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Cell phases

Repeated attempts to obtain the band at 1030 cm 1 in spectra of the respective solids of various compositions did not furnish the desired result. Nevertheless, the band was observed in IR transmission spectra of gaseous components that separated from molten K2NbF7 and were collected in a standard gas phase cell with Csl windows appropriate for IR measurements. Fig. 85 presents the structure of the band and exact wave numbers of its components. Storage of the gas in the cell for several days resulted in a yellow deposit on the windows due to oxidation and subsequent separation of iodine. Analysis of available reported data [364 - 367] enables to assign the band observed at -1030 cm 1 to vibrations of OF radicals. It should be emphasized that a single mode was observed for OF in the argon matrix while in the case of nitrogen, two modes were indicated [367]. [Pg.190]

Once there is an appreciable amount of cells and they are growing very rapidly, the cell number exponentially increases. The optical cell density of a culture can then be easily detected that phase is known as the exponential growth phase. The rate of cell synthesis sharply increases the linear increase is shown in the semi-log graph with a constant slope representing a constant rate of cell population. At this stage carbon sources are utilised and products are formed. Finally, rapid utilisation of substrate and accumulation of products may lead to stationary phase where the cell density remains constant. In this phase, cell may start to die as the cell growth rate balances the death rate. It is well known that the biocatalytic activities of the cell may gradually decrease as they age, and finally autolysis may take place. The dead cells and cell metabolites in the fermentation broth may create... [Pg.82]

Gx to S phase cell-cycle transition. Transition is required for the onset of IL-2 induced T-cell proliferation. Additionally, SRL also attenuates growth factor induced proliferation of several nonimmune cells and also inhibits metastatic tumor growth and angiogenesis. [Pg.620]

FIG. 3 MD simulation of the heptane-water interface, (a) Configuration of solvent molecules in a two-phase cell (b) density vs. distance profile along the axis from aqueous phase to heptane phase. [Pg.364]

Roovers, K. and Assoian, R. K., Integrating the MAP kinase signal into the G, phase cell cycle machinery, Bioessays, 22, 818-826, 2000. [Pg.268]

A simple rocking device was tested for routine determination of distribution coefficients [9], Sample cells were constructed for two-phase [9] and three-phase [10] systems. The investigators claim that the rocking action causes the shape of each phase to vary slowly and constantly and that the precision associated with the distribution coefficient is similar to that for shake-out methods. The three-phase cell was tested as an in vitro model to simulate factors involved in the absorption process. Rates of drug transfer and equilibrium drug distribution were evaluated under conditions in which one aqueous phase was maintained at pH 7.4 and the other phase was maintained at another pH. [Pg.108]

Rocking device with two- and three-phase cells (free boundary method) Nonemulsifying method for determining partition coefficient 9,10... [Pg.121]

HU is an inhibitor of ribonucleotide reductase, a rate-limiting enzyme which catalyzes the conversion of ribonucleotides into deoxyribonucleotides. HU is thus a cytotoxic agent as it has the ability to inhibit DNA synthesis. Consequently, H U can affect only cells that are actively synthesizing DNA and, therefore, a drug of S-phase cell-cycle specific. Moreover, HU-mediated inhibition of ribonucleotide reductase is reversible, implying that the action of HU will exhibit a relatively straight forward concentration-time course dependence [2—4-]. [Pg.235]

Two groups demonstrated that BRCA-1- and BRCA-2-deficient cells are acutely sensitive to PARPi [11,12]. Potent inhibitors like KU0058684 (5), KU0058948 (6), and AG14361 (26) were cytotoxic at nanomolar concentrations in HR-defective cells, and displayed excellent selectivity for BRCA-1- and BRCA-2-deficient cells over wild-type cells. After 24 h of exposure, 5 elicited G2 or M phase cell cycle arrest and a tetraploid DNA content. The applicability of this discovery was revealed when BRCA-2-deficient and BRCA-2-proficient cells were injected into mice and tumors were allowed to develop. Daily treatment with 5 or 26 had no effect on the BRCA-2 wild-type cells however, when BRCA-2-deficient cells were treated with PARPi, no tumors developed. [Pg.231]

Xu X, Hamhouyia F, Thomas SD, Burke TJ, Girvan AC, McGregor WG, Trent JO, Miller DM, Bates PJ (2001) Inhibition of DNA replication and induction of S phase cell cycle arrest by G-rich oligonucleotides. J Biol Chem 276 43221-43230... [Pg.144]

Pollitt SK, Pallos J, Shao J, Desai UA, Ma AA, Thompson LM, Marsh JL, Diamond MI (2003) A rapid cellular FRET assay of polyglutamine aggregation identifies a novel inhibitor. Neuron 40(4) 685-694 Ranganathan S, Bowser, R (2003) Alterations in G(l) to S phase cell-cycle regulators during amyotrophic lateral sclerosis. Am J Pathol 162(3) 823—835... [Pg.291]

Plitidepsin (Aplidin) (203) Cyclic depsipeptide Plitidepsin (Aplidin ) (203) Oncology Inhibitor to VEGF, VEGFRLandGl/ G2 phase cell cycle Phase II PharmaMar 934-936... [Pg.84]

Dolastatin 15 (213) Depsipeptide Tasidotin (Synthadotin, ILX-651) (214) Oncology Induces G2/M phase cell cycle arrest by inhibiting tubulin assembly Phase II Genzyme 952-954... [Pg.85]

A single optimal CPD introduced into Sicl (called Sicl ) restores recognition and ubiquitination by SCF in vitro and degradation in vivo. However, in individual G1 phase cells, Sicl is eliminated well before cells pass Start, resulting in premature DNA replication, genome instability and lethality in a cdhl deletion background. [Pg.54]


See other pages where Cell phases is mentioned: [Pg.71]    [Pg.447]    [Pg.43]    [Pg.9]    [Pg.60]    [Pg.39]    [Pg.76]    [Pg.374]    [Pg.105]    [Pg.94]    [Pg.26]    [Pg.169]    [Pg.170]    [Pg.327]    [Pg.40]    [Pg.46]    [Pg.88]    [Pg.88]    [Pg.90]    [Pg.90]    [Pg.94]    [Pg.94]    [Pg.96]    [Pg.97]    [Pg.271]    [Pg.495]    [Pg.194]    [Pg.58]    [Pg.343]    [Pg.23]    [Pg.154]    [Pg.154]    [Pg.476]    [Pg.216]    [Pg.105]   
See also in sourсe #XX -- [ Pg.109 , Pg.121 , Pg.184 , Pg.371 ]

See also in sourсe #XX -- [ Pg.693 ]




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Cell , biological phase diagram

Cell accelerating phase

Cell batch culture phases

Cell cycle Mitotic phase

Cell cycle phases

Cell cycles S phase

Cell decelerating phase

Cell exponential phase

Cell growth accelerating phase

Cell growth decelerating phase

Cell growth declining phase

Cell growth phases

Cell growth phases Death phase

Cell growth phases Stationary phase

Cell growth stationary phase

Cell membrane phase transition temperature

Cell single-phase flow

Cell stationary phase

Cells Involved in the Inflammatory Phase

Cells in phase space

Contrast structures phase plane cell

Diffusion cell experiments, phase

Double Cell Phase Change Dichroic LCD

Electrochemical cell phases

Equilibrium between Phases in Electrochemical Cell

G2/M phase cell cycle

Galvanic cells mobile phases

Growth Phases of Cells

Hybrid solar cells phases

M-phase of cell cycle

Mast cells late phase inflammatory reaction

Microbial stationary phase cells

Mixed-phase cell

PECS cells with solution-phase storage

Phase space cell

S-phase of cell cycle

Selective killing of cells in particular phases

Solid-phase cell immobilization

Stationary phase cells and aminopterin

Tropochemical cell-twinned phases

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