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Biomedical subjects

J W Shands

Publications and source records attributed to J W Shands.

At least 37 records · Page 2Linked to original sources
PubMed1983

Endotoxin fails to induce procoagulant in C3H/HeJ exudate macrophages.

Monocytes and macrophages from a variety of animal species produce procoagulants upon stimulation with endotoxin in vitro. While C3H/HeJ mice and their cells have exhibited refractoriness to known effects of phenol-water extracted endotoxin, two recent reports indicate that the cells of these mice produce procoagulants in a normal manner in response to endotoxin. This study compares the responsiveness of cells of C3H/HeJ and C3H/HeN mice to phenol-water extracted endotoxin and to disrupted gram-negative cell walls. Phenol-water extracted endotoxin had no mitogenic effect on spleen cells and failed to elicit procoagulant synthesis in exudate macrophages from C3H/HeJ mice. In contrast it was an effective stimulant for spleen cells and exudate macrophages of C3H/HeN mice. Gram-negative cell walls were an effective stimulant for spleen cells and macrophages from both mouse strains. I conclude that exudate macrophages of C3H/HeJ mice do not respond to endotoxin by producing procoagulant.

Animals↗
PubMed1983

The endotoxin-induced procoagulant of mouse exudate macrophages: a factor-X activator.

The properties of mouse macrophage procoagulant induced by endotoxin in vitro were studied by the acceleration of clotting and by chromogenic assays using as substrates human plasma and bovine components, which are not activated by mouse tissue factor. Maximal macrophage procoagulant activity occurred when activated cells were lysed in culture supernatant fluids, suggesting the interaction of cellular and supernatant factors. This procoagulant was clearly able to activate bovine factor X. The procoagulant also appeared to have prothrombinase activity. However, additional experiments suggested that the bulk of this activity was due to the activation of factor X contaminating the prothrombin. The production of the procoagulant was inhibited by warfarin (5 microM). Its activity was inhibited by 1 mM diisopropylfluorophosphate and unaffected by iodoacetamide, indicating that the procoagulant is a serine protease. Macrophage culture supernatants contained factor-VII-like activity. Neither mouse tissue factor nor macrophage culture supernatants alone activated bovine factor X. The two combined served as an efficient factor-X activator. Active supernatant factor (factor-VII-like) was not produced by macrophages cultured in the presence of warfarin, while the production of the macrophage cellular factor was unaffected by the presence of warfarin. I conclude that exudate macrophages cultured in vitro make and secrete factor VII or a factor-VII-like substance into the culture supernatant. When activated macrophages are lysed in this supernatant, the interaction of a cellular factor (? tissue factor) and factor VII gives rise to a factor-X activator.

Animals↗
PubMed1981

Comparative efficacy of piperacillin and penicillin G in treatment of gonococcal urethritis.

The comparative efficacy of 2 g of piperacillin and 4.8 X 10(6) U of penicillin G in the treatment of uncomplicated gonococcal urethritis was assessed in a randomized prospective study. Sixty-five evaluable patients received piperacillin, and 55 received penicillin G. All patients received either therapy were cured of gonorrhea. We conclude that piperacillin is as efficacious as aqueous procaine penicillin G in the therapy of uncomplicated gonococcal urethritis.

Gonorrhea↗
PubMed1980

The dispersion of gram-negative lipopolysaccharide by deoxycholate. Subunit molecular weight.

The lipopolysaccharide (LPS) was isolated from three strains of Salmonella typhimurium, a "smooth" strain, STM 7, the Ra mutant, TV 119, and the Re mutant, SL 1102. The effect of depletion of divalent cations on structure and the effect of deoxycholate on hydrodynamic behavior were studied. The results confirmed previous work by others that divalent cations and hydrophobic forces are important factors influencing LPS size and morphology. The binding of deoxycholate to LPS was measured. When the weight average molecular weights of the deoxycholate-dissociated LPS were determined by sedimentation equilibrium and corrected for bound deoxycholate, the values 5,555, 10,607, and 15,592, respectively, for Re, Ra, and "smooth" LPS were in good agreement with calculated formula weights. Although others have suggested that the basic LPS subunit is a trimer, our results suggest that it exists in the dimeric form.

Binding Sites↗
PubMed1980

Heat treatment for certain chronic granulomatous skin infections.

Four cases of chronic granulomatous skin infections (two due to Sporothrix schenckii and two to Mycobacterium marinum) were treated primarily by the intermittent application of local hyperthermia. This treatment was initiated either because of intolerance to conventional iodide therapy for sporotrichosis or as interim therapy while awaiting diagnosis of the mycobacterial infections. The response indicated that the application of heat is a useful adjunct to the therapy of these infections. Our experience, and that of others, suggests that in some cases heat alone may be curative.

Adult↗
PubMed1980

Adherence of Pseudomonas aeruginosa to tracheal cells injured by influenza infection or by endotracheal intubation.

Adherence of Pseudomonas aeruginosa to normal, injured, and regenerating tracheal mucosa was examined by scanning electron microscopy. Uninfected and influenza-infected murine tracheas were exposed to six strains of P. aeruginosa isolated from human sources and one strain of platn origin. All of the strains tested adhered to desquamating cells of the infected tracheas, but not to normal mucosa, the basal cell layer, or the regenerating epithelium. Adherence increased when the incubation time of the bacteria with the trachea was prolonged. Strains isolated from human tracheas appeared to adhere better than strains derived from the urinary tract. After endotracheal intubation of ferrets, P. aeruginosa adhered only to the injured cells and to areas of exposed basement membrane. We call this phenomenon "opportunistic adherence" and propose that alteration of the cell surfaces or cell injury facilitates the adherence of this bacterium and that adherence to injured cells may be a key to the pathogenesis of opportunistic Pseudomonas infections.

Animals↗
PubMed1979

Depressed mitogen responsiveness of lymphocytes at skin temperature.

The responsiveness of murine lymphocytes and human peripheral blood lymphocytes to phytohemagglutinin, concanavalin A, pokeweed mitogen, and endotoxin was tested in vitro at 32, 35, and 37 degrees C. The responses at 32 degrees C were delayed and often depressed. Mouse cells responded equally well at 35 and 37 degrees C. Human lymphocytes often responded more rapidly at 37 than at 35 degrees C. Since skin temperature, particularly that of the distal extremities, is usually 32 degrees C or less, a relative deficiency in cell-mediated immunity may exist in these sites. This may be part of the reason for the usual localization of certain infections, such as sporotrichosis, to these coller areas.

Animals↗
PubMed1979

Serum antibody prevents lethal murine influenza pneumonitis but not tracheitis.

This paper reports studies showing the effects of serum antibody upon influenza infection at two different sites: the trachea and lung. Tracheal desquamation, pulmonary consolidation, death, and virus shedding were examined after infection of mice with a lethal A/Port Chalmers/1/73 (H3N2) influenza virus. Immune serum administered intraperitoneally before infection prevented death and pulmonary consolidation and also significantly lowered lung virus shedding as compared with controls receiving normal serum. However, this protection did not extend to the ciliated epithelium of the trachea because serum antibody did not prevent desquamation of the trachea or significantly decrease viral yield from the trachea. These results indicate that serum antibody is protective against severe pulmonary parenchymal disease but not for disease of the ciliated epithelium.

Animals↗
PubMed1979

Murine influenzal tracheitis: a model for the study of influenza and tracheal epithelial repair.

The murine model of influenza virus infection is generally a lethal pneumonitis produced by a highly mouse-adapted virus. However, we infected mice with a less adapted virus and produced a nonlethal disease that involved the airways without producing gross pneumonitis. Changes that occurred in the tracheal epithelium were studied by scanning and transmission electron microscopy. Complete desquamation of the epithelium occurred within 3 days after infection, regeneration began within 5 days, and repair was complete within 2 wk after infection. This model is proposed as an alternative to the lethal pneumonitis for the study of murine influenza and also as a model for the study of repair of the respiratory ciliated epithelium.

Animals↗
PubMed1978

Legionnaires' disease. A sporadic case.

A patient with Legionnaires' disease developed consolidated pneumonia with severe hypoxemia and mental confusion; his condition improved with therapy with positive end-expiratory pressure, steroids, and chloramphenicol. The retrospective diagnosis was made by a fourfold rise in indirect fluorescent antibody titers. The chest x-ray films showed bilateral alveolar infiltrates and air bronchograms.

Adult↗
PubMed1977

Commitment to deoxyribonulceic acid synthesis and the cell cycle in endotoxin-stimulated murine spleen cells.

Events associated with endotoxin-induced mitogenesis in murine spleen cells were investigated. Commitment to deoxyribonucleic acid (DNA) synthesis, the onset of DNA synthesis, and phases of cell cycle were timed. Increased levels of DNA synthesis in murine spleen cells stimulated with endotoxin were observed 12 to 16 h after the addition of the mitogen. The total cell cycle time of stimulated B-cells was 11 to 14 h. The S-phase was 8 h. The G2-phase was 1 h, and the combined M-plus G1-phase of cycling cells was 2 to 5 h. A 1- to 4-h exposure to lipopolysaccharide elicited a significant increase in DNA synthesis. Progressively longer exposures to lipopolysaccharide, up to 24 h, produced further increases in first-cycle DNA synthesis. Polymyxin B, when added with endotoxin to cultures from the outset, inhibited first-cycle DNA synthesis. However, if addition of the antibiotic was delayed, progressive increases in first-cycle dna synthesis were observed. These data indicate a heterogeneity among B-cells in their responsiveness to endotoxin.

Animals↗
PubMed1976

Endotoxin-stimulated spleen cells: dissociation between DNA synthesis and IgM production at the cellular level.

LPS stimulation of mouse spleen cells in the presence of Hu resulted in almost total suppression of [3H]thymidine incorporation without affecting the percentage of cells induced to produce IgM. Utilizing a method which permitted the simultaneous measurement of IgM production and [3H]thymidine incorporation in individual cells, it was demonstrated directly that LPS stimulation of IgM production can occur in the absence of DNA synthesis.

Animals↗