Radiative Decay of a Long-Lived Particle and Big-Bang Nucleosynthesis

The effects of radiatively decaying, long-lived particles on big-bang nucleosynthesis (BBN) are discussed. If high-energy photons are emitted after BBN, they may change the abundances of the light elements through photodissociation processes, which may result in a significant discrepancy between the BBN theory and observation. We calculate the abundances of the light elements, including the effects of photodissociation induced by a radiatively decaying particle, but neglecting the hadronic branching ratio. Using these calculated abundances, we derive a constraint on such particles by comparing our theoretical results with observations. Taking into account the recent controversies regarding the observations of the light-element abundances, we derive constraints for various combinations of the measurements. We also discuss several models which predict such radiatively decaying particles, and we derive constraints on such models.Comment: Published version in Phys. Rev. D. Typos in figure captions correcte

Assessing Big-Bang Nucleosynthesis

Systematic uncertainties in the light-element abundances and their evolution make a rigorous statistical assessment difficult. However, using Bayesian methods we show that the following statement is robust: the predicted and measured abundances are consistent with 95\% credibility only if the baryon-to-photon ratio is between $2\times 10^{-10}$ and $6.5\times 10^{-10}$ and the number of light neutrino species is less than 3.9. Our analysis suggests that the $^4$He abundance may have been systematically underestimated.Comment: 7 pages, LaTeX(2.09), 6 postscript figures (attached). A postscript version with figures can be found at ftp://astro.uchicago.edu/pub/astro/copi/assessing_BBN . (See the README file for details

Characterisation of 2-arachidonylglycerol-induced platelet aggregation in rat whole blood and the influence of gender"leave in review"

The endocannabinoid, 2-AG, is released from activated platelets and can modulate aggregation in man (Maccarrone et al., 2001). This study aimed to characterise the effects of 2-AG, and its interactions with other agonists, on platelet aggregation in rat whole blood. Male Sprague Dawley rats (300-500g) were anaesthetized with isoflurane and the carotid artery cannulated to allow blood withdrawal. Whole blood aggregometry was used to study the effects of 2-AG, ADP and the interactions among 2-AG, ADP and 5-HT (n=6-7). Data are expressed as mean ± SEM and compared with an unpaired Student’s t-test or a repeated measure 2-way ANOVA (*P<0.05). 2-AG caused slowly developing aggregation that peaked at 10 min in contrast to the response to ADP which peaked at 2 min. Maximal responses to 2-AG 75, 150 and 300 µM were 9.8±3.4, 13.2±0.9 and 14.0±0.7Omega. Aggregation induced by 150 µM 2-AG was reduced to 2.0±1.7*Omega by 1 µM AM251 (CB1 antagonist) and to 0.6±0.5*Omega by 1 µM AM630 (CB2 antagonist). In further experiments, the TP antagonist ICI 192,605 markedly reduced aggregation induced by 150 µM 2-AG from 9.3±2.4 to -0.5±0.1*Omega. 5-HT did not cause platelet aggregation but it potentiated the response to 75 µM 2-AG at 5 min from 5.1±2.8 to 12.4±0.7*Omega. 2-AG prolonged and enhanced the aggregatory response to ADP and this effect was attenuated by ICI 192,605. This study demonstrated that the endocannabinoid, 2-AG, caused platelet aggregation in rat whole blood and interacted with other agonists to modulate aggregation through several mechanisms