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Function of cholesterol concentration

Fig. 16. Isothermal compressibility data of DPPC-cholesterol mixtures as a function of cholesterol concentration and pressure at T= 50 °C [98]. Fig. 16. Isothermal compressibility data of DPPC-cholesterol mixtures as a function of cholesterol concentration and pressure at T= 50 °C [98].
In an attempt to compare the physical state of the bilayers with the extent of hydrogen bonding to the keto group of 9HP, as a function of cholesterol concentration, we studied the temperature dependence of the CH2 symmetric stretching vibrational modes, (CH2). (24)... [Pg.65]

Figure 2 Encapsulation as a function of ethanol concentration. Oligonucleotides were added to distearoyl-phosphatidyl-choline/cholesterol/l-0-(2 -(co-methoxy-poly-ethylene-glycol)succinoyl)-2-iV-myristoyl-sphingosine /1,2-dioleoyl-3-dimethylam-monium propane liposomes in varying concentrations of ethanol at an initial oligonucleotide-to-lipid ratio of 0.24mg/mg. Abbreviations AS, antisense oligonucleotide %EtOH(v/v), percentage of ethanol in volume/volume. Figure 2 Encapsulation as a function of ethanol concentration. Oligonucleotides were added to distearoyl-phosphatidyl-choline/cholesterol/l-0-(2 -(co-methoxy-poly-ethylene-glycol)succinoyl)-2-iV-myristoyl-sphingosine /1,2-dioleoyl-3-dimethylam-monium propane liposomes in varying concentrations of ethanol at an initial oligonucleotide-to-lipid ratio of 0.24mg/mg. Abbreviations AS, antisense oligonucleotide %EtOH(v/v), percentage of ethanol in volume/volume.
The organisation and function of cholesterol in biological membranes and the possible interactions with other Upids and proteins need to be clarified in order to achieve an understanding of many ceUular functions at the molecular level. Various disease conditions have been linked with abnormal cholesterol concentrations in cell membranes. Recently the evolutionary development of cholesterol and its role in membrane speciaUsation have become of some interest. [Pg.151]

Figure 8 (a) Binding of cholesterol to cholesterol-imprinted and control polymers, from a 2 mM solution of cholesterol in hexane, as a function of polymer concentration, (b) Binding of cholesterol and various cholesterol analogues (2 mM) to the cholesterol-imprinted polymer, prepared by the sacrificial spacer method. Reprinted with permission from Journal of the American Chemical Society. Copyright 1995 American Chemical Society (Ref. 10). [Pg.101]

Phenylalanine and related metabolites inhibit activity of 3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase (Fig. 9.2). This aizyme is critical for proper synthesis of cholesterol in phenylalanine-sensitive oligodendrocytes located in the frontal brain, especially in the prefrontal cortex. Locally synthesized cholesterol makes up approximately 30 % of all myelin lipids of the brain tissue. The function of cholesterol is not only structural but is also required for proper neuronal signal transmission [50]. Inhibition of HMG-CoA reductase by phaiylalanine is partially reversible in some individuals. This explains the improvement in myelination observed in MRl scans of poorly controlled patients who have returned to diet and have lowered their blood phenylalanine concentrations. The reduction in phenylalanine allows for proper myelin production in the phenylalanine-sensitive oligodendrocyte population [50,57,58] (Fig. 9.3). [Pg.94]

Iodine is one of the most effective substances in the presence of which the conductance of phospholipid bilayers increases. Various interpretations of the results of measurements of the conductance of bilayers in the presences of the I /I systems have been the subject of discussion. A number of authors believed that in the presence of iodine electron conductance is possible in the membrane as a result of the formation of iodine complexes with phospholipids. In contrast to this view, it was claimed that only ionic conductance is possible. The impedence of bilayers in the presence of iodine was first measured by Louger et aL By measuring the impedance of bilayers it is possible to detect the motion of ions inside the membrane, during the measurement of the impedance at a sufficiently high frequency which would not give ions to pass from the membrane into the solution. the impedance of a bilayer membrane formed from egg lecithin with cholesterol in the presence of 10" MI2 in an aqueous solution, measured by Lebedev et al is given in Figs. 16a and 16b as a function of the concentration of KI added to the solution. [Pg.148]

Figure 24 shows the variation of nanoparticle size as a function of the concentration of cholesterol in the same microemulsion system. Contrary to the previous graph (Fig. 22), no minimum appears. The size of the particles is thus controlled by a thermodynamic stabilization with the molecules of the surfactant. [Pg.378]

CETP exchanges cholesteryl esters of HDL with triglycerides of VLDL, IDL, and LDL. The HDL-derived cholesteryl esters are subsequently removed from the circulation via the LDL receptor pathway [28, 91]. Absence of functional CETP results in pronounced elevations of plasma concentrations of HDL cholesterol (2.5-8 mmol/1) and apoA-I. In parallel, plasma concentrations of LDL cholesterol and apoB are relatively low. Heterozygous CETP deficiency is associated with a milder elevation of HDL cholesterol. Most patients with CETP deficiency do not present with specific clinical symptoms. Some were reported to exhibit corneal opacities. CETP deficiency has been claimed to reduce the risk of atherosclerotic vascular disease and to prolong life expectancy. However, in some situations (e.g., in hypertriglyceridemia or in the absence of high HDL cholesterol), CETP deficiency may also increase cardiovascular risk [15, 28,91]. [Pg.540]

Although elevated levels of cholesterol and LDL in human plasma are linked to an increased incidence of cardiovascular disease, recent data have shown that an increase in concentration of HDL in plasma is correlated with a lowered risk of coronary artery disease. Why does an elevated HDL level in plasma appear to protect against cardiovascular disease, whereas an elevated LDL level seems to cause this disease The answer to this question is not known. An explanation currently favored is that HDL functions in the removal of cholesterol from nonhepatic tissues and the return of cholesterol to the liver, where it is metabolized and secreted. The net effect would be a decrease in the amount of plasma cholesterol available for deposit in arteries (see... [Pg.472]

Figure 6. Observed 23Na quadrupole splitting for lamellar mesophase samples of dimyristoyllecithin-cholesterol-2H20 as a function of the cholesterol concentration at four different temperatures 16°C ( ), 30°C (V), 40°C ( ), and 48°C (O). In all samples the salt solution (0.8M NaCl in 2H20) accounted for 25% of the total sample weight. The concentration of cholesterol is expressed as the percentage (by weight) of cholesterol in the lecithin-cholesterol mixture. Figure 6. Observed 23Na quadrupole splitting for lamellar mesophase samples of dimyristoyllecithin-cholesterol-2H20 as a function of the cholesterol concentration at four different temperatures 16°C ( ), 30°C (V), 40°C ( ), and 48°C (O). In all samples the salt solution (0.8M NaCl in 2H20) accounted for 25% of the total sample weight. The concentration of cholesterol is expressed as the percentage (by weight) of cholesterol in the lecithin-cholesterol mixture.

See other pages where Function of cholesterol concentration is mentioned: [Pg.58]    [Pg.65]    [Pg.46]    [Pg.56]    [Pg.58]    [Pg.58]    [Pg.65]    [Pg.46]    [Pg.56]    [Pg.58]    [Pg.156]    [Pg.78]    [Pg.148]    [Pg.148]    [Pg.172]    [Pg.172]    [Pg.408]    [Pg.268]    [Pg.343]    [Pg.63]    [Pg.167]    [Pg.227]    [Pg.26]    [Pg.155]    [Pg.247]    [Pg.24]    [Pg.163]    [Pg.161]    [Pg.230]    [Pg.170]    [Pg.265]    [Pg.147]    [Pg.18]    [Pg.966]    [Pg.210]    [Pg.530]    [Pg.543]    [Pg.888]    [Pg.353]    [Pg.401]    [Pg.155]   
See also in sourсe #XX -- [ Pg.65 , Pg.66 , Pg.67 , Pg.68 ]

See also in sourсe #XX -- [ Pg.65 , Pg.66 , Pg.67 , Pg.68 ]




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