Radiative corrections to low energy neutrino reactions

We show that the radiative corrections to charged current (CC) nuclear reactions with an electron(positron) in the final state are described by a universal function. The consistency of our treatment of the radiative corrections with the procedure used to extract the value of the axial coupling constant $g_A$ is discussed. To illustrate we apply our results to (anti)neutrino deuterium disintegration and to $pp$ fusion in the sun. The limit of vanishing electron mass is considered, and a simple formula valid for E_{obs}\gsim 1 MeV is obtained. The size of the nuclear structure-dependent effects is also discussed. Finally, we consider CC transitions with an electron(positron) in the initial state and discuss some applications to electron capture reactions.Comment: 23 pages, 5 figure

Standard Neutrino Spectrum from B-8 Decay

We present a systematic evaluation of the shape of the neutrino energy spectrum produced by beta-decay of $^8$B. We place special emphasis on determining the range of uncertainties permitted by existing laboratory data and theoretical ingredients (such as forbidden and radiative corrections). We review and compare the available experimental data on the $^8$B$(\beta^+){}^8$Be$(2\alpha)$ decay chain. We analyze the theoretical and experimental uncertainties quantitatively. We give a numerical representation of the best-fit (standard-model) neutrino spectrum, as well as two extreme deviations from the standard spectrum that represent the total (experimental and theoretical) effective $\pm3\sigma$ deviations. Solar neutrino experiments that are currently being developed will be able to measure the shape of the $^8$B neutrino spectrum above about 5 MeV. An observed distortion of the $^8$B solar neutrino spectrum outside the range given in the present work could be considered as evidence, at an effective significance level greater than three standard deviations, for physics beyond the standard electroweak model. We use the most recent available experimental data on the Gamow--Teller strengths in the $A=37$ system to calculate the $^8$B neutrino absorption cross section on chlorine: $\sigma_{\rm Cl}=(1.14\pm0.11)\times10^{-42}$~cm$^2$ ($\pm3\sigma$ errors). The chlorine cross section is also given as a function of the neutrino energy. The $^8$B neutrino absorption cross section in gallium is $\sigma_{\rm Ga}=(2.46^{+2.1}_{-1.1})\times10^{-42}$ cm$^2$ ($\pm3\sigma$ errors).Comment: Revised version, to appear in Phys. Rev.

Bremsstrahlung emission during α\alpha-decay of 226Ra^{226}{\rm Ra}

We obtained the spectrum of probability of the bremsstrahlung emission accompanying the $\alpha$-decay of $^{226}{\rm Ra}$ (E$_{\alpha}$=4.8 MeV) by measuring the $\alpha$-$\gamma$ coincidences and using the model presented in our previous study on the $\alpha-$decay of $^{214}{\rm Po}$ (E$_{\alpha}$=7.7 MeV). We compare the experimental data with the quantum mechanical calculation and find a good agreement between theory and experiment. We discuss the differences between the photon spectra connected with the $\alpha$-decay of the $^{226}{\rm Ra}$ and $^{214}{\rm Po}$ nuclei. For the two mentioned nuclei we analyze the bremsstrahlung emission contributions from the tunneling and external regions of the nucleus barrier into the total spectrum, and we find the destructive interference between these contributions. We also find that the emission of photons during tunneling of the $\alpha$-particle gives an important contribution to the bremsstrahlung spectrum in the whole E$_{\gamma}$ energy range of the studied $^{226}$Ra nucleus

Multipolar model of bremsstrahlung accompanying proton-decay of nuclei

Emission of bremsstrahlung photons accompanying proton decay of nuclei is studied. The new improved multipolar model describing such a process is presented. The angular formalism of calculations of the matrix elements is stated in details. The bremsstrahlung probabilities for the $^{157}{\rm Ta}$, $^{161}{\rm Re}$, $^{167}{\rm Ir}$ and $^{185}{\rm Bi}$ nuclei decaying from the $2s_{1/2}$ state, the $^{109}_{53}{\rm I}_{56}$ and $^{112}_{55}{\rm Cs}_{57}$ nuclei decaying from the $1d_{5/2}$ state, the $^{146}_{69}{\rm Tm}_{77}$ and $^{151}_{71}{\rm Lu}_{80}$ nuclei decaying from the $0h_{11/2}$ state are predicted. Such spectra have orders of values similar to the experimental data for the bremsstrahlung photons emitted during the $\alpha$-decay. This indicates on real possibility to study bremsstrahlung photons during proton decay experimentally and perform further measurements.Comment: 14 pages, 6 figure

Continuous Multi-Parameter Heart Rate Variability Analysis Heralds Onset of Sepsis in Adults

BACKGROUND: Early diagnosis of sepsis enables timely resuscitation and antibiotics and prevents subsequent morbidity and mortality. Clinical approaches relying on point-in-time analysis of vital signs or lab values are often insensitive, non-specific and late diagnostic markers of sepsis. Exploring otherwise hidden information within intervals-in-time, heart rate variability (HRV) has been documented to be both altered in the presence of sepsis, and correlated with its severity. We hypothesized that by continuously tracking individual patient HRV over time in patients as they develop sepsis, we would demonstrate reduced HRV in association with the onset of sepsis. METHODOLOGY/PRINCIPAL FINDINGS: We monitored heart rate continuously in adult bone marrow transplant (BMT) patients (n = 21) beginning a day before their BMT and continuing until recovery or withdrawal (12+/-4 days). We characterized HRV continuously over time with a panel of time, frequency, complexity, and scale-invariant domain techniques. We defined baseline HRV as mean variability for the first 24 h of monitoring and studied individual and population average percentage change (from baseline) over time in diverse HRV metrics, in comparison with the time of clinical diagnosis and treatment of sepsis (defined as systemic inflammatory response syndrome along with clinically suspected infection requiring treatment). Of the 21 patients enrolled, 4 patients withdrew, leaving 17 patients who completed the study. Fourteen patients developed sepsis requiring antibiotic therapy, whereas 3 did not. On average, for 12 out of 14 infected patients, a significant (25%) reduction prior to the clinical diagnosis and treatment of sepsis was observed in standard deviation, root mean square successive difference, sample and multiscale entropy, fast Fourier transform, detrended fluctuation analysis, and wavelet variability metrics. For infected patients (n = 14), wavelet HRV demonstrated a 25% drop from baseline 35 h prior to sepsis on average. For 3 out of 3 non-infected patients, all measures, except root mean square successive difference and entropy, showed no significant reduction. Significant correlation was present amongst these HRV metrics for the entire population. CONCLUSIONS/SIGNIFICANCE: Continuous HRV monitoring is feasible in ambulatory patients, demonstrates significant HRV alteration in individual patients in association with, and prior to clinical diagnosis and treatment of sepsis, and merits further investigation as a means of providing early warning of sepsis

Ndfip1 mediates peripheral tolerance to self and exogenous antigen by inducing cell cycle exit in responding CD4(+) T cells

The NDFIP1 (neural precursor cell expressed, developmentally down-regulated protein 4 family-interacting protein 1) adapter for the ubiquitin ligase ITCH is genetically linked to human allergic and autoimmune disease, but the cellular mechanism by which these proteins enable foreign and self-antigens to be tolerated is unresolved. Here, we use two unique mouse strains—an Ndfip1-YFP reporter and an Ndfip1-deficient strain—to show that Ndfip1 is progressively induced during T-cell differentiation and activation in vivo and that its deficiency causes a cell-autonomous, Forkhead box P3-independent failure of peripheral CD4+ T-cell tolerance to self and exogenous antigen. In small cohorts of antigen-specific CD4+ cells responding in vivo, Ndfip1 was necessary for tolerogen-reactive T cells to exit cell cycle after one to five divisions and to abort Th2 effector differentiation, defining a step in peripheral tolerance that provides insights into the phenomenon of T-cell anergy in vivo and is distinct from the better understood process of Bcl2-interacting mediator of cell death-mediated apoptosis. Ndfip1 deficiency precipitated autoimmune pancreatic destruction and diabetes; however, this depended on a further accumulation of nontolerant anti-self T cells from strong stimulation by exogenous tolerogen. These findings illuminate a peripheral tolerance checkpoint that aborts T-cell clonal expansion against allergens and autoantigens and demonstrate how hypersensitive responses to environmental antigens may trigger autoimmunity.John A. Altin, Stephen R. Daley, Jason Howitt, Helen J. Rickards, Alison K. Batkin, Keisuke Horikawa, Simon J. Prasad, Keats A. Nelms, Sharad Kumar, Lawren C. Wu, Seong-Seng Tan, Matthew C. Cook, and Christopher C. Goodno