[Energy transfer between electric polymer PVK and terbium complex and its transmission electronmicroscope (TME) study].

A chloroform-soluble terbium complex, which is confirmed to be Tb(aspirin)3 phen using element analysis and FT-IR spectroscopy, was synthesized. Photoluminescent investigation on the terbium complex and PVK-terbium complex composite was conducted. Förster energy transfer occurred between the terbium complex and the PVK matrix. There are no overlap between UV spectrum of the complex and the emission spectrum of PVK, however, overlap is observed between the excitation spectrum of the complex and the emission spectrum of PVK. Therefore, we suggest that the necessary condition of Förster energy transfer should be overlap between the excitation (not UV) spectrum of one complex and the emission spectrum of polymer matrix. Further investigation indicates that the emission of PVK can be suppressed at different extents by doping various amount of Tb(aspirin)3 phen into PVK films. The ratio of Tb(aspirin)3 phen: PVK = 1:2 (wt%) are regarded as an optimized ratio for limiting the emission of PVK. TEM images of PVK/Tb(aspirin)3 phen films reveal that nanoparticles of the Tb complex are dispersed in the PVK matrix. The size of the aggregated complex in PVK matrix is 20-30 nm. The film is not homogeneous as dark regions co-exist with light region in the TEM images. This phenomenon may be related to the short lifetime of electroluminescent devices.

Synthesis of oligosaccharides containing beta-D-Gal-(1-->3)-O-(6-O-sulfo-beta-D-GlcNAc) as a terminal unit.

The chemical synthesis of beta-D-Gal-(1-->3)-6-O-SO3Na-beta-D-GlcNAc-(1-->6)-alpha-D-Man-O-+ ++C6H4NO2 (1) and beta-D-Gal-(1-->3)-6-O-SO3Na-beta-D-GlcNAc-(1-->2)-alpha-D-Man-OMe (2) is reported using a key glycosyl donor, phenyl O-(2,3,4,6-tetra-O-acetyl-beta-D-galactopyranosyl)-(1-->3)-4,6-di-O- chloroacetyl-2-deoxy-2-phthalimido-1-thio-beta-D-glucopyranoside (3).

Synthesis and in vitro antitumor activity of some amino-deoxy 7-hexofuranosylpyrrolo[2,3-d]pyrimidines.

7-(6-amino-6-deoxy-beta-D-glucofuranosyl)-5-cyanopyrrolo[2,3 -d]pyrimidine (22) and 7-(3-amino-methyl-3-deoxy-beta-D-allofuranosyl)-5- cyanopyrrolo[2,3-d]pyrimidine (28) were synthesized by sequentially coupling silylated 4-amino-6-bromo-5- cyanopyrrolo[2,3-d]pyrimidine with the corresponding protected sugars 9 and 17, followed by deblocking and catalytic hydrogenation. Conversion of the 5-nitrile in 22 and 28 into a carboxamide gave the corresponding sangivamycin derivatives 23 and 29. Whereas 5'-aminomethyl nucleosides 22 and 23 inhibited the growth of four different human tumor cell lines at microM concentrations, the 3'-aminomethyl analogs 28 and 29 were much less active against these cells.

Inhibition of L- and P-selectin by a rationally synthesized novel core 2-like branched structure containing GalNAc-Lewisx and Neu5Acalpha2-3Galbeta1-3GalNAc sequences.

The selectins interact in important normal and pathological situations with certain sialylated, fucosylated glycoconjugate ligands containing sialyl Lewisx(Neu5Acalpha2-3Galbeta1-4(Fucalpha1-3)GlcN Ac). Much effort has gone into the synthesis of sialylated and sulfated Lewisxanalogs as competitive ligands for the selectins. Since the natural selectin ligands GlyCAM-1 and PSGL-1 carry sialyl Lewisxas part of a branched Core 2 O-linked structure, we recently synthesized Galbeta1-4(Fucalpha1-3)GlcNAcbeta1-6(SE-3Galbeta1++ +-3)GalNAc1alphaOMe and found it to be a moderately superior ligand for L and P-selectin (Koenig et al. , Glycobiology 7, 79-93, 1997). Other studies have shown that sulfate esters can replace sialic acid in some selectin ligands (Yeun et al. , Biochemistry, 31, 9126-9131, 1992; Imai et al. , Nature, 361, 555, 1993). Based upon these observations, we hypothesized that Neu5Acalpha2-3Galbeta1-3GalNAc might have the capability of interacting with L- and P-selectin. To examine this hypothesis, we synthesized Galbeta1-4(Fucalpha1-3)GlcNAcbeta1-6(Neu5Acalpha2++ +-3Galbeta1-3)-GalNAc alpha1-OB, which was found to be 2- to 3-fold better than sialyl Lexfor P and L selectin, respectively. We also report the synthesis of an unusual structure GalNAcbeta1-4(Fucalpha1- 3)GlcNAcbeta1-OMe (GalNAc-Lewisx-O-methyl glycoside), which also proved to be a better inhibitor of L- and P-selectin than sialyl Lewisx-OMe. Combining this with our knowledge of Core 2 branched structures, we have synthesized a molecule that is 5- to 6-fold better at inhibiting L- and P-selectin than sialyl Lewisx-OMe, By contrast to unbranched structures, substitution of a sulfate ester group for a sialic acid residue in such a molecule resulted in a considerable loss of inhibition ability. Thus, the combination of a sialic acid residue on the primary (beta1-3) arm, and a modified Lexunit on the branched (beta1-6) arm on an O-linked Core 2 structure generated a monovalent synthetic oliogosaccharide inhibitor superior to SLexfor both L- and P-selectin.