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Biomedical subjects

H Hahn

Publications and source records attributed to H Hahn.

At least 235 records · Page 13Linked to original sources

[Resistance spectrum of various bacteria against cefotiam in 3 Berlin clinics].

The in vitro activity of Cefotiam (Spizef) was tested using the agar diffusion test method according to DIN 58940 and compared with the antibacterial activity of 12 other routinely tested antibacterial chemotherapeutics. A total of 3000 strains from patients' specimens from the University Hospital of the Free University of Berlin and the Municipal Wenckebach Hospital, West Berlin, was tested. Cefotiam proved effective against strains of Staphylococcus aureus in 99,4%, Escherichia coli in 99,7%, Klebsiella species in 97,8%, Enterobacter species in 90,3%, Proteus mirabilis in 98,7%, indolpositive Proteus species in 91,7%, Citrobacter in 92,6%, and beta-hemolytic Streptococci in 99,3% of all strains tested. There were only few sensitive strains of Enterococci and of Pseudomonas aeruginosa.

Anti-Bacterial Agents↗

[Spectrum of resistance of various bacteria against cefotiam in 3 Berlin clinics].

The in vitro activity of Cefotiam ( Spizef ) was tested using the agar diffusion test method according to DIN 58940 and compared with the antibacterial activity of 12 other routinely tested antibacterial chemotherapeutics. A total of 3000 strains from patients' specimens from the University Hospital of the Free University of Berlin and the Municipal Wenckebach Hospital, West Berlin, was tested. Cefotiam proved effective against strains of Staphylococcus aureus in 99,4%, Escherichia coli in 99,7%, Klebsiella species in 97,8%, Enterobacter species in 91,7%, Citrobacter in 92,6%, and beta-hemolytic Streptococci in 99,3% of all strains tested. There were only few sensitive strains of Enterococci and of Pseudomonas aeruginosa.

Berlin↗

Intravenous injection of mice with bacteroides fragilis and Escherichia coli: role of Thioglycollate medium in the infectious process.

Mice were intravenously infected with E. coli, B. fragilis, and combinations of both, and the bacterial contents of livers, kidneys, and spleens were monitored from the first up to the 9th day postinfection. If Thioglycollate medium was added to otherwise sublethal doses of E. coli, the inoculum was able to induce severe and for some animals lethal infections. B. fragilis was not capable to produce prolonged infections; however, when given together with E. coli and Thioglycollate medium, both bacteria were recovered from some animal organs even on day 9 postinfection. Employing this experimental model of a mixed anaerobic/facultative bacterial infection, previous reports attributing animal lethality to E. coli were confirmed, but a synergism between E. coli and B. fragilis could not be demonstrated.

Animals↗

Biological functions of t cell lines with specificity for the intracellular bacterium Listeria monocytogenes in vitro and in vivo.

Peritoneal exudate T lymphocytes from mice immunized with live Listeria monocytogenes were cloned in double-layer soft agar containing heat-killed L. monocytogenes (lower layer) and syngeneic accessory cells (upper layer). Colony-derived T cells were propagated in vitro in the presence of listerial antigen, syngeneic accessory cells, and T cell growth factor. In vitro proliferation, interleukin secretion, and bystander help for B cells of six such T cell lines and several sublines derived from them were found to be antigen dependent and restricted by the H-2IA locus of the major histocompatibility complex. In vivo, these T cell lines conferred delayed-type hypersensitivity to listerial antigen and protection to live L. monocytogenes. It is concluded that different biological functions of acquired antibacterial immunity can be mediated by a single T cell population.

Animals↗

Phagocytosis of C3b-coated sheep red blood cells by guinea-pig macrophages in the absence of antibody.

C1 was passively attached to tannic-acid-treated SRBC in the absence of antibody. EC1,4,2,3 were prepared by the stepwise reaction of EC1 with C4, C2, and C3. Contamination with IgM or IgG antibodies of the complement components used could not be detected by immunochemical methods; furthermore, possibly contaminating traces of antibody were removed by careful absorption of all preparations with erythrocytes. The C3b-opsonized SRBC were ingested by unstimulated guinea-pig peritoneal macrophages and PMN leukocytes. Addition of purified IgM to the C3b-opsonized SRBC did not substantially enhance particle uptake. It is concluded that C3b alone can act as an opsonin and triggers phagocytosis in the absence of antibody.

Animals↗

T lymphocyte-macrophage interactions in cellular antibacterial immunity.

Acquired resistance to facultative intracellular bacteria depends on a bicellular mechanism whereby specific T lymphocytes activate macrophages for enhanced bacteriocidal capacity. In vivo, protection is paralleled by delayed-type hypersensitivity. In vitro correlates are specific T lymphocyte proliferation and interleukin induction. Macrophage activation results from complex cell interactions involving both T lymphocytes and macrophages. Although such interactions are not yet fully understood, it appears likely that interleukin-facilitated collaboration between Lyt 1 and Lyt 123 T lymphocytes is required. Most probably, H2-restricted interactions between antigen-presenting mononuclear phagocytes and Lyt 1 T lymphocytes induce secretion of interleukins which further recruit additional Lyt 1 T lymphocytes from the Lyt 123 T lymphocyte set. In this way, the pool of Lyt 1 T lymphocytes capable of attracting and activating macrophages at the site of bacterial and implantation via lymphokines (macrophage activating factor, migration inhibition factor) could be markedly enhanced.

Animals↗

The use of the three-phase bone scan in the early diagnosis of heterotopic ossification (HO) and in the evaluation of Didronel therapy.

The purpose of this study is to investigate the use of a three-phase bone scan for early detection of HO formation and as a method of evaluating Didronel treatment. A marked vascular blush and blood pool was noted about the hips sometimes with a normal bone scan and normal X-ray of the hips. This appeared to represent the precursor phase of HO formation since, on repeat scans, the bone scan showed accumulation of the bone-seeking radionuclide usually in 2 to 4 weeks and the X-ray revealed ossification. Fifty-two patients treated with Didronel between October 1978 and December 1979 were reviewed to determine the value of Didronel treatment. There were 23 patients in the series who either showed HO by X-ray on admission or developed HO on follow-up X-rays before beginning Didronel therapy. A three-phase bone scan revealed increased vascularity and accumulation of radioactivity on the bone scan in all areas of ossification on the X-ray and in some areas that did not appear to be involved. The other 29 patients had serial three-phase bone scans, X-ray study, and an alkaline phosphatase determination at approximately 2-week intervals. Didronel treatment was started as soon as the precursor phase of HO was demonstrated on the three-phase bone scan in most of these patients. Nine have not developed ossification that could be seen in X-rays during 3 months of continuing study. Six patients seen at follow-Up during the past year had known HO of 4 to 7 years duration. The three-phase bone scan was used to predict the maturity of HO in these patients. Our study in indicates that increased vascularity precedes rather than being secondary to HO formation as is suggested in the literature. Didronel treatment appears to be most effective if initiated during this precursor phase.

Diphosphonates↗

T-cell subsets induced in Listeria monocytogenes-immune mice. Ly phenotypes of T cells interacting with macrophages in vitro.

Interactions of peritoneal exudate T lymphocytes from listeria-immune mice with macrophages from normal mice in the presence of heat-killed listeriae result in the induction of interleukins. The data show that Ly 1+, 23- T cells specific for listeria antigens are essential for interleukin induction and make it likely that, in addition, Ly 1+, 23+ T cells are required for optimal responses.

Animals↗

Interleukin 2 induction in Lyt 1+ 23- T cells from Listeria monocytogenes-immune mice.

Peritoneal exudate T lymphocytes from mice experimentally infected with the intracellular bacterium Listeria monocytogenes secreted high interleukin 2 activities after interaction with syngeneic normal macrophage presenting listerial antigen in vitro. L. monocytogenes-immune cells secreting IL 2 were radioresistant and bore the phenotype Thy 1(+) Lyt 1(+)23(-).

Animals↗

Regulatory interactions between macrophages and T-cell subsets in Listeria monocytogenes-specific T-cell activation.

Peritoneal exudate T lymphocytes from Listeria monocytogenes-immune mice in the presence of the homologous antigen (heat-killed L. monocytogenes) and normal macrophages showed L. monocytogenes-specific proliferative responses. Proliferation was inhibited by macrophages from L. monocytogenes- or Corynebacterium parvum-pretreated mice as well as by exogenous prostaglandin E(2). Macrophage-dependent inhibition of T-cell proliferation-at least in part-could be reversed by addition of indomethacin. When selected L. monocytogenes-immune Lyt T-cell subsets were cultured in the presence of inhibitory macrophages, pretreatment with anti-Lyt 1 antiserum plus complement completely abrogated proliferation and pretreatment with anti-Lyt 2 and anti-Lyt 3 antisera plus complement markedly reduced proliferation. However, a mixture (1:1) of the two preselected Lyt T-cell subsets resulted in complete reconstitution of proliferative responses. In contrast, when L. monocytogenes-immune peritoneal exudate T lymphocytes were treated with anti-Lyt antisera plus complement after culture, only treatment with anti-Lyt 1 antiserum plus complement affected proliferation, suggesting regulatory interactions between Lyt 1(+)23(-) and Lyt 1(-)23(+) T cells during in vitro culture which result in proliferation within the Lyt 1(+)23(-) T-cell subset. After rigorous depletion of residual macrophages and in the presence of indomethacin, pretreatment with anti-Lyt 1 antiserum plus complement, but not with anti-Lyt 2 and 3 antisera plus complement, eliminated proliferation. The data presented indicate that interactions between macrophages and Lyt T-cell subsets regulate L. monocytogenes-specific T-cell activation.

Animals↗

[Protective effect of Pseudomonas-specific immunoglobulin from the rabbit and of active immunization in experimental Pseudomonas sepsis in mice].

Using the model of an experimental Pseudomonas septicemia in mice, the protective effect of specific antipseudomonal immunoglobulin from rabbits was examined. During bacterial spreading in the bloodstream, a protective effect could be demonstrated under certain conditions. The degree of protection was equivalent to that achieved by active immunization. After bacterial colonization and replication in parenchymal organs no further therapeutic effect could be detected.

Animals↗

[Acquired resistance to facultative intracellular bacteria: as to the identity of the cell mediating protection and delayed hypersensitivity (author's transl)].

Acquired resistance to facultative intracellular bacteria depends on two interacting classes of cells: antigen specific T lymphocytes and mononuclear phagocytes. After specific interaction with antigen, T lymphocytes are capable of activating mononuclear phagocytes to form granulomas and to acquire enhanced bacteriocidal capacity. In general, protection is paralleled by delayed hypersensitivity to bacterial antigens. Although Robert Koch had already postulated that protection against Mycobacterium tuberculosis and delayed hypersensitivity to tuberculin in principle depend on an identical mechanism, this question has been unresolved thus far. Recently it has become possible (a) to select heterogeneous T cell subpopulations by serologic methods and (b) to clone and propagate homogeneous T cell lines in a biologically active form. Applying these techniques, we could show that a single T cell population specific for the intracellular bacterium, Listeria monocytogenes, is capable of mediating both antibacterial protection and delayed hypersensitivity. These data show that both functions in principle depend on an identical mechanism thus resolving the problem in Robert Koch's original sense.

Bacteria↗

Carbohydrate surface constituents of T cells mediating delayed-type hypersensitivity that control entry into sites of antigen deposition.

Peritoneal exudate T lymphocytes (PETLs) that mediate delayed-type hypersensitivity (DTH) to sheep red blood cells in mice were modified by in vitro treatment methods which modify surface carbohydrate constituents. Neuraminidase treatment resulted in the release of both N-acetylneuraminic acid and N-glycolyl-neuraminic acid, and periodate treatment in the formation of the corresponding C7 analogues. Treatment of PETLs with neuraminidase led to a transient reduction of DTH reactions in syngeneic cell recipients. After treatment with neuraminidase plus galactose oxidase, adoptive mediation of DTH was more markedly reduced. Incubation of PETLs with periodate caused a permanent loss of DTH transferring capacity. The oxidation-induced effects following treatment of PETLs with neuraminidase plus galactose oxidase or with periodate could be reversed by subsequent reduction with borohydride of the previously formed aldehyde moieties. Decreased DTH reactions observed after the various treatment procedures were paralleled by reduced immigration of PETLs into sites of antigen deposition, indicating that the reduction/oxidation state of cell surface carbohydrates is crucial for induction of inflammatory processes by T cells. Trapping of PETLs in the liver could not be the sole mechanism since neuraminidase- and periodate-treated PETLs, but not neuraminidase plus galactose oxidase-treated PETLs, accumulated in the liver. It therefore appears that alterations in the reduction/oxidation state of the cell surface can lead to unresponsiveness of T cells to inflammatory signals.

Animals↗