Cholesterol calcium

Biliary sludge A deposit of tiny stones or crystals made up of cholesterol, calcium bilirubinate, and other calcium salts. The cholesterol and calcium bilirubinate crystals in biliary sludge can lead to gallstone formation. 

Components of gallstones Cholesterol, calcium bilirubinate, and bile... 

Edwards et al. (1958) have used infrared spectroscopy in the qualitative analysis of 30 specimens of human biliary calculi. The spectra of cholesterol, calcium bilirubinate, and calcium carbonate display prominent and characteristic bands that do not overlap in certain areas of the spectrum. Bands at 3380, 2910, and 1055cm" indicate the presence of cholesterol, a doublet at 1670 and 1630 cm" is characteristic of calcium bilirubinate, and a sharp band at 875 cm is produced by calcium carbonate. It is thus possible to verify the principal constituents of biliary calculi—whether they are (1) pure gallstones that are composed of either cholesterol, calcium bilirubinate, or calcium carbonate, or are (2) mixed gallstones that are composed chiefly of two or three of these components, or are (3) combined llstones with a nucleus of one kind and a shell of another substance. 

The pathogenesis of gallstones can essentially be reduced to a matter of solubility of the various solutes that constitute the stone—cholesterol in cholesterol stones and cholesterol, calcium carbonate, phosphate, or bilirubinate in mixed stones. 

Age group Dry matter Nitrogen Cholesterol Calcium Potassium... 

Later, the vascularized scars of the cornea often contain deposits of cholesterol, calcium, and fat (Giraud, 1917 WHO, 1970 Balali-Mood and Navaeian, 1986 Balali-Mood et al., 1986 Balali-Mood and Hefazi, 2005). 

Two nucleation processes important to many people (including some surface scientists ) occur in the formation of gallstones in human bile and kidney stones in urine. Cholesterol crystallization in bile causes the formation of gallstones. Cryotransmission microscopy (Chapter VIII) studies of human bile reveal vesicles, micelles, and potential early crystallites indicating that the cholesterol crystallization in bile is not cooperative and the true nucleation time may be much shorter than that found by standard clinical analysis by light microscopy [75]. Kidney stones often form from crystals of calcium oxalates in urine. Inhibitors can prevent nucleation and influence the solid phase and intercrystallite interactions [76, 77]. Citrate, for example, is an important physiological inhibitor to the formation of calcium renal stones. Electrokinetic studies (see Section V-6) have shown the effect of various inhibitors on the surface potential and colloidal stability of micrometer-sized dispersions of calcium oxalate crystals formed in synthetic urine [78, 79]. 

A 0-9% salt solution is considered to be isotonic with blood. Other electrolytes present include bicarbonate ions (HCOj ) and small amounts of potassium, calcium, magnesium, phosphate, sulphate and organic acid ions. Included among the complex compounds and present in smaller amounts are phospholipids, cholesterols, natural fats, proteins, glucose and amino acids. Under normal conditions the extracellular body fluid is slightly alkaline with a pH of 7-4. ... 

Biochemical characteristics (plasma levels of alanine and aspartate transminases, alkaline phosphatase, triglycerides, cholesterol, urea, uric acid, allantoin, glucose, protein, albumin, sodium, potassium, calcium, magnesium, phosphorus urine levels of protein and glucose). 

Angiotensin II binds to specific adrenal cortex glomerulosa cell receptors. The hormone-receptor interaction does not activate adenylyl cyclase, and cAMP does not appear to mediate the action of this hormone. The actions of angiotensin II, which are to stimulate the conversion of cholesterol to pregnenolone and of corticosterone to 18-hydroxycorticosterone and aldosterone, may involve changes in the concentration of intracellular calcium and of phospholipid metabolites by mechanisms similar to those described in Chapter 43. 

Napoli et al. [286] found that the nifedipine treatment of stroke-prone spontaneously hypertensive rats (SPSHR) suppressed the plasma and LDL oxidation and the formation of oxidation-specific epitopes and increased the survival of rats independently of blood pressure modification. Their results suggest that the protective effects of calcium blockers of dihydro-pyridine-type on cerebral ischemia and stroke may, at least in part, depend on their antioxidant activity. In vivo antioxidant effect of nilvadipine on LDL oxidation has been studied in hypertensive patients with high risk of atherosclerosis [287], It was found that there was a significant decrease in the level of LDL cholesterol oxidation in patients after nilvadipine treatment. 

A few enzymes, such as the previously mentioned CNP, are believed to be fairly specific for myelin/oligodendro-cytes. There is much more in the CNS than in peripheral nerve, suggesting some function more specialized to the CNS. In addition, a unique pH 7.2 cholesterol ester hydrolase is also enriched in myelin. On the other hand, there are many enzymes that are not myelin-specific but appear to be intrinsic to myelin and not contaminants. These include cAMP-stimulated kinase, calcium/calmodulin-dependent kinase, protein kinase C, a neutral protease activity and phosphoprotein phosphatases. The protein kinase C and phosphatase activities are presumed to be responsible for the rapid turnover of MBP phosphate groups, and the PLP acylation enzyme activity is also intrinsic to myelin. 

Experimental. A second study was conducted with nine postmenopausal women age 51-65 yr. The subjects were fed standardized meals for 19 weeks. The mean composition for the 7-day menus of natural foods as % of total calories was 15% protein, 50% carbohydrate, 35% fat with a P/S ratio of 0.7, 10 g/day crude fiber, and less than 300 mg/day cholesterol. In addition, the diets supplied 1289 mg calcium, 1832 mg phosphorus, 2561 mg sodium and 5099 mg potassium daily. The diets met the RDA for all other nutrients. Calorie levels were adjusted to maintain body weight. The experimental meals were fed during the last six weeks of this 19-week period. No more than one liquid meal was consumed by each subject in one week. Fasting and postprandial samples of blood and urine were collected as in the previous study. Diuresis was induced by scheduled consumption of water. 

In the studies discussed, wheat bran, cellulose, and psyllium fiber feeding resulted in increased fecal fat losses and in lowered blood serum cholesterol and triglyceride levels (14,15,32,41) as well as increased fecal losses of calcium. Possible involvement of dietary fat with high or low dietary fiber intake has not been extensively investigated. However, that calcium is involved in intestinal fat absorption is generally accepted (42-45). 

As shown in Table III, mean fecal calcium losses tended to be higher when the higher fat diet was fed in comparison to results when the lower fat diet was fed. Therefore, apparent calcium absorption was higher when the low fat diet was fed. These differences were significant at only the P< 0.075 level hence, only a trend was illustrated. In this study no attempt was made to equalize fatty acid proportionality patterns or cholesterol intake. These or other dietary or non-dietary factors may have influenced the observed apparent trends. Other studies with human adults have not demonstrated any apparent influence on level of dietary fat on calcium absorption. 

Chetty KN, Walker J, Brown K, et al. 1993a. The effects of dietary calcium and chlordecone on cholinesterase, triglycerides, low density lipoproteins, and cholesterol in serum of rat. Arch Environ Contam Toxicol 24 365-367. 

An old hypothesis is based on the observations of Dahlen et al. (D3), who demonstrated that above a certain concentration in plasma, Lp(a) could bind to glycosaminoglycans in the arterial wall (B12). Colocalization of Lp(a) and fibrin on the arterial wall can lead to oxidative changes in the lipid moiety of Lp(a) and induce the formation of oxidatively modified cholesterol esters, which in turn can influence the interaction of Lp(a) and its receptors on macrophages. This process is promoted by the presence of calcium ions. Cushing (C14), Loscalzo (L22), and Rath (R3) reported a colocalization of undegraded Lp(a) and apo-Bl00 in the extracellular space of the arterial wall. In contrast to LDL, Lp(a) is a substrate for tissue transglutaminase and Factor XUIa and can be altered to products that readily interact with cell surface structures (B21). 

Very often, vaccines are formulated with certain substances to enhance the immune response. These substances are called adjuvants (from the Latin adju-vare, which means to help ). The most common adjuvants for human use are aluminum hydroxide, aluminum phosphate, and calcium phosphate. Other adjuvants being used include bacteria and cholesterol. Mineral oil emulsions are normally the adjuvants used in animal studies. The adjuvant known as Freund s complete adjuvant consists of killed tubercle bacilli in water-inmineral oil emulsion, and Freund s incomplete adjuvant is a water-in-oil emulsion. Both these adjuvants are effective in stimulating an immune response, but they cause unacceptable side effects in humans (see Table 4.2). 

Cholesterol reducer in 10,20,40, and 80 mg doses Active ingredient Atorvastatin calcium... 

Lipitor is currently one of the best selling drugs for lowering cholesterol. Searching in WDI for Lipitor produces the page shown in Figure 10.1 [46]. The preferred name is Atorvastatin Calcium . WDI has information about the pharmacology, indications, interactions, and so on, hyperlinked for keyword search. 

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