Hydrogen Burning of 17-O in Classical Novae

We report on the observation of a previously unknown resonance at E=194.1+/-0.6 keV (lab) in the 17-O(p,alpha)14-N reaction, with a measured resonance strength omega_gamma(p,alpha)=1.6+/-0.2 meV. We studied in the same experiment the 17-O(p,gamma)18-F reaction by an activation method and the resonance-strength ratio was found to be omega_gamma(p,alpha)/omega_gamma(p,gamma)=470+/-50. The corresponding excitation energy in the 18-F compound nucleus was determined to be 5789.8+/-0.3 keV by gamma-ray measurements using the 14-N(alpha,gamma)18-F reaction. These new resonance properties have important consequences for 17-O nucleosynthesis and gamma-ray astronomy of classical novae.Comment: 4 pages, 4 figures. Accepted for publication in Physical Review Letter

A new experiment for the determination of the 18F(p,alpha) reaction rate at nova temperatures

The 18F(p,alpha) reaction was recognized as one of the most important for gamma ray astronomy in novae as it governs the early 511 keV emission. However, its rate remains largely uncertain at nova temperatures. A direct measurement of the cross section over the full range of nova energies is impossible because of its vanishing value at low energy and of the short 18F lifetime. Therefore, in order to better constrain this reaction rate, we have performed an indirect experiment taking advantage of the availability of a high purity and intense radioactive 18F beam at the Louvain La Neuve RIB facility. We present here the first results of the data analysis and discuss the consequences.Comment: Contribution to the Classical Novae Explosions conference, Sitges, Spain, 20-24 May 2002, 5 pages, 3 figure

Cross sections relevant to gamma-ray line emission in solar flares:3^3He-induced reactions on 16^{16}O nuclei

Gamma-ray production cross sections have been measured for gamma-ray lines copiously emitted in the $^3$He bombardment of $^{16}$O nuclei: the 937, 1042 and 1081 keV lines of $^{18}$F and the 1887 keV line of $^{18}$Ne. Four Ge detectors with BGO shielding for Compton suppression were used to measure the angular distributions of the gamma-rays. The excitation functions have been obtained for $^3$He bombarding energies from 3.7 to 36 MeV. Total cross sections are tabulated for calculations relevant to gamma-ray astronomy. The importance of these lines as diagnosis for the presence and properties of accelerated $^3$He in solar flares is discussed in light of the measured cross sections.Comment: Phys. Rev. C68 (2003) 0258XX, in pres

Low energy measurement of the 7Be(p,gamma)8B cross section

We have measured the cross section of the 7Be(p,gamma)8B reaction for E_cm = 185.8 keV, 134.7 keV and 111.7 keV using a radioactive 7Be target (132 mCi). Single and coincidence spectra of beta^+ and alpha particles from 8B and 8Be^* decay, respectively, were measured using a large acceptance spectrometer. The zero energy S factor inferred from these data is 18.5 +/- 2.4 eV b and a weighted mean value of 18.8 +/- 1.7 eV b (theoretical uncertainty included) is deduced when combining this value with our previous results at higher energies.Comment: Accepted for publication in Phys. Rev. Let

D(18F,pa)15N reaction applied to nova gamma-ray emission

The 18F(p,alpha)15O reaction is recognized to be one of the most important reactions for nova gamma-ray astronomy as it governs the early E <= 511keV gamma emission. However in the nova temperature regime, its rate remains largely uncertain due to unknown low-energy resonance strengths. We report here the measurement of the D(18F,p)19F(alpha)15N one-nucleon transfer reaction, induced by a 14 MeV 18F radioactive beam impinging on a CD2 target; outgoing protons and 15N (or alpha-particles) were detected in coincidence in two silicon strip detectors. A DWBA analysis of the data resulted in new limits to the contribution of low-energy resonances to the rate of the 18F(p,alpha)15O reaction.Comment: Rapid Communication to appear in Phys. Rev. C., 4 pages and 4 figure

Systemic approach to the role and regulation of hepcidin by quantifying its circulating form : extra-hepatic expression in obesity : discrepancy between systemic regulation and local expression in Gaucher disease : protection against iron overload in hemolysis

L’homéostasie du fer est régulée par l’hepcidine, peptide hyposidérémiant d’origine essentiellement hépatique, qui agit par inhibition de l’absorption intestinale du fer et de son recyclage par les macrophages. Ce travail propose de mettre en évidence l’intérêt d’une approche du rôle et de la régulation de l’hepcidine en pathologie, à partir de sa quantification dans la circulation. Après une mise point du dosage par spectrométrie de masse en tandem et une validation dans des modèles pathologiques chez l’homme et la souris, nous avons étudié les anomalies du métabolisme du fer dans plusieurs pathologies. Dans un modèle murin d’obésité, nous avons montré qu’une augmentation de l’hepcidine circulante due à la contribution du tissu adipeux permet d’expliquer les phénotypes décrits chez l’homme, une carence martiale et/ou une surcharge en fer, tout en ouvrant la perspective d’une nouvelle voie de régulation. Cependant une diminution de l’absorption intestinale en fer serait en partie indépendante de l’hepcidine. Chez des patients atteints de maladie de Gaucher, l’absence de modulation de l’hepcidine sérique, malgré une hyperferritinémie fréquemment observée, a révélé une séquestration locale de fer. Enfin, la variation des taux d’hepcidine sérique dans un modèle murin d’hémolyse chronique selon le fond génétique a permis d’illustrer l’impact de l’hepcidine circulante sur le phénotype de surcharge martiale. Au travers de ces différentes applications nous avons montré comment la quantification de l’hepcidine sérique peut aider à la compréhension d’anomalies de l’homéostasie du fer chez l’homme et l’animal.Iron homeostasis is regulated by hepcidin, a negative iron regulator peptide, mainly produced by hepatocytes, which acts by inhibiting the intestinal iron absorption and its recycling by macrophages. This work proposes to highlight the interest of approach to the role and regulation of hepcidin in pathology, from its quantification in blood. After developing a tandem mass spectrometry assay and validating it in human and mice disease patterns, we studied iron metabolism disorders in several pathologies. In a mouse model of obesity, we showed that an increase of circulating hepcidin due to the adipose tissue contribution helps explaining phenotypes described in humans, iron deficiency and / or iron overload, while opening the prospect of a new regulatory pathway. However a decrease in intestinal iron absorption is partly independent of hepcidin. In Gaucher disease patients, the absence of modulation in serum hepcidin despite frequently high ferritinemia observed, revealed a local iron sequestration. Finally, the change in serum hepcidin levels in a chronic hemolysis mouse model, according to the genetic background, has illustrated the impact of circulating hepcidin on iron overload phenotype. Through these different applications we showed how quantification of serum hepcidin may help understanding iron homeostasis abnormalities in humans and animals

La coproporphyrie héréditaire (investigations cliniques, biochimiques et moléculaires)

CHATENAY M.-PARIS 11-BU Pharma. (920192101) / SudocSudocFranceF

Extrahepatic hepcidin production: The intriguing outcomes of recent years

International audienceHepcidin is the hyposideremic hormone regulating iron metabolism. It is a defensin-like disulfide-bonded peptide with antimicrobial activity. The main site of hepcidin production is the liver where its synthesis is modulated by iron, inflammation and erythropoietic signaling. However, hepcidin locally produced in several peripheral organs seems to be an important actor for the maintenance of iron homeostasis in these organs. This review highlights the presence of peripheral hepcidin and its potential functions. Understanding the role of extrahepatic hepcidin could be of great physiological and therapeutic importance for several specific pathologies