The authors separately studied the epidemiology (risk and risk factors) of Kaposi's sarcoma occurring as an initial acquired immunodeficiency syndrome (AIDS) outcome (early Kaposi's sarcoma) and later after a different initial AIDS outcome (later Kaposi's sarcoma) in a cohort of 2,591 human immunodeficiency virus type 1-infected gay men of the Multicenter AIDS Cohort Study between 1984 and 1992. Among 844 AIDS cases, 202 presented with early Kaposi's sarcoma, 101 subsequently developed later Kaposi's sarcoma, and 541 were not diagnosed with Kaposi's sarcoma. Overall, 37.4% of AIDS cases were diagnosed with Kaposi's sarcoma prior to death. Kaposi's sarcoma diagnosed on the skin was significantly more common with early Kaposi's sarcoma (77.3%) than with later Kaposi's sarcoma (65.1%). Men presenting with an AIDS outcome other than Kaposi's sarcoma were at high risk for later Kaposi's sarcoma. Later Kaposi's sarcoma onset in men with a previous AIDS outcome was associated with the following characteristics: 1) lower immune status prior to AIDS and 2) longer post-AIDS survival. A Kaposi's sarcoma diagnosis in a man with a previous AIDS illness approximately doubled the risk (hazard) for death. Histories of urethral gonorrhea and scabies prior to study entry were more common in early Kaposi's sarcoma cases than in later Kaposi's sarcoma cases. However, self-reported sexual activity at study entry and prior to AIDS onset was highest in the later Kaposi's sarcoma group. In this cohort, cigarette smoking had a protective association against all Kaposi's sarcoma in univariate and multivariate models. Only 21.0% of the later Kaposi's sarcoma and 25.0% of the early Kaposi's sarcoma men smoked at least one-half pack of cigarettes daily at study entry compared with 33.8% of non-Kaposi's sarcoma and 35.5% of seroprevalent men still AIDS free. The reasons for this surprising association are unclear. However, other evidence which documents that habitual smoking alters the immune system (and possibly cytokine levels) in ways that could perhaps influence Kaposi's sarcoma pathogenesis should be considered.

Previous studies in human asthmatics have suggested a defect in the beta-adrenergic pathway leading to cyclic adenosine monophosphate (cAMP) generation. Although these studies have suggested normal or increased numbers of beta-adrenergic receptors, limitations in the quantity of tissue available have not allowed further delineation of the biochemical or molecular mechanisms of human asthma. The basenji-greyhound (BG) dog model of nonspecific airway hyperreactivity displays similarities to human asthma, and altered functional response to beta-adrenergic agonists has been previously shown in airway tissue from this model. We have now correlated this functional impairment in beta-adrenergic response with a decreased generation of cAMP in response to isoproterenol. Organ bath studies and adenylyl cyclase assays of trachealis muscle revealed impaired responses to isoproterenol in the BG dog as compared with control dogs. Pretreatment of muscle strips from BG dogs with isoproterenol had no effect on subsequent dose-response curves to methacholine (pD2 = 7.17 +/- 0.13, 7.34 +/- 0.12, and 7.14 +/- 0.17 for control, 10(-6) M isoproterenol, and 10(-5) M isoproterenol, respectively), while muscle strips from mongrel dogs had a significant shift in methacholine responses after isoproterenol pretreatment (pD2 = 7.91 +/- 0.23, 7.48 +/- 0.29, and 6.98 +/- 0.33 for control, 10(-6) M isoproterenol, and 10(-5) M isoproterenol, respectively). Adenylyl cyclase activity in response to isoproterenol was 54% in the BG trachealis membranes as compared with mongrels. Functional and biochemical responses to forskolin, NaF, prostaglandin, and dibutyryl cAMP, and the quantity of G,alpha were similar in the BG and control dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Aims This study aimed to determine if macrophages can attach and directly affect the oxide layers of 316L stainless steel, titanium alloy (Ti6Al4V), and cobalt-chromium-molybdenum alloy (CoCrMo) by releasing components of these alloys. Methods Murine peritoneal macrophages were cultured and placed on stainless steel, CoCrMo, and Ti6Al4V discs into a 96-well plate. Cells were activated with interferon gamma and lipopolysaccharide. Macrophages on stainless steel discs produced significantly more nitric oxide (NO) compared to their control counterparts after eight to ten days and remained elevated for the duration of the experiment. Results On stainless steel, both nonactivated and activated cell groups were shown to have a significant increase in metal ion release for Cr, Fe, and Ni (p < 0.001, p = 0.002, and p = 0.020 respectively) compared with medium only and showed macrophage-sized corrosive pits on the stainless steel surface. On titanium alloy discs there was a significant increase in aluminum (p < 0.001) among all groups compared with medium only. Conclusion These results indicated that macrophages were able to attach to and affect the oxide surface of stainless steel and titanium alloy discs. Cite this article: Bone Joint J 2020;102-B(7 Supple B):116–121.

We selected two inbred strains of mice based on their different in vivo lung responses to intravenous acetylcholine for studies on the in vitro tracheal responses to contractile and relaxing agents. In addition, we studied the role of cyclooxygenase products on the in vitro responses. Tracheal rings were contracted with increasing concentrations of carbachol and KCl and relaxed with increasing concentrations of isoproterenol after contraction with carbachol at the concentration that produced 30, 50, and 70% of the maximal contraction (EC30, EC50, and EC70, respectively) and KCl at the EC50. Half the tracheae simultaneously underwent the same protocols after pretreatment with indomethacin (3 X 10(-6) M). Despite a severalfold difference in the maximal response to cholinergic agents in vivo, there were no significant differences between the strains in the tracheal responses to carbachol (P = 0.78) or KCl (P = 0.13) in vitro. Both strains showed inhibition of the isoproterenol relaxation by carbachol (P less than 0.0001). Multiple linear regression analysis showed that the strain that was more sensitive to carbachol in vivo was also more sensitive to isoproterenol in vitro after carbachol contraction (P = 0.014). The greater isoproterenol sensitivity of the tracheae from this strain was not present after contraction with KCl, nor were these tracheae more sensitive to relaxation with sodium nitroprusside. Indomethacin pretreatment of the tissues in vitro augmented the maximal response and the sensitivity to carbachol (P less than 0.001) and KCl (P = 0.0006), and this effect was similar in both strains. Evaluation of isoproterenol relaxation after indomethacin pretreatment was confounded by the lower concentrations of carbachol needed for contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract