82 research outputs found
signals at LEP2 energies in the Minimal Supersymmetric Standard Model
In this paper we compare and into four-fermion production
at centre-of-mass energies typical of LEP2 and somewhat larger. The theoretical
framework considered is the Minimal Supersymmetric Standard Model. The interest
in exploiting the CERN collider at values of greater than
192 GeV could come from the discovery of Supersymmetric signals during runs at
lower energy. If these indicate that a charged Higgs boson exists in the mass
range \MH\approx95-105 GeV, then a few years of running at
GeV and nominal luminosity could make the detection of such scalars feasible,
in the purely leptonic channel and, for small
\tb's, also in the semi-hadronic(leptonic) one . Charged
Higgs bosons of the above nature cannot be produced by the beam energies
approved at present for LEP2. However, if runs beyond the so-called `192 GeV
cryogenic limit' will be approved by the CERN Council, our selection procedure
will enable us to establish the presence, or otherwise, of charged Higgs bosons
in the mentioned mass rangeComment: 30 pages, latex, epsfig, 12 postscript figures, complete paper
available at ftp://axpa.hep.phy.cam.ac.uk/stefano/cavendish_9615 and at
http://www.hep.phy.cam.ac.uk/theory/papers
The Anisotropic Elasticity of the Human Vocal Fold
A review of the work carried out jointly with UKE Hamburg, which demostrated the anisotropic nature of the human vocal folds. This additional work presents collagen and elastin stains to support that research.
APC paid for Open AccessObjective: To verify the anisotropic nature of the vocal folds by
reproducing an experiment led by Rholfs that measured vocal fold
elasticity in the transverse and longitudinal directions. To present
a physiological explanation of the measured phenomena using
immunochemical results.
Methods: 6 cadaveric human excised larynges were hemi-sectioned
in the mid-sagittal plane exposing the vocal folds, and orthogonal
measurements of tension made at 3 equally spaced points.
Immunohistochemistry carried out by Ichiro Tateya was used to
visualise collagens and elastins in the deep layer of the lamina propria.
Results: The LSR results indicate that the measured elasticity of
the vocal folds are highly anisotropic. The immunohistochemistry
results show that there is a strong alignment of collagens and
elastins along the longitudinal axis of human vocal folds.
Conclusion: The measured anisotropic behaviour is due to the
alignment of collagens & elastins in the lamina propri
ALPGEN, a generator for hard multiparton processes in hadronic collisions
This paper presents a new event generator, ALPGEN, dedicated to the study of
multiparton hard processes in hadronic collisions. The code performs, at the
leading order in QCD and EW interactions, the calculation of the exact matrix
elements for a large set of parton-level processes of interest in the study of
the Tevatron and LHC data. The current version of the code describes the
following final states: (W -> ffbar') QQbar+ N jets (Q being a heavy quark, and
f=l,q), with N f fbar)+QQbar+Njets (f=l,nu), with N
ffbar') + charm + N jets (f=l,q), N f fbar') + N jets (f=l,q) and
(Z/gamma* -> f fbar)+ N jets (f=l,nu), with N<=6; nW+mZ+lH+N jets, with
n+m+l+N<=8 and N<=3 including all 2-fermion decay modes of W and Z bosons, with
spin correlations; Q Qbar+N jets (N b f fbar' decays and relative
spin correlations included if Q=t; Q Qbar Q' Qbar'+N jets, with Q and Q' heavy
quarks (possibly equal) and N b f fbar'
decays and relative spin correlations included if Q=t; N jets, with N<=6.
Parton-level events are generated, providing full information on their colour
and flavour structure, enabling the evolution of the partons into fully
hadronised final states.Comment: 1+38 pages, uses JHEP.cls. Documents code version 1.2: extended list
of processes, updated documentation and bibliograph
Chemerin regulates Ξ²-cell function in mice
Although various function of chemerin have been suggested, its physiological role remains to be elucidated. Here we show that chemerin-deficient mice are glucose intolerant irrespective of exhibiting reduced macrophage accumulation in adipose tissue. The glucose intolerance was mainly due to increased hepatic glucose production and impaired insulin secretion. Chemerin and its receptor ChemR23 were expressed in Ξ²-cell. Studies using isolated islets and perfused pancreas revealed impaired glucose-dependent insulin secretion (GSIS) in chemerin-deficient mice. Conversely, chemerin transgenic mice revealed enhanced GSIS and improved glucose tolerance. Expression of MafA, a pivotal transcriptional factor for Ξ²-cell function, was downregulated in chemerin-deficient islets and a chemerin-ablated Ξ²-cell line and rescue of MafA expression restored GSIS, indicating that chemerin regulates Ξ²-cell function via maintaining MafA expression. These results indicate that chemerin regulates Ξ²-cell function and plays an important role in glucose homeostasis in a tissue-dependent manner
Standard Model Large-E_T Processes and Searches for New Physics at HERA
Existing and missing calculations of standard model processes producing large
transverse energy in electron-proton interactions at HERA are reviewed. The
adequacy of the existing standard model Monte Carlo programs for generic
searches of exotic processes is analyzed.Comment: 9 pages, LaTeX, uses iop style files, Contribution to the 3rd UK
Phenomenology Workshop on HERA Physics, September 1998, Durha
Apolipoprotein A-I Attenuates Palmitate-Mediated NF-ΞΊB Activation by Reducing Toll-Like Receptor-4 Recruitment into Lipid Rafts
While high-density lipoprotein (HDL) is known to protect against a wide range of inflammatory stimuli, its anti-inflammatory mechanisms are not well understood. Furthermore, HDL's protective effects against saturated dietary fats have not been previously described. In this study, we used endothelial cells to demonstrate that while palmitic acid activates NF-ΞΊB signaling, apolipoprotein AβI, (apoA-I), the major protein component of HDL, attenuates palmitate-induced NF-ΞΊB activation. Further, vascular NF-ΞΊB signaling (IL-6, MCP-1, TNF-Ξ±) and macrophage markers (CD68, CD11c) induced by 24 weeks of a diabetogenic diet containing cholesterol (DDC) is reduced in human apoA-I overexpressing transgenic C57BL/6 mice compared to age-matched WT controls. Moreover, WT mice on DDC compared to a chow diet display increased gene expression of lipid raft markers such as Caveolin-1 and Flotillin-1, and inflammatory Toll-like receptors (TLRs) (TLR2, TLR4) in the vasculature. However apoA-I transgenic mice on DDC show markedly reduced expression of these genes. Finally, we show that in endothelial cells TLR4 is recruited into lipid rafts in response to palmitate, and that apoA-I prevents palmitate-induced TLR4 trafficking into lipid rafts, thereby blocking NF-ΞΊB activation. Thus, apoA-I overexpression might be a useful therapeutic tool against vascular inflammation
The Prosensory Function of Sox2 in the Chicken Inner Ear Relies on the Direct Regulation of Atoh1
The proneural gene Atoh1 is crucial for the development of inner ear hair cells and it requires the function of the transcription factor Sox2 through yet unknown mechanisms. In the present work, we used the chicken embryo and HEK293T cells to explore the regulation of Atoh1 by Sox2. The results show that hair cells derive from Sox2-positive otic progenitors and that Sox2 directly activates Atoh1 through a transcriptional activator function that requires the integrity of Sox2 DNA binding domain. Atoh1 activation depends on Sox transcription factor binding sites (SoxTFBS) present in the Atoh1 3β² enhancer where Sox2 directly binds, as shown by site directed mutagenesis and chromatin immunoprecipitation (ChIP). In the inner ear, Atoh1 enhancer activity is detected in the neurosensory domain and it depends on Sox2. Dominant negative competition (Sox2HMG-Engrailed) and mutation of the SoxTFBS abolish the reporter activity in vivo. Moreover, ChIP assay in isolated otic vesicles shows that Sox2 is bound to the Atoh1 enhancer in vivo. However, besides activating Atoh1, Sox2 also promotes the expression of Atoh1 negative regulators and the temporal profile of Atoh1 activation by Sox2 is transient suggesting that Sox2 triggers an incoherent feed-forward loop. These results provide a mechanism for the prosensory function of Sox2 in the inner ear. We suggest that sensory competence is established early in otic development through the activation of Atoh1 by Sox2, however, hair cell differentiation is prevented until later stages by the parallel activation of negative regulators of Atoh1 function
MCP-1 Upregulates Amylin Expression in Murine Pancreatic Ξ² Cells through ERK/JNK-AP1 and NF-ΞΊB Related Signaling Pathways Independent of CCR2
BACKGROUND: Amylin is the most abundant component of islet amyloid implicated in the development of type 2 diabetes. Plasma amylin levels are elevated in individuals with obesity and insulin resistance. Monocyte chemoattractant protein-1 (MCP-1, CCL2) is involved in insulin resistance of obesity and type 2 diabetes. We investigated the effect of MCP-1 on amylin expression and the underlying mechanisms with murine pancreatic Ξ²-cell line MIN6 and pancreatic islets. METHODOLOGY/PRINCIPAL FINDINGS: We found that MCP-1 induced amylin expression at transcriptional level and increased proamylin and intermediate forms of amylin at protein level in MIN6 cells and islets. However, MCP-1 had no effect on the expressions of proinsulin 1 and 2, as well as prohormone convertase (PC) 1/3 and PC2, suggesting that MCP-1 specifically induces amylin expression in Ξ²-cells. Mechanistic studies showed that although there is no detectable CCR2 mRNA in MIN6 cells and islets, pretreatment of MIN6 cells with pertussis toxin inhibited MCP-1 induced amylin expression, suggesting that alternative Gi-coupled receptor(s) mediates the inductive effect of MCP-1. MCP-1 rapidly induced ERK1/2 and JNK phosphorylation. Inhibitors for MEK1/2 (PD98059), JNK (SP600125) or AP1 (curcumin) significantly inhibited MCP-1-induced amylin mRNA expression. MCP-1 failed to induce amylin expression in pancreatic islets isolated from Fos knockout mice. EMSA showed that JNK and ERK1/2 were involved in MCP-1-induced AP1 activation. These results suggest that MCP-1 induces murine amylin expression through AP1 activation mediated by ERK1/2 or JNK. Further studies showed that treatment of MIN6 cells with NF-ΞΊB inhibitor or overexpression of IΞΊBΞ± dominant-negative construct in MIN6 cells significantly inhibited MCP-1-induced amylin expression, suggesting that NF-ΞΊB related signaling also participates in MCP-1-induced murine amylin expression. CONCLUSIONS/SIGNIFICANCE: MCP-1 induces amylin expression through ERK1/2/JNK-AP1 and NF-ΞΊB related signaling pathways independent of CCR2. Amylin upregulation by MCP-1 may contribute to elevation of plasma amylin in obesity and insulin resistance
A Patient-Specific in silico Model of Inflammation and Healing Tested in Acute Vocal Fold Injury
The development of personalized medicine is a primary objective of the medical community and increasingly also of funding and registration agencies. Modeling is generally perceived as a key enabling tool to target this goal. Agent-Based Models (ABMs) have previously been used to simulate inflammation at various scales up to the whole-organism level. We extended this approach to the case of a novel, patient-specific ABM that we generated for vocal fold inflammation, with the ultimate goal of identifying individually optimized treatments. ABM simulations reproduced trajectories of inflammatory mediators in laryngeal secretions of individuals subjected to experimental phonotrauma up to 4 hrs post-injury, and predicted the levels of inflammatory mediators 24 hrs post-injury. Subject-specific simulations also predicted different outcomes from behavioral treatment regimens to which subjects had not been exposed. We propose that this translational application of computational modeling could be used to design patient-specific therapies for the larynx, and will serve as a paradigm for future extension to other clinical domains
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