Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Resistance of cells

Figure 6. Comparison of internal resistance of cells with different /T-Al20, electrolyte geometries. Figure 6. Comparison of internal resistance of cells with different /T-Al20, electrolyte geometries.
First, we have tried to evaluate the resistance of cells toward pH changes without a change of osmolar-ity. This major precaution has to be taken, because, otherwise, the results would have been changed by two different parameters. [Pg.85]

Figure 22-1 An electrolytic cell for determining (a) Current = 0.00 mA. (b) Schematic of cell in (a) with internal resistance of cell represented by a 15.0 n resistor and fiappued increased to give a current of 2.00 mA. Figure 22-1 An electrolytic cell for determining (a) Current = 0.00 mA. (b) Schematic of cell in (a) with internal resistance of cell represented by a 15.0 n resistor and fiappued increased to give a current of 2.00 mA.
On the other hand, owing to the high diffusion resistance of cell and subcellular membranes, sensors based on HIS compare less favorably with enzyme sensors with respect to sensitivity and measuring time. Figure 104 presents a comparison of the basic characteristics of HIS sensors with those of enzyme sensors. [Pg.231]

Cell Hardware. Cell jars are constructed almost exclusively of injection-molded plastics, which are resistant to the strong alkali electrolyte. The most generally used materials are modified styrenes or copolymers of styrene and acrylonitrile (SAN). Another material that has been found to increase shock resistance of cells is ABS plastic (acrylonitrile—butadiene—styrene). All of these plastics can be injection-molded, are solvent-sealable and, in general, meet operating temperature ranges up to about 70°C. For applications that require greater resistance to temperature, some of the more recent plastics such as polysulfone and poly(phenylene oxide) (PPO) injection-moldable materials able to withstand operating temperatures up to 150°C are used. [Pg.555]

Finally, the QCM can not only be used in a sensory mode but also as an actuator. It has been recently shown by Dultsev and coworkers [57] that virus particles deposited on the resonator surface may be displaced by increasing the shear amplitude of the resonator. Thus, it seems plausible that the resistance of cell-substrate interactions to lateral shear forces may be inferred from QCM measurements when the shear amplitude is increased to invasive magnitudes. The ease of the measurement, which can be automated and multiplexed, the rather simple experimental design, as well as the unique experimental access to the interface between living cells and technical substrates is very likely to create growing interest within the cell culture community for these new experimental options. [Pg.336]

Figure 18.9 Apoptosis resistance is a hallmark of cancer. Multiple genetic lesions results In an Increased apoptotic threshold that accompanies the cancerous phenotype. The relative resistance of cells to apoptosis Is Indicated by the thickness of the arrow and the key genes involved In setting the apoptotic threshold are shown. The function of these genes can be affected by either genetic mutations (such as loss of heterozygosity, LOH) or direct inhibition of their function by cellular Inhibitors (such as Bcl-2, lAP, or heath shock (HSP) proteins). The ultimate outcome is the inability of cancer cells to undergo apoptosis despite exposure to potent cell death triggers (such as In case of therapeutic inten/ention with chemo- or radiation therapy). Figure 18.9 Apoptosis resistance is a hallmark of cancer. Multiple genetic lesions results In an Increased apoptotic threshold that accompanies the cancerous phenotype. The relative resistance of cells to apoptosis Is Indicated by the thickness of the arrow and the key genes involved In setting the apoptotic threshold are shown. The function of these genes can be affected by either genetic mutations (such as loss of heterozygosity, LOH) or direct inhibition of their function by cellular Inhibitors (such as Bcl-2, lAP, or heath shock (HSP) proteins). The ultimate outcome is the inability of cancer cells to undergo apoptosis despite exposure to potent cell death triggers (such as In case of therapeutic inten/ention with chemo- or radiation therapy).
The relative ratios of anti- and pro-apoptotic Bcl-2-family proteins dictate the ultimate sensitivity to or resistance of cells to various apoptotic stimuli, including hypoxia, radiation, anticancer drugs, oxidants, Ca2+ overload, ceramide, and growth-factor/neurotrophin deprivation [25]. [Pg.148]

Saifuddin M, Parker CJ, Peeples ME, Gorny MK, Zolla-Pazner S, Ghassemi M, Rooney lA, Atkinson JP, Spear GT (1995) Role of virion-associated glycosylphosphatidylinositol-linked proteins CD55 and CD59 in complement resistance of cell line-derived and primary isolates of HIV-1. J Exp Med 182 501-509... [Pg.202]

It is noteworthy that a change of heat resisteince was also observed in hypothermal conditions. Thus at 20 C an increase was observed both of cold- and heat resistance of the above also of thermostability of PSA membranes. But the dynamics of the above values has its own characteristics if the cold resistance of cells increased monotonically during the whole experiment, the other two reached their ma-ximtun on the 2-3d day and then decreased. [Pg.3418]

On the other hand, inhibitors such as ABA (abscisic acid) are used in the further stages of somatic embryogenesis. They cause the maturation of somatic embryos through globular, heart-shaped, torpedo and cotyledonary stages (Fig. 1), and in the final stage -their development into the seedling. Moreover, ABA increases the resistance of cells to stress conditions. [Pg.427]

Recent data suggests that poly(ADP-ribose) metabolism may be involved in the expression of radiation sensitivity and in the repair of radiation damage (4-11). Therefore, ADP-ribosylation is a likely candidate for one of the biochemical mechanisms involved in the repair of radiation damage, and in the intrinsic radiation sensitivity (resistance) of cells. [Pg.520]

Builenweg JR, Rutten WLC, Willems WPA, Van Nieuwkasteele JW (1998) Measurement of sealing resistance of cell-electrode interfaces in neuronal cultures using impedance spectroscopy. Med Biol Eng Comput 36 630-637... [Pg.506]

Interestingly, CPT does not bind to topoisomerase I and only weakly to B-DNA under physiological conditions [5], so both biomolecules and CPT are needed to form stable ternary complex 50. Additional evidence supporting such mechanism comes from the observation of resistance of cell lines toward CPT which have specific mutations of enzyme [180-182] (for medical consequences of CPT resistance, see [4, 183]). Similarly, deletion of gene coding topoisomerase I from yeast (Saccharomyces cerevisiae) resulted in fuU resistance of viable cells to CPT, with restoration of sensitivity to CPT after expression of human or yeast topoisomerase I [184, 185]. The schematic mechanism of CPT action is given in Fig. 22.6. [Pg.4306]


See other pages where Resistance of cells is mentioned: [Pg.597]    [Pg.12]    [Pg.610]    [Pg.265]    [Pg.497]    [Pg.26]    [Pg.46]    [Pg.177]    [Pg.16]    [Pg.349]    [Pg.83]    [Pg.91]    [Pg.160]    [Pg.219]    [Pg.306]    [Pg.61]    [Pg.93]    [Pg.47]    [Pg.35]    [Pg.209]    [Pg.316]    [Pg.798]    [Pg.63]    [Pg.684]    [Pg.127]    [Pg.463]    [Pg.297]    [Pg.786]    [Pg.425]    [Pg.1881]    [Pg.3418]    [Pg.136]    [Pg.597]    [Pg.570]    [Pg.350]   
See also in sourсe #XX -- [ Pg.5 ]




SEARCH



Cell resistance

Resistant cells

© 2024 chempedia.info