Surgical treatment of mycotic aneurysms.
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Biomedical subjects
Publications and source records attributed to R F SMITH.
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Intradermal injection of a simple hapten (e.g., 1-fluoro-2,4-dinitrobenzene) in water-in-oil emulsion results in contact hypersensitivity to surface application of the homologous hapten and, after appearance of circulating antibody, in Arthus type hypersensitivity to a conjugate of homologous hapten with guinea pig serum. Intradermal administration of this conjugate induces delayed and subsequently Arthus hypersensitivity to the conjugate, but no evidence of a contact reaction to the hapten alone. When a conjugate of hapten plus solubilized guinea pig skin is used as the sensitizing antigen, both contact hypersensitivity to the hapten and delayed and/or Arthus reactions to the conjugate develop. These observations are consistent with the hypothesis that the specificity of contact sensitivity is directed toward some particular protein of the skin which has been modified by combination with hapten.
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Guinea pigs sensitized with either hen, duck, or goose egg albumin showed delayed hypersensitivity followed by Arthus reactions to the homologous antigen, but tended to have much weaker delayed responses and slower antibody formation to heterologous antigens. Guinea pigs with delayed hypersensitivity to one of the avian antigens had a slower antibody response to a secondary injection of heterologous antigen than to one of the homologous antigen. Sensitization with a protein conjugated with a hapten such as picryl chloride (Pi) or dinitrofluorobenzene (DFB) resulted in delayed hypersensitivity to the homologous conjugate, the homologous protein, and the homologous protein with a heterologous hapten. Circulating antibody and Arthus reactions occurred subsequently to the homologous conjugate, as well as to the homologous hapten attached to a heterologous protein. Delayed hypersensitivity thus seemed associated with the protein moiety, and Arthus responses with the hapten. Anamnestic responses followed injection of an antigen causing delayed hypersensitivity, but not of a hapten not causing delayed reactions. Thus, animals sensitized initially with Pi.HEA, DFB.HEA, or HEA produced antibodies sooner after a secondary injection of Pi.HEA than did unsensitized animals. No anamnestic response resulted when animals sensitized to Pi.BGG were injected with Pi.HEA. Thus, delayed hypersensitivity is indicated to be a preliminary and immature step in the immune process, with specificity directed against broad, more general features of the protein antigen. This intermediate step is followed by production of circulating antibody to any antigen having a similar basic structure, with the specificity of the antibody also directed against smaller immunologically active sites on the antigen molecule.
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Intravenous administration of 5-hydroxytryptamine to rabbits and guinea pigs is shown to bring about changes very similar to those produced by (+) air ions, including (1) decreased ciliary rate, (2) contraction of the posterior tracheal wall, (3) exaggerated response of the tracheal mucosa to trauma, (4) marked vasoconstriction in the tracheal wall, and (5) increased respiratory rate. These effects are reversed by (-) air ions. Iproniazid, which raises 5-hydroxytryptamine levels in the animal by blocking monamine oxidase, produces similar but non-reversible effects. Reserpine, which depletes 5-hydroxytryptamine in the animal, causes changes that resemble those produced by (-) air ions, including (1) increased ciliary rate, (2) relaxed posterior sulcus, (3) hyperemia of the tracheal mucosa, (4) lowered respiratory rate, and (5) increased volume and rate of mucus flow. On the basis of these facts, the hypothesis is advanced that (+) air ion effects are mediated by the release of free 5-hydroxytryptamine, while (-) air ion effects depend on the ability of (-) ions to accelerate the enzymatic oxidation of 5-hydroxytryptamine.
Negative air ions are shown to decrease 5-hydroxytryptamine concentrations in extirpated strips of rabbit trachea and in the respiratory tracts of living mice. An initial exposure of guinea pigs to (-) air ions causes a transient rise in urinary 5-hydroxyindoleacetic acid excretion which is not observed upon subsequent exposures. These findings are compatible with the hypothesis advanced earlier that (-) air ion effects depend on the ability of (-) ions to accelerate enzymatic oxidation of 5-hydroxytryptamine.
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A. Duration of Effects Groups of mice exposed to high densities of unipolar light air ions for 72 hours exhibited persistent alterations in the functional efficiency of their tracheas. These effects lasted at least 4 weeks, and in the case of animals treated with (+) ions included diminished ciliary activity, pale and contracted tracheal mucosa, and enhanced vulnerability to trauma. Following treatment with (-) ions, animals displayed increased ciliary activity with no other detectable changes. It required at least 60 minutes of exposure to ions to induce such "permanent" functional changes. B. Minimal Effective Ion Densities The minimal ion densities producing changes in ciliary activity within an arbitrary period of 30 minutes were determined with extirpated tracheal strips from rabbits and guinea pigs. The threshold value for (-) ions was approximately 2.5 x 10(3) ions/cm.(2)/sec. and that for (+) ions was in the range between 1 x 10(4) and 2.5 x 10(5) ions/cm.(2)/sec.The minimal ion densities producing changes in ciliary activity within an arbitrary period of 30 minutes were determined with extirpated tracheal strips from rabbits and guinea pigs. The threshold value for (-) ions was approximately 2.5 x 10(3) ions/cm.(2)/sec. and that for (+) ions was in the range between 1 x 10(4) and 2.5 x 10(5) ions/cm.(2)/sec. The evidence indicates that ion-induced functional changes in the ciliated epithelium of the pulmonary tree are the results of direct contact of ions with surface cells and do not involve participation of the central nervous system or circulation. So far as ciliary activity is concerned, the number of ions required to produce a change in rate is very small.
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The induction of delayed type of hypersensitivity to diphtheria toxoid in the guinea pig was not inhibited by total body irradiation up to 300 r in intensity. X-ray doses of 200 to 300 r administered about 18 hours before sensitization caused the period of delayed hypersensitivity to be extended to the 19th to 21st day postsensitization in. the absence of circulating antibody. X-ray doses of 50 to 100 r caused a decrease in the titer of circulating antibody, although delayed hypersensitivity lasted for a normal time. When 300 r irradiation was administered 18 hours after sensitization, delayed hypersensitivity lasted for the usual period and circulating antibody first appeared at the usual 13 to 14 days after sensitization. Introduction of normal serum or leucocytes into irradiated animals apparently did not reduce damage to the mechanism regulating the rate of antibody synthesis.
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