The interaction of IgE antibody with human alveolar macrophages and its participation in the inflammatory processes of lung allergy

After the initial observation that human and animal mononuclear phagocytes can be activated into specific killer cells against larvae of the parasite Schistosoma mansoni by seric IgE antibody from infected patients, a possible interaction of IgE with human alveolar macrophages in asthmatic patients was investigated. In vitro, alveolar macrophages from non-atopic individuals can bind monoclonal IgE molecules, as well as IgE antibody from the serum of patients with respiratory allergy. A subsequent contact with anti-IgE antibody or with the specific allergen induces the extracellular release of a variety of mediators, such as lysosomal enzymes, neutral proteases, or superoxide anion. Due to the presence of allergen-specific IgE antibody on the macrophage surface in situ, the same results were obtained in vitro with freshly purified alveolar macrophages from allergic patients. Disodium cromoglycate, corticosteroids, or beta-adrenergic stimulants are strong inhibitors of this specific exocytosis of physiological mediators. The atopic cells formed rosettes with allergen-coated erythrocytes at 4 degrees C, except after pretreatment with aggregated monoclonal IgE or with the allergen.     

In vitro activity of 9 antibiotics and 3 beta-lactamase inhibitors against 107 clinical isolates of Acinetobacter baumanii

Twenty eight of 227 patients undergoing restorative proctocolectomy for inflammatory bowel disease, familial adenomatous polyposis or functional disease were over the age of 50 years: ages 50 to 60 (n = 13), 60 to 70 (n = 10), and over 70 (n = 5). Major complications occurred in 5 patients over the age of 50 (18%) compared with 43 patients under the age of 50 (23%). Three patients above the age of 50 had their pouch excised (11%) compared with 23 under the age of 50 (12%). Functional outcome was assessed with a 12 point symptom score. This was similar in all age bands: under 50 years (mean = 2.2; sd +/- 2.2; n = 109), 50 to 60 years (mean = 2.5; sd +/- 2.5; n = 12), 60 to 70 years (mean = 2.8; sd +/- 2.3; n = 7) and over 70 years (mean = 4.0; sd +/- 3.7; n = 5): P > 0.05). When analysed for ulcerative colitis alone, no significant differences were seen between the two age groups. Restorative proctocolectomy in the elderly gives results which are comparable to the younger population.     

Idiopathic thrombocytopenic purpura in a liver transplant recipient with previous primary biliary cirrhosis

The loss of immunotolerance has been implicated in the pathogenesis of both primary biliary cirrhosis (PBC) and idiopathic, immune-mediated thrombocytopenic purpura (ITP). An association between these two autoimmune diseases has been well described. We describe a 41-year-old woman in whom ITP developed 457 days after liver transplantation for PBC while receiving immunosuppressive medications sufficient to maintain allograft function. Our case report, the first to describe post-transplant ITP in association with PBC, demonstrates the persistence of the underlying immune dysregulation of PBC after transplantation. The practice of decreasing the dosage of immunosuppressive medication to maintenance levels after transplantation may unmask the effects of this defect in immunotolerance.     

Heterogeneity of glomerular perfusion and filtration induced by epinephrine and norepinephrine

The role of catecholamines in the distribution of intrarenal blood flow and in single-nephron glomerular filtration rate (SNGFR) was evaluated in anesthetized Wistar rats by the Hanssen technique. Epinephrine (EPI) and norepinephrine (NOR) were infused to produce elevations of 20-30 mmHg in mean arterial pressure. Superficial and juxtamedullary nephron perfusion and filtration were determined by the presence of Prussian blue dye. In the control group, 100% of the nephrons presented a homogeneous pattern of perfusion and filtration. In contrast, a heterogeneous distribution of the dye was found even in the larger arteries (arciform and radial), indicating variable perfusion and filtration in both superficial and juxtamedullary nephrons. The effects of EPI and NOR were also evaluated in the superficial cortex by the micropuncture technique in two additional groups of Munich-Wistar rats. Mean SNGFR was 27% and 54% lower in the EPI- and NOR-treated groups, respectively. No change in mean intraglomerular hydraulic pressure was observed after EPI or NOR infusion in spite of a highly scattered pattern, indicating an important variability in perfusion along the superficial cortex, and/or different sensitivity of the pre- and post-glomerular arterioles. The present data suggest that EPI and NOR may affect intrarenal hemodynamics by modifying perfusion and filtration in both superficial and juxtamedullary glomeruli and not by shifting blood flow from superficial to juxtamedullary nephrons. The heterogeneous pattern of perfusion was a consequence of differential vasoconstriction along the intrarenal arteries, probably due to different density and/or sensitivity of the adrenergic receptor subtypes present in the intrarenal vascular tree.     

Characterization of unconventional MYO6, the human homologue of the gene responsible for deafness in Snell's waltzer mice

Deafness is the most common form of sensory impairment in humans. Mutations in unconventional myosins have been found to cause deafness in humans and mice. The mouse recessive deafness mutation, Snell's waltzer, contains an intragenic deletion in an unconventional myosin, myosin VI (locus designation, Myo6). The requirement for Myo6 for proper hearing in mice makes this gene an excellent candidate for a human deafness disorder. Here we report the cloning and characterization of the human unconventional myosin VI (locus designation, MYO6) cDNA. The MYO6 gene maps to human chromosome 6q13. The isolation of the human gene makes it now possible to determine if mutations in MYO6 contribute to the pathogenesis of deafness in the human population.