PACS. 71.55 -i -Impurity and defect levels. PACS. 72.20Ht -High field and nonlinear effects.PACS. 72.40 + w -Photoconduction and photovoltaic effects: photodielectric effects.Abstract. -The ionisation of deep impurity centres in germanium has been observed with radiation in the terahertz range where the photon energy is much less than the binding energy of the impurities. It is shown that for not too high radiation intensities the ionisation is caused by the Poole-Frenkel effect. As in the well-known case of d.c. fields, the electric field of the highfrequency radiation lowers the Coulomb potential barrier and enhances the thermal emission of carriers.

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Cardiovascular diseases remain the leading cause of death in the United States. Two factors associated with a decreased risk of developing cardiovascular disease are elevated HDL levels and sexspecifically, a decreased risk is found in premenopausal women. HDL and estrogen stimulate eNOS and the production of nitric oxide, which has numerous protective effects in the vascular system including vasodilation, antiadhesion, and anti-inflammatory effects. We tested the hypothesis that HDL binds to its receptor, scavenger receptor class B type I (SR-BI), and delivers estrogen to eNOS, thereby stimulating the enzyme. HDL isolated from women stimulated eNOS, whereas HDL isolated from men had minimal activity. Studies with ovariectomized and ovariectomized/estrogen replacement mouse models demonstrated that HDL-associated estradiol stimulation of eNOS is SR-BI dependent. Furthermore, female HDL, but not male HDL, promoted the relaxation of muscle strips isolated from C57BL/6 mice but not SR-BI null mice. Finally, HDL isolated from premenopausal women or postmenopausal women receiving estradiol replacement therapy stimulated eNOS, whereas HDL isolated from postmenopausal women did not stimulate eNOS. We conclude that HDL-associated estrodial is capable of the stimulating eNOS. These studies establish a new paradigm for examining the cardiovascular effects of HDL and estrogen.

We previously demonstrated that in Chinese hamster ovary cells scavenger receptor, class B, type I-dependent selective cholesteryl ester uptake occurs in caveolae. In the present study we hypothesized that cholesteryl ester is transported from caveolae through the cytosol to an internal membrane by a caveolin chaperone complex similar to the one we originally described for the transport of newly synthesized cholesterol. Caveolae are plasma membrane domains found in most types of cells and are identified biochemically by the presence of a 22-kDa protein called caveolin (1). Caveolin plays a pivotal role in the formation, structural integrity, and function of caveolae (1). Caveolin has multiple functions, but the function of caveolin relevant to the present studies is its role in the trafficking of intracellular sterol. Caveolin can directly bind to cholesterol (2, 3), and in an earlier study, we demonstrated that acylation of caveolin was required for the binding of cholesterol to caveolin (4). We speculated that the acylation of caveolin, which occurs adjacent to the hydrophobic membrane domain of caveolin, forms a binding pocket that sequesters cholesterol from the aqueous environment (4). These studies were extended to demonstrate that caveolin is part of a lipid-protein chaperone complex that transports newly synthesized cholesterol from the endoplasmic reticulum directly to caveolae (2). The lipid-protein complex consists of cholesterol, caveolin, heat shock protein 56 (HSP56), 1 cyclophilin 40, and cyclophilin A. Acylation of caveolin at cysteine residues 143 and 156, but not at 133, was required for cholesterol to associate with caveolin (4) and for the assembly of the lipid-protein complex. The lipid-protein complex rapidly (ϳ10 min) transported newly synthesized cholesterol to caveolae where it remained for some time before diffusing throughout the plasma membrane (2) or was effluxed to extracellular acceptors (5, 6). Pharmacological disruption of the lipid-protein complex with cyclosporin A or rapamycin prevented the rapid translocation of newly synthesized cholesterol to caveolae and resulted in a net decrease in the mass of cholesterol associated with caveolae over time. The decrease in caveolae cholesterol mass was presumably caused by the diffusion of cholesterol from caveolae to the rest of the plasma membrane without replenishing the cholesterol from intracellular stores.We recently demonstrated that caveolae in CHO cells are also involved in the selective uptake of exogenous cholesteryl esters from HDL (7,8). Selective uptake refers to the uptake of cholesteryl esters without the internalization and degradation of the entire lipoprotein particle (9). The scavenger receptor, class B, type I (SR-BI) is a physiological receptor for HDL that facilitates the selective uptake of HDL cholesteryl esters (10). Babitt et al. (11) demonstrated that SR-BI is preferentially localized to caveolae in CHO cells, and we recently demonstrated that HDL-derived cholesteryl ester is initially transferred to caveolae...

Illinois 601 15. USC M S . received 14th M a y 1970Ahtract. Starting from bare-ion pseudopotentials, net crystal potentials are evalutiied in direct space by (a) the usual linear screening technique and (b) the Thomas-Fermi method. For the metals considered (Na and AI), the potentials are quite similar, crossing outside the cores and never differing by more than 0.02 a.u. in the case of Na nor by more than 0.2 a.u. in the case of Al. The similarity of the results based on (a) and (b) suggest the use of the pseudopotential concept in conjunction with the rather general method (b) under conditions when (a) is questionable, that is whenever the zeroth order uniform electron gas solution is a poor physical approximation to the actual system under study (specific examples being molecules, insulating solids and interfaces).Methods (a) and (bj both yield shallower wells than those most often used as input information in band structure calculations and obtained by superposing atomic data.

There is evidence that dietary fat can modify the cytotoxicity of polychlorinated biphenyls (PCBs) and that coplanar PCBs can induce inflammatory processes critical in the pathology of vascular diseases. To test the hypothesis that the interaction of PCBs with dietary fat is dependent on the type of fat, low-density lipoprotein receptor–deficient (LDL-R−/−) mice were fed diets enriched with either olive oil or corn oil for 4 weeks. Half of the animals from each group were injected with PCB-77. Vascular cell adhesion molecule-1 (VCAM-1) expression in aortic arches was non-detectable in the olive-oil–fed mice but was highly expressed in the presence of PCB-77. PCB treatment increased liver neutral lipids and decreased serum fatty acid levels only in mice fed the corn-oil–enriched diet. PCB treatment increased mRNA expression of genes involved in inflammation, apoptosis, and oxidative stress in all mice. Upon PCB treatment, mice in both olive- and corn-oil–diet groups showed induction of genes involved in fatty acid degradation but with up-regulation of different key enzymes. Genes involved in fatty acid synthesis were reduced only upon PCB treatment in corn-oil–fed mice, whereas lipid transport/export genes were altered in olive-oil–fed mice. These data suggest that dietary fat can modify changes in lipid metabolism induced by PCBs in serum and tissues. These findings have implications for understanding the interactions of nutrients with environmental contaminants on the pathology of inflammatory diseases such as atherosclerosis.

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Low zinc concentration can be associated with an increased risk of cardiovascular diseases. In the current study, we hypothesize that zinc deficiency can increase and zinc supplementation can decrease proatherosclerotic events in LDL receptor knock-out (LDL-R-/-) mice fed a moderate-fat diet. Mice were fed either a zinc-deficient (0 micromol Zn/g), a control (0.45 micromol Zn/g), or a zinc-supplemented (1.529 micromol Zn/g) diet for 4 wk. Mice fed the zinc-deficient diet had significantly increased concentrations of cholesterol and triacylglycerides in the VLDL and HDL fractions. Zinc supplementation decreased these lipid variables compared with control mice. We detected significantly higher concentrations of glutathione reductase mRNA in the thoracic aortae of zinc-deficient mice. Furthermore, inflammatory markers, such as nuclear factor-kappaB and vascular cell adhesion molecule-1, were significantly increased in zinc-deficient mice compared with mice of the control or supplemented groups. In addition, zinc deficiency significantly reduced the DNA binding activity of peroxisome proliferator activate receptors (PPARs) in liver extracts. Interestingly, mRNA expression levels of PPARgamma were significantly increased in thoracic aortae of zinc-deficient mice, indicating an adaptation process to decreased PPAR signaling. These data provide in vivo evidence of zinc deficiency inducing proinflammatory events in an atherogenic mouse model. These data also suggest that adequate zinc may be a critical component in protective PPAR signaling during atherosclerosis.