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Long formation

Due to this low pore filling and long formation times, hydrates should be considered a nonrenewable resource from which the recovery of gas is much more difficult than that from a normal gas reservoir. In addition, while an energy balance of the dissociation of pure hydrates is highly favorable, hydrates may be sparsely dispersed in sediment so economic recovery will be problematic. However, before turning to the production of gas from hydrates, consider first the locations of hydrate reserves, and requirements for formation. [Pg.543]

Today the majority of polymeric porous flat membranes used in microfiltration, ultrafiltration, and dialysis are prepared from a homogenous polymer solution by the wet-phase inversion method [59-66]. This method involves casting of a polymer solution onto an inert support followed by immersion of the support with the cast film into a bath filled with a non-solvent for the polymer. The contact between the solvent and the non-solvent causes the solution to be phase separated. This process involves the use of organic solvents that must be expensively removed from the membrane with posttreatments, since residual solvents can cause potential problems for use in biomedical apphcations (i.e., dialysis). Moreover, long formation times and a limited versatihty (reduced possibUity to modulate cell size and membrane stmcture) characterize this process. [Pg.189]

QUANTIFICATION OF THE BCL-2 FAMILY ACTIVITIES USING THE CYTOCHOME C RELEASE LONG-FORMAT ASSAY... [Pg.122]

A Long format 180+ minutes B Short format 35 minutes... [Pg.123]

Fig. 2. Schematic showing the long-format (A) and short-format (B) cytochrome c release assays. Fig. 2. Schematic showing the long-format (A) and short-format (B) cytochrome c release assays.
Fig. 3. Quantification of Bcl-2 family activities with the long-format cytochrome c release assay. Results are the average of duplicate measurements in (A) and are averages of triplicate measurements +/-SEM in (B-D) (many error bars in panels [B-D] are obscured by the symbols). In panels (A-D) open circles indicate cytochrome c detected when Triton X-100 was added to mitochondria and open diamonds indicate cytochrome c detected when no Bcl-2 family proteins were added to mitochondria. All incubations of mitochondria except those in (B) were for 30 min. (A) Recombinant human Bid (solid circles) and caspase-8-cleaved human Bid (squares) induce release of cytochrome c from isolated mouse liver mitochondria in a dose- dependent manner. (B) Kinetics of 52 nM (solid squares) and 5.2 nM (solid circles) human cleaved Bid-induced cytochrome c release from isolated mouse liver mitochondria. (C) Bcl-xL inhibition of caspase-8-cleaved human Bid and cleaved mouse Bid induced cytochrome c release. Mitochondria were incubated with 52 nM cleaved human Bid without (solid diamond) or with ( solid squares) the indicated concentrations of mouse Bcl-xL. Mitochondria were also incubated with 17 nM cleaved mouse Bid without (open square) or with (solid circles) the indicated concentrations of mouse Bcl-xL. (D) A synthetic peptide (GQVGRQLAIIGDDINR) corresponding to the amino acid 72-87 BH3 region of Bak prevents Bcl-xL from inhibiting caspase-8-cleaved mouse Bid induction of cytochrome c release. Mitochondria were incubated with 17 nM caspase-8-cleaved mouse Bid without (triangle) or with (open square) 155 nM mouse Bcl-xL and the indicated concentrations of Bak-BH3 (solid circle) or the corresponding Bak peptide (GQVGRQAAIIGDDINR) with a L to A substitution (solid squares). Fig. 3. Quantification of Bcl-2 family activities with the long-format cytochrome c release assay. Results are the average of duplicate measurements in (A) and are averages of triplicate measurements +/-SEM in (B-D) (many error bars in panels [B-D] are obscured by the symbols). In panels (A-D) open circles indicate cytochrome c detected when Triton X-100 was added to mitochondria and open diamonds indicate cytochrome c detected when no Bcl-2 family proteins were added to mitochondria. All incubations of mitochondria except those in (B) were for 30 min. (A) Recombinant human Bid (solid circles) and caspase-8-cleaved human Bid (squares) induce release of cytochrome c from isolated mouse liver mitochondria in a dose- dependent manner. (B) Kinetics of 52 nM (solid squares) and 5.2 nM (solid circles) human cleaved Bid-induced cytochrome c release from isolated mouse liver mitochondria. (C) Bcl-xL inhibition of caspase-8-cleaved human Bid and cleaved mouse Bid induced cytochrome c release. Mitochondria were incubated with 52 nM cleaved human Bid without (solid diamond) or with ( solid squares) the indicated concentrations of mouse Bcl-xL. Mitochondria were also incubated with 17 nM cleaved mouse Bid without (open square) or with (solid circles) the indicated concentrations of mouse Bcl-xL. (D) A synthetic peptide (GQVGRQLAIIGDDINR) corresponding to the amino acid 72-87 BH3 region of Bak prevents Bcl-xL from inhibiting caspase-8-cleaved mouse Bid induction of cytochrome c release. Mitochondria were incubated with 17 nM caspase-8-cleaved mouse Bid without (triangle) or with (open square) 155 nM mouse Bcl-xL and the indicated concentrations of Bak-BH3 (solid circle) or the corresponding Bak peptide (GQVGRQAAIIGDDINR) with a L to A substitution (solid squares).
Results typical of those obtained when mitochondria, HRP-conjugated detection antibody, and Bcl-2 family members were incubated in assay buffer in wells of the ELISA plate for 30 min at 30°C are shown in Fig. 4A. Caspase-8 cleaved human Bid was used to demonstrate that the short format detects protein-induced cytochrome c release (Fig. 4A). Bcl-xL was added with cleaved Bid to demonstrate that the short format detects inhibition of a pro-apoptotic Bcl-2 family member by an anti-apoptotic member (Fig. 4A). In the 35-min assay, Bid-induced release of cytochrome c was concentration-dependent with an EC50 of 38 nM (Fig. 4B). The difference between the EC50 of 38 nM determined in the 35-min short-format assay was not statistically different (z test, p < 0.05) from the EC50 of 30 +/- 4 nM determined in the 3-h long format assay (Fig. 3A). Appreciable release caused by cleaved Bid can also be detected in a 15-min short-format assay conducted in the well of the ELISA plate (Fig. 4C) and inhibition of Bid was apparent when Bcl-xL was included in the 15-min short-format assay (Fig. 4C). [Pg.127]

Advantages of the Long-Format and Short-Format Assays... [Pg.127]

Ritchie claims that formation of lead—acid batteries could reach close to the theoretical electric charge, 241 Ah kg PbO, if conducted with weak current for a period of at least two weeks. However, battery manufacturers cannot afford such a long formation time. The general strive is to complete the formation process within 15—30 h, and even less. This is associated with 1.7—2.5-fold increase in electricity consumed per 1 kg of dry paste. New formation current and voltage algorithms are aimed to reduce substantially the above energy consumption. [Pg.511]

As described in section 2, OBDec shifts two windows over the hits produced hy OBDem one for the long format telegram and another one for the short format telegram. These two windows have different lengths. The shift used for each window influences the value of Fp. The way the windows are built also... [Pg.2187]

The window shift is 300 bits for both windows. The numbers between brackets indicate the positions of the first and last bits of the window within the bit-stream. The windows of the short format version and long format version are s3mchronized by forcing both windows to have the same bit as last bit. Note that three short format windows are built before the first long format window is built. [Pg.2189]

It can be observed that not all the dec bits are used to build the windows. The short format version does not use the last bits, because they are not enough to build a short format window. The long format version does not use bits from both the beginning and the end of the bit-stream. [Pg.2189]

Figure 7 shows the state transitions for the long format version decoding algorithm of the example in section 4.2.1. The states are labelled as S(i, n, where... [Pg.2190]

The first segment has 262 bits and it is not used to build any long format window. Therefore, there is a transition to a state S 0,0) with probability 1. [Pg.2190]

In any case, the smaller frie bound given by equation 4 is, the smaller the number of windows that OBDec can buM. The smaller the number of windows that OBDec can build, the smaller the probability to have an error free window is. Therefore, the values of TV, Tlhi and Ttho obtained for each scenario can be used in equation 4 to identify the worse balise passage scenario. The worse bahse passage scenario yields dec 2134 and corresponds to a long format telegram transmission. [Pg.2191]

To locate the other site of anion action the saitples were incubated for longer time in formate medium. Long formate-treatment of Chlamvdomonas cells (3 h under N2 gas) slowed down the decay of Q , as monitored by the decay of Chi a variable fluorescence. The similarity between the decay of Q of both formate and DCMCJ-treated cells, after the third actinic flash, is shown in Fig. 3. This shows that formate, like DOyiU, slows down the Q reoxidation by the secondary plastoquinone Qg (or Qg ). HCO3 addition accelerates this decay suggesting the oxidation of Q . We call this site 2. This is the first measurement of bicarbonate-reversible formate effect on to Qg reaction in an intact eukaryotic cell. [Pg.512]


See other pages where Long formation is mentioned: [Pg.27]    [Pg.501]    [Pg.122]    [Pg.126]    [Pg.126]    [Pg.127]    [Pg.2186]    [Pg.2186]    [Pg.2188]    [Pg.2189]    [Pg.2191]    [Pg.2191]    [Pg.190]    [Pg.511]    [Pg.57]    [Pg.206]    [Pg.280]    [Pg.990]   
See also in sourсe #XX -- [ Pg.980 ]




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Formation of Long-Chain Molecules

Long-chain branch formation

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