Near syncope and chest tightness after administration of apraclonidine before argon laser iridotomy.
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Biomedical subjects
Publications and source records attributed to D W Richards.
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Mouse zygotes were cultured in medium containing follicular fluid from patients who had follicles containing oocytes which fertilized, did not fertilize, or were atretic and who did or did not become pregnant after in vitro fertilization and embryo replacement. The inhibitory effect was least with the follicular fluid from follicles in which the oocytes subsequently fertilized, greater when the oocytes did not fertilize, and most inhibitory when the follicle contained an atretic oocyte. More mouse zygotes developed to blastocysts when culture medium was supplemented with follicular fluid from patients who became pregnant compared to those who did not become pregnant. There was no difference in pregnancy outcome when an oocyte which subsequently fertilized was obtained from the follicle. These results indicate that follicles contain a substance(s) which inhibits mouse zygote development in vitro and that the inhibitory activity is related to the developmental potential of the oocyte in the follicle.
Over a period of three years, Salmonella dublin was isolated occasionally from the faeces of nine adult cattle in a closed dairy herd. The organism was also isolated from 12 of the samples collected after parturition; isolations were made from newborn calves on 11 occasions, from a vaginal swab once and from a milk sample once. Nine of the isolations from the calves were made from swabs obtained within 24 hours of birth. Throughout the investigation isolations were made from heifers, steers and older calves and 11 infected animals were detected. S. dublin was widespread in the farm environment and it was concluded that environmental contamination was an important source of infection for animals of all ages, some of which may have become latent carriers. The family history of one cow, seven of whose offspring were infected with S dublin, suggested the possibility of vertical transmission. Without reliable tests to detect latent carriers, it is suggested that control of this infection must be based on improved hygiene and the use of vaccination to improve the immunity of the herd.
A new method is described for obtaining cross-sectional images of the anterior chamber. Photographs are obtained with a Scheimpflug slit-lamp camera. After cornea, iris, and lens surfaces are digitized, mathematical corrections are made for the camera distortion and for the refractive effects of the cornea. The reproducibility and accuracy of the method were tested and found to be adequate for clinical study of human eyes in physiologic or diseased states.
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We evaluated local and systemic humoral responses to inhalational challenges with ovalbumin (OA) by measuring IgA and IgG isotypic antibodies to OA in serum and bronchoalveolar wash fluids (BAW), and by quantitating cells containing IgA, IgG, and anti-OA in lung, lymph nodes, spleen, and gut. Rabbit models of acute hypersensitivity pneumonitis and chronically-challenged "desensitized" animals were studied along with appropriate control animals. Systemic (via a toe pad) immunization or acute aerosol challenge with OA resulted in only trace amounts of IgG anti-OA antibodies in BAW and no apparent anti-OA-containing cells in the lung itself. Acute aerosol challenge of systemically immunized rabbits caused alveolitis, increased IgG anti-OA-containing cells in mediastinal and popliteal lymph nodes, and increased IgG anti-OA in BAW attributable to transudation from serum. Thrice-weekly inhalational challenge with aerosolized OA resulted in waning alveolitis, elevated concentrations of IgA and IgG anti-OA in BAW and serum, and increased concentrations of IgG and IgA anti-OA cells in the lung, but not in other tissues, including the gut. We conclude that these experiments have implicated IgG as well as IgA antibodies in local humoral responses to inhaled antigen, have not substantiated the notion of a common mucosal immune system involving lung and gut, have failed to demonstrate humoral tolerogenesis after inhalation of antigen, and have shown an effect of systemic priming on subsequent pulmonary immune responses in the models examined.
Rabbits that had been prepared to develop acute alveolitis after aerosol challenge with simple protein antigens did not develop chronic alveolitis but rather gradually recovered despite continued challenge. Immunologic accompaniments of waning disease were compared in this model to those associated with intravenous injections of antigen causing "desensitization." We also studied the effects of aerosol challenge prior to systemic immunization, antigen specificity, and the duration of desensitization by aerosolized and intravenous antigen. We found that repeated aerosol or intravenous challenges produced antigen-specific desensitization in this model, and the effect lasted several weeks. Prior exposure to aerosolized antigen was not protective. Neither aerosol nor intravenous desensitization maneuvers abrogated antigen-specific lymphocyte blastogenesis, although an early transient fall did occur. Humoral responses were boosted. These findings suggest that chronic alveolitis is prevented in this model by specific desensitization, without the induction of true tolerance or of nonspecific anergy. Such immunoregulation may result from development of antigen-specific blockade or blocking factors (e.g., lymphokines), antigen-antibody complexes, or suppressor cells affecting specific effector cells. Evaluation of these mechanisms may have implications for diagnosis and prognosis in human hypersensitivity pneumonitis.
The pathogenesis of hypersensitivity pneumonitis is incompletely understood; cell-mediated hypersensitivity mechanisms may be involved, but in vitro correlates have been studied in humans with inconclusive results. We used a rabbit model of hypersensitivity pneumonitis to study systemic and local antigen-specific lymphocyte responses as measured by in vitro incorporation of 3H-thymidine. Groups of animals were systemically immunized with ovalbumin and acutely or repeatedly challenged with aerosolized ovalbumin. Lymphocyte responses were measured in peripheral blood, mediastinal and popliteal lymph nodes, bronchus-associated lymphoid tissue, and bronchoalveolar wash fluids in these groups and in appropriate control animals. Lymphocyte proliferative responses to specific antigen, shown previously to be a T-cell response in this system, occurred after systemic or inhalation exposure to antigen. Acute alveolitis was associated with a decrease in peripheral blood lymphocyte responses and the presence of responsive lymphocytes in bronchoalveolar was fluids. Repeated inhalation challenge thrice weekly for 1 month, with waning of alveolitis, was not associated with significant changes in lymphocyte responsiveness. Antigen-specific lymphocyte blastogenesis did not define animals capable of developing alveolitis after aerosol challenge and did not appear, therefore, to distinguish effector cell activity in this model.
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Guinea pig basophils were tested against chemotactic factor(s) generated from homologous and heterologous sera. An "under agarose" method of quantitating leukocyte chemotaxis was adapted to measure serum-derived basophil chemotactic factor(s) (BCF). The method was found to be simple, reproducible, and sparing of time and reagents and it provided simultaneous controls. Because of the economy of reagents compared with the Boyden chamber technique, basophils from individual guinea pigs could be studied and were found to be variable in responsiveness. A definite difference in the response of guinea pig basophils to zymosan-activated sera of various other species was demonstrated. Guinea pig basophils responded to zymosan-activated serum from guinea pig and rat but failed to respond to zymosan-activated serum from human, hamster, rabbit, or cow. Optimal conditions were determined for cell numbers, serum activation and dilution, and migration times for studies of guinea pig BCF. The under agarose technique provides a practical alternative to chamber methods for the study of basophil chemotaxis. Although guinea pig basophils do not respond to human serum-derived BCF, the economy of reagents with this technique gives promise toward adaptation of the method to studies of human basophil chemotaxis.
Strychnine intoxication is manifested by agitation, muscle spasms, and convulsions. We report a case in which intractable convulsions led to severe lactic acidosis which secondarily resulted in visceral (lung, heart, kidney, liver, and brain) collapse and death. Aggressive therapy instituted in the emergency department and aimed at control of seizure activity and lactic acidosis may be lifesaving.
The effects on the lungs of chronic aerosol and intravenous antigen challenges in preimmunized and control rabbits were studied. Soluble and particulate antigens included ovalbumin, keyhole limpet hemocyanin, antigen-adsorbed latex particles, glutaraldehyde cross-linked ovalbumin, and killed bacille Calmette-Guérin (BCG). Despite the development of acute alveolitis in sensitized animals, chronic aerosol challenge with both soluble and particulate antigens failed to produce chronic interstitial lung disease. Chronic intravenous challenge with killed BCG, but not other particulate antigens, resulted in a progressive interstitial pneumonitis, with evidence of fibrogenesis in animals that had been presensitized to tuberculin by toepad injection of complete Freund's adjuvant. Adaptive alveolar clearance mechanisms thus appear to protect rabbits from chronically inhaled antigen. Pulmonary circulatory clearance of BCG, however, results in an interstitial pneumonitis that is dependent on previous sensitization.
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