Transfer of phosphatidylcholine facilitated by a component of human plasma.

A constituent of lipoprotein-free (p greater than 1.21) human plasma from normolipemic donors facilitates the transfer of diacyl phosphatidylcholine from unilamellar egg yolk phosphatidylcholine liposomes to liver mitochondria. The active component is heat labile, has a hydrated density greater than 1.25 and an apparent molecular weight of more than 100 000. The presence of this protein in plasma may facilitate movement of diacylphospholipids between the surfaces of lipid-containing particles such as lipoproteins and erythrocytes. Knowledge of the properties and behavior of this protein are important in designing methods of drug therapy based on encapsulation in biodegradable lipid vesicles.

Interaction of a human plasma lipid transfer protein complex with lipid monolayers.

The interaction of a purified human plasma lipid transfer complex with cholesteryl ester, triacylglycerol and phosphatidylcholine in binary and ternary lipid monolayers was investigated. The lipid transfer complex, designated LTC, catalyzes the removal of cholesteryl oleate and triacylglycerol from phosphatidylcholine monolayers. Preincubation of LTC with p-chloromercuriphenyl sulfonate inhibits LTC-catalyzed removal of triacylglycerol; cholesteryl ester removal is not affected. The rate of LTC-facilitated removal of cholesteryl oleate from a phosphatidylcholine monolayer depends on the amount of LTC added to the subphase up to 100 micrograms protein. In addition, the rate of the LTC-catalyzed transfer of cholesteryl oleate to the subphase increases linearly as the amount of cholesteryl oleate in the monolayer increases to 6 mol%. LTC also removes cholesterol from phosphatidylcholine-cholesterol monolayers, albeit at a rate which is 15% of that for removal of cholesteryl oleate. The ability of LTC to facilitate triacylglycerol and cholesteryl ester removal depends on the composition of the monolayer. Phosphatidylcholine supports cholesteryl ester transfer whereas sphingomyelin-cholesteryl ester monolayers are almost refractory to LTC. In contrast, LTC removes triacylglycerol from either a phosphatidylcholine or a sphingomyelin monolayer. The results suggest the existence of at least two lipid transfer proteins, one of which catalyzes the removal of cholesteryl ester and the other triacylglycerol. The role of these proteins as they relate to lipoprotein metabolism is discussed.

Ineffective immune enhancement by IL-12 in tumor-bearing mice whose immune depression is mediated by suppressive granulocyte-macrophage progenitor cells.

Lewis lung carcinoma (LLC-LN7) tumors stimulate myelopoiesis and induce immunosuppressive granulocyte-macrophage (GM)-progenitor cells. Treating mice having palpable tumors with IL-12 enhanced the frequency of GM-progenitors and did not diminish GM-suppressor activity. Proliferation of splenic T-cells of tumor-bearers to Con-A or to anti-CD3 plus IL-2 was suppressed; this was not enhanced by IL-12 treatment. Also not stimulated was T-cell secretion of IL-2 in response to autologous tumor, or the intratumoral T-cell content. IL-12 slightly increased splenic IFN-gamma secretion, and increased cytotoxicity of lymph node (but not spleen) cells toward autologous tumor. In these tumor-bearing mice that were immune depressed as a result of GM-suppressor cells, immune modulatory effects of IL-12 were marginal and did not affect tumor size or metastasis.

Vitamin D3 treatment of tumor bearers can stimulate immune competence and reduce tumor growth when treatment coincides with a heightened presence of natural suppressor cells.

By secreting granulocyte-macrophage colony-stimulating factor (GM-CSF), Lewis lung carcinoma tumors induce immune suppressive granulocyte-macrophage progenitor cells. Treating mice having established tumors and high levels of suppressor activity with vitamin D3 eliminated suppressor activity, increased anti-tumor immunity, induced an immune stimulatory cell population, and reduced tumor growth. When instead, the vitamin D3 treatment was initiated earlier, when implanted tumors first became detectable and when natural suppressor activity was less prominent, the treatment had no effect. Thus, vitamin D3 treatment can stimulate the immune competence of tumor bearers when treatment is targeted to coincide with a heightened presence of GM-CSF-induced suppressor cells.

Defects, quasibound states, and quantum conductance in metallic carbon nanotubes

The effects of impurities and local structural defects on the conductance of metallic carbon nanotubes are calculated using an ab initio pseudopotential method within the Landauer formalism. Substitutionally doped boron or nitrogen produces quasibound impurity states of a definite parity and reduces the conductance by a quantum unit (2e(2)/h) via resonant backscattering. These resonant states show strong similarity to acceptor or donor states in semiconductors. The Stone-Wales defect also produces quasibound states and exhibits quantized conductance reduction. In the case of a vacancy, the conductance shows a much more complex behavior than the prediction from the widely used pi-electron tight-binding model.

Effect of aminoguanidine on lipid peroxidation in streptozotocin-induced diabetic rats.

Diabetes mellitus is postulated to be associated with increased lipid peroxidation, which may contribute to vascular complications. One potential mechanism of the increased lipid peroxidation in diabetes is lipid-linked advanced glycosylation and oxidation. Aminoguanidine (AMGN), the prototype inhibitor of advanced glycosylation end product (AGE) formation, has been recently shown to prevent oxidative modification of low-density lipoprotein (LDL) in vitro at a moderate concentration. It is unknown whether AMGN may act as an antioxidant against lipid peroxidation under hyperglycemia in vivo. To investigate the in vivo effect of AMGN on lipid peroxidation in diabetes, we administered AMGN (1 g/L in drinking water) or vitamin E (400 mg/d for 5 d/wk) to streptozotocin (STZ)-induced diabetic rats for 9 weeks and measured plasma lipid hydroperoxides by ferrous oxidation with xylenol orange II (FOX method) and red blood cell (RBC) membrane malondialdehyde (MDA) and related aldehydes as thiobarbituric acid-reactive substances (TBARS). Plasma lipid hydroperoxide was higher in STZ-induced diabetic rats versus control rats (mean +/- SD, 7.53 +/- 2.03 v 5.62 +/- 0.44 micromol/L, P < .05; n = 8 to 14). RBC membrane TBARS were also higher in STZ-induced diabetic rats than in control rats (2.67 +/- 0.46 v 1.81 +/- 0.19 nmol/mL, P < .05). Plasma lipid hydroperoxide was lower in AMGN-treated (6.23 +/- 0.59 micromol/L, P < .05) and vitamin E-treated (5.29 +/- 0.27 micromol/L, P < .05) diabetic rats than in untreated diabetic rats. RBC membrane TBARS were also lower in AMGN-treated (1.93 +/- 0.12 nmol/mL, P < .05) diabetic rats than in untreated diabetic rats. There was no significant difference in plasma glucose, cholesterol, and triglyceride levels among diabetic groups. Although the mechanism(s) of action of AMGN on lipid peroxidation in vivo should be studied further, these results suggest that AMGN may have an additional beneficial effect as an antioxidant against lipid peroxidation in a prevention trial for diabetic vascular complications.

Galactosylated chitosan (GC)-graft-poly(vinyl pyrrolidone) (PVP) as hepatocyte-targeting DNA carrier. Preparation and physicochemical characterization of GC-graft-PVP/DNA complex (1).

Galactosylated chitosan was conjugated with poly(vinyl pyrrolidone) (PVP) as a hydrophilic group. The complex formation of GC-graft-PVP (GCPVP)/DNA complexes was confirmed by agarose gel electrophoresis. The morphology of the complex observed by atomic force microscopy had a compact and spherical shape, around 40 nm particle sizes at a charge ratio of 3. The binding strength of GCPVP 10K/DNA complex measured by ethidium bromide binding assay was superior to that of the GCPVP 50K/DNA one, probably attributable to its higher flexibility due to the smaller size, whereas the DNase I protection of GCPVP 10K/DNA complex was inferior to that of the GCPVP 50K/DNA one. This indicated that effective complex formation required both higher binding strength and minimal molecular weight of polycation enough to induce the condensation of DNA. The DNA-binding property of GCPVP mainly depended on the molecular weight of chitosan and composition of PVP.

Atomic and electronic structures of amorphous Ge(2)Sb(2)Te(5); melt-quenched versus ideal glasses.

To investigate an amorphous structure of Ge(2)Sb(2)Te(5) that satisfies the 8-N rule (so-called 'ideal glass'), we perform alternative melt-quench simulations on Si(2)As(2)Se(5) and replace atoms in the final structure with Ge-Sb-Te. The resulting structures have salient features of the 8-N rule such as the tetrahedral configuration for all Ge atoms and the localized Te lone pairs at the valence top. In addition, the average Ge-Te and Sb-Te distances are in good agreement with experiment. The energetic stability of the ideal glass supports the existence of this amorphous structure that is distinct from the melt-quenched glass. From the analysis of electronic structures and optical dielectric constants, it is concluded that the electronic character of the melt-quenched amorphous Ge(2)Sb(2)Te(5) lies in between the resonant p-bonding of the crystalline phase and the covalent bonding of the ideal glass.