Cell-surviving fraction

Cell surviving fractions after irradiation PadS-linear quadratic... 

Pad6 approximant for cell surviving fractions in radiobiological modelings... 

Figure 4.12 Cell survival fractions SF(D) as a function of absorbed radiation dose D in Gy (top panel). The bottom panel is the so-called reactivity R(D) given by product of the reciprocal dose D-1 and the negative natural logarithm of SF(D), as the ordinate versus D as the abscissa. Experiment (symbols) the mean clonogenic surviving fractions SF(D) (top panel) and R(D) = — (1/D) ln(SF) (bottom panel) for the Chinese hamster cells grown in culture and irradiated by 50 kV X-ray [73]. Theories solid curve - PLQ (Pads Linear Quadratic) model and dotted curve - LQ model (the straight line a + /SD on the bottom panel).

D2. Belkic, Cell surviving fractions after irradiation novel radiobiological models with the Michaelis-Menten enzyme kinetics and the Lambert W function, J. Math. Chem. 49 (2011) 1618. 

SCE increases absolute colony number and surviving fraction of CEU-E, CEU-G, and CEU-GM in kradiated human BM. An increase in the fraction of CDSd cells in the radioresistant S-phase has been noted, which suggests a possible mechanism (184). A cautionary note has been sounded about attempting to predict interactions between SCE and CSEs in hemopoieticaHy deprived individuals (185). Although SCE synergizes with GM-CSE or GM-CSE and lL-3 to increase CEU-GM in vitro, no such effect has been found in vivo. 

Not all neurons have NFs. Indeed, one entire phylum in the animal kingdom, arthropods, expresses only type V nuclear lamins so arthropod cells have no IF cytoskeletal structures at all. In addition, mature oligodendrocytes lack IFs although their embryonic precursors contain vimentin. Clearly, the IFs are not essential for cell survival. Yet, in large myelinated fibers, NFs make up the bulk of axonal volume and represent a substantial fraction of the total protein in brain. In most organisms, IFs in both glia... 

It has been postulated that radiation may act as a potentiator of fluoropyrimidine-medi-cated cytotoxicity. This possibility is borne out of the observation that fluoropyrimidine-induced radiosensitization of human colon cancer cells tends to occur under conditions that produce at least some cytotoxicity by the drug alone (15,33,36,37). This hypothesis is further supported by the data employing FdUrd treatment in HT29 cells, which showed that enhancement ratio was significantly greater when surviving fraction was <0.7 than when the surviving fraction was >0.7 (p < 0.05 by t test) (Fig. 6). 

Fig. 3. Effect of gemcitabine on the sensitivity of HT-29 cells to radiation. Cells were incubated with no drug, 3 nM, 10 nM, and 30 nM gemcitabine for 24 h followed by radiation. Surviving fraction was corrected for cell survival in the absence of radiation. From Shewach et al. Cancer Res 1994 54 3218-3223.

Exposure of rat primary mixed hippocampal cell cultures to either sodium nitroprusside (SNP 100 xM) or 3-morpholinosydnonimine resulted in both a decrease in cell survival and an increase in free-radical accumulation. These SNP-induced events were blocked by either EGb 761 (10 to 100 pg/ml) or its flavonoid fraction CP 205 (25 pg/ml), as well as by inhibitors of protein kinase C (PKC chelerythrine) and 1-type calcium channels (nitrendipine). In contrast, the terpenoid constituents of EGb 761, known as bilobalide and ginkgolide B, as well as inhibitors of phospholipases A [3-[4-octadecyl)benzoyl]acrylic acid (OBAA)] and C (U-73122), failed to display any significant effects. Moreover, EGb 761 (50 pg/ml), CP 205 (25 pg/ml), and chelerythrine were also able to rescue hippocampal cells preexposed to SNP (up to 1 mM). Finally, EGb 761 (100 g/ml) was shown to block the activation of PKC induced by SNP (100 xM). These data suggest that the protective and rescuing abilities of EGb 761 are not only attributable to the antioxidant properties of its flavonoid constituents but also by their ability to inhibit NO-stimulated PKC activity (Figure 36.1). 

It can be mentioned the work of Cerecetto et al. [ 133,134] where the anti-7 cruzi activities of a series of QDO and its vanadyl complexes were correlated with theoretical physicochemical descriptors. On the one hand, a clear two-variable correlation was found between both QDO-antiparasite activity and theoretical lipophilicity and LUMO energy [133]. The equation confirms some previously observed aspects, i.e., that the presence of an electron-withdrawing substituent, like halogen, in 5-8-positions produces more active compounds. On the other hand, it was found that the anti-T. cruzi response of a family of QDO-vanadyl complexes depends on the lipophilic properties and the electronic properties, am, of 6-7-substituents [134], Another QSAR study involving PDO derivatives with selective hypoxic cytotoxicity was performed by these researchers [145]. In this case, electrochemical properties, expressed as pc, together with lipophilicity correlated to the fraction of cell survival in hypoxia finding that when the redox potential of the N-oxidc moiety decreases the hypoxic cytotoxicity increase. 

When the surviving fraction of bacterial cells are plotted against concentration, with a common contact interval, the chlorination studies present a typical logistic-type curve ozone produces an inunediate kill at the critical concentration. 

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