Fresh Extraction of the Proton Charge Radius from Electron Scattering.

We present a novel method for extracting the proton radius from elastic electron-proton (ep) scattering data. The approach is based on interpolation via continued fractions augmented by statistical sampling and avoids any assumptions on the form of function used for the representation of data and subsequent extrapolation onto Q^{2}≃0. Applying the method to extant modern ep datasets, we find that all results are mutually consistent and, combining them, we arrive at r_{p}=0.847(8) fm. This result compares favorably with values obtained from contemporary measurements of the Lamb shift in muonic hydrogen, transitions in electronic hydrogen, and muonic deuterium spectroscopy.

Completing the Picture of the Roper Resonance.

We employ a continuum approach to the three valence-quark bound-state problem in relativistic quantum field theory to predict a range of properties of the proton's radial excitation and thereby unify them with those of numerous other hadrons. Our analysis indicates that the nucleon's first radial excitation is the Roper resonance. It consists of a core of three dressed quarks, which expresses its valence-quark content and whose charge radius is 80% larger than the proton analogue. That core is complemented by a meson cloud, which reduces the observed Roper mass by roughly 20%. The meson cloud materially affects long-wavelength characteristics of the Roper electroproduction amplitudes but the quark core is revealed to probes with Q(2)≳3m(N)(2).

Revealing dressed quarks via the proton's charge distribution.

The proton is arguably the most fundamental of nature's readily detectable building blocks. It is at the heart of every nucleus and has never been observed to decay. It is nevertheless a composite object, defined by its valence-quark content: u+u+d--i.e., two up (u) quarks and one down (d) quark; and the manner by which they influence, inter alia, the distribution of charge and magnetization within this bound state. Much of novelty has recently been learned about these distributions; and it now appears possible that the proton's momentum-space charge distribution possesses a zero. Experiments in the coming decade should answer critical questions posed by this and related advances; we explain how such new information may assist in charting the origin and impact of key emergent phenomena within the strong interaction. Specifically, we show that the possible existence and location of a zero in the proton's electric form factor are a measure of nonperturbative features of the quark-quark interaction in the standard model, with particular sensitivity to the running of the dressed-quark mass.

Dressed-quark anomalous magnetic moments.

Perturbation theory predicts that a massless fermion cannot possess a measurable magnetic moment. We explain, however, that the nonperturbative phenomenon of dynamical chiral symmetry breaking generates a momentum-dependent anomalous chromomagnetic moment for dressed light quarks, which is large at infrared momenta, and demonstrate that consequently these same quarks also possess an anomalous electromagnetic moment with similar magnitude and opposite sign.

Phase diagram and critical end point for strongly interacting quarks.

We introduce a method based on chiral susceptibility, which enables one to draw a phase diagram in the chemical-potential-temperature plane for strongly interacting quarks whose interactions are described by any reasonable gap equation, even if the diagrammatic content of the quark-gluon vertex is unknown. We locate a critical end point at (µ(E),T(E))∼(1.0,0.9)T(c), where T(c) is the critical temperature for chiral-symmetry restoration at µ=0, and find that a domain of phase coexistence opens at the critical end point whose area increases as a confinement length scale grows.

Interaction between the second messengers cAMP and Ca2+ in mouse presynaptic taste cells.

The second messenger, 3',5'-cyclic adenosine monophosphate (cAMP), is known to be modulated in taste buds following exposure to gustatory and other stimuli. Which taste cell type(s) (Type I/glial-like cells, Type II/receptor cells, or Type III/presynaptic cells) undergo taste-evoked changes of cAMP and what the functional consequences of such changes are remain unknown. Using Fura-2 imaging of isolated mouse vallate taste cells, we explored how elevating cAMP alters Ca(2+) levels in identified taste cells. Stimulating taste buds with forskolin (Fsk; 1 microm) + isobutylmethylxanthine (IBMX; 100 microm), which elevates cellular cAMP, triggered Ca(2+) transients in 38% of presynaptic cells (n = 128). We used transgenic GAD-GFP mice to show that cAMP-triggered Ca(2+) responses occur only in the subset of presynaptic cells that lack glutamic acid decarboxylase 67 (GAD). We never observed cAMP-stimulated responses in receptor cells, glial-like cells or GAD-expressing presynaptic cells. The response to cAMP was blocked by the protein kinase A inhibitor H89 and by removing extracellular Ca(2+). Thus, the response to elevated cAMP is a PKA-dependent influx of Ca(2+). This Ca(2+) influx was blocked by nifedipine (an inhibitor of L-type voltage-gated Ca(2+) channels) but was unperturbed by omega-agatoxin IVA and omega-conotoxin GVIA (P/Q-type and N-type channel inhibitors, respectively). Single-cell RT-PCR on functionally identified presynaptic cells from GAD-GFP mice confirmed the pharmacological analyses: Ca(v)1.2 (an L-type subunit) is expressed in cells that display cAMP-triggered Ca(2+) influx, while Ca(v)2.1 (a P/Q subunit) is expressed in all presynaptic cells, and underlies depolarization-triggered Ca(2+) influx. Collectively, these data demonstrate cross-talk between cAMP and Ca(2+) signalling in a subclass of taste cells that form synapses with gustatory fibres and may integrate tastant-evoked signals.

Intravascular food reward.

Consumption of calorie-containing sugars elicits appetitive behavioral responses and dopamine release in the ventral striatum, even in the absence of sweet-taste transduction machinery. However, it is unclear if such reward-related postingestive effects reflect preabsorptive or postabsorptive events. In support of the importance of postabsorptive glucose detection, we found that, in rat behavioral tests, high concentration glucose solutions administered in the jugular vein were sufficient to condition a side-bias. Additionally, a lower concentration glucose solution conditioned robust behavioral responses when administered in the hepatic-portal, but not the jugular vein. Furthermore, enteric administration of glucose at a concentration that is sufficient to elicit behavioral conditioning resulted in a glycemic profile similar to that observed after administration of the low concentration glucose solution in the hepatic-portal, but not jugular vein. Finally using fast-scan cyclic voltammetry we found that, in accordance with behavioral findings, a low concentration glucose solution caused an increase in spontaneous dopamine release events in the nucleus accumbens shell when administered in the hepatic-portal, but not the jugular vein. These findings demonstrate that the postabsorptive effects of glucose are sufficient for the postingestive behavioral and dopaminergic reward-related responses that result from sugar consumption. Furthermore, glycemia levels in the hepatic-portal venous system contribute more significantly for this effect than systemic glycemia, arguing for the participation of an intra-abdominal visceral sensor for glucose.

Sketching the Bethe-Salpeter kernel.

An exact form is presented for the axial-vector Bethe-Salpeter equation, which is valid when the quark-gluon vertex is fully dressed. A Ward-Takahashi identity for the Bethe-Salpeter kernel is derived therefrom and solved for a class of dressed quark-gluon-vertex models. The solution provides a symmetry-preserving closed system of gap and vertex equations. The analysis can be extended to the vector equation. This enables a comparison between the responses of pseudoscalar and scalar meson masses to nonperturbatively dressing the quark-gluon vertex. The result indicates that dynamical chiral symmetry breaking enhances spin-orbit splitting in the meson spectrum.

Imaging cyclic AMP changes in pancreatic islets of transgenic reporter mice.

Cyclic AMP (cAMP) and Ca(2+) are two ubiquitous second messengers in transduction pathways downstream of receptors for hormones, neurotransmitters and local signals. The availability of fluorescent Ca(2+) reporter dyes that are easily introduced into cells and tissues has facilitated analysis of the dynamics and spatial patterns for Ca(2+) signaling pathways. A similar dissection of the role of cAMP has lagged because indicator dyes do not exist. Genetically encoded reporters for cAMP are available but they must be introduced by transient transfection in cell culture, which limits their utility. We report here that we have produced a strain of transgenic mice in which an enhanced cAMP reporter is integrated in the genome and can be expressed in any targeted tissue and with tetracycline induction. We have expressed the cAMP reporter in beta-cells of pancreatic islets and conducted an analysis of intracellular cAMP levels in relation to glucose stimulation, Ca(2+) levels, and membrane depolarization. Pancreatic function in transgenic mice was normal. In induced transgenic islets, glucose evoked an increase in cAMP in beta-cells in a dose-dependent manner. The cAMP response is independent of (in fact, precedes) the Ca(2+) influx that results from glucose stimulation of islets. Glucose-evoked cAMP responses are synchronous in cells throughout the islet and occur in 2 phases suggestive of the time course of insulin secretion. Insofar as cAMP in islets is known to potentiate insulin secretion, the novel transgenic mouse model will for the first time permit detailed analyses of cAMP signals in beta-cells within islets, i.e. in their native physiological context. Reporter expression in other tissues (such as the heart) where cAMP plays a critical regulatory role, will permit novel biomedical approaches.