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Saturation damage formation

Sometimes it may become necessary to shut-in a gas well when the demand for gas is low. In such instances, the well is shut-in for an indefinite period, after which it is reopened and production is resumed. It often has been found that the production rate of gas from the reopened well is substantially less than it was before the well was shut-in. During production, the inner wall of the production tubing will be coated with a film of condensed freshwater because of the geothermal gradient. This water flows down when production is interrupted and can cause formation damage. This may occur because clays are normally saturated with brine water and not with freshwater. This swelling can be prevented with the injection of some additive, for example, sodium chloride, potassium chloride, calcium chloride, or an alcohol or a similar organic material [1853]. [Pg.63]

Fluid loss from the wellbore to the formation may be reduced using the less permeability damaging drilling fluid loss additives described above. In saturated brines, carefully sized sodium chloride particles have been used to temporarily plug the formation face (35). The particles may be dissolved by pumping a less saline fluid down the wellbore. [Pg.15]

Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone. Figure 22.6 How various factors increase the risk of atherosclerosis, thrombosis and myocardial infarction. The diagram provides suggestions as to how various factors increase the risk of development of the trio of cardiovascular problems. The factors include an excessive intake of total fat, which increases activity of clotting factors, especially factor VIII an excessive intake of saturated or trans fatty acids that change the structure of the plasma membrane of cells, such as endothelial cells, which increases the risk of platelet aggregation or susceptibility of the membrane to injury excessive intake of salt - which increases blood pressure, as does smoking and low physical activity a high intake of fat or cholesterol or a low intake of antioxidants, vitamin 6 2 and folic acid, which can lead either to direct chemical damage (e.g. oxidation) to the structure of LDL or an increase in the serum level of LDL, which also increases the risk of chemical damage to LDL. A low intake of folate and vitamin B12 also decreases metabolism of homocysteine, so that the plasma concentration increases, which can damage the endothelial membrane due to formation of thiolactone.
Figure 7.10 Metabolism of paracetamol. With therapeutic doses, paracetamol is metabolised to the glucuronide and sulphate conjugates. With higher doses these pathways become saturated and metabolism proceeds via die P-450-mediated route, with the formation of the toxic metabolite benzoquinone. This is normally metabolised by conjugation with glutathione. When glutathione is depleted benzoquinone is free to interact with cellular macromolecules, leading to cellular damage. Figure 7.10 Metabolism of paracetamol. With therapeutic doses, paracetamol is metabolised to the glucuronide and sulphate conjugates. With higher doses these pathways become saturated and metabolism proceeds via die P-450-mediated route, with the formation of the toxic metabolite benzoquinone. This is normally metabolised by conjugation with glutathione. When glutathione is depleted benzoquinone is free to interact with cellular macromolecules, leading to cellular damage.
Mechanistically, the formation of malonaldehyde and TBA-active DNA-bound material is not yet fully understood. While free malonaldehyde increases linearly with dose (G = 0.1 x 10 7 mol J 1 = 1.7% of OH), the efficiency of forming TBA-active DNA-bound material markedly decreases with increasing dose, that is when the integrity of the DNA is getting lost upon damage accumulation. At one stage, 02- seems to play a role, since the yield of total TBA-active material is G = 0.3 x 10"7 mol J-1 in N20/02-saturated and 0.2 x 10"7 mol J 1 in ( -saturated solution (at 100 Gy). As compared to N20/02, the OH yield is about half in 02-saturated solutions, but the 02 yield is markedly enhanced (Chap. 2.2). This could point to hydroperoxides as precursors of the TBA-active material, but details remain open. Yet, a G value of 0.2 x 10"7 mol J 1 (02-saturated) indicates that this type of lesion is not an unimportant one, about 7% of OH. [Pg.388]

Ward JF (1988) DNA damage produced by ionizing radiation in mammalian cells identities, mechanisms of formation, and repairability. Progr Nucleic Acid Res Mol Biol 35 95-125 Ward JF, Kuo I (1976) Strand breaks, base release and postirradiation changes in DNA y-irradiated in dilute 02-saturated aqueous solution. Radiat Res 66 485-498 Ward JF, Mora-Arellano VO (1984) Pulse radiolysis studies of WR-1065. Int J Radiat One Biol Phys 10 1533-1536... [Pg.479]

Shimizu and Oku (1957) studied the effects of salts on the solubility of wool in 0.1 M KOH. At low salt concentrations the effects of various ions followed the Hofmeister series. Similarly, McPhee (1958b, 1959) has shown that whereas 56 % of wool was dissolved by 1.286 N NaOH at 25°C in 2 hr, only 2 % dissolved when the solution was first saturated with NaCl. There was a corresponding decrease in formation of primary amino groups and in loss of cystine. Not all salts were equally effective in protecting wool against alkali damage. The effectiveness of 2 M solutions of the sodium salts decreased in the order 8203 > SO3 > citrate > COs" > SO 4 > acetate > Cl > Br > NOs" > I > CNS . Cations followed the order Li+, Na+ > K+. Similar rates of alkali uptake were obtained with all salts at a concentration oi 2 M. [Pg.278]

The new material composition on the CSPE base with Structure 5.1 and vulcanized by a water solution of MAs provides the formation of a saturated polymer vulcanized net. This makes it possible to obtain impenetrable crack-resistant coatings for metal, concrete, plastic, and other substrates, protecting them from damaging effects of the environment. [Pg.180]

Guanosine triphosphate and ribulose-5-phosphate are recruited in a 1 2 stoichiometric ratio by GTP cyclohydrolase II and DHBP synthase, respectively, for riboflavin biosynthesis. Since at substrate saturation the activity of B. subtilis DHBP is twice the activity of B. suhtilis cyclohydrolase II (DSM, unpublished observations) and since both enzymatic activities are associated with the same bifunctional protein encoded by rihA, the balanced formation of the pyrimidinedione and the dihydroxybutanone intermediates is ensured. However, the ifg.s constant of DHBP synthase ( 1 mmol is about 100-fold higher than the ifg.s constant of GTP cyclohydrolase II imposing the risk of excessive synthesis of the pyrimidinone and pyrimidinedione intermediates in case of reduced intracellular concentrations of pentose phosphate pathway intermediates. This can be expected, for instance, in glucose-limited fed-batch fermentations, which are frequentiy used in industrial applications. The pyrimidinone and pyrimidinedione intermediates are highly reactive, oxidative compounds, which can do serious damage on the bacteria. [Pg.128]


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See also in sourсe #XX -- [ Pg.602 ]




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Formation damage

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