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Biomedical subjects

S D Miller

Publications and source records attributed to S D Miller.

At least 181 records · Page 10Linked to original sources
PubMed1989

Optical differences in cases of multiple personality disorder.

Nine patients diagnosed with multiple personality disorder (MPD) and nine control subjects role-playing MPD were given complete ophthalmological examinations to test whether the MPD subjects would show greater variability in visual functioning across alter personalities than would control subjects role-playing MPD. An analysis of variability of eight optical measures in four prominent areas of vision was performed by comparing two covariance matrices for equality. The test on the equality of the two covariance matrices showed that the two groups were significantly different (p less than .05). That is, MPD subjects had significantly more variability in visual functioning across alter personalities than did control subjects. Because the test of equality of the two covariance matrices rejected the null hypothesis, univariate analyses of variance were performed on the eight individual ophthalmological measures that comprised the matrix. The results of these analyses showed that MPD subjects had significantly more variability across alter personalities than did their control counterparts on measures of visual acuity with correction, visual acuity without correction, visual fields, manifest refraction, and eye muscle balance. The data were also analyzed for clinical significance. Blind ratings of the data were performed by comparing the results of the individual dependent measures across the alter personalities of individual MPD and control subjects according to established ophthalmological criteria. The ratings for clinical significance showed that the MPD subjects had 4.5 times the average number of changes in optical functioning between alter personalities of the control subjects, with a mean of 2.56 clinically significant changes for the MPD subjects and .55 clinically significant changes for the control subjects. This difference was also statistically significant (p less than .01).

Adult↗
PubMed1989

Ulceroglandular tularemia: a typical case of relapse.

Tularemia is an infectious disease that continues to occur sporadically and in epidemics in the United States. It is characterized as an acute febrile illness with constitutional symptoms associated with skin, glandular, respiratory, or gastrointestinal involvement. Tularemia usually can be treated effectively with streptomycin. Relapse most often occurs when patients are treated with bacteriostatic agents such as chloramphenicol or tetracycline. We present a case of ulceroglandular tularemia distinguished by its relapse after initial streptomycin/doxycycline therapy and subsequent slow response to additional streptomycin.

Adult↗
PubMed1988

Specific immune regulation of chronic-relapsing experimental allergic encephalomyelitis in mice.

These studies were designed to examine immunologic means of regulating the clinical course of murine chronic-relapsing experimental allergic encephalomyelitis (R-EAE). We asked whether induction of specific immune tolerance to the major CNS myelin proteins, myelin basic protein (MBP) and proteolipid protein (PLP), could inhibit the development of R-EAE. Neuroantigen-specific tolerance was induced in SJL/J mice in a dose-dependent manner by the i.v. injection of mouse spinal cord homogenate-coupled syngeneic splenocytes (MSCH-SP) on day -7 relative to immunization on days 0 and +7. Sham-tolerized controls developed significant MBP- and PLP-specific DTH responses before the onset of clinical R-EAE. In contrast, MSCH-SP tolerized mice exhibited a dramatically reduced incidence of clinical and histologic signs of disease which correlated with the failure to develop MBP- and PLP-specific DTH responses. In 10 separate experiments, 118/149 (79%) of control mice, but only 22/137 (16%) of tolerized mice developed clinical R-EAE. Tolerance took time to develop and lasted at least 4 wk as mice injected with Ag-coupled splenocytes on day -1 relative to immunization remained susceptible to R-EAE, whereas mice injected on days -7, -14, or -28 were resistant. Tolerance induction required neuroantigens as injection of splenocytes coupled with a syngeneic mouse kidney homogenate failed to significantly alter the incidence of R-EAE or the development of neuroantigen-specific DTH responses. Thus, induction of R-EAE can be specifically and significantly regulated after the i.v. injection of splenocytes coupled with a crude, heterogeneous mixture of neuroantigens (i.e. MSCH).

Animals↗
PubMed1988

Hand infections. Bacteriology and treatment: a prospective study.

In a prospective, double-blind study, 193 patients hospitalized for established hand infections were randomized to receive either cefamandole intravenously followed by cephalexin by mouth or methicillin intravenously followed by dicloxacillin by mouth. Careful aerobic and anaerobic cultures were performed. Multiple organisms grew in cultures from 84% of the patients (over three isolates per infection on average). Human bite wounds contained anaerobes 43% of the time compared with 12% for other wounds. The majority of wounds (72%) required operative treatment. In 128 patients assessable for treatment outcome, results were unsatisfactory in 11 (9%). There was no difference in outcome between cefamandole (6/59, 10%) and methicillin (5/59, 8%). The presence of anaerobes, Eikenella corrodens, human bites, or an increasing number of organisms was associated with an unsatisfactory response. The presence of Staphylococcus aureus and/or beta-hemolytic streptococci was associated with a favorable response. The incidence of antibiotic-resistant isolates did not correlate with outcome.

Adolescent↗
PubMed1988

Risk of infection after open fracture of the arm or leg.

Two hundred forty consecutive patients admitted for operative treatment of an open fracture of the arm or leg were followed up prospectively for the development of fracture infection. The independent risk of fracture infection was increased in patients with grade IIIB or IIIC fractures, internal or external fixation, lower-leg fracture, any blood transfusion, or injuries resulting from motorcycle accidents or motor vehicle-pedestrian accidents. By stepwise multivariate logistic regression, the most significant risk factors were the grade of the fracture, internal or external fixation, and fractures of the lower leg. These risk factors all represent local wound characteristics, and we conclude that the most important actions by the surgeon to prevent infection involve local wound care. There was no relation between the timing of antibiotic administration or duration of antibiotic therapy and infection risk.

Arm Injuries↗
PubMed1988

Conductive hearing loss in autistic, learning-disabled, and normal children.

Katz (1978) has suggested that mild, fluctuating conductive hearing loss due to middle-ear anomalies may account for the language and attention problems of learning-disabled children. His position was extended here to include autism. Normal, learning-disabled, and autistic children received repeated impedance measures over 5 weeks. A repeated-measures ANOVA of central tendency and variability values led to the conclusions that (1) fluctuating, negative middle-ear pressure greater than normal characterizes both autistic and learning-disabled children, (2) the negative pressure is greater in autistic than in learning-disabled children, and (3) the condition is typically bilateral for autistic children.

Acoustic Impedance Tests↗
PubMed1988

Antimicrobial susceptibilities of southern African isolates of Haemophilus ducreyi.

We determined the antimicrobial susceptibilities of 122 recent clinical isolates of Haemophilus ducreyi to 24 antimicrobial agents. All isolates produced beta-lactamase and were resistant to penicillins. The majority of strains were also resistant to tetracycline, doxycycline, and sulfamethoxazole. All isolates were susceptible to macrolides, quinolones, extended-spectrum cephalosporins, spectinomycin, rifampin, and amoxycillin-clavulanate. Reduced susceptibility to minocycline, co-trimoxazole, and kanamycin was noted. Chloramphenicol and thiamphenicol resistance was noted for the first time among southern African strains.

Anti-Bacterial Agents↗
PubMed1988

Fatal infection caused by a multiply resistant type 3 pneumococcus.

The most virulent pneumococcal serotype (type 3) has not to date been associated with multiple antimicrobial resistance. We report an unusual gastrointestinal presentation of fatal septicemia caused by a multiply resistant type 3 pneumococcus in a setting of increasing prevalence of multiple resistance, including resistance to erythromycin, clindamycin, and tetracycline.

Adolescent↗
PubMed1987

Class II-restricted T cell responses in Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease. I. Cross-specificity among TMEV substrains and related picornaviruses, but not myelin proteins.

Following intracerebral inoculation of Theiler's murine encephalomyelitis virus (TMEV), susceptible mouse strains develop a chronic demyelinating disease characterized by mononuclear cell-rich infiltrates in the central nervous system. Current evidence strongly supports an immune-mediated basis for myelin breakdown, with an effector role proposed for TMEV-specific, major histocompatibility class II-restricted delayed-type hypersensitivity, which temporally correlates with disease onset and remains chronically elevated in susceptible mice. This study examined the fine specificity of class II-restricted T cell responses in TMEV-infected mice to better define the relevant virus-encoded T cell determinant(s) responsible for triggering the demyelinating process, and to determine if class II-restricted neuroantigen-specific autoimmune responses could be detected in mice with TMEV-induced demyelination. The data clearly show that T cell responses in TMEV-infected mice are directed against determinants shared by closely related TMEV strains and are cross-reactive with related picornaviruses, such as encephalomyocarditis virus. In contrast, class II-restricted autoimmune responses against syngeneic mouse spinal cord homogenate and the two major protein components of myelin, myelin basic protein and proteolipid protein, are not demonstrable in susceptible SJL/J mice undergoing chronic TMEV-induced demyelinating disease, but are readily seen in SJL/J mice displaying chronic, relapsing experimental allergic encephalomyelitis. Cross-reactivity (or lack thereof), as determined by functional T cell analyses, was found to correlate with the extent of exact amino acid homology between the TMEV capsid proteins, the two neuroantigens, and related picornaviruses. The data thus do not support a major role for autoimmune responses against myelin proteins in TMEV-induced demyelinating disease, but are consistent with our previously proposed hypothesis that TMEV-specific T cell responses constitute a major effector mechanism of myelin breakdown.

Animals↗
PubMed1987

The Theiler's murine encephalomyelitis virus (TMEV) model for multiple sclerosis shows a strong influence of the murine equivalents of HLA-A, B, and C.

Following intracerebral inoculation of Theiler's murine encephalomyelitis virus (TMEV), susceptible mouse strains develop a chronic demyelinating disease characterized histologically by mononuclear cell-rich infiltrates in the central nervous system (CNS). An immune-mediated basis for this disease is strongly supported by previous studies demonstrating a correlation between clinical disease susceptibility, the presence of particular H-2 region genotypes, and the development of chronically elevated levels of TMEV-specific, MHC class II-restricted delayed-type hypersensitivity (DTH). The present study compared disease susceptibility in (B10.S X SJL)F1 and (B10.S(26R) X SJL)F1 mice which differ only at the D region of the H-2 complex. The data conclusively demonstrates a major influence for homozygosity of H-2s alleles at the H-2D region (the murine equivalent of the human class I HLA-A, B, and C genes) in determining disease susceptibility, as measured by either clinical or histopathological endpoints. In addition, disease susceptibility strongly correlated with the development of high levels of TMEV-specific DTH in the susceptible (B10.S X SJL)F1 strain. However, disease susceptibility did not appear to correlate with TMEV titers in the CNS, TMEV-specific humoral (ELISA and neutralizing) immune responses, or virus-specific splenic T cell proliferative responses. These findings lend additional support to our hypothesis that CNS myelin damage is mediated by a TMEV-specific DTH response. The possible role of class I-restricted responses in the demyelinating process is discussed and murine TMEV-induced demyelinating disease is compared with experimental allergic encephalomyelitis as relevant animal models for human multiple sclerosis.

Alleles↗
PubMed1987

Monoclonal antibody-induced inhibition of relapsing EAE in SJL/J mice correlates with inhibition of neuroantigen-specific cell-mediated immune responses.

Relapsing experimental allergic encephalomyelitis (R-EAE) in SJL/J mice was examined in relation to the development of neuroantigen-specific T cell proliferative (Tprlf) and delayed-type hypersensitivity (DTH) responses. R-EAE was induced by injecting syngeneic mouse spinal cord homogenate in CFA on days 0 and 7 over the shaved flanks of female SJL/J mice. Mice primed in this manner exhibited significant Tprlf and DTH responses specific for both major myelin proteins, myelin basic protein (MBP) and proteolipid protein (PLP). A time course comparison between the induction of R-EAE and the development of neuroantigen-specific cell-mediated immune (CMI) responses (Tprlf and DTH) revealed that the MBP- and PLP-specific Tprlf and DTH responses peaked prior to the onset of initial clinical symptoms and the DTH responses remained at significant levels throughout the relapsing course of the disease. Monoclonal antibodies were used to determine whether in vivo inhibition of class II-restricted Tprlf and DTH responses correlated with inhibition of R-EAE. In vivo administration of a total of 100 micrograms anti-L3T4 antibody, but not anti-Lyt-2 antibody, resulted in delayed onset and reduced severity of clinical signs of R-EAE concomitant with significantly reduced levels of MBP- and PLP-specific Tprlf and DTH responses. Treatment with a total of 300 micrograms of purified anti-L3T4 resulted in total abrogation of R-EAE induction and neuroantigen-specific CMI. Thus, clinical signs of R-EAE were found to correlate with the activity of neuroantigen-specific, class II-restricted T cells.

Animals↗
PubMed1987

Class II-restricted T cell responses in Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease. II. Survey of host immune responses and central nervous system virus titers in inbred mouse strains.

Previous studies using mouse strains with limited genetic differences and H-2 haplotypes demonstrated that susceptibility to Theiler's murine encephalomyelitis virus (TMEV)-induced demyelinating disease strongly correlated with chronically high levels of TMEV-specific delayed-type hypersensitivity (DTH), but not with TMEV-specific T cell proliferation (Tprlf), serum antibody responses, or with CNS virus titers. To determine if this correlation would be supported by analysis of these parameters in a more thorough genetic survey, ten inbred mouse strains, representing a wide variety of genetic backgrounds and H-2 haplotypes, were inoculated intracerebrally (i.c.) with the BeAn strain of TMEV. Significant TMEV-specific DTH was observed in all highly susceptible strains, but was not detectable in intermediate and resistant strains. TMEV-specific serum antibody titers also appeared to correlate with susceptibility to demyelinating disease, however even resistant strains had high antibody responses. Significant differences in CNS TMEV titers existed between strains, but did not correlate with disease susceptibility. DTH and Tprlf responses were observed in 3/4 resistant strains following peripheral immunization with UV-inactivated TMEV indicating that most resistant strains are genetically capable of mounting virus-specific cell-mediated immune (CMI) responses. The data extends our knowledge of host immune responses and virus titers in many different inbred mouse strains persistently infected with TMEV, supports the hypothesis that the demyelination in highly susceptible mice involves a TMEV-specific DTH response, and suggests that the genetic ability to mount specific DTH responses is necessary, but not sufficient for development of the demyelinating disease.

Animals↗
PubMed1987

Characterization and specificity of humoral immune responses to Theiler's murine encephalomyelitis virus capsid proteins.

Humoral antibody responses to Theiler's murine encephalomyelitis virus (TMEV) capsid proteins were examined. Rabbit antisera produced against the native BeAn strain of TMEV and against the isolated capsid proteins (VP1, VP2 and VP3) were tested for their ability to bind or neutralize virus and to inhibit the virus-induced haemagglutination of human O+ erythrocytes. Western immunoblotting analysis showed that isolated VP1, VP2 and VP3 each primed for a specific antibody response, but that native virions primed for antibodies specific for VP1 and VP2, but not VP3. Virus neutralization studies revealed that a dominant TMEV neutralizing determinant(s) lay on VP1, as did the haemagglutinating determinant. The possible location of the neutralizing epitopes are discussed on the basis of molecular modelling of the predicted amino acid sequence of TMEV from that of the closely related Mengo virus for which the three-dimensional structure is known.

Animals↗
PubMed1987

In vitro and in vivo correlates of hybrid tumor resistance.

Tumorigenicity of 2 sublines, TU1 and TM5, of the C.B6-H-2dm4 (dm4) mouse tumor, TDM4, was tested in dm4 and F1 hybrid mice (from crosses of dm4 with a variety of other strains) to determine the genetics of hybrid resistance to these 2 tumor sublines. Resistance to TU1 was associated with at least 3 genes and required heterozygosity in the H-2D region, with secondary effects attributable to H-2K genes and non-H-2 genes. Resistance to TM5, however, did not require H-2D region heterozygosity, whereas H-2K and non-H-2 genes appeared to have significant effects. For evaluation of possible mechanisms for hybrid resistance, 4 assay systems were used. Comparison of natural killer cell activity in dm4 and various hybrid mice revealed no consistent activity against either TU1 or TM5. Little correlation was seen between resistance and generation of strong T-lymphocyte proliferative responses to the sublines. Likewise, cytotoxic T-lymphocyte (CTL) activity, particularly against TU1, was not associated with increased resistance. In contrast, delayed-type hypersensitivity (DTH) was consistently greater in hybrids with increased resistance to either subline. These results suggest a strong association between DTH responsiveness and hybrid resistance. Furthermore, the association, in some hybrids, of CTL activity with resistance to the TM5 subline, but not to TU1, may mean that different sublines of the same tumor can induce different sets of immune responses.

Animals↗