QuotationFinder - Searching for Quotations and Allusions in Greek and Latin Texts and Establishing the Degree to Which a Quotation or Allusion Matches Its Source

The software programs generally used with the TLG (Thesaurus Linguae Graecae) and the CLCLT (CETEDOC Library of Christian Latin Texts) CD-ROMs are not well suited for finding quotations and allusions. QuotationFinder uses more sophisticated criteria as it ranks search results based on how closely they match the source text, listing search results with literal quotations first and loose verbal parallels last

CaMKII-dependent regulation of cardiac Na(+) homeostasis.

Na(+) homeostasis is a key regulator of cardiac excitation and contraction. The cardiac voltage-gated Na(+) channel, NaV1.5, critically controls cell excitability, and altered channel gating has been implicated in both inherited and acquired arrhythmias. Ca(2) (+)/calmodulin-dependent protein kinase II (CaMKII), a serine/threonine kinase important in cardiac physiology and disease, phosphorylates NaV1.5 at multiple sites within the first intracellular linker loop to regulate channel gating. Although CaMKII sites on the channel have been identified (S516, T594, S571), the relative role of each of these phospho-sites in channel gating properties remains unclear, whereby both loss-of-function (reduced availability) and gain-of-function (late Na(+) current, INa L) effects have been reported. Our review highlights investigating the complex multi-site phospho-regulation of NaV1.5 gating is crucial to understanding the genesis of acquired arrhythmias in heart failure (HF) and CaMKII activated conditions. In addition, the increased Na(+) influx accompanying INa L may also indirectly contribute to arrhythmia by promoting Ca(2) (+) overload. While the precise mechanisms of Na(+) loading during HF remain unclear, and quantitative analyses of the contribution of INa L are lacking, disrupted Na(+) homeostasis is a consistent feature of HF. Computational and experimental observations suggest that both increased diastolic Na(+) influx and action potential prolongation due to systolic INa L contribute to disruption of Ca(2) (+) handling in failing hearts. Furthermore, simulations reveal a synergistic interaction between perturbed Na(+) fluxes and CaMKII, and confirm recent experimental findings of an arrhythmogenic feedback loop, whereby CaMKII activation is at once a cause and a consequence of Na(+) loading

Wilson coefficients for Higgs boson production and decoupling relations to O(αs4)\mathcal{O}\left(\alpha_s^4\right)

An important ingredient for the calculation of Higgs boson properties in the infinite top quark mass limit is the knowledge of the effective coupling between the Higgs bosons and gluons, i.e. the Wilson coefficients $C_H$ and $C_{HH}$ for one and two Higgs bosons, respectively. In this work we calculate for the first time $C_{HH}$ to four loops in a direct, diagrammatic way, discussing in detail all issues arising due to the renormalization of operator products. Furthermore, we also calculate the Wilson coefficient $C_H$ for the coupling of a single Higgs boson to gluons as well as all four loop decoupling relations in QCD with general SU$(N_c)$ colour factors. The latter are related to $C_H$ and $C_{HH}$ via low-energy theorems.Comment: 23 page

Real-virtual corrections to Higgs boson pair production at NNLO: three closed top quark loops

We compute the real-radiation corrections to Higgs boson pair production at next-to-next-to-leading order in QCD, in an expansion for large top quark mass. We concentrate on the radiative corrections to the interference contribution from the next-to-leading order one-particle reducible and the leading order amplitudes. This is a well defined and gauge invariant subset of the full real-virtual corrections to the inclusive cross section. We obtain analytic results for all phase-space master integrals both as an expansion around the threshold and in an exact manner in terms of Goncharov polylogarithms.Comment: 25 page