Enamel shear bond strengths after vital bleaching.

This study examined the shear bond strengths of enamel bond formed at specific time intervals after the termination of vital bleaching. A total of 160 extracted human anterior teeth were divided into three bleaching treatment (BTx) groups (Superoxol, Proxigel, White & Brite), two bonding agent (BA) subgroups (Scotchbond Dual Cure, Scotchbond 2) and two BA control groups. After BTx for 30 days, bonds were formed at 1, 6 and 24 hours; 3 and 7 days (time interval, TI) post-termination of BTx. A total of 32 groups of n = 5 were used. Bonds were formed in nylon tubes with selected BA and Silux Plus, and ruptured 24 hours later with Instron and cable/loop to measure enamel shear bond strength (SBS). A 3 x 2 x 5 factorial ANOVA and Tukey 95% confidence interval (TCI) detected significant differences between BTx (F = 3.54; TCI = 2.7 MPa), BA (F = 9.73; TCI = 1.8 MPa) and TI (F = 9.39; TCI = 4.1 MPa). The interaction between BTx and TI was slightly significant (F = 2.02); other interactions were not significant. Post-hoc analysis showed 80% of bonds failed at the interface or by mixed cohesive composite/interfacial failure. Scanning electron microscope observations suggested association of increased density of voids in bond area at TI with lowest mean bond strengths. SBS ranged from 42.3 to 106.8% of control.

Studies of the mechanism by which gangliosides inhibit the proliferative response of murine splenocytes to concanavalin A.

Gangliosides are known to inhibit the proliferative response of murine and human lymphocytes to antigens and mitogens in vitro. In this study the response of murine spleen cells to concanavalin A (Con A) was used as a model system. Analysis of the cellular events by flow cytometry revealed that during the first 24 hr of culture the effect of gangliosides on Con A-treated cells was minimal. At 48 hr, however, more of the ganglioside-treated cells were in G0/G1, the cells contained more RNA, and fewer cells were in S phase. These data indicate that gangliosides inhibit the transition of the cells from G0/G1 into the S phase of the cell cycle. Expression of the interleukin 2 (IL-2) receptor, as measured by the binding of a monoclonal antibody to the receptor, was not inhibited by the gangliosides. Binding of 125I-labeled recombinant IL-2 to cells cultured for 48 hr with Con A was inhibited by ganglioside GD1a but not by asialo GM1. Inhibition was much more effective if the gangliosides were preincubated with IL-2 before addition of cells, but no inhibition was observed if the cells were preincubated with gangliosides and the unbound gangliosides were washed out prior to addition of the IL-2. These data suggest that interference with the binding of IL-2 to the high-affinity IL-2 receptor of activated T lymphocytes plays an important role in the inhibition of Con A-induced proliferation.

Glycosphingolipids of human plasma.

A number of glycosphingolipids, including 10 gangliosides, not previously identified in human plasma have been characterized. The plasma contains 2 micrograms of lipid-bound sialic acid/ml plasma and 54% of the gangliosides are monosialo, 30% disialo, 10% trisialo, and 6% tetrasialo. Individual glycosphingolipids were purified by high-performance liquid chromatography and thin-layer chromatography, and were characterized on the basis of their chromatographic mobility, carbohydrate composition, hydrolysis by glycosidases, methylation analysis, and immunostaining with anti-glycosphingolipid antibodies. The monosialogangliosides were identified as GM3, GM2, sialosyl(2-3)- and sialosyl(2-6)lactoneotetraosylceramides, sialosyllacto-N-nor-hexaosylceramide, and sialosyllacto-N-isooctaosylceramide. The major gangliosides in the polysialo fractions contained a ganglio-N-tetraose backbone and were identified as GD3, GD1a, GD1b, and GQ1b. The most abundant neutral glycosphingolipids were glucosyl, lactosyl, globotriaosyl, globotetraosyl and lactoneotetraosylceramides. The other neutral glycosphingolipids, tentatively identified by immunostaining with monoclonal antibodies, contained H1, Lea, Leb, and lacto-N-fucopentose III (X hapten) structures.

Antibodies to glycosphingolipids in patients with multiple sclerosis.

Antibodies to one or more glycosphingolipids were detected by means of a liposome lysis assay in the sera of 60/81 patients with multiple sclerosis, 24/42 patients with systemic lupus erythematosus and in the majority of patients with cranial trauma or cerebrovascular accidents. Antibodies against ganglioside GM1 and asialo GM1 were found most commonly and they were frequently present in the same sera. Among patients whose sera contained antibodies to glycolipids, anti-GM1 alone occurred more frequently in patients with multiple sclerosis (14/59) than in systemic lupus erythematosus (1/22; p = 0.045) and antiasialo GM1 alone was more common in patients with lupus (9/22) than in patients with multiple sclerosis (8/59, p = 0.007). In 10 sera analyzed, all of the antibodies against these two glycolipids were of the IgM class, and some fluctuation in antibody titers was noted over a three-month period. The role of these antibodies in the initiation or perpetuation of inflammatory diseases of the central nervous system remains to be determined.