Study of Spin and Decay-Plane Correlations of W Bosons in the e+e- -> W+W- Process at LEP

Data collected at LEP at centre-of-mass energies \sqrt(s) = 189 - 209 GeV are used to study correlations of the spin of W bosons using e+e- -> W+W- -> lnqq~ events. Spin correlations are favoured by data, and found to agree with the Standard Model predictions. In addition, correlations between the W-boson decay planes are studied in e+e- -> W+W- -> lnqq~ and e+e- -> W+W- -> qq~qq~ events. Decay-plane correlations, consistent with zero and with the Standard Model predictions, are measured

Ultrarelativistic sources in nonlinear electrodynamics

The fields of rapidly moving sources are studied within nonlinear electrodynamics by boosting the fields of sources at rest. As a consequence of the ultrarelativistic limit the delta-like electromagnetic shock waves are found. The character of the field within the shock depends on the theory of nonlinear electrodynamics considered. In particular, we obtain the field of an ultrarelativistic charge in the Born-Infeld theory.Comment: 10 pages, 3 figure

Measurement of the Cross Section for Open-Beauty Production in Photon-Photon Collisions at LEP

The cross section for open-beauty production in photon-photon collisions is measured using the whole high-energy and high-luminosity data sample collected by the L3 detector at LEP. This corresponds to 627/pb of integrated luminosity for electron-positron centre-of-mass energies from 189GeV to 209GeV. Events containing b quarks are identified through their semi-leptonic decay into electrons or muons. The e+e- -> e+e-b b~X cross section is measured within our fiducial volume and then extrapolated to the full phase space. These results are found to be in significant excess with respect to Monte Carlo predictions and next-to-leading order QCD calculations

Depletion of stromal cells expressing fibroblast activation protein-α from skeletal muscle and bone marrow results in cachexia and anemia.

Fibroblast activation protein-α (FAP) identifies stromal cells of mesenchymal origin in human cancers and chronic inflammatory lesions. In mouse models of cancer, they have been shown to be immune suppressive, but studies of their occurrence and function in normal tissues have been limited. With a transgenic mouse line permitting the bioluminescent imaging of FAP(+) cells, we find that they reside in most tissues of the adult mouse. FAP(+) cells from three sites, skeletal muscle, adipose tissue, and pancreas, have highly similar transcriptomes, suggesting a shared lineage. FAP(+) cells of skeletal muscle are the major local source of follistatin, and in bone marrow they express Cxcl12 and KitL. Experimental ablation of these cells causes loss of muscle mass and a reduction of B-lymphopoiesis and erythropoiesis, revealing their essential functions in maintaining normal muscle mass and hematopoiesis, respectively. Remarkably, these cells are altered at these sites in transplantable and spontaneous mouse models of cancer-induced cachexia and anemia. Thus, the FAP(+) stromal cell may have roles in two adverse consequences of cancer: their acquisition by tumors may cause failure of immunosurveillance, and their alteration in normal tissues contributes to the paraneoplastic syndromes of cachexia and anemia