A new domestic procedure is described for the installation of “Atlant” anchor piles. Characteristic features and advantages over other procedures are presented.
The strength of adhesion of a reinforcing element to cement stone during anchor-pile installation, and its dependence on the composition of the cement grout and the surface condition of the ...reinforcing tube is examined.
We report four narrow peaks in the Ξ_{b}^{0}K^{-} mass spectrum obtained using pp collisions at center-of-mass energies of 7, 8, and 13 TeV, corresponding to a total integrated luminosity of 9 ...fb^{-1} recorded by the LHCb experiment. Referring to these states by their mass, the mass values are mΩ_{b}(6316)^{-}=6315.64±0.31±0.07±0.50 MeV, mΩ_{b}(6330)^{-}=6330.30±0.28±0.07±0.50 MeV, mΩ_{b}(6340)^{-}=6339.71±0.26±0.05±0.50 MeV, mΩ_{b}(6350)^{-}=6349.88±0.35±0.05±0.50 MeV, where the uncertainties are statistical, systematic, and the last is due to the knowledge of the Ξ_{b}^{0} mass. The natural widths of the three lower mass states are consistent with zero, and the 90% confidence-level upper limits are determined to be ΓΩ_{b}(6316)^{-}<2.8 MeV, ΓΩ_{b}(6330)^{-}<3.1 MeV and ΓΩ_{b}(6340)^{-}<1.5 MeV. The natural width of the Ω_{b}(6350)^{-} peak is 1.4_{-0.8}^{+1.0}±0.1 MeV, which is 2.5σ from zero and corresponds to an upper limit of 2.8 MeV. The peaks have local significances ranging from 3.6σ to 7.2σ. After accounting for the look-elsewhere effect, the significances of the Ω_{b}(6316)^{-} and Ω_{b}(6330)^{-} peaks are reduced to 2.1σ and 2.6σ, respectively, while the two higher mass peaks exceed 5σ. The observed peaks are consistent with expectations for excited Ω_{b}^{-} resonances.
Four members of the tumor necrosis factor (TNF) ligand family, TNF-α,
LT-α, LT-β, and LIGHT, interact with four receptors of the TNF/nerve
growth factor family, the p55 TNF receptor (CD120a), the p75 ...TNF receptor
(CD120b), the lymphotoxin beta receptor (LTβR), and herpes virus entry
mediator (HVEM) to control a wide range of innate and adaptive immune response
functions. Of these, the most thoroughly studied are cell death induction and
regulation of the inflammatory process. Fas/Apo1 (CD95), a receptor of the TNF
receptor family activated by a distinct ligand, induces death in cells through
mechanisms shared with CD120a. The last four years have seen a proliferation in
knowledge of the proteins participating in the signaling by the TNF system and
CD95. The downstream signaling molecules identified so far-caspases,
phospholipases, the three known mitogen activated protein (MAP) kinase
pathways, and the NF-κB activation cascade-mediate the effects of
other inducers as well. However, the molecules that initiate these signaling
events, including the death domain- and TNF receptor associated factor (TRAF)
domain-containing adapter proteins and the signaling enzymes associated with
them, are largely unique to the TNF/nerve growth factor receptor family.
We sought to describe the responses of patients to clopidogrel using ex vivo measures of platelet aggregation and activation in a large, heterogeneous population.
Recently, a number of reports, using ...various definitions, have dichotomized patients who are treated with clopidogrel into a minority of “non-responders” and a majority of “responders.” Such classifications imply that treatment leads to an all-or-none response, with potentially important clinical implications.
We conducted secondary post-hoc analyses of a dataset consisting of volunteers (n = 94) and patients after coronary stenting (n = 405), with heart failure (n = 25), and after stroke (n = 20).
The response of subjects to clopidogrel followed a normal, bell-shaped distribution, with a mean and standard deviation of 41.9 ± 20.8% when aggregation was induced by 5 μmol/l of adenosine diphosphate. When hyporesponsiveness and hyper-responsiveness to clopidogrel were considered to be two standard deviations less than and greater than the mean, respectively, the prevalence of hyporesponsiveness and hyper-responsiveness in these patients was 4.2% and 4.8%, respectively. Pretreatment platelet activity and clinical characteristics were not associated with responsiveness to clopidogrel.
Individuals receiving clopidogrel exhibit a wide variability in response that follows a normal distribution. The clinical implications of this variability are unknown but potentially are important. Clinical trials are needed to define whether hyporesponders to clopidogrel are at increased risk for thrombotic events and whether hyper-responders are at increased risk for bleeding. If so, the individualization of antiplatelet therapy, including clopidogrel dosing, may be possible in the future but will require the ability to easily and reproducibly measure responsiveness by a method that has been proven to be predictive of clinical events.
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