Analysis of the superdefomed rotational bands

All available experimental data for the $\Delta I=2$ transition energies in superdeformed bands are analyzed by using a new one-point formula. The existence of deviations from the smooth behavior is confirmed in many bands. However, we stress that one cannot necessarily speak about staggering patterns as they are mostly irregular. Simulations of the experimental data suggest that the irregularities may stem from the presence of irregular kinks in the rotational spectra. This could be a clue but, at the moment, where such kinks come from is an open question.Comment: 6 pages, RevTex, 7 p.s. figures, submitted to P.R.

Period of the gamma-ray staggering in the 150Gd superdeformed region

It has been previously proposed to explain gamma-ray staggerings in the deexcitation of some superdeformed bands in the $^{150}$Gd region in terms of a coupling between global rotation and intrinsic vortical modes. The observed 4$\hbar$ period for the phenomenon is suggested from our microscopic Routhian calculations using the Skyrme SkM* effective interaction.Comment: 4 pages, LaTeX with RevTeX, 4 included figures, submitted to Phys. Rep. C (revised version

Smooth Termination of Rotational Bands in 62Zn: Evidence for a Loss of Collectivity

Two sets of strongly coupled rotational bands have been identified in Zn-62. These bands have been observed up to the terminating states of their respective configurations. Lifetime measurements indicate that the transition quadrupole moments in these bands decrease as termination is approached. These results establish the first terminating states of rotational bands in the A similar to 60 mass region and confirm the predicted loss of collectivity associated with smooth band termination

Decay Out of the Doubly Magic Superdeformed Band in the N=Z Nucleus 60Zn

The doubly magic superdeformed band in the N = Z nucleus Zn-60 has been identified. Linking transitions connecting this band to the yrast line provide the first spin, parity, and excitation energy measurements for superdeformed states in the A similar to 60 region. The stretched-E2 character and relatively large B(E2) values of these transitions suggest a nonstatistical decay-out process

The Sudbury Neutrino Observatory

The Sudbury Neutrino Observatory is a second generation water Cherenkov detector designed to determine whether the currently observed solar neutrino deficit is a result of neutrino oscillations. The detector is unique in its use of D2O as a detection medium, permitting it to make a solar model-independent test of the neutrino oscillation hypothesis by comparison of the charged- and neutral-current interaction rates. In this paper the physical properties, construction, and preliminary operation of the Sudbury Neutrino Observatory are described. Data and predicted operating parameters are provided whenever possible.Comment: 58 pages, 12 figures, submitted to Nucl. Inst. Meth. Uses elsart and epsf style files. For additional information about SNO see http://www.sno.phy.queensu.ca . This version has some new reference

UCP2-induced fatty acid synthase promotes NLRP3 inflammasome activation during sepsis

Cellular lipid metabolism has been linked to immune responses; however, the precise mechanisms by which de novo fatty acid synthesis can regulate inflammatory responses remain unclear. The NLRP3 inflammasome serves as a platform for caspase-1-dependent maturation and secretion of proinflammatory cytokines. Here, we demonstrated that the mitochondrial uncoupling protein-2 (UCP2) regulates NLRP3-mediated caspase-1 activation through the stimulation of lipid synthesis in macrophages. UCP2-deficient mice displayed improved survival in a mouse model of polymicrobial sepsis. Moreover, UCP2 expression was increased in human sepsis. Consistently, UCP2-deficient mice displayed impaired lipid synthesis and decreased production of IL-1β and IL-18 in response to LPS challenge. In macrophages, UCP2 deficiency suppressed NLRP3-mediated caspase-1 activation and NLRP3 expression associated with inhibition of lipid synthesis. In UCP2-deficient macrophages, inhibition of lipid synthesis resulted from the downregulation of fatty acid synthase (FASN), a key regulator of fatty acid synthesis. FASN inhibition by shRNA and treatment with the chemical inhibitors C75 and cerulenin suppressed NLRP3-mediated caspase-1 activation and inhibited NLRP3 and pro-IL-1β gene expression in macrophages. In conclusion, our results suggest that UCP2 regulates the NLRP3 inflammasome by inducing the lipid synthesis pathway in macrophages. These results identify UCP2 as a potential therapeutic target in inflammatory diseases such as sepsis