Triple-Product Correlations in B -> V1 V2$ Decays and New Physics

In this paper we examine T-violating triple-product correlations (TP's) in B -> V1 V2 decays. TP's are excellent probes of physics beyond the standard model (SM) for two reasons: (i) within the SM, most TP's are expected to be tiny, and (ii) unlike direct CP asymmetries, TP's are not suppressed by the small strong phases which are expected in B decays. TP's are obtained via the angular analysis of B -> V1 V2. In a general analysis based on factorization, we demonstrate that the most promising decays for measuring TP's in the SM involve excited final-state vector mesons, and we provide estimates of such TP's. We find that there are only a handful of decays in which large TP's are possible, and the size of these TP's depends strongly on the size of nonfactorizable effects. We show that TP's which vanish in the SM can be very large in models with new physics. The measurement of a nonzero TP asymmetry in a decay where none is expected would specifically point to new physics involving large couplings to the right-handed b-quark.Comment: 42 pages, LaTeX, no figures. Title changed, several explanatory paragraphs added, references added, analysis and conclusions unchange

Triangulations and Severi varieties

We consider the problem of constructing triangulations of projective planes over Hurwitz algebras with minimal numbers of vertices. We observe that the numbers of faces of each dimension must be equal to the dimensions of certain representations of the automorphism groups of the corresponding Severi varieties. We construct a complex involving these representations, which should be considered as a geometric version of the (putative) triangulations

Mathematical modelling of clostridial acetone-butanol-ethanol fermentation

Clostridial acetone-butanol-ethanol (ABE) fermentation features a remarkable shift in the cellular metabolic activity from acid formation, acidogenesis, to the production of industrial-relevant solvents, solventogensis. In recent decades, mathematical models have been employed to elucidate the complex interlinked regulation and conditions that determine these two distinct metabolic states and govern the transition between them. In this review, we discuss these models with a focus on the mechanisms controlling intra- and extracellular changes between acidogenesis and solventogenesis. In particular, we critically evaluate underlying model assumptions and predictions in the light of current experimental knowledge. Towards this end, we briefly introduce key ideas and assumptions applied in the discussed modelling approaches, but waive a comprehensive mathematical presentation. We distinguish between structural and dynamical models, which will be discussed in their chronological order to illustrate how new biological information facilitates the ‘evolution’ of mathematical models. Mathematical models and their analysis have significantly contributed to our knowledge of ABE fermentation and the underlying regulatory network which spans all levels of biological organization. However, the ties between the different levels of cellular regulation are not well understood. Furthermore, contradictory experimental and theoretical results challenge our current notion of ABE metabolic network structure. Thus, clostridial ABE fermentation still poses theoretical as well as experimental challenges which are best approached in close collaboration between modellers and experimentalists

Prognostic model to predict postoperative acute kidney injury in patients undergoing major gastrointestinal surgery based on a national prospective observational cohort study.

Background: Acute illness, existing co-morbidities and surgical stress response can all contribute to postoperative acute kidney injury (AKI) in patients undergoing major gastrointestinal surgery. The aim of this study was prospectively to develop a pragmatic prognostic model to stratify patients according to risk of developing AKI after major gastrointestinal surgery. Methods: This prospective multicentre cohort study included consecutive adults undergoing elective or emergency gastrointestinal resection, liver resection or stoma reversal in 2-week blocks over a continuous 3-month period. The primary outcome was the rate of AKI within 7 days of surgery. Bootstrap stability was used to select clinically plausible risk factors into the model. Internal model validation was carried out by bootstrap validation. Results: A total of 4544 patients were included across 173 centres in the UK and Ireland. The overall rate of AKI was 14·2 per cent (646 of 4544) and the 30-day mortality rate was 1·8 per cent (84 of 4544). Stage 1 AKI was significantly associated with 30-day mortality (unadjusted odds ratio 7·61, 95 per cent c.i. 4·49 to 12·90; P < 0·001), with increasing odds of death with each AKI stage. Six variables were selected for inclusion in the prognostic model: age, sex, ASA grade, preoperative estimated glomerular filtration rate, planned open surgery and preoperative use of either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. Internal validation demonstrated good model discrimination (c-statistic 0·65). Discussion: Following major gastrointestinal surgery, AKI occurred in one in seven patients. This preoperative prognostic model identified patients at high risk of postoperative AKI. Validation in an independent data set is required to ensure generalizability

The epigenetic evolution of glioma is determined by the IDH1 mutation status and treatment regimen

Tumor adaptation or selection is thought to underlie therapy resistance in glioma. To investigate longitudinal epigenetic evolution of gliomas in response to therapeutic pressure, we performed an epigenomic analysis of 132 matched initial and recurrent tumors from patients with IDH-wildtype (IDHwt) and IDH-mutant (IDHmut) glioma. IDHwt gliomas showed a stable epigenome over time with relatively low levels of global methylation. The epigenome of IDHmut gliomas showed initial high levels of genome-wide DNA methylation that was progressively reduced to levels similar to those of IDHwt tumors. Integration of epigenomics, gene expression, and functional genomics identified HOXD13 as a master regulator of IDHmut astrocytoma evolution. Furthermore, relapse of IDHmut tumors was accompanied by histological progression that was associated with survival, as validated in an independent cohort. Finally, the initial cell composition of the tumor microenvironment varied between IDHwt and IDHmut tumors and changed differentially following treatment, suggesting increased neo-angiogenesis and T-cell infiltration upon treatment of IDHmut gliomas. This study provides one of the largest cohorts of paired longitudinal glioma samples with epigenomic, transcriptomic, and genomic profiling and suggests that treatment of IDHmut glioma is associated with epigenomic evolution towards an IDHwt-like phenotype

Thermostable Direct Hemolysin Downregulates Human Colon Carcinoma Cell Proliferation with the Involvement of E-Cadherin, and β-Catenin/Tcf-4 Signaling

BACKGROUND: Colon cancers are the frequent causes of cancer mortality worldwide. Recently bacterial toxins have received marked attention as promising approaches in the treatment of colon cancer. Thermostable direct hemolysin (TDH) secreted by Vibrio parahaemolyticus causes influx of extracellular calcium with the subsequent rise in intracellular calcium level in intestinal epithelial cells and it is known that calcium has antiproliferative activity against colon cancer. KEY RESULTS: In the present study it has been shown that TDH, a well-known traditional virulent factor inhibits proliferation of human colon carcinoma cells through the involvement of CaSR in its mechanism. TDH treatment does not induce DNA fragmentation, nor causes the release of lactate dehydrogenase. Therefore, apoptosis and cytotoxicity are not contributing to the TDH-mediated reduction of proliferation rate, and hence the reduction appears to be caused by decrease in cell proliferation. The elevation of E-cadherin, a cell adhesion molecule and suppression of β-catenin, a proto-oncogene have been observed in presence of CaSR agonists whereas reverse effect has been seen in presence of CaSR antagonist as well as si-RNA in TDH treated cells. TDH also triggers a significant reduction of Cyclin-D and cdk2, two important cell cycle regulatory proteins along with an up regulation of cell cycle inhibitory protein p27(Kip1) in presence of CaSR agonists. CONCLUSION: Therefore TDH can downregulate colonic carcinoma cell proliferation and involves CaSR in its mechanism of action. The downregulation occurs mainly through the involvement of E-cadherin-β-catenin mediated pathway and the inhibition of cell cycle regulators as well as upregulation of cell cycle inhibitors

Supersymmetric QCD corrections to e+e−→tbˉH−e^+e^-\to t\bar{b}H^- and the Bernstein-Tkachov method of loop integration

The discovery of charged Higgs bosons is of particular importance, since their existence is predicted by supersymmetry and they are absent in the Standard Model (SM). If the charged Higgs bosons are too heavy to be produced in pairs at future linear colliders, single production associated with a top and a bottom quark is enhanced in parts of the parameter space. We present the next-to-leading-order calculation in supersymmetric QCD within the minimal supersymmetric SM (MSSM), completing a previous calculation of the SM-QCD corrections. In addition to the usual approach to perform the loop integration analytically, we apply a numerical approach based on the Bernstein-Tkachov theorem. In this framework, we avoid some of the generic problems connected with the analytical method.Comment: 14 pages, 6 figures, accepted for publication in Phys. Rev.

Jet modification via π 0 -hadron correlations in Au+Au collisions at √sNN = 200 GeV

High-momentum two-particle correlations are a useful tool for studying jet-quenching effects in the quark-gluon plasma. Angular correlations between neutral-pion triggers and charged hadrons with transverse momenta in the range 4–12 GeV/c and 0.5–7 GeV/c, respectively, have been measured by the PHENIX experiment in 2014 for Au+Au collisions at √sNN = 200 GeV. Suppression is observed in the yield of high-momentum jet fragments opposite the trigger particle, which indicates jet suppression stemming from in-medium partonic energy loss, while enhancement is observed for low-momentum particles. The ratio and differences between the yield in Au+Au collisions and p+p collisions, IAA and ∆AA, as a function of the trigger-hadron azimuthal separation, ∆ϕ, are measured for the first time at the Relativistic Heavy Ion Collider. These results better quantify how the yield of low-pT associated hadrons is enhanced at wide angle, which is crucial for studying energy loss as well as medium-response effects

Systematic study of nuclear effects in p+Al, p+Au, d+Au, and 3He+Au collisions at √sNN = 200 GeV using π 0 production

The PHENIX collaboration presents a systematic study of inclusive π 0 production from p+p, p+Al, p+Au, d+Au, and 3He+Au collisions at √sNN = 200 GeV. Measurements were performed with different centrality selections as well as the total inelastic, 0%–100%, selection for all collision systems. For 0%–100% collisions, the nuclear-modification factors, RxA, are consistent with unity for pT above 8 GeV/c, but exhibit an enhancement in peripheral collisions and a suppression in central collisions. The enhancement and suppression characteristics are similar for all systems for the same centrality class. It is shown that for high-pT -π 0 production, the nucleons in the d and 3He interact mostly independently with the Au nucleus and that the counter intuitive centrality dependence is likely due to a physical correlation between multiplicity and the presence of a hard scattering process. These observations disfavor models where parton energy loss has a significant contribution to nuclear modifications in small systems. Nuclear modifications at lower pT resemble the Cronin effect – an increase followed by a peak in central or inelastic collisions and a plateau in peripheral collisions. The peak height has a characteristic ordering by system size as p+Au > d+Au > 3He+Au > p+Al. For collisions with Au ions, current calculations based on initial state cold nuclear matter effects result in the opposite order, suggesting the presence of other contributions to nuclear modifications, in particular at lower pT