Design, Commissioning and Performance of the PIBETA Detector at PSI

We describe the design, construction and performance of the PIBETA detector built for the precise measurement of the branching ratio of pion beta decay, pi+ -> pi0 e+ nu, at the Paul Scherrer Institute. The central part of the detector is a 240-module spherical pure CsI calorimeter covering 3*pi sr solid angle. The calorimeter is supplemented with an active collimator/beam degrader system, an active segmented plastic target, a pair of low-mass cylindrical wire chambers and a 20-element cylindrical plastic scintillator hodoscope. The whole detector system is housed inside a temperature-controlled lead brick enclosure which in turn is lined with cosmic muon plastic veto counters. Commissioning and calibration data were taken during two three-month beam periods in 1999/2000 with pi+ stopping rates between 1.3*E3 pi+/s and 1.3*E6 pi+/s. We examine the timing, energy and angular detector resolution for photons, positrons and protons in the energy range of 5-150 MeV, as well as the response of the detector to cosmic muons. We illustrate the detector signatures for the assorted rare pion and muon decays and their associated backgrounds.Comment: 117 pages, 48 Postscript figures, 5 tables, Elsevier LaTeX, submitted to Nucl. Instrum. Meth.

New perspectives on the ecology and evolution of siboglinid tubeworms

Siboglinids are tube-dweling annelids that are important members of deep-sea chemosynthetic communities, which include hydrothermal vents, cold seeps, whale falls and reduced sediments. As adults, they lack a functional digestive system and rely on microbial endosymbionts for their energetic needs. Recent years have seen a revolution in our understanding of these fascinating worms. Molecular systematic methods now place these animals, formerly known as the phyla Pogonophora and Vestimentifera, within the polychaete clade Siboglinidae. Furthermore, an entirely new radiation of siboglinids, Osedax, has just recently been discovered living on whale bones. The unique and intricate evolutionary association of siboglinids with both geology, in the formation of spreading centres and seeps, and biology with the evolution of large whales, offers opportunities for studies of vicariant evolution and the calibration of molecular clocks. Moreover, new advances in our knowledge of siboglinid anatomy coupled with molecular characterization of microbial symbiont communities are revolutionizing our knowledge of host-symbiont relationships in the Metazoa. Despite these advances, considerable debate persists concerning the evolutionary history of siboglinids. Here we review the morphological, molecular, ecological and fossil data in order to address when and how siboglinids evolved. We discuss the role of ecological conditions in the evolution of siboglinids and present possible scenarios of the evolutionary origin of the symbiotic relationships between siboglinids and their endosymbiotic bacteria

Effector T-cell trafficking between the leptomeninges and the cerebrospinal fluid

In multiple sclerosis, brain-reactive T cells invade the central nervous system (CNS) and induce a self-destructive inflammatory process. T-cell infiltrates are not only found within the parenchyma and the meninges, but also in the cerebrospinal fluid (CSF) that bathes the entire CNS tissue 1,2 . How the T cells reach the CSF, their functionality, and whether they traffic between the CSF and other CNS compartments remains hypothetical 3–6 . Here we show that effector T cells enter the CSF from the leptomeninges during Lewis rat experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. While moving through the three-dimensional leptomeningeal network of collagen fibres in a random Brownian walk, T cells were flushed from the surface by the flow of the CSF. The detached cells displayed significantly lower activation levels compared to T cells from the leptomeninges and CNS parenchyma. However, they did not represent a specialized non-pathogenic cellular sub-fraction, as their gene expression profile strongly resembled that of tissue-derived T cells and they fully retained their encephalitogenic potential. T-cell detachment from the leptomeninges was counteracted by integrins VLA-4 and LFA-1 binding to their respective ligands produced by resident macrophages. Chemokine signalling via CCR5/CXCR3 and antigenic stimulation of T cells in contact with the leptomeningeal macrophages enforced their adhesiveness. T cells floating in the CSF were able to reattach to the leptomeninges through steps reminiscent of vascular adhesion in CNS blood vessels, and invade the parenchyma. The molecular/cellular conditions for T-cell reattachment were the same as the requirements for detachment from the leptomeningeal milieu. Our data indicate that the leptomeninges represent a checkpoint at which activated T cells are licensed to enter the CNS parenchyma and non-activated T cells are preferentially released into the CSF, from where they can reach areas of antigen availability and tissue damage