1,400 research outputs found
On Glauber modes in Soft-Collinear Effective Theory
Gluon interactions involving spectator partons in collisions at hadronic
machines are investigated. We find a class of examples in which a mode, called
Glauber gluons, must be introduced to the effective theory for consistency.Comment: 19 pages, three figures. Uses JHEP3.cl
Sudden infant death syndrome due to long QT syndrome: a brief review of the genetic substrate and prevalence
Next-to-eikonal corrections to soft gluon radiation: a diagrammatic approach
We consider the problem of soft gluon resummation for gauge theory amplitudes
and cross sections, at next-to-eikonal order, using a Feynman diagram approach.
At the amplitude level, we prove exponentiation for the set of factorizable
contributions, and construct effective Feynman rules which can be used to
compute next-to-eikonal emissions directly in the logarithm of the amplitude,
finding agreement with earlier results obtained using path-integral methods.
For cross sections, we also consider sub-eikonal corrections to the phase space
for multiple soft-gluon emissions, which contribute to next-to-eikonal
logarithms. To clarify the discussion, we examine a class of log(1 - x) terms
in the Drell-Yan cross-section up to two loops. Our results are the first steps
towards a systematic generalization of threshold resummations to
next-to-leading power in the threshold expansion.Comment: 66 pages, 19 figure
Parton Fragmentation within an Identified Jet at NNLL
The fragmentation of a light parton i to a jet containing a light energetic
hadron h, where the momentum fraction of this hadron as well as the invariant
mass of the jet is measured, is described by "fragmenting jet functions". We
calculate the one-loop matching coefficients J_{ij} that relate the fragmenting
jet functions G_i^h to the standard, unpolarized fragmentation functions D_j^h
for quark and gluon jets. We perform this calculation using various IR
regulators and show explicitly how the IR divergences cancel in the matching.
We derive the relationship between the coefficients J_{ij} and the quark and
gluon jet functions. This provides a cross-check of our results. As an
application we study the process e+ e- to X pi+ on the Upsilon(4S) resonance
where we measure the momentum fraction of the pi+ and restrict to the dijet
limit by imposing a cut on thrust T. In our analysis we sum the logarithms of
tau=1-T in the cross section to next-to-next-to-leading-logarithmic accuracy
(NNLL). We find that including contributions up to NNLL (or NLO) can have a
large impact on extracting fragmentation functions from e+ e- to dijet + h.Comment: expanded introduction, typos fixed, journal versio
Non-global Structure of the O({\alpha}_s^2) Dijet Soft Function
High energy scattering processes involving jets generically involve matrix
elements of light- like Wilson lines, known as soft functions. These describe
the structure of soft contributions to observables and encode color and
kinematic correlations between jets. We compute the dijet soft function to
O({\alpha}_s^2) as a function of the two jet invariant masses, focusing on
terms not determined by its renormalization group evolution that have a
non-separable dependence on these masses. Our results include non-global single
and double logarithms, and analytic results for the full set of non-logarithmic
contributions as well. Using a recent result for the thrust constant, we
present the complete O({\alpha}_s^2) soft function for dijet production in both
position and momentum space.Comment: 55 pages, 8 figures. v2: extended discussion of double logs in the
hard regime. v3: minor typos corrected, version published in JHEP. v4: typos
in Eq. (3.33), (3.39), (3.43) corrected; this does not affect the main
result, numerical results, or conclusion
Inhibition of cerebrovascular raf activation attenuates cerebral blood flow and prevents upregulation of contractile receptors after subarachnoid hemorrhage
<p>Abstract</p> <p>Background</p> <p>Late cerebral ischemia carries high morbidity and mortality after subarachnoid hemorrhage (SAH) due to reduced cerebral blood flow (CBF) and the subsequent cerebral ischemia which is associated with upregulation of contractile receptors in the vascular smooth muscle cells (SMC) via activation of mitogen-activated protein kinase (MAPK) of the extracellular signal-regulated kinase (ERK)1/2 signal pathway. We hypothesize that SAH initiates cerebrovascular ERK1/2 activation, resulting in receptor upregulation. The raf inhibitor will inhibit the molecular events upstream ERK1/2 and may provide a therapeutic window for treatment of cerebral ischemia after SAH.</p> <p>Results</p> <p>Here we demonstrate that SAH increases the phosphorylation level of ERK1/2 in cerebral vessels and reduces the neurology score in rats in additional with the CBF measured by an autoradiographic method. The intracisternal administration of SB-386023-b, a specific inhibitor of raf, given 6 h after SAH, aborts the receptor changes and protects the brain from the development of late cerebral ischemia at 48 h. This is accompanied by reduced phosphorylation of ERK1/2 in cerebrovascular SMC. SAH per se enhances contractile responses to endothelin-1 (ET-1), 5-carboxamidotryptamine (5-CT) and angiotensin II (Ang II), upregulates ET<sub>B</sub>, 5-HT<sub>1B </sub>and AT<sub>1 </sub>receptor mRNA and protein levels. Treatment with SB-386023-b given as late as at 6 h but not at 12 h after the SAH significantly decreased the receptor upregulation, the reduction in CBF and the neurology score.</p> <p>Conclusion</p> <p>These results provide evidence for a role of the ERK1/2 pathway in regulation of expression of cerebrovascular SMC receptors. It is suggested that raf inhibition may reduce late cerebral ischemia after SAH and provides a realistic time window for therapy.</p
Quantification of the response of circulating epithelial cells to neodadjuvant treatment for breast cancer: a new tool for therapy monitoring
INTRODUCTION: In adjuvant treatment for breast cancer there is no tool available with which to measure the efficacy of the therapy. In contrast, in neoadjuvant therapy reduction in tumour size is used as an indicator of the sensitivity of tumour cells to the agents applied. If circulating epithelial (tumour) cells can be shown to react to therapy in the same way as the primary tumour, then this response may be exploited to monitor the effect of therapy in the adjuvant setting. METHOD: We used MAINTRAC(® )analysis to monitor the reduction in circulating epithelial cells during the first three to four cycles of neoadjuvant therapy in 30 breast cancer patients. RESULTS: MAINTRAC(® )analysis revealed a patient-specific response. Comparison of this response with the decline in size of the primary tumour showed that the reduction in number of circulating epithelial cells accurately predicted final tumour reduction at surgery if the entire neoadjuvant regimen consisted of chemotherapy. However, the response of the circulating tumour cells was unable to predict the response to additional antibody therapy. CONCLUSION: The response of circulating epithelial cells faithfully reflects the response of the whole tumour to adjuvant therapy, indicating that these cells may be considered part of the tumour and can be used for therapy monitoring
Anti-müllerian hormone is not associated with cardiometabolic risk factors in adolescent females
<p>Objectives: Epidemiological evidence for associations of Anti-Müllerian hormone (AMH) with cardiometabolic risk factors is lacking. Existing evidence comes from small studies in select adult populations, and findings are conflicting. We aimed to assess whether AMH is associated with cardiometabolic risk factors in a general population of adolescent females.</p>
<p>Methods: AMH, fasting insulin, glucose, HDLc, LDLc, triglycerides and C-reactive protein (CRP) were measured at a mean age 15.5 years in 1,308 female participants in the Avon Longitudinal Study of Parents and Children (ALSPAC). Multivariable linear regression was used to examine associations of AMH with these cardiometabolic outcomes.</p>
<p>Results: AMH values ranged from 0.16–35.84 ng/ml and median AMH was 3.57 ng/ml (IQR: 2.41, 5.49). For females classified as post-pubertal (n = 848) at the time of assessment median (IQR) AMH was 3.81 ng/ml (2.55, 5.82) compared with 3.25 ng/ml (2.23, 5.05) in those classed as early pubertal (n = 460, P≤0.001). After adjusting for birth weight, gestational age, pubertal stage, age, ethnicity, socioeconomic position, adiposity and use of hormonal contraceptives, there were no associations with any of the cardiometabolic outcomes. For example fasting insulin changed by 0% per doubling of AMH (95%CI: −3%,+2%) p = 0.70, with identical results if HOMA-IR was used. Results were similar after additional adjustment for smoking, physical activity and age at menarche, after exclusion of 3% of females with the highest AMH values, after excluding those that had not started menarche and after excluding those using hormonal contraceptives.</p>
<p>Conclusion: Our results suggest that in healthy adolescent females, AMH is not associated with cardiometabolic risk factors.</p>
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