1,437 research outputs found
QCD
We discuss QCD studies that will be possible at LEP2. We examine both
experimental and theoretical aspects of jets, fragmentation functions,
multiplicities and particle spectra.Comment: 44 pages, Latex, epsfig, 18 figures, to appear on the Report of the
Workshop on Physics at LEP2, CERN 96-01, vol. 1, 199
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Fibroblast Growth Factorâ23 and Cardiac Structure and Function
Background: Fibroblast growth factorâ23 (FGFâ23) is a phosphaturic factor previously associated with left ventricular hypertrophy and systolic dysfunction among individuals with chronic kidney disease. Whether FGFâ23 acts directly to induce left ventricular hypertrophy, potentially independent of its klotho coreceptor, remains uncertain. We investigated associations of FGFâ23 with cardiac structural abnormalities among individuals with a broad range of kidney function and explored potential biological mechanisms using cardiac magnetic resonance imaging and histology in klothoânull mice, an established model of constitutively elevated FGFâ23. Methods and Results: Among 887 participants with coronary artery disease in the Heart and Soul Study, FGFâ23 was modestly associated with worse left ventricular ejection fraction (â1.0% per standard deviation increase in lnFGFâ23; standard error, 0.4%), but was not associated with the overall prevalence of concentric hypertrophy (odds ratio, 1.5; CI, 0.9 to 2.4) or eccentric hypertrophy (odds ratio, 1.1; CI, 0.9 to 1.3). FGFâ23 was only associated with concentric hypertrophy among individuals with diminished kidney function (eGFR <60 mL/min per 1.73 m2; odds ratio, 2.3; CI, 1.0 to 5.3; Pâinteraction=0.28). Comparing klothoânull with wildâtype mice, null mice did not have greater left ventricular mass (P=0.37) or a lower ejection fraction (P=0.94). Conclusions: Together, our results suggest that FGFâ23 is unlikely to have major effects on cardiovascular structure and function among patients free of substantial chronic kidney disease, and these effects may not be independent of the klotho coreceptor
The skeletal phenotype of chondroadherin deficient mice
Chondroadherin, a leucine rich repeat extracellular matrix protein with functions in cell to matrix interactions, binds cells via their a2b1 integrin as well as via cell surface proteoglycans, providing for different sets of signals to the cell. Additionally, the protein acts as an anchor to the matrix by binding tightly to collagens type I and II as well as type VI. We generated mice with inactivated chondroadherin gene to provide integrated studies of the role of the protein. The null mice presented distinct phenotypes with affected cartilage as well as bone. At 3â6 weeks of age the epiphyseal growth plate was widened most pronounced in the proliferative zone. The proteome of the femoral head articular cartilage at 4 months of age showed some distinct differences, with increased deposition of cartilage intermediate layer protein 1 and fibronectin in the chondroadherin deficient mice, more pronounced in the female. Other proteins show decreased levels in the deficient mice, particularly pronounced for matrilin-1, thrombospondin-1 and notably the members of the a1-antitrypsin family of proteinase inhibitors as well as for a member of the bone morphogenetic protein growth factor family. Thus, cartilage homeostasis is distinctly altered. The bone phenotype was expressed in several ways. The number of bone sialoprotein mRNA expressing cells in the proximal tibial metaphysic was decreased and the osteoid surface was increased possibly indicating a change in mineral metabolism. Micro-CT revealed lower cortical thickness and increased structure model index, i.e. the amount of plates and rods composing the bone trabeculas. The structural changes were paralleled by loss of function, where the null mice showed lower femoral neck failure load and tibial strength during mechanical testing at 4 months of age. The skeletal phenotype points at a role for chondroadherin in both bone and cartilage homeostasis, however, without leading to altered longitudinal growth
Deletion of PTH Rescues Skeletal Abnormalities and High Osteopontin Levels in Klothoâ/â Mice
Maintenance of normal mineral ion homeostasis is crucial for many biological activities, including proper mineralization of the skeleton. Parathyroid hormone (PTH), Klotho, and FGF23 have been shown to act as key regulators of serum calcium and phosphate homeostasis through a complex feedback mechanism. The phenotypes of Fgf23â/â and Klothoâ/â (Klâ/â) mice are very similar and include hypercalcemia, hyperphosphatemia, hypervitaminosis D, suppressed PTH levels, and severe osteomalacia/osteoidosis. We recently reported that complete ablation of PTH from Fgf23â/â mice ameliorated the phenotype in Fgf23â/â/PTHâ/â mice by suppressing serum vitamin D and calcium levels. The severe osteomalacia in Fgf23â/â mice, however, persisted, suggesting that a different mechanism is responsible for this mineralization defect. In the current study, we demonstrate that deletion of PTH from Klâ/â (Klâ/â/PTHâ/â or DKO) mice corrects the abnormal skeletal phenotype. Bone turnover markers are restored to wild-type levels; and, more importantly, the skeletal mineralization defect is completely rescued in Klâ/â/PTHâ/â mice. Interestingly, the correction of the osteomalacia is accompanied by a reduction in the high levels of osteopontin (Opn) in bone and serum. Such a reduction in Opn levels could not be observed in Fgf23â/â/PTHâ/â mice, and these mice showed sustained osteomalacia. This significant in vivo finding is corroborated by in vitro studies using calvarial osteoblast cultures that show normalized Opn expression and rescued mineralization in Klâ/â/PTHâ/â mice. Moreover, continuous PTH infusion of Klâ/â mice significantly increased Opn levels and osteoid volume, and decreased trabecular bone volume. In summary, our results demonstrate for the first time that PTH directly impacts the mineralization disorders and skeletal deformities of Klâ/â, but not of Fgf23â/â mice, possibly by regulating Opn expression. These are significant new perceptions into the role of PTH in skeletal and disease processes and suggest FGF23-independent interactions of PTH with Klotho
Genetic Evidence of Serum Phosphate-Independent Functions of FGF-23 on Bone
Maintenance of physiologic phosphate balance is of crucial biological importance, as it is fundamental to cellular function, energy metabolism, and skeletal mineralization. Fibroblast growth factor-23 (FGF-23) is a master regulator of phosphate homeostasis, but the molecular mechanism of such regulation is not yet completely understood. Targeted disruption of the Fgf-23 gene in mice (Fgf-23â/â) elicits hyperphosphatemia, and an increase in renal sodium/phosphate co-transporter 2a (NaPi2a) protein abundance. To elucidate the pathophysiological role of augmented renal proximal tubular expression of NaPi2a in Fgf-23â/â mice and to examine serum phosphateâindependent functions of Fgf23 in bone, we generated a new mouse line deficient in both Fgf-23 and NaPi2a genes, and determined the effect of genomic ablation of NaPi2a from Fgf-23â/â mice on phosphate homeostasis and skeletal mineralization. Fgf-23â/â/NaPi2aâ/â double mutant mice are viable and exhibit normal physical activities when compared to Fgf-23â/â animals. Biochemical analyses show that ablation of NaPi2a from Fgf-23â/â mice reversed hyperphosphatemia to hypophosphatemia by 6 weeks of age. Surprisingly, despite the complete reversal of serum phosphate levels in Fgf-23â/â/NaPi2aâ/â, their skeletal phenotype still resembles the one of Fgf23â/â animals. The results of this study provide the first genetic evidence of an in vivo pathologic role of NaPi2a in regulating abnormal phosphate homeostasis in Fgf-23â/â mice by deletion of both NaPi2a and Fgf-23 genes in the same animal. The persistence of the skeletal anomalies in double mutants suggests that Fgf-23 affects bone mineralization independently of systemic phosphate homeostasis. Finally, our data support (1) that regulation of phosphate homeostasis is a systemic effect of Fgf-23, while (2) skeletal mineralization and chondrocyte differentiation appear to be effects of Fgf-23 that are independent of phosphate homeostasis
Search for Yukawa Production of a Light Neutral Higgs Boson at LEP
Within a Two-Higgs-Doublet Model (2HDM) a search for a light Higgs boson in
the mass range of 4-12 GeV has been performed in the Yukawa process e+e- -> b
bbar A/h -> b bbar tau+tau-, using the data collected by the OPAL detector at
LEP between 1992 and 1995 in e+e- collisions at about 91 GeV centre-of-mass
energy. A likelihood selection is applied to separate background and signal.
The number of observed events is in good agreement with the expected
background. Within a CP-conserving 2HDM type II model the cross-section for
Yukawa production depends on xiAd = |tan beta| and xihd = |sin alpha/cos beta|
for the production of the CP-odd A and the CP-even h, respectively, where tan
beta is the ratio of the vacuum expectation values of the Higgs doublets and
alpha is the mixing angle between the neutral CP-even Higgs bosons. From our
data 95% C.L. upper limits are derived for xiAd within the range of 8.5 to 13.6
and for xihd between 8.2 to 13.7, depending on the mass of the Higgs boson,
assuming a branching fraction into tau+tau- of 100%. An interpretation of the
limits within a 2HDM type II model with Standard Model particle content is
given. These results impose constraints on several models that have been
proposed to explain the recent BNL measurement of the muon anomalous magnetic
moment.Comment: 24 pages, 9 figures, Submitted to Euro. Phys. J.
Search for the Standard Model Higgs Boson with the OPAL Detector at LEP
This paper summarises the search for the Standard Model Higgs boson in e+e-
collisions at centre-of-mass energies up to 209 GeV performed by the OPAL
Collaboration at LEP. The consistency of the data with the background
hypothesis and various Higgs boson mass hypotheses is examined. No indication
of a signal is found in the data and a lower bound of 112.7GeV/C^2 is obtained
on the mass of the Standard Model Higgs boson at the 95% CL.Comment: 51 pages, 21 figure
Tests of model of color reconnection and a search for glueballs using gluon jets with a rapidity gap
Gluon jets with a mean energy of 22 GeV and purity of 95% are selected from
hadronic Z0 decay events produced in e+e- annihilations. A subsample of these
jets is identified which exhibits a large gap in the rapidity distribution of
particles within the jet. After imposing the requirement of a rapidity gap, the
gluon jet purity is 86%. These jets are observed to demonstrate a high degree
of sensitivity to the presence of color reconnection, i.e. higher order QCD
processes affecting the underlying color structure. We use our data to test
three QCD models which include a simulation of color reconnection: one in the
Ariadne Monte Carlo, one in the Herwig Monte Carlo, and the other by Rathsman
in the Pythia Monte Carlo. We find the Rathsman and Ariadne color reconnection
models can describe our gluon jet measurements only if very large values are
used for the cutoff parameters which serve to terminate the parton showers, and
that the description of inclusive Z0 data is significantly degraded in this
case. We conclude that color reconnection as implemented by these two models is
disfavored. The signal from the Herwig color reconnection model is less clear
and we do not obtain a definite conclusion concerning this model. In a separate
study, we follow recent theoretical suggestions and search for glueball-like
objects in the leading part of the gluon jets. No clear evidence is observed
for these objects.Comment: 42 pages, 18 figure
Scaling violations of quark and gluon jet fragmentation functions in e+e- annihilations at sqrt(s) = 91.2 and 183-209 GeV
Flavour inclusive, udsc and b fragmentation functions in unbiased jets, and
flavour inclusive, udsc, b and gluon fragmentation functions in biased jets are
measured in e+e- annihilations from data collected at centre-of-mass energies
of 91.2, and 183-209 GeV with the OPAL detector at LEP. The unbiased jets are
defined by hemispheres of inclusive hadronic events, while the biased jet
measurements are based on three-jet events selected with jet algorithms.
Several methods are employed to extract the fragmentation functions over a wide
range of scales. Possible biases are studied in the results are obtained. The
fragmentation functions are compared to results from lower energy e+e-
experiments and with earlier LEP measurements and are found to be consistent.
Scaling violations are observed and are found to be stronger for the
fragmentation functions of gluon jets than for those of quarks. The measured
fragmentation functions are compared to three recent theoretical
next-to-leading order calculations and to the predictions of three Monte Carlo
event generators. While the Monte Carlo models are in good agreement with the
data, the theoretical predictions fail to describe the full set of results, in
particular the b and gluon jet measurements.Comment: 46 pages, 17 figures, Submitted to Eur. Phys J.
Measurement of the Hadronic Cross-Section for the Scattering of Two Virtual Photons at LEP
The interaction of virtual photons is investigated using the reaction e+e- ->
e+e- hadrons based on data taken by the OPAL experiment at e+e- centre-of-mass
energies sqrt(s_ee)=189-209 GeV, for W>5 GeV and at an average Q^2 of 17.9
GeV^2. The measured cross-sections are compared to predictions of the Quark
Parton Model (QPM), to the Leading Order QCD Monte Carlo model PHOJET to the
NLO prediction for the reaction e+e- -> e+e-qqbar, and to BFKL calculations.
PHOJET, NLO e+e- -> e+e-qqbar, and QPM describe the data reasonably well,
whereas the cross-section predicted by a Leading Order BFKL calculation is too
large.Comment: 30 pages, 10 figures, Submitted to Eur.Phys.J.
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