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Peripheral cells

Proteases are crucial enzymes induced by HIV to alter the physiology of the central nervous system. Indeed, proteases participate in brain infection, helping infected peripheral cells to cross the blood-brain barrier, as well as in the viral neuropathogenesis as will be later discussed. We will first describe examples of... [Pg.153]

Morphologically, the lens is arranged so that dedifferentiated or disorientated lens fibres are not eliminated but are pushed to the core (Spector, 1984,). Damage to the cell-fibre membranes or to the proteins they contain is irreversible. The lens is therefore dependent on the peripheral cells of the epithelial layer for protection against insult. [Pg.130]

Richardson You say that the stem cells are dividing much more slowly than the peripheral cells. Why is this ... [Pg.246]

ApoA-I is the major apo-lipoprotein of HDL (Tserentsoodol et al., 2006a Zannis et al., 2006), which is involved in lipid efflux from peripheral cells and its transport to the liver. Also, free ApoA-I has been shown to act as an acceptor for cholesterol secreted from cells and to stimulate its efflux. [Pg.319]

Calcium ions play a critical role in regulating the synthesis and release of neurotransmitters, in neuronal excitability, and in long-term neuroplastic events, and it is thus not surprising that a number of studies have investigated intracellular Ca2+ in peripheral cells, particularly in bipolar disorder. [Pg.899]

LDL particles are transported through the plasma and taken into peripheral cells by apoB receptor... [Pg.164]

Dubovsky SL, Thomas M, Hijazi A, et al Intracellular calcium signalhng in peripheral cells of patients with bipolar affective disorder. Eur Arch Psychiatry Clin Neurosci 243 229-234, 1994... [Pg.628]

Fig. 5.2.1 The major metabolic pathways of the lipoprotein metabolism are shown. Chylomicrons (Chylo) are secreted from the intestine and are metabolized by lipoprotein lipase (LPL) before the remnants are taken up by the liver. The liver secretes very-low-density lipoproteins (VLDL) to distribute lipids to the periphery. These VLDL are hydrolyzed by LPL and hepatic lipase (HL) to result in intermediate-density lipoproteins (IDL) and low-density lipoproteins (LDL), respectively, which then is cleared from the blood by the LDL receptor (LDLR). The liver and the intestine secrete apolipoprotein AI, which forms pre-jS-high-density lipoproteins (pre-jl-HDL) in blood. These pre-/ -HDL accept phospholipids and cholesterol from hepatic and peripheral cells through the activity of the ATP binding cassette transporter Al. Subsequent cholesterol esterification by lecithinxholesterol acyltransferase (LCAT) and transfer of phospholipids by phospholipid transfer protein (PLTP) transform the nascent discoidal high-density lipoproteins (HDL disc) into a spherical particle and increase the size to HDL2. For the elimination of cholesterol from HDL, two possible pathways exist (1) direct hepatic uptake of lipids through scavenger receptor B1 (SR-BI) and HL, and (2) cholesteryl ester transfer protein (CfiTP)-mediated transfer of cholesterol-esters from HDL2 to chylomicrons, and VLDL and hepatic uptake of the lipids via the LDLR pathway... Fig. 5.2.1 The major metabolic pathways of the lipoprotein metabolism are shown. Chylomicrons (Chylo) are secreted from the intestine and are metabolized by lipoprotein lipase (LPL) before the remnants are taken up by the liver. The liver secretes very-low-density lipoproteins (VLDL) to distribute lipids to the periphery. These VLDL are hydrolyzed by LPL and hepatic lipase (HL) to result in intermediate-density lipoproteins (IDL) and low-density lipoproteins (LDL), respectively, which then is cleared from the blood by the LDL receptor (LDLR). The liver and the intestine secrete apolipoprotein AI, which forms pre-jS-high-density lipoproteins (pre-jl-HDL) in blood. These pre-/ -HDL accept phospholipids and cholesterol from hepatic and peripheral cells through the activity of the ATP binding cassette transporter Al. Subsequent cholesterol esterification by lecithinxholesterol acyltransferase (LCAT) and transfer of phospholipids by phospholipid transfer protein (PLTP) transform the nascent discoidal high-density lipoproteins (HDL disc) into a spherical particle and increase the size to HDL2. For the elimination of cholesterol from HDL, two possible pathways exist (1) direct hepatic uptake of lipids through scavenger receptor B1 (SR-BI) and HL, and (2) cholesteryl ester transfer protein (CfiTP)-mediated transfer of cholesterol-esters from HDL2 to chylomicrons, and VLDL and hepatic uptake of the lipids via the LDLR pathway...
Watson, S.A., Sanders, E.H., Wakely, R.D., and Williams, C.B. 1955. Peripheral cells of the endosperms of grain sorghum and corn and their influence on starch purification. Cereal Chem. 32 165-170. [Pg.678]

The metabolism of HDL probably involves interaction with both hepatic and peripheral cells, as well as with other lipoproteins. HDL may remove cholesterol from tissues, the "scavenger hypothesis (11,12). The cholesterol may then be esterifed by the action of lecithin cholesterol acyl transferase. HDL may provide cholesterol to the liver for bile acid synthesis (13) and some HDL may be catabolized by the liver in the process. HDL has not been found to interfere with the binding of LDL in cultured human fibroblasts (6). However, in cultured human arterial cells, porcine or rat hepatocytes, and rat adrenal gland, there appears to be some competition of HDL with LDL binding sites, suggesting the presence of a "lipoprotein-binding" site (14). [Pg.267]

Among the different peripheral cells expressing APP, platelets are particularly interesting because they show concentrations of its isoforms equivalent to those found in the brain [96]. Some differences between these two cellular populations are nevertheless present both at mRNA and at protein levels the isoform 695, lacking the Kuntiz Protease Inhibitor (KPI) domain, is by far the most abundant in neuronal tissue, whereas its expression is nearly undetectable in platelets in whom the major isoform is APP 770 [97]. After the platelets are activated, soluble forms of cleaved APP are released, analogous to processing in neurons. [Pg.120]

Feeney-Bums, L., Hilderbrand, E.S., and Eldridge, S. Aging human RPE Morphometric analysis of macular, equatorial, and peripheral cells, Invest. Ophthalmol. Vis. Sci., 25(2), 195-200,1984. [Pg.106]

After treatment of U. avenae with triadimefon, nuarimol or other compounds with the same mode of action, several distinct morphological changes could be seen at the ultrastructural level. This mainly consisted of thickening of the peripheral cell wall and of incomplete formation of septa, resulting in a lack of cell division of a multi-branched mycelium. [Pg.74]

Therefore, the three vitamin deficiencies so far studied in detail appear to affect amino acid transport and accumulation in similar but indirect ways. The accumulation defect is most pronounced in vitamin B6-deficient cells, for which there is also strong evidence implicating an abnormality in cell wall composition as a likely source of the change in transport activity. Direct evidence for a cell wall change in biotin- and pantothenate-deficient cells has not yet been obtained. The possibility remains, therefore, that the change in accumulation activity may be caused by an abnormality in some other structural component such as the peripheral cell membrane. [Pg.134]

It is apparent that at this stage of development definitive conclusions are premature, and that this aspect of amino acid and lipide metabolism will be pursued vigorously in the near future. It is of considerable interest to us that biotin and pantothenic acid deficiencies affect amino acid transport in L. arabinosus, since both vitamins are known to play a prominent role in lipide biosynthesis. We are currently reexamining the turnover of lipide fractions in nutritionally normal and vitamin-deficient cell types to determine whether there is some relation between this aspect of metabolism and amino acid transport. In any case, the nature of the catalytic steps involved in amino acid transport is still unknown to us. They probably occur in the peripheral cell membrane, but even this elementary and widely accepted belief will require additional study before it can be accepted beyond doubt as an established fact. [Pg.138]

Inhalation anesthetics are nonselective in their action. That is, in addition to their clinically important effect on the central nervous system (CNS), they also alter the function of various peripheral cell types. The fact that chemically unrelated molecules produce a state of general anesthesia argues against a specific anesthetic receptor. Further, whereas anesthetics alter the function of receptors for neurotransmitters (for example, y-aminobutyric acid, glutamate),... [Pg.123]

The weight of evidence supports the conclusion that the more expressed inhibition of HMG-CoA reductase by a higher statin blood level reduces the concentrations of other essential products, primarily of isoprenylated proteins and possibly ubiquinone, synthetized downstream from mevalonic acid within the peripheral cells. In parallel, it was also recognized that statins exert pleiotropic effects in various cells far beyond the originally described inhibition of hepatic cholesterol synthesis. All of these effects are considered to be class-specific for the statins. It is important to emphasize that the frequency of untoward side effects observed with the various statins can be related to their potency, the number of metabolic inter-... [Pg.137]


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See also in sourсe #XX -- [ Pg.130 , Pg.143 , Pg.152 , Pg.156 ]




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