Vascular endothelial and smooth muscle cells in culture selectively release adenine nucleotides.

Endothelial cells in culture can modulate platelet aggregation and vascular tone, in part by producing prostacyclin (PGI2), a powerful vasodilator and inhibitor of platelet aggregation, but also by their ecto-ADPase activity, which initiates the conversion of pro-aggregating ADP to adenosine, a potent vasodilator and platelet inhibitor. We have now demonstrated that cultured aortic endothelial cells exposed to trypsin, thrombin or other stimuli can liberate a high proportion of their adenine nucleotides without substantial loss of lactate dehydrogenase. ADP rapidly accumulates extracellularly, reaching biologically active concentrations before there is further breakdown to adenosine. Whether this selective release of nucleotides is a response to damage, or whether it represents a specific secretory mechanism remains to be resolved. Cultured aortic smooth muscle cells can secrete adenine nucleotides in a similar manner, but extracellular conversion to adenosine occurs much faster.     

Effects of injury on the concentration ofα 1 andα 2 in the plasmas of male and female rats

Summary The effects of injury on the concentration of ₁-macroglobulin and ₂-macroglobulin in the plasmas of male and female rats has been investigated. At 5 days after injury to the male rats the ₁-macroglobulin concentration increased to 131% of its preinjury value. The ₂-macroglobulin concentration increased more rapidly to a maximum of 86 times its initial value. In the female rats ₂-macroglobulin increased only slightly and ₁-macroglobulin not at all.     

Effects of injury on the concentration of alpha1-macroglobulin and alpha2-macroglobulin in the plasmas of male and remale rats.

The effects of injury on the concentration of alpha1-macroglobulin and alpha2-macroglobulin in the plasmas of male and remale rats has been investigates. At 5 days after injury to the male rats the alpha1-macroglobulin concentration increased to 131% of its preinjury value. The alpha2-macroglobulin concentration increased more rapidly to a maximum of 86 times its initial value. In the female rats alpha2-macroglobulin increased only slightly and alpha1-macroglobulin not at all.     

Transfer of diabetes in mice prevented by blockade of adhesion-promoting receptor on macrophages

Insulin-dependent diabetes mellitus (IDDM) is a disease with an autoimmune aetiology. The non-obese diabetic mouse is a good spontaneous animal model of the human disease, with IDDM developing in 50-80% of female mice by the age of 6 months. The disease can be transferred by splenic T cells from diabetic donors and is prevented by T-cell depletion. The mechanism(s) by which the beta cell is specifically destroyed is not known, but T cells and macrophages have both been implicated, based on the presence of macrophages in the infiltrated islet and the ability of chronic silica treatment to prevent disease. The monoclonal antibody 5C6 is specific for the myelomonocytic adhesion-promoting type-3 complement receptor (CR3 or CD11b/CD18) and does not bind to T cells. Here we show that blockade of macrophage CR3 in vivo prevents intra-islet infiltration by both macrophages and T cells and inhibits development of IDDM. We conclude that both T cells and macrophages have an essential role in the onset of IDDM.     

Selective effects of cyclosporin A on colony-forming lymphoid and myeloid cells in man

THE properties of the fungus metabolite, cyclosporin A, have suggested its potential as a clinically valuable immunosup-pressive agent(1,2). Experiments in animals have demonstrated that its suppressive action against cell-mediated and humoral immunity is not accompanied by any appreciable myelotoxicity(3,4). In this respect, cyclosporin A contrasts with other immunosuppressants in current use, such as antilymphocyte globulin and azathioprine. There are, however, few data to substantiate a selective toxicity of cyclosporin A against human lymphocytes. Here, we have compared its effects against human lymphoid and myeloid cells, using colony formation by the different cell types as the end point. We found that the compound exhibited far greater toxicity towards a sub-population of T cells than towards either B lymphocytes or haematopoietic precursor cells.     

Shigella sonnei genome sequencing and phylogenetic analysis indicate recent global dissemination from Europe

Shigella are human-adapted Escherichia coli that have gained the ability to invade the human gut mucosa and cause dysentery, spreading efficiently via low-dose fecal-oral transmission. Historically, S. sonnei has been predominantly responsible for dysentery in developed countries but is now emerging as a problem in the developing world, seeming to replace the more diverse Shigella flexneri in areas undergoing economic development and improvements in water quality. Classical approaches have shown that S. sonnei is genetically conserved and clonal. We report here whole-genome sequencing of 132 globally distributed isolates. Our phylogenetic analysis shows that the current S. sonnei population descends from a common ancestor that existed less than 500 years ago and that diversified into several distinct lineages with unique characteristics. Our analysis suggests that the majority of this diversification occurred in Europe and was followed by more recent establishment of local pathogen populations on other continents, predominantly due to the pandemic spread of a single, rapidly evolving, multidrug-resistant lineage.     

Solvent Extraction in Hydrometallurgy： Present and Future

Introduction Solvent extraction as applied to refining operations, particularly uranium, commenced in the late 1940s. These plants were small by present plant sizes. Shortly after, and almost 50 years ago now, the first solvent extraction plant was installed to treat hydrometallurgi-cal solutions at the mine site for the recovery of ura-nium. The success in this first generation of uranium operations in the 1950s and 1960s eventually led to the application of solvent extraction to copper opera…