Compliance with breast self-examination instruction in high school students.

In a prospective study, we measured compliance with breast self-examination, using an anonymous questionnaire, in suburban high school students three months (n = 85) and eight months (n = 54) after group instruction. Post-instruction proficiency in performing the procedure and personal health beliefs regarding breast cancer were also evaluated. At three months, 40% of the group reported practicing breast self-examination at some time since instruction; 12% had performed the procedure timed correctly with their menstrual cycle. At eight months, only two girls (4%) had practiced breast self-examination at least once since the three-month evaluation. Proficiency scores overall were high, with 77% scoring 12 points or above on a 15-item questionnaire; however, scores were significantly lower in the 15-year-olds than in the older adolescents. No significant relationships were found between compliance and most personal health beliefs, previous instruction, or level of knowledge of the procedure. Attention should be directed toward assessing the ability and willingness to practice preventive health behaviors before instruction programs are instituted in this age group.

Compliance with breast self-examination instruction in healthy adolescents.

Compliance with breast self-examination was prospectively assessed in three groups of healthy outpatient adolescents 6 weeks, 3 months, and 6 months after instruction. Although 87%, 59%, and 71% of the three respective groups reported sporadic practice of breast self-examination, only 39%, 9%, and 18%, respectively, performed the procedure timed correctly with the menstrual cycle. Those adolescents tested at 6 weeks demonstrated a high degree of proficiency in replicating the procedure on a silicone model. There was no significant difference between demographic variables or personal health beliefs regarding breast cancer and breast self-examination compliance. Our findings suggest that adolescents can effectively perform breast self-examination, but their practice is erratic. Thus, we recommend that when instruction in breast self-examination is given, the examination schedule should be reinformed at a follow-up visit.

Autogenous bone grafts for atrophic edentulous mandibles: a final report.

While autogenous bone augmentations for atrophic edentulous mandibles are not the ideal solution for this problem, we do not share the pessimism of other investigators. The average loss of bone over the 92-month observation period was 60% for this small sample of eight patients. However, there was an 81% gain in bone height in the premolar-molar regions when compared with presurgical measurements. Seven of the eight patients believed these procedures were beneficial.

Possible relationship between antigenic properties and isolation history of HSV-1 strains.

29 monoclonal anti-herpes simplex virus (HSV)-1 antibodies were produced and characterized with regard to virus neutralizing activity, intracellular or cell-surface location of viral antigens and, where possible, molecular weight of the viral protein recognized. 13 antibodies recognized viral antigens expressed on the surface of infected cells and 16 were directed to intracellular viral components. Only two antibodies exhibited virus neutralizing activity. Application of these antibodies to an antigenic comparison of standard laboratory HSV-1 strains F, HFEM, mP, Glasgow-17 and MAC revealed unique antigenic differences among these strains. The antibodies were further used in an antigenic comparison of 45 human HSV-1 isolates with defined isolation history. Except for two paired isolates from left and right trigeminal ganglia of two human cadavers, the antibody panel revealed antigenic differences among all isolates, including paired isolates from three additional cadavers. Overall, isolates from different human donors showed greater antigenic dissimilarity from each other in cell-surface associated than in intracellular antigens. The data suggest the possibility of a correlation between antigenic and biologic properties of HSV-1.

Molecular mimicry in virus infection: crossreaction of measles virus phosphoprotein or of herpes simplex virus protein with human intermediate filaments.

Using monoclonal antibodies, we demonstrate that the phosphoprotein of measles virus and a protein of herpes simplex virus type 1 crossreact with an intermediate filament protein of human cells. This intermediate filament protein, probably vimentin, has a molecular weight of 52,000, whereas the molecular weights of the measles viral phosphoprotein and the herpes virus protein are 70,000 and 146,000, respectively. Crossreactivity was shown by immunofluorescent staining of infected and uninfected cells and by immunoblotting. The monoclonal antibody against measles virus phosphoprotein did not react with herpes simplex virus protein and vice versa, indicating that these monoclonal antibodies recognize different antigenic determinants on the intermediate filament molecule. The significance of these results in explaining the appearance of autoantibodies during virus infections in humans is discussed.

Antigenic structure of influenza virus haemagglutinin defined by hybridoma antibodies.

The recurrence of influenza virus infection in man is attributed primarily to changes occurring in the antigenic structure of the viral surface glycoproteins, especially of the haemagglutinin (HA) molecule. Comparative antigenic analysis of epidemic influenza virus strains has allowed the description of 'strain-specific' and 'cross-reactive' antigenic determinants. However, the interpretation of these findings remained ambiguous, because the specificity of the applied antisera was insufficiently defined and because the antigenic differences among the HA molecules of various epidemic virus strains resulted presumably from a large number of amino acid substitutions. Thus, in characterizing the antigenic structure of the HA molecule, our approach has been (1) to generate a panel of monoclonal anti-HA hybridoma antibodies, (2) to use some of these antibodies to select mutants of the influenza A/PR/8/34 (PR8) virus expressing antigenically altered HA molecules, and (3) to construct an operational antigenic map of the HA molecule by comparative antigenic analysis of the mutant viruses with the monoclonal antibodies. As we report here, analysis of the 34 mutant viruses selected has enabled us to define four antigenic sites on the HA molecule. Our observation that these sites have undergone antigenic drift to a different extent in nature implies that the mechanisms responsible for antigenic drift act selectively on distinct structures of the HA molecule.

A monoclonal antibody to viral glycoprotein blocks virus-immune effector T cells operating at H-2Dd but not at H-2Kd1.

A particular monoclonal antibody that binds to the influenza virus HA molecule inhibits HA-specific thymus-derived lymphocytes mediating cytotoxicity in the context of H-2Dd but not of H-2Kd. Another monoclonal antibody blocks both sets of HA-specific effector T cells. This observation, together with related findings from other laboratories, is considered to support the idea that T cell recognition is directed against some association of viral and H-2 glycoproteins, as proposed in the original formulation of the "altered self" concept.

Inhibition of influenza-immune T cell effector function by virus-specific hybridoma antibody.

The in vitro activity of influenza-specific cytotoxic T cells can be inhibited by incubation of the target cells with monoclonal anti-influenza antibodies. Hybridoma antibodies that bind to the virus HA inhibit the cytotoxic activity of TDL for the virus-infected target by as much as 80%, whereas these same antibodies never reduce splenic T cell function by more than 40%. This reflects the fact that TDL from anti-influenza strain A/WSN/33 (HON1) are highly subtype-specific, whereas splenic effector cells from the same mice are cross-reactive for target cells infected with heterologous influenza A viruses. These findings are discussed in the light of previous failures to block virus-immune T cell effector function with heterogeneous antisera produced in vivo, and are considered to favor the idea that at least some of the "virus-immune" T cells are indeed recognizing viral antigens.

Antigenic drift in type A influenza virus: peptide mapping and antigenic analysis of A/PR/8/34 (HON1) variants selected with monoclonal antibodies.

Variants of A/PR/8/34 (HON1) influenza virus, having hemagglutinin molecules with probably a single altered antigenic determinant, were isolated by growing the virus in the presence of the monoclonal hybridoma antibody PEG-1. The variants were analyzed by peptide mapping and characterized antigenically by using PEG-1 and four other monoclonal hybridoma antibodies to PR8 hemagglutinin. Peptide maps of the large hemagglutinin polypeptide, HA1, from 8 out of 10 variants showed a single changed peptide. This peptide from two of the variants was analyzed, and in each case a serine residue in the wild-type hemagglutinin was replaced by leucine in the variant. Although these eight variants showed identical peptide maps, one could be discriminated antigenically from the others with one of the hybridomas. (The peptide maps represented about one-third of the HA1 molecule.) Of the other two variants, one gave the same HA1 map as the wild type, but could be distinguished antigenically from wild-type virus by two of the hybridomas. The other was unique, and could be distinguished, both antigenically and by peptide mapping, from the other variants. Since a large number of the variants selected with PEG-1 showed the same peptide change, it is likely that this alteration in amino acid sequence (serine to leucine) was responsible for the inability of the variants to bind PEG-1 monoclonal antibody. We do not know, however, whether the changed amino acids were located within the antigenic sites or whether the change occurred somewhere else in the hemagglutinin molecule and altered the determinants through conformational changes.