Abstract We present results of the first calculation of next-to-leading-order electroweak corrections to W-boson pair production at the LHC that fully takes into account leptonic W-boson decays and ...off-shell effects. Employing realistic event selections, we discuss the corrections in situations that are typical for the study of W-boson pairs as a signal process or of Higgs-boson decays H arrow right WW, to which W-boson pair production represents an irreducible background. In particular, we compare the full off-shell results, obtained treating the W-boson resonances in the complex-mass scheme, to previous results in the so-called double-pole approximation, which is based on an expansion of the loop amplitudes about the W resonance poles. At small and intermediate scales, i.e. in particular in angular and rapidity distributions, the two approaches show the expected agreement at the level of fractions of a percent, but larger differences appear in the TeV range. For transverse-momentum distributions, the differences can even exceed the 10% level in the TeV range where "background diagrams" with one instead of two resonant W bosons gain in importance because of recoil effects.
We present results of the first calculation of next-to-leading-order electroweak corrections to W-boson pair production at the LHC that fully takes into account leptonic W-boson decays and off-shell ...effects. Employing realistic event selections, we discuss the corrections in situations that are typical for the study of W-boson pairs as a signal process or of Higgs-boson decays H arrow right WW super(), to which W-boson pair production represents an irreducible background. In particular, we compare the full off-shell results, obtained treating the W-boson resonances in the complex-mass scheme, to previous results in the so-called double-pole approximation, which is based on an expansion of the loop amplitudes about the W resonance poles. At small and intermediate scales, i.e. in particular in angular and rapidity distributions, the two approaches show the expected agreement at the level of fractions of a percent, but larger differences appear in the TeV range. For transverse-momentum distributions, the differences can even exceed the 10% level in the TeV range where "background diagrams" with one instead of two resonant W bosons gain in importance because of recoil effects.
Dopamine plays important functional roles in the vertebrate retina. Here we show that functional D2 dopamine receptors are present on mammalian retinal Müller (glial) cells. Using an antiserum ...directed to two oligopeptides predicted from rat D2 receptor DNA, patchy label was demonstrated immunocytochemically on virtually all Müller cells enzymatically isolated from guinea-pig and rat retinae. Application of exogeneous dopamine to voltage-clamped isolated living guinea-pig Müller cells caused either a decrease (40%), an increase (32%), or no change (28%) of the input resistance of the membrane. The D2 receptor agonist quinelorane caused an increase of the membrane's input resistance in 100% of the cells. This effect was completely blocked by the D2 receptor antagonist S(-)-sulpiride. When all voltage-activated K+ channels except the delayed rectifiers were blocked by Ba2+, quinelorane had no effect. Further, the reversal potentials of the responses were near the potassium equilibrium potential. We conclude that the activation of Müller cell D2 receptors closes (inwardly rectifying) K+ channels. The presence of functional dopamine receptors on mammalian Müller cells may have important consequences for retinal K+ clearance, and thus, for information processing in the retina.
To detect the presence of voltage-gated Ca(2+) channels in the plasma membranes of freshly isolated Müller glial cells from the human retina and their modulation by GABA(B) receptor agonists.
Whole ...cell voltage-clamp recordings were made to study Ca( 2+), Ba(2+), and Na(+) currents through voltage-gated Ca(2+) channels.
The vast majority of the investigated cells displayed no resolvable currents through Ca(2+) channels when Ca(2+) ions (2 mM) were present in the extracellular solution. Small-amplitude inwardly directed currents ( approximately 0.6 pA/pF) were detected when Ba(2+) ions (20 mM) were used as charge carrier. However, when Na(+) ions were used as charge carrier in divalent cation-free external solution, currents of large amplitudes ( approximately 7.5 pA/pF) through voltage-gated Ca(2+) channels were detected. Human Müller cells displayed currents through both transient, low voltage-activated Ca(2+) channels and long-lasting, high voltage-activated channels. The Na(+) fluxes through low voltage-activated Ca( 2+) channels were inhibited in a voltage-independent manner in the presence of GABA(B) receptor agonists.
Human Müller glial cells express different kinds of voltage-gated Ca(2+) channels in their plasma membranes that can be activated only under certain physiological or pathophysiological conditions. The record of Na(+) fluxes in divalent cation-free solutions may be a technique to detect the presence of "hidden" voltage-gated Ca(2+) channels in Müller glial cells.
Vascular endothelial cells form the interface between recipient tissues and circulating alloreactive donor T cells after allogeneic stem cell transplantation. Vascular injury has been seen in ...patients with acute graft versus host disease (GVHD) in the skin. We aimed to see whether vascular injury mediated by cytotoxic T lymphocytes and microvessel loss arises in patients with chronic GVHD.
We investigated eight patients with acute GVHD and ten with chronic GVHD for signs of endothelial injury and microvessel loss by measurement of von Willebrand factor (vWF) in plasma and blood vessel density in biopsy samples taken from lesional skin. Controls consisted of nine patients without GVHD who survived for longer than 100 days and nine healthy people. Inflammation and endothelial injury were assessed in selected samples by immunostaining for CD8 T cells, activated cytotoxic T lymphocytes, and vascular endothelial cells.
We identified more extensive loss of microvessels in the skin of patients with GVHD (median 66 capilllaries/mm2; IQR 16–98) than of healthy controls (205 capilllaries/mm2; 157–226; p=0·005). Patients with GVHD had higher concentrations of vWF (238%; 168–288) than did those without GVHD (102%; 88–118; p=0·0005). Perivascular CD8 T cell infiltrates in skin correlated with vWF plasma concentrations in patients with GVHD (p=0·01), and activated cytotoxic T lymphocytes and endothelial injury were present in these same samples.
Host endothelial cells are a target of alloreactive donor cytotoxic T lymphocytes. Substantial blood vessel loss may lead to impaired blood perfusion and tissue fibrosis, the hallmark lesion of chronic GVHD.
Gliosis of retinal Mueller glial cells may have both beneficial and detrimental effects on neurons. To investigate the role of purinergic signaling in ischemia-induced reactive gliosis, transient ...retinal ischemia was evoked by elevation of the intraocular pressure in wild-type (Wt) mice and in mice deficient in the glia-specific nucleotide receptor P2Y sub(1) (P2Y sub(1) receptor-deficient (P2Y1R-KO)). While control retinae of P2Y1R-KO mice displayed reduced cell numbers in the ganglion cell and inner nuclear layers, ischemia induced apoptotic death of cells in all retinal layers in both, Wt and P2Y1R-KO mice, but the damage especially on photoreceptors was more pronounced in retinae of P2Y1R-KO mice. In contrast, gene expression profiling and histological data suggest an increased survival of amacrine cells in the postischemic retina of P2Y1R-KO mice. Interestingly, measuring the ischemia-induced downregulation of inwardly rectifying potassium channel (Kir)-mediated K super(+) currents as an indicator, reactive Mueller cell gliosis was found to be weaker in P2Y1R-KO (current amplitude decreased by 18%) than in Wt mice (decrease by 68%). The inner retina harbors those neurons generating action potentials, which strongly rely on an intact ion homeostasis. This may explain why especially these cells appear to benefit from the preserved Kir4.1 expression in Mueller cells, which should allow them to keep up their function in the context of spatial buffering of potassium. Especially under ischemic conditions, maintenance of this Mueller cell function may dampen cytotoxic neuronal hyperexcitation and subsequent neuronal cell loss. In sum, we found that purinergic signaling modulates the gliotic activation pattern of Mueller glia and lack of P2Y sub(1) has janus-faced effects. In the end, the differential effects of a disrupted P2Y sub(1) signaling onto neuronal survival in the ischemic retina call the putative therapeutical use of P2Y sub(1)-antagonists into question.
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