QCD and strongly coupled gauge theories : challenges and perspectives

We highlight the progress, current status, and open challenges of QCD-driven physics, in theory and in experiment. We discuss how the strong interaction is intimately connected to a broad sweep of physical problems, in settings ranging from astrophysics and cosmology to strongly coupled, complex systems in particle and condensed-matter physics, as well as to searches for physics beyond the Standard Model. We also discuss how success in describing the strong interaction impacts other fields, and, in turn, how such subjects can impact studies of the strong interaction. In the course of the work we offer a perspective on the many research streams which flow into and out of QCD, as well as a vision for future developments.Peer reviewe

38 Nu clear Tech nol ogy & Ra di a tion Pro tec tion –1/2005 X-RAY PHOTOELECTRON SPECTROSCOPY STUDY OF INTERACTION OF Np 5+ WITH GOETHITE a-FeOOH by

n+ com plexes on the sur face of goethite a-(FeOOH) re sulted from the in ter ac tion of neptunyl ni trate (NpO 2NO 3, 10-6 M) in the aque ous me dia with the back ground elec tro lyte (NaClO 4) of ionic force 0.1 M (pH = 7.0 � 0.2) were formed and stud ied with the X-ray pho to elec tron spec tros copy. The X-ray pho to elec tron spec-tros copy ionic and el e men tal quan ti ta tive anal y sis of the goethite and prod ucts of its in ter ac tion with neptunyl and plutonyl ni trates was car ried out. It was es tab lished that dur ing the stud ied neptunyl ni trate – goethite in ter ac tion Np 4+ and Np 6+ com pounds did not to form, while the com plexes of neptunyl group NpO

Pathogenesis and therapeutic interventions for ANCA-associated vasculitis.

Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) affects systemic small vessels and is accompanied by the presence of ANCAs in the serum. This disease entity includes microscopic polyangiitis, granulomatosis with polyangiitis, eosinophilic granulomatosis with polyangiitis and drug-induced AAV. Similar to other autoimmune diseases, AAV develops in patients with a predisposing genetic background who have been exposed to causative environmental factors. The mechanism by which ANCAs cause vasculitis involves ANCA-mediated excessive activation of neutrophils that subsequently release inflammatory cytokines, reactive oxygen species and lytic enzymes. In addition, this excessive activation of neutrophils by ANCAs induces formation of neutrophil extracellular traps (NETs). Although NETs are essential elements in innate immunity, excessive NET formation is harmful to small vessels. Moreover, NETs are involved not only in ANCA-mediated vascular injury but also in the production of ANCAs themselves. Therefore, a vicious cycle of NET formation and ANCA production is considered to be involved in the pathogenesis of AAV. In addition to this role of NETs in AAV, some other important discoveries have been made in the past few years. Incorporating these new insights into our understanding of the pathogenesis of AAV is needed to fully understand and ultimately overcome this disease

Osteobiology, strain, and microgravity. Part II: studies at the tissue level.

Loading microgravity, and/or defective mechanical strain-forces have important effects on bone cells and bone quality and quantity. The complex mechanisms induced by strain and microgravity on bone cells have been reviewed in Part I of this paper. In Part II, we have considered the data on the alterations induced by unloading and microgravity on the skeleton and the mechanisms that are involved at the tissue level in animals and humans.Journal ArticleResearch Support, Non-U.S. Gov'tReviewinfo:eu-repo/semantics/publishe