Irrational constants in positronium decays

We establish irrational constants, that contribute to the positronium lifetime at $O(\alpha)$ and $O(\alpha^2)$ order. In particular we show, that a new type of constants appear, which are not related to Euler--Zagier sums or multiple $\zeta$ values.Comment: Presented at 9th Workshop on Elementary Particle Theory: Loops and Legs in Quantum Field Theory, Sondershausen, 20-25 Apr 2008. 6 pages, 3 figure

Two-loop corrections to the decay rate of parapositronium

Order $\alpha^2$ corrections to the decay rate of parapositronium are calculated. A QED scattering calculation of the amplitude for electron-positron annihilation into two photons at threshold is combined with the technique of effective field theory to determine an NRQED Hamiltonian, which is then used in a bound state calculation to determine the decay rate. Our result for the two-loop correction is $5.1243(33)$ in units of $(\alpha/\pi)^2$ times the lowest order rate. This is consistent with but more precise than the result $5.1(3)$ of a previous calculation.Comment: 26 pages, 7 figure

Combination epigenetic therapy in metastatic colorectal cancer (mCRC) with subcutaneous 5-azacitidine and entinostat: A phase 2 consortium/stand up 2 cancer study

PURPOSE: Therapy with demethylating agent 5-azacitidine and histone deacetylase inhibitor entinostat shows synergistic re-expression of tumor-suppressor genes and growth inhibition in colorectal (CRC) cell lines and in vivo studies. EXPERIMENTAL DESIGN: We conducted a phase II, multi-institutional study of the combination in metastatic CRC patients. Subcutaneous azacitidine was administered at 40 mg/m2 days 1-5 and 8-10 and entinostat was given 7 mg orally on days 3 and 10. An interim analysis indicated toxicity crossed the pre-specified safety boundary but was secondary to disease. A 2nd cohort with added eligibility restrictions was accrued: prior therapies were limited to no more than 2 or 3 (KRAS-mutated and KRAS-wildtype cancers, respectively) and \u3c30% of liver involvement. The primary endpoint was RECIST response. Serial biopsies were performed at baseline and after 2 cycles of therapy. RESULTS: Forty-seven patients were enrolled (24:Cohort 1, 23:Cohort 2). Patients were heavily pre-treated (median prior therapies 4: Cohort 1 and 2.5: cohort 2). No responses were observed. Median progression-free survival was 1.9 months; overall survival was 5.6 and 8.3 months in Cohorts 1 and 2, respectively. Toxicity was tolerable and as expected. Unsupervised cluster analysis of serial tumor biopsies suggested greater DNA demethylation in patients with PFS above the median. CONCLUSION: In this first trial of CRC patients with combination epigenetic therapy, we show tolerable therapy without significant clinical activity as determined by RECIST responses. Reversal of hypermethylation was seen in a subset of patients and correlated with improved PFS

alpha^2 corrections to parapositronium decay: a detailed description

We present details of our recent calculation of alpha^2 corrections to the parapositronium decay into two photons. These corrections are rather small and our final result for the parapositronium lifetime agrees well with the most recent measurement. Implications for orthopositronium decays are briefly discussed.Comment: 18 pages, late

Radiative Corrections to One-Photon Decays of Hydrogenic Ions

Radiative corrections to the decay rate of n=2 states of hydrogenic ions are calculated. The transitions considered are the M1 decay of the 2s state to the ground state and the E1(M2) decays of the $2p_{1/2}$ and $2p_{3/2}$ states to the ground state. The radiative corrections start in order $\alpha (Z \alpha)^2$, but the method used sums all orders of $Z\alpha$. The leading $\alpha (Z\alpha)^2$ correction for the E1 decays is calculated and compared with the exact result. The extension of the calculational method to parity nonconserving transitions in neutral atoms is discussed.Comment: 22 pages, 2 figure

Order alpha^3 ln(1/alpha) Corrections to Positronium Decays

The logarithmically enhanced alpha^3 ln(1/alpha) corrections to the para- and orthopositronium decay widths are calculated in the framework of dimensionally regularized nonrelativistic quantum electrodynamics.In the case of parapositronium, the correction is negative, approximately doubles the effect of the leading logarithmic alpha^3 ln^2(1/alpha) one, and is comparable to the nonlogarithmic O(alpha^2) one. As for orthopositronium, the correction is positive and almost cancels the alpha^3 ln^2(1/alpha) one. The uncertainties in the theoretical predictions for the decay widths are reduced.Comment: 10 pages (Latex); missing term added, corrected coefficient B_p used, numerical results insignificantly change

Decays of ℓ=1\ell=1 Baryons --- Quark Model versus Large-NcN_c

We study nonleptonic decays of the orbitally excited, \su6 \rep{70}-plet baryons in order to test the hypothesis that the successes of the nonrelativistic quark model have a natural explanation in the large-$N_c$ limit of QCD. By working in a Hartree approximation, we isolate a specific set of operators that contribute to the observed s- and d-wave decays in leading order in $1/N_c$. We fit our results to the current experimental decay data, and make predictions for a number of allowed but unobserved modes. Our tentative conclusion is that there is more to the nonrelativistic quark model of baryons than large-$N_c$.Comment: LaTeX 49pp. (38 pp. landscape), PicTex, PrePicTex, PostPicTex required for 3 figures, Harvard Preprint HUTP-94/A008. (Two additional operators are included, but conclusions are unchanged.

Multiscale, multimodal analysis of tumor heterogeneity in IDH1 mutant vs wild-type diffuse gliomas.

Glioma is recognized to be a highly heterogeneous CNS malignancy, whose diverse cellular composition and cellular interactions have not been well characterized. To gain new clinical- and biological-insights into the genetically-bifurcated IDH1 mutant (mt) vs wildtype (wt) forms of glioma, we integrated data from protein, genomic and MR imaging from 20 treatment-naïve glioma cases and 16 recurrent GBM cases. Multiplexed immunofluorescence (MxIF) was used to generate single cell data for 43 protein markers representing all cancer hallmarks, Genomic sequencing (exome and RNA (normal and tumor) and magnetic resonance imaging (MRI) quantitative features (protocols were T1-post, FLAIR and ADC) from whole tumor, peritumoral edema and enhancing core vs equivalent normal region were also collected from patients. Based on MxIF analysis, 85,767 cells (glioma cases) and 56,304 cells (GBM cases) were used to generate cell-level data for 24 biomarkers. K-means clustering was used to generate 7 distinct groups of cells with divergent biomarker profiles and deconvolution was used to assign RNA data into three classes. Spatial and molecular heterogeneity metrics were generated for the cell data. All features were compared between IDH mt and IDHwt patients and were finally combined to provide a holistic/integrated comparison. Protein expression by hallmark was generally lower in the IDHmt vs wt patients. Molecular and spatial heterogeneity scores for angiogenesis and cell invasion also differed between IDHmt and wt gliomas irrespective of prior treatment and tumor grade; these differences also persisted in the MR imaging features of peritumoral edema and contrast enhancement volumes. A coherent picture of enhanced angiogenesis in IDHwt tumors was derived from multiple platforms (genomic, proteomic and imaging) and scales from individual proteins to cell clusters and heterogeneity, as well as bulk tumor RNA and imaging features. Longer overall survival for IDH1mt glioma patients may reflect mutation-driven alterations in cellular, molecular, and spatial heterogeneity which manifest in discernable radiological manifestations

The hr1 and Fusion Peptide Regions of the Subgroup B Avian Sarcoma and Leukosis Virus Envelope Glycoprotein Influence Low pH-Dependent Membrane Fusion

The avian sarcoma and leukosis virus (ASLV) envelope glycoprotein (Env) is activated to trigger fusion by a two-step mechanism involving receptor-priming and low pH fusion activation. In order to identify regions of ASLV Env that can regulate this process, a genetic selection method was used to identify subgroup B (ASLV-B) virus-infected cells resistant to low pH-triggered fusion when incubated with cells expressing the cognate TVB receptor. The subgroup B viral Env (envB) genes were then isolated from these cells and characterized by DNA sequencing. This led to identification of two frequent EnvB alterations which allowed TVB receptor-binding but altered the pH-threshold of membrane fusion activation: a 13 amino acid deletion in the host range 1 (hr1) region of the surface (SU) EnvB subunit, and the A32V amino acid change within the fusion peptide of the transmembrane (TM) EnvB subunit. These data indicate that these two regions of EnvB can influence the pH threshold of fusion activation