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Physical retardation

Physically retarding acid reaction is accomphshed by thickening (viscosifying) the acid used. Viscous acids include polymer-gelled, surfactant-gelled, emulsified, and foamed acids. Combinations can also be used in addition, surfactant-retarded acid can be gelled or foamed. The intent of viscosifying acid is to slow the rate of acid diffusion outward, to the rock surfaces, and to reduce the rate of fluid loss from wormhole to unreacted matrix. Both of these effects work to increase live acid penetration distance. [Pg.162]

As in fracture acidizing, the retarded acid system that provides the deepest live acid penetration is an oil-external emulsified acid. The high friction pressures experienced with such systems are especially limiting in matrix stimulation, however. [Pg.162]

Foamed acids can be effective in improving contact with longer treatment intervals. As in fracture acidizing, most foams are 60-75 quality. The lightness of foam makes it an effective stimulation fluid for damaged gas wells. As with emulsions, the pumping of foam at high rates is not always possible. [Pg.162]

Surfactant-gelled acid systems (also known as viscoelastic acid systems) represent a more recent development. Such systems have found success in carbonate matrix acidizing applications in particular. Certain special surfactant formulations can be added to acid that is above a certain concentration (e.g., 15% HCl) at which the surfactant does not impart appreciable viscosity. However, as the acid is injected and reacts in the formation, the surfactant generates viscosity (as a function of dissolved chloride ion and pH), thereby retarding reaction and providing, potentially, in situ diversion. As acid spends further, viscosity breaks back to reduced level (in the ideal case). [Pg.163]

Currently, the commercial systems available that will result in the deepest penetration of acid are emulsified acid and, perhaps, surfactant-gelled acid. Viscous acids may contain a fluid-loss additive, such as an oil-soluble resin or polymer, to reduce leak-off. Particulate diverters are not effective in fracture acidizing, but in matrix treatments, they can make a difference. [Pg.164]


Filtration. The filtration process depends on the physical retardation of microorganisms from a fluid by a filter membrane or similarly effective medium. The effectiveness of this process is also influenced by the bioburden (6). HoUow-fiber membranes (qv) are most often employed. The resultant... [Pg.409]

The hypercalcemia resulting from hypervitaminosis D is responsible for toxic symptoms such as muscle weakness, bone pain, anorexia, ectopic calcification, hypertension, and cardiac arrhythmias. Toxicity in infants can result in mental and physical retardation, renal failure, and death. [Pg.779]

While defects in protein XPD often cause typical XP symptoms, some defects in the same protein lead to trichothiodystrophy (TTD, brittle hair disease). The hair is sulfur deficient, and scaly skin (ichthyosis, Box 8-F), mental retardation, and other symptoms are observed.0 Like their yeast counterparts (proteins RAD3 and RAD25), XPB and XPD are both DNA helicases.0 They also constitute distinct subunits of the human transcription factor TFIIHP, which is discussed in Chapter 28. It seems likely that XPD is involved in transcription-coupled repair (TCR) of DNA.° °i-s This is a subpathway of the nucleotide excision repair (NER) pathway, which allows for rapid repair of the transcribed strand of DNA. This is important in tissues such as skin, where the global NER process may be too slow to keep up with the need for rapid protein synthesis. Transcription-coupled repair also appears to depend upon proteins CSA and CSB, defects which may result in the rare cockayne syndrome.13 0 4 11 Patients are not only photosensitive but have severe mental and physical retardation including skeletal defects and a wizened appearance. [Pg.1585]

Although alcaptonuria is a relatively harmless condition, such is not the case with other errors in amino acid metabolism. In maple syrup urine disease, the oxidative decarboxylation of a-ketoacids derived from valine, isoleucine, and leucine is blocked because the branched-chain dehydrogenase is missing or defective. Hence, the levels of these a-ketoacids and the branched-chain amino acids that give rise to them are markedly elevated in both blood and urine. Indeed, the urine of patients has the odor of maple syrup—hence the name of the disease (also called branched-chain ketoaciduria). Maple syrup urine disease usually leads to mental and physical retardation unless the patient is placed on a diet low in valine. [Pg.974]

Branched-chain ketoaciduria (commonly known as Maple Syrup Urine Disease MSUD) is another ailment that may be caused by thiamine deficiency. In MSUD, the oxidative decarboxylation of alpha-keto acids derived from, i.e. valine, isoleucine, and leucine, is blocked due to an inadequate supply of the coenzyme thiamine pyrophosphate (TPP). Clinical symptoms of MSUD include mental and physical retardation. Describe briefly the structure of Riboflavin (Vitamin B-2) and its biochemical role. [Pg.244]

Another example of a maternal condition that contributes to birth defects is low circulating iodine. Cretinism is one of the most profound, but completely preventable, syndromes of malformation known. Characteristic consequences of prenatal iodine deficiency include pervasive mental and physical retardation, deaf-mutism (due to primary malformation of the inner ear), lack of muscle tone with a spastic or rigid walk, and failure to attain a height at maturity of more than 1 m. Today, this condition (known as endemic cretinism) is most prevalent in impoverished areas of African and East Asian countries. Prior to implementation of a national program of iodized salt in the early part of the twentieth century, endemic cretinism was commonplace in Switzerland. After institution of iodized salt, deaf-mutism declined 50% within 8 years and no cretins have been born in that country since 1930. [Pg.756]

Of the 11 known cases, 10 are female and 1 male. The prognosis is poor. Three have died, one in the second year of life (H5) and two in the seventh year of life (L8). On the other hand, one child, a girl aged 4 years, on a very low protein diet, is well and of normal intelligence (LIO). Another child, a boy also on a low protein intake, has developed normally and has a normal IQ (L6). Other children, although still alive, have gross mental and physical retardation (C13, L3). The only adult with this condition so far diagnosed is quite normal apart from an elevated plasma ammonia (L3). [Pg.89]

W5. Wellby, M. L., Defective thyroid biosynthesis A cause of mental and physical retardation. Aust. J. Ment. Retard. 1, 191-195 (1971). [Pg.171]

Formaminotransferase (EC 2.1.2.5). Increased urinary formamino-glutamate after oral histidine load, despite adequate serum folate. Mental and physical retardation. Neurological abnormalities. See Histidine. [Pg.315]

Thyroxine (also known as Levothyroxine or T4) is the ultimate metabolism regulator. Its reactions and products influence carbohydrate metabolism, protein synthesis and breakdown, and cardiovascular, renal, and brain function. Thyroxine is essential to an animal s functions and it is essential for development in the young. Tadpoles won t develop into frogs, for example. Untreated human babies will develop cretinism, a condition marked by severe mental and physical retardation. Adult humans with low thyroxine levels (hypothyroidism) suffer mental slowness, weight gain, depression, and fatigue. ... [Pg.1084]

Characteristic clinical Progressive mental and physical retardation + + + +... [Pg.94]

Niemann-Piek disaase Isphingomyelin lipidesis) (Also see FATS AND OTHER LIPIOS.I taifficiBizt levels of the enzyme sphingomyelinase. Accumulation chiefly ol sphingomyelin and lecithin in the livei. spleen, and central nervous system, enlarged liver and sple mental and physical retardation cherry red spot on retina of eye. None of value. [Pg.574]

Orotic aciduria insufficient levels of the enzyme orotidylic pyrophosphorylase orotidylic decarboxylase. Very rare appears first year or so of life severe megobiestic anemia rosisiam to usual treatments mental and physical retardation excreta large quantities of ortic acid in urine needle-shaped crystals in urine. Dietary supplementation with large doses of uridine improves eoemia and mental and physical development. Lady diagnosis essential. [Pg.575]

At least 1 billion people live in iodine-deficient areas, and 200 million suffer from goiter (Onuma Okezie 1998). A severe iodine deficiency during pregnancy can cause extreme and irreversible mental and physical retardation, known as cretinism. Iodine is essential for the synthesis of thyroxin, and tri-iodothyronine or thyroid hormones necessary for normal cell metabolism. Its deficiency affects approximately 6 million people worldwide, and can be averted by early diagnosis and treatment. A worldwide effort to provide iodized salt has been very successful in preventing cretinism. [Pg.573]

In all three conditions the first signs commonly appear within 48 h of birth. The infant ceases to suck, becomes drowsy and may have convulsions. At this time marked ketosis appears in ketotic glycinaemia and methylmalonic acidaemia. Most affected infants go rapidly downhill and die within a few days or weeks of birth. In some cases the onset of symptoms is later, up to four months of age, and the disease runs a slower course with survival for several years. The survivors show mental and physical retardation (I.Q. seizures, E.E.G. abnormalities,... [Pg.240]


See other pages where Physical retardation is mentioned: [Pg.311]    [Pg.317]    [Pg.26]    [Pg.32]    [Pg.173]    [Pg.175]    [Pg.228]    [Pg.81]    [Pg.311]    [Pg.453]    [Pg.161]    [Pg.162]    [Pg.180]    [Pg.161]    [Pg.162]    [Pg.1]    [Pg.342]    [Pg.419]   
See also in sourсe #XX -- [ Pg.162 ]

See also in sourсe #XX -- [ Pg.162 ]




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