The United Nations and the Bed of the Sea

Worldwide sentiment is growing that the bed of the sea, which occupies seventy percent of the Earth\u27s surface, as yet unclaimed, should be reserved from national claims of sovereignty and regarded as a common heritage of mankind. It should be reserved for peaceful purposes only. All nations, maritime, landlocked and developing, have an equity in this heritage. An authority of the United Nations should so administer it. For common ownership of this vast area to be recognized, and for it to be internationally administered, would be one of the greatest advances in the history of world organization. Instead of national rivalry, a power struggle and a colonial race, this concept would enable mankind, working together, to develop new forms of international cooperation

The Seabed Question in Context: One of Many Issues Massing for the 1973 Conference

A Comment on the evolution the United Nation\u27s Seabed Committee

Solubility studies of ultra pure transition elements in ultra pure alkali metals

Solubility of pure iron, molybdenum, niobium, and tantalum in liquid potassiu

Collision rate constants for polarizable ions

AbstractLangevin described a model for the interaction between an ion and a neutral nearly a century ago and since then, many modifications have been introduced to adjust for specific circumstances. This work discusses the induced dipole–induced dipole interaction between an ion and a neutral without a permanent dipole and introduces an anisotropic adjustment. A point polarizable ion model (PPI) and an orientation dependent polarizable ion model (ODPI) are discussed and applied to systems where the ion is highly polarizable and the neutral is only weakly polarizable. Significant deviations from classical Langevin rate constants and significant differences between PPI and ODPI are observed

Pulmonary dendritic cells and alveolar macrophages are regulated by γδ T cells during the resolution of S. pneumoniae-induced inflammation

γδ T cells commonly associate with mucosal and epithelial sites, fulfilling a variety of immunoregulatory functions. While lung γδ T cells have well-characterized pro-inflammatory activity, their potential role in the resolution of lung inflammation has yet to be explored in any detail. Indeed, given the importance of minimizing inflammation, the cellular mechanisms driving the resolution of lung inflammation are poorly understood. Using a murine model of acute Streptococcus pneumoniae-mediated lung inflammation, we now show that resolution of inflammation following bacterial clearance is associated with a > 30-fold increase in γδ T-cell number. Although inflammation eventually resolves in TCRδ−/− mice, elevated numbers of alveolar macrophages and pulmonary dendritic cells, and the appearance of well-formed granulomas in lungs of TCRδ−/− mice, together indicated a role for γδ T cells in regulating mononuclear phagocyte number. Ex vivo, both alveolar macrophages and pulmonary dendritic cells were susceptible to lung γδ T cell-mediated cytotoxicity, the first demonstration of such activity against a dendritic cell population. These findings support a model whereby expansion of γδ T cells helps restore mononuclear phagocyte numbers to homeostatic levels, protecting the lung from the consequences of inappropriate inflammation. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd

Adequação da infraestrutura, dos equipamentos, das acomodações e das condições ambientais dos laboratórios da Embrapa à norma ABNT NBR ISO/IEC 17.025:2005.

Editores técnicos: Joseani Mesquita Antunes, Ana Lídia Variani Bonato, Márcia Barrocas Moreira Pimentel

Antibody contributes to heterosubtypic protection against influenza A-induced tachypnea in cotton rats

<p>Abstract</p> <p>Background</p> <p>Influenza virus infection or vaccination evokes an antibody response to viral hemagglutinin (HA) and neuraminidase (NA) surface glycoproteins, which results in immunity against influenza A viruses of the same HA and NA subtype. A heterosubtypic immune response that offers some protection against different influenza A subtypes has been suggested from epidemiologic studies in human influenza outbreaks, and has been induced in experimental animal models. Original studies of such cross-protection showed that cytotoxic T lymphocytes (CTL) protect H3N2-immune mice from a lethal H1N1 infection. More recent studies in mice demonstrate that antibodies also contribute to heterosubtypic immunity (HSI). We previously demonstrated that HSI in cotton rats (<it>Sigmodon hispidus</it>) is characterized by protection of H3N2-immune animals from influenza H1N1-induced increase in respiratory rate (tachypnea). Alternatively, H1N1-immune animals are protected from H3N2-induced tachypnea. The experiments described in this report were designed to elucidate the immune mechanism that prevents this very early sign of disease.</p> <p>Results</p> <p>Our results show that cotton rats provided with H1N1-immune serum prior to challenge with an H3N2 virus were protected from influenza-associated tachypnea, with the degree of protection correlating with the antibody titer transferred. Immunization with an inactivated preparation of virus delivered intramuscularly also provided some protection suggesting that CTL and/or mucosal antibody responses are not required for protection. Antibodies specific for conserved epitopes present on the virus exterior are likely to facilitate this protection since prophylactic treatment of cotton rats with anti-M2e (the extracellular domain of M2) but not anti-nucleoprotein (NP) reduced virus-induced tachypnea.</p> <p>Conclusion</p> <p>In the cotton rat model of heterosubtypic immunity, humoral immunity plays a role in protecting animals from influenza-induced tachypea. Partial protection against respiratory disease caused by different influenza A subtypes can be attained with either live virus administered intranasally or inactivated virus delivered intramuscularly suggesting that either vaccine regimen may provide some protection against potential pandemic outbreaks in humans.</p