1,047 research outputs found
TLR4-dependent claudin-1 internalization and secretagogue-mediated chloride secretion regulate irinotecan-induced diarrhea
Published OnlineFirst August 22, 2016Abstract not availableHannah R.Wardill, Joanne M. Bowen, Ysabella Z.A. Van Sebille, Kate R. Secombe, Janet K. Coller, Imogen A. Ball, Richard M. Logan, and Rachel J Gibso
Irinotecan-induced gastrointestinal dysfunction and pain are mediated by common TLR4-dependent mechanisms
Published Online First March 29, 2016Abstract not availableHannah R. Wardill, Rachel J. Gibson, Ysabella Z.A. Van Sebille, Kate R. Secombe, Janet K. Coller, Imogen A. White, Jim Manavis, Mark R. Hutchinson, Vasiliki Staikopoulos, Richard M. Logan, and Joanne M. Bowe
Measurement of the branching ratios of the Z0 into heavy quarks
We measure the hadronic branching ratios of the Z0 boson into heavy quarks:
Rb=Gamma(Z0->bb)/Gamma(Z0->hadrons) and Rc=Gamma(Z0->cc/Gamma(Z0->hadrons)
using a multi-tag technique. The measurement was performed using about 400,000
hadronic Z0 events recorded in the SLD experiment at SLAC between 1996 and
1998. The small and stable SLC beam spot and the CCD-based vertex detector were
used to reconstruct bottom and charm hadron decay vertices with high efficiency
and purity, which enables us to measure most efficiencies from data. We obtain,
Rb=0.21604 +- 0.00098(stat.) +- 0.00073(syst.) -+ 0.00012(Rc) and, Rc= 0.1744
+- 0.0031(stat.) +- 0.0020(syst.) -+ 0.0006(Rb)Comment: 37 pages, 8 figures, to be submitted to Phys. Rev. D version 2:
changed title to ratios, used common D production fractions for Rb and Rc and
corrected Zgamma interference. Identical to PRD submissio
Direct Measurements of A_b and A_c using Vertex/Kaon Charge Tags at SLD
Exploiting the manipulation of the SLC electron-beam polarization, we present
precise direct measurements of the parity violation parameters A_c and A_b in
the Z boson - c quark and Z boson - b quark coupling. Quark/antiquark
discrimination is accomplished via a unique algorithm that takes advantage of
the precise SLD CCD vertex detector, employing the net charge of displaced
vertices as well as the charge of kaons that emanate from those vertices. From
the 1996-98 sample of 400,000 Z decays, produced with an average beam
polarization of 73.4%, we find A_c = 0.673 +/- 0.029 (stat.) +/- 0.023 (syst.)
and A_b = 0.919 +/- 0.018 (stat.) +/- 0.017 (syst.).Comment: 11 pages, 2 figures, 2 tables, to be submitted to Physical Review
Letters; version 2 reflects changes suggested by the refere
A Search for Jet Handedness in Hadronic Decays
We have searched for signatures of polarization in hadronic jets from decays using the ``jet handedness'' method. The polar angle
asymmetry induced by the high SLC electron-beam polarization was used to
separate quark jets from antiquark jets, expected to be left- and
right-polarized, respectively. We find no evidence for jet handedness in our
global sample or in a sample of light quark jets and we set upper limits at the
95% C.L. of 0.063 and 0.099 respectively on the magnitude of the analyzing
power of the method proposed by Efremov {\it et al.}Comment: Revtex, 8 pages, 2 figure
Platelets generated from human embryonic stem cells are functional in vitro and in the microcirculation of living mice
Platelets play an essential role in hemostasis and atherothrombosis. Owing to their short storage time, there is constant demand for this life-saving blood component. In this study, we report that it is feasible to generate functional megakaryocytes and platelets from human embryonic stem cells (hESCs) on a large scale. Differential-interference contrast and electron microscopy analyses showed that ultrastructural and morphological features of hESC-derived platelets were indistinguishable from those of normal blood platelets. In functional assays, hESC-derived platelets responded to thrombin stimulation, formed microaggregates, and facilitated clot formation/retraction in vitro. Live cell microscopy demonstrated that hESC-platelets formed lamellipodia and filopodia in response to thrombin activation, and tethered to each other as observed in normal blood. Using real-time intravital imaging with high-speed video microscopy, we have also shown that hESC-derived platelets contribute to developing thrombi at sites of laser-induced vascular injury in mice, providing the first evidence for in vivo functionality of hESC-derived platelets. These results represent an important step toward generating an unlimited supply of platelets for transfusion. Since platelets contain no genetic material, they are ideal candidates for early clinical translation involving human pluripotent stem cells
Dental management considerations for the patient with an acquired coagulopathy. Part 1: Coagulopathies from systemic disease
Current teaching suggests that many patients are at risk for prolonged bleeding during and following invasive dental procedures, due to an acquired coagulopathy from systemic disease and/or from medications. However, treatment standards for these patients often are the result of long-standing dogma with little or no scientific basis. The medical history is critical for the identification of patients potentially at risk for prolonged bleeding from dental treatment. Some time-honoured laboratory tests have little or no use in community dental practice. Loss of functioning hepatic, renal, or bone marrow tissue predisposes to acquired coagulopathies through different mechanisms, but the relationship to oral haemostasis is poorly understood. Given the lack of established, science-based standards, proper dental management requires an understanding of certain principles of pathophysiology for these medical conditions and a few standard laboratory tests. Making changes in anticoagulant drug regimens are often unwarranted and/or expensive, and can put patients at far greater risk for morbidity and mortality than the unlikely outcome of postoperative bleeding. It should be recognised that prolonged bleeding is a rare event following invasive dental procedures, and therefore the vast majority of patients with suspected acquired coagulopathies are best managed in the community practice setting
The mTOR-Regulated Phosphoproteome Reveals a Mechanism of mTORC1-Mediated Inhibition of Growth Factor Signaling
September 21 Author ManuscriptThe mammalian target of rapamycin (mTOR) protein kinase is a master growth promoter that nucleates two complexes, mTORC1 and mTORC2. Despite the diverse processes controlled by mTOR, few substrates are known. We defined the mTOR-regulated phosphoproteome by quantitative mass spectrometry and characterized the primary sequence motif specificity of mTOR using positional scanning peptide libraries. We found that the phosphorylation response to insulin is largely mTOR dependent and that mTOR exhibits a unique preference for proline, hydrophobic, and aromatic residues at the +1 position. The adaptor protein Grb10 was identified as an mTORC1 substrate that mediates the inhibition of phosphoinositide 3-kinase typical of cells lacking tuberous sclerosis complex 2 (TSC2), a tumor suppressor and negative regulator of mTORC1. Our work clarifies how mTORC1 inhibits growth factor signaling and opens new areas of investigation in mTOR biology.National Institutes of Health (U.S.) (Grant CA103866)National Institutes of Health (U.S.) (Grant AI47389)United States. Department of Defense (W81XWH-07-0448)W. M. Keck FoundationLAM FoundationAmerican Cancer SocietyHoward Hughes Medical Institute (Investigator
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