purine and pyrimidine nucleotides. [Pg.299]

Fig. 14.1. The Thl/Th2 balance is central to the regulation of normal wound repair. Tissue injury results in the initiation of an inflammatory response, mediated by a variety of cells and their by-products. Immune cells are recruited and cross-regulate the Thl/ Th2 balance that occurs in response to the cytokine environment. This balance is in turn cross-regulated by the chemokine/chemokine-receptor expression profile, which functions to amplify the inflammatory process. Cells residing in the injured tissue release profibrotic mediators, which promote fibroblast activation, proliferation, and differentiation to the myofibroblast phenotype. Myofibroblasts produce collagen to repair damaged tissue, which is an event that is favored by the inhibition of MMP activity. The Thl/Th2 balance is central to whether a normal or aberrant wound-repair process is established A Thl environment promotes normal tissue resolution (fibrinolysis), whereas a Th2 environment maintains the progression of fibrotic disease (excessive collagen deposition). Fig. 14.1. The Thl/Th2 balance is central to the regulation of normal wound repair. Tissue injury results in the initiation of an inflammatory response, mediated by a variety of cells and their by-products. Immune cells are recruited and cross-regulate the Thl/ Th2 balance that occurs in response to the cytokine environment. This balance is in turn cross-regulated by the chemokine/chemokine-receptor expression profile, which functions to amplify the inflammatory process. Cells residing in the injured tissue release profibrotic mediators, which promote fibroblast activation, proliferation, and differentiation to the myofibroblast phenotype. Myofibroblasts produce collagen to repair damaged tissue, which is an event that is favored by the inhibition of MMP activity. The Thl/Th2 balance is central to whether a normal or aberrant wound-repair process is established A Thl environment promotes normal tissue resolution (fibrinolysis), whereas a Th2 environment maintains the progression of fibrotic disease (excessive collagen deposition).
Latham, J.A. and Dent, S.Y. (2007) Cross-regulation of histone modifications. Nature Structural S, Molecular Biology, 14, 1017-1024. [Pg.20]

Induction of CYP3A enzymes is primarily mediated by PXR. However, CAR also plays a prominent role because several ligands that bind PXR also bind CAR. There is further cross-regulation at the level of response elements for these two nuclear receptors (16,19,47,150,151). The abundance of PXR itself is correlated with the level of expression of CYP3A4, CYP3A5, and CYP transcripts and CYP3A proteins in human liver (152). Three additional nuclear receptors, GR, LXR, and YDR, exert modulatory roles in CYP3A induction (Table 3). [Pg.183]

There may also be feedback activators, especially where cross-regulation occurs the product of one pathway activates another pathway. Thus, in purine biosynthesis (Chapter 10),... [Pg.112]

B. L. Wanner (1995). Signal transduction and cross regulation in the E. coli phosphate regulon PhoR. CreC and acetyl phosphate. In J. A. Hoch and T. J. Silhavy (Eds), Two Component Signal Transduction, American Society of Microbiology, Washington, DC, USA, pp. 203-221. [Pg.264]

IL-12 is considered as a counterbalancing cytokine to IL-4 as it cross regulates it. IL-13 has been identified as having... [Pg.668]

Cytotoxic activity of both NK cells and Tc lymphocytes is enhanced by IL-12 (it acts synergistically with IL-2 to induce IFNy synthesis by these cells and is considered as the most potent NK-ceH stimulator known). This cytotoxic enhancement occurs in parallel with depression of IgE production and reduction of IL-4 secretion (IL-12 and IL-4 cross regulate one another s activities). IL-12 effects are only seen early, whereas IL-4 effects are maintained. Studies have suggested a molecular basis for these temporal differences... [Pg.684]

Bouaboula M, Desnoyer N, Carayon P, Combes T, CaseUas P (1999a) Gi protein modulation induced by a selective inverse agonist for the peripheral cannabinoid receptor CB2 impUcation for intraceUular signalization cross-regulation. Mol Pharmacol 55 473-480... [Pg.107]

Hursh, D., Padgett, R., and Gelbart, W. (1993). Cross regulation of decapentaplegic and Ultrabithorax transcription in the embryonic visceral mesoderm of Drosophila. Development 777 1211-1222. [Pg.43]

Gould, A., Morrison, A., Sproat, G., White, R.A.H., Krumlauf, R. 1997. Positive cross-regulation and enhancer sharing-two mechanisms for specifying overlapping Hox expression patterns. Genes Dev. 11, 900-913. [Pg.35]

Maconochie, M.K., Nonchev, S., Studer, M., Chan, S.-K., Popperl, H., Sham, M.H., Mann, R.S., Krumlauf, R. 1997. Cross-regulation in the mouse HoxB complex the expression of Hoxb2 in rhombomere 4 is regulated by Hoxbl. Genes Dev. 11, 1885-1895. [Pg.38]


See other pages where Cross-regulation is mentioned: [Pg.274]    [Pg.55]    [Pg.61]    [Pg.320]    [Pg.328]    [Pg.303]    [Pg.113]    [Pg.113]    [Pg.593]    [Pg.299]    [Pg.304]    [Pg.11]    [Pg.327]    [Pg.39]    [Pg.173]    [Pg.80]    [Pg.47]    [Pg.47]    [Pg.30]    [Pg.42]    [Pg.109]    [Pg.253]    [Pg.85]    [Pg.86]    [Pg.375]    [Pg.381]    [Pg.14]    [Pg.21]    [Pg.374]    [Pg.84]   
See also in sourсe #XX -- [ Pg.55 , Pg.61 ]

See also in sourсe #XX -- [ Pg.85 ]




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