Radiative Capture of Protons by Be9

The gamma rays from the capture in Be9 of protons of energy between 0.27 and 1.2 Mev have been studied using large scintillation crystals. Excitation functions of the gamma rays leading to the 0-, 0.72-, 1.74-, 2.15-, 3.58-, and 5.16-Mev states of B10 were computed from the measured gamma-ray spectra. In addition to the resonances previously known to exist at 0.33-, 0.99-, and 1.086-Mev proton energy [corresponding to (1-) 6.88-, (2-) 7.48-, and (0+) 7.56-Mev states in B10], evidence was found only for the p-wave resonance near 1 Mev [(2+) 7.5-Mev state in B10] postulated by Mozer and by Dearnaly and for the influence of higher lying states. This work leaves unexplained the large isotopic-spin impurity of the 6.88-Mev level. Appreciable nonresonant capture was found for the transitions to the 0-, 0.72-, 3.58-, and 5.16-Mev states, which is probably not s-wave for the latter two transitions. Accurate energy measurements and coincidence work showed that the 5.16-Mev level of B10 is populated in preference to the 5.11-Mev level, contradicting earlier work of Clegg. Also, experimental evidence has been found which appears to be in contradiction to the 0+ spin assignment for the 7.56-Mev level of B10 and raises doubts about the 2+ spin assignment of the 5.16-Mev level

Density effect in Cu K-shell ionization by 5.1-GeV electrons

We have made an absolute measurement of the Cu K-shell impact ionization cross section by 5.1-GeV electrons, which demonstrates directly a density effect predicted by Fermi in 1940. By determining the ratio of the K x-ray yield from a thin front and back layer of the target by a novel grazing emission method, we have verified the effect of transition radiation on the x-ray production, suggested by Sorensen and reported by Bak et al

Two-body Photodisintegration of 4^{4}He with Full Final State Interaction

The cross sections of the processes $^4$He($\gamma,p$)$^3$H and $^4$He($\gamma,n$)$^3$He are calculated taking into account the full final state interaction via the Lorentz integral transform (LIT) method. This is the first consistent microscopic calculation beyond the three--body breakup threshold. The results are obtained with a semirealistic central NN potential including also the Coulomb force. The cross sections show a pronounced dipole peak at 27 MeV which lies within the rather broad experimental band. At higher energies, where experimental uncertainties are considerably smaller, one finds a good agreement between theory and experiment. The calculated sum of three-- and four--body photodisintegration cross sections is also listed and is in fair agreement with the data.Comment: 18 pages, 6 figure

Insights into the Binding of Phenyltiocarbamide (PTC) Agonist to Its Target Human TAS2R38 Bitter Receptor

Humans' bitter taste perception is mediated by the hTAS2R subfamily of the G protein-coupled membrane receptors (GPCRs). Structural information on these receptors is currently limited. Here we identify residues involved in the binding of phenylthiocarbamide (PTC) and in receptor activation in one of the most widely studied hTAS2Rs (hTAS2R38) by means of structural bioinformatics and molecular docking. The predictions are validated by site-directed mutagenesis experiments that involve specific residues located in the putative binding site and trans-membrane (TM) helices 6 and 7 putatively involved in receptor activation. Based on our measurements, we suggest that (i) residue N103 participates actively in PTC binding, in line with previous computational studies. (ii) W99, M100 and S259 contribute to define the size and shape of the binding cavity. (iii) W99 and M100, along with F255 and V296, play a key role for receptor activation, providing insights on bitter taste receptor activation not emerging from the previously reported computational models

The perception of quinine taste intensity is associated with common genetic variants in a bitter receptor cluster on chromosome 12

The perceived taste intensities of quinine HCl, caffeine, sucrose octaacetate (SOA) and propylthiouracil (PROP) solutions were examined in 1457 twins and their siblings. Previous heritability modeling of these bitter stimuli indicated a common genetic factor for quinine, caffeine and SOA (22–28%), as well as separate specific genetic factors for PROP (72%) and quinine (15%). To identify the genes involved, we performed a genome-wide association study with the same sample as the modeling analysis, genotyped for approximately 610 000 single-nucleotide polymorphisms (SNPs). For caffeine and SOA, no SNP association reached a genome-wide statistical criterion. For PROP, the peak association was within TAS2R38 (rs713598, A49P, P = 1.6 × 10−104), which accounted for 45.9% of the trait variance. For quinine, the peak association was centered in a region that contains bitter receptor as well as salivary protein genes and explained 5.8% of the trait variance (TAS2R19, rs10772420, R299C, P = 1.8 × 10−15). We confirmed this association in a replication sample of twins of similar ancestry (P = 0.00001). The specific genetic factor for the perceived intensity of PROP was identified as the gene previously implicated in this trait (TAS2R38). For quinine, one or more bitter receptor or salivary proline-rich protein genes on chromosome 12 have alleles which affect its perception but tight linkage among very similar genes precludes the identification of a single causal genetic variant

Expression of taste receptors in Solitary Chemosensory Cells of rodent airways

<p>Abstract</p> <p>Background</p> <p>Chemical irritation of airway mucosa elicits a variety of reflex responses such as coughing, apnea, and laryngeal closure. Inhaled irritants can activate either chemosensitive free nerve endings, laryngeal taste buds or solitary chemosensory cells (SCCs). The SCC population lies in the nasal respiratory epithelium, vomeronasal organ, and larynx, as well as deeper in the airway. The objective of this study is to map the distribution of SCCs within the airways and to determine the elements of the chemosensory transduction cascade expressed in these SCCs.</p> <p>Methods</p> <p>We utilized a combination of immunohistochemistry and molecular techniques (rtPCR and in situ hybridization) on rats and transgenic mice where the Tas1R3 or TRPM5 promoter drives expression of green fluorescent protein (GFP).</p> <p>Results</p> <p>Epithelial SCCs specialized for chemoreception are distributed throughout much of the respiratory tree of rodents. These cells express elements of the taste transduction cascade, including Tas1R and Tas2R receptor molecules, α-gustducin, PLCβ2 and TrpM5. The Tas2R bitter taste receptors are present throughout the entire respiratory tract. In contrast, the Tas1R sweet/umami taste receptors are expressed by numerous SCCs in the nasal cavity, but decrease in prevalence in the trachea, and are absent in the lower airways.</p> <p>Conclusions</p> <p>Elements of the taste transduction cascade including taste receptors are expressed by SCCs distributed throughout the airways. In the nasal cavity, SCCs, expressing Tas1R and Tas2R taste receptors, mediate detection of irritants and foreign substances which trigger trigeminally-mediated protective airway reflexes. Lower in the respiratory tract, similar chemosensory cells are not related to the trigeminal nerve but may still trigger local epithelial responses to irritants. In total, SCCs should be considered chemoreceptor cells that help in preventing damage to the respiratory tract caused by inhaled irritants and pathogens.</p