Simplicity in interim tooth-supported removable partial denture construction.
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Biomedical subjects
Publications and source records attributed to C C Chien.
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The antibody response to the inulin [(In), beta-(2 leads to 1) fructosan] determinant of bacterial levan [(BL), a beta-(2 leads to 6) polyfructosan that contains beta-(2 leads to 1) branch points] requires the presence of the a haplotype of the Igh gene complex. BALB/c (Igh a) mice immunized with BL produce IgG anti-In antibodies of a single spectrotype by isoelectric focusing analysis. C57BL/6 mice, which possess the b haplotype of the Igh gene complex and which fail to produce anti-In antibodies, nevertheless possess a gene, spectrotype regulation gene 1 (Sr-1), that regulates the isoelectric focusing (IEF) pattern of anti-In antibodies in mice of the a haplotype. Thus, the IEF patterns of anti-In antibodies of (BALB/c x C57BL/6)F1 mice and of B.C8 mice (C57BL/Ka . Igh-Ca) are considerably more complex than those of BALB/c. Backcross analysis indicates that Sr-1 is not linked to the Igh complex, the major histocompatibility complex, or to the genes that code for coat color. Studies of the heterogeneity of anti-In antibodies in recombinant inbred lines and their progeny from matings to BALB/c and C.B20 (BALB/c . Igh-Cb) suggest the existence of other regulatory genes.
Anti-inulin [beta-(2 --> 1) polyfructosan Brucella abortus (InuBA)] and anti-grass levan [beta-(2 --> 6) polyfructosan] antibody responses in BALB/c and C57BL mice and in their F(1) and backcross progeny, as well as in immunoglobulin congenic and Bailey recombinant inbred strains derived from BALB/c and C57BL mice, were examined. The anti-inulin antibodies could accommodate both beta-(2 --> 1)- and beta-(2 --> 6)-linked polyfructosans, and 97% of the anti-inulin plaque-forming cells (PFC) from BALB/c mice expressed the cross-reactive idiotypes (InuIdX) shared by the BALB/c inulin- and levan-binding myeloma proteins. Of the C57BL mice, only 25% produced high anti-inulin response, and none exhibited the InuIdX of BALB/c anti-inulin antibodies. The percentages of InuIdX(+) anti-inulin PFC were also examined in other strains with high anti-inulin response. In C58 and AL mice, 80% of anti-inulin PFC were InuIdX(+), whereas in A/He and RIII mice, only 40% were InuIdX(+). All strains examined developed high anti-grass levan response, and the antibodies were specific for beta-(2 --> 6) structures and did not exhibit InuIdX. Comparison of the magnitude of the anti-inulin antibody titers in response to InuBA in BALB/c, C57BL, and their F(1) and backcross progeny, as well as in immunoglobulin congenic (i.e., B.C-8, BAB-14, and C.B-20) and recombinant inbred strains derived from BALB/c and C57BL mice, showed that all mice having the IgCH(a)(BALB/c) allotype gave high anti-inulin response. In addition to the InuIdX structural genes, the effects of allotype-linked or unlinked "regulatory" genes were also indicated by the lower anti-inulin response in B.C-8 and BAB-14 mice compared with BALB/c mice and the higher anti-inulin response in C.B-20 mice compared with C57BL mice. A multigene interaction in controlling the production of the anti-inulin antibodies was implicated.
A method is described for preparing derivatives of alkali-stable polysaccharides for coupling to immunogen carriers or to sheep red blood cells (SRBC) for use in hemagglutination (HA) and plaque-forming cell (PFC) assays. Inulin, a beta (2 leads to 1)-linked polyfructosan was partially derivatized with carboxyl, aminoethyl or (p-aminophenyl)butyryl groups; the latter derivative was coupled to SRBC following diazotization. Optimal conditions for the sensitization of SRBC with inulin were given. The immunological reactivity of the inulin molecule was unaffected by the derivatization reactions, and high, reproducible anti-inulin HA titers for inulin-binding myeloma proteins were found using these specifically sensitized SRBC. The sensitized SRBC were stable for assays for over 2 weeks. Problems with spontaneous agglutination or distortion of sensitized SRBC, normally seen in other procedures, e.g., methods using stearoyl-inulin, were not encountered.
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Idiotypes of inulin-binding myeloma proteins (InuBMP) were determined primarly by variable region light chains (VL) or by variable region heavy chains (VH) but needed both chains to be expressed. Recombinant molecules were used to show that individual idiotypes (IdI) of U61, E109, T957, and A4 InuBMP and cross-specific idiotypes (IdXB) of U61 were primarily determined by VL while cross-specific idiotype (IdXA) of A4 was determined mainly by VH. The assignment of genes controlling idiotypes to VH based on allotype linkage (e.g., IdXB) is dubious until the role of the L chain in determining that idiotype is assessed. IdXB has been shown to be a VL-VH marker which presumably is controlled by two unlinked genes. However IdXB can be used as a L chain marker in combinations of strains differing in their L chain genes but having the same permissive H chain genes. Conversely IdXB can be used as a H chain marker in strains having the same permissive L chain genes but differing in their H chain genes.
Rabbits of allotype a1a3 were injected on days 0, 2, and 4 with mixtures containing equal amounts of pigeon erythrocytes (Prbc) coupled to para-azobenzenearsonate (AA) and to para-azobenzene-N-trimethylammonium (TMA). On day 6, the allotypes of antibody from plaque-forming cells (PFC) of the blood were determined by observing the inhibition of plaque formation by anti-allotype sera. Anti-AA PFC appeared to consist for the most part of cells making antibody of allotype a1 since 65% of them were inhibited by anti-a1 serum and only 8% by anti-a3. Anti-TMA PFC, on the other hand, appeared to consist mostly of cells making antibody of allotype a3, since less than 1% of them were inhibited by anti-a1 but 47% by anti-a3. Antibody allotype for spleen PFC was also determined on day 6 and was similar to that found for blood PFC. Anti-AA PFC were inhibited 74% by anti-a1 serum and 15% by anti-a3 whereas anti-TMA PFC were inhibited 19% by anti-a1 and 43% by anti-a3. Serum hemolysin specific for AA hapten from a1a3 animals was also strongly inhibited by anti-a1 serum but not by anti-a3 whereas the converse was true for hemolysin against TMA hapten. The a1a3 rabbits, in whcih the anti-AA was restricted to allotype a1, were mated to produced homozygous a3a3 animals. When the PFC and serum antibodies of these a3a3 offspring were examined by specific inhibition, the anti-AA activity was found to be of allotype a3 rather than being a-negative. The number of anti-AA PFC in the blood of a3a3 rabbits was lower than that in blood of a1a3 or a1a1 animals. In addition, the TMA hapten appeared to inhibit the response to the AA hapten. Thus a1a3 rabbits immunized with AA-Prbc alone had 14-fold more anti-AA PFC or 18-fold higher anti-AA hemolysin titer than a3a3 animals immunized with both AA-Prbc and TMA-Prbc. Our results are discussed in relation to various explanations which have been offered for an imbalance of allotypes in a given antibody.
The serum from non-immunized mice of strains BALB/c, C58, A/He, and RIII contained hemagglutinins for stearoyl inulin-coated SRBC. Immunization with bacterial levan slightly elevated these titers. These same sera also carried cross-specific idiotypic determinants (IdX) that are associated only with inulin-binding myeloma proteins (INBMP) of BLAB/c mice. Three InuldX specificities, A, B, and G, were identified. The InuIdX phenotypes of strains BALB/c, C58, and A/He were InuIdXA+B+G+; strain RIII was InuIdX A+B-G+; strain C57BL/6, C57BL/10, DBA/2, AKR and NH were A-B-G-. Strains CBA, C3H, PL, and C57L could not be typed because of low and inconsistent levels of InuIdX and anti-inulin hemagglutinins. The InuIdXA+B+G+ phenotype was used as a genetic marker in immunoglobulin congenic strains CB-20, BAB-14, and BC-8 and in Bailey RI strains which are derived from crosses of BALB/c (InuIdXA+B+G+) and C57BL/ka or C57BL/6, respectively (InuldXA-B-G-). Linkage of the IdXA+B+G+ to the BALB/c a allotype locus was demonstrated. In addition, the InuldXA+B+G+ marker was used as a phenotype in an analysis of 168 first generation backcorss progeny (C57BL X (C57BL X BALB/c) F). Linkage of the marker to the BALB/c allotype was found again. Two proven recombinant mice having the C57BL a allotype and the InuIdxA+B+G+ markers were identified and progeny tested. Four other potential crossover types are still being progeny-tested.
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