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Biomedical subjects

D Bauer

Publications and source records attributed to D Bauer.

At least 73 records · Page 4Linked to original sources
PubMed1987

Active immunization of NMRI mice against Serratia marcescens. II. K-antigen extracts.

The minimal active immunogenic doses (intraperitoneal administration) of crude K-antigen extracts of Serratia marcescens for NMRI mice were 80 ng. Following ultracentrifugation (300,000 x g, 16 h), supernatant fluids of three K-antigen extracts were free of contaminating DNA, RNA, and 2-keto-3-deoxy-D-manno-octonic acid (KDO), and the contents of Limulus amoebocyte lysate-reactive lipopolysaccharide (LPS) had been reduced from 100- to 1000-fold. The minimal active immunogenic doses of two ultracentrifuged K-antigen extracts were 2 and 10 micrograms, respectively. A mucoid strain of S. marcescens (SM 20-M; serotype O6/O14:H12) yielded nonmucoid (= SM 29-NM) variants that had lost most of the O6/O14 O-antigen (LPS) and all of the SM 29-M K-antigen extract reactivity (ELISA test) and which were ca. 5-fold less mouse-virulent. Crude K-antigen extracts from S. marcescens strain SM 29-M and variant SM 29-NM failed to protect NMRI mice against strain SM 29-M.

Animals↗
PubMed1987

Growth curves of Clostridium perfringens in Schaedler and brain heart infusion broths.

Four Clostridium perfringens strains recovered from clinical specimens, four strains obtained from faecal specimens of healthy adults, and control strain ATCC 13124 were inoculated into Schaedler and Brain Heart Infusion broths, respectively, and incubated anaerobically at 35 degrees C for 24 h. The exponential growth phase usually lasted from 2 to 6 h following inoculation; the generation times averaged 23 min at 2 to 4 h and 27 min between 4 and 6 h of incubation. The early stationary growth phase (generation time between 6 and 8 h = 89 min) was reached at 8 h following inoculation. All strains displayed essentially identical in vitro growth rates, even though they differed in murine virulence.

Animals↗
PubMed1987

Active immunization of NMRI mice against Serratia marcescens. I. Phenol-water lipopolysaccharide fractions and purified metalloproteases.

The minimal intraperitoneal (i.p.) immunogenic doses of phenol-hot water lipopolysaccharide (P-W- LPS) preparations from three strains of Serratia marcescens for juvenile NMRI mice ranged from 3.2 to 16 ng following i.p. challenge infection with homologous strains. Dual autoclaving (121 degrees C, 15 min) abolished the cross-immunogenicity of two selected P-W LPS extracts. Four purified metalloproteases from S. marcescens strains SF 178, SH 186, SV O1, and SE 182 shared the following properties: a) inhibition of proteolytic (azocasein hydrolysis) activity by 50 mM of EDTA; b) heat-lability (60 degrees C, 15 min); c) identical molecular weights (54,000 Daltons = 54 K) as documented with the SDS-PAGE procedure; d) close serologic relatedness (ELISA technique, polyclonal rabbit immune sera); and e) uniform reactivity of the 54 K polypeptide bands with polyclonal rabbit anti-metalloprotease immune sera (Western blots). The minimal immunogenic dose of metalloprotease SF 178, the sole significantly murine immunogenic enzyme, was 1000 ng = 1 microgram.

Animals↗
PubMed1987

Interactions of purified Serratia marcescens metalloproteases with fresh human serum and with purified human serum proteins.

Exposure of fresh human serum to two purified metalloproteases of S. marcescens strains SF 178 and SH 186 (both of serotype O6/O14:H12) at 35 degrees C, 3 h, resulted in altered electrophoretic mobility of the protease inhibitors alpha 1-antitrypsin and alpha 2-macroglobulin, alpha 2-HS-glycoprotein, and complement (C) components C1q, C1s, C3a, C3c, C4, C5, and C9, but not C6, C7, C8, and properdin, as determined with electroimmunoassays (Laurell technique). Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) documented the partial degradation of the heavy (H) chain of purified human immunoglobulin IgG by the metalloproteases of S. marcescens strains SF 178 and SV O1 (serotype O13/O19:H1), but not by the metalloproteases of strains SH 186 and SE 182 (serotype O9B:H11) following extended incubation (35 degrees C, 22 h). Human IgA and IgM were refractory. Purified human C components, C3, C4, C5, C6, C7, C8, and C9, as well as purified human alpha 1-antitrypsin, alpha 2-macroglobulin, transferrin, and lactoferrin were attacked by the S. marcescens metalloproteases SF 178 and SH 186 at 35 degrees C for 5 h, as demonstrated with the SDS-PAGE procedure; haptoglobin and C-reactive protein were resistant.

Acute-Phase Proteins↗
PubMed1987

Outer membrane protein alterations in Serratia marcescens resistant against aminoglycoside and beta-lactam antibiotics.

Six isolates of Serratia marcescens were recovered sequentially from the respiratory tract of a single patient. The first three isolates were of the 'opaque' (wild-type) colony type and were susceptible to amikacin, cefotaxime, and lamoxactam. The following three isolates were of the small, 'gray' colony variety, significantly less susceptible to the three antibiotics, and revealed three altered outer membrane proteins, as determined with the SDS-PAGE procedure.

Aminoglycosides↗
PubMed1987

Gentamicin- and methicillin-resistant Staphylococcus aureus: in vitro susceptibility to antimicrobial drugs.

Thirteen nosocomially significant, gentamicin- and methicillin-resistant (GRMR) Staphylococcus aureus isolates, all of phage group III/M (lysotype 42E/47/53/54/75/77/83A/84/85/94/96), were uniformly resistant against augmentin, erythromycin, fosfomycin, gentamicin, methicillin, oxacillin, penicillin G, tetracycline, and tobramycin, but differed in susceptibility to cefamandole, ciprofloxacin, clindamycin, imipenem, josamycin, the synthetic chinolone Ro 23-6240, and ofloxacin. All isolates were susceptible to chloramphenicol, coumermycin, fusidic acid, novobiocin, rifampin, teicoplanin, trimethoprim-sulfamethoxazole (cotrimoxazole), and vancomycin. One isolate was of intermediate susceptibility to netilmicin. On a weight-for-weight basis, the 7 most active drugs were rifampin, coumermycin, cotrimoxazole, novobiocin, teicoplanin, fusidic acid, and vancomycin (in decreasing order) in terms of minimal inhibitory concentrations. With regard to minimal bactericidal concentrations, coumermycin, rifampin, vancomycin, teicoplanin, cotrimoxazole, ofloxacin, and ciprofloxacin (in decreasing order) were the 7 most potent antimicrobial drugs. Freshly defibrinated human blood [65% (v/v)] combined with chloramphenicol and rifampin, respectively, resulted in a weak additive effect (time kill curves). Indifferent effects were observed following combination of blood with ciprofloxacin, cotrimoxazole, coumermycin, fusidic acid, imipenem, netilmicin, novobiocin, ofloxacin, compound Ro 23-6240, teicoplanin, and vancomycin. Rifampin combined with novobiocin, teicoplanin, and vancomycin, respectively, in the presence of 65% (v/v) human blood, resulted in an additive effect. Combinations of rifampin with 9 other antimicrobial drugs in blood yielded essentially indifferent effects.

Anti-Bacterial Agents↗
PubMed1987

Tentative inhibition zone criteria (Bauer-Kirby agar disk diffusion method) for rifampin against staphylococci.

Two of 359 (0.6%) clinical isolates of Staphylococcus aureus and 12 of 218 (5.5%) clinical isolates of coagulase-negative staphylococci were resistant or of intermediate susceptibility against rifampin as based on minimal inhibitory concentration (MIC) breakpoints obtained with the agar dilution method: MIC greater than or equal to 2 micrograms/ml = resistant; MIC 0.25-1 microgram/ml = intermediate susceptible; MIC less than 0.125 microgram/ml = susceptible. The following inhibition zone criteria with 2 micrograms rifampin disks were proposed for staphylococcal isolates utilizing the Bauer-Kirby agar disk diffusion test: diameter of inhibition zones less than or equal to 13 mm = resistant; diameter 14-21 mm = intermediate susceptible; diameter greater than or equal to 22 mm = susceptible.

Drug Resistance, Microbial↗
PubMed1986

In vitro additive effect of imipenem combined with vancomycin against multiple-drug resistant, coagulase-negative Staphylococci.

Imipenem combined with vancomycin resulted in a marked additive effect in vitro against 9 clinical isolates of multiple-drug resistant (MDR), coagulase-negative staphylococci, including strains resistant against imipenem. The additive effect was documented with the aid of checkerboard MIC determinations and with time kill curve experiments. In contrast, imipenem combined with vancomycin merely yielded weak additive or indifferent effects against 10 MDR isolates of Staphylococcus aureus, all of which were susceptible to imipenem.

Coagulase↗
PubMed1986

Intraphagocytic bactericidal activity of ofloxacin compared with that of aztreonam and ceftriaxone against Serratia marcescens.

Addition of phenylbutazone (2 mg/ml) to 55 vol % of fresh defibrinated human blood permitted leukocytic ingestion of serum-resistant Serratia marcescens bacteria, but blocked phagocytic killing activity. The group A (phage tail) bacteriocin bA+ 16 served to kill extraphagocytic test bacteria. At greater than or equal to 2 X MBC, the DNA gyrase inhibitor ofloxacin revealed potent intraphagocytic bactericidal activity against S. marcescens test bacteria (99% kill; 3 h observation period) which corresponded to that of the control drug rifampin (97% kill). The monobactam aztreonam (11% kill) and the third generation cephalosporin ceftriaxone (14% kill) corresponded to cefotaxime (26% kill) in terms of suboptimal intraphagocytic activity. Ofloxacin and aztreonam yielded additive effects following combination of supra-(2 X MIC) and inhibitory (MIC), but not sub-inhibitory (0.5 X MIC) concentrations with 55 vol % of defibrinated human blood against S. marcescens and Escherichia coli control strain ATCC 25922; sub- and inhibitory concentrations of ceftriaxone yielded indifferent effects.

Aztreonam↗
PubMed1986

Streptococcus faecalis: in vitro susceptibility to antimicrobial drugs, single and combined, with and without defibrinated human blood.

Ampicillin, fusidic acid, gentamicin, imipenem, mezlocillin, ofloxacin, penicillin G, piperacillin, and vancomycin were examined for inhibitory and bactericidal activity in various broth media against 7 clinical isolates of Streptococcus faecalis. On a weight-for-weight basis, ampicillin, imipenem, mezlocillin, and ofloxacin proved to be more efficacious. All enterococcal isolates were resistant against gentamicin; fusidic acid and vancomycin lacked bactericidal activity. The combinations of either ampicillin, imipenem, mezlocillin, ofloxacin, piperacillin, or vancomycin with a subinhibitory concentration (4 micrograms/ml) of gentamicin, with or without added 65% (v/v) fresh defibrinated human blood, respectively, yielded additive effects against all enterococcal isolates. The addition of fresh human blood failed to enhance the antienterococcal activity of 4 micrograms/ml of gentamicin; in contrast, addition of 65% (v/v) fresh or heat-inactivated (56 degrees C, 30 min) normal rabbit, bovine, and human sera augmented the activity of gentamicin, an effect that was ablated through the addition of either 0.005 M DTT or 0.01 M MgCl2 + 0.01 M EGTA + 0.01 M CaCl2, supplements known to antagonize human serum beta-lysin, but not lysozyme activity.

Animals↗
PubMed1986

The reliability of a historical interview with physically disabled respondents.

This study investigated the reliability of a historical interview with 20 respondents with physical disabilities. An existing interview, the Occupational Role History, was modified and a companion rating scale was developed. Analysis of the test-retest and interrater reliabilities suggest that a stable clinical judgment can be formed from data gathered in a historical interview.

Adolescent↗
PubMed1986

Verapamil-mediated sensitization of doxorubicin-selected pleiotropic resistance in human sarcoma cells: selectivity for drugs which produce DNA scission.

The effects of verapamil on the cytotoxicity and accumulation of multiple drugs were studied in a model of pleiotropic resistance generated by doxorubicin (DOX) selection of the human sarcoma cell line MES-SA. The in vitro sensitivity of the DOX-resistant variant (named Dx5), which is 50- to 100-fold resistant to DOX compared to MES-SA, was enhanced approximately 7-fold by verapamil (3 micrograms/ml). In addition, the cytotoxicity of several agents to which the Dx5 line displays cross-resistance, i.e., daunorubicin, dactinomycin, mitoxantrone, and etoposide, was also enhanced 2- to 14-fold by verapamil. These agents share the properties of DNA intercalation and/or interaction with topoisomerase II. In contrast, verapamil did not alter the sensitivity of Dx5 to several other agents to which cross-resistance had been demonstrated, i.e., vincristine, vinblastine, colchicine, mitomycin C, and melphalan; nor did verapamil enhance the cytotoxicity of DOX or other agents against the DOX-sensitive parent, MES-SA. The sensitizing effect of verapamil did not correlate well with its effects on intracellular drug accumulation. [14C]DPX accumulation was increased by 30-40% in Dx5 but not in MES-SA cells in the presence of verapamil. [3H]Vinblastine accumulation was increased by 24-72% in both MES-SA and Dx5 cells in the presence of verapamil, although cytotoxicity of the Vinca alkaloids was not affected. In this human sarcoma model of DOX-selected pleiotropic resistance, verapamil partially reversed the resistance to DOX, as well as four of the nine drugs for which cross-resistance had been demonstrated in Dx5. The potentiation by verapamil of the cytotoxicity of some but not all of these antitumor agents suggests that factors other than altered drug transport may be responsible. The pattern of sensitization, restricted to agents which produce DNA strand scission by interaction with topoisomerase II, suggests that verapamil may be acting to promote the formation or inhibit the repair of such DNA strand breaks.

Animals↗
PubMed1985

Active immunization of NMRI mice against Serratia marcescens.

Phenol-hot water lipopolysaccharide (LPS) extracts of Serratia marcescens strains CDC O3:H1, CDC O6:H3, NEW CDC O14:H12, and SH 186 (serotype O6/O14:H12) significantly protected NMRI mice against intraperitoneal challenge with the more mouse virulent homologous strains; overall, there was moderate cross-protection against the minority of heterologous challenge strains. Trichloroacetic acid LPS extracts and K-antigen extracts of strains NEW CDC O14:H12 and SH 186 also proved protective antigens. The purified metalloproteases of strains SH 186 and SF 178 (serotype O6/O14:H12) effected active murine immunization. Neither active nor passive immunization of NMRI mice with E. coli Rc mutant J5 afforded significant protection against various challenge strains of S. marcescens.

Animals↗
PubMed1985

Learning preferences, values, and student satisfaction.

This study sought to determine the relative importance of values and learning preferences for educational satisfaction and to examine differences in value and learning preferences among undergraduate and graduate occupational therapy students and undergraduate physical therapy students. Although all three groups conformed to a profile of preferring teacher-structured, concrete, interpersonal learning, the graduate occupational therapy students appeared to give greater emphasis to universal social values and to have a stronger preference for abstract learning than both groups of undergraduates. The undergraduates expressed significantly greater satisfaction with their education than the graduate occupational therapy students; for each of the three groups educational satisfaction correlated with a different set of values or learning preferences.

Adult↗
PubMed1984

[Problems in the biological monitoring of benzene exposure].

The biological monitoring of workers exposed to benzene containing mixtures by phenol analysis in urine is complicated by the facts that varying amounts of phenolic compounds are also produced by other precursors than benzene and that coexposure with other chemicals can cause interactions in metabolism and elimination rates. In order to overcome these difficulties it is proposed a) to abandon the colorimetric methods and to use only gas chromatography as a standard and reference method, b) as an overall monitoring concept always to determine phenol pre-exposure values as well as the cresol and creatinine concentrations in urine, and to combine biological monitoring whenever possible with personal air sampling.

Benzene↗
PubMed1984

Gentamicin- and methicillin-resistant, clinical isolates of Staphylococcus aureus: comparative in vitro and in vivo efficacy of alternative antimicrobial drugs.

Six representative clinical isolates of gentamicin- and methicillin-resistant (GRMR) Staphylococcus aureus, constituting phage groups II and III, were susceptible only to amikacin, cefamandole, clindamycin, fosfomycin, fusidic acid, netilmicin, nitrofurantoin, trimethoprim-sulfamethoxazole, and vancomycin (Bauer-Kirby test). With few exceptions, the minimal bactericidal concentrations of the beta-lactam and aminoglycoside antibiotics tested, fusidic acid, and irregularly those of vancomycin, but not those of fosfomycin and rifampin, exceeded minimal inhibitory concentrations values by at least 8-fold. In vitro, combinations of rifampin with cefamandole, cefazolin, cefotaxime, erythromycin, fosfomycin, fusidic acid, netilmicin, and vancomycin yielded indifferent effects. The GRMR S. aureus strains were refractory against 50, 65, and 80 vol% of fresh defibrinated blood; following reduction of viable counts at 2 h (greater than or equal to 90%), rebound growth invariably occurred within 4 h after exposure. Combined human blood (55 vol%)-antibiotic assays revealed rifampin as the most effective drug, followed by vancomycin, fusidic acid, and cefamandole, in that order. Blood plus cefotaxime, cefazolin, or netilmicin yielded indifferent effects; fosfomycin failed in vitro. In terms of speed of recovery and survival data (chi 2 test), cyclophosphamide-pretreated, i.e., leukopenic NMRI mice responded best to chemotherapy with rifampin, followed by vancomycin, cefamandole, netilmicin, and fosfomycin, in that order; cefazolin yielded variable results.

Animals↗