Prevalence of Superior Semicircular Canal Dehiscence on High-Resolution CT Imaging in Patients without Vestibular or Auditory Abnormalities.

BACKGROUND AND PURPOSE: Prior studies of radiologic superior semicircular canal dehiscence have suggested that CT may overcall dehiscence. However, many of those studies were performed before the advent of multichannel helical CT. Furthermore, there are limited data investigating the prevalence of radiologic superior semicircular canal dehiscence in asymptomatic individuals. The purpose of this study was to determine the rate of radiologic superior semicircular canal dehiscence in an asymptomatic population using 64-channel helical CT. MATERIALS AND METHODS: We retrospectively enrolled 500 consecutive adult patients without symptoms of superior semicircular canal dehiscence who had undergone CT of the temporal bones in the emergency department of a tertiary academic center between February 2012 and June 2017. The superior semicircular canals were evaluated bilaterally by 2 dedicated head and neck radiologists and subjectively classified as either dehiscent or nondehiscent. A secondary group of 110 scans of patients with symptoms consistent with superior semicircular canal dehiscence was similarly interpreted, and the rate of radiologic superior semicircular canal dehiscence was calculated for each group. RESULTS: Ten of the 500 asymptomatic patients (2.0%; 95% CI, 1.1%-3.6%) had CT evidence of superior semicircular canal dehiscence, compared with 15 of 110 symptomatic patients (13.6%; 95% CI, 7.8%-21.5%). There was excellent interobserver agreement (κ = 0.91). CONCLUSIONS: Only 2% of asymptomatic patients had radiologic evidence of superior semicircular canal dehiscence on 64-detector row helical CT. This is markedly lower than previous reports and approaches the postmortem rate of asymptomatic superior semicircular canal dehiscence. We therefore recommend that asymptomatic patients with CT evidence of superior semicircular canal dehiscence undergo audiologic evaluation because the rate of false-positive scans is extremely low.

Observational study of the extent of driving while suspended for alcohol impaired driving.

OBJECTIVE: To determine the proportion of first time driving while alcohol impaired (DWI) offenders who drive while their driver's license is suspended. DESIGN: Systematic, unobtrusive observations were conducted by surveillance professionals from Pinkerton Investigative Services, Inc, of first time offenders in the City of Milwaukee, Wisconsin, and Bergen County, New Jersey. Observations included two four hour periods during suspension (one weekday morning, one Friday/Saturday evening) and two four hour periods after license reinstatement (matched by day of week and time of day). Focus groups of first time offenders were conducted in each site. SETTING: New Jersey laws pertaining to license suspension for DWI and driving while suspended are stronger than Wisconsin laws. SUBJECTS: 93 recently convicted first time DWI offenders (57 in Milwaukee and 36 in Bergen County). MAIN OUTCOME MEASURES: Proportion of subjects observed driving during suspension and after license reinstatement, with reference to all subjects and subjects observed traveling by any means. RESULTS: Of subjects observed traveling while suspended, 88% of Milwaukee subjects compared with 36% of Bergen County subjects drove. Five percent of Milwaukee subjects and 78% of Bergen County subjects reinstated their driver's license. Bergen County subjects were significantly more likely to drive after reinstatement (54%) than during suspension (25%). CONCLUSION: Prevalence of driving while suspended among first time offenders is high and can vary substantially between jurisdictions. However, the license suspension can have a positive impact on the driving patterns of offenders during suspension, relative to after license reinstatement. Lower prevalence of driving while suspended in New Jersey may partly be attributable to that state's tougher laws.

[Regional differences in the utilization of early cancer screening 1985]. / Regional unterschiedliche Inanspruchnahme der Krebsfrüherkennung 1985.

Analysis of attendance of the German Cancer Screening Programme according to sex, age and federal state ("Land") reveals noticeable regional differences whereas in general participation is decreasing. It is shown that attendance is above average in the city states, Hesse, and Baden-Württemberg. The remaining Länder should, therefore, improve their rates. A decline in preventive activities and a reluctant attitude towards cancer screening must be taken seriously and be considered when developing the programme further.

The role of complement receptor positive and complement receptor negative B cells in the primary and secondary immune response to thymus independent type 2 and thymus dependent antigens.

Both complement receptor positive (CR+) and complement receptor negative (CR-) B cells have been shown to be involved in the primary immune response to PC-Hy (phosphocholine conjugated hemocyanin), a thymus dependent (TD) antigen which preferentially induces antibody secretion in Lyb-5+ B cells during a primary adoptive transfer assay. CR+ and CR- B cells also responded in a primary adoptive transfer assay to TNP-Ficoll, a thymus independent type 2 (TI-2) antigen which activates only Lyb-5+ B cells. When the secondary immune response to PC-Hy and TNP-Ficoll were analyzed, it was found that most of the immune memory to both antigens was present in the CR- B cell subset. The CR- B cell subset also dominated the secondary immune response to PC-Hy in immune defective (CBA/N X DBA/2N)F1 male mice. These data indicate that CR- B cells dominate the memory response in both the Lyb-5+ and Lyb-5- B cell subsets of normal and xid immune defective mice and suggest that Lyb-5+ and Lyb-5- B cells can be subdivided into CR+ and CR- subsets.

Recognition and response to alloantigens in vivo. I. Negative and positive selection of MLR reactivity in murine peripheral blood lymphocytes to major histocompatibility complex and Mls antigens.

Specific mixed lymphocyte reaction (MLR) responsiveness to allogeneic major histocompatibility complex (MHC), or minor lymphocyte-stimulating (Mls) determinants, was depleted in the peripheral blood lymphocytes (PBL) obtained from mice 24 to 48 hr after i.v. injection of 5 to 7.5 X 10(7) MHC or Mlsa-incompatible spleen cells, respectively. Results of cell mixture experiments suggest that the generation of suppressor cells was not the explanation for this specific reduction in MLR proliferation occurring with these PBL responder cells. To gain additional insight into parameters involved in the recognition of allodeterminants in vivo, experimental manipulations of the host environment and donor cell inoculum utilized in the negative selection procedure were employed. For example, removal of the spleen in the recipient animal, an anatomic site in which injected allogeneic cells and corresponding host antigen-reactive cells (ARC) are trapped, still permitted the specific depletion in murine PBL of host ARC for donor foreign MHC antigens. This finding may implicate other sites such as the liver where unprimed host alloreactive clones are trapped. In addition, irradiation of allogeneic donor cells significantly reduced their capacity to trap alloreactive T cell clones in vivo, whereas heat treatment of the donor cells completely eliminated this ability, even though the Ia determinants were still expressed, measured by flow cytometry. After the negative selection period, kinetic analysis of proliferation showed that 3, 4, or 5 days after injection of MHC-incompatible allogeneic spleen cells, the PBL of the recipient showed specific hyperresponsiveness to the MHC-haplotype of the donor cells. Interestingly, these primed PBL responder cells had the volume distribution of small resting cells; thoracic duct lymphocytes (TDL), positively selected by adoptive transfer of T cells to irradiated semiallogeneic recipients, are reported to be mainly blast cells. In contrast to the MLR hyperresponsiveness that results from priming with MHC-incompatible splenocytes, PBL, obtained at these later time points from mice primed with Mlsa-incompatible, H-2-compatible splenocytes, showed complete unresponsiveness in MLR to these Mlsa-bearing stimulator cells, as well as some nonspecific reduction in proliferation to MHC-incompatible stimulator cells regardless of their Mls genotype.(ABSTRACT TRUNCATED AT 400 WORDS)

Development of B lymphocytes in the mouse; studies of the frequency and distribution of surface IgM and IgD in normal and immune-defective CBA/N F1 mice.

Affinity-purified anti-mouse mu and delta antibodies and flow microfluorometric techniques were utilized to study the frequency and distribution of sIgM and sIgD on adult and neonatal B lymphocytes of immunologically normal mice and mice with the immune-defect characteristic of the CBA/N strain. Neonatal normal B lymphocytes can be distinguished from their adult counterparts by the presence of increased amounts of sIgM on sIgM+ cells and by the increased number of sIgM+IgD- cells. The most primitive B lymphocytes of immunologically normal mice appear to reside in the bone marrow of 1- to 2-wk-old mice and are distinguished from splenic B lymphocytes at this time by their relatively low amounts of sIgM. However, in the adult, splenic and bone marrow B lymphocytes are indistinguishable with regard to the quantities of their sIgM or sIgD. Adult immune-defective mice have increased amounts of sIgM on their B lymphocytes, although the number of sIgM+ IgD- cells in these mice is not increased. During development, however, larger than normal numbers of sIgM+ IgD- cells are found in the spleen and bone marrow of these mice; and the low frequency of such cells seen in normal adults is not achieved in immune defectives until after the 56th day of life. Thereafter, immune-defective mice have low frequencies of B lymphocytes with high relative amounts of sIgM, even after 1 yr or age.

Augmentation of in vitro humoral immune responses in the mouse by an antibody to IgD.

Heterologous anti-delta-chain antibodies have an adjuvant effect on specific in vivo humoral immune responses to simultaneously, or subsequently, injected antigens in the rat and rhesus monkey. We have used a hybridoma-secreted antibody that binds murine delta-chain of the allotype (4.22aM delta a) to study this phenomenon in the mouse and to investigate the mechanism of this effect. Injection of 4.22aM delta a into BALB/c mice removes almost all surface IgD (sIgD) from splenic B lymphocites. sIgD does not reappear until the serum level of 4.22aM delta a decreased 5-7 d after injection. 4.22aM delta a fails to induce detectable proliferation or to raise total serum Ig levels substantially above control values. However, 4.22aM dalta a injected 24 h before antigen elicits an approximately twofold enhancement of serum IgM and a 3- to 10-fold enhancement of serum IgG anti-trintriphenyl (TNP) antibodies in response to immunization with optimal doses of TNP-Ficoll or TNP-sheep red blood cells (TNP-SRBC). 4.22aM delta a injected 1 wk before or 3 d after TNP-SRBC, however, has no effect on IgG anti-TNP levels. The adjuvant effect of anti-delta-chain antibody was markedly decreased when suboptimal antigen doses were used. Furthermore, even in the case of TNP-Ficoll, a relatively T-independent antigen, the ability of 4.22aM dalta a to enhance the anti-TNP antibody response was T cell dependent. Our data suggest that the binding of anti-delta-chain antibody to cell sIgD may partially activate B lymphocytes and make them more capable of differentiating into antibody-secreting cells when stimulated by antigen-specific T cell help.

Mapping of the X-linked immune deficiency mutation (xid) of CBA/N mice.

CBA/N mice carry a recessive mutation at the X-linked immune deficiency (xid) locus that precludes their response to certain thymus-independent (TI) antigens. We have determined that xid is situated on the X-chromosome between the genes Ta (tabby) and Hyp (hypophosphatemia), genetic distances being Ta-6.6 +/- 1.8-xid-12.2 +/- 2.3-Hyp.

X-linked B-lymphocyte immune defect in CBA/N mice. II. Studies of the mechanisms underlying the immune defect.

The mechanisms underlying the X-linked thymus-independent (B) lymphocyte functional defect in the CBA/N (CN) mice and their F1 progeny were studied. Immune defective mice were unable to respond to the T-independent antigen 2,4-dinitrophenyl-lysyl-derivative of Ficoll (DNP-lys-Ficoll) but were able to form antibody against the highly cross-reactive hapten (trinitrophenyl) when it was coupled to an erythrocyte carrier. Immune defective CN X DBA/2N (DN) F1 male mice, which do not normally respond to T-independent antigens, were able to respond to both polyribosinic-polyribocytidylic acid and DNP-lys-Ficoll after the administration of CN X DN F1 female spleen cells even if these cells had been depleted of T lymphocytes. In addition, it was shown that the inability of the CN mice and their F1 progeny to respond to T-independent antigens was not due to an intrinsic abnormality of their microenvironment or the suppressive actions of a T lymphocyte. Our data present evidence that the X-linked defect in the CN mice is due to an intrinsic defect in B-lymphocyte development.

The immune response to a synthetic amino acid terpolymer in man: relationship to HL-A type.

The immune response to the synthetic amino acid terpolymer (L-glutamic acid-55 L-lysine-33 L-tyrosine15)n (GLT) was studied in normal human volunteers. Delayed skin test reactivity to this antigen was seen in 34 of 61 subjects immunized with 150 mug of GLT. No antibody to GLT was detected in these responding individuals. There was a close correlation between the in vivo skin reactivity of volunteers to GLT and the ability of their lymphocytes to produce migration inhibitory factor (MIF) in response to GLT in vitro. However, a similar correlation was not seen when the in vitro proliferative response of lymphocytes to GLT, as measured by [methyl-3H] thymidine ([3H] T dR) incorporation, was assayed. HL-A typing of volunteers was studied to determine if responsiveness to GLT was correlated to HL-A type. No statistical association was seen after correction was made for the number of individual HL-A antigens.